Common Hand and Wrist Conditions: Symptoms and Characteristics

Ulnar Nerve Entrapment
Ulnar neuropathy is a common condition where the ulnar nerve is compressed at or near the elbow. Patients experience numbness and tingling in the fifth finger and ulnar half of the fourth finger, along with weakness of grip and potential muscle wasting. In severe cases, a claw hand deformity may occur.

De Quervain’s Tenosynovitis
Also known as mother’s wrist, this condition is caused by tendinitis in the tendons of the first dorsal compartment of the wrist. Patients experience pain during thumb and wrist movement, along with tenderness and thickening at the radial styloid. Finkelstein’s test causes sharp pain at the first dorsal compartment, and a prominent radial styloid may be visible. There is no associated sensory loss.

Carpal Tunnel Syndrome
This condition occurs when the median nerve is compressed as it passes through the carpal tunnel at the wrist. Symptoms include numbness and tingling in the thumb and radial fingers, aching and pain in the anterior wrist and forearm, and potential weakness and clumsiness in the hand. Risk factors include female sex, pregnancy, hypothyroidism, connective tissue disease, obesity, trauma, dialysis, and repetitive stress.

Dupuytren’s Contracture
This progressive fibrous tissue contracture of the palmar fascia mainly affects men over 40 with a family history. Patients experience difficulty with manual dexterity, palmar nodules, and eventually flexion contractures in the fourth and fifth fingers. There is no sensory deficit. Risk factors include smoking, alcohol, heavy manual labor, trauma, and diabetes.

Radial Nerve Palsy
Radial nerve palsy results in wrist drop and loss of triceps reflex, along with potential sensory loss in the dorsal thumb and forearm. The radial nerve does not supply sensory innervation to the fourth and fifth fingers.

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.

Friedreich’s ataxia is a common inherited progressive ataxia in the UK that typically presents in childhood or adolescence. The earliest symptom is gait ataxia, followed by limb ataxia, absent lower limb reflexes, and later weakness and wasting of the limbs. Other common features include reduced or absent vibration sense and proprioception, spasticity, dysarthria, dysphagia, cardiac abnormalities, scoliosis, pes cavus, equinovarus, sleep apnea, and urinary frequency/urgency. The history is classic for this condition, and the ECG may show left ventricular hypertrophy. Charcot-Marie-Tooth disease, Huntington’s disease, and multiple sclerosis are not consistent with this history, while vitamin B12 deficiency may cause similar symptoms but is generally a condition of adults and does not fit the clinical picture as well as Friedreich’s ataxia.

Neurological Conditions and Upper Motor Neurone Signs

Upper motor neurone signs, such as spasticity, hyperreflexia, clonus, and the Babinski reflex, are indicative of certain neurological conditions. Multiple sclerosis, a demyelinating disease, is one such condition that causes these signs. On the other hand, a stroke in a young person is relatively unlikely to cause upper motor neurone signs. Cerebral venous thrombosis could cause these signs, but it would be highly unlikely without a headache and normal fundoscopy. Guillain–Barré syndrome (GBS) is a relatively symmetrical, ascending lower motor neurone disease that does not typically present with blurred vision and speech disturbances. Poliomyelitis, a lower motor neurone condition, is characterised by hypotonia and hyporeflexia and would not cause the Babinski reflex.

Understanding Upper Motor Neurone Signs in Neurological Conditions

The Importance of Neuroimaging in the Diagnosis of Dementia

Neuroimaging plays a crucial role in the diagnosis of dementia and ruling out reversible causes of cognitive decline. Structural imaging should be offered to assist with subtype diagnosis and exclude other reversible conditions unless dementia is well established and the subtype is clear. In primary care, a blood screen is usually sent to exclude reversible causes, while in secondary care, neuroimaging is performed to provide information on aetiology to guide prognosis and management. Focal neurology and cardiovascular abnormalities are not indications for performing structural imaging of the brain. However, neuroimaging is required in the workup of dementia in all age groups, including patients over 75 years old and those under 65 years old with suspected early-onset dementia. The 2011 National Institute for Health and Care Excellence (NICE) guidelines state that structural imaging is essential in the investigation of dementia.

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.

Ramsey Hunt syndrome can be diagnosed based on the presence of a vesicular rash near the ear, which is often accompanied by hyperacusis in approximately one-third of patients.

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.

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.

Management of Transient Visual Loss and Carotid Artery Stenosis

Transient visual loss can be caused by various factors, including retinal ischemia and emboli from atherosclerotic carotid arteries. In cases where Doppler ultrasound shows 40% stenosis of the internal carotid artery, surgery is not recommended. Instead, best medical treatment should be administered, including control of blood pressure, antiplatelet agents, cholesterol-lowering drugs, and lifestyle advice. Acute treatment with 300 mg aspirin is recommended, followed by high-dose treatment for two weeks before initiating long-term antithrombotic treatment.

Prednisolone is used in the treatment of giant cell arteritis, which can also cause transient visual loss. Diagnosis requires three out of five criteria, including age over 50, new headache, temporal artery abnormality, elevated ESR, and abnormal artery biopsy.

Carotid artery angioplasty may be considered as an alternative to carotid endarterectomy for revascularization in select cases. However, there are concerns regarding stent placement and the risk of stroke. Surgical management is only indicated for carotid artery stenosis over 50%.

Anticoagulation treatment is not routinely used for the treatment of acute stroke. It may be considered for those in atrial fibrillation or at high risk of venous thromboembolism. For patients with a history of transient ischemic attack, high-dose aspirin is recommended for two weeks post-event, followed by long-term secondary prevention with aspirin and modified-release dipyridamole or clopidogrel.

Management of Transient Visual Loss and Carotid Artery Stenosis

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.