Transient Global Amnesia

Transient global amnesia (TGA) is a condition characterized by anterograde amnesia without any loss of personal identity or clouding of consciousness. The cognitive impairment is limited to amnesia, with no apraxia or aphasia. TGA is not associated with recent head trauma or seizures in the preceding two years. There are no focal neurologic signs or features suggesting temporal lobe epilepsy or depression.

The most common symptom of TGA is disorientation to time and place, with repetitive questioning such as Where am I? lasting throughout the attack. Most attacks last one to eight hours, with a mean duration of 4.2 hours. The exact cause of TGA is not clear, but studies have shown that blood flow to specific brain areas involved in memory, such as the thalamus and mesial temporal structures (amygdala and hippocampus), may be disrupted transiently during an attack.

In conclusion, TGA is a temporary condition that affects memory and can cause disorientation. While the exact cause is not known, studies have shown that specific brain areas involved in memory may be affected.

Urgent Assessment and Referral for Anterior Cord Syndrome

This patient is showing symptoms and signs of anterior cord syndrome, which is likely caused by an acute disc herniation at the C5/C6 level. The lower limb is displaying upper motor neuron weakness and spinothalamic disruption, while the upper limb is showing lower motor neuron signs at the C5/C6 level, such as absent biceps/supinator jerks and weak elbow flexion, and upper motor neuron signs below this level. There is also evidence of spinothalamic disruption affecting C6-T1 bilaterally.

To properly diagnose and treat this condition, the patient needs urgent assessment with MRI imaging and referral to a neurosurgeon for decompression. It is important to rule out other conditions such as anterior spinal artery infarct, Brown-Séquard syndrome, central cord syndrome, and cervical myelopathy.

Anterior spinal artery infarct primarily affects the lower limb and causes a sensory level. Brown-Séquard syndrome results in ipsilateral loss of dorsal column and corticospinal function with contralateral loss of pain and temperature below the level of the lesion. Central cord syndrome, or syringomyelia, causes greater LMN weakness in the arms than UMN weakness in the legs, and dissociated pain and temperature loss in the arms. Cervical myelopathy at C7 is unlikely to have such a sudden onset and does not account for all the signs in the upper limb.

Encephalitis is a serious condition that can have a variety of causes. One possibility is West Nile disease, which is caused by a virus transmitted by mosquitoes. While this disease was once considered tropical, it has become more common in recent years, with thousands of cases reported in the US alone. Symptoms can include fever, myalgia, nausea, vomiting, and a rash, and neurological involvement is possible, particularly in older individuals or those with weakened immune systems. Other potential causes of encephalitis include Lyme disease, which is associated with tick bites, and TB meningitis, which is characterized by lymphocytic inflammation. Lassa fever, a viral hemorrhagic fever endemic to West Africa, is another possibility. While there is no cure for most forms of encephalitis, early diagnosis and treatment can help manage symptoms and improve outcomes.

According to NICE guidelines, this woman should be prescribed atorvastatin for secondary prevention of stroke within 48 hours of her ischaemic episode. This is because early administration of statins has been linked to a risk of haemorrhagic transformation. Anti-embolism stockings are not recommended for stroke patients as they do not provide any additional benefit in preventing embolic events during the acute phase.

The Royal College of Physicians (RCP) and NICE have published guidelines on the diagnosis and management of patients following a stroke. The guidelines provide recommendations for the management of acute stroke, including maintaining normal levels of blood glucose, hydration, oxygen saturation, and temperature. Blood pressure should not be lowered in the acute phase unless there are complications. Aspirin should be given as soon as possible if a haemorrhagic stroke has been excluded. Anticoagulants should not be started until brain imaging has excluded haemorrhage, and usually not until 14 days have passed from the onset of an ischaemic stroke. If the cholesterol is > 3.5 mmol/l, patients should be commenced on a statin.

Thrombolysis with alteplase should only be given if it is administered within 4.5 hours of onset of stroke symptoms and haemorrhage has been definitively excluded. There are absolute and relative contraindications to thrombolysis, including previous intracranial haemorrhage, intracranial neoplasm, and active bleeding. Mechanical thrombectomy is a new treatment option for patients with an acute ischaemic stroke. NICE recommends considering thrombectomy together with intravenous thrombolysis for people last known to be well up to 24 hours previously.

Secondary prevention recommendations from NICE include the use of clopidogrel and dipyridamole. Clopidogrel is recommended ahead of combination use of aspirin plus modified-release dipyridamole in people who have had an ischaemic stroke. Aspirin plus MR dipyridamole is recommended after an ischaemic stroke only if clopidogrel is contraindicated or not tolerated. MR dipyridamole alone is recommended after an ischaemic stroke only if aspirin or clopidogrel are contraindicated or not tolerated. Carotid artery endarterectomy should only be considered if carotid stenosis is greater than 70% according to ECST criteria or greater than 50% according to NASCET criteria.

Diagnosis and Differential Diagnosis of a Patient with Brain Metastases and Lepto-meningeal Carcinomatosis

The patient in question presents with symptoms, signs, and investigations that suggest a diagnosis of brain metastases and lepto-meningeal carcinomatosis, possibly originating from a left breast carcinoma. Lung metastases and lymphadenopathy are also present. Bacterial meningitis is unlikely due to the prolonged history, focal neurology, and normal white cell count and inflammatory markers. Neurosarcoidosis and granulomatosis with polyangiitis are also unlikely based on the patient’s symptoms and history. There is no indication of a risk of tuberculosis. Male breast cancer is a rare disease that may be a risk factor in this case, given the patient’s age and other factors. Overall, the most likely diagnosis is brain metastases and lepto-meningeal carcinomatosis, with a possible origin in breast cancer.

Ramsay Hunt Syndrome: A Herpes Zoster Infection

Ramsay Hunt syndrome is a condition characterized by a lower motor neurone facial palsy on one side of the face, often caused by herpes zoster infection of the geniculate ganglion. While a vesicular eruption in the external auditory canal, cranial integument, and oropharynx is typically present, it may not appear immediately or at all. The eighth cranial nerve may also be affected, leading to deafness and vertigo. The virus can be detected through exudates collected from the skin of the pinna and analyzed through PCR. Treatment with a combination of prednisolone and acyclovir is effective if started within seven days of symptom onset. Left-sided acoustic neuroma is unlikely due to the absence of hearing loss and tinnitus, while herpes simplex infection leads to cold sores rather than facial palsy. Atypical migraine may cause paralysis, but the absence of headache and other symptoms rules it out as a diagnosis.

This man has experienced two crescendo TIAs within a week, which puts him at high risk and requires urgent treatment. He needs to be admitted and undergo a CT head and carotid doppler within 24 hours. Although his ABCD score is 3, which would typically classify him as low-risk, the presence of crescendo episodes makes this score irrelevant. Thrombolysis is not necessary as his neurology has resolved. An outpatient TIA clinic and imaging and dopplers within a week are also not appropriate due to the crescendo episodes.

A transient ischaemic attack (TIA) is a brief period of neurological deficit caused by a vascular issue, lasting less than an hour. The original definition of a TIA was based on time, but it is now recognized that even short periods of ischaemia can result in pathological changes to the brain. Therefore, a new ’tissue-based’ definition is now used. The clinical features of a TIA are similar to those of a stroke, but the symptoms resolve within an hour. Possible features include unilateral weakness or sensory loss, aphasia or dysarthria, ataxia, vertigo, or loss of balance, visual problems, sudden transient loss of vision in one eye (amaurosis fugax), diplopia, and homonymous hemianopia.

NICE recommends immediate antithrombotic therapy, giving aspirin 300 mg immediately unless the patient has a bleeding disorder or is taking an anticoagulant. If aspirin is contraindicated, management should be discussed urgently with the specialist team. Specialist review is necessary if the patient has had more than one TIA or has a suspected cardioembolic source or severe carotid stenosis. Urgent assessment within 24 hours by a specialist stroke physician is required if the patient has had a suspected TIA in the last 7 days. Referral for specialist assessment should be made as soon as possible within 7 days if the patient has had a suspected TIA more than a week previously. The person should be advised not to drive until they have been seen by a specialist.

Neuroimaging should be done on the same day as specialist assessment if possible. MRI is preferred to determine the territory of ischaemia or to detect haemorrhage or alternative pathologies. Carotid imaging is necessary as atherosclerosis in the carotid artery may be a source of emboli in some patients. All patients should have an urgent carotid doppler unless they are not a candidate for carotid endarterectomy.

Antithrombotic therapy is recommended, with clopidogrel being the first-line treatment. Aspirin + dipyridamole should be given to patients who cannot tolerate clopidogrel. Carotid artery endarterectomy should only be considered if the patient has suffered a stroke or TIA in the carotid territory and is not severely disabled. It should only be recommended if carotid stenosis is greater

Andexanet alfa can reverse the effects of rivaroxaban and apixaban, which is important in the case of this patient who has suffered a traumatic intracranial hemorrhage. The first step in treatment is to ensure a clear airway and attempt to stop the bleeding to prevent increased intracranial pressure. Cryoprecipitate, which contains various clotting factors, can be used to treat fibrinogen deficiency in cases of hemorrhage, trauma, invasive procedures, or disseminated intravascular coagulation. Dexamethasone may be given to treat increased intracranial pressure, but it is not the initial treatment in this case as there is no evidence of cerebral edema or midline shift. Idarucizumab is not indicated as it is a specific reversal agent for dabigatran, which the patient is not taking.

Direct oral anticoagulants (DOACs) are medications used to prevent stroke in non-valvular atrial fibrillation (AF), as well as for the prevention and treatment of venous thromboembolism (VTE). To be prescribed DOACs for stroke prevention, patients must have certain risk factors, such as a prior stroke or transient ischaemic attack, age 75 or older, hypertension, diabetes mellitus, or heart failure. There are four DOACs available, each with a different mechanism of action and method of excretion. Dabigatran is a direct thrombin inhibitor, while rivaroxaban, apixaban, and edoxaban are direct factor Xa inhibitors. The majority of DOACs are excreted either through the kidneys or the liver, with the exception of apixaban and edoxaban, which are excreted through the feces. Reversal agents are available for dabigatran and rivaroxaban, but not for apixaban or edoxaban.

Differential Diagnosis for Progressive CNS Dysfunction in Late Childhood

subacute sclerosing panencephalitis (SSPE) is a rare condition that could explain the progressive CNS dysfunction in a patient with a history of measles in early life. SSPE typically presents with a decline in school proficiency, followed by myoclonic jerks, seizures, visual deterioration, pyramidal signs, rigidity, and unresponsiveness, ultimately leading to death within 1-3 years. Neurosarcoidosis, lipid storage disease, Schilder’s demyelinative disease, and ceroid lipofuscinosis are other potential differential diagnoses, but their clinical features do not match the patient’s presentation. It is important to consider SSPE in cases of progressive CNS dysfunction in late childhood, especially in patients with a history of measles.

The patient is most likely suffering from motor neuron disease. He is a male in his 50s and has shown signs of bulbar involvement without any peripheral or sensory issues. The chronic nature of his symptoms makes a stroke unlikely, while his age, sex, and progressive symptoms make multiple sclerosis less probable. The absence of arm weakness or sensory loss makes syringobulbia less likely, and myotonic dystrophy would present with more peripheral signs. Therefore, the most likely diagnosis is motor neuron disease with bulbar features.

Motor neuron disease is a neurological condition that is not yet fully understood. It can manifest with both upper and lower motor neuron signs and is rare before the age of 40. There are different patterns of the disease, including amyotrophic lateral sclerosis, progressive muscular atrophy, and bulbar palsy. Some of the clues that may indicate a diagnosis of motor neuron disease include fasciculations, the absence of sensory signs or symptoms, a combination of lower and upper motor neuron signs, and wasting of small hand muscles or tibialis anterior.

Other features of motor neuron disease include the fact that it does not affect external ocular muscles and there are no cerebellar signs. Abdominal reflexes are usually preserved, and sphincter dysfunction is a late feature if present. The diagnosis of motor neuron disease is made based on clinical presentation, but nerve conduction studies can help exclude a neuropathy. Electromyography may show a reduced number of action potentials with increased amplitude. MRI is often used to rule out cervical cord compression and myelopathy as differential diagnoses. It is important to note that while vague sensory symptoms may occur early in the disease, sensory signs are typically absent.

The patient is displaying symptoms and signs of myasthenia gravis that were previously undetected. The stress of surgery has triggered a myasthenic crisis, resulting in type 2 respiratory failure, tachycardia, tachypnea, and decreased forced vital capacity. The top priority in managing this situation is to transfer the patient to an intensive care unit for respiratory support.

Corticosteroids and pyridostigmine are the primary treatments for myasthenia gravis, with intravenous immunoglobulin used in severe cases. However, these treatments cannot be expected to quickly restore respiratory muscle function in this emergency scenario.

The patient does not have a history of obstructive lung disease, and the type 2 respiratory failure is due to respiratory muscle weakness causing ventilation failure. Therefore, reducing the percentage of supplemental oxygen would not be helpful and would only worsen hypoxia.

Exacerbating Factors of Myasthenia Gravis

Myasthenia gravis is a neuromuscular disorder that is characterized by fatigability, which is worsened by exertion. This means that symptoms become more pronounced as the day progresses. In addition to exertion, certain drugs can also exacerbate myasthenia gravis. These drugs include penicillamine, quinidine, procainamide, beta-blockers, lithium, and certain antibiotics such as gentamicin, macrolides, quinolones, and tetracyclines. It is important for individuals with myasthenia gravis to be aware of these exacerbating factors and to avoid them whenever possible in order to manage their symptoms effectively. By doing so, they can improve their quality of life and minimize the impact of this condition on their daily activities.

To diagnose multiple sclerosis, it is necessary to confirm the presence of the disease in different areas and at different times.

To establish dissemination in space, there must be at least one T2 bright lesion in two or more of the following locations: periventricular, juxtacortical, infratentorial, or spinal cord.

To establish dissemination in time, there are two options:
1) A new lesion compared to a previous scan, regardless of timing, that is either T2 bright or gadolinium-enhancing.
2) The presence of an asymptomatic enhancing lesion and a non-enhancing T2 bright lesion on any one scan, indicating two lesions of different ages that meet the criteria for dissemination in space.

Investigating Multiple Sclerosis

Diagnosing multiple sclerosis (MS) requires the identification of lesions that are disseminated in both time and space. There are several methods used to investigate MS, including magnetic resonance imaging (MRI), cerebrospinal fluid (CSF) analysis, and visual evoked potentials (VEP).

MRI is a commonly used tool to identify MS lesions. High signal T2 lesions and periventricular plaques are often observed, as well as Dawson fingers, which are hyperintense lesions perpendicular to the corpus callosum. CSF analysis can also aid in diagnosis, as it may reveal oligoclonal bands that are not present in serum and an increased intrathecal synthesis of IgG.

VEP testing can also be used to diagnose MS. This test measures the electrical activity in the visual pathway and can reveal a delayed but well-preserved waveform in MS patients.

Overall, a combination of these methods is often used to diagnose MS and demonstrate the dissemination of lesions in time and space.

The Effects of Vitamin B Deficiencies

Vitamin B deficiencies can have various effects on the body. Chronic alcohol use can lead to Wernicke-Korsakoff syndrome, which is characterized by ataxia, opthalmoplegia, and disorientation due to thiamine (vitamin B1) deficiency. Riboflavin (vitamin B2) deficiency can cause angular cheilitis, glossitis, and seborrhoeic dermatitis. Niacin (vitamin B3) deficiency can result in dermatitis, dementia, and diarrhoea (pellagra). Folic acid (vitamin B9) deficiency can cause macrocytic anaemia, while vitamin B12 deficiency can lead to macrocytic anaemia, peripheral neuropathy, and cognitive impairment. It is important to maintain a balanced diet to prevent these deficiencies and their associated health problems.

This image displays a significant bleeding outside the dura mater, which is likely the result of a middle meningeal artery rupture.

There are different types of traumatic brain injury, including focal (contusion/haematoma) or diffuse (diffuse axonal injury). Diffuse axonal injury occurs due to mechanical shearing following deceleration, causing disruption and tearing of axons. Intracranial haematomas can be extradural, subdural or intracerebral, while contusions may occur adjacent to (coup) or contralateral (contre-coup) to the side of impact. Secondary brain injury occurs when cerebral oedema, ischaemia, infection, tonsillar or tentorial herniation exacerbates the original injury.

Although the absence of cardiac symptoms is evident, the presence of ST elevation in this man could be indicative of subarachnoid haemorrhage. While it is possible that this is simply benign early re-polarisation, the severity of his headache suggests otherwise. Additionally, his slender build may suggest Marfan’s syndrome, which is known to cause cerebral aneurysms. It is unlikely that he has experienced a silent myocardial infarction, especially given his young age and lack of other symptoms such as difficulty breathing.

Understanding Subarachnoid Haemorrhage

Subarachnoid haemorrhage (SAH) is a type of intracranial haemorrhage where blood is present in the subarachnoid space, which is located deep to the subarachnoid layer of the meninges. Spontaneous SAH is caused by various factors such as intracranial aneurysm, arteriovenous malformation, pituitary apoplexy, arterial dissection, mycotic aneurysms, and perimesencephalic. The most common symptom of SAH is a sudden-onset headache, which is severe and occipital. Other symptoms include nausea, vomiting, meningism, coma, seizures, and sudden death. SAH can be confirmed through a CT head scan or lumbar puncture. Treatment for SAH depends on the underlying cause, and most intracranial aneurysms are treated with a coil by interventional neuroradiologists. Complications of aneurysmal SAH include re-bleeding, vasospasm, hyponatraemia, seizures, hydrocephalus, and death. Predictive factors for SAH include conscious level on admission, age, and the amount of blood visible on CT head.

Femoral Neuropathy: Causes and Symptoms

Femoral neuropathy is a condition that primarily affects the quadriceps, causing weakness in this muscle group. The femoral nerve is formed by the L2-4 roots as part of the lumbar plexus and is susceptible to compression within the psoas muscle. This compression can occur due to haemorrhage into the muscle caused by haemophilia, anticoagulation therapy, or trauma.

The main motor component of the femoral nerve innervates the iliopsoas and quadriceps muscles. The motor branch to the iliopsoas originates in the pelvis proximal to the inguinal ligament. The sensory branch of the femoral nerve, known as the saphenous nerve, innervates the skin of the medial thigh and the anterior and medial aspects of the calf.

Diabetic patients are more prone to femoral and proximal mononeuropathies. However, the obturator nerve, which innervates the adductors of the hip, and the sciatic nerve, which innervates the hip extensors and all muscle compartments below the knee, are both intact in patients with femoral neuropathy.

While a lumbar plexopathy could potentially cause similar physical signs, deep-seated excruciating pain is common. An L1 root lesion would not explain weakness of hip flexion and knee extension. the causes and symptoms of femoral neuropathy is crucial for proper diagnosis and treatment.

Visual Disturbances Caused by Anti-Epileptic Medications

Visual disturbances are a common side effect of anti-epileptic medications. However, only vigabatrin has been linked to visual field loss, with patients experiencing blurred vision, tunnel vision, oscillopsia, and difficulty in navigation. Despite these symptoms, visual acuity remains intact.

Other anti-epileptic medications have been associated with different visual disturbances. Carbamazepine has been linked to abnormal color perception and reduced contrast sensitivity, while levetiracetam can cause diplopia. Topiramate has been associated with closed angle glaucoma, and sodium valproate can cause abnormal color perception and altered visual evoked potentials.

It is important for patients to be aware of the potential visual side effects of their anti-epileptic medication and to report any changes in vision to their healthcare provider. Regular eye exams may also be recommended for patients taking these medications.

The CT scan reveals a widespread bleeding in the subarachnoid space.

There are different types of traumatic brain injury, including focal (contusion/haematoma) or diffuse (diffuse axonal injury). Diffuse axonal injury occurs due to mechanical shearing following deceleration, causing disruption and tearing of axons. Intracranial haematomas can be extradural, subdural or intracerebral, while contusions may occur adjacent to (coup) or contralateral (contre-coup) to the side of impact. Secondary brain injury occurs when cerebral oedema, ischaemia, infection, tonsillar or tentorial herniation exacerbates the original injury.

MELAS (Mitochondrial Encephalopathy with Lactic Acidosis and Stroke) is a rare genetic disorder that is inherited through the mitochondria. It is characterized by short stature, recurrent migraines, vomiting, muscle weakness, seizures, and the development of multiple strokes at an early age, typically before the age of 40. Progressive dementia is also a common symptom, and there is a raised level of lactic acid in the blood. A skeletal muscle biopsy will show ragged red fibers.

Based on the given information, it is possible that the patient’s mother had the same condition, as mitochondrial inheritance is typical. The patient may have also experienced a posterior stroke that was not treated, as he had sudden onset cerebellar symptoms and is now left with an intention tremor and nystagmus. While cerebellar infarcts may not always show up on CT scans, MRI is the best modality for viewing the posterior fossa. Although the patient’s MMSE score is normal, a score of 25/30 for a young man is a potential concern in the clinical context.

While CADASIL may also present with migraines and stroke at an early age, lactic acidosis is not a feature, and subcortical infarct would be more typical. The patient’s high cholesterol is not high enough for a diagnosis of familial hypercholesterolemia and would not explain the muscle weakness, vomiting, and lactic acidosis. Carbamazepine poisoning could explain the cerebellar symptoms, but not the other symptoms.

Mitochondrial diseases are caused by a small amount of double-stranded DNA present in the mitochondria, which encodes protein components of the respiratory chain and some special types of RNA. These diseases are inherited only via the maternal line, as the sperm contributes no cytoplasm to the zygote. None of the children of an affected male will inherit the disease, while all of the children of an affected female will inherit it. Mitochondrial diseases generally encode rare neurological diseases, and there is poor genotype-phenotype correlation due to heteroplasmy, which means that within a tissue or cell, there can be different mitochondrial populations. Muscle biopsy typically shows red, ragged fibers due to an increased number of mitochondria. Examples of mitochondrial diseases include Leber’s optic atrophy, MELAS syndrome, MERRF syndrome, Kearns-Sayre syndrome, and sensorineural hearing loss.

Cluster Headaches: Symptoms and Treatment Options

Cluster headaches are a type of headache that primarily affects men in their 30s and 40s. These headaches occur in clusters, usually at night. Autonomic symptoms such as nasal congestion, lacrimation, conjunctival injection, ptosis, and eyelid edema are common during these attacks.

The treatment of choice for acute attacks is either high flow oxygen or subcutaneous sumatriptan. Verapamil is the most commonly used prophylactic agent, but lithium and Epilim valproate are also options. It is important to avoid long-term treatment with ergotamine due to serious side effects such as retroperitoneal fibrosis.

Trigeminal neuralgia is treated with carbamazepine, while propranolol is the preferred treatment for migraine.

The patient’s ileal resection indicates that they are unable to absorb the vitamin B12-intrinsic factor complex, resulting in a deficiency of vitamin B12 (also known as cobalamin deficiency) and subsequent subacute combined degeneration. The presence of macrocytic anaemia with hypersegmented neutrophils further confirms this diagnosis. While folate deficiency can also cause a similar blood film appearance, it does not typically result in neurological symptoms.

Subacute Combined Degeneration of Spinal Cord

Subacute combined degeneration of spinal cord is a condition that occurs due to a deficiency of vitamin B12. The dorsal columns and lateral corticospinal tracts are affected, leading to the loss of joint position and vibration sense. The first symptoms are usually distal paraesthesia, followed by the development of upper motor neuron signs in the legs, such as extensor plantars, brisk knee reflexes, and absent ankle jerks. If left untreated, stiffness and weakness may persist.

This condition is a serious concern and requires prompt medical attention. It is important to maintain a healthy diet that includes sufficient amounts of vitamin B12 to prevent the development of subacute combined degeneration of spinal cord.

Urgent Treatment for Venous Sinus Thrombosis Peri-Partum

This woman is experiencing symptoms of headache, photophobia, and vomiting due to venous sinus thrombosis peri-partum. The condition has caused a small occipital bleed due to venous congestion, and urgent treatment with low molecular weight heparin (LWMH) is necessary to prevent clot propagation and further complications.

It is important to note that her symptoms are not caused by a subarachnoid aneurysm, so aneurysm coiling and nimodipine are not appropriate treatments. Additionally, a lumbar puncture is not necessary as she does not have idiopathic intracranial hypertension. Migraine is also not the cause of her symptoms, so a triptan is not an appropriate treatment option.

In summary, this woman requires immediate treatment with LWMH to address her venous sinus thrombosis peri-partum and prevent further complications.

Parkinson-Plus Syndromes: Understanding Corticobasal Degeneration

Corticobasal degeneration (CBD) is a type of Parkinson-plus syndrome that typically affects adults. It is characterized by unilateral symptoms that can progress to both sides of the body. Along with rigidity and bradykinesia, patients may experience myoclonus, apraxia, or dystonia of a limb. One of the most distinctive features of CBD is the development of an alien limb phenomenon, where a limb, usually an arm, appears to move on its own. Cognitive impairment, including progressive non-fluent aphasia, may also occur. Unfortunately, there is no cure for CBD.

Other Parkinson-plus syndromes include Wilson’s disease, which presents with neuropsychiatric symptoms or asymptomatic rise in transaminases in the late teenage/early twenties time frame. Progressive supranuclear palsy is another Parkinson-plus syndrome, but it lacks the gaze palsy that is characteristic of CBD. Dementia with Lewy bodies is characterized by features of parkinsonism accompanied by memory impairment, confusion, and visual hallucinations. Multiple system atrophy is associated with autonomic dysfunction such as postural hypotension, fainting episodes, and signs of parkinsonism.

The CT scan of the brain shows that a meningioma primary brain tumor is present, which is characterized by homogeneous contrast enhancement. This finding is more consistent with meningioma than with neuroblastoma, metastatic lung cancer, or aspergilloma. While the patient had a history of active tuberculosis in the past, there was no evidence of active or latent infection upon arrival in the UK, which rules out the possibility of reactivation due to immunosuppressive medications. A screening CT scan of the chest, abdomen, and pelvis may be necessary to exclude metastatic lung cancer.

Brain tumours can be classified into different types based on their location, histology, and clinical features. Metastatic brain cancer is the most common form of brain tumours, which often cannot be treated with surgical intervention. Glioblastoma multiforme is the most common primary tumour in adults and is associated with a poor prognosis. Meningioma is the second most common primary brain tumour in adults, which is typically benign and arises from the arachnoid cap cells of the meninges. Vestibular schwannoma is a benign tumour arising from the eighth cranial nerve, while pilocytic astrocytoma is the most common primary brain tumour in children. Medulloblastoma is an aggressive paediatric brain tumour that arises within the infratentorial compartment, while ependymoma is commonly seen in the 4th ventricle and may cause hydrocephalus. Oligodendroma is a benign, slow-growing tumour common in the frontal lobes, while haemangioblastoma is a vascular tumour of the cerebellum. Pituitary adenoma is a benign tumour of the pituitary gland that can be either secretory or non-secretory, while craniopharyngioma is a solid/cystic tumour of the sellar region that is derived from the remnants of Rathke’s pouch.

Differential Diagnosis for Sudden Onset Symptoms

When a patient presents with sudden onset symptoms, it is important to consider a range of potential diagnoses. In the case of severe neck pain, vertigo, nausea, and vomiting, a likely diagnosis is vertebral artery dissection. This condition can be caused by trauma, such as rifle shooting, or may occur spontaneously. It is often associated with infarction in the territory of the posterior inferior cerebellar artery.

Other potential diagnoses to consider include extradural bleed, which typically presents with a brief lucid interval followed by rapid reduction in GCS, and Subarachnoid hemorrhage, which presents with sudden onset severe headache rather than neck pain. Carotid artery dissection may present with headache, Horner syndrome, and anterior circulation ischemic stroke, while basilar artery occlusion may result in motor and bulbar symptoms and even locked-in syndrome.

In summary, when faced with sudden onset symptoms, it is important to consider a range of potential diagnoses and to carefully evaluate the patient’s symptoms and medical history to arrive at an accurate diagnosis.

The patient’s diagnosis of trigeminal neuralgia needs to be reviewed due to several red-flag features, including limited response to carbamazepine, simultaneous bilateral pain, and soft neurological signs suggestive of CNS lesions. Multiple sclerosis is the most likely alternative diagnosis, and the best investigation to assess for differentials is standard protocol MRI brain with contrast. Specialised MRI protocols for observing vascular contacts are not normally performed.

Understanding Trigeminal Neuralgia

Trigeminal neuralgia is a type of pain syndrome that is characterized by severe pain on one side of the face. While most cases are idiopathic, some may be caused by compression of the trigeminal roots due to tumors or vascular problems. According to the International Headache Society, trigeminal neuralgia is defined as a disorder that causes brief electric shock-like pains that are limited to one or more divisions of the trigeminal nerve. The pain is often triggered by light touch, such as washing, shaving, or brushing teeth, and can occur spontaneously. Certain areas of the face may be more susceptible to pain, known as trigger areas, and the pain may remit for varying periods.

It is important to note that there are red flag symptoms and signs that may suggest a serious underlying cause, such as sensory changes, ear problems, history of skin or oral lesions, pain only in the ophthalmic division of the trigeminal nerve, optic neuritis, a family history of multiple sclerosis, or onset before the age of 40.

The first-line treatment for trigeminal neuralgia is carbamazepine. However, if there is a failure to respond to treatment or atypical features are present, such as onset before the age of 50, referral to neurology may be necessary. Understanding the symptoms and management of trigeminal neuralgia can help individuals seek appropriate treatment and improve their quality of life.

The patient’s medical history and physical examination suggest that they may be suffering from normal pressure hydrocephalus, which is characterized by the triad of new onset dementia, urinary incontinence, and gait disturbance. The results of the investigations suggest that a ventriculoperitoneal shunt may be a suitable treatment option for the patient. Specifically, the CSF infusion test revealed a raised CSF resistance, indicating impaired CSF absorption, which is a positive indicator for surgical intervention. Additionally, the patient’s significant gait disturbance further supports the potential success of surgical treatment.

Understanding Normal Pressure Hydrocephalus

Normal pressure hydrocephalus is a type of dementia that is reversible and commonly seen in elderly patients. It is believed to be caused by a reduction in the absorption of cerebrospinal fluid (CSF) at the arachnoid villi, which may be due to head injury, subarachnoid hemorrhage, or meningitis. The condition is characterized by a classical triad of symptoms, including urinary incontinence, dementia and bradyphrenia, and gait abnormality that may resemble Parkinson’s disease. These symptoms usually develop over a few months, and around 60% of patients will have all three features at the time of diagnosis.

Imaging studies typically show hydrocephalus with ventriculomegaly, which is an enlargement of the ventricles in the brain, in the absence of or out of proportion to sulcal enlargement. The management of normal pressure hydrocephalus involves ventriculoperitoneal shunting, which can help alleviate symptoms. However, around 10% of patients who undergo shunting may experience significant complications such as seizures, infection, and intracerebral hemorrhages. Therefore, careful consideration and monitoring are necessary when deciding on treatment options for patients with normal pressure hydrocephalus.

The MRI results indicate that the patient has multiple sclerosis. The scan shows numerous high T2 regions in the periventricular, juxtacortical, post fossa, and upper cervical cord areas. The lesions vary in contrast enhancement and restricted diffusion, indicating recent or active demyelination. These findings meet the diagnostic criteria for multiple sclerosis, including separation in time and space.

Investigating Multiple Sclerosis

Diagnosing multiple sclerosis (MS) requires the identification of lesions that are disseminated in both time and space. There are several methods used to investigate MS, including magnetic resonance imaging (MRI), cerebrospinal fluid (CSF) analysis, and visual evoked potentials (VEP).

MRI is a commonly used tool to identify MS lesions. High signal T2 lesions and periventricular plaques are often observed, as well as Dawson fingers, which are hyperintense lesions perpendicular to the corpus callosum. CSF analysis can also aid in diagnosis, as it may reveal oligoclonal bands that are not present in serum and an increased intrathecal synthesis of IgG.

VEP testing can also be used to diagnose MS. This test measures the electrical activity in the visual pathway and can reveal a delayed but well-preserved waveform in MS patients.

Overall, a combination of these methods is often used to diagnose MS and demonstrate the dissemination of lesions in time and space.

The Chiari type I malformation is evident on the MRI, with the cerebellar tonsils protruding through the foramen magnum.

Understanding Arnold-Chiari Malformation

Arnold-Chiari malformation is a condition where the cerebellar tonsils are pushed downwards through the foramen magnum. This can occur either due to a congenital defect or as a result of trauma. The condition can lead to non-communicating hydrocephalus, which is caused by the obstruction of cerebrospinal fluid outflow. Patients with Arnold-Chiari malformation may experience headaches and syringomyelia, which is a condition where fluid-filled cysts form in the spinal cord.

Diagnosis and Management of Idiopathic Intracranial Hypertension

Idiopathic intracranial hypertension (IIH) is a condition that commonly affects young overweight women. It is characterized by raised intracranial pressure, which can lead to bilateral papilloedema. To confirm the diagnosis, magnetic resonance imaging of the brain and a lumbar puncture are required. The lumbar puncture will show raised pressure but normal contents of the cerebrospinal fluid. Management options include weight loss, diuretics, therapeutic lumbar punctures, optic nerve fenestration, or a shunt from the CSF to the peritoneum. Goldmann perimetry can be useful in assessing the response to treatment. Other investigations, such as cerebral angiogram, EEG, and serum cortisol, are not helpful in the diagnosis of IIH.