Neurology Flashcards
How long do TIA symptoms last for?
< 24 hours.
What is a TIA?
An acute loss of cerebral or ocular function with symptoms lasting less than 24 hours. Caused by an inadequate cerebral or ocular blood supply due to reduced blood flow, ischaemia or embolism associated with disease of the blood vessels or heart. Complete recovery and no evidence of infarction on imaging.
What percentage of strokes are preceded by TIA?
15%.
What is the main cause of TIA?
Main cause is atherothromboembolism from the carotid artery.
What are the causes of TIA?
Main cause is atherothromboembolism from the carotid artery.
Other causes:
• Small vessel occlusion
• Cardioembolism resulting in microemboli from mural thrombosis post MI, valve disease, prosthetic valve, AF
• AF: no blood flow in or out of the atrial appendage in the left atrium. Results in the stasis of and pooling of blood which is a point on Virchow’s triangle. Forms a clot and if it dislodges, it may be carried as an embolus. The path of least resistance if the carotid arteries but emboli go elsewhere in the body too.
• Endocarditis
• Hyperviscosity e.g. polycythaemia, sickle cell anaemia, myeloma, very high white cell count.
What are the risk factors for a TIA?
Age, hypertension, smoking, diabetes, heart disease e.g. valvular, ischaemic, AF, previous TIA, peripheral arterial disease.
What is the pathophysiology of a TIA?
Commonest cause is cerebral ischaemia so lack of oxygen to brain and cerebral dysfunction. Ischaemia is short-lived and symptoms only last a maximum of 15 minutes after onset. Then resolves before irreversible cell death occurs. Gradual progression of symptoms suggests a different pathology e.g. demyelination, tumour or migraine.
What percentage of TIAs are in the anterior circulation (carotid artery)?
90%.
What percentage of TIAs are in the posterior circulation (vertebrobasilar artery)?
10%.
What are the symptoms of an anterior (carotid artery) circulation TIA?
- Amaurosis fugax: “fleeting darkness” described as a “curtain descending”. Most likely is an embolus in the internal carotid artery and then in the retinal/opthalmic arteries
- Aphasia: inability to formulate and/or understand speech
- Hemiparesis: weakness or inability to move on one side of the body
- Hemisensory loss
- Hemianopic visual loss: visual field loss on the left or right side of the vertical midline, affecting one eye or both eyes
- Dysphasia: inability to produce speech.
What are the symptoms of a posterior (vertebrobasilar artery) circulation TIA?
- Diplopia (double vision)
- Vertigo
- Vomiting
- Choking and dysarthria (muscles used to produce speech are damaged)
- Ataxia: many symptoms mimic being drunk
- Hemisensory loss
- Hemianopic or bilateral visual loss
- Tetraparesis: all four limbs are weak
- Loss of consciousness: rare
- Transient global amnesia possibly.
What are the signs of a TIA?
- Aphasia
- Carotid bruit (whooshing noise over artery)
- Dysarthria
- Ataxia
- Hemisensory loss
- Hemaniopic or bilateral vidual loss
- Tetraparesis.
What are the investigations in a TIA?
- Carotid artery imaging: Doppler ultrasound of the internal carotid arteries and MR/CT angiography to look for stenosis
- Cardiac echo
- ECG and 24 hour ECG
- MRI brain
- Bloods: FBC, ESR, U&E, glucose, lipids.
What artery is blocked in amaurosis fugax?
Most likely is an embolus in the internal carotid artery and then in the retinal/opthalmic arteries.
What are the differential diagnoses in a TIA?
It is impossible to differentiate from a stroke until there is a full recovery.
• Hypoglycaemia
• Mass lesions produce identical events e.g. subdural haematoma, cerebral abscess tumours
• Focal epilepsy: positive features e.g. limb jerking and loss of consciousness which are less common in TIA. Progression of symptoms over minutes
• Migraine aura: visual loss and dysphasia common in both. Headache and positive visual phenomena e.g. shimmering are typical of migraine aura but not TIA. The onset and evolution of symptoms is slower in migraine aura and limb weakness is unlikely (develops over minutes rather than seconds)
• Hyperventilation
• Retinal bleeds
• Cerebral amyloid angiopathy
• Postural weakness (Todd’s paralysis)
• Malignant hypertension (rare).
Not a TIA is syncope, dizziness, temporary loss of consciousness, temporary memory loss, gradual onset.
When does a low risk TIA patient need to be referred?
Refer for specialist assessment within 7 days of the onset of symptoms.
What is the management in a TIA?
- Refer for specialist assessment within 24 hours/7 days of the onset of symptoms
- Start aspirin immediately and them move to clopidogrel or continue current standard dose if already on an antiplatelet (unless on an anticoagulant)
- Start an anticoagulant if cardiac source of emboli
- Statin
- ACE-i/ARB for blood pressure
- No driving until seen by a specialist.
Modify risk factors e.g. stop smoking, less alcohol, exercise, diet, BP (aim for <145/85), hyperlipidaemia, diabetes mellitus.
Surgery: carotid endarterectomy to remove build-up of fatty deposits (plaque). If tolerated, preferred to angioplasty with stenting as less chance of stroke from procedure.
When does a low risk TIA patient need to be referred?
24 hours.
How long should someone not drive for after a TIA?
Should not drive for 1 month. If no residual defect after 1 month e.g. visual field defect, do not have to inform DVLA. If recurrent, a 3 month free period is needed.
What score is used to assess the risk of a stroke after a TIA?
ABCD2 to assess risk of stroke: max score is 7
• Age >=60 = 1 point
• Blood pressure at presentation >=140/90 = 1 point
• Clinical features:
• Unilateral weakness= 2 points
• Speech disturbance without weakness= 1 point
• Duration >=60 minutes= 2 points, 10-59 minutes= 1 point.
• Diabetes= 1 point.
High risk is ABCD2 >=4, AF, >1 TIA in one week, TIA whilst on anti-coagulation.
Low risk is none of the above, present >1 week after their last symptoms has resolved.
What is the prognosis of a TIA?
After 5 years, 30% have a stroke (1/3 in the first year). 1 in 12 go on to have a stroke within 1 week. 15% suffer from an MI.
What is a stroke?
A syndrome of rapidly developing onset neurological deficit caused by focal cerebral, spinal or retinal infarction or haemorrhage.
What are the types of stroke?
- Ischaemic (85%)
- Haemorrhagic (10%): intracerebral and subarachnoid
- Other (5%): arterial dissection, venous sinus thrombosis, vasculitis.
50% are cerebral, 25% are brainstem and 25% are lacunar.
What are the causes of ischaemic stroke?
Atherosclerosis, thrombosis, embolus, shock:
• Thrombosis
• Large artery stenosis: acts as an embolic source
• Cardio-embolic: AF, MI, endocarditis, prosthetic valves, patent foramen ovale (allow passage of thrombosis from right atrium to left)/septal defects, valve disease
• Athereothromboembolism e.g. from carotid artery
• Shock: reduced blood flow through body
• Small-vessel disease: occlusive vasculopathy (lipohyalinosis) that leads to small infarcts called ‘lacunes’ and/or gradual accumulation of diffuse ischaemic change in deep white matter (consequence of hypertension)
• Hypoperfusion e.g. severe hypotension such as in cardiac arrest, may lead to border-zone infarction in the watershed areas between vascular territories (parieto-occipital area between MCA and PCA vulnerable)
• Vasculitis.
What are the causes of haemorrhage stroke?
- Brain bleeds: trauma, aneurysm rupture causing subarachnoid haemorrhage, anticoagulation, thrombolysis, carotid artery dissection
- Atherothromboembolism
- Vasculitis.
What are the risk factors of stroke?
Increased blood pressure, smoking, diabetes mellitus, heart disease (vascular, ischaemic, AF), peripheral vascular disease, age, smoking, drinking alcohol, increased lipids, obesity, increased clotting (increased plasma fibrinogen and decreased antithrombin), combined pill, increased homocysteine, increased packed cell volume, carotid bruit, syphilis, past TIA, ethnicity (black or Asian).
What is the pathophysiology of an ischaemic stroke?
Usually atherosclerotic plaque or clot in large artery ruptures, travels downstream, and gets trapped in narrower artery of the brain. Ischaemia -> infarction -> death of neural tissue -> loss of functionality. Embolic strokes are common complications of AF and atherosclerosis of carotids.
What is the pathophysiology of haemorrhagic stroke?
Bleeding from a single vessel within the brain, high blood pressure being the main cause.
What are the symptoms for a stroke?
Anterior circulation infarcts (middle cerebral artery, anterior cerebral artery, internal carotid, ophthalmic arteries):
• MCA infarction: contralateral hemiplegia (muscle weakness/paralysis) on one side of the body, facial weakness, contralateral sensory loss, dysphagia (speech problems only if stroke is in dominant hemisphere, Broca’s), aphasia (inability to understand is Wernicke’s or produce speech is Broca’s, in dominant hemisphere stroke), facial droop, eye deviation towards the affected eye
• ICA infarction: similar to MCA but collateral circulation may reduce the infarct size
• ACA infarction: less common than MCA, hemiparesis affecting the leg more than the arm (contralateral weakness and sensory loss of the lower limb) truncal ataxia, incontinence, drowsiness, logical thinking, personality, frontal lobe deficits e.g. apathy or apraxia.
• Cerebral hemisphere infarcts: most commonly occlusion of branch of MCA, with collateral circulation protecting the cortex, leading to infarction of the internal capsule (deep structures).
Posterior circulation infarcts:
• PCA infarction: contralateral hemianopia from unilateral lesions, cortical blindness from bilateral lesions (Anton’s syndrome), confusion or memory impairment because the PCA supplies the thalamus and posteromedial temporal lobe
• Posterior circulation (vertebrobasilar artery): more catastrophic due to wide region supplied. Disorders of balance and coordination
• Basilar artery thrombosis: high lesions cause midbrain infarction including coma and locked-in syndrome.
• Cerebellar infarcts
• Brainstem infarcts: includes basilar artery thrombosis. Also lateral medullary syndrome (Wallenberg’s syndrome) which is caused by occlusion of posterior inferior cerebellar artery. Presents with sudden vomiting and vertigo, Horner’s syndrome, ipsilateral facial numbness, dysarthria, limb ataxia, dysphagia and contralateral loss of pain and temperature
• Lacunar infarcts (basal ganglia, internal capsule, thalamus and pons): often symptomless.
Haemorrhage: headaches, altered mental status, seizures, nausea and vomiting.
Watershed/border zone infarctions: causes by severe cerebral hypoperfusion such as hypotension after cardiac arrest. Ischaemia in the border zones between areas supplied by the ACA, MCA and PCA. Affects the parieto-occipito cortex, hippocampi and motor pathways. Complex patterns of visual loss e.g. Balint’s syndrome, memory loss, intellectual impairment, motor deficits and a vegetative state in prolonged cerebral hypoperfusion.
Signs
- Slurred speech
- Arm/leg weakness
- Facial drooping.
What is the treatment for a stroke?
Immediate (within 1 hour):
• CT scan
• Bloods: FBC (look for thrombocytopenia and polycythaemia), blood glucose (rule out hypoglycaemia), clotting studies if anticoagulated.
Further (within 24 hours):
• Bloods: FBC, ESR, glucose, lipids, clotting studies
• ECG and later 24 hour ECG: look for AF and cardioembolic stroke
• Carotid Doppler studies: in patients with anterior circulation stroke.
Others:
• CT or MR angiography for carotid artery stenosis
• MRI brain scan with dissection protocol
• Cardiac monitoring
• Vasculitis screen: increased ESR, ANCA, VDRL test for syphilis
• Antiphospholipid antibodies (antiphospholipid syndrome is prothrombotic)
• Thrombophilia screen
• Genetics for CADASIL and mitochondrial disorders
• Alpha-galactosidase for Fabry’s disease
• Drugs of abuse screen e.g. cocaine
• Chest X-ray to look for cardiomegaly (enlarged left atrium)
• Hypertension: look for retinopathy, nephropathy or cardiomegaly
• Look for hypoglycaemia, hyperglycaemia, dyslipidaemia, hyperhomocysteinaemia
• Check for hyperviscosity: e.g. polycythaemia, sickle-cell disease
• Check for thrombocytopenia and other bleeding disorders.
What is the management for a stroke?
Low risk:
• Refer for specialist assessment within 7 days of the onset of symptoms
• Start aspirin immediately and them move to clopidogrel or continue current standard dose if already on an antiplatelet (unless on an anticoagulant)
• Start an anticoagulant if cardiac source of emboli
• Statin
• ACE-i/ARB for blood pressure
• No driving until seen by a specialist.
High risk:
• Assessment within 24 hours
• As above.
Modify risk factors e.g. stop smoking, less alcohol, exercise, diet, BP (aim for <145/85), hyperlipidaemia, diabetes mellitus.
Surgery: carotid endarterectomy to remove build-up of fatty deposits (plaque). If tolerated, preferred to angioplasty with stenting as less chance of stroke from procedure.
- Immediate general medical measures: airway, oxygen by mask, monitor blood pressure
- Determine if thromboprophylaxis is appropriate: if so, immediate brain imaging
- Brain imaging: CT to exclude haemorrhage and will show other pathology and sometimes infarction (<1 hour). MRI is best for acute infarct
- If CT excludes haemorrhage, give immediate thrombolytic therapy (should be <4.5 hours after onset of symptoms), alteplase therapy. CI if stroke or head injury in last 3 months, history of intracranial haemorrhage, GI bleed in the last 21 days, major surgery in the last 14 days. IV alteplase is a tissue plasminogen activator. If CI, give aspirin. If CT confirms haemorrhage, give no drugs that could interfere with clotting.
- Admit to MDT stroke unit: assess swallowing, start thromboembolism prophylaxis.
What is a migraine?
A recurrent throbbing headache often preceded by an aura and associated with nausea, vomiting and visual changes.
What is the most common cause of episodic (recurrent) headache?
Migraine.
When does the incidence of migraines increase?
In females in reproductive years, suggesting hormones have an influence.
What is a migraine with aura?
May affect the patient’s eyesight with visual phenomena such as fortification spectra (zig-zag lines), shimmering or scotomas (black holes in visual field) but may also result in pins and needles, dysphagia and rarely weakness of limbs and motor function.
What is a variant migraine?
Unilateral motor or sensory symptoms resembling a stroke.
What are the triggers of migraine?
Remember CHOCOLATE: • C hocolate • H angovers • O rgasms • C heese • O ral contraceptives • L ie-ins • A lcohol • T umult (loud noise) • E xercise.
What is the pathophysiology of a migraine?
Changes in the arterial brainstem blood flow which causes unstable trigeminal nerve nuclei in the basal thalamus and causes release of vasoactive neuropeptides (CGRP and substance P). Leads to neurogenic inflammation, vasodilation and plasma protein extravasation.
In aura, the cortical spreading depression is a self propagating wave of neuronal and glial depolarisation that spreads across the cortex.
What are the 4 diagnostic symptoms of migraine without aura?
A. 5 attacks fulfilling B-D B. Attacks last 4-72 hours C. Two of the following: Unilateral Pulsing Moderate/severe Aggravated by routine physical exercise D. During headache at least one of: Nausea and/or vomiting Photophobia (light sensitive) and phonophobia (sound sensitive). These are often premenstrual.
What are the 3 diagnostic criteria of migraine with aura?
A. At least 2 attacks fulfilling B and C
B. One or more reversible aura symptom:
Visual: zigzags, spots
Unilateral sensory: tingling numbness
Motor weakness: known as ‘hemiplegic migraine’ so rule out stroke and TIA
C. Two or more of the following 4:
One or more aura symptoms spread gradually over 5 minutes and/or two or more aura symptoms occurring in succession
Each aura symptom lasts 5-60 minutes
One or more aura symptom is unilateral
Aura accompanies/followed within 60 minutes by headache.
What is prodrome?
Prodrome occurs a while before the migraine and is a weird feeling of: yawning, cravings, mood/sleep changes.
What are the investigations of a migraine?
Mainly based on clinical diagnosis.
Neuroimaging.
Examine:
• Eyes for papilloedema and other eye issues
• Blood pressure
• Head and neck.
Exclude other causes (including mass lesions):
• Lab tests for CRP and ESR
Neuroimaging indications red flags:
• Worst/severe thunderclap headache: subarachnoid haemorrhage
• Change in pattern of migraine
• Abnormal neurological exam
• Onset over 50 years
• Epilepsy
• Posteriorly located headache.
Lumbar puncture indications:
• Worst headache of life, thunderclap: subarachnoid haemorrhage
• Severe rapid onset headache, progressive headaches, unresponsible headaches.
What are the differentials for migraine?
- Tension headache (bilateral, tight band around head)
- Cluster headache
- Medication over-use headache
- Meningitis (fever, photophobia, stiff neck, purpuric rash, coma)
- Subarachnoid haemorrhage (‘worst headache ever’, often occipital. neck stiff, focal signs, decreased consciousness)
- Tumour
- Cervical spondylosis
- TIAs may mimic migraine aura
- Encephalitis (fever, odd behaviour, fits or reduced consciousness).
What is the management of a migraine?
Conservative: avoid triggers and ensure analgesic rebound headache s not a problem.
Acute attacks:
• Mild: NSAID/paracetamol +/- anti-emetic
• Severe: oral triptan e.g. sumatriptan or nasal in 12-17 year olds.
Non-pharmalogical: warm or cold packs to the head, or rebreathing into paper bag (increase PaCO2) may help abort attacks. Butterbur extracts or riboflaxin supplementation. Transcutaneous nerve stimulation may help.
What is the prophylaxis of a migraine?
- Propranolol (beta-blocker) or Topiramate (anti-convulsant)
- Acupuncture (10 sessions over 5-8 weeks)
- Amitriptyline (tricyclic anti-depressant)
- Botulinum toxin type A (only if not responded to at least 3 prior pharnalogical therapies and whose condition is appropriately managed for medication overdose).
When do migraines often improve?
Migraine often improves in pregnancy but if not they are associated with greater risk of pre-eclampsia and cardiovascular complications. First line is paracetamol. Triptans and NSAIDs can be used but discuss risks. Don’t use aspirin if breastfeeding . Anti-emetic: cyclizine or promethazine.
What increases the incidence of migraine?
Incidence of migraine usually with aura and ischaemic stroke is increased by use of combined oral contraceptive pill.
What should be used in perimenstrural migraine on the days a migraine is expected?
If uncontrolled with standard treatment and predictable, consider use of frovatriptan or zolmitriptan on the days migraine is expected.
What are the types of tension headaches?
Can be episodic (<15 days per month) or chronic (>15 days per month for at least 3 months).
What are the types of headache?
Primary (syndromes based on symptoms): • Migraine • Cluster • Tension. Secondary (associated with something else): • Meningitis • Subarachnoid haemorrhage • Giant cell arteritis • Idiopathic intracranial hypertension • Medication overuse headache. Other: • Trigeminal Neuralgia (facial pain).
What causes tension headaches?
Neurovascular irritation which refers to scalp muscles and soft tissues. Remember MC SCOLD: • Missed meals • Conflict • Stress • Clenched jaw • Overexertion • Lack of sleep • Depression.
What are the symptoms of a tension headache?
A. 10 or more attacks occurring less than 1 day per month (less than 12 days per year) and fulfilling B-D
B. Headache lasting 30 minutes to 7 days
C. Headache has two of the following:
Bilateral
Pressing/tightening (non-pulsatile) quality
Mild or moderate intensity/pain
Not aggravated by routine physical activity (e.g. walking or climbing stairs)
D. Both of the following:
No nausea or vomiting (anorexia may occur)
No more than one of photophobia and phonophobia
E. Not attributed to another disorder.
What is the management of a tension headache?
- Reassurance and lifestyle advice
- Stress relief by massage or acupuncture
- Avoidance of cause
- Medication e.g. paracetamol, NSAIDs (ibuprofen, diclofenac) or aspirin
- Tricyclic anti-depressants e.g. amitriptyline
- Avoid opioids
- Limit analgesics to no more than 6 days per month to reduce risk of medication overuse headaches.
What is the most disabling of the primary headache disorders?
Cluster headaches.
What are the types of cluster headache?
Episodic: 2 or more cluster periods lasting 7 days to 1 year (usually 2-3 weeks) separated by pain free periods lasting one or more months.
Chronic: attack occurring for one or more years without remission or with remission lasting less than one month.
What are the triggers of cluster headaches?
Remember CHOCOLATE: • C hocolate • H angovers • O rgasms • C heese • O ral contraceptives • L ie-ins • A lcohol • T umult (loud noise) • E xercise.
What is the diagnostic criteria for cluster headache?
A. At least 5 headache attacks fulfilling B-D
B. Severe or very severe unilateral orbital, supraorbital and/or temporal pain lasting 15-180 minutes if untreated and rises to crescendo
C. Headache is accompanied by ipsilateral cranial autonomic features and/or sense of restlessness or agitation
D. Attacks have a frequency from 1 every other day to 8 per day.
What are the symptoms of a cluster headache?
Rapid onset of excruciating pain around one eye that may become watery and bloodshot. Deemed to have a boring/hot poker characteristic.
Associated with ipsilateral eye lacrimation and redness, facial flushing, rhinorrhoea (blocked nose), miosis (excessive pupil constriction) and/or ptosis (drooping or falling of upper eyelid).
Usually occur in the middle of the night or morning hours. Occurs once or twice a day, usually at the same time.
Pain raises to a crescendo over a few minutes and lasts for 15-180 minutes (average 30-100).
