Week 12 - Neurology Flashcards
What is the most common cause of radial nerve palsy? How does it present?
Entrapment at spiral groove - i.e. Saturday night palsy or sleeping with someone resting on your arm.
Wrist and finger drop, usually painless, sensory change over back of thumb index and middle finger.
What is the most common cause of ulnar nerve palsy? How does it present?
Entrapment at ulnar groove (medial epicondyle of humerus.)
May be history of trauma at the elbow, sensory disturbance over front and back of pinkie and ring finger, weak grip, usually painless.
What is the most common cause of median nerve palsy? What are the presenting symptoms?
Entrapment within carpal tunnel at wrist.
Presenting symptoms: history of intermittent nocturnal pain, numbness and tingling often relieved by shaking the hand. Patient may complain of weak grip, positive tinel’s sign (parasthesia in the distribution of the nerve when it is gently percussed.
What is the most common cause of palsy of the Anterior Interosseous branch of the median nerve?
Trauma to forearm.
History of forearm pain, patient may complain of weak grip of keys, positive tinel’s sign, no sensory change.
What is the most common cause of femoral nerve palsy? What are the presenting symptoms?
Cause: haemorrhage, trauma.
Presenting symptoms: weakness of quadriceps, weakness of hip flexion, numbness in medial shin (from thigh down to leg).
What is the most common cause of palsy of the common peroneal nerve? What are the presenting symptoms?
Entrapment at fibular head.
History of trauma, surgery or external compression.
Acute onset of foot drop or sensory disturbance (lateral top of leg), usually painless.
What is mononeuritis multiplex? What are the common causes?
Simultaneous or sequential development of palsy of 2 or more nerves.
Diabetes, vasculitic causes, rheumatological (i.e. RA), infective (i.e. Hep C, HIV), sarcoidosis, lymphoma.
What are the protective connective tissue layers surrounding peripheral nerves in fascicles?
Endoneurium
Perineurium
Epineurium
What is the function of large myelinated fibres in the PNS?
Motor nerves
Proprioception, vibration, light touch,
How does neuropathy present in:
- Motor fibres
- Sensory fibres
- Autonomic fibres
Motor - muscle weakness and atrophy
Sensory:
Large (myelinated fibres) sensory ataxia, loss of vibratory sense +/- tingling. Small (thinly myelinated/myelinated) fibres - impaired pin prick, temperature, painful burning, numbness and tingling.
Autonomic - postural hypotension, erectile dysfunction, GI disturbance, abnormal sweating.
Describe the features of length dependant axonal neuropathy.
Diffuse involvement of peripheral nerves. Length dependant - starts in toes/feet. Symmetrical. Slowly progressive. No significant sensory ataxia. Any weakness is distal and mild.
What are the causes of length-dependent axonal
neuropathy?
Diabetes, alcohol, nutritional (folate, B12, thiamine, B6 deficiency), immune related (RA, lupus), renal failure, hypothyroidism, drugs (isoniazid, amiodarone), infectious (HIV, hepatitis B and C), inherited, myeloma.
Describe the features of guillain-barre syndrome. How is it treated?
Progressive, ascending (starts in hands and feet) weakness, numbness and pain over days.
Flaccid quadraparesis with areflexia.
+/- respiratory/bulbar/autonomic involvement.
Post infectious autoimmune aetiology (e.g. campylobacter, EBV)
Treated with IVIG or apheresis.
Chronic form (steroid and IVIG responsive)
What are the clinical features of muscle disease in the following systems:
- Limbs
- Face
- Eyes
- Bulbar
- Neck and spine
- Respiratory
- Myocardial
Proximal limb weakness - difficulty raising arms above head, arising from seat.
Facial weakness - characterisic myopathic facies, drooling.
Eyes - ptosis, opthalamoplegia.
Bulbar - dysarthria (speech difficulty), dysphagia.
Neck and spine - head drop, scoliosis.
Respiratory - breathlessness (especially when lying flat).
Myocardial - exercise intolerance, palpitations.
What are some of the causes of muscle disease?
Muscular dystrophies i.e. duchenne, becker.
Inflammatory muscle disease i.e. polymyositis, dermatomyositis.
Neuromuscular junction disorders - myasthenia gravis.
Metabolic muscle disorders - glycogen storage diseases.
What is Myasthenia Gravis and its pathogenesis?
Autoimmune disorder: antibodies to acetylcholine receptor at post synaptic NMJ.
Fatiguable weakness of ocular, bulbar, neck, respiratory and/or limb muscles.
How is it investigated and managed?
Investigation - antibodies to AChr present in 85% of cases.
Single fibre EMG (electromyography) and repetitive nerve stimulation also abnormal.
Managed with pyridostigmine (anti-acetylcholine esterase) and immunosuppressive therapies (e.g. steroids and IVIG)
Define primary and secondary headache and give a few examples of each.
Primary headache - the headache and it’s associated features is the disorder (no underlying cause) i.e. migraine, tension-type headache, cluster headache.
Secondary headache - the headache is secondary to an underlying cause i.e. subarachnoid haemorrhage,, space occupying lesion, meningitis, temporal arteritis, high/low intracranial pressure, drug induced.
What are some of the red flag features of secondary headache?
Age >50 years, thunderclap headache, focal/non-focal neurological deficit, worsening of symptoms with posture, valsava or physical exertion.
Early morning headaches.
Systemic symptoms - fever, weight loss.
Seizures, meningism.
Temporal artery tenderness, jaw claudication.
Specific situations - cancer, pregnancy, post partum, HIV/immunosuppression.
Abnormal signs in a clinical examination of a patient with a headache suggests a secondary cause of the headache. What abnormal signs may be present?
General/systemic - reduced conscious level, reduced BP, pyrexia, menignism, skin rash, temporal artery tenderness.
Cranial nerve - pupillary responses, visual fields +/- blind spot, eye movements, fundoscopy.
What is the clinical features of a migraine headache?
Prodrome - reported 40-60%, up to 48 hours before headache, variable symptoms - mood disturbance, photophobia, hyperosmia, restlessness, diarrhoea.
Aura - develops 5-20 minutes and lasts <60 mins. Visual aura most common, sensory aura often starts in hand and migrates up arm.
Headache - throbbing/pulsatile, moderate-severe intensity, duration 4-72 hours, unilateral in 60% of cases, aggravated by routine physical activity.
Associated symptoms - nausea and vomiting, photophobia, phonophobia, osmophobia, mood disturbance, diarrhoea, autonomic disturbance: lacrimation, conjunctival injection, nasal stuffiness.
What is the investigation and management of migraine?
Good history and normal clinical examination does not require further investigation. Cranial imaging if red flags or aura >24 hours.
Avoid triggers, reduce alcohol and caffeine, regular meals and sleep patterns. Simple analgesia (i.e. paracetamol, aspirin, NSAIDs.) Triptans, antiemetics (i.e. metoclopramide). Prophylaxis: beta blockers, tricyclic antidepressants (i.e. amitriptyline), anti-epilepsy drugs (topiramate).
What is a medication overuse headache (MOH)?
Headache of 15+ days per month associated with frequent use of acute relief medications (e.g. NSAIDs).
What is a thunderclap headache? What should it be treated as until proven otherwise?
Abrupt-onset of severe headache which reaches maximal intensity <5mins (and lasts >1hr). Subarachnoid haemorrhage.
What are the causes of thunderclap?
Subarachnoid haemorrhage
Intracerebral haemorrhage;
Arterial dissection (vertebral or carotid);
Cerebral venous sinus thrombosis;
Bacterial meningitis;
Rare – spontaneous intracranial hypotension,
pituitary apoplexy;
Primary headaches (eg. migraine, exertional
headache, cluster headache) – diagnosis of
exclusion
How is a thunderclap headache investigated?
Bloods - U&E. LFT, glucose, FBC, coagulation screen, CRP. Blood cultures if pyrexial.
12 lead ECG
Urgent CT brain
Lumbar puncture - after 12 hours to look for xanthochromia.
What is a normal intra cranial pressure?
7-15 mmHg
Why is raised intracranial pressure a problem?
Because global brain perfusion is reduced when ICP is raised and therefore cerebral metabolism is reduced.
What features of the history would indicate a raised pressure headache?
Worse when lying flat, worse in the morning, persistent nausea and vomiting, worse of valsalva (coughing, laughing, straining), worse with physical exertion, transient visual obscuration with change in posture.
