Neurology Flashcards
Antiplatelet therapy as secondary prevention of stroke or transient ischaemic attack
For initial antiplatelet therapy, use:
aspirin 100 mg orally, once daily OR clopidogrel 75 mg orally, once daily OR dipyridamole modified-release+aspirin 200+25 mg orally, twice daily
Clopidogrel is a thienopyridine antiplatelet drug and selectively inhibits the binding of adenosine phosphate to its platelet receptor.
Dipyridamole has both antiplatelet and vasodilating
properties and is thought to inhibit the uptake of adenosine (a potent inhibitor
of platelet activation and aggregation) into blood and vascular cells.
adenosine is a potent inhibitor of platelet activation and aggregation
What is mononeuritis multiplex?
Vasculitic neuropathy which classically presents as multiple mononeuropathy, which refers to an anatomic pattern of peripheral neuropathy that affects two or more noncontiguous named nerves simultaneously or sequentially
What is normal pressure hydrocephalus and what is the traid of symptoms?
Normal pressure hydrocephalus is a reversible cause of dementia seen in elderly patients. It is thought to be secondary to reduced CSF absorption at the arachnoid villi. These changes may be secondary to head injury, subarachnoid haemorrhage or meningitis.
Triad:
Dementia (bradyphrenia –> slow thinking/cognitive decline), urinary incontinence, Gait problems (ataxia)
It is thought around 60% of patients will have all 3 features at the time of diagnosis. Symptoms typically develop over a few months.
Imaging
hydrocephalus with an enlarged fourth ventricle
in addition to the ventriculomegaly there is typically an absence of substantial sulcal atrophy
Management
ventriculoperitoneal shunting
around 10% of patients who have shunts experience significant complications such as seizures, infection and intracerebral haemorrhages
What does the common peroneal nerve supply?
Features of common peroneal nerve lesion?
Muscles of the peroneal and anterior compartment of the leg and sensation to the dorsum of the foot.
The sciatic nerve divides into the tibial and common peroneal nerves. Injury often occurs at the neck of the fibula
The most characteristic feature of a common peroneal nerve lesion is foot drop.
Other features include:
weakness of foot dorsiflexion
weakness of foot eversion
weakness of extensor hallucis longus
sensory loss over the dorsum of the foot and the lower lateral part of the leg
wasting of the anterior tibial and peroneal muscles
Features of 3rd nerve palsy
- eye is deviated ‘down and out’
- ptosis
- pupil may be dilated
Signs of damage to median nerve at wrist & elbow
Damage at wrist
e.g. carpal tunnel syndrome
paralysis and wasting of thenar eminence muscles and opponens pollicis (ape hand deformity)
sensory loss to palmar aspect of lateral (radial) 2 ½ fingers
Damage at elbow, as above plus:
unable to pronate forearm
weak wrist flexion
ulnar deviation of wrist
Anterior interosseous nerve (branch of median nerve)
leaves just below the elbow
results in loss of pronation of forearm and weakness of long flexors of thumb and index finger
Clues for motor neurone disease
fasciculations
the absence of sensory signs/symptoms*
the mixture of lower motor neuron and upper motor neuron signs
wasting of the small hand muscles/tibialis anterior is common
What signs do you get in ALS?
Amyotrophic lateral sclerosis (ALS) is a type of motor neurone disease (MND).
Degeneration of neurones in the motor cortex and in the ventral spinal cord produces mixed UMN and LMN signs.
There are no associated sensory deficits.
GBS signs and symptoms
Inflammation of peripheral nervous system
No upper motor neurone signs
Assoc w recent infection
GBS is often accompanied by sensory disturbances
(both motor and sensory nerves of the peripheral nervous system are attacked by the immune system).
What is an essential tremor?
Essential tremor is an autosomal dominant condition which usually affects both upper limbs.
Worse when arms outstretched
Better with alcohol and rest
Common cause of titubation
Treatment with propranalol
Anaesthetic agents in myasthenia gravis
Rocuronium and suxamethonium are both neuromuscular blocking drugs (NMBDs), however they act in different ways.
Rocuronium is a non-depolarising NMBD, acting as an antagonist the post-synaptic receptor and leaving fewer receptors available for acetylcholine. In MG, there are already fewer functional receptors available and therefore patients with MG will be more sensitive to rocuronium and will require a lower dose for paralysis.
Suxamethonium is a depolarising NMBD - it acts by binding to and activating the receptor, at first causing muscle contraction, then paralysis. Again, due to a decreased number of available receptors, MG patients are typically resistant to depolarising NMBDs and may require significantly higher doses.
What is myasthenia gravis?
Myasthenia gravis (MG) is caused by autoantibodies to postsynaptic nicotinic acetylcholine receptors at the neuromuscular junction.
Multiple sclerosis features
Patient’s with multiple sclerosis (MS) may present with non-specific features, for example around 75% of patients have significant lethargy.
Diagnosis can be made on the basis of two or more relapses and either objective clinical evidence of two or more lesions or objective clinical evidence of one lesion together with reasonable historical evidence of a previous relapse.
Visual
optic neuritis: common presenting feature
optic atrophy
Uhthoff’s phenomenon: worsening of vision following rise in body temperature
internuclear ophthalmoplegia
Sensory pins/needles numbness trigeminal neuralgia Lhermitte's syndrome: paraesthesiae in limbs on neck flexion
Motor
spastic weakness: most commonly seen in the legs
Cerebellar
ataxia: more often seen during an acute relapse than as a presenting symptom
tremor
Others
urinary incontinence
sexual dysfunction
intellectual deterioration
Immediate treatment for acute ischaemic stroke
IV thrombolysis
- alteplase within 4.5 hours
- aim BP <185/100 (consider using GTN, labetalol)
- monitor BP and neurological status for 24 hours, withold aspirin for 24 hours
Endovascular thrombectomy
- due to occlusion of a large vessel (ie distal internal carotid artery, proximal middle cerebral artery [M1 segment], basilar artery—ususally detected by computed tomography angiography)
- perform within 6 hours of symptom onset
- If 6-24 hours: must have occluded large vessel (as defined above) and salvageable brain tissue on CT/MRI
- Can be used when patients present late between 4.5-6 hours and is not eligible for alteplase therapy
Antiplatelet therapy for acute ischaemic stroke
- If no ICH and within 48 hours, aspirin 300 mg orally or via nasogastric tube or rectally, on the first day. Reduce dose to 100 mg daily on the second day and continue daily therapy indefinitely.
General tips on management of ischaemic stroke:
- BP is often raised after an acute ischaemic stroke, but usually reduces spontaneously
- Avoid lowering blood pressure in the acute phase of ischaemic stroke (first 48 hours); exceptions can include patients with malignant hypertension or hypertensive encephalopathy, or patients receiving alteplase
- Cautious use of blood pressure–lowering drugs (preferably oral) is recommended for patients with markedly raised blood pressure (systolic blood pressure greater than 220 mmHg, diastolic blood pressure greater than 110 mmHg)—the aim is to reduce the blood pressure by about 20%. in a day
- Give supplemental oxygen to patients who are hypoxic—routine use of oxygen is not supported. Lower fever with paracetamol.
- Hyperglycaemia is associated with a worse outcome after stroke, so avoid intravenous fluids containing glucose. About 20% of patients admitted with acute stroke have unrecognised diabetes. Monitor the blood glucose concentration and maintain euglycaemia, but avoid aggressive management of blood glucose.
- Early mobilisation, adequate hydration
- Consider LMWH or apply intermittent pneumatic compression pump
Secondary prevention of stroke/ TIA
- Stroke patients are at high risk of a cardiovascular event (especially ischaemic heart disease)—monitor closely for symptoms of myocardial ischaemia.
- Lifestyle: diabetes + SNAP
- aspirin/ clopidogrel/ dypyridamole (The combination of dipyridamole and aspirin is marginally more effective than aspirin alone, but has more adverse effects. It should be considered in patients who have recurrent cerebral ischaemic events despite aspirin therapy)
- BP: Aim SBP 120-130
- Cholesterol: Consider starting a statin in all patients whose stroke or TIA is presumed to be due to atherosclerotic disease, regardless of the initial cholesterol concentration
Carotid stenosis: If the patient with recent mild stroke or TIA has a high-grade ipsilateral carotid stenosis (more than or equal to 70%), refer for urgent carotid endarterectomy.
AF/ mural thrombus after MI: consider starting anticoagulants. Stroke Foundation guidelines [Note 6] recommend starting anticoagulation immediately after a TIA or minor stroke, after 5 days for a moderate stroke, and after 10 days for a severe stroke.