Understanding Guillain-Barre Syndrome: Symptoms and Features

Guillain-Barre syndrome is a condition that affects the peripheral nervous system and is caused by an immune-mediated demyelination. It is often triggered by an infection, with Campylobacter jejuni being a common culprit. The initial symptoms of the illness include back and leg pain, which is experienced by around 65% of patients. The characteristic feature of Guillain-Barre syndrome is a progressive, symmetrical weakness of all the limbs, with the weakness typically starting in the legs and ascending upwards. Reflexes are reduced or absent, and sensory symptoms tend to be mild, with very few sensory signs.

Other features of Guillain-Barre syndrome may include a history of gastroenteritis, respiratory muscle weakness, cranial nerve involvement, diplopia, bilateral facial nerve palsy, oropharyngeal weakness, and autonomic involvement. Autonomic involvement may manifest as urinary retention or diarrhea. Less common findings may include papilloedema, which is thought to be secondary to reduced CSF resorption.

To diagnose Guillain-Barre syndrome, a lumbar puncture may be performed, which can reveal a rise in protein with a normal white blood cell count (albuminocytologic dissociation) in 66% of cases. Nerve conduction studies may also be conducted, which can show decreased motor nerve conduction velocity due to demyelination, prolonged distal motor latency, and increased F wave latency. Understanding the symptoms and features of Guillain-Barre syndrome is crucial for prompt diagnosis and treatment.

To minimize the risk of errors, brain death testing must be conducted by two experienced doctors on different occasions. The testing involves evaluating the patient’s history, pupil reactions, reflexes, pain response, and respiratory effort. Once brain death is confirmed, life support can be discontinued, and the patient may be considered for organ donation, which can take place before the withdrawal of life support.

Criteria and Testing for Brain Stem Death

Brain death occurs when the brain and brain stem cease to function, resulting in irreversible loss of consciousness and vital functions. To determine brain stem death, certain criteria must be met and specific tests must be performed. The patient must be in a deep coma of known cause, with reversible causes excluded and no sedation. Electrolyte levels must be normal.

The testing for brain stem death involves several assessments. The pupils must be fixed and unresponsive to changes in light intensity. The corneal reflex must be absent, and there should be no response to supraorbital pressure. The oculo-vestibular reflexes must be absent, which is tested by injecting ice-cold water into each ear. There should be no cough reflex to bronchial stimulation or gagging response to pharyngeal stimulation. Finally, there should be no observed respiratory effort in response to disconnection from the ventilator for at least five minutes, with adequate oxygenation ensured.

It is important that the testing is performed by two experienced doctors on two separate occasions, with at least one being a consultant. Neither doctor can be a member of the transplant team if organ donation is being considered. These criteria and tests are crucial in determining brain stem death and ensuring that the patient is beyond recovery.

Assessment and Investigations for Stroke

Whilst diagnosing a stroke may be straightforward in some cases, it can be challenging when symptoms are vague. The FAST screening tool, which stands for Face/Arms/Speech/Time, is a well-known tool used by the general public to identify stroke symptoms. However, medical professionals use a validated tool called the ROSIER score, recommended by the Royal College of Physicians. The ROSIER score assesses for loss of consciousness or syncope, seizure activity, and new, acute onset of asymmetric facial, arm, or leg weakness, speech disturbance, or visual field defect. A score of greater than zero indicates a likely stroke.

When investigating suspected stroke, a non-contrast CT head scan is the first line radiological investigation. The key question to answer is whether the stroke is ischaemic or haemorrhagic, as this determines the appropriate management. Ischaemic strokes may show areas of low density in the grey and white matter of the territory, while haemorrhagic strokes typically show areas of hyperdense material surrounded by low density. It is important to identify the type of stroke promptly, as thrombolysis and thrombectomy play an increasing role in acute stroke management. In rare cases, a third pathology such as a tumour may also be detected.

Treatment Options for Metastatic Spinal Cord Compression

Metastatic spinal cord compression (MSCC) is a serious condition that requires urgent medical attention. Red flags for lower back pain include associated lower limb pain, limb weakness, paraesthesia/numbness, and reduced perianal tone. If these features are present, especially in a patient with an oncological past medical history, urgent magnetic resonance imaging (MRI) should be performed to rule out spinal cord compression.

Patients with MSCC should be referred urgently to the oncology and neurosurgical teams for immediate treatment and consideration of surgical intervention to relieve the compression. Management should include high-dose oral dexamethasone and urgent oncological assessment for consideration of radiotherapy or surgery. Diclofenac is not indicated in MSCC treatment, and high-dose prednisolone is not the corticosteroid of choice.

Intravenous ceftriaxone is not effective in treating MSCC, as it is used to treat meningitis. Intravenous immunoglobulin therapy is also not indicated in MSCC treatment, as it is used to treat conditions such as immune thrombocytopenia, Kawasaki disease, and Guillain–Barré syndrome.

In conclusion, early recognition and prompt treatment of MSCC are crucial to prevent permanent neurological damage. High-dose dexamethasone and urgent oncological assessment for consideration of radiotherapy or surgery are the recommended treatment options for MSCC.

The patient’s symptoms suggest Guillain-Barré syndrome, an acute inflammatory polyneuropathy that often occurs after a viral or bacterial infection. This condition is characterized by progressive, bilateral, ascending weakness that typically starts in the legs and spreads to the arms, respiratory muscles, and bulbar muscles. Areflexia is also present. Treatment may involve respiratory support, intravenous immunoglobulins, and plasma exchange. Most patients recover completely or almost completely, but the mortality rate is around 10%.

Mononeuritis multiplex is a rare condition that affects multiple peripheral and/or cranial nerves. Symptoms are usually asymmetrical and evolve at different times and with different degrees of severity. Diabetes is a common cause, but other systemic disorders can also be implicated. The patient’s symmetrical weakness affecting both legs at the same time is more consistent with a polyneuropathy than mononeuritis multiplex.

The patient’s symptoms do not fit with a diagnosis of multiple sclerosis, which typically presents with relapsing-remitting disease characterized by acute flairs and some improvement between flairs. MS is more common in females and onset peaks between 20 and 40 years. The patient’s symmetrical distribution of symptoms and rapid progression to affect knees and hips make MS unlikely.

Myasthenia gravis is an autoimmune disorder associated with antibodies to acetylcholine receptors at the neuromuscular junction. Patients typically display weakness of the periocular, facial, bulbar, and girdle muscles, with symptoms worsening with prolonged use. The patient’s symmetrical distal weakness is atypical for myasthenia gravis, which tends to affect proximal muscles first.

Polymyositis is a connective tissue disease that affects striated muscle, with symmetrical proximal muscle/limb girdle weakness being a prominent feature. Muscle tenderness and atrophy may also be present. The patient’s distal muscle weakness is not consistent with polymyositis.

The classic signs associated with basilar skull fractures are periorbital bruising, which is bruising around the eye also known as Raccoon eyes, and post-auricular bruising, which is bruising of the mastoid also known as Battle’s sign. Therefore, the correct answer for this question is basilar skull fracture.

NICE Guidelines for Investigating Head Injuries in Adults

Head injuries can be serious and require prompt medical attention. The National Institute for Health and Care Excellence (NICE) has provided clear guidelines for healthcare professionals to determine which adult patients need further investigation with a CT head scan. Patients who require immediate CT head scans include those with a Glasgow Coma Scale (GCS) score of less than 13 on initial assessment, suspected open or depressed skull fractures, signs of basal skull fractures, post-traumatic seizures, focal neurological deficits, and more than one episode of vomiting.

For patients with any loss of consciousness or amnesia since the injury, a CT head scan within 8 hours is recommended for those who are 65 years or older, have a history of bleeding or clotting disorders, experienced a dangerous mechanism of injury, or have more than 30 minutes of retrograde amnesia of events immediately before the head injury. Additionally, patients on warfarin who have sustained a head injury with no other indications for a CT head scan should also receive a scan within 8 hours of the injury.

It is important for healthcare professionals to follow these guidelines to ensure that patients receive appropriate and timely care for their head injuries. By identifying those who require further investigation, healthcare professionals can provide the necessary treatment and support to prevent further complications and improve patient outcomes.

This question assesses the candidate’s understanding of TIA risk stratification. The individual meets the criteria for crescendo TIAs, having experienced two TIAs within a week. This necessitates prompt evaluation and imaging. Admission is recommended for any patient with a score of more than 4 on the ABCD2 scale or crescendo TIA.

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, and sudden transient loss of vision in one eye (amaurosis fugax).

NICE recommends immediate antithrombotic therapy with aspirin 300 mg unless the patient has a bleeding disorder or is taking an anticoagulant. If the patient has had more than one TIA or has a suspected cardioembolic source or severe carotid stenosis, specialist review is necessary. Urgent assessment is required within 24 hours for patients who have had a suspected TIA in the last 7 days. Referral for specialist assessment is necessary as soon as possible within 7 days for patients who have had a suspected TIA more than a week previously. Neuroimaging and carotid imaging are recommended, and antithrombotic therapy is necessary. Carotid artery endarterectomy should only be considered if the carotid stenosis is greater than 70% according to ECST criteria or greater than 50% according to NASCET criteria.

The following factors increase the risk of ischaemic stroke: age, hypertension, smoking, hyperlipidaemia, diabetes mellitus, and atrial fibrillation. However, gout, recurrent UTIs, and dementia do not have an impact on stroke risk. Taking aspirin can lower the risk of stroke.

Understanding Stroke: A Basic Overview

Stroke is a significant cause of morbidity and mortality, with over 150,000 cases reported annually in the UK alone. It is the fourth leading cause of death in the country, killing twice as many women as breast cancer each year. However, the prevention and treatment of strokes have undergone significant changes in the past decade. What was once considered an untreatable condition is now viewed as a brain attack that requires emergency assessment to determine if patients can benefit from new treatments such as thrombolysis.

A stroke, also known as a cerebrovascular accident (CVA), occurs when there is a sudden interruption in the vascular supply of the brain. This interruption can lead to irreversible damage as neural tissue is entirely dependent on aerobic metabolism. There are two main types of strokes: ischaemic and haemorrhagic. Ischaemic strokes occur when there is a blockage in the blood vessel that stops blood flow, while haemorrhagic strokes happen when a blood vessel bursts, leading to a reduction in blood flow.

Symptoms of a stroke include motor weakness, speech problems, swallowing difficulties, visual field defects, and balance problems. The Oxford Stroke Classification is a formal system used to classify strokes based on initial symptoms. Patients with suspected stroke require emergency neuroimaging to determine if they are suitable for thrombolytic therapy to treat early ischaemic strokes. If the stroke is haemorrhagic, neurosurgical consultation should be considered for advice on further management.

In conclusion, understanding the basics of stroke is crucial in identifying and managing the condition. Early intervention and treatment can significantly improve outcomes for patients.

A blockage in the left middle cerebral artery (MCA) is a common cause of cerebral infarction. The symptoms experienced will depend on the extent of the infarct and which hemisphere of the brain is dominant. In right-handed individuals, over 95% have left-sided dominance. Symptoms may include weakness on the opposite side of the body, particularly in the face and arm, as well as sensory loss and homonymous hemianopia. If the left MCA is affected, the patient may experience expressive dysphasia in the anterior MCA territory (Broca’s area) if it is their dominant side, or neglect if it is their non-dominant side. A tumour in the left cerebral hemisphere or thalamus would have a more gradual onset of symptoms, while an occlusion of the right anterior cerebral artery would produce left-sided weakness. The region affected and presentation of each type of artery involvement is summarized in a table.

The diagnosis of an ear infection is unlikely based on the patient’s symptoms and the results of their ear exam.

Understanding Bell’s Palsy

Bell’s palsy is a sudden, one-sided facial nerve paralysis of unknown cause. It is more common in individuals aged 20-40 years and pregnant women. The condition is characterized by lower motor neuron facial nerve palsy, which affects the forehead. Unlike upper motor neuron lesions, the upper face is spared. Patients may also experience post-auricular pain, altered taste, dry eyes, and hyperacusis.

The management of Bell’s palsy has been a subject of debate. However, it is now widely accepted that all patients should receive oral prednisolone within 72 hours of onset. The addition of antiviral medications is still a matter of discussion, but it may be beneficial for severe facial palsy. Eye care is also crucial to prevent exposure keratopathy, and patients should be prescribed artificial tears and eye lubricants. If they are unable to close their eyes at bedtime, they should tape them closed using microporous tape.

If the paralysis shows no sign of improvement after three weeks, an urgent referral to ENT is necessary. Patients with long-standing weakness may require a referral to plastic surgery. The prognosis for Bell’s palsy is generally good, with most patients making a full recovery within 3-4 months. However, untreated patients may experience permanent moderate to severe weakness in around 15% of cases.

The correct answer is cubital tunnel syndrome. This condition is characterized by ulnar nerve neuropathy, which affects the sensory innervation of the palmar and dorsal aspects of 1.5 fingers medially. It can also cause wasting and paralysis of intrinsic hand muscles (except lateral two lumbricals) and the hypothenar muscles. To test for ulnar neuropathy, Froment’s test can be used to assess the function of the adductor pollicis muscle.

Axillary nerve neuropathy is not the correct answer. The axillary nerve has both motor and sensory functions, innervating the deltoid and teres minor muscles, as well as providing sensory innervation to the skin over the lower two-thirds of the posterior part of the deltoid and the long head of the triceps brachii.

C8/T1 radiculopathy is also not the correct answer. While it can mimic ulnar nerve neuropathy, the preserved sensation of the forearm would suggest cubital tunnel syndrome instead. The medial antebrachial cutaneous nerve (C8 and T1) provides sensation to the medial forearm, not the ulnar nerve.

Carpal tunnel syndrome is also not the correct answer. This condition is caused by median nerve dysfunction, resulting in sensory loss over the lateral 3.5 digits and loss of motor function to the flexor muscles of the forearm and hand, as well as those responsible for thumb movement.

The Ulnar Nerve: Overview, Branches, and Patterns of Damage

The ulnar nerve is a nerve that arises from the medial cord of the brachial plexus, specifically from the C8 and T1 spinal nerves. It provides motor innervation to several muscles in the hand, including the medial two lumbricals, adductor pollicis, interossei, hypothenar muscles (abductor digiti minimi, flexor digiti minimi), and flexor carpi ulnaris. It also provides sensory innervation to the medial 1 1/2 fingers on both the palmar and dorsal aspects.

The ulnar nerve travels through the posteromedial aspect of the upper arm before entering the palm of the hand via the Guyon’s canal, which is located superficial to the flexor retinaculum and lateral to the pisiform bone. The nerve has several branches, including the muscular branch, palmar cutaneous branch, dorsal cutaneous branch, superficial branch, and deep branch. These branches supply various muscles and skin areas in the hand.

Damage to the ulnar nerve can occur at the wrist or elbow. When damaged at the wrist, it can result in a claw hand deformity, which involves hyperextension of the metacarpophalangeal joints and flexion at the distal and proximal interphalangeal joints of the 4th and 5th digits. There may also be wasting and paralysis of intrinsic hand muscles (except lateral two lumbricals) and hypothenar muscles, as well as sensory loss to the medial 1 1/2 fingers. When damaged at the elbow, the same symptoms may occur, but with the addition of radial deviation of the wrist. It is important to note that in distal lesions, the clawing may be more severe, which is known as the ulnar paradox.

When it comes to managing chronic pain, drugs for neuropathic pain are typically used alone. If they are not effective, it is recommended to switch to a different drug rather than adding another one. This question may also bring attention to poorly controlled acute pain, but it is important to note that morphine sulfate is not ideal for chronic pain management due to its potential side effects, dependence, and worsening of chronic pain. Tramadol is a better option for managing breakthrough pain in neuropathic pain patients, but it does not change the overall management of chronic pain. The recommended drugs for neuropathic pain include duloxetine, gabapentinoids, and amitriptyline (a tricyclic antidepressant).

Understanding Neuropathic Pain and its Management

Neuropathic pain is a type of pain that occurs due to damage or disruption of the nervous system. It is a complex condition that is often difficult to treat and does not respond well to standard painkillers. Examples of neuropathic pain include diabetic neuropathy, post-herpetic neuralgia, trigeminal neuralgia, and prolapsed intervertebral disc.

To manage neuropathic pain, the National Institute for Health and Care Excellence (NICE) updated their guidance in 2013. The first-line treatment options include amitriptyline, duloxetine, gabapentin, or pregabalin. If the first-line drug treatment does not work, patients may try one of the other three drugs. Unlike standard painkillers, drugs for neuropathic pain are typically used as monotherapy, meaning that if they do not work, patients should switch to a different drug rather than adding another one.

Tramadol may be used as rescue therapy for exacerbations of neuropathic pain, while topical capsaicin may be used for localized neuropathic pain, such as post-herpetic neuralgia. Pain management clinics may also be useful for patients with resistant problems. However, it is important to note that for some specific conditions, such as trigeminal neuralgia, the guidance may vary, and carbamazepine may be used as a first-line treatment. Overall, understanding neuropathic pain and its management is crucial for improving the quality of life for patients suffering from this condition.

The recommended target time for thrombectomy in acute ischaemic stroke is within 6 hours of symptom onset.

Thrombectomy is the preferred treatment for this patient who has presented with symptoms of left-sided paralysis and paraesthesia, along with vascular risk factors and confirmatory CT imaging indicating an ischaemic stroke. While aspirin may be given initially, thrombectomy is the most definitive treatment option within the 6-hour timeframe. Clopidogrel is used for secondary prevention, and thrombolysis is only indicated within 4.5 hours of symptom onset, making them incorrect choices for this patient.

The Royal College of Physicians (RCP) and NICE have published guidelines on the diagnosis and management of patients following a stroke. The management of acute stroke includes 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. Thrombolysis with alteplase should only be given if administered within 4.5 hours of onset of stroke symptoms and haemorrhage has been definitively excluded. Mechanical thrombectomy is a new treatment option for patients with an acute ischaemic stroke. NICE recommends thrombectomy for people who have acute ischaemic stroke and confirmed occlusion of the proximal anterior circulation demonstrated by computed tomographic angiography or magnetic resonance angiography. Secondary prevention includes the use of clopidogrel and dipyridamole. 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.

Patients with newly diagnosed Parkinson’s who experience motor symptoms that negatively impact their quality of life should be provided with levodopa.

Management of Parkinson’s Disease: Medications and Considerations

Parkinson’s disease is a complex condition that requires specialized expertise in movement disorders for diagnosis and management. However, all healthcare professionals should be familiar with the medications used to treat Parkinson’s disease due to its prevalence. The National Institute for Health and Care Excellence (NICE) published guidelines in 2017 to aid in the management of Parkinson’s disease.

For first-line treatment, levodopa is recommended if motor symptoms are affecting the patient’s quality of life. If motor symptoms are not affecting the patient’s quality of life, dopamine agonists (non-ergot derived), levodopa, or monoamine oxidase B (MAO-B) inhibitors may be used. NICE provides tables to aid in decision-making regarding the use of these medications, taking into account their effects on motor symptoms, activities of daily living, motor complications, and adverse events.

If a patient continues to have symptoms despite optimal levodopa treatment or has developed dyskinesia, NICE recommends the addition of a dopamine agonist, MAO-B inhibitor, or catechol-O-methyl transferase (COMT) inhibitor as an adjunct. Other considerations in Parkinson’s disease management include the risk of acute akinesia or neuroleptic malignant syndrome if medication is not taken or absorbed, the potential for impulse control disorders with dopaminergic therapy, and the need to adjust medication if excessive daytime sleepiness or orthostatic hypotension develops.

Specific medications used in Parkinson’s disease management include levodopa, dopamine receptor agonists, MAO-B inhibitors, amantadine, COMT inhibitors, and antimuscarinics. Each medication has its own set of benefits and potential adverse effects, which should be carefully considered when selecting a treatment plan. Overall, the management of Parkinson’s disease requires a comprehensive approach that takes into account the individual needs and circumstances of each patient.

If a patient has a lacunar stroke, they may experience a purely motor, purely sensory, or mixed motor and sensory deficit. A total anterior circulation infarct would cause unilateral weakness in the face, arm, and leg, as well as a homonymous hemianopia and symptoms of higher cerebral dysfunction. A posterior circulation infarct could result in a cerebellar or brainstem syndrome, loss of consciousness, or an isolated homonymous hemianopia. A partial anterior circulation infarct would lead to two of the following: unilateral weakness, homonymous hemianopia, and higher cerebral dysfunction. The absence of hemorrhage on a CT scan suggests that this is most likely a lacunar infarct, as there is only a purely sensory deficit.

Lacunar stroke is a type of ischaemic stroke that accounts for approximately 20-25% of all cases. It occurs when a single penetrating branch of a large cerebral artery becomes blocked, leading to damage in the internal capsule, thalamus, and basal ganglia. The symptoms of lacunar stroke can vary depending on the location of the blockage, but they typically involve either purely motor or purely sensory deficits. Other possible presentations include sensorimotor stroke, ataxic hemiparesis, and dysarthria-clumsy hand syndrome. Unlike other types of stroke, lacunar syndromes tend to lack cortical findings such as aphasia, agnosia, neglect, apraxia, or hemianopsia.

The patient is displaying typical symptoms of hypocalcaemia, including perioral paraesthesia, cramps, tetany, and convulsions. This condition can be a side effect of taking phenytoin, and if left untreated, it can lead to seizures due to changes in neuromuscular excitability. Mild cases of hypocalcaemia can be managed with oral supplementation, while more severe cases may require intravenous replacement.

It’s important to note that hypercalcaemia can cause bone pain, renal calculi, constipation, polyuria, fatigue, depression, and confusion. However, the patient does not display any of these symptoms.

Hyperkalaemia can cause muscle weakness and cardiac arrhythmias, but the patient does not have these symptoms. Hypokalaemia can also cause muscle weakness and cardiac arrhythmias, but the patient’s symptoms do not fit this condition.

Finally, hypernatraemia can cause nausea, vomiting, headache, and confusion, but the patient is not experiencing these symptoms.

Hypocalcaemia: Symptoms and Signs

Hypocalcaemia is a condition characterized by low levels of calcium in the blood. Since calcium is essential for proper muscle and nerve function, many of the symptoms and signs of hypocalcaemia are related to neuromuscular excitability. The most common features of hypocalcaemia include muscle twitching, cramping, and spasms, as well as perioral paraesthesia. In chronic cases, patients may experience depression and cataracts.

An electrocardiogram (ECG) may show a prolonged QT interval, while Trousseau’s sign may be present when the brachial artery is occluded by inflating the blood pressure cuff and maintaining pressure above systolic. This causes wrist flexion and fingers to be drawn together, and is seen in around 95% of patients with hypocalcaemia and around 1% of normocalcaemic people. Chvostek’s sign, which is seen in around 70% of patients with hypocalcaemia and around 10% of normocalcaemic people, involves tapping over the parotid gland to cause facial muscles to twitch.

In summary, hypocalcaemia can cause a range of symptoms and signs related to neuromuscular excitability, including muscle twitching, cramping, and spasms, as well as perioral paraesthesia, depression, and cataracts. Trousseau’s sign and Chvostek’s sign are also commonly observed in patients with hypocalcaemia.

Weight gain can be a side effect of taking sodium valproate.

Sodium Valproate: Uses and Adverse Effects

Sodium valproate is a medication commonly used to manage epilepsy, particularly for generalised seizures. Its mechanism of action involves increasing the activity of GABA in the brain. However, the use of sodium valproate during pregnancy is strongly discouraged due to its teratogenic effects, which can lead to neural tube defects and neurodevelopmental delays in children. Women of childbearing age should only use this medication if it is absolutely necessary and under the guidance of a specialist neurological or psychiatric advisor.

Aside from its teratogenic effects, sodium valproate can also inhibit P450 enzymes, leading to gastrointestinal issues such as nausea, increased appetite, and weight gain. Other adverse effects include alopecia, ataxia, tremors, hepatotoxicity, pancreatitis, thrombocytopenia, hyponatremia, and hyperammonemic encephalopathy. In cases where hyperammonemic encephalopathy develops, L-carnitine may be used as a treatment option.

Overall, while sodium valproate can be an effective medication for managing epilepsy, its use should be carefully considered and monitored due to its potential adverse effects, particularly during pregnancy.

Phenytoin is recognized to cause peripheral neuropathy as a side effect.

Phenytoin: Mechanism of Action and Adverse Effects

Phenytoin is a medication used to manage seizures. Its mechanism of action involves binding to sodium channels, which increases their refractory period. However, the drug is associated with a large number of adverse effects, which can be categorized as acute, chronic, idiosyncratic, and teratogenic. Acute effects include dizziness, diplopia, nystagmus, slurred speech, ataxia, confusion, and seizures. Chronic effects include gingival hyperplasia, hirsutism, coarsening of facial features, drowsiness, megaloblastic anemia, peripheral neuropathy, enhanced vitamin D metabolism causing osteomalacia, lymphadenopathy, and dyskinesia. Idiosyncratic effects include fever, rashes, hepatitis, Dupuytren’s contracture, aplastic anemia, and drug-induced lupus. Teratogenic effects are associated with cleft palate and congenital heart disease. Although routine monitoring of phenytoin levels is not necessary, trough levels should be checked before dosing in cases of dose adjustment, suspected toxicity, or non-adherence to the prescribed medication.

For women of childbearing age who suffer from migraines, propranolol is a better option than topiramate. This is because NICE recommends both drugs for migraine prophylaxis, but the combined oral contraceptive pill cannot be used due to the patient’s migraine history. While zolmitriptan can be used to stop attacks, it is not effective for prophylaxis.

Managing Migraines: Guidelines and Treatment Options

Migraines can be debilitating and affect a significant portion of the population. To manage migraines, it is important to understand the different treatment options available. According to the National Institute for Health and Care Excellence (NICE) guidelines, acute treatment for migraines involves a combination of an oral triptan and an NSAID or paracetamol. For young people aged 12-17 years, a nasal triptan may be preferred. If these measures are not effective, non-oral preparations of metoclopramide or prochlorperazine may be considered, along with a non-oral NSAID or triptan.

Prophylaxis should be given if patients are experiencing two or more attacks per month. NICE recommends topiramate or propranolol, depending on the patient’s preference, comorbidities, and risk of adverse events. Propranolol is preferred in women of childbearing age as topiramate may be teratogenic and reduce the effectiveness of hormonal contraceptives. Acupuncture and riboflavin may also be effective in reducing migraine frequency and intensity for some people. For women with predictable menstrual migraines, frovatriptan or zolmitriptan may be recommended as a type of mini-prophylaxis.

Specialists may consider other treatment options, such as candesartan or monoclonal antibodies directed against the calcitonin gene-related peptide (CGRP) receptor, like erenumab. However, pizotifen is no longer recommended due to common adverse effects like weight gain and drowsiness. It is important to exercise caution with young patients as acute dystonic reactions may develop. By following these guidelines and considering various treatment options, migraines can be effectively managed.

Misconceptions about Dementia: Debunking Common Myths

Dementia is a complex and often misunderstood condition. Here are some common misconceptions about dementia that need to be debunked:

1. In Creutzfeldt-Jakob disease an EEG may be characteristic: An EEG is abnormal in approximately 90% of cases of Creutzfeldt-Jakob disease, showing characteristic changes (i.e. periodic sharp wave complexes).

2. A multi-infarct aetiology is more common than the Alzheimer disease type: Multi-infarct dementia is the second most common type of dementia in people aged over 65 years.

3. A CT scan will reliably distinguish between Alzheimer disease and multi-infarct dementia: The diagnosis of both AD and multi-infarct dementia remains essentially a clinical one (and can only be definitively confirmed at autopsy).

4. In Alzheimer disease a gait disorder is seen at an early stage: Gait disturbances are usually a late sign of AD.

5. Visual hallucinations are typical of Alzheimer’s disease: Visual hallucinations, often very vivid and colourful, are typical of dementia with Lewy bodies (DLB) and Parkinson’s disease dementia (PDD), not of AD.