Typical symptoms of Parkinson’s include bradykinesia, postural instability, and initially unilateral symptoms. On the other hand, alcohol can alleviate essential tremor symptoms.

Understanding Essential Tremor

Essential tremor, also known as benign essential tremor, is a genetic condition that typically affects both upper limbs. The most common symptom is a postural tremor, which worsens when the arms are outstretched. However, the tremor can be improved by rest and alcohol consumption. Essential tremor is also the leading cause of head tremors, known as titubation.

When it comes to managing essential tremor, the first-line treatment is propranolol. This medication can help reduce the severity of the tremors. In some cases, primidone may also be used to manage the condition. It’s important to note that essential tremor is a lifelong condition, but with proper management, individuals can lead a normal life. By understanding the symptoms and treatment options, those with essential tremor can take control of their condition and improve their quality of life.

Managing Frontotemporal Dementia: Treatment Options and Referrals

Frontotemporal dementia (FTD) is a progressive neurodegenerative disorder that affects behavior, language, and executive function. While there is no cure for FTD, management strategies can help alleviate symptoms and provide support for patients and their families.

One important step in managing FTD is to stop any drugs that may be exacerbating memory problems or confusion, such as anticholinergics or central nervous system drugs. Multidisciplinary health and social care is also crucial, involving referrals to geriatric medicine, psychiatry, psychology, social work, occupational therapy, speech and language therapy, physiotherapy, and community nursing.

However, certain treatment options should be avoided or used with caution in FTD patients. Benzodiazepines, for example, are associated with cognitive worsening and fall-related injuries. Anticholinesterase inhibitors, typically used in mild to moderate Alzheimer’s disease, have shown disappointing results in FTD patients who do not have cholinergic loss. Memantine, used in moderate to severe Alzheimer’s disease, has not been shown to be effective in FTD and may even have a detrimental effect on cognition in some individuals.

Antipsychotics should only be used cautiously and when other options have failed, as FTD patients are at higher risk of extrapyramidal side effects. Overall, a personalized and coordinated approach to FTD management is essential for optimizing patient outcomes.

The man is experiencing acute confusion and impaired consciousness, which is indicative of delirium rather than dementia. The presence of dehydration and a smell of urine suggests a possible urinary tract infection as a trigger for the delirium. Korsakoff syndrome is unlikely as it is an amnestic disorder caused by thiamine deficiency associated with prolonged alcohol ingestion. The symptoms described are more likely to be mistaken for Wernicke’s encephalopathy, which can also cause confusion and altered consciousness. There is no evidence to suggest an acute psychotic episode. Treatment for Wernicke’s encephalopathy involves thiamine replacement.

Delirium vs. Dementia: Understanding the Differences

Delirium and dementia are two conditions that are often confused with each other. While both can cause confusion and cognitive impairment, there are some key differences between the two. Delirium is a sudden onset of confusion and disorientation, often accompanied by changes in consciousness and perception. Dementia, on the other hand, is a gradual decline in cognitive function that occurs over time.

Factors that can help distinguish delirium from dementia include the acute onset of symptoms, impairment of consciousness, fluctuation of symptoms (such as being worse at night or having periods of normality), abnormal perception (such as illusions and hallucinations), agitation, fear, and delusions. These symptoms are often more pronounced in delirium than in dementia.

It is important to understand the differences between delirium and dementia, as they require different approaches to treatment. Delirium is often reversible if the underlying cause can be identified and treated, while dementia is a progressive condition that cannot be cured.

Myotonic dystrophy is a genetic disorder that causes muscle stiffness and wasting. It is inherited in an autosomal dominant pattern and typically presents between the ages of 15 and 40. The disease progresses slowly and can lead to cataracts, hypogonadism, frontal balding, and cardiac issues. Patients may experience weakness, wasting, and myotonia in affected muscles, particularly in the face and limbs. Other symptoms include hollowing of the cheeks, swan neck appearance, and difficulty releasing a handshake. This patient’s presentation is consistent with myotonic dystrophy and likely inherited from her father.

Myasthenia gravis is an autoimmune disorder that causes weakness, particularly in the periocular, facial, bulbar, and girdle muscles. Fatigue is a hallmark symptom, and dysphagia may occur in advanced cases. Temporalis atrophy is not a feature.

Motor neurone disease is a rare condition that typically presents with mixed upper and lower motor neuron signs in the same limb. Symptoms may include weakness, wasting, cramps, stiffness, and problems with speech and swallowing. Dysphagia and speech problems become more common as the disease progresses. MND is unlikely in a woman of this age, and there is typically no familial link.

Multiple sclerosis is a more common condition in women that typically presents with transient episodes of optic neuritis or limb weakness/paraesthesiae. Only a small percentage of sufferers have a family history of MS.

Polymyositis is a connective tissue disease that causes proximal muscle weakness and tenderness. Atrophy is a late feature, and patients may have difficulty rising from chairs. Dysphagia may occur in advanced cases, but ptosis and temporalis wasting are not features. Polymyositis is not typically inherited.

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.

The Addenbrookes Cognitive Exam (ACE-3) is a reliable tool for detecting dementia, with a score of 82 or less indicating a strong likelihood of dementia. The exam assesses five domains: Memory, Attention, Fluency, Language, and Visuospatial. Alzheimer’s dementia typically results in a global deficit across all domains, with later deficits in memory and attention due to damage in the medial temporal lobe. Frontotemporal dementia primarily affects fluency and language due to damage in the frontal lobe. Vascular dementia deficits vary depending on the location and severity of previous strokes, and there is no consistent pattern seen in ACE-3 examinations. Mild cognitive impairment (MCI) is a precursor to many forms of dementia, with an ACE-3 score of 82-88 indicating MCI. In this scenario, the patient’s score of 68 rules out MCI as a diagnosis.

Alzheimer’s disease is a type of dementia that gradually worsens over time and is the most common form of dementia in the UK. The risk factors for Alzheimer’s disease include increasing age, family history of the disease, and certain genetic mutations. Inherited forms of the disease are caused by mutations in the amyloid precursor protein, presenilin 1, and presenilin 2 genes. Additionally, the apoprotein E allele E4 and Caucasian ethnicity are also risk factors for Alzheimer’s disease.

The pathological changes associated with Alzheimer’s disease include widespread cerebral atrophy, particularly in the cortex and hippocampus. Microscopically, cortical plaques and intraneuronal neurofibrillary tangles are present due to the deposition of type A-Beta-amyloid protein and abnormal aggregation of the tau protein. The hyperphosphorylation of the tau protein has been linked to Alzheimer’s disease. Furthermore, there is a deficit of acetylcholine due to damage to an ascending forebrain projection.

Neurofibrillary tangles are partly made from a protein called tau, which interacts with tubulin to stabilize microtubules and promote tubulin assembly into microtubules. In Alzheimer’s disease, tau proteins are excessively phosphorylated, impairing their function.

Diagnostic Tests for Acoustic Tumours: Importance of MRI with Contrast

Acoustic tumours require accurate diagnosis for effective treatment. The most definitive diagnostic test is gadolinium-enhanced magnetic resonance imaging (MRI) of the cerebellopontine angle. This test can detect tumours as small as 1-2 mm in diameter, while fine-cut computed tomography (CT) scanning may miss tumours as large as 1.5 cm even with intravenous contrast enhancement.

Audiometry is also important, but only 5% of patients with acoustic tumours will have a normal audiogram. If MRI is contraindicated, air-contrast cisternography can detect relatively small intracanalicular tumours with high sensitivity.

Fine-cut CT scanning of the internal auditory canal with contrast can rule out medium to large tumours, but cannot reliably detect tumours smaller than 1-1.5 cm. CT scanning without contrast can rule out medium-sized tumours, but is not reliable for detecting smaller tumours.

It is critical to use gadolinium contrast in MRI of the cerebellopontine angle, as non-enhanced MRI may miss small tumours. Therefore, MRI with contrast is the most important diagnostic test for acoustic tumours.

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.

Immediate admission for imaging to rule out a hemorrhage is necessary if a patient with suspected TIA is on warfarin, a DOAC, or has a bleeding disorder.

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 recommended initial treatments for spasticity in multiple sclerosis are baclofen and gabapentin.

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.