Spasticity in multiple sclerosis is caused by demyelination along the nerves that control movement, resulting in stiffness that can sometimes be helpful but can also become painful. Physiotherapy exercises are the simplest and most effective treatment, but first-line medications such as baclofen and gabapentin are also recommended. Gabapentin is an anticonvulsant that can be effective against muscle spasms, while diazepam is a muscle relaxant that may be more useful at night due to side effects at higher doses. Botulinum toxin and dantrolene sodium can be considered if conventional treatments prove ineffective, but are not used as first-line for spasticity. The NICE multiple sclerosis guideline recommends gabapentin as one of the first drugs to try in the treatment of spasms and spasticity.

Multiple sclerosis is a condition that cannot be cured, but its treatment aims to reduce the frequency and duration of relapses. In the case of an acute relapse, high-dose steroids may be administered for five days to shorten its length. However, it is important to note that steroids do not affect the degree of recovery. Disease-modifying drugs are used to reduce the risk of relapse in patients with MS. These drugs are typically indicated for patients with relapsing-remitting disease or secondary progressive disease who have had two relapses in the past two years and are able to walk a certain distance unaided. Natalizumab, ocrelizumab, fingolimod, beta-interferon, and glatiramer acetate are some of the drugs used to reduce the risk of relapse in MS.

Fatigue is a common problem in MS patients, and amantadine is recommended by NICE after excluding other potential causes such as anaemia, thyroid problems, or depression. Mindfulness training and CBT are other options for managing fatigue. Spasticity is another issue that can be addressed with first-line drugs such as baclofen and gabapentin, as well as physiotherapy. Cannabis and botox are currently being evaluated for their effectiveness in managing spasticity. Bladder dysfunction is also a common problem in MS patients, and anticholinergics may worsen symptoms in some patients. Ultrasound is recommended to assess bladder emptying, and intermittent self-catheterisation may be necessary if there is significant residual volume. Gabapentin is the first-line treatment for oscillopsia, which is a condition where visual fields appear to oscillate.

Understanding Wernicke’s Encephalopathy

Wernicke’s encephalopathy is a condition that affects the brain and is caused by a deficiency in thiamine. This condition is commonly seen in individuals who abuse alcohol, but it can also be caused by persistent vomiting, stomach cancer, or dietary deficiencies. The classic triad of symptoms associated with Wernicke’s encephalopathy includes oculomotor dysfunction, gait ataxia, and encephalopathy. Other symptoms may include peripheral sensory neuropathy and confusion.

When left untreated, Wernicke’s encephalopathy can lead to the development of Korsakoff’s syndrome. This condition is characterized by antero- and retrograde amnesia and confabulation in addition to the symptoms associated with Wernicke’s encephalopathy.

To diagnose Wernicke’s encephalopathy, doctors may perform a variety of tests, including a decreased red cell transketolase test and an MRI. Treatment for this condition involves urgent replacement of thiamine. With prompt treatment, individuals with Wernicke’s encephalopathy can recover fully.

It is probable that the patient experienced cataplexy, as indicated by their laughter and history of excessive sleepiness during classes, which suggests a potential diagnosis of narcolepsy. While cardiac syncope is a possibility, further investigations such as an ECG and transthoracic echocardiogram would be necessary to rule it out. Absence seizures are unlikely due to the absence of blank staring, and generalized epilepsy is also improbable as it typically involves longer-lasting tonic-clonic seizures with a slower recovery time.

Understanding Cataplexy

Cataplexy is a condition characterized by a sudden and temporary loss of muscle control triggered by intense emotions such as laughter or fear. It is commonly associated with narcolepsy, with around two-thirds of patients experiencing cataplexy. The symptoms of cataplexy can vary from mild buckling of the knees to complete collapse.

This condition can be debilitating and can significantly impact a person’s quality of life. It can also be challenging to diagnose, as the symptoms can be mistaken for other conditions such as seizures or fainting spells. Treatment options for cataplexy include medication and lifestyle changes, such as avoiding triggers that can cause emotional responses.

Understanding the Clinical Features of Idiopathic Intracranial Hypertension (IIH)

Idiopathic intracranial hypertension (IIH) is a condition that presents with non-specific complaints, making it difficult to diagnose. However, there are several clinical features that can help identify the condition. The most common symptom is a severe daily headache, often described as pulsatile, that may be associated with nausea and vomiting. Other symptoms include pulse-synchronous tinnitus, transient visual obscurations, visual loss, neck and back pain, diplopia, and photophobia. IIH can occur in any age group but is most commonly seen in women of childbearing age. Horizontal diplopia occurs in about 33% of patients with IIH, while hearing loss is a rare presentation. Tinnitus is described by two-thirds of patients, with pulse-synchronous tinnitus being a relatively specific symptom for elevated intracranial pressure. By understanding these clinical features, healthcare professionals can better diagnose and manage IIH.

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.

The patient is likely suffering from Becker’s muscular dystrophy, a milder form of the condition compared to Duchenne muscular dystrophy (DMD). Both conditions are caused by mutations in the DMD gene, but Becker’s tends to present later in childhood or adolescence with slower progression of symptoms. The patient’s normal childhood development followed by slow onset of proximal weakness fits the typical picture of Becker’s. Limb-girdle muscular dystrophy (LGMD) is a possibility, but less likely given the patient’s presentation. DMD is unlikely as it typically presents in early childhood with rapid progression of symptoms. Facioscapulohumeral dystrophy is characterized by weakness and wasting of the face, scapula, and upper arms, and would not typically present with gait disturbance or lower limb weakness in childhood. Myasthenia gravis is also unlikely given the patient’s history.

Contraindications and Considerations for the Use of Donepezil

Donepezil is a medication used to treat Alzheimer’s disease. However, there are certain contraindications and considerations that healthcare professionals should keep in mind when prescribing this medication.

Bradycardia, a condition where the heart beats too slowly, is a relative contraindication for the use of donepezil. This medication may cause bradycardia and atrioventricular node block, so caution should be taken in patients with other cardiac abnormalities. Additionally, patients with asthma, chronic obstructive pulmonary disease, supraventricular conduction abnormalities, susceptibility to peptic ulcers, and sick-sinus syndrome should also be closely monitored when taking donepezil.

Concurrent use of simvastatin, a medication used to lower cholesterol levels, is not a concern when taking donepezil. General anxiety disorder (GAD) and diabetes mellitus type II are also not contraindications for the use of donepezil.

However, elderly patients with a known history of persistent bradycardia, heart block, recurrent unexplained syncope, or concurrent treatment with drugs that reduce heart rate should avoid donepezil. A history of ischaemic heart diseases alone is not a contraindication for donepezil.

In summary, healthcare professionals should carefully consider a patient’s medical history and current medications before prescribing donepezil. Close monitoring is necessary in patients with certain cardiac abnormalities and caution should be taken in elderly patients with a history of bradycardia or heart block.

Understanding Carpal Tunnel Syndrome: Symptoms and Examination Findings

Carpal tunnel syndrome (CTS) is a condition caused by compression of the median nerve in the carpal tunnel. One of the symptoms of CTS is the wasting of the thenar eminence, which is innervated by the median nerve. It is important to note that the hypothenar eminence, which is innervated by the ulnar nerve, is not affected by CTS.

During examination, weakness of thumb abduction (abductor pollicis brevis) is a common finding in CTS. Tapping along the problematic nerve causes paraesthesia, which is known as Tinel’s sign. Flexion of the wrist also causes symptoms, which is known as Phalen’s sign.

Treatment for CTS may include a corticosteroid injection, wrist splints at night, and surgical decompression through flexor retinaculum division.

Overall, understanding the symptoms and examination findings of CTS can help with early diagnosis and appropriate treatment.

Patients with Bell’s palsy should receive oral prednisolone within 72 hours of onset, regardless of the severity of their symptoms or any improvement since onset. This is important to differentiate Bell’s palsy from other conditions such as cerebral events and Ramsay-Hunt syndrome. Eye protection with lid taping or lubricating eye drops should also be considered. Therefore, the correct answer is oral prednisolone and artificial tears. Oral aciclovir alone is not sufficient as it does not provide steroids or eye protection. Reassurance only and advice to return if symptoms persist after 2 weeks is not appropriate as treatment should be offered within the 72-hour window. Urgent referral to ENT is not necessary as the diagnosis can be made and managed in primary care, but non-urgent referral may be necessary in severe or prolonged cases or where the diagnosis is unclear.

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.

Lifelong use of aspirin and dipyridamole. Age: 55.

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.

The woman is experiencing migraines with aura, a condition that can be exacerbated by the use of COCP. If a woman has migraine with aura, it is recommended that she discontinue the use of the pill immediately. This is because the oestrogen component of COCP can increase the risk of ischaemic stroke. The only alternative contraceptive medication that can be prescribed is a progesterone-only contraceptive pill, as other options contain oestrogen.

Counselling for Women Considering the Combined Oral Contraceptive Pill

Women who are considering taking the combined oral contraceptive pill (COC) should receive counselling on the potential harms and benefits of the pill. The COC is highly effective if taken correctly, with a success rate of over 99%. However, there is a small risk of blood clots, heart attacks, and strokes, as well as an increased risk of breast and cervical cancer.

In addition to discussing the potential risks and benefits, women should also receive advice on how to take the pill. If the COC is started within the first 5 days of the menstrual cycle, there is no need for additional contraception. However, if it is started at any other point in the cycle, alternative contraception should be used for the first 7 days. Women should take the pill at the same time every day and should be aware that intercourse during the pill-free period is only safe if the next pack is started on time.

There have been recent changes to the guidelines for taking the COC. While it was previously recommended to take the pill for 21 days and then stop for 7 days to mimic menstruation, it is now recommended to discuss tailored regimes with women. This is because there is no medical benefit to having a withdrawal bleed, and options include never having a pill-free interval or taking three 21-day packs back-to-back before having a 4 or 7 day break.

Women should also be informed of situations where the efficacy of the pill may be reduced, such as vomiting within 2 hours of taking the pill, medication that induces diarrhoea or vomiting, or taking liver enzyme-inducing drugs. It is also important to discuss sexually transmitted infections and precautions that should be taken with enzyme-inducing antibiotics such as rifampicin.

Overall, counselling for women considering the COC should cover a range of topics to ensure that they are fully informed and able to make an informed decision about their contraceptive options.

The patient in the scenario has non-fluent speech, normal comprehension, and impaired repetition, which is indicative of Broca’s dysphasia. This type of speech abnormality is associated with a lesion in the frontal lobe affecting Broca’s area. When responding to a conversation, the signal travels from the ear to Wernicke’s area for comprehension, then along the arcuate fasciculus to Broca’s area for speech coordination. A lesion in the cerebellum, occipital lobe, parietal lobe, or temporal lobe would not be associated with Broca’s dysphasia.

Understanding the Different Types of Aphasia

Aphasia is a language disorder that affects a person’s ability to communicate effectively. There are different types of aphasia, each with its own set of symptoms and causes. Wernicke’s aphasia is caused by a lesion in the superior temporal gyrus, which is responsible for forming speech before sending it to Broca’s area. This type of aphasia results in sentences that make no sense, word substitution, and neologisms, but speech remains fluent. On the other hand, Broca’s aphasia is caused by a lesion in the inferior frontal gyrus, resulting in non-fluent, laboured, and halting speech. Repetition is impaired, but comprehension is normal.

Conduction aphasia is caused by a stroke affecting the arcuate fasiculus, the connection between Wernicke’s and Broca’s area. Speech is fluent, but repetition is poor, and the person is aware of the errors they are making. Comprehension is normal. Global aphasia is the most severe type, affecting all three areas and resulting in severe expressive and receptive aphasia. However, the person may still be able to communicate using gestures.

Understanding the different types of aphasia is crucial in providing appropriate treatment and support for individuals with this language disorder. It is important to note that dysarthria is different from aphasia and refers to a motor speech disorder.

The P450 system is inhibited by 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.

Guillain-Barre syndrome is a condition where the immune system attacks the peripheral nervous system, leading to demyelination. It is often triggered by an infection and causes rapidly advancing ascending motor neuropathy. Proximal muscles are more affected than distal muscles.

A stroke or transient ischaemic attack usually has a sudden onset and causes unilateral symptoms such as facial droop, arm weakness, and slurred speech.

Raynaud’s disease causes numbness and pain in the fingers and toes, typically in response to cold weather or stress.

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.

Understanding Multiple Sclerosis

Multiple sclerosis is a chronic autoimmune disorder that affects the central nervous system, causing demyelination. It is more common in women and typically diagnosed in individuals aged 20-40 years. Interestingly, it is much more prevalent in higher latitudes, with a five-fold increase compared to tropical regions. Genetics play a role in the development of multiple sclerosis, with a 30% concordance rate in monozygotic twins and a 2% concordance rate in dizygotic twins.

There are several subtypes of multiple sclerosis, including relapsing-remitting disease, which is the most common form and accounts for around 85% of patients. This subtype is characterized by acute attacks followed by periods of remission. Secondary progressive disease describes relapsing-remitting patients who have deteriorated and developed neurological signs and symptoms between relapses. Gait and bladder disorders are commonly seen in this subtype, and around 65% of patients with relapsing-remitting disease go on to develop secondary progressive disease within 15 years of diagnosis. Finally, primary progressive disease accounts for 10% of patients and is characterized by progressive deterioration from onset, which is more common in older individuals. Understanding the different subtypes of multiple sclerosis is crucial for proper diagnosis and management of the disease.

Differential diagnosis for a patient with subacute cerebellar dysfunction and normal imaging

Paraneoplastic cerebellum syndrome, multiple sclerosis, cerebellar metastasis, malignant meningitis, and Wernicke’s encephalopathy are among the possible diagnoses for a patient presenting with subacute onset of cerebellar signs and normal imaging.

Paraneoplastic cerebellum syndrome is a rare immune-mediated complication of many cancers, which may be diagnosed before the underlying tumour. Symptoms develop rapidly and include dizziness, nausea, vertigo, nystagmus, ataxia, oscillopsia, dysarthria, tremor, dysphagia, and blurry vision. MRI may be normal, but CSF may show raised protein and anti-neuronal antibodies.

Multiple sclerosis is more common in women and usually presents with transient episodes of visual change or limb weakness/paraesthesiae, as well as bladder and cerebellar dysfunction. MRI may visualise plaques of demyelination, and CSF shows oligoclonal bands.

Cerebellar metastasis could occur in breast cancer, but it would be visualised on MRI.

Malignant meningitis occurs when cancer spreads to the meninges and presents with confusion, headaches, and weakness. Imaging and CSF would be abnormal.

Wernicke’s encephalopathy is due to thiamine deficiency, typically seen in alcoholics, and presents with acute confusional state, ophthalmoplegia, and gait ataxia. Dysarthria is not usually a feature. Thiamine deficiency is not suggested by this patient’s history.

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.

The gradual decline in cognitive function, along with hypertension and smoking as risk factors for cerebrovascular disease, suggest a diagnosis of vascular dementia. This type of dementia is caused by damage to the brain from reduced blood flow or bleeding due to cerebrovascular disease. In contrast, Alzheimer’s dementia progresses slowly over time, while frontotemporal dementia affects personality, behavior, language, and attention. Lewy body dementia is characterized by hallucinations and Parkinsonian symptoms, while Parkinson’s dementia occurs in patients with Parkinson’s disease and affects their mental function and memory, along with physical signs of PD.

Understanding Vascular Dementia: Causes, Symptoms, and Management

Vascular dementia is a type of cognitive impairment that is caused by different mechanisms resulting from cerebrovascular disease. It is the second most common form of dementia after Alzheimer’s disease. Vascular dementia is often recognized as the most severe form of the spectrum of deficits encompassed by the term vascular cognitive impairment. Early detection and an accurate diagnosis are crucial in preventing vascular dementia.

The prevalence of vascular dementia is estimated to be around 17% of dementia cases in the UK. The incidence of vascular dementia increases with age and is often associated with a history of stroke or transient ischemic attack, atrial fibrillation, hypertension, diabetes mellitus, hyperlipidemia, smoking, obesity, coronary heart disease, and a family history of stroke or cardiovascular disease. Rarely, vascular dementia can be inherited as in the case of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy.

Patients with vascular dementia typically present with a sudden or stepwise deterioration of cognitive function, focal neurological abnormalities, difficulty with attention and concentration, seizures, memory disturbance, gait disturbance, speech disturbance, and emotional disturbance. Diagnosis is made based on a comprehensive history and physical examination, formal screening for cognitive impairment, medical review to exclude medication cause of cognitive decline, and MRI scan.

Treatment for vascular dementia is mainly symptomatic with the aim to address individual problems and provide support to the patient and carers. It is important to detect and address cardiovascular risk factors to slow down the progression of the disease. Non-pharmacological management is tailored to the individual and may include cognitive stimulation programs, multisensory stimulation, music and art therapy, and animal-assisted therapy. Pharmacological management is limited, and there is no specific pharmacological treatment approved for cognitive symptoms. Only consider AChE inhibitors or memantine for people with vascular dementia if they have suspected comorbid Alzheimer’s disease, Parkinson’s disease dementia, or dementia with Lewy bodies. There is no evidence that aspirin is effective in treating patients with a diagnosis of vascular dementia, and no randomized trials have evaluated statins for vascular dementia.

Cervico-cerebral arterial dissections (CADs) are a common cause of strokes in younger patients, accounting for almost 20% of strokes in those under 45 years old. The majority of cases involve the extracranial internal carotid artery, while extracranial vertebral dissections make up about 15% of cases. A high level of suspicion is necessary to diagnose CAD, and confirmation can be obtained through various imaging techniques such as Doppler ultrasonography, magnetic resonance imaging/magnetic resonance angiography (MRA), computed tomography angiography (CTA), or catheter angiography. CTA can reveal several characteristic features of CAD, including an abnormal vessel contour, enlargement of the dissected artery, an intimal flap, and a dissecting aneurysm. The traditional method of diagnosing arterial dissections is catheter angiography, which typically shows a long segment of narrowed lumen known as the string sign. Other conditions such as carotid-artery pseudoaneurysm, carotid-artery aneurysm, carotid-artery occlusion, and carotid-artery stenosis can also be identified through imaging techniques, but they are not evident in this particular angiogram.

Driving Restrictions Following a Stroke or TIA

After experiencing a transient ischaemic attack (TIA) or stroke, patients must not drive for at least one month, regardless of the severity. If clinical recovery is satisfactory, non-HGV drivers may resume driving after one month. However, if residual neurological deficits persist after one month, including visual field defects, cognitive defects, and impaired limb function, patients must not drive until these signs have fully resolved. Minor limb weakness alone does not require notification to the DVLA unless restriction to certain types of vehicles is needed.

If a patient has only minor weakness to the hand, they can resume driving after one month. However, if they wish to drive a group 2 vehicle, such as a large goods vehicle (LGV), they must wait at least two years. The DVLA may refuse or revoke a license for one year following a stroke or TIA, but patients can be considered for licensing after this period if there is no residual impairment likely to affect safe driving and no other significant risk factors. Licensing may be subject to satisfactory medical reports, including exercise electrocardiographic (ECG) testing.

In cases of doubt, driving assessments may be carried out at specialist rehabilitation centers. It is essential to contact the DVLA for an overview of the main restrictions for drivers with neurological and other conditions.