Gait disorders can be caused by a variety of conditions, including neurological, muscular, and structural abnormalities. One common gait disorder is hemiplegic gait, which is characterized by unilateral weakness on the affected side, with the arm flexed, adducted, and internally rotated, and the leg on the same side in extension with plantar flexion of the foot and toes. When walking, the patient may hold their arm to one side and drag their affected leg in a semicircle (circumduction) due to weakness of leg flexors and extended foot. Hemiplegic gait is often seen in patients who have suffered a stroke.

Other gait disorders include ataxic gait, spastic gait, and steppage gait, each with their own unique characteristics and associated conditions. Accurate diagnosis and treatment of gait disorders is important for improving mobility and quality of life for affected individuals.

Non-Dominant Parietal Lobe Dysfunction

The non-dominant parietal lobe is typically the right lobe in most individuals. Dysfunction in this area can lead to various symptoms, including the inability to recognize one’s own illness (anosognosia), neglect of half the body (hemiasomatognosia), difficulty dressing (dressing apraxia), trouble with spatial awareness and construction (constructional dyspraxia), difficulty recognizing familiar places (geographical agnosia), and altered perception of sensory stimuli (allesthesia). It’s important to note that agraphia, a symptom seen in Gerstmann’s syndrome, is caused by dysfunction in the dominant parietal lobe, not the non-dominant lobe.

There is no correlation between multiple sclerosis and raised intraocular pressure, which is known as glaucoma when accompanied by visual field loss.

Multiple Sclerosis: An Overview

Multiple sclerosis is a neurological disorder that is classified into three categories: primary progressive, relapsing-remitting, and secondary progressive. Primary progressive multiple sclerosis affects 5-10% of patients and is characterized by a steady progression with no remissions. Relapsing-remitting multiple sclerosis affects 20-30% of patients and presents with a relapsing-remitting course but does not lead to serious disability. Secondary progressive multiple sclerosis affects 60% of patients and initially presents with a relapsing-remitting course but is then followed by a phase of progressive deterioration.

The disorder typically begins between the ages of 20 and 40 and is characterized by multiple demyelinating lesions that have a preference for the optic nerves, cerebellum, brainstem, and spinal cord. Patients with multiple sclerosis present with a variety of neurological signs that reflect the presence and distribution of plaques. Ocular features of multiple sclerosis include optic neuritis, internuclear ophthalmoplegia, and ocular motor cranial neuropathy.

Multiple sclerosis is more common in women than in men and is seen with increasing frequency as the distance from the equator increases. It is believed to be caused by a combination of genetic and environmental factors, with monozygotic concordance at 25%. Overall, multiple sclerosis is a predominantly white matter disease that can have a significant impact on a patient’s quality of life.

Actin is the primary component of Hirano bodies, which are indicative of neurodegeneration but lack specificity.

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.

Nissl bodies are sizable granules present in neurons that contain rough endoplasmic reticulum and free ribosomes, where protein synthesis occurs. These structures were named after Franz Nissl and exhibit a distinctive purple-blue hue when exposed to Cresyl violet solution, although the reason for this selective staining remains unknown.

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.

Motor Neuron Lesions

Signs of an upper motor neuron lesion include weakness, increased reflexes, increased tone (spasticity), mild atrophy, an upgoing plantar response (Babinski reflex), and clonus. On the other hand, signs of a lower motor neuron lesion include atrophy, weakness, fasciculations, decreased reflexes, and decreased tone. It is important to differentiate between the two types of lesions as they have different underlying causes and require different treatment approaches. A thorough neurological examination can help identify the location and extent of the lesion, which can guide further diagnostic testing and management.

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.

Multiple Sclerosis: An Overview

Multiple sclerosis is a neurological disorder that is classified into three categories: primary progressive, relapsing-remitting, and secondary progressive. Primary progressive multiple sclerosis affects 5-10% of patients and is characterized by a steady progression with no remissions. Relapsing-remitting multiple sclerosis affects 20-30% of patients and presents with a relapsing-remitting course but does not lead to serious disability. Secondary progressive multiple sclerosis affects 60% of patients and initially presents with a relapsing-remitting course but is then followed by a phase of progressive deterioration.

The disorder typically begins between the ages of 20 and 40 and is characterized by multiple demyelinating lesions that have a preference for the optic nerves, cerebellum, brainstem, and spinal cord. Patients with multiple sclerosis present with a variety of neurological signs that reflect the presence and distribution of plaques. Ocular features of multiple sclerosis include optic neuritis, internuclear ophthalmoplegia, and ocular motor cranial neuropathy.

Multiple sclerosis is more common in women than in men and is seen with increasing frequency as the distance from the equator increases. It is believed to be caused by a combination of genetic and environmental factors, with monozygotic concordance at 25%. Overall, multiple sclerosis is a predominantly white matter disease that can have a significant impact on a patient’s quality of life.

The Papez Circuit: A Neural Pathway for Emotion

James Papez was the first to describe a neural pathway in the brain that mediates the process of emotion. This pathway is known as the ‘Papez circuit’ and is located on the medial surface of the brain. It is bilateral, symmetrical, and links the cortex to the hypothalamus.

According to Papez, information about emotion passes through several structures in the brain, including the hippocampus, the Mammillary bodies of the hypothalamus, the anterior nucleus of the thalamus, the cingulate cortex, and the entorhinal cortex. Finally, the information passes through the hippocampus again, completing the circuit.

The Papez circuit was one of the first descriptions of the limbic system, which is responsible for regulating emotions, motivation, and memory. Understanding the Papez circuit and the limbic system has important implications for understanding and treating emotional disorders such as anxiety and depression.

The anterior lobe of the pituitary gland secretes adrenocorticotropic hormone.

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.

Understanding Prosopagnosia: The Inability to Recognize Faces

Prosopagnosia, also known as face blindness, is a condition where individuals are unable to recognize faces. This complex process involves various areas of the brain, with the fusiform gyrus in the temporal lobe being the most significant. The inability to recognize faces can be caused by damage to this area of the brain of can be a result of a developmental disorder.

The condition can be challenging for individuals as it can affect their ability to recognize familiar faces, including family members and friends. It can also impact their social interactions and make it difficult to navigate social situations. While there is no cure for prosopagnosia, individuals can learn to use other cues such as voice, clothing, and context to recognize people.

Understanding prosopagnosia is crucial in providing support and accommodations for individuals who experience this condition. It is essential to raise awareness and promote research to develop effective interventions to help individuals with face blindness.

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.

Abnormal Motor Behaviours Associated with Utilization Behaviour

Utilization behaviour (UB) is a condition where patients exhibit exaggerated and inappropriate motor responses to environmental cues and objects. This behaviour is automatic and instrumentally correct, but not contextually appropriate. For instance, a patient may start brushing their teeth when presented with a toothbrush, even in a setting where it is not expected. UB is caused by frontal lobe lesions that result in a loss of inhibitory control.

Other motor abnormalities associated with UB include imitation behaviour, where patients tend to imitate the examiner’s behaviour, and the alien hand sign, where patients experience bizarre hand movements that they cannot control. Manual groping behaviour is also observed, where patients automatically manipulate objects placed in front of them. The grasp reflex, which is normal in infants, should not be present in children and adults. It is an automatic tendency to grip objects of stimuli, such as the examiner’s hand.

Environmental Dependency Syndrome is another condition associated with UB. It describes deficits in personal control of action and an overreliance on social and physical environmental stimuli to guide behaviour in a social context. For example, a patient may start commenting on pictures in an examiner’s office, believing it to be an art gallery.

Frontal lobe damage can be best detected through tests of verbal fluency, such as the FAS Verbal Fluency Test, as the anterior cerebral artery supplies the frontal lobes and medial aspects of the parietal and occipital lobes, which are responsible for this function.

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.

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.

Parkinson plus syndromes, including multisystem atrophy, exhibit a limited efficacy towards Parkinson’s treatment, such as levodopa.

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.

The blood supply to the caudate nucleus primarily comes from the deep penetrators of the anterior and middle cerebral arteries. The effects of caudate infarcts can differ depending on the study, but typically include behavioral symptoms such as abulia and agitation, loss of executive function, and motor weakness.

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.

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.

The inability to carry out complex instructions is referred to as Ideational Apraxia, while the inability to perform previously learned actions with the appropriate tools is known as Ideomotor Apraxia.

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.

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.

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.

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.

EEG Waveform Frequencies

Delta waves have the lowest frequency among the EEG waveforms, ranging from 0.5 to 4 Hz. Theta waves follow with a frequency range of 4 to 8 Hz, while alpha waves have a frequency range of 8 to 14 Hz. Beta waves have a frequency range of 14 to 32 Hz, and gamma waves have a frequency range of 32 to 48+ Hz. In a normal awake adult EEG, alpha waves are the most prominent waveform.

The Cerebral Cortex and Neocortex

The cerebral cortex is the outermost layer of the cerebral hemispheres and is composed of three parts: the archicortex, paleocortex, and neocortex. The neocortex accounts for 90% of the cortex and is involved in higher functions such as thought and language. It is divided into 6-7 layers, with two main cell types: pyramidal cells and nonpyramidal cells. The surface of the neocortex is divided into separate areas, each given a number by Brodmann (e.g. Brodmann’s area 17 is the primary visual cortex). The surface is folded to increase surface area, with grooves called sulci and ridges called gyri. The neocortex is responsible for higher cognitive functions and is essential for human consciousness.

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 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.

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.

Motor Neuron Lesions

Signs of an upper motor neuron lesion include weakness, increased reflexes, increased tone (spasticity), mild atrophy, an upgoing plantar response (Babinski reflex), and clonus. On the other hand, signs of a lower motor neuron lesion include atrophy, weakness, fasciculations, decreased reflexes, and decreased tone. It is important to differentiate between the two types of lesions as they have different underlying causes and require different treatment approaches. A thorough neurological examination can help identify the location and extent of the lesion, which can guide further diagnostic testing and management.