Parietal Lobe Dysfunction: Types and Symptoms

The parietal lobe is a part of the brain that plays a crucial role in processing sensory information and integrating it with other cognitive functions. Dysfunction in this area can lead to various symptoms, depending on the location and extent of the damage.

Dominant parietal lobe dysfunction, often caused by a stroke, can result in Gerstmann’s syndrome, which includes finger agnosia, dyscalculia, dysgraphia, and right-left disorientation. Non-dominant parietal lobe dysfunction, on the other hand, can cause anosognosia, dressing apraxia, spatial neglect, and constructional apraxia.

Bilateral damage to the parieto-occipital lobes, a rare condition, can lead to Balint’s syndrome, which is characterized by oculomotor apraxia, optic ataxia, and simultanagnosia. These symptoms can affect a person’s ability to shift gaze, interact with objects, and perceive multiple objects at once.

In summary, parietal lobe dysfunction can manifest in various ways, and understanding the specific symptoms can help diagnose and treat the underlying condition.

Normal Pressure Hydrocephalus

Normal pressure hydrocephalus is a type of chronic communicating hydrocephalus, which occurs due to the impaired reabsorption of cerebrospinal fluid (CSF) by the arachnoid villi. Although the CSF pressure is typically high, it remains within the normal range, and therefore, it does not cause symptoms of high intracranial pressure (ICP) such as headache and nausea. Instead, patients with normal pressure hydrocephalus usually present with a classic triad of symptoms, including incontinence, gait ataxia, and dementia, which is often referred to as wet, wobbly, and wacky. Unfortunately, this condition is often misdiagnosed as Parkinson’s of Alzheimer’s disease.

The classic triad of normal pressure hydrocephalus, also known as Hakim’s triad, includes gait instability, urinary incontinence, and dementia. On the other hand, non-communicating hydrocephalus results from the obstruction of CSF flow in the third of fourth ventricle, which causes symptoms of raised intracranial pressure, such as headache, vomiting, hypertension, bradycardia, altered consciousness, and papilledema.

Electroencephalography

Electroencephalography (EEG) is a clinical test that records the brain’s spontaneous electrical activity over a short period of time using multiple electrodes placed on the scalp. It is mainly used to rule out organic conditions and can help differentiate dementia from other disorders such as metabolic encephalopathies, CJD, herpes encephalitis, and non-convulsive status epilepticus. EEG can also distinguish possible psychotic episodes and acute confusional states from non-convulsive status epilepticus.

Not all abnormal EEGs represent an underlying condition, and psychotropic medications can affect EEG findings. EEG abnormalities can also be triggered purposely by activation procedures such as hyperventilation, photic stimulation, certain drugs, and sleep deprivation.

Specific waveforms are seen in an EEG, including delta, theta, alpha, sigma, beta, and gamma waves. Delta waves are found frontally in adults and posteriorly in children during slow wave sleep, and excessive amounts when awake may indicate pathology. Theta waves are generally seen in young children, drowsy and sleeping adults, and during meditation. Alpha waves are seen posteriorly when relaxed and when the eyes are closed, and are also seen in meditation. Sigma waves are bursts of oscillatory activity that occur in stage 2 sleep. Beta waves are seen frontally when busy of concentrating, and gamma waves are seen in advanced/very experienced meditators.

Certain conditions are associated with specific EEG changes, such as nonspecific slowing in early CJD, low voltage EEG in Huntington’s, diffuse slowing in encephalopathy, and reduced alpha and beta with increased delta and theta in Alzheimer’s.

Common epileptiform patterns include spikes, spike/sharp waves, and spike-waves. Medications can have important effects on EEG findings, with clozapine decreasing alpha and increasing delta and theta, lithium increasing all waveforms, lamotrigine decreasing all waveforms, and valproate having inconclusive effects on delta and theta and increasing beta.

Overall, EEG is a useful tool in clinical contexts for ruling out organic conditions and differentiating between various disorders.

The Significance of 5-HIAA in Depression and Aggression

During the 1980s, there was a brief period of interest in 5-hydroxyindoleacetic acid (5-HIAA), a serotonin metabolite. Studies found that up to a third of people with depression had low concentrations of 5-HIAA in their cerebrospinal fluid (CSF), while very few normal controls did. This suggests that 5-HIAA may play a role in depression.

Furthermore, individuals with low CSF levels of 5-HIAA have been found to respond less effectively to antidepressants and are more likely to commit suicide. This finding has been replicated in multiple studies, indicating the significance of 5-HIAA in depression.

Low levels of 5-HIAA are also associated with increased levels of aggression. This suggests that 5-HIAA may play a role in regulating aggressive behavior. Overall, the research on 5-HIAA highlights its potential importance in understanding and treating depression and aggression.

Electroencephalography

Electroencephalography (EEG) is a clinical test that records the brain’s spontaneous electrical activity over a short period of time using multiple electrodes placed on the scalp. It is mainly used to rule out organic conditions and can help differentiate dementia from other disorders such as metabolic encephalopathies, CJD, herpes encephalitis, and non-convulsive status epilepticus. EEG can also distinguish possible psychotic episodes and acute confusional states from non-convulsive status epilepticus.

Not all abnormal EEGs represent an underlying condition, and psychotropic medications can affect EEG findings. EEG abnormalities can also be triggered purposely by activation procedures such as hyperventilation, photic stimulation, certain drugs, and sleep deprivation.

Specific waveforms are seen in an EEG, including delta, theta, alpha, sigma, beta, and gamma waves. Delta waves are found frontally in adults and posteriorly in children during slow wave sleep, and excessive amounts when awake may indicate pathology. Theta waves are generally seen in young children, drowsy and sleeping adults, and during meditation. Alpha waves are seen posteriorly when relaxed and when the eyes are closed, and are also seen in meditation. Sigma waves are bursts of oscillatory activity that occur in stage 2 sleep. Beta waves are seen frontally when busy of concentrating, and gamma waves are seen in advanced/very experienced meditators.

Certain conditions are associated with specific EEG changes, such as nonspecific slowing in early CJD, low voltage EEG in Huntington’s, diffuse slowing in encephalopathy, and reduced alpha and beta with increased delta and theta in Alzheimer’s.

Common epileptiform patterns include spikes, spike/sharp waves, and spike-waves. Medications can have important effects on EEG findings, with clozapine decreasing alpha and increasing delta and theta, lithium increasing all waveforms, lamotrigine decreasing all waveforms, and valproate having inconclusive effects on delta and theta and increasing beta.

Overall, EEG is a useful tool in clinical contexts for ruling out organic conditions and differentiating between various disorders.

The question specifically requests the sensory aspect.

Cranial Nerve Reflexes

When it comes to questions on cranial nerve reflexes, it is important to match the reflex to the nerves involved. Here are some examples:

– Pupillary light reflex: involves the optic nerve (sensory) and oculomotor nerve (motor).
– Accommodation reflex: involves the optic nerve (sensory) and oculomotor nerve (motor).
– Jaw jerk: involves the trigeminal nerve (sensory and motor).
– Corneal reflex: involves the trigeminal nerve (sensory) and facial nerve (motor).
– Vestibulo-ocular reflex: involves the vestibulocochlear nerve (sensory) and oculomotor, trochlear, and abducent nerves (motor).

Another example of a cranial nerve reflex is the gag reflex, which involves the glossopharyngeal nerve (sensory) and the vagus nerve (motor). This reflex is important for protecting the airway from foreign objects of substances that may trigger a gag reflex. It is also used as a diagnostic tool to assess the function of these nerves.

Neurodevelopment: Understanding Brain Development

The development of the central nervous system begins with the neuroectoderm, a specialized region of ectoderm. The embryonic brain is divided into three areas: the forebrain (prosencephalon), midbrain (mesencephalon), and hindbrain (rhombencephalon). The prosencephalon further divides into the telencephalon and diencephalon, while the hindbrain subdivides into the metencephalon and myelencephalon.

The telencephalon, of cerebrum, consists of the cerebral cortex, underlying white matter, and the basal ganglia. The diencephalon includes the prethalamus, thalamus, hypothalamus, subthalamus, epithalamus, and pretectum. The mesencephalon comprises the tectum, tegmentum, ventricular mesocoelia, cerebral peduncles, and several nuclei and fasciculi.

The rhombencephalon includes the medulla, pons, and cerebellum, which can be subdivided into a variable number of transversal swellings called rhombomeres. In humans, eight rhombomeres can be distinguished, from caudal to rostral: Rh7-Rh1 and the isthmus. Rhombomeres Rh7-Rh4 form the myelencephalon, while Rh3-Rh1 form the metencephalon.

Understanding neurodevelopment is crucial in comprehending brain development and its complexities. By studying the different areas of the embryonic brain, we can gain insight into the formation of the central nervous system and its functions.

Headache, nausea, vomiting, papilledema, and ocular palsies are symptoms of increased intracranial pressure, which are not typically present in cases of normal pressure hydrocephalus.

Normal Pressure Hydrocephalus

Normal pressure hydrocephalus is a type of chronic communicating hydrocephalus, which occurs due to the impaired reabsorption of cerebrospinal fluid (CSF) by the arachnoid villi. Although the CSF pressure is typically high, it remains within the normal range, and therefore, it does not cause symptoms of high intracranial pressure (ICP) such as headache and nausea. Instead, patients with normal pressure hydrocephalus usually present with a classic triad of symptoms, including incontinence, gait ataxia, and dementia, which is often referred to as wet, wobbly, and wacky. Unfortunately, this condition is often misdiagnosed as Parkinson’s of Alzheimer’s disease.

The classic triad of normal pressure hydrocephalus, also known as Hakim’s triad, includes gait instability, urinary incontinence, and dementia. On the other hand, non-communicating hydrocephalus results from the obstruction of CSF flow in the third of fourth ventricle, which causes symptoms of raised intracranial pressure, such as headache, vomiting, hypertension, bradycardia, altered consciousness, and papilledema.

Brain Structures and Functions

The brain is a complex organ that is responsible for controlling various bodily functions. Among the important structures in the brain are the substantia nigra, hippocampus, hypothalamus, pituitary gland, and thalamus.

The substantia nigra is a part of the basal ganglia located in the midbrain. It contains dopamine-producing neurons that regulate voluntary movement and mood. Parkinson’s disease is associated with the degeneration of the melanin-containing cells in the pars compacta of the substantia nigra.

The hippocampus is a part of the limbic system that is involved in memory, learning, attention, and information processing.

The hypothalamus is located at the base of the brain near the pituitary gland. It regulates thirst, hunger, circadian rhythm, emotions, and body temperature. It also controls the pituitary gland by secreting hormones.

The pituitary gland is a small endocrine organ located below the hypothalamus in the middle of the base of the brain. It controls many bodily functions through the action of hormones and is divided into an anterior lobe, intermediate lobe, and posterior lobe.

The thalamus is located above the brainstem and processes and relays sensory and motor information.

Electroencephalography

Electroencephalography (EEG) is a clinical test that records the brain’s spontaneous electrical activity over a short period of time using multiple electrodes placed on the scalp. It is mainly used to rule out organic conditions and can help differentiate dementia from other disorders such as metabolic encephalopathies, CJD, herpes encephalitis, and non-convulsive status epilepticus. EEG can also distinguish possible psychotic episodes and acute confusional states from non-convulsive status epilepticus.

Not all abnormal EEGs represent an underlying condition, and psychotropic medications can affect EEG findings. EEG abnormalities can also be triggered purposely by activation procedures such as hyperventilation, photic stimulation, certain drugs, and sleep deprivation.

Specific waveforms are seen in an EEG, including delta, theta, alpha, sigma, beta, and gamma waves. Delta waves are found frontally in adults and posteriorly in children during slow wave sleep, and excessive amounts when awake may indicate pathology. Theta waves are generally seen in young children, drowsy and sleeping adults, and during meditation. Alpha waves are seen posteriorly when relaxed and when the eyes are closed, and are also seen in meditation. Sigma waves are bursts of oscillatory activity that occur in stage 2 sleep. Beta waves are seen frontally when busy of concentrating, and gamma waves are seen in advanced/very experienced meditators.

Certain conditions are associated with specific EEG changes, such as nonspecific slowing in early CJD, low voltage EEG in Huntington’s, diffuse slowing in encephalopathy, and reduced alpha and beta with increased delta and theta in Alzheimer’s.

Common epileptiform patterns include spikes, spike/sharp waves, and spike-waves. Medications can have important effects on EEG findings, with clozapine decreasing alpha and increasing delta and theta, lithium increasing all waveforms, lamotrigine decreasing all waveforms, and valproate having inconclusive effects on delta and theta and increasing beta.

Overall, EEG is a useful tool in clinical contexts for ruling out organic conditions and differentiating between various disorders.

The Cerebellum: Anatomy and Function

The cerebellum is a part of the brain that consists of two hemispheres and a median vermis. It is separated from the cerebral hemispheres by the tentorium cerebelli and connected to the brain stem by the cerebellar peduncles. Anatomically, it is divided into three lobes: the flocculonodular lobe, anterior lobe, and posterior lobe. Functionally, it is divided into three regions: the vestibulocerebellum, spinocerebellum, and cerebrocerebellum.

The vestibulocerebellum, located in the flocculonodular lobe, is responsible for balance and spatial orientation. The spinocerebellum, located in the medial section of the anterior and posterior lobes, is involved in fine-tuned body movements. The cerebrocerebellum, located in the lateral section of the anterior and posterior lobes, is involved in planning movement and the conscious assessment of movement.

Overall, the cerebellum plays a crucial role in motor coordination and control. Its different regions and lobes work together to ensure smooth and precise movements of the body.

Glial Cells: The Support System of the Central Nervous System

The central nervous system is composed of two basic cell types: neurons and glial cells. Glial cells, also known as support cells, play a crucial role in maintaining the health and function of neurons. There are several types of glial cells, including macroglia (astrocytes and oligodendrocytes), ependymal cells, and microglia.

Astrocytes are the most abundant type of glial cell and have numerous functions, such as providing structural support, repairing nervous tissue, nourishing neurons, contributing to the blood-brain barrier, and regulating neurotransmission and blood flow. There are two main types of astrocytes: protoplasmic and fibrous.

Oligodendrocytes are responsible for the formation of myelin sheaths, which insulate and protect axons, allowing for faster and more efficient transmission of nerve impulses.

Ependymal cells line the ventricular system and are involved in the circulation of cerebrospinal fluid (CSF) and fluid homeostasis in the brain. Specialized ependymal cells called choroid plexus cells produce CSF.

Microglia are the immune cells of the CNS and play a crucial role in protecting the brain from infection and injury. They also contribute to the maintenance of neuronal health and function.

In summary, glial cells are essential for the proper functioning of the central nervous system. They provide structural support, nourishment, insulation, and immune defense to neurons, ensuring the health and well-being of the brain and spinal cord.

Neurofibrillary tangles consist of insoluble clumps of Tau protein, which are made up of multiple strands. Since Tau is a microtubule-associated protein that plays a role in the structural processes of neurons, these tangles are always found within the cell.

Alzheimer’s disease is characterized by both macroscopic and microscopic changes in the brain. Macroscopic changes include cortical atrophy, ventricular dilation, and depigmentation of the locus coeruleus. Microscopic changes include the presence of senile plaques, neurofibrillary tangles, gliosis, degeneration of the nucleus of Meynert, and Hirano bodies. Senile plaques are extracellular deposits of beta amyloid in the gray matter of the brain, while neurofibrillary tangles are intracellular inclusion bodies that consist primarily of hyperphosphorylated tau. Gliosis is marked by increases in activated microglia and reactive astrocytes near the sites of amyloid plaques. The nucleus of Meynert degenerates in Alzheimer’s, resulting in a decrease in acetylcholine in the brain. Hirano bodies are actin-rich, eosinophilic intracytoplasmic inclusions which have a highly characteristic crystalloid fine structure and are regarded as a nonspecific manifestation of neuronal degeneration. These changes in the brain contribute to the cognitive decline and memory loss seen in Alzheimer’s disease.

Alzheimer’s disease is not characterized by significant frontal lobe atrophy, but rather by early medial temporal lobe atrophy (MTA) on MRI, particularly in the hippocampus, entorhinal cortex, amygdala, and parahippocampus. In contrast, frontotemporal lobar degeneration (FTLD) typically affects the frontal and anterior temporal lobes in behavioral variant frontotemporal dementia (bvFTD of Pick’s disease), the left anterior temporal lobe in semantic dementia (SD), and the left perisylvian fissure in progressive nonfluent aphasia (PNFA).

Frontotemporal Lobar Degeneration (FTLD) is a pathological term that refers to a group of neurodegenerative disorders that affect the frontal and temporal lobes of the brain. FTLD is classified into several subtypes based on the main protein component of neuronal and glial abnormal inclusions and their distribution. The three main proteins associated with FTLD are Tau, TDP-43, and FUS. Each FTD clinical phenotype has been associated with different proportions of these proteins. Macroscopic changes in FTLD include atrophy of the frontal and temporal lobes, with focal gyral atrophy that resembles knives. Microscopic changes in FTLD-Tau include neuronal and glial tau aggregation, with further sub-classification based on the existence of different isoforms of tau protein. FTLD-TDP is characterized by cytoplasmic inclusions of TDP-43 in neurons, while FTLD-FUS is characterized by cytoplasmic inclusions of FUS.

Apraxia: Understanding the Inability to Carry Out Learned Voluntary Movements

Apraxia is a neurological condition that affects a person’s ability to carry out learned voluntary movements. It is important to note that this condition assumes that everything works and the person is not paralyzed. There are different types of apraxia, each with its own set of symptoms and characteristics.

Limb kinetic apraxia is a type of apraxia that affects a person’s ability to make fine of delicate movements. This can include tasks such as buttoning a shirt of tying shoelaces.

Ideomotor apraxia, on the other hand, is an inability to carry out learned tasks when given the necessary objects. For example, a person with ideomotor apraxia may try to write with a hairbrush instead of using it to brush their hair.

Constructional apraxia affects a person’s ability to copy a picture of combine parts of something to form a whole. This can include tasks such as building a puzzle of drawing a picture.

Ideational apraxia is an inability to follow a sequence of actions in the correct order. For example, a person with ideational apraxia may struggle to take a match out of a box and strike it with their left hand.

Finally, oculomotor apraxia affects a person’s ability to control eye movements. This can make it difficult for them to track moving objects of read smoothly.

Overall, apraxia can have a significant impact on a person’s ability to carry out everyday tasks. However, with the right support and treatment, many people with apraxia are able to improve their abilities and maintain their independence.

Neurotransmitters are substances used by neurons to communicate with each other and with target tissues. They are synthesized and released from nerve endings into the synaptic cleft, where they bind to receptor proteins in the cellular membrane of the target tissue. Neurotransmitters can be classified into different types, including small molecules (such as acetylcholine, dopamine, norepinephrine, serotonin, and GABA) and large molecules (such as neuropeptides). They can also be classified as excitatory or inhibitory. Receptors can be ionotropic or metabotropic, and the effects of neurotransmitters can be fast of slow. Some important neurotransmitters include acetylcholine, dopamine, GABA, norepinephrine, and serotonin. Each neurotransmitter has a specific synthesis, breakdown, and receptor type. Understanding neurotransmitters is important for understanding the function of the nervous system and for developing treatments for neurological and psychiatric disorders.

The sphenoid bone contains a saddle-shaped depression known as the sella turcica. The anterior cranial fossa is formed by the frontal, ethmoid, and a portion of the sphenoid bones. The middle cranial fossa is formed by the sphenoid and temporal bones, while the posterior cranial fossa is formed by the occipital and temporal bones.

Tauopathies exhibit tangles, but vascular dementia is not classified as one.

Alzheimer’s disease is characterized by both macroscopic and microscopic changes in the brain. Macroscopic changes include cortical atrophy, ventricular dilation, and depigmentation of the locus coeruleus. Microscopic changes include the presence of senile plaques, neurofibrillary tangles, gliosis, degeneration of the nucleus of Meynert, and Hirano bodies. Senile plaques are extracellular deposits of beta amyloid in the gray matter of the brain, while neurofibrillary tangles are intracellular inclusion bodies that consist primarily of hyperphosphorylated tau. Gliosis is marked by increases in activated microglia and reactive astrocytes near the sites of amyloid plaques. The nucleus of Meynert degenerates in Alzheimer’s, resulting in a decrease in acetylcholine in the brain. Hirano bodies are actin-rich, eosinophilic intracytoplasmic inclusions which have a highly characteristic crystalloid fine structure and are regarded as a nonspecific manifestation of neuronal degeneration. These changes in the brain contribute to the cognitive decline and memory loss seen in Alzheimer’s disease.

Serotonin: Synthesis and Breakdown

Serotonin, also known as 5-Hydroxytryptamine (5-HT), is synthesized in the central nervous system (CNS) in the raphe nuclei located in the brainstem, as well as in the gastrointestinal (GI) tract in enterochromaffin cells. The amino acid L-tryptophan, obtained from the diet, is used to synthesize serotonin. L-tryptophan can cross the blood-brain barrier, but serotonin cannot.

The transformation of L-tryptophan into serotonin involves two steps. First, hydroxylation to 5-hydroxytryptophan is catalyzed by tryptophan hydroxylase. Second, decarboxylation of 5-hydroxytryptophan to serotonin (5-hydroxytryptamine) is catalyzed by L-aromatic amino acid decarboxylase.

Serotonin is taken up from the synapse by a monoamine transporter (SERT). Substances that block this transporter include MDMA, amphetamine, cocaine, TCAs, and SSRIs. Serotonin is broken down by monoamine oxidase (MAO) and then by aldehyde dehydrogenase to 5-Hydroxyindoleacetic acid (5-HIAA).

Overview of Cranial Nerves and Their Functions

The cranial nerves are a complex system of nerves that originate from the brain and control various functions of the head and neck. There are twelve cranial nerves, each with a specific function and origin. The following table provides a simplified overview of the cranial nerves, including their origin, skull exit, modality, and functions.

The first cranial nerve, the olfactory nerve, originates from the telencephalon and exits through the cribriform plate. It is a sensory nerve that controls the sense of smell. The second cranial nerve, the optic nerve, originates from the diencephalon and exits through the optic foramen. It is a sensory nerve that controls vision.

The third cranial nerve, the oculomotor nerve, originates from the midbrain and exits through the superior orbital fissure. It is a motor nerve that controls eye movement, pupillary constriction, and lens accommodation. The fourth cranial nerve, the trochlear nerve, also originates from the midbrain and exits through the superior orbital fissure. It is a motor nerve that controls eye movement.

The fifth cranial nerve, the trigeminal nerve, originates from the pons and exits through different foramina depending on the division. It is a mixed nerve that controls chewing and sensation of the anterior 2/3 of the scalp. It also tenses the tympanic membrane to dampen loud noises.

The sixth cranial nerve, the abducens nerve, originates from the pons and exits through the superior orbital fissure. It is a motor nerve that controls eye movement. The seventh cranial nerve, the facial nerve, also originates from the pons and exits through the internal auditory canal. It is a mixed nerve that controls facial expression, taste of the anterior 2/3 of the tongue, and tension on the stapes to dampen loud noises.

The eighth cranial nerve, the vestibulocochlear nerve, originates from the pons and exits through the internal auditory canal. It is a sensory nerve that controls hearing. The ninth cranial nerve, the glossopharyngeal nerve, originates from the medulla and exits through the jugular foramen. It is a mixed nerve that controls taste of the posterior 1/3 of the tongue, elevation of the larynx and pharynx, and swallowing.

The tenth cranial nerve, the vagus nerve, also originates from the medulla and exits through the jugular foramen. It is a mixed nerve that controls swallowing, voice production, and parasympathetic supply to nearly all thoracic and abdominal viscera. The eleventh cranial nerve, the accessory nerve, originates from the medulla and exits through the jugular foramen. It is a motor nerve that controls shoulder shrugging and head turning.

The twelfth cranial nerve, the hypoglossal nerve, originates from the medulla and exits through the hypoglossal canal. It is a motor nerve that controls tongue movement. Overall, the cranial nerves play a crucial role in controlling various functions of the head and neck, and any damage of dysfunction can have significant consequences.

The BOLD technique is used by fMRI to non-invasively map cortical activation, while PET and SPECT require the administration of a radioactive isotope and are invasive. Although all three magnetic imaging techniques are non-invasive, fMRI stands out for its use of the BOLD technique.

Cerebral Asymmetry in Planum Temporale and its Implications in Language and Auditory Processing

The planum temporale, a triangular region in the posterior superior temporal gyrus, is a highly lateralized brain structure involved in language and music processing. Studies have shown that the planum temporale is up to ten times larger in the left cerebral hemisphere than the right, with this asymmetry being more prominent in men. This asymmetry can be observed in gestation and is present in up to 70% of right-handed individuals.

Recent research suggests that the planum temporale also plays an important role in auditory processing, specifically in representing the location of sounds in space. However, reduced planum temporale asymmetry has been observed in individuals with dyslexia, stuttering, and schizophrenia. These findings highlight the importance of cerebral asymmetry in the planum temporale and its implications in language and auditory processing.

Gliosis is a discovery that can only be observed under a microscope.

Alzheimer’s disease is characterized by both macroscopic and microscopic changes in the brain. Macroscopic changes include cortical atrophy, ventricular dilation, and depigmentation of the locus coeruleus. Microscopic changes include the presence of senile plaques, neurofibrillary tangles, gliosis, degeneration of the nucleus of Meynert, and Hirano bodies. Senile plaques are extracellular deposits of beta amyloid in the gray matter of the brain, while neurofibrillary tangles are intracellular inclusion bodies that consist primarily of hyperphosphorylated tau. Gliosis is marked by increases in activated microglia and reactive astrocytes near the sites of amyloid plaques. The nucleus of Meynert degenerates in Alzheimer’s, resulting in a decrease in acetylcholine in the brain. Hirano bodies are actin-rich, eosinophilic intracytoplasmic inclusions which have a highly characteristic crystalloid fine structure and are regarded as a nonspecific manifestation of neuronal degeneration. These changes in the brain contribute to the cognitive decline and memory loss seen in Alzheimer’s disease.

Sleep Stages

Sleep is divided into two distinct states called rapid eye movement (REM) and non-rapid eye movement (NREM). NREM is subdivided into four stages.

Sleep stage
Approx % of time spent in stage
EEG findings
Comment

I
5%
Theta waves (4-7 Hz)
The dozing off stage. Characterized by hypnic jerks: spontaneous myoclonic contractions associated with a sensation of twitching of falling.

II
45%
Theta waves, K complexes and sleep spindles (short bursts of 12-14 Hz activity)
Body enters a more subdued state including a drop in temperature, relaxed muscles, and slowed breathing and heart rate. At the same time, brain waves show a new pattern and eye movement stops.

III
15%
Delta waves (0-4 Hz)
Deepest stage of sleep (high waking threshold). The length of stage 3 decreases over the course of the night.

IV
15%
Mixed, predominantly beta
High dream activity.

The percentage of REM sleep decreases with age.

It takes the average person 15-20 minutes to fall asleep, this is called sleep latency (characterised by the onset of stage I sleep). Once asleep one descends through stages I-II and then III-IV (deep stages). After about 90 minutes of sleep one enters REM. The rest of the sleep comprises of cycles through the stages. As the sleep progresses the periods of REM become greater and the periods of NREM become less. During an average night’s sleep one spends 25% of the sleep in REM and 75% in NREM.

REM sleep has certain characteristics that separate it from NREM

Characteristics of REM sleep

– Autonomic instability (variability in heart rate, respiratory rate, and BP)
– Loss of muscle tone
– Dreaming
– Rapid eye movements
– Penile erection

Deafness:

(No information provided on deafness in relation to sleep stages)

Melanin

Melanin is a pigment found in various parts of the body, including the skin, hair, and eyes. It is produced by specialized cells called melanocytes, which are located in the skin’s basal layer. The function of melanin in the body is not fully understood, but it is thought to play a role in protecting the skin from the harmful effects of ultraviolet (UV) radiation from the sun. Additionally, melanin may be a by-product of neurotransmitter synthesis, although this function is not well established. Overall, the role of melanin in the body is an area of ongoing research.

The base of the skull contains a sizable opening called the foramen magnum, which permits the spinal cord to pass through.

Cranial Fossae and Foramina

The cranium is divided into three regions known as fossae, each housing different cranial lobes. The anterior cranial fossa contains the frontal lobes and includes the frontal and ethmoid bones, as well as the lesser wing of the sphenoid. The middle cranial fossa contains the temporal lobes and includes the greater wing of the sphenoid, sella turcica, and most of the temporal bones. The posterior cranial fossa contains the occipital lobes, cerebellum, and medulla and includes the occipital bone.

There are several foramina in the skull that allow for the passage of various structures. The most important foramina likely to appear in exams are listed below:

– Foramen spinosum: located in the middle fossa and allows for the passage of the middle meningeal artery.
– Foramen ovale: located in the middle fossa and allows for the passage of the mandibular division of the trigeminal nerve.
– Foramen lacerum: located in the middle fossa and allows for the passage of the small meningeal branches of the ascending pharyngeal artery and emissary veins from the cavernous sinus.
– Foramen magnum: located in the posterior fossa and allows for the passage of the spinal cord.
– Jugular foramen: located in the posterior fossa and allows for the passage of cranial nerves IX, X, and XI.

Understanding the location and function of these foramina is essential for medical professionals, as they play a crucial role in the diagnosis and treatment of various neurological conditions.

Electroencephalography

Electroencephalography (EEG) is a clinical test that records the brain’s spontaneous electrical activity over a short period of time using multiple electrodes placed on the scalp. It is mainly used to rule out organic conditions and can help differentiate dementia from other disorders such as metabolic encephalopathies, CJD, herpes encephalitis, and non-convulsive status epilepticus. EEG can also distinguish possible psychotic episodes and acute confusional states from non-convulsive status epilepticus.

Not all abnormal EEGs represent an underlying condition, and psychotropic medications can affect EEG findings. EEG abnormalities can also be triggered purposely by activation procedures such as hyperventilation, photic stimulation, certain drugs, and sleep deprivation.

Specific waveforms are seen in an EEG, including delta, theta, alpha, sigma, beta, and gamma waves. Delta waves are found frontally in adults and posteriorly in children during slow wave sleep, and excessive amounts when awake may indicate pathology. Theta waves are generally seen in young children, drowsy and sleeping adults, and during meditation. Alpha waves are seen posteriorly when relaxed and when the eyes are closed, and are also seen in meditation. Sigma waves are bursts of oscillatory activity that occur in stage 2 sleep. Beta waves are seen frontally when busy of concentrating, and gamma waves are seen in advanced/very experienced meditators.

Certain conditions are associated with specific EEG changes, such as nonspecific slowing in early CJD, low voltage EEG in Huntington’s, diffuse slowing in encephalopathy, and reduced alpha and beta with increased delta and theta in Alzheimer’s.

Common epileptiform patterns include spikes, spike/sharp waves, and spike-waves. Medications can have important effects on EEG findings, with clozapine decreasing alpha and increasing delta and theta, lithium increasing all waveforms, lamotrigine decreasing all waveforms, and valproate having inconclusive effects on delta and theta and increasing beta.

Overall, EEG is a useful tool in clinical contexts for ruling out organic conditions and differentiating between various disorders.

Agnosia is a condition where a person loses the ability to recognize objects, persons, sounds, shapes, of smells, despite having no significant memory loss of defective senses. There are different types of agnosia, such as prosopagnosia (inability to recognize familiar faces), anosognosia (inability to recognize one’s own condition/illness), autotopagnosia (inability to orient parts of the body), phonagnosia (inability to recognize familiar voices), simultanagnosia (inability to appreciate two objects in the visual field at the same time), and astereoagnosia (inability to recognize objects by touch).

Functions of the Hypothalamus

The hypothalamus is a vital part of the brain that plays a crucial role in regulating various bodily functions. It receives and integrates sensory information about the internal environment and directs actions to control internal homeostasis. The hypothalamus contains several nuclei and fiber tracts, each with specific functions.

The suprachiasmatic nucleus (SCN) is responsible for regulating circadian rhythms. Neurons in the SCN have an intrinsic rhythm of discharge activity and receive input from the retina. The SCN is considered the body’s master clock, but it has multiple connections with other hypothalamic nuclei.

Body temperature control is mainly under the control of the preoptic, anterior, and posterior nuclei, which have temperature-sensitive neurons. As the temperature goes above 37ºC, warm-sensitive neurons are activated, triggering parasympathetic activity to promote heat loss. As the temperature goes below 37ºC, cold-sensitive neurons are activated, triggering sympathetic activity to promote conservation of heat.

The hypothalamus also plays a role in regulating prolactin secretion. Dopamine is tonically secreted by dopaminergic neurons that project from the arcuate nucleus of the hypothalamus into the anterior pituitary gland via the tuberoinfundibular pathway. The dopamine that is released acts on lactotrophic cells through D2-receptors, inhibiting prolactin synthesis. In the absence of pregnancy of lactation, prolactin is constitutively inhibited by dopamine. Dopamine antagonists result in hyperprolactinemia, while dopamine agonists inhibit prolactin secretion.

In summary, the hypothalamus is a complex structure that regulates various bodily functions, including circadian rhythms, body temperature, and prolactin secretion. Dysfunction of the hypothalamus can lead to various disorders, such as sleep-rhythm disorder, diabetes insipidus, hyperprolactinemia, and obesity.

The middle cerebral artery is the most frequent location for cerebral infarction, resulting in contralateral paralysis and sensory loss. If the dominant hemisphere is affected, language impairment such as Broca’s of Wernicke’s aphasia may occur. Bilateral anterior cerebellar artery blockage is uncommon but can lead to akinetic mutism, which is characterized by a loss of speech and movement. Non-dominant middle cerebral artery blockage can cause contralateral neglect, as well as motor and sensory dysfunction, but language is typically unaffected. The occlusion of the posterior inferior cerebellar artery can result in lateral medullary syndrome, also known as Wallenberg syndrome, which is characterized by crossed contralateral and trunk sensory deficits and ipsilateral sensory deficits affecting the face and cranial nerves. Emboli in the ophthalmic artery can cause temporary vision loss, also known as amaurosis fugax, which is more commonly caused by emboli originating in the carotid artery.

The frontal part of the brain responsible for motor function is supplied by the anterior cerebral artery.

Aphasia is a language impairment that affects the production of comprehension of speech, as well as the ability to read of write. The areas involved in language are situated around the Sylvian fissure, referred to as the ‘perisylvian language area’. For repetition, the primary auditory cortex, Wernicke, Broca via the Arcuate fasciculus (AF), Broca recodes into articulatory plan, primary motor cortex, and pyramidal system to cranial nerves are involved. For oral reading, the visual cortex to Wernicke and the same processes as for repetition follows. For writing, Wernicke via AF to premotor cortex for arm and hand, movement planned, sent to motor cortex. The classification of aphasia is complex and imprecise, with the Boston Group classification and Luria’s aphasia interpretation being the most influential. The important subtypes of aphasia include global aphasia, Broca’s aphasia, Wernicke’s aphasia, conduction aphasia, anomic aphasia, transcortical motor aphasia, and transcortical sensory aphasia. Additional syndromes include alexia without agraphia, alexia with agraphia, and pure word deafness.

Aphasia is a language impairment that affects the production of comprehension of speech, as well as the ability to read of write. The areas involved in language are situated around the Sylvian fissure, referred to as the ‘perisylvian language area’. For repetition, the primary auditory cortex, Wernicke, Broca via the Arcuate fasciculus (AF), Broca recodes into articulatory plan, primary motor cortex, and pyramidal system to cranial nerves are involved. For oral reading, the visual cortex to Wernicke and the same processes as for repetition follows. For writing, Wernicke via AF to premotor cortex for arm and hand, movement planned, sent to motor cortex. The classification of aphasia is complex and imprecise, with the Boston Group classification and Luria’s aphasia interpretation being the most influential. The important subtypes of aphasia include global aphasia, Broca’s aphasia, Wernicke’s aphasia, conduction aphasia, anomic aphasia, transcortical motor aphasia, and transcortical sensory aphasia. Additional syndromes include alexia without agraphia, alexia with agraphia, and pure word deafness.

An infarction to the left posterior cerebral artery typically results in pure alexia, also known as alexia without agraphia, which is characterized by the inability to read but the ability to write.

Brain Blood Supply and Consequences of Occlusion

The brain receives blood supply from the internal carotid and vertebral arteries, which form the circle of Willis. The circle of Willis acts as a shunt system in case of vessel damage. The three main vessels arising from the circle are the anterior cerebral artery (ACA), middle cerebral artery (MCA), and posterior cerebral artery (PCA). Occlusion of these vessels can result in various neurological deficits. ACA occlusion may cause hemiparesis of the contralateral foot and leg, sensory loss, and frontal signs. MCA occlusion is the most common and can lead to hemiparesis, dysphasia/aphasia, neglect, and visual field defects. PCA occlusion may cause alexia, loss of sensation, hemianopia, prosopagnosia, and cranial nerve defects. It is important to recognize these consequences to provide appropriate treatment.

Hormones and their functions:

Dopamine, also known as prolactin inhibitory factor, is released from the hypothalamus. Antipsychotics, which are dopamine antagonists, are often linked to increased prolactin levels.

Oxytocin, released from the posterior pituitary, plays a crucial role in sexual reproduction.

Substance P is present throughout the brain and is essential in pain perception.

Vasopressin, a peptide hormone, is released from the posterior pituitary.

The medial temporal lobe, comprising the hippocampus and parahippocampal gyrus, exhibits the earliest neuropathological alterations.

Alzheimer’s disease is characterized by both macroscopic and microscopic changes in the brain. Macroscopic changes include cortical atrophy, ventricular dilation, and depigmentation of the locus coeruleus. Microscopic changes include the presence of senile plaques, neurofibrillary tangles, gliosis, degeneration of the nucleus of Meynert, and Hirano bodies. Senile plaques are extracellular deposits of beta amyloid in the gray matter of the brain, while neurofibrillary tangles are intracellular inclusion bodies that consist primarily of hyperphosphorylated tau. Gliosis is marked by increases in activated microglia and reactive astrocytes near the sites of amyloid plaques. The nucleus of Meynert degenerates in Alzheimer’s, resulting in a decrease in acetylcholine in the brain. Hirano bodies are actin-rich, eosinophilic intracytoplasmic inclusions which have a highly characteristic crystalloid fine structure and are regarded as a nonspecific manifestation of neuronal degeneration. These changes in the brain contribute to the cognitive decline and memory loss seen in Alzheimer’s disease.

Inflammatory Cytokines and Mental Health

Research has suggested that an imbalance in the immune system, particularly the pro-inflammatory cytokines, may play a significant role in the development of common mental disorders. The strongest evidence is found in depression, where studies have shown increased levels of inflammatory markers, such as interleukin-6 (IL-6), tumour necrosis factor-α (TNF-α), and c-reactive protein (CRP), in depressed individuals compared to healthy controls (Santoft, 2020).

While most studies have focused on the differences in inflammatory markers between depressed and healthy individuals, some have also found a correlation between higher levels of inflammation and more severe depressive symptoms. The underlying cause of this chronic low-grade inflammation is not yet fully understood, but potential factors include psychosocial stress, physical inactivity, poor diet, smoking, obesity, altered gut permeability, disturbed sleep, and vitamin D deficiency.

Ventricular enlargement is a common finding in individuals with schizophrenia.

Schizophrenia is a pathology that is characterized by a number of structural and functional brain alterations. Structural alterations include enlargement of the ventricles, reductions in total brain and gray matter volume, and regional reductions in the amygdala, parahippocampal gyrus, and temporal lobes. Antipsychotic treatment may be associated with gray matter loss over time, and even drug-naïve patients show volume reductions. Cerebral asymmetry is also reduced in affected individuals and healthy relatives. Functional alterations include diminished activation of frontal regions during cognitive tasks and increased activation of temporal regions during hallucinations. These findings suggest that schizophrenia is associated with both macroscopic and functional changes in the brain.

Multisystem Atrophy: A Parkinson Plus Syndrome

Multisystem atrophy is a type of Parkinson plus syndrome that is characterized by three main features: Parkinsonism, autonomic failure, and cerebellar ataxia. It can present in three different ways, including Shy-Drager Syndrome, Striatonigral degeneration, and Olivopontocerebellar atrophy, each with varying degrees of the three main features.

Macroscopic features of multisystem atrophy include pallor of the substantia nigra, greenish discoloration and atrophy of the putamen, and cerebellar atrophy. Microscopic features include the presence of Papp-Lantos bodies, which are alpha-synuclein inclusions found in oligodendrocytes in the substantia nigra, cerebellum, and basal ganglia.

Overall, multisystem atrophy is a complex and debilitating condition that affects multiple systems in the body, leading to a range of symptoms and challenges for patients and their caregivers.

Neurotransmitters are substances used by neurons to communicate with each other and with target tissues. They are synthesized and released from nerve endings into the synaptic cleft, where they bind to receptor proteins in the cellular membrane of the target tissue. Neurotransmitters can be classified into different types, including small molecules (such as acetylcholine, dopamine, norepinephrine, serotonin, and GABA) and large molecules (such as neuropeptides). They can also be classified as excitatory or inhibitory. Receptors can be ionotropic or metabotropic, and the effects of neurotransmitters can be fast of slow. Some important neurotransmitters include acetylcholine, dopamine, GABA, norepinephrine, and serotonin. Each neurotransmitter has a specific synthesis, breakdown, and receptor type. Understanding neurotransmitters is important for understanding the function of the nervous system and for developing treatments for neurological and psychiatric disorders.

Understanding the sylvian (lateral) sulcus is crucial in comprehending the perisylvian language area and distinguishing between perisylvian and extrasylvian types of aphasias.

Aphasia is a language impairment that affects the production of comprehension of speech, as well as the ability to read of write. The areas involved in language are situated around the Sylvian fissure, referred to as the ‘perisylvian language area’. For repetition, the primary auditory cortex, Wernicke, Broca via the Arcuate fasciculus (AF), Broca recodes into articulatory plan, primary motor cortex, and pyramidal system to cranial nerves are involved. For oral reading, the visual cortex to Wernicke and the same processes as for repetition follows. For writing, Wernicke via AF to premotor cortex for arm and hand, movement planned, sent to motor cortex. The classification of aphasia is complex and imprecise, with the Boston Group classification and Luria’s aphasia interpretation being the most influential. The important subtypes of aphasia include global aphasia, Broca’s aphasia, Wernicke’s aphasia, conduction aphasia, anomic aphasia, transcortical motor aphasia, and transcortical sensory aphasia. Additional syndromes include alexia without agraphia, alexia with agraphia, and pure word deafness.

Functions of the Hypothalamus

The hypothalamus is a vital part of the brain that plays a crucial role in regulating various bodily functions. It receives and integrates sensory information about the internal environment and directs actions to control internal homeostasis. The hypothalamus contains several nuclei and fiber tracts, each with specific functions.

The suprachiasmatic nucleus (SCN) is responsible for regulating circadian rhythms. Neurons in the SCN have an intrinsic rhythm of discharge activity and receive input from the retina. The SCN is considered the body’s master clock, but it has multiple connections with other hypothalamic nuclei.

Body temperature control is mainly under the control of the preoptic, anterior, and posterior nuclei, which have temperature-sensitive neurons. As the temperature goes above 37ºC, warm-sensitive neurons are activated, triggering parasympathetic activity to promote heat loss. As the temperature goes below 37ºC, cold-sensitive neurons are activated, triggering sympathetic activity to promote conservation of heat.

The hypothalamus also plays a role in regulating prolactin secretion. Dopamine is tonically secreted by dopaminergic neurons that project from the arcuate nucleus of the hypothalamus into the anterior pituitary gland via the tuberoinfundibular pathway. The dopamine that is released acts on lactotrophic cells through D2-receptors, inhibiting prolactin synthesis. In the absence of pregnancy of lactation, prolactin is constitutively inhibited by dopamine. Dopamine antagonists result in hyperprolactinemia, while dopamine agonists inhibit prolactin secretion.

In summary, the hypothalamus is a complex structure that regulates various bodily functions, including circadian rhythms, body temperature, and prolactin secretion. Dysfunction of the hypothalamus can lead to various disorders, such as sleep-rhythm disorder, diabetes insipidus, hyperprolactinemia, and obesity.

The Basal Ganglia: Functions and Disorders

The basal ganglia are a group of subcortical structures that play a crucial role in controlling movement and some cognitive processes. The components of the basal ganglia include the striatum (caudate, putamen, nucleus accumbens), subthalamic nucleus, globus pallidus, and substantia nigra (divided into pars compacta and pars reticulata). The putamen and globus pallidus are collectively referred to as the lenticular nucleus.

The basal ganglia are connected in a complex loop, with the cortex projecting to the striatum, the striatum to the internal segment of the globus pallidus, the internal segment of the globus pallidus to the thalamus, and the thalamus back to the cortex. This loop is responsible for regulating movement and cognitive processes.

However, problems with the basal ganglia can lead to several conditions. Huntington’s chorea is caused by degeneration of the caudate nucleus, while Wilson’s disease is characterized by copper deposition in the basal ganglia. Parkinson’s disease is associated with degeneration of the substantia nigra, and hemiballism results from damage to the subthalamic nucleus.

In summary, the basal ganglia are a crucial part of the brain that regulate movement and some cognitive processes. Disorders of the basal ganglia can lead to significant neurological conditions that affect movement and other functions.

Functional Imaging Techniques

Functional imaging techniques are used to study brain activity by detecting changes in blood flow and oxygenation levels. One such technique is functional magnetic resonance imaging (fMRI), which measures the concentration of oxygenated haemoglobin in the blood. When neural activity increases in a specific area of the brain, blood flow to that area increases, leading to a higher concentration of haemoglobin.

Magnetic resonance imaging (MRI) is another technique that uses magnetic fields to create images of the brain’s structure. Magnetic resonance spectroscopy (MRS) is a related technique that can detect several odd-numbered nuclei.

To obtain a more accurate anatomical location for functional information, single photon emission computed tomography (SPECT) and positron emission tomography (PET) are used. SPECT and PET both provide information about brain activity by detecting the emission of particles. However, SPECT emits a single particle, while PET emits two particles. These techniques are useful for studying brain function in both healthy individuals and those with neurological disorders.

Neurodevelopment: Understanding Brain Development

The development of the central nervous system begins with the neuroectoderm, a specialized region of ectoderm. The embryonic brain is divided into three areas: the forebrain (prosencephalon), midbrain (mesencephalon), and hindbrain (rhombencephalon). The prosencephalon further divides into the telencephalon and diencephalon, while the hindbrain subdivides into the metencephalon and myelencephalon.

The telencephalon, of cerebrum, consists of the cerebral cortex, underlying white matter, and the basal ganglia. The diencephalon includes the prethalamus, thalamus, hypothalamus, subthalamus, epithalamus, and pretectum. The mesencephalon comprises the tectum, tegmentum, ventricular mesocoelia, cerebral peduncles, and several nuclei and fasciculi.

The rhombencephalon includes the medulla, pons, and cerebellum, which can be subdivided into a variable number of transversal swellings called rhombomeres. In humans, eight rhombomeres can be distinguished, from caudal to rostral: Rh7-Rh1 and the isthmus. Rhombomeres Rh7-Rh4 form the myelencephalon, while Rh3-Rh1 form the metencephalon.

Understanding neurodevelopment is crucial in comprehending brain development and its complexities. By studying the different areas of the embryonic brain, we can gain insight into the formation of the central nervous system and its functions.

Lewy body dementia is a neurodegenerative disorder that is characterized by both macroscopic and microscopic changes in the brain. Macroscopically, there is cerebral atrophy, but it is less marked than in Alzheimer’s disease, and the brain weight is usually in the normal range. There is also pallor of the substantia nigra and the locus coeruleus, which are regions of the brain that produce dopamine and norepinephrine, respectively.

Microscopically, Lewy body dementia is characterized by the presence of intracellular protein accumulations called Lewy bodies. The major component of a Lewy body is alpha synuclein, and as they grow, they start to draw in other proteins such as ubiquitin. Lewy bodies are also found in Alzheimer’s disease, but they tend to be in the amygdala. They can also be found in healthy individuals, although it has been suggested that these may be pre-clinical cases of dementia with Lewy bodies. Lewy bodies are also found in other neurodegenerative disorders such as progressive supranuclear palsy, corticobasal degeneration, and multiple system atrophy.

In Lewy body dementia, Lewy bodies are mainly found within the brainstem, but they are also found in non-brainstem regions such as the amygdaloid nucleus, parahippocampal gyrus, cingulate cortex, and cerebral neocortex. Classic brainstem Lewy bodies are spherical intraneuronal cytoplasmic inclusions, characterized by hyaline eosinophilic cores, concentric lamellar bands, narrow pale halos, and immunoreactivity for alpha synuclein and ubiquitin. In contrast, cortical Lewy bodies typically lack a halo.

Most brains with Lewy body dementia also show some plaques and tangles, although in most instances, the lesions are not nearly as severe as in Alzheimer’s disease. Neuronal loss and gliosis are usually restricted to brainstem regions, particularly the substantia nigra and locus ceruleus.

HPA Axis Dysfunction in Mood Disorders

The HPA axis, which includes regulatory neural inputs and a feedback loop involving the hypothalamus, pituitary, and adrenal glands, plays a central role in the stress response. Excessive secretion of cortisol, a glucocorticoid hormone, can lead to disruptions in cellular functioning and widespread physiologic dysfunction. Dysregulation of the HPA axis is implicated in mood disorders such as depression and bipolar affective disorder.

In depressed patients, cortisol levels often do not decrease as expected in response to the administration of dexamethasone, a synthetic corticosteroid. This abnormality in the dexamethasone suppression test is thought to be linked to genetic of acquired defects of glucocorticoid receptors. Tricyclic antidepressants have been shown to increase expression of glucocorticoid receptors, whereas this is not the case for SSRIs.

Early adverse experiences can produce long standing changes in HPA axis regulation, indicating a possible neurobiological mechanism whereby childhood trauma could be translated into increased vulnerability to mood disorder. In major depression, there is hypersecretion of cortisol, corticotropin-releasing factor (CRF), and ACTH, and associated adrenocortical enlargement. HPA abnormalities have also been found in other psychiatric disorders including Alzheimer’s and PTSD.

In bipolar disorder, dysregulation of ACTH and cortisol response after CRH stimulation have been reported. Abnormal DST results are found more often during depressive episodes in the course of bipolar disorder than in unipolar disorder. Reduced pituitary volume secondary to LHPA stimulation, resulting in pituitary hypoactivity, has been observed in bipolar patients.

Overall, HPA axis dysfunction is implicated in mood disorders, and understanding the underlying mechanisms may lead to new opportunities for treatments.

The typical EEG pattern for CJD includes periodic sharp wave complexes, which is a diagnostic criterion. Lewy body dementia may show generalized slow wave activity, but if it is more prominent in the temporal and parietal regions, it may indicate Alzheimer’s disease. Toxic encephalopathies, such as lithium toxicity, may show periodic triphasic waves on EEG. For more information, see Smith SJ’s article EEG in neurological conditions other than epilepsy: when does it help, what does it add? (2005).

The parahippocampal gyrus is located surrounding the hippocampus and is involved in memory processing. Asymmetry in this area has also been observed in individuals with schizophrenia.

Aphasia is a language impairment that affects the production of comprehension of speech, as well as the ability to read of write. The areas involved in language are situated around the Sylvian fissure, referred to as the ‘perisylvian language area’. For repetition, the primary auditory cortex, Wernicke, Broca via the Arcuate fasciculus (AF), Broca recodes into articulatory plan, primary motor cortex, and pyramidal system to cranial nerves are involved. For oral reading, the visual cortex to Wernicke and the same processes as for repetition follows. For writing, Wernicke via AF to premotor cortex for arm and hand, movement planned, sent to motor cortex. The classification of aphasia is complex and imprecise, with the Boston Group classification and Luria’s aphasia interpretation being the most influential. The important subtypes of aphasia include global aphasia, Broca’s aphasia, Wernicke’s aphasia, conduction aphasia, anomic aphasia, transcortical motor aphasia, and transcortical sensory aphasia. Additional syndromes include alexia without agraphia, alexia with agraphia, and pure word deafness.

Apraxia: Understanding the Inability to Carry Out Learned Voluntary Movements

Apraxia is a neurological condition that affects a person’s ability to carry out learned voluntary movements. It is important to note that this condition assumes that everything works and the person is not paralyzed. There are different types of apraxia, each with its own set of symptoms and characteristics.

Limb kinetic apraxia is a type of apraxia that affects a person’s ability to make fine of delicate movements. This can include tasks such as buttoning a shirt of tying shoelaces.

Ideomotor apraxia, on the other hand, is an inability to carry out learned tasks when given the necessary objects. For example, a person with ideomotor apraxia may try to write with a hairbrush instead of using it to brush their hair.

Constructional apraxia affects a person’s ability to copy a picture of combine parts of something to form a whole. This can include tasks such as building a puzzle of drawing a picture.

Ideational apraxia is an inability to follow a sequence of actions in the correct order. For example, a person with ideational apraxia may struggle to take a match out of a box and strike it with their left hand.

Finally, oculomotor apraxia affects a person’s ability to control eye movements. This can make it difficult for them to track moving objects of read smoothly.

Overall, apraxia can have a significant impact on a person’s ability to carry out everyday tasks. However, with the right support and treatment, many people with apraxia are able to improve their abilities and maintain their independence.

Appetite Control Hormones

The regulation of appetite is influenced by various hormones in the body. Neuropeptide Y, which is produced by the hypothalamus, stimulates appetite. On the other hand, leptin, which is produced by adipose tissue, suppresses appetite. Ghrelin, which is mainly produced by the gut, increases appetite. Cholecystokinin (CCK), which is also produced by the gut, reduces appetite. These hormones play a crucial role in maintaining a healthy balance of food intake and energy expenditure.

Kluver-Bucy Syndrome: Causes and Symptoms

Kluver-Bucy syndrome is a neurological disorder that results from bilateral medial temporal lobe dysfunction, particularly in the amygdala. This condition is characterized by a range of symptoms, including hyperorality (a tendency to explore objects with the mouth), hypersexuality, docility, visual agnosia, and dietary changes.

The most common causes of Kluver-Bucy syndrome include herpes, late-stage Alzheimer’s disease, frontotemporal dementia, trauma, and bilateral temporal lobe infarction. In some cases, the condition may be reversible with treatment, but in others, it may be permanent and require ongoing management. If you of someone you know is experiencing symptoms of Kluver-Bucy syndrome, it is important to seek medical attention promptly to determine the underlying cause and develop an appropriate treatment plan.

Serotonin: Synthesis and Breakdown

Serotonin, also known as 5-Hydroxytryptamine (5-HT), is synthesized in the central nervous system (CNS) in the raphe nuclei located in the brainstem, as well as in the gastrointestinal (GI) tract in enterochromaffin cells. The amino acid L-tryptophan, obtained from the diet, is used to synthesize serotonin. L-tryptophan can cross the blood-brain barrier, but serotonin cannot.

The transformation of L-tryptophan into serotonin involves two steps. First, hydroxylation to 5-hydroxytryptophan is catalyzed by tryptophan hydroxylase. Second, decarboxylation of 5-hydroxytryptophan to serotonin (5-hydroxytryptamine) is catalyzed by L-aromatic amino acid decarboxylase.

Serotonin is taken up from the synapse by a monoamine transporter (SERT). Substances that block this transporter include MDMA, amphetamine, cocaine, TCAs, and SSRIs. Serotonin is broken down by monoamine oxidase (MAO) and then by aldehyde dehydrogenase to 5-Hydroxyindoleacetic acid (5-HIAA).

The nervous system in embryos develops from the neural plate, which is a thickening of the ectoderm. The first step in this process is the formation of the neural groove, which is then surrounded by neural folds. These folds gradually come together and fuse to form the neural tube. The neural crest, which is made up of parts of the neural ectoderm, is formed from the rolled-up sides of the neural tube and helps in the development of the peripheral nervous system. The mesencephalon, of midbrain, is formed from the second vesicle of the neural tube. This process of neural development is essential for the proper functioning of the nervous system in later life.

Neurotransmitters and their functions:

Orexin, which is derived from the Greek word for ‘appetite’, is responsible for regulating arousal, wakefulness, and appetite. It is also known as hypocretin and is produced in the hypothalamus. Orexin increases the craving for food.

Glutamate is an excitatory amino acid that plays a crucial role in the nervous system. It is responsible for transmitting signals between nerve cells and is involved in learning and memory.

Prolactin is a neurotransmitter produced by the hypothalamus. It is also known as ‘dopamine inhibitory factor’ and is important in the regulation of sexual function. Prolactin levels increase during pregnancy and breastfeeding.

Serotonin is a monoamine neurotransmitter that has a range of actions, including decreasing appetite. It is involved in regulating mood, sleep, and appetite. Low levels of serotonin have been linked to depression and anxiety.

Senile plaques and neurofibrillary tangles contain accumulations of hyperphosphorylated tau, while Hirano bodies are primarily composed of actin. The cytoskeleton is made up of microtubules (composed of tubulin), actin filaments, and intermediate filaments. Lewy bodies are characterized by the presence of insoluble aggregates of α-Synuclein, a protein that plays a role in regulating synaptic vesicle trafficking and neurotransmitter release.

Alzheimer’s disease is characterized by both macroscopic and microscopic changes in the brain. Macroscopic changes include cortical atrophy, ventricular dilation, and depigmentation of the locus coeruleus. Microscopic changes include the presence of senile plaques, neurofibrillary tangles, gliosis, degeneration of the nucleus of Meynert, and Hirano bodies. Senile plaques are extracellular deposits of beta amyloid in the gray matter of the brain, while neurofibrillary tangles are intracellular inclusion bodies that consist primarily of hyperphosphorylated tau. Gliosis is marked by increases in activated microglia and reactive astrocytes near the sites of amyloid plaques. The nucleus of Meynert degenerates in Alzheimer’s, resulting in a decrease in acetylcholine in the brain. Hirano bodies are actin-rich, eosinophilic intracytoplasmic inclusions which have a highly characteristic crystalloid fine structure and are regarded as a nonspecific manifestation of neuronal degeneration. These changes in the brain contribute to the cognitive decline and memory loss seen in Alzheimer’s disease.

Brain Anatomy

The brain is a complex organ with various regions responsible for different functions. The major areas of the cerebrum (telencephalon) include the frontal lobe, parietal lobe, occipital lobe, temporal lobe, insula, corpus callosum, fornix, anterior commissure, and striatum. The cerebrum is responsible for complex learning, language acquisition, visual and auditory processing, memory, and emotion processing.

The diencephalon includes the thalamus, hypothalamus and pituitary, pineal gland, and mammillary body. The thalamus is a major relay point and processing center for all sensory impulses (excluding olfaction). The hypothalamus and pituitary are involved in homeostasis and hormone release. The pineal gland secretes melatonin to regulate circadian rhythms. The mammillary body is a relay point involved in memory.

The cerebellum is primarily concerned with movement and has two major hemispheres with an outer cortex made up of gray matter and an inner region of white matter. The cerebellum provides precise timing and appropriate patterns of skeletal muscle contraction for smooth, coordinated movements and agility needed for daily life.

The brainstem includes the substantia nigra, which is involved in controlling and regulating activities of the motor and premotor cortical areas for smooth voluntary movements, eye movement, reward seeking, the pleasurable effects of substance misuse, and learning.

Alzheimer’s disease is associated with the presence of Hirano bodies.

Schizophrenia is a pathology that is characterized by a number of structural and functional brain alterations. Structural alterations include enlargement of the ventricles, reductions in total brain and gray matter volume, and regional reductions in the amygdala, parahippocampal gyrus, and temporal lobes. Antipsychotic treatment may be associated with gray matter loss over time, and even drug-naïve patients show volume reductions. Cerebral asymmetry is also reduced in affected individuals and healthy relatives. Functional alterations include diminished activation of frontal regions during cognitive tasks and increased activation of temporal regions during hallucinations. These findings suggest that schizophrenia is associated with both macroscopic and functional changes in the brain.

Microglia serve as the immune cells of the central nervous system and perform functions similar to macrophages. When a microglial cell engulfs infectious material, it is referred to as a Gitter cell.

Glial Cells: The Support System of the Central Nervous System

The central nervous system is composed of two basic cell types: neurons and glial cells. Glial cells, also known as support cells, play a crucial role in maintaining the health and function of neurons. There are several types of glial cells, including macroglia (astrocytes and oligodendrocytes), ependymal cells, and microglia.

Astrocytes are the most abundant type of glial cell and have numerous functions, such as providing structural support, repairing nervous tissue, nourishing neurons, contributing to the blood-brain barrier, and regulating neurotransmission and blood flow. There are two main types of astrocytes: protoplasmic and fibrous.

Oligodendrocytes are responsible for the formation of myelin sheaths, which insulate and protect axons, allowing for faster and more efficient transmission of nerve impulses.

Ependymal cells line the ventricular system and are involved in the circulation of cerebrospinal fluid (CSF) and fluid homeostasis in the brain. Specialized ependymal cells called choroid plexus cells produce CSF.

Microglia are the immune cells of the CNS and play a crucial role in protecting the brain from infection and injury. They also contribute to the maintenance of neuronal health and function.

In summary, glial cells are essential for the proper functioning of the central nervous system. They provide structural support, nourishment, insulation, and immune defense to neurons, ensuring the health and well-being of the brain and spinal cord.

Dementia Pugilistica: A Neurodegenerative Condition Resulting from Neurotrauma

Dementia pugilistica, also known as chronic traumatic encephalopathy (CTE), is a neurodegenerative condition that results from neurotrauma. It is commonly seen in boxers and NFL players, but can also occur in anyone with neurotrauma. The condition is characterized by symptoms such as gait ataxia, slurred speech, impaired hearing, tremors, disequilibrium, neurobehavioral disturbances, and progressive cognitive decline.

Most cases of dementia pugilistica present with early onset cognitive deficits, and behavioral signs exhibited by patients include aggression, suspiciousness, paranoia, childishness, hypersexuality, depression, and restlessness. The progression of the condition leads to more prominent behavioral symptoms such as difficulty with impulse control, irritability, inappropriateness, and explosive outbursts of aggression.

Neuropathological abnormalities have been identified in CTE, with the most unique feature being the abnormal accumulation of tau in neurons and glia in an irregular, focal, perivascular distribution and at the depths of cortical sulci. Abnormalities of the septum pellucidum, such as cavum and fenestration, are also a common feature.

While the condition has become increasingly rare due to the progressive improvement in sports safety, it is important to recognize the potential long-term consequences of repeated head injuries and take steps to prevent them.

When the parietal lobe is not functioning properly, it can cause constructional apraxia. This condition makes it difficult for individuals to replicate the intersecting pentagons, which is a common cognitive test included in Folstein’s mini-mental state examination.

The individual’s age, behavioral changes, disinhibition, and fatuous giggling suggest a diagnosis of frontal lobe dementia, which is further supported by their physical examination. The absence of focal abnormalities on EEG rules out the possibility of vascular dementia. Typically, EEG results are normal during the early stages of this condition and remain so until the advanced stages.

When a stroke affects the thalamus, it can cause loss of sensation on the opposite side of the body and intense burning pain that can be treated with tricyclics. This type of sensory loss is commonly seen in conditions that affect the brain stem, thalamus, of cortex. In addition, a stroke in the thalamogeniculate artery can result in temporary paralysis on the opposite side of the body, followed by ataxia, and involuntary movements. Facial expression may also be affected. Treatment for these patients is similar to that for other stroke patients.

Neurotransmitters are substances used by neurons to communicate with each other and with target tissues. They are synthesized and released from nerve endings into the synaptic cleft, where they bind to receptor proteins in the cellular membrane of the target tissue. Neurotransmitters can be classified into different types, including small molecules (such as acetylcholine, dopamine, norepinephrine, serotonin, and GABA) and large molecules (such as neuropeptides). They can also be classified as excitatory or inhibitory. Receptors can be ionotropic or metabotropic, and the effects of neurotransmitters can be fast of slow. Some important neurotransmitters include acetylcholine, dopamine, GABA, norepinephrine, and serotonin. Each neurotransmitter has a specific synthesis, breakdown, and receptor type. Understanding neurotransmitters is important for understanding the function of the nervous system and for developing treatments for neurological and psychiatric disorders.

Primary progressive aphasia is a specific type of frontotemporal dementia that is characterized by the degeneration of the left perisylvian region. Frontotemporal dementia can be divided into two subtypes: behavioral, which involves atrophy of the frontal region, and language, which includes primary progressive aphasia and semantic dementia. The language subtypes of frontotemporal dementia typically exhibit more severe atrophy on the left side of the brain. Semantic dementia is characterized by greater atrophy in the anterior temporal lobe compared to the posterior temporal lobe. In contrast, Alzheimer’s dementia is associated with bilateral hippocampal atrophy, while vascular dementia is characterized by diffuse white matter lesions.

Cannabis attaches to cannabinoid receptors, while heroin acts as an opioid agonist and alters the function of dopamine.

Serotonin: Synthesis and Breakdown

Serotonin, also known as 5-Hydroxytryptamine (5-HT), is synthesized in the central nervous system (CNS) in the raphe nuclei located in the brainstem, as well as in the gastrointestinal (GI) tract in enterochromaffin cells. The amino acid L-tryptophan, obtained from the diet, is used to synthesize serotonin. L-tryptophan can cross the blood-brain barrier, but serotonin cannot.

The transformation of L-tryptophan into serotonin involves two steps. First, hydroxylation to 5-hydroxytryptophan is catalyzed by tryptophan hydroxylase. Second, decarboxylation of 5-hydroxytryptophan to serotonin (5-hydroxytryptamine) is catalyzed by L-aromatic amino acid decarboxylase.

Serotonin is taken up from the synapse by a monoamine transporter (SERT). Substances that block this transporter include MDMA, amphetamine, cocaine, TCAs, and SSRIs. Serotonin is broken down by monoamine oxidase (MAO) and then by aldehyde dehydrogenase to 5-Hydroxyindoleacetic acid (5-HIAA).

Depression, suicidality, and aggression have been linked to decreased levels of 5-HIAA in the CSF.

The Significance of 5-HIAA in Depression and Aggression

During the 1980s, there was a brief period of interest in 5-hydroxyindoleacetic acid (5-HIAA), a serotonin metabolite. Studies found that up to a third of people with depression had low concentrations of 5-HIAA in their cerebrospinal fluid (CSF), while very few normal controls did. This suggests that 5-HIAA may play a role in depression.

Furthermore, individuals with low CSF levels of 5-HIAA have been found to respond less effectively to antidepressants and are more likely to commit suicide. This finding has been replicated in multiple studies, indicating the significance of 5-HIAA in depression.

Low levels of 5-HIAA are also associated with increased levels of aggression. This suggests that 5-HIAA may play a role in regulating aggressive behavior. Overall, the research on 5-HIAA highlights its potential importance in understanding and treating depression and aggression.

When under stress, the paraventricular nucleus of the hypothalamus releases two hormones: corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP).

HPA Axis Dysfunction in Mood Disorders

The HPA axis, which includes regulatory neural inputs and a feedback loop involving the hypothalamus, pituitary, and adrenal glands, plays a central role in the stress response. Excessive secretion of cortisol, a glucocorticoid hormone, can lead to disruptions in cellular functioning and widespread physiologic dysfunction. Dysregulation of the HPA axis is implicated in mood disorders such as depression and bipolar affective disorder.

In depressed patients, cortisol levels often do not decrease as expected in response to the administration of dexamethasone, a synthetic corticosteroid. This abnormality in the dexamethasone suppression test is thought to be linked to genetic of acquired defects of glucocorticoid receptors. Tricyclic antidepressants have been shown to increase expression of glucocorticoid receptors, whereas this is not the case for SSRIs.

Early adverse experiences can produce long standing changes in HPA axis regulation, indicating a possible neurobiological mechanism whereby childhood trauma could be translated into increased vulnerability to mood disorder. In major depression, there is hypersecretion of cortisol, corticotropin-releasing factor (CRF), and ACTH, and associated adrenocortical enlargement. HPA abnormalities have also been found in other psychiatric disorders including Alzheimer’s and PTSD.

In bipolar disorder, dysregulation of ACTH and cortisol response after CRH stimulation have been reported. Abnormal DST results are found more often during depressive episodes in the course of bipolar disorder than in unipolar disorder. Reduced pituitary volume secondary to LHPA stimulation, resulting in pituitary hypoactivity, has been observed in bipolar patients.

Overall, HPA axis dysfunction is implicated in mood disorders, and understanding the underlying mechanisms may lead to new opportunities for treatments.

During sleep, strokes are more likely to occur as blood pressure decreases and areas of the brain with poor blood flow (caused by arterial damage in arteriopaths) become oxygen-deprived. Women with pre-existing cardiovascular disease should avoid taking oral contraceptives as they can raise the risk of stroke and DVTs.

Cerebrovascular accidents (CVA), also known as strokes, are defined by the World Health Organization as a sudden onset of focal neurological symptoms lasting more than 24 hours and presumed to be of vascular origin. Strokes can be caused by either infarction of hemorrhage, with infarction being more common. Hemorrhagic strokes tend to be more severe. Intracranial hemorrhage can be primary, caused mainly by hypertension, of subarachnoid, caused by the rupture of an aneurysm of angioma. Primary intracranial hemorrhage is most common in individuals aged 60-80 and often occurs during exertion. Infarction can be caused by thrombosis of embolism, with thrombosis being more common. Atherosclerosis, often caused by hypertension, is the main cause of infarction. CT scanning is the preferred diagnostic tool during the first 48 hours after a stroke as it can distinguish between infarcts and hemorrhages. Recovery from embolism is generally quicker and more complete than from thrombosis due to the availability of collateral channels.

Simultagnosia is a condition where an individual is unable to focus on more than one aspect of a complex scene at a time. This condition, along with optic ataxia and oculomotor apraxia, is part of Balint’s syndrome.

Gerstmann syndrome is characterized by four symptoms: dysgraphia/agraphia, dyscalculia/acalculia, finger agnosia, and left-right disorientation. This syndrome is linked to a lesion in the dominant parietal lobe, specifically the left side of the angular and supramarginal gyri. It is rare for an individual to present with all four symptoms of the tetrad.

The blood retinal barrier refers to the membrane that separates the aqueous humour from the blood.

Understanding the Blood Brain Barrier

The blood brain barrier (BBB) is a crucial component of the brain’s defense system against harmful chemicals and ion imbalances. It is a semi-permeable membrane formed by tight junctions of endothelial cells in the brain’s capillaries, which separates the blood from the cerebrospinal fluid. However, certain areas of the BBB, known as circumventricular organs, are fenestrated to allow neurosecretory products to enter the blood.

When it comes to MRCPsych questions, the focus is on the following aspects of the BBB: the tight junctions between endothelial cells, the ease with which lipid-soluble molecules pass through compared to water-soluble ones, the difficulty large and highly charged molecules face in passing through, the increased permeability of the BBB during inflammation, and the theoretical ability of nasally administered drugs to bypass the BBB.

It is important to remember the specific circumventricular organs where the BBB is fenestrated, including the posterior pituitary and the area postrema. Understanding the BBB’s function and characteristics is essential for medical professionals to diagnose and treat neurological disorders effectively.

The Edinger-Westphal nucleus is the motor nucleus of the third cranial nerve, while the putamen and globus pallidus comprise the lenticular nucleus, which is part of the basal ganglia. The basal ganglia play a role in motor control and use the inhibitory neurotransmitter GABA. The components of the basal ganglia can be classified in various ways, with the corpus striatum (caudate nucleus, putamen, nucleus accumbens, and globus pallidus) and the striatum of neostriatum (caudate, putamen, and globus pallidus) being common groupings.

Neuroimaging techniques can be divided into structural and functional types, although this distinction is becoming less clear as new techniques emerge. Structural techniques include computed tomography (CT) and magnetic resonance imaging (MRI), which use x-rays and magnetic fields, respectively, to produce images of the brain’s structure. Functional techniques, on the other hand, measure brain activity by detecting changes in blood flow of oxygen consumption. These include functional MRI (fMRI), emission tomography (PET and SPECT), perfusion MRI (pMRI), and magnetic resonance spectroscopy (MRS). Some techniques, such as diffusion tensor imaging (DTI), combine both structural and functional information to provide a more complete picture of the brain’s anatomy and function. DTI, for example, uses MRI to estimate the paths that water takes as it diffuses through white matter, allowing researchers to visualize white matter tracts.

Sleep Stages

Sleep is divided into two distinct states called rapid eye movement (REM) and non-rapid eye movement (NREM). NREM is subdivided into four stages.

Sleep stage
Approx % of time spent in stage
EEG findings
Comment

I
5%
Theta waves (4-7 Hz)
The dozing off stage. Characterized by hypnic jerks: spontaneous myoclonic contractions associated with a sensation of twitching of falling.

II
45%
Theta waves, K complexes and sleep spindles (short bursts of 12-14 Hz activity)
Body enters a more subdued state including a drop in temperature, relaxed muscles, and slowed breathing and heart rate. At the same time, brain waves show a new pattern and eye movement stops.

III
15%
Delta waves (0-4 Hz)
Deepest stage of sleep (high waking threshold). The length of stage 3 decreases over the course of the night.

IV
15%
Mixed, predominantly beta
High dream activity.

The percentage of REM sleep decreases with age.

It takes the average person 15-20 minutes to fall asleep, this is called sleep latency (characterised by the onset of stage I sleep). Once asleep one descends through stages I-II and then III-IV (deep stages). After about 90 minutes of sleep one enters REM. The rest of the sleep comprises of cycles through the stages. As the sleep progresses the periods of REM become greater and the periods of NREM become less. During an average night’s sleep one spends 25% of the sleep in REM and 75% in NREM.

REM sleep has certain characteristics that separate it from NREM

Characteristics of REM sleep

– Autonomic instability (variability in heart rate, respiratory rate, and BP)
– Loss of muscle tone
– Dreaming
– Rapid eye movements
– Penile erection

Deafness:

(No information provided on deafness in relation to sleep stages)

Prions are responsible for causing Creutzfeldt-Jakob disease (CJD), a fatal and uncommon condition that leads to progressive neurodegeneration. The disease is characterized by swiftly advancing dementia as one of its primary symptoms.

Perseveration: The Clinical Symptoms in Chronic Schizophrenia and Organic Dementia

Perseveration is a common behavior observed in patients with organic brain involvement. It is characterized by the conscious continuation of an act of an idea. This behavior is frequently seen in patients with delirium, epilepsy, dementia, schizophrenia, and normal individuals under extreme fatigue of drug-induced states.

In chronic schizophrenia and organic dementia, perseveration is a prominent symptom. Patients with these conditions tend to repeat the same words, phrases, of actions over and over again, even when it is no longer appropriate of relevant to the situation. This behavior can be frustrating for caregivers and family members, and it can also interfere with the patient’s ability to communicate effectively.

In schizophrenia, perseveration is often associated with disorganized thinking and speech. Patients may jump from one topic to another without any logical connection, and they may repeat the same words of phrases in an attempt to express their thoughts. In organic dementia, perseveration is a sign of cognitive decline and memory impairment. Patients may repeat the same stories of questions, forgetting that they have already asked of answered them.

Overall, perseveration is a common symptom in patients with organic brain involvement, and it can have a significant impact on their daily functioning and quality of life. Understanding this behavior is essential for effective management and treatment of these conditions.

Tyrosine is converted to L-DOPA by the enzyme tyrosine hydroxylase. L-DOPA is then converted to dopamine by the enzyme dopa decarboxylase.

Neurotransmitters are substances used by neurons to communicate with each other and with target tissues. They are synthesized and released from nerve endings into the synaptic cleft, where they bind to receptor proteins in the cellular membrane of the target tissue. Neurotransmitters can be classified into different types, including small molecules (such as acetylcholine, dopamine, norepinephrine, serotonin, and GABA) and large molecules (such as neuropeptides). They can also be classified as excitatory or inhibitory. Receptors can be ionotropic or metabotropic, and the effects of neurotransmitters can be fast of slow. Some important neurotransmitters include acetylcholine, dopamine, GABA, norepinephrine, and serotonin. Each neurotransmitter has a specific synthesis, breakdown, and receptor type. Understanding neurotransmitters is important for understanding the function of the nervous system and for developing treatments for neurological and psychiatric disorders.

The presence of a gradual onset may indicate non-epileptic attacks, while other symptoms suggest genuine generalised tonic clonic seizures. Additional characteristics of pseudoseizures include a higher incidence in females (8:1), a history of previous illness behavior, and childhood physical and/of sexual abuse. Diagnosis can be challenging, but video EEG can be a useful tool in confirming the presence of pseudoseizures.

Development of the cerebellum commences from the metencephalon in the sixth week.

Neurodevelopment: Understanding Brain Development

The development of the central nervous system begins with the neuroectoderm, a specialized region of ectoderm. The embryonic brain is divided into three areas: the forebrain (prosencephalon), midbrain (mesencephalon), and hindbrain (rhombencephalon). The prosencephalon further divides into the telencephalon and diencephalon, while the hindbrain subdivides into the metencephalon and myelencephalon.

The telencephalon, of cerebrum, consists of the cerebral cortex, underlying white matter, and the basal ganglia. The diencephalon includes the prethalamus, thalamus, hypothalamus, subthalamus, epithalamus, and pretectum. The mesencephalon comprises the tectum, tegmentum, ventricular mesocoelia, cerebral peduncles, and several nuclei and fasciculi.

The rhombencephalon includes the medulla, pons, and cerebellum, which can be subdivided into a variable number of transversal swellings called rhombomeres. In humans, eight rhombomeres can be distinguished, from caudal to rostral: Rh7-Rh1 and the isthmus. Rhombomeres Rh7-Rh4 form the myelencephalon, while Rh3-Rh1 form the metencephalon.

Understanding neurodevelopment is crucial in comprehending brain development and its complexities. By studying the different areas of the embryonic brain, we can gain insight into the formation of the central nervous system and its functions.

Dhat is a syndrome that is specific to Indian culture and affects men. Those who suffer from it experience anxiety about the presence of semen in their urine, which they believe leads to a loss of energy.

Creutzfeldt-Jakob Disease: Differences between vCJD and CJD

Creutzfeldt-Jakob Disease (CJD) is a prion disease that includes scrapie, BSE, and Kuru. However, there are important differences between sporadic (also known as classic) CJD and variant CJD. The table below summarizes these differences.

vCJD:
– Longer duration from onset of symptoms to death (a year of more)
– Presents with psychiatric and behavioral symptoms before neurological symptoms
– MRI shows pulvinar sign
– EEG shows generalized slowing
– Originates from infected meat products
– Affects younger people (age 25-30)

CJD:
– Shorter duration from onset of symptoms to death (a few months)
– Presents with neurological symptoms
– MRI shows bilateral anterior basal ganglia high signal
– EEG shows biphasic and triphasic waves 1-2 per second
– Originates from genetic mutation (bad luck)
– Affects older people (age 55-65)

Overall, understanding the differences between vCJD and CJD is important for diagnosis and treatment.

While alpha (α) and beta (β) activity are typical in adults who are awake and at rest, delta activity (δ) may suggest the presence of a brain tumor. Mu (μ) activity is linked to movement, and theta activity (θ) is uncommon in the waking adult population, occurring briefly in only 15% of individuals.

Located in the epithalamus at the center of the brain, the pineal gland is an endocrine gland. The basal ganglia, also known as basal nuclei, consist of four primary components: the caudate, nucleus accumbens, putamen, globus pallidus, subthalamic nucleus, and substantia nigra. The lenticular (of lentiform) nucleus is formed by the globus pallidus and putamen.

Overview of Cranial Nerves and Their Functions

The cranial nerves are a complex system of nerves that originate from the brain and control various functions of the head and neck. There are twelve cranial nerves, each with a specific function and origin. The following table provides a simplified overview of the cranial nerves, including their origin, skull exit, modality, and functions.

The first cranial nerve, the olfactory nerve, originates from the telencephalon and exits through the cribriform plate. It is a sensory nerve that controls the sense of smell. The second cranial nerve, the optic nerve, originates from the diencephalon and exits through the optic foramen. It is a sensory nerve that controls vision.

The third cranial nerve, the oculomotor nerve, originates from the midbrain and exits through the superior orbital fissure. It is a motor nerve that controls eye movement, pupillary constriction, and lens accommodation. The fourth cranial nerve, the trochlear nerve, also originates from the midbrain and exits through the superior orbital fissure. It is a motor nerve that controls eye movement.

The fifth cranial nerve, the trigeminal nerve, originates from the pons and exits through different foramina depending on the division. It is a mixed nerve that controls chewing and sensation of the anterior 2/3 of the scalp. It also tenses the tympanic membrane to dampen loud noises.

The sixth cranial nerve, the abducens nerve, originates from the pons and exits through the superior orbital fissure. It is a motor nerve that controls eye movement. The seventh cranial nerve, the facial nerve, also originates from the pons and exits through the internal auditory canal. It is a mixed nerve that controls facial expression, taste of the anterior 2/3 of the tongue, and tension on the stapes to dampen loud noises.

The eighth cranial nerve, the vestibulocochlear nerve, originates from the pons and exits through the internal auditory canal. It is a sensory nerve that controls hearing. The ninth cranial nerve, the glossopharyngeal nerve, originates from the medulla and exits through the jugular foramen. It is a mixed nerve that controls taste of the posterior 1/3 of the tongue, elevation of the larynx and pharynx, and swallowing.

The tenth cranial nerve, the vagus nerve, also originates from the medulla and exits through the jugular foramen. It is a mixed nerve that controls swallowing, voice production, and parasympathetic supply to nearly all thoracic and abdominal viscera. The eleventh cranial nerve, the accessory nerve, originates from the medulla and exits through the jugular foramen. It is a motor nerve that controls shoulder shrugging and head turning.

The twelfth cranial nerve, the hypoglossal nerve, originates from the medulla and exits through the hypoglossal canal. It is a motor nerve that controls tongue movement. Overall, the cranial nerves play a crucial role in controlling various functions of the head and neck, and any damage of dysfunction can have significant consequences.

Agnosia is a condition where a person loses the ability to recognize objects, persons, sounds, shapes, of smells, despite having no significant memory loss of defective senses. There are different types of agnosia, such as prosopagnosia (inability to recognize familiar faces), anosognosia (inability to recognize one’s own condition/illness), autotopagnosia (inability to orient parts of the body), phonagnosia (inability to recognize familiar voices), simultanagnosia (inability to appreciate two objects in the visual field at the same time), and astereoagnosia (inability to recognize objects by touch).

Cranial Nerve Reflexes

When it comes to questions on cranial nerve reflexes, it is important to match the reflex to the nerves involved. Here are some examples:

– Pupillary light reflex: involves the optic nerve (sensory) and oculomotor nerve (motor).
– Accommodation reflex: involves the optic nerve (sensory) and oculomotor nerve (motor).
– Jaw jerk: involves the trigeminal nerve (sensory and motor).
– Corneal reflex: involves the trigeminal nerve (sensory) and facial nerve (motor).
– Vestibulo-ocular reflex: involves the vestibulocochlear nerve (sensory) and oculomotor, trochlear, and abducent nerves (motor).

Another example of a cranial nerve reflex is the gag reflex, which involves the glossopharyngeal nerve (sensory) and the vagus nerve (motor). This reflex is important for protecting the airway from foreign objects of substances that may trigger a gag reflex. It is also used as a diagnostic tool to assess the function of these nerves.

The midbrain contains a section called the pars compacta, which is made up of neurons that produce dopamine and is situated next to the pars reticulata. Parkinson’s disease is identified by the loss of these dopamine-producing neurons in this area.

Parkinson’s Disease Pathology

Parkinson’s disease is a neurodegenerative disorder that affects the central nervous system. The pathology of Parkinson’s disease is very similar to that of Lewy body dementia. The macroscopic features of Parkinson’s disease include pallor of the substantia nigra (midbrain) and locus coeruleus (pons). The microscopic changes include the presence of Lewy bodies, which are intracellular aggregates of alpha-synuclein. Additionally, there is a loss of dopaminergic cells from the substantia nigra pars compacta. These changes contribute to the motor symptoms of Parkinson’s disease, such as tremors, rigidity, and bradykinesia. Understanding the pathology of Parkinson’s disease is crucial for developing effective treatments and improving the quality of life for those affected by this condition.

Creutzfeldt-Jakob disease is characterized by a slow background rhythm accompanied by paroxysmal sharp waves on EEG, while the remaining options are typical EEG features of the aging process.

If the individual were to experience impaired consciousness during the attack, this would be classified as a complex partial seizure. However, based on the current symptoms, it appears to be a simple partial seizure with retained consciousness.

Neurotransmitters are substances used by neurons to communicate with each other and with target tissues. They are synthesized and released from nerve endings into the synaptic cleft, where they bind to receptor proteins in the cellular membrane of the target tissue. Neurotransmitters can be classified into different types, including small molecules (such as acetylcholine, dopamine, norepinephrine, serotonin, and GABA) and large molecules (such as neuropeptides). They can also be classified as excitatory or inhibitory. Receptors can be ionotropic or metabotropic, and the effects of neurotransmitters can be fast of slow. Some important neurotransmitters include acetylcholine, dopamine, GABA, norepinephrine, and serotonin. Each neurotransmitter has a specific synthesis, breakdown, and receptor type. Understanding neurotransmitters is important for understanding the function of the nervous system and for developing treatments for neurological and psychiatric disorders.

Neurotransmitters are substances used by neurons to communicate with each other and with target tissues. They are synthesized and released from nerve endings into the synaptic cleft, where they bind to receptor proteins in the cellular membrane of the target tissue. Neurotransmitters can be classified into different types, including small molecules (such as acetylcholine, dopamine, norepinephrine, serotonin, and GABA) and large molecules (such as neuropeptides). They can also be classified as excitatory or inhibitory. Receptors can be ionotropic or metabotropic, and the effects of neurotransmitters can be fast of slow. Some important neurotransmitters include acetylcholine, dopamine, GABA, norepinephrine, and serotonin. Each neurotransmitter has a specific synthesis, breakdown, and receptor type. Understanding neurotransmitters is important for understanding the function of the nervous system and for developing treatments for neurological and psychiatric disorders.

Alpha-Secretase: A Potential Treatment for Alzheimer’s Disease

Alpha-secretase is a promising avenue for preventing and treating Alzheimer’s disease. When amyloid precursor protein (APP) crosses the cell membrane, it can be cleaved by various enzymes. Alpha-secretase cleaves APP in a way that produces non-toxic protein fragments. However, beta and gamma-secretase are two other enzymes that can cleave APP, resulting in shorter, stickier fragments called beta-amyloid. These fragments can join together to form insoluble amyloid plaques. Researchers are developing drugs that can either stimulate alpha-secretase of block beta- and gamma-secretase, with the hope of preventing or treating Alzheimer’s disease.

White matter is the cabling that links different parts of the CNS together. There are three types of white matter cables: projection tracts, commissural tracts, and association tracts. Projection tracts connect higher centers of the brain with lower centers, commissural tracts connect the two hemispheres together, and association tracts connect regions of the same hemisphere. Some common tracts include the corticospinal tract, which connects the motor cortex to the brainstem and spinal cord, and the corpus callosum, which is the largest white matter fiber bundle connecting corresponding areas of cortex between the hemispheres. Other tracts include the cingulum, superior and inferior occipitofrontal fasciculi, and the superior and inferior longitudinal fasciculi.

Neuroimaging techniques can be divided into structural and functional types, although this distinction is becoming less clear as new techniques emerge. Structural techniques include computed tomography (CT) and magnetic resonance imaging (MRI), which use x-rays and magnetic fields, respectively, to produce images of the brain’s structure. Functional techniques, on the other hand, measure brain activity by detecting changes in blood flow of oxygen consumption. These include functional MRI (fMRI), emission tomography (PET and SPECT), perfusion MRI (pMRI), and magnetic resonance spectroscopy (MRS). Some techniques, such as diffusion tensor imaging (DTI), combine both structural and functional information to provide a more complete picture of the brain’s anatomy and function. DTI, for example, uses MRI to estimate the paths that water takes as it diffuses through white matter, allowing researchers to visualize white matter tracts.

Dura Mater

The dura mater is one of the three membranes, known as meninges, that cover the brain and spinal cord. It is the outermost and most fibrous layer, with the pia mater and arachnoid mater making up the remaining layers. The pia mater is the innermost layer.

The dura mater is folded at certain points, including the falx cerebri, which separates the two cerebral hemispheres of the brain, the tentorium cerebelli, which separates the cerebellum from the cerebrum, the falx cerebelli, which separates the cerebellar hemispheres, and the sellar diaphragm, which covers the pituitary gland and forms a roof over the hypophyseal fossa.

– Dement and Kleitman (1957) classified sleep into five stages.
– Normal adults spend the majority of their sleep in Stage 2 (55%).
– Non-REM sleep is divided into four stages: Stage 1 (5%), Stage 2 (55%), Stage 3 (5%), and Stage 4 (10%).
– REM sleep is Stage 5 and normal adults spend 25% of their sleep in this stage.

The strongest association with HIV dementia is the infiltration of monocytes and activation of microglia in the brain. While the presence of HIV encephalopathy is somewhat linked to HIV associated dementia, the extent of monocyte infiltration and microglial activation is the best indicator of AIDS dementia. Microglia can cause damage to neurons by releasing oxidative radicals, nitric oxide, and cytokines. The correlation between viral load and HAD is not significant. Astrocytes have limited susceptibility to HIV infection, and neuronal infection is rare and unlikely to have a significant impact on HIV-related CNS disorders.

This question is presented in two variations on the exam, with one implying that auras are primarily linked to temporal lobe epilepsy and the other to complex partial seizures. In reality, partial seizures are most commonly associated with auras compared to other types of seizures. While partial seizures can originate in any lobe of the brain, those that arise in the temporal lobe are most likely to produce an aura. Therefore, both versions of the question are accurate.

Epilepsy and Aura

An aura is a subjective sensation that is a type of simple partial seizure. It typically lasts only a few seconds and can help identify the site of cortical onset. There are eight recognized types of auras, including somatosensory, visual, auditory, gustatory, olfactory, autonomic, abdominal, and psychic.

In about 80% of cases, auras precede temporal lobe seizures. The most common auras in these seizures are abdominal and psychic, which can cause a rising epigastric sensation of feelings of fear, déjà vu, of jamais vu. Parietal lobe seizures may begin with a contralateral sensation, usually of the positive type, such as an electrical sensation of tingling. Occipital lobe seizures may begin with contralateral visual changes, such as colored lines, spots, of shapes, of even a loss of vision. Temporal-parietal-occipital seizures may produce more formed auras.

Complex partial seizures are defined by impairment of consciousness, which means decreased responsiveness and awareness of oneself and surroundings. During a complex partial seizure, a patient is unresponsive and does not remember events that occurred.

Cerebral Dysfunction: Lobe-Specific Features

When the brain experiences dysfunction, it can manifest in various ways depending on the affected lobe. In the frontal lobe, dysfunction can lead to contralateral hemiplegia, impaired problem solving, disinhibition, lack of initiative, Broca’s aphasia, and agraphia (dominant). The temporal lobe dysfunction can result in Wernicke’s aphasia (dominant), homonymous upper quadrantanopia, and auditory agnosia (non-dominant). On the other hand, the non-dominant parietal lobe dysfunction can lead to anosognosia, dressing apraxia, spatial neglect, and constructional apraxia. Meanwhile, the dominant parietal lobe dysfunction can result in Gerstmann’s syndrome. Lastly, occipital lobe dysfunction can lead to visual agnosia, visual illusions, and contralateral homonymous hemianopia.

Serotonin: Synthesis and Breakdown

Serotonin, also known as 5-Hydroxytryptamine (5-HT), is synthesized in the central nervous system (CNS) in the raphe nuclei located in the brainstem, as well as in the gastrointestinal (GI) tract in enterochromaffin cells. The amino acid L-tryptophan, obtained from the diet, is used to synthesize serotonin. L-tryptophan can cross the blood-brain barrier, but serotonin cannot.

The transformation of L-tryptophan into serotonin involves two steps. First, hydroxylation to 5-hydroxytryptophan is catalyzed by tryptophan hydroxylase. Second, decarboxylation of 5-hydroxytryptophan to serotonin (5-hydroxytryptamine) is catalyzed by L-aromatic amino acid decarboxylase.

Serotonin is taken up from the synapse by a monoamine transporter (SERT). Substances that block this transporter include MDMA, amphetamine, cocaine, TCAs, and SSRIs. Serotonin is broken down by monoamine oxidase (MAO) and then by aldehyde dehydrogenase to 5-Hydroxyindoleacetic acid (5-HIAA).

Excitatory neurotransmitters include glutamate, histamine, acetylcholine, and noradrenaline, as they increase ion flow and the likelihood of action potential in neurons. However, GABA functions as an inhibitory neurotransmitter, reducing ion flow and decreasing the probability of action potential.

The septum pellucidum is a thin layer that divides the front sections of the left and right lateral ventricles in the brain. It extends as a flat structure from the corpus callosum to the fornix.

Dementia Pugilistica: A Neurodegenerative Condition Resulting from Neurotrauma

Dementia pugilistica, also known as chronic traumatic encephalopathy (CTE), is a neurodegenerative condition that results from neurotrauma. It is commonly seen in boxers and NFL players, but can also occur in anyone with neurotrauma. The condition is characterized by symptoms such as gait ataxia, slurred speech, impaired hearing, tremors, disequilibrium, neurobehavioral disturbances, and progressive cognitive decline.

Most cases of dementia pugilistica present with early onset cognitive deficits, and behavioral signs exhibited by patients include aggression, suspiciousness, paranoia, childishness, hypersexuality, depression, and restlessness. The progression of the condition leads to more prominent behavioral symptoms such as difficulty with impulse control, irritability, inappropriateness, and explosive outbursts of aggression.

Neuropathological abnormalities have been identified in CTE, with the most unique feature being the abnormal accumulation of tau in neurons and glia in an irregular, focal, perivascular distribution and at the depths of cortical sulci. Abnormalities of the septum pellucidum, such as cavum and fenestration, are also a common feature.

While the condition has become increasingly rare due to the progressive improvement in sports safety, it is important to recognize the potential long-term consequences of repeated head injuries and take steps to prevent them.

Understanding the Blood Brain Barrier

The blood brain barrier (BBB) is a crucial component of the brain’s defense system against harmful chemicals and ion imbalances. It is a semi-permeable membrane formed by tight junctions of endothelial cells in the brain’s capillaries, which separates the blood from the cerebrospinal fluid. However, certain areas of the BBB, known as circumventricular organs, are fenestrated to allow neurosecretory products to enter the blood.

When it comes to MRCPsych questions, the focus is on the following aspects of the BBB: the tight junctions between endothelial cells, the ease with which lipid-soluble molecules pass through compared to water-soluble ones, the difficulty large and highly charged molecules face in passing through, the increased permeability of the BBB during inflammation, and the theoretical ability of nasally administered drugs to bypass the BBB.

It is important to remember the specific circumventricular organs where the BBB is fenestrated, including the posterior pituitary and the area postrema. Understanding the BBB’s function and characteristics is essential for medical professionals to diagnose and treat neurological disorders effectively.

Norepinephrine: Synthesis, Release, and Breakdown

Norepinephrine is synthesized from tyrosine through a series of enzymatic reactions. The first step involves the conversion of tyrosine to L-DOPA by tyrosine hydroxylase. L-DOPA is then converted to dopamine by DOPA decarboxylase. Dopamine is further converted to norepinephrine by dopamine beta-hydroxylase. Finally, norepinephrine is converted to epinephrine by phenylethanolamine-N-methyltransferase.

The primary site of norepinephrine release is the locus coeruleus, also known as the blue spot, which is located in the pons. Once released, norepinephrine is broken down by two enzymes: catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO). These enzymes play a crucial role in regulating the levels of norepinephrine in the body.

Hemiballismus is an uncommon condition that arises following a stroke affecting the basal ganglia, particularly the subthalamic nucleus. It is typically identified by uncontrolled flinging movements of the limbs, which can be forceful and have a broad range of motion. These movements are unpredictable and ongoing, and may affect either the proximal or distal muscles on one side of the body.

The Basal Ganglia: Functions and Disorders

The basal ganglia are a group of subcortical structures that play a crucial role in controlling movement and some cognitive processes. The components of the basal ganglia include the striatum (caudate, putamen, nucleus accumbens), subthalamic nucleus, globus pallidus, and substantia nigra (divided into pars compacta and pars reticulata). The putamen and globus pallidus are collectively referred to as the lenticular nucleus.

The basal ganglia are connected in a complex loop, with the cortex projecting to the striatum, the striatum to the internal segment of the globus pallidus, the internal segment of the globus pallidus to the thalamus, and the thalamus back to the cortex. This loop is responsible for regulating movement and cognitive processes.

However, problems with the basal ganglia can lead to several conditions. Huntington’s chorea is caused by degeneration of the caudate nucleus, while Wilson’s disease is characterized by copper deposition in the basal ganglia. Parkinson’s disease is associated with degeneration of the substantia nigra, and hemiballism results from damage to the subthalamic nucleus.

In summary, the basal ganglia are a crucial part of the brain that regulate movement and some cognitive processes. Disorders of the basal ganglia can lead to significant neurological conditions that affect movement and other functions.

The trigeminal nerve, which is the largest cranial nerve, serves both sensory and motor functions. It is composed of three primary branches, namely the ophthalmic, maxillary, and mandibular branches. This nerve is responsible for providing sensory information to the face and head, while also controlling the muscles involved in chewing. On the other hand, the facial nerve is responsible for controlling the muscles that enable facial expressions and transmitting information from the front two-thirds of the tongue.

Overview of Cranial Nerves and Their Functions

The cranial nerves are a complex system of nerves that originate from the brain and control various functions of the head and neck. There are twelve cranial nerves, each with a specific function and origin. The following table provides a simplified overview of the cranial nerves, including their origin, skull exit, modality, and functions.

The first cranial nerve, the olfactory nerve, originates from the telencephalon and exits through the cribriform plate. It is a sensory nerve that controls the sense of smell. The second cranial nerve, the optic nerve, originates from the diencephalon and exits through the optic foramen. It is a sensory nerve that controls vision.

The third cranial nerve, the oculomotor nerve, originates from the midbrain and exits through the superior orbital fissure. It is a motor nerve that controls eye movement, pupillary constriction, and lens accommodation. The fourth cranial nerve, the trochlear nerve, also originates from the midbrain and exits through the superior orbital fissure. It is a motor nerve that controls eye movement.

The fifth cranial nerve, the trigeminal nerve, originates from the pons and exits through different foramina depending on the division. It is a mixed nerve that controls chewing and sensation of the anterior 2/3 of the scalp. It also tenses the tympanic membrane to dampen loud noises.

The sixth cranial nerve, the abducens nerve, originates from the pons and exits through the superior orbital fissure. It is a motor nerve that controls eye movement. The seventh cranial nerve, the facial nerve, also originates from the pons and exits through the internal auditory canal. It is a mixed nerve that controls facial expression, taste of the anterior 2/3 of the tongue, and tension on the stapes to dampen loud noises.

The eighth cranial nerve, the vestibulocochlear nerve, originates from the pons and exits through the internal auditory canal. It is a sensory nerve that controls hearing. The ninth cranial nerve, the glossopharyngeal nerve, originates from the medulla and exits through the jugular foramen. It is a mixed nerve that controls taste of the posterior 1/3 of the tongue, elevation of the larynx and pharynx, and swallowing.

The tenth cranial nerve, the vagus nerve, also originates from the medulla and exits through the jugular foramen. It is a mixed nerve that controls swallowing, voice production, and parasympathetic supply to nearly all thoracic and abdominal viscera. The eleventh cranial nerve, the accessory nerve, originates from the medulla and exits through the jugular foramen. It is a motor nerve that controls shoulder shrugging and head turning.

The twelfth cranial nerve, the hypoglossal nerve, originates from the medulla and exits through the hypoglossal canal. It is a motor nerve that controls tongue movement. Overall, the cranial nerves play a crucial role in controlling various functions of the head and neck, and any damage of dysfunction can have significant consequences.

The use of HAART has led to a complete elimination of new cases of toxoplasmosis in individuals who are HIV positive. Studies conducted on the Edinburgh cohort have revealed a significant decrease in the occurrence of CMV by 50% during autopsy, a 68% reduction in HIVE, and complete eradication of toxoplasmosis. However, there has been a slight increase in the incidence of PML and lymphoma in this group and other samples.

Hirano bodies, Pick bodies, Lewy bodies, Negri bodies, and Barr bodies are all types of inclusion bodies that can be seen in various cells. Hirano bodies are rod-shaped structures found in the cytoplasm of neurons, composed of actin and other proteins. They are commonly seen in the hippocampus, along with granulovacuolar degeneration, which may represent lysosomal accumulations within neuronal cytoplasm. The clinical significance of these microscopic features is not yet fully understood. Pick bodies are masses of cytoskeletal elements seen in Pick’s disease, while Lewy bodies are abnormal protein aggregates that develop in nerve cells in Lewy body disease. Negri bodies are inclusion bodies seen in rabies, and Barr bodies are inactive X chromosomes in a female somatic cell.

Delta waves are typically observed during stages III and IV of deep sleep and their presence outside of these stages can indicate diffuse slowing and encephalopathy.

Electroencephalography

Electroencephalography (EEG) is a clinical test that records the brain’s spontaneous electrical activity over a short period of time using multiple electrodes placed on the scalp. It is mainly used to rule out organic conditions and can help differentiate dementia from other disorders such as metabolic encephalopathies, CJD, herpes encephalitis, and non-convulsive status epilepticus. EEG can also distinguish possible psychotic episodes and acute confusional states from non-convulsive status epilepticus.

Not all abnormal EEGs represent an underlying condition, and psychotropic medications can affect EEG findings. EEG abnormalities can also be triggered purposely by activation procedures such as hyperventilation, photic stimulation, certain drugs, and sleep deprivation.

Specific waveforms are seen in an EEG, including delta, theta, alpha, sigma, beta, and gamma waves. Delta waves are found frontally in adults and posteriorly in children during slow wave sleep, and excessive amounts when awake may indicate pathology. Theta waves are generally seen in young children, drowsy and sleeping adults, and during meditation. Alpha waves are seen posteriorly when relaxed and when the eyes are closed, and are also seen in meditation. Sigma waves are bursts of oscillatory activity that occur in stage 2 sleep. Beta waves are seen frontally when busy of concentrating, and gamma waves are seen in advanced/very experienced meditators.

Certain conditions are associated with specific EEG changes, such as nonspecific slowing in early CJD, low voltage EEG in Huntington’s, diffuse slowing in encephalopathy, and reduced alpha and beta with increased delta and theta in Alzheimer’s.

Common epileptiform patterns include spikes, spike/sharp waves, and spike-waves. Medications can have important effects on EEG findings, with clozapine decreasing alpha and increasing delta and theta, lithium increasing all waveforms, lamotrigine decreasing all waveforms, and valproate having inconclusive effects on delta and theta and increasing beta.

Overall, EEG is a useful tool in clinical contexts for ruling out organic conditions and differentiating between various disorders.

Multisystem Atrophy: A Parkinson Plus Syndrome

Multisystem atrophy is a type of Parkinson plus syndrome that is characterized by three main features: Parkinsonism, autonomic failure, and cerebellar ataxia. It can present in three different ways, including Shy-Drager Syndrome, Striatonigral degeneration, and Olivopontocerebellar atrophy, each with varying degrees of the three main features.

Macroscopic features of multisystem atrophy include pallor of the substantia nigra, greenish discoloration and atrophy of the putamen, and cerebellar atrophy. Microscopic features include the presence of Papp-Lantos bodies, which are alpha-synuclein inclusions found in oligodendrocytes in the substantia nigra, cerebellum, and basal ganglia.

Overall, multisystem atrophy is a complex and debilitating condition that affects multiple systems in the body, leading to a range of symptoms and challenges for patients and their caregivers.

Anton’s syndrome, also known as Anton-Babinski syndrome, is a condition that results from damage to the occipital lobe. People with this syndrome are cortically blind, but they are not aware of it and deny having any problem, a condition known as anosognosia. They may start falling over furniture as they cannot see, but they believe they can still see and describe their surroundings in detail, even though their descriptions are incorrect (confabulation). This syndrome is characterized by a lack of awareness of visual impairment, which can lead to significant difficulties in daily life.

The Cerebellum: Anatomy and Function

The cerebellum is a part of the brain that consists of two hemispheres and a median vermis. It is separated from the cerebral hemispheres by the tentorium cerebelli and connected to the brain stem by the cerebellar peduncles. Anatomically, it is divided into three lobes: the flocculonodular lobe, anterior lobe, and posterior lobe. Functionally, it is divided into three regions: the vestibulocerebellum, spinocerebellum, and cerebrocerebellum.

The vestibulocerebellum, located in the flocculonodular lobe, is responsible for balance and spatial orientation. The spinocerebellum, located in the medial section of the anterior and posterior lobes, is involved in fine-tuned body movements. The cerebrocerebellum, located in the lateral section of the anterior and posterior lobes, is involved in planning movement and the conscious assessment of movement.

Overall, the cerebellum plays a crucial role in motor coordination and control. Its different regions and lobes work together to ensure smooth and precise movements of the body.

The striatum is composed of the caudate nucleus and putamen, which are part of the basal ganglia. The basal ganglia is the largest subcortical structure in the brain and consists of a group of grey matter nuclei located in the subcortical area. In contrast, the mammillary bodies are small round bodies that are part of the hypothalamus and play a crucial role in the Papez circuit as a component of the limbic system.

Medial temporal lobe atrophy (MTA) is prevalent in 80% to 90% of individuals diagnosed with Alzheimer’s dementia, and can also be present in other forms of dementia, albeit less frequently and severely. MTA is an early and relatively reliable indicator of Alzheimer’s disease, although it is not exclusive to this condition.

The Basal Ganglia: Functions and Disorders

The basal ganglia are a group of subcortical structures that play a crucial role in controlling movement and some cognitive processes. The components of the basal ganglia include the striatum (caudate, putamen, nucleus accumbens), subthalamic nucleus, globus pallidus, and substantia nigra (divided into pars compacta and pars reticulata). The putamen and globus pallidus are collectively referred to as the lenticular nucleus.

The basal ganglia are connected in a complex loop, with the cortex projecting to the striatum, the striatum to the internal segment of the globus pallidus, the internal segment of the globus pallidus to the thalamus, and the thalamus back to the cortex. This loop is responsible for regulating movement and cognitive processes.

However, problems with the basal ganglia can lead to several conditions. Huntington’s chorea is caused by degeneration of the caudate nucleus, while Wilson’s disease is characterized by copper deposition in the basal ganglia. Parkinson’s disease is associated with degeneration of the substantia nigra, and hemiballism results from damage to the subthalamic nucleus.

In summary, the basal ganglia are a crucial part of the brain that regulate movement and some cognitive processes. Disorders of the basal ganglia can lead to significant neurological conditions that affect movement and other functions.

Norepinephrine: Synthesis, Release, and Breakdown

Norepinephrine is synthesized from tyrosine through a series of enzymatic reactions. The first step involves the conversion of tyrosine to L-DOPA by tyrosine hydroxylase. L-DOPA is then converted to dopamine by DOPA decarboxylase. Dopamine is further converted to norepinephrine by dopamine beta-hydroxylase. Finally, norepinephrine is converted to epinephrine by phenylethanolamine-N-methyltransferase.

The primary site of norepinephrine release is the locus coeruleus, also known as the blue spot, which is located in the pons. Once released, norepinephrine is broken down by two enzymes: catechol-O-methyltransferase (COMT) and monoamine oxidase (MAO). These enzymes play a crucial role in regulating the levels of norepinephrine in the body.

Broca’s aphasia is also known as non-fluent aphasia, while Wernicke’s aphasia is referred to as fluent aphasia.

Broca’s and Wernicke’s are two types of expressive dysphasia, which is characterized by difficulty producing speech despite intact comprehension. Dysarthria is a type of expressive dysphasia caused by damage to the speech production apparatus, while Broca’s aphasia is caused by damage to the area of the brain responsible for speech production, specifically Broca’s area located in Brodmann areas 44 and 45. On the other hand, Wernicke’s aphasia is a type of receptive of fluent aphasia caused by damage to the comprehension of speech, while the actual production of speech remains normal. Wernicke’s area is located in the posterior part of the superior temporal gyrus in the dominant hemisphere, within Brodmann area 22.

Neurotransmitters are substances used by neurons to communicate with each other and with target tissues. They are synthesized and released from nerve endings into the synaptic cleft, where they bind to receptor proteins in the cellular membrane of the target tissue. Neurotransmitters can be classified into different types, including small molecules (such as acetylcholine, dopamine, norepinephrine, serotonin, and GABA) and large molecules (such as neuropeptides). They can also be classified as excitatory or inhibitory. Receptors can be ionotropic or metabotropic, and the effects of neurotransmitters can be fast of slow. Some important neurotransmitters include acetylcholine, dopamine, GABA, norepinephrine, and serotonin. Each neurotransmitter has a specific synthesis, breakdown, and receptor type. Understanding neurotransmitters is important for understanding the function of the nervous system and for developing treatments for neurological and psychiatric disorders.

Overview of Cranial Nerves and Their Functions

The cranial nerves are a complex system of nerves that originate from the brain and control various functions of the head and neck. There are twelve cranial nerves, each with a specific function and origin. The following table provides a simplified overview of the cranial nerves, including their origin, skull exit, modality, and functions.

The first cranial nerve, the olfactory nerve, originates from the telencephalon and exits through the cribriform plate. It is a sensory nerve that controls the sense of smell. The second cranial nerve, the optic nerve, originates from the diencephalon and exits through the optic foramen. It is a sensory nerve that controls vision.

The third cranial nerve, the oculomotor nerve, originates from the midbrain and exits through the superior orbital fissure. It is a motor nerve that controls eye movement, pupillary constriction, and lens accommodation. The fourth cranial nerve, the trochlear nerve, also originates from the midbrain and exits through the superior orbital fissure. It is a motor nerve that controls eye movement.

The fifth cranial nerve, the trigeminal nerve, originates from the pons and exits through different foramina depending on the division. It is a mixed nerve that controls chewing and sensation of the anterior 2/3 of the scalp. It also tenses the tympanic membrane to dampen loud noises.

The sixth cranial nerve, the abducens nerve, originates from the pons and exits through the superior orbital fissure. It is a motor nerve that controls eye movement. The seventh cranial nerve, the facial nerve, also originates from the pons and exits through the internal auditory canal. It is a mixed nerve that controls facial expression, taste of the anterior 2/3 of the tongue, and tension on the stapes to dampen loud noises.

The eighth cranial nerve, the vestibulocochlear nerve, originates from the pons and exits through the internal auditory canal. It is a sensory nerve that controls hearing. The ninth cranial nerve, the glossopharyngeal nerve, originates from the medulla and exits through the jugular foramen. It is a mixed nerve that controls taste of the posterior 1/3 of the tongue, elevation of the larynx and pharynx, and swallowing.

The tenth cranial nerve, the vagus nerve, also originates from the medulla and exits through the jugular foramen. It is a mixed nerve that controls swallowing, voice production, and parasympathetic supply to nearly all thoracic and abdominal viscera. The eleventh cranial nerve, the accessory nerve, originates from the medulla and exits through the jugular foramen. It is a motor nerve that controls shoulder shrugging and head turning.

The twelfth cranial nerve, the hypoglossal nerve, originates from the medulla and exits through the hypoglossal canal. It is a motor nerve that controls tongue movement. Overall, the cranial nerves play a crucial role in controlling various functions of the head and neck, and any damage of dysfunction can have significant consequences.

CJD has several subtypes, including familial (fCJD), iatrogenic (iCJD), sporadic (sCJD), and new variant (vCJD). The most common subtype is sCJD, which makes up 85% of cases. sCJD can be further classified based on the MV polymorphisms at codon 129 of the PRNP gene, with sCJDMM1 and sCJDMV1 being the most prevalent subtypes. fCJD is the most common subtype after sCJD, while vCJD and iCJD are rare and caused by consuming contaminated food of tissue contamination from other humans, respectively.

Tyrosine is converted to L-DOPA by the enzyme tyrosine hydroxylase. L-DOPA is then converted to dopamine by the enzyme dopa decarboxylase.

Neurotransmitters are substances used by neurons to communicate with each other and with target tissues. They are synthesized and released from nerve endings into the synaptic cleft, where they bind to receptor proteins in the cellular membrane of the target tissue. Neurotransmitters can be classified into different types, including small molecules (such as acetylcholine, dopamine, norepinephrine, serotonin, and GABA) and large molecules (such as neuropeptides). They can also be classified as excitatory or inhibitory. Receptors can be ionotropic or metabotropic, and the effects of neurotransmitters can be fast of slow. Some important neurotransmitters include acetylcholine, dopamine, GABA, norepinephrine, and serotonin. Each neurotransmitter has a specific synthesis, breakdown, and receptor type. Understanding neurotransmitters is important for understanding the function of the nervous system and for developing treatments for neurological and psychiatric disorders.

The pituitary gland is situated in the sella turcica, while the suprachiasmatic nucleus regulates circadian rhythms. Serotonin release in the brain is primarily sourced from the neurons of the raphe nuclei, which are located along the midline of the brainstem. The choroid plexus produces cerebrospinal fluid, and enterochromaffin cells in the gut contain the majority of the body’s serotonin.

Serotonin: Synthesis and Breakdown

Serotonin, also known as 5-Hydroxytryptamine (5-HT), is synthesized in the central nervous system (CNS) in the raphe nuclei located in the brainstem, as well as in the gastrointestinal (GI) tract in enterochromaffin cells. The amino acid L-tryptophan, obtained from the diet, is used to synthesize serotonin. L-tryptophan can cross the blood-brain barrier, but serotonin cannot.

The transformation of L-tryptophan into serotonin involves two steps. First, hydroxylation to 5-hydroxytryptophan is catalyzed by tryptophan hydroxylase. Second, decarboxylation of 5-hydroxytryptophan to serotonin (5-hydroxytryptamine) is catalyzed by L-aromatic amino acid decarboxylase.

Serotonin is taken up from the synapse by a monoamine transporter (SERT). Substances that block this transporter include MDMA, amphetamine, cocaine, TCAs, and SSRIs. Serotonin is broken down by monoamine oxidase (MAO) and then by aldehyde dehydrogenase to 5-Hydroxyindoleacetic acid (5-HIAA).

Gerstmann’s Syndrome: Symptoms and Brain Lesions

Gerstmann’s syndrome is a condition that is characterized by several symptoms, including dyscalculia, dysgraphia, finger agnosia, and right-left disorientation. Patients with this syndrome have been found to have lesions in areas such as the left frontal posterior, left parietal, temporal, and occipital lobes. The left angular gyrus, which is located at the junction of the temporal, occipital, and parietal lobes, seems to be the main area of overlap. Although the function of the angular gyrus is not well understood, it is believed to be involved in various functions such as calculation, spatial reasoning, understanding of ordinal concepts, and comprehension of metaphors.

Posterior inferior cerebellar artery occlusion/infarct, also known as Wallenberg’s syndrome of lateral medullary syndrome, can cause a sudden onset of dizziness and vomiting. It can also result in ipsilateral facial sensory loss, specifically for pain and temperature, and contralateral sensory loss for pain and temperature of the limbs and trunk. Nystagmus to the side of the lesion, ipsilateral limb ataxia, dysphagia, and dysarthria are also common symptoms. Additionally, this condition can cause ipsilateral pharyngeal and laryngeal paralysis.

Brain Blood Supply and Consequences of Occlusion

The brain receives blood supply from the internal carotid and vertebral arteries, which form the circle of Willis. The circle of Willis acts as a shunt system in case of vessel damage. The three main vessels arising from the circle are the anterior cerebral artery (ACA), middle cerebral artery (MCA), and posterior cerebral artery (PCA). Occlusion of these vessels can result in various neurological deficits. ACA occlusion may cause hemiparesis of the contralateral foot and leg, sensory loss, and frontal signs. MCA occlusion is the most common and can lead to hemiparesis, dysphasia/aphasia, neglect, and visual field defects. PCA occlusion may cause alexia, loss of sensation, hemianopia, prosopagnosia, and cranial nerve defects. It is important to recognize these consequences to provide appropriate treatment.

Lurasidone may cause akathisia and sedation as common side effects, which can vary based on the dosage. Its metabolic profile is neutral. However, doses lower than 37 mg are unlikely to produce desired results.

This question is a common one, but it is worded in various ways each time.

Neuroimaging Findings in Obsessive-Compulsive Disorder (OCD)

Obsessive-compulsive disorder (OCD) is a mental disorder characterized by intrusive thoughts (obsessions) and repetitive behaviors (compulsions). Neuroimaging studies have been conducted to investigate the underlying neural mechanisms of OCD. Two commonly used techniques are 18 Fluorodeoxyglucose PET (FDG-PET) and Technetium-99m (99mTc)-hexamethylpropyleneamine-oxime SPECT (HMPAO-SPECT).

Studies using FDG-PET have reported increased glucose metabolism in several brain regions among OCD patients, including the orbitofrontal cortex (OFC), caudate, thalamus, prefrontal cortex, and anterior cingulate. These regions are involved in cognitive and emotional processing, decision-making, and motor control. The increased activity in these regions may contribute to the symptoms of OCD, such as repetitive behaviors and difficulty controlling intrusive thoughts.

On the other hand, studies using HMPAO-SPECT have found both increased and decreased blood flow to various brain regions in OCD patients compared to normal controls. These regions include the OFC, caudate, various areas of the cortex, and thalamus. The inconsistent findings may be due to differences in the severity and subtype of OCD, as well as the specific task of stimulus used in the imaging studies.

Overall, neuroimaging studies have provided valuable insights into the neural mechanisms of OCD. However, further research is needed to better understand the complex interactions between different brain regions and how they contribute to the development and maintenance of OCD symptoms.

Kluver-Bucy Syndrome: Causes and Symptoms

Kluver-Bucy syndrome is a neurological disorder that results from bilateral medial temporal lobe dysfunction, particularly in the amygdala. This condition is characterized by a range of symptoms, including hyperorality (a tendency to explore objects with the mouth), hypersexuality, docility, visual agnosia, and dietary changes.

The most common causes of Kluver-Bucy syndrome include herpes, late-stage Alzheimer’s disease, frontotemporal dementia, trauma, and bilateral temporal lobe infarction. In some cases, the condition may be reversible with treatment, but in others, it may be permanent and require ongoing management. If you of someone you know is experiencing symptoms of Kluver-Bucy syndrome, it is important to seek medical attention promptly to determine the underlying cause and develop an appropriate treatment plan.

Serotonin: Synthesis and Breakdown

Serotonin, also known as 5-Hydroxytryptamine (5-HT), is synthesized in the central nervous system (CNS) in the raphe nuclei located in the brainstem, as well as in the gastrointestinal (GI) tract in enterochromaffin cells. The amino acid L-tryptophan, obtained from the diet, is used to synthesize serotonin. L-tryptophan can cross the blood-brain barrier, but serotonin cannot.

The transformation of L-tryptophan into serotonin involves two steps. First, hydroxylation to 5-hydroxytryptophan is catalyzed by tryptophan hydroxylase. Second, decarboxylation of 5-hydroxytryptophan to serotonin (5-hydroxytryptamine) is catalyzed by L-aromatic amino acid decarboxylase.

Serotonin is taken up from the synapse by a monoamine transporter (SERT). Substances that block this transporter include MDMA, amphetamine, cocaine, TCAs, and SSRIs. Serotonin is broken down by monoamine oxidase (MAO) and then by aldehyde dehydrogenase to 5-Hydroxyindoleacetic acid (5-HIAA).

Frontotemporal lobar degeneration results in the specific shrinking of the frontal and temporal lobes.

Frontotemporal Lobar Degeneration (FTLD) is a pathological term that refers to a group of neurodegenerative disorders that affect the frontal and temporal lobes of the brain. FTLD is classified into several subtypes based on the main protein component of neuronal and glial abnormal inclusions and their distribution. The three main proteins associated with FTLD are Tau, TDP-43, and FUS. Each FTD clinical phenotype has been associated with different proportions of these proteins. Macroscopic changes in FTLD include atrophy of the frontal and temporal lobes, with focal gyral atrophy that resembles knives. Microscopic changes in FTLD-Tau include neuronal and glial tau aggregation, with further sub-classification based on the existence of different isoforms of tau protein. FTLD-TDP is characterized by cytoplasmic inclusions of TDP-43 in neurons, while FTLD-FUS is characterized by cytoplasmic inclusions of FUS.

Cerebrospinal Fluid: Formation, Circulation, and Composition

Cerebrospinal fluid (CSF) is produced by ependymal cells in the choroid plexus of the lateral, third, and fourth ventricles. It is constantly reabsorbed, so only a small amount is present at any given time. CSF occupies the space between the arachnoid and pia mater and passes through various foramina and aqueducts to reach the subarachnoid space and spinal cord. It is then reabsorbed by the arachnoid villi and enters the dural venous sinuses.

The normal intracerebral pressure (ICP) is 5 to 15 mmHg, and the rate of formation of CSF is constant. The composition of CSF is similar to that of brain extracellular fluid (ECF) but different from plasma. CSF has a higher pCO2, lower pH, lower protein content, lower glucose concentration, higher chloride and magnesium concentration, and very low cholesterol content. The concentration of calcium and potassium is lower, while the concentration of sodium is unchanged.

CSF fulfills the role of returning interstitial fluid and protein to the circulation since there are no lymphatic channels in the brain. The blood-brain barrier separates CSF from blood, and only lipid-soluble substances can easily cross this barrier, maintaining the compositional differences.

Pancreatic Hormones: Functions and Production

The pancreas serves as both an exocrine and endocrine gland. Its endocrine function involves the production of four distinct hormones from the islets of Langerhans. These hormones include somatostatin, insulin, pancreatic polypeptide, and glucagon. Somatostatin is also produced by the brain, specifically the hypothalamus, where it inhibits the secretion of thyroid-stimulating hormone and growth hormone from somatotroph cells.

Kluver-Bucy syndrome is a neurological disorder that results from dysfunction in both the right and left medial temporal lobes of the brain. This condition is characterized by a range of symptoms, including docility, altered dietary habits, hyperorality, and changes in sexual behavior. Additionally, individuals with Kluver-Bucy syndrome may experience visual agnosia, which is a condition that impairs their ability to recognize and interpret visual stimuli.

Sigma waves are typically observed during stage 2 sleep and are considered a normal occurrence during sleep. They usually follow muscle twitches and are believed to help maintain a peaceful state during sleep. These waves are produced in the reticular nucleus of the thalamus and arise from the interplay between the thalamus and the cortex. However, in familial fatal insomnia (a prion disease), the absence of sigma waves is a characteristic feature.

Electroencephalography

Electroencephalography (EEG) is a clinical test that records the brain’s spontaneous electrical activity over a short period of time using multiple electrodes placed on the scalp. It is mainly used to rule out organic conditions and can help differentiate dementia from other disorders such as metabolic encephalopathies, CJD, herpes encephalitis, and non-convulsive status epilepticus. EEG can also distinguish possible psychotic episodes and acute confusional states from non-convulsive status epilepticus.

Not all abnormal EEGs represent an underlying condition, and psychotropic medications can affect EEG findings. EEG abnormalities can also be triggered purposely by activation procedures such as hyperventilation, photic stimulation, certain drugs, and sleep deprivation.

Specific waveforms are seen in an EEG, including delta, theta, alpha, sigma, beta, and gamma waves. Delta waves are found frontally in adults and posteriorly in children during slow wave sleep, and excessive amounts when awake may indicate pathology. Theta waves are generally seen in young children, drowsy and sleeping adults, and during meditation. Alpha waves are seen posteriorly when relaxed and when the eyes are closed, and are also seen in meditation. Sigma waves are bursts of oscillatory activity that occur in stage 2 sleep. Beta waves are seen frontally when busy of concentrating, and gamma waves are seen in advanced/very experienced meditators.

Certain conditions are associated with specific EEG changes, such as nonspecific slowing in early CJD, low voltage EEG in Huntington’s, diffuse slowing in encephalopathy, and reduced alpha and beta with increased delta and theta in Alzheimer’s.

Common epileptiform patterns include spikes, spike/sharp waves, and spike-waves. Medications can have important effects on EEG findings, with clozapine decreasing alpha and increasing delta and theta, lithium increasing all waveforms, lamotrigine decreasing all waveforms, and valproate having inconclusive effects on delta and theta and increasing beta.

Overall, EEG is a useful tool in clinical contexts for ruling out organic conditions and differentiating between various disorders.

Glutamate is the primary neurotransmitter responsible for excitatory signaling in the brain.

Glutamate: The Most Abundant Neurotransmitter in the Brain

Glutamate is a neurotransmitter that is found in abundance in the brain. It is always excitatory and can act through both ionotropic and metabotropic receptors. This neurotransmitter is believed to play a crucial role in learning and memory processes. Its ability to stimulate neurons and enhance synaptic plasticity is thought to be responsible for its role in memory formation. Glutamate is also involved in various other brain functions, including motor control, sensory perception, and emotional regulation. Its importance in the brain makes it a target for various neurological disorders, including Alzheimer’s disease, Parkinson’s disease, and epilepsy.

White matter is the cabling that links different parts of the CNS together. There are three types of white matter cables: projection tracts, commissural tracts, and association tracts. Projection tracts connect higher centers of the brain with lower centers, commissural tracts connect the two hemispheres together, and association tracts connect regions of the same hemisphere. Some common tracts include the corticospinal tract, which connects the motor cortex to the brainstem and spinal cord, and the corpus callosum, which is the largest white matter fiber bundle connecting corresponding areas of cortex between the hemispheres. Other tracts include the cingulum, superior and inferior occipitofrontal fasciculi, and the superior and inferior longitudinal fasciculi.

Neurotransmitters are substances used by neurons to communicate with each other and with target tissues. They are synthesized and released from nerve endings into the synaptic cleft, where they bind to receptor proteins in the cellular membrane of the target tissue. Neurotransmitters can be classified into different types, including small molecules (such as acetylcholine, dopamine, norepinephrine, serotonin, and GABA) and large molecules (such as neuropeptides). They can also be classified as excitatory or inhibitory. Receptors can be ionotropic or metabotropic, and the effects of neurotransmitters can be fast of slow. Some important neurotransmitters include acetylcholine, dopamine, GABA, norepinephrine, and serotonin. Each neurotransmitter has a specific synthesis, breakdown, and receptor type. Understanding neurotransmitters is important for understanding the function of the nervous system and for developing treatments for neurological and psychiatric disorders.

Nitric Oxide and Depression

Recent research has indicated that nitric oxide (NO) may play a role in the development of depression. Inhibitors of NO synthase have been found to exhibit antidepressant-like effects in preclinical studies, suggesting that NO may be involved in the pathogenesis of depression. These findings suggest that targeting NO signaling pathways may be a potential therapeutic approach for treating depression. Further research is needed to fully understand the role of NO in depression and to develop effective treatments based on this knowledge.

This question is presented in two variations on the exam, with one implying that auras are primarily linked to temporal lobe epilepsy and the other to complex partial seizures. In reality, partial seizures are most commonly associated with auras compared to other types of seizures. While partial seizures can originate in any lobe of the brain, those that arise in the temporal lobe are most likely to produce an aura. Therefore, both versions of the question are accurate.

Epilepsy and Aura

An aura is a subjective sensation that is a type of simple partial seizure. It typically lasts only a few seconds and can help identify the site of cortical onset. There are eight recognized types of auras, including somatosensory, visual, auditory, gustatory, olfactory, autonomic, abdominal, and psychic.

In about 80% of cases, auras precede temporal lobe seizures. The most common auras in these seizures are abdominal and psychic, which can cause a rising epigastric sensation of feelings of fear, déjà vu, of jamais vu. Parietal lobe seizures may begin with a contralateral sensation, usually of the positive type, such as an electrical sensation of tingling. Occipital lobe seizures may begin with contralateral visual changes, such as colored lines, spots, of shapes, of even a loss of vision. Temporal-parietal-occipital seizures may produce more formed auras.

Complex partial seizures are defined by impairment of consciousness, which means decreased responsiveness and awareness of oneself and surroundings. During a complex partial seizure, a patient is unresponsive and does not remember events that occurred.

The Neuroscience of Morality

Morality is a process that involves both instinctive feelings and rational judgement. The ventromedial prefrontal cortex (PFC) is responsible for the emotional baseline, while the dorsolateral PFC is involved in cognitive control and problem solving. Studies have shown that the ventromedial PFC is activated during the solving of moral problems, particularly when responding to emotionally charged scenarios. On the other hand, the dorsolateral PFC is involved in tamping down our innate, reactionary moral system. These findings suggest that morality is a dual process event that involves both emotional and cognitive systems in the brain.

The density of striatal dopamine transporters in individuals with ADHD is influenced by their prior exposure to psychostimulants. ADHD is a complex disorder that involves dysfunction in multiple neurotransmitter systems, including dopamine, adrenergic, cholinergic, and serotonergic systems. Dopamine systems have received significant attention due to their role in regulating psychomotor activity, motivation, inhibition, and attention. Psychostimulants increase dopamine availability by blocking striatal dopamine transporters. Individuals with untreated ADHD have lower levels of dopamine transporters, while those who have received psychostimulants have higher levels.

Neurofibrillary tangles and neuritic (senile) plaques are commonly found in the brains of elderly individuals, but they are not present in Lewy body dementia. Pick’s disease is characterized by the presence of Pick’s bodies and knife blade atrophy. Creutzfeldt-Jakob disease (CJD) is identified by the spongy appearance of the grey matter in the cerebral cortex due to multiple vacuoles. If an individual experiences short-term memory problems that affect their daily life, it may indicate the presence of dementia. Alzheimer’s disease is characterized by extensive tangles and plaques in the brain.

Neurotransmitters are substances used by neurons to communicate with each other and with target tissues. They are synthesized and released from nerve endings into the synaptic cleft, where they bind to receptor proteins in the cellular membrane of the target tissue. Neurotransmitters can be classified into different types, including small molecules (such as acetylcholine, dopamine, norepinephrine, serotonin, and GABA) and large molecules (such as neuropeptides). They can also be classified as excitatory or inhibitory. Receptors can be ionotropic or metabotropic, and the effects of neurotransmitters can be fast of slow. Some important neurotransmitters include acetylcholine, dopamine, GABA, norepinephrine, and serotonin. Each neurotransmitter has a specific synthesis, breakdown, and receptor type. Understanding neurotransmitters is important for understanding the function of the nervous system and for developing treatments for neurological and psychiatric disorders.

Depression, suicidality, and aggression have been linked to low levels of 5-HIAA in the CSF.

The Significance of 5-HIAA in Depression and Aggression

During the 1980s, there was a brief period of interest in 5-hydroxyindoleacetic acid (5-HIAA), a serotonin metabolite. Studies found that up to a third of people with depression had low concentrations of 5-HIAA in their cerebrospinal fluid (CSF), while very few normal controls did. This suggests that 5-HIAA may play a role in depression.

Furthermore, individuals with low CSF levels of 5-HIAA have been found to respond less effectively to antidepressants and are more likely to commit suicide. This finding has been replicated in multiple studies, indicating the significance of 5-HIAA in depression.

Low levels of 5-HIAA are also associated with increased levels of aggression. This suggests that 5-HIAA may play a role in regulating aggressive behavior. Overall, the research on 5-HIAA highlights its potential importance in understanding and treating depression and aggression.

The trigeminal nerve is responsible for controlling the muscles involved in chewing, while the glossopharyngeal nerves consist of both motor and sensory fibers that originate from nuclei in the medulla oblongata. The motor fibers of the glossopharyngeal nerves stimulate the pharyngeal muscles and parotid gland secretory cells, while the sensory fibers transmit impulses from the posterior third of the tongue, tonsils, and pharynx to the cerebral cortex.

Overview of Cranial Nerves and Their Functions

The cranial nerves are a complex system of nerves that originate from the brain and control various functions of the head and neck. There are twelve cranial nerves, each with a specific function and origin. The following table provides a simplified overview of the cranial nerves, including their origin, skull exit, modality, and functions.

The first cranial nerve, the olfactory nerve, originates from the telencephalon and exits through the cribriform plate. It is a sensory nerve that controls the sense of smell. The second cranial nerve, the optic nerve, originates from the diencephalon and exits through the optic foramen. It is a sensory nerve that controls vision.

The third cranial nerve, the oculomotor nerve, originates from the midbrain and exits through the superior orbital fissure. It is a motor nerve that controls eye movement, pupillary constriction, and lens accommodation. The fourth cranial nerve, the trochlear nerve, also originates from the midbrain and exits through the superior orbital fissure. It is a motor nerve that controls eye movement.

The fifth cranial nerve, the trigeminal nerve, originates from the pons and exits through different foramina depending on the division. It is a mixed nerve that controls chewing and sensation of the anterior 2/3 of the scalp. It also tenses the tympanic membrane to dampen loud noises.

The sixth cranial nerve, the abducens nerve, originates from the pons and exits through the superior orbital fissure. It is a motor nerve that controls eye movement. The seventh cranial nerve, the facial nerve, also originates from the pons and exits through the internal auditory canal. It is a mixed nerve that controls facial expression, taste of the anterior 2/3 of the tongue, and tension on the stapes to dampen loud noises.

The eighth cranial nerve, the vestibulocochlear nerve, originates from the pons and exits through the internal auditory canal. It is a sensory nerve that controls hearing. The ninth cranial nerve, the glossopharyngeal nerve, originates from the medulla and exits through the jugular foramen. It is a mixed nerve that controls taste of the posterior 1/3 of the tongue, elevation of the larynx and pharynx, and swallowing.

The tenth cranial nerve, the vagus nerve, also originates from the medulla and exits through the jugular foramen. It is a mixed nerve that controls swallowing, voice production, and parasympathetic supply to nearly all thoracic and abdominal viscera. The eleventh cranial nerve, the accessory nerve, originates from the medulla and exits through the jugular foramen. It is a motor nerve that controls shoulder shrugging and head turning.

The twelfth cranial nerve, the hypoglossal nerve, originates from the medulla and exits through the hypoglossal canal. It is a motor nerve that controls tongue movement. Overall, the cranial nerves play a crucial role in controlling various functions of the head and neck, and any damage of dysfunction can have significant consequences.

Glial Cells: The Support System of the Central Nervous System

The central nervous system is composed of two basic cell types: neurons and glial cells. Glial cells, also known as support cells, play a crucial role in maintaining the health and function of neurons. There are several types of glial cells, including macroglia (astrocytes and oligodendrocytes), ependymal cells, and microglia.

Astrocytes are the most abundant type of glial cell and have numerous functions, such as providing structural support, repairing nervous tissue, nourishing neurons, contributing to the blood-brain barrier, and regulating neurotransmission and blood flow. There are two main types of astrocytes: protoplasmic and fibrous.

Oligodendrocytes are responsible for the formation of myelin sheaths, which insulate and protect axons, allowing for faster and more efficient transmission of nerve impulses.

Ependymal cells line the ventricular system and are involved in the circulation of cerebrospinal fluid (CSF) and fluid homeostasis in the brain. Specialized ependymal cells called choroid plexus cells produce CSF.

Microglia are the immune cells of the CNS and play a crucial role in protecting the brain from infection and injury. They also contribute to the maintenance of neuronal health and function.

In summary, glial cells are essential for the proper functioning of the central nervous system. They provide structural support, nourishment, insulation, and immune defense to neurons, ensuring the health and well-being of the brain and spinal cord.

Dementia pugilistica, also known as CTE, is categorized as a tauopathy, which is a type of neurodegenerative disease that involves the accumulation of tau protein into NFTs of gliofibrillary tangles in the brain. While it commonly occurs due to repeated brain injuries, it can also develop from a single traumatic event, as reported by Smith in 2013.

Dementia Pugilistica: A Neurodegenerative Condition Resulting from Neurotrauma

Dementia pugilistica, also known as chronic traumatic encephalopathy (CTE), is a neurodegenerative condition that results from neurotrauma. It is commonly seen in boxers and NFL players, but can also occur in anyone with neurotrauma. The condition is characterized by symptoms such as gait ataxia, slurred speech, impaired hearing, tremors, disequilibrium, neurobehavioral disturbances, and progressive cognitive decline.

Most cases of dementia pugilistica present with early onset cognitive deficits, and behavioral signs exhibited by patients include aggression, suspiciousness, paranoia, childishness, hypersexuality, depression, and restlessness. The progression of the condition leads to more prominent behavioral symptoms such as difficulty with impulse control, irritability, inappropriateness, and explosive outbursts of aggression.

Neuropathological abnormalities have been identified in CTE, with the most unique feature being the abnormal accumulation of tau in neurons and glia in an irregular, focal, perivascular distribution and at the depths of cortical sulci. Abnormalities of the septum pellucidum, such as cavum and fenestration, are also a common feature.

While the condition has become increasingly rare due to the progressive improvement in sports safety, it is important to recognize the potential long-term consequences of repeated head injuries and take steps to prevent them.

Neurotransmitters are substances used by neurons to communicate with each other and with target tissues. They are synthesized and released from nerve endings into the synaptic cleft, where they bind to receptor proteins in the cellular membrane of the target tissue. Neurotransmitters can be classified into different types, including small molecules (such as acetylcholine, dopamine, norepinephrine, serotonin, and GABA) and large molecules (such as neuropeptides). They can also be classified as excitatory or inhibitory. Receptors can be ionotropic or metabotropic, and the effects of neurotransmitters can be fast of slow. Some important neurotransmitters include acetylcholine, dopamine, GABA, norepinephrine, and serotonin. Each neurotransmitter has a specific synthesis, breakdown, and receptor type. Understanding neurotransmitters is important for understanding the function of the nervous system and for developing treatments for neurological and psychiatric disorders.

Glial Cells: The Support System of the Central Nervous System

The central nervous system is composed of two basic cell types: neurons and glial cells. Glial cells, also known as support cells, play a crucial role in maintaining the health and function of neurons. There are several types of glial cells, including macroglia (astrocytes and oligodendrocytes), ependymal cells, and microglia.

Astrocytes are the most abundant type of glial cell and have numerous functions, such as providing structural support, repairing nervous tissue, nourishing neurons, contributing to the blood-brain barrier, and regulating neurotransmission and blood flow. There are two main types of astrocytes: protoplasmic and fibrous.

Oligodendrocytes are responsible for the formation of myelin sheaths, which insulate and protect axons, allowing for faster and more efficient transmission of nerve impulses.

Ependymal cells line the ventricular system and are involved in the circulation of cerebrospinal fluid (CSF) and fluid homeostasis in the brain. Specialized ependymal cells called choroid plexus cells produce CSF.

Microglia are the immune cells of the CNS and play a crucial role in protecting the brain from infection and injury. They also contribute to the maintenance of neuronal health and function.

In summary, glial cells are essential for the proper functioning of the central nervous system. They provide structural support, nourishment, insulation, and immune defense to neurons, ensuring the health and well-being of the brain and spinal cord.

The Dopamine Hypothesis is a theory that suggests that dopamine and dopaminergic mechanisms are central to schizophrenia. This hypothesis was developed based on observations that antipsychotic drugs provide at least some degree of D2-type dopamine receptor blockade and that it is possible to induce a psychotic episode in healthy subjects with pharmacological dopamine agonists. The hypothesis was further strengthened by the finding that antipsychotic drugs’ clinical effectiveness was directly related to their affinity for dopamine receptors. Initially, the belief was that the problem related to an excess of dopamine in the brain. However, later studies showed that the relationship between hypofrontality and low cerebrospinal fluid (CSF) dopamine metabolite levels indicates low frontal dopamine levels. Thus, there was a move from a one-sided dopamine hypothesis explaining all facets of schizophrenia to a regionally specific prefrontal hypodopaminergia and a subcortical hyperdopaminergia. In summary, psychosis appears to result from excessive dopamine activity in the striatum, while the negative symptoms seen in schizophrenia appear to result from too little dopamine activity in the frontal lobe. Antipsychotic medications appear to help by countering the effects of increased dopamine by blocking postsynaptic D2 receptors in the striatum.

While ventricular enlargement is often observed in individuals with schizophrenia, it is not a definitive indicator of the condition as it can also be present in other disorders.

Schizophrenia is a pathology that is characterized by a number of structural and functional brain alterations. Structural alterations include enlargement of the ventricles, reductions in total brain and gray matter volume, and regional reductions in the amygdala, parahippocampal gyrus, and temporal lobes. Antipsychotic treatment may be associated with gray matter loss over time, and even drug-naïve patients show volume reductions. Cerebral asymmetry is also reduced in affected individuals and healthy relatives. Functional alterations include diminished activation of frontal regions during cognitive tasks and increased activation of temporal regions during hallucinations. These findings suggest that schizophrenia is associated with both macroscopic and functional changes in the brain.

Serotonin (5-hydroxytryptamine, 5-HT) receptors are primarily G protein receptors, except for 5-HT3, which is a ligand-gated receptor. It is important to remember that 5-HT3 is most commonly associated with nausea. Additionally, 5-HT7 is linked to circadian rhythms. The stimulation of 5-HT2 receptors is believed to be responsible for the side effects of insomnia, agitation, and sexual dysfunction that are associated with the use of selective serotonin reuptake inhibitors (SSRIs).