Neuro CBL Flashcards
How should suspected stroke be evaluated in ED?
ABC, blood glucose
A good history is key - when were they last seen well or time of onset?
Did they have a seizure?
Medical history that may predispose to stroke
Medication e.g. oral anti-coags
IV access - blood tests
Diff dx of stroke?
Migraine Seizure Hypoglycaemia Tumour or space occupying lesion Peripheral neuropathy Syncope Functional weakness
Total anterior circulation syndrome (TACS)
Contra-lateral hemiparesis
Contra-lateral hemianopia
Higher dysfunction - e.g. dysphagia
Posterior anterior circulation stroke (PACS)
When 2 out of 3 of TACS present -
Contra-lateral hemiparesis
Contra-lateral hemianopia
Higher dysfunction - e.g. dysphagia
or isolated dysphagia
Different lacunar stroke presentations
Pure motor/hemiparesis
Ataxic hemiparesis
Dysarthria/clumsy hand
Pure sensory stroke
Posterior circulation stroke (POCS) symptoms
Cranial nerve palse with contralateral motor/sensory defect
Bilateral motor or sensory defect
Eye movement disorder
Cerebellar signs
Isolated homonymous hemianopia
Which tests requested in stroke?
FBC, UE, CRP, LFT, Lipid profile, glucose, coag profile
Exclusion of hypoglycaemia is mandatory - treatment of hyperglycaemic px with thrombolysis is detrimental!
12 lead ECG
Cranial imaging
Role of imaging in stroke?
To exlude mimics (tumours)
Distinguish ischaemic vs haemorrhagic
Identify site of thrombus
Which imaging used in stroke?
CT first line - non contrast CT can be supplemented by CT angiogram
MRI first line in advanced centres or for minor strokes where it wont be picked up by CT - MRI sequence known as diffusion weighted imaging is v. sensitive for detection of stroke
What should a px with acute stroke be managed with?
A CT scan showed occlusion
<4.5 hr time window for intra-venous thrombolysis
Alteplase is the licensed thrombolytic drug
If px presents early, could consider IVT followed by MT
Px should be admitted to stroke unit!! (easy marks)
Recombinant tissue plasminogen activator (rtPA) - effect?
Precipates reperfusion of a potentially salvageable tissue
Most feared complication of IVT?
Secondary haemorrhagic transformation
What are the cascade of events when blood flow to the brain drops below a critical threshold?
1) excitotoxity
2) peri-infarct depolarisation
3) oxidative stress
4) inflammation
5) apoptosis
Mechanism of cell death after stroke?
Tissue doesn’t immediately die - there is a time window when the tissue is compromised but is potentially salvagable.
Ischaemia vs infarction?
Hypoperfused and hypoxic tissue = ischaemic, doesn’t necessarily imply reverisble tamage
Only when infarction ensues is the ischaemic region irreversibly damaged
Day 2 after stroke - CT angiogram - calcified atheroma affecting carotid arteries and arch of aorta.
Echocardiogram showed left ventricular hypertrophy
Total cholesterol 6
What medications should now be commenced?
Antiplatelets -
evidence of aspirin being effective (not until 24hrs after IVT)
clopidogrel 75mg once daily
Aspirin 75mg and dipyridamole considered if px intolerant to clopidogrel
Statins - prevent further stroke - atorvastatin and simvastatin
Antihypertensives - not given in acute period, once px is stable - ACE inhibitor and thiazide diuretic
Which other therapies can be given after stroke?
Physio Occ health Speech therapy Smoking cessation Dietician
Which other therapies can be given after stroke?
Physio Occ health Speech therapy Smoking cessation Dietician
Uthoff’s phenomenon
Seen in demyelination - symptoms are worse with exercise (heat)
Significance of PMH of optic neuritis?
Inflammation of optic nerve presents with pain on eye movement and visual blurring
MS presents with optic neuritis in 20% of cases - 50% of those with MS will have it at some stage
Important history questions for MS diagnosis?
Tick bites? - lyme disease is an MS mimic
Illicit drugs
Do they drive? DVLA needs to be informed
Signs of optic neuritis?
Red desaturation
Relative afferent pupillary defect
Optic disc pallor (implies atrophy)
Hoffman’s sign
Upper motor neuron (UMN) sign - parallels the extensor plantar sign in the lower limb
It is positive when there is flexion of the ipsilateral thumb after tapping the nail bed of the third finger
UMN lesion signs?
Increased tone Weakness hyper-reflexia Clonus Extensor plantars Positive hoffmans sign
Dx of MS
Exlude mimics (bloods and MRI)
MS diagnosed based on clinical hx supported by findings and investigations
CSF
signs and symptoms of MS
Can affect optic nerve (optic neuritis), brainstem (ataxia, swallowing), cord (bladder problems, constipation) and white matter (motor and sensory problems)
What is found in the CSF of px with MS?
Positive oligoclonal bands (also seen in sarcoidosis)
Increase WCC
Differential dx to exclude for MS?
Lyme disease
B12 deficiency
Vasculitis
PML
What are VERS and what do they show?
Visual evoked responses - the speed at which impulses travel along the optic nerve.
Role of MRI in dx of MS?
Can detect a lesion of MS - demonstrated as bright with lesions on T2-weighted MRI
McDonald criteria require dissemination in space, a lesion in at least two of:
Periventricular
Juxtacortical
Infratentorial
Spinal cord
Dissemination in time - 2 clinical attacks or MRI lesions of different ages
Acute tx options for an MS relapse?
IV steroids - do not affect long term tissue damage
PPI given with steroids
Physiotherapists and occupational therapists
Disease modifying therapies
Aetiology of MS
Exercise can worsen symptoms - heat - also hot showers? (uhthoff’s phenomenon)
Multi-factorial
Vit D deficiency, low levels of sunlight, viral infections (EBV?), genetics, smoking
First line disease modifying treatments for MS?
Injectable tx -
Beta interferons and glatiramer acetate
Oral -
Dimethyl fumerate suppresses the immune system and reduces lymphocyte counts
Teriflunomide suppresses immune system
Induction therapy -
Alemtuzumab
Tx for progressive MS?
Targeted at symptom control -
Fatigue - Antidepressant or modafinil?
Urinary - tamsulosin?
Spasticity - physio/OT, baclofen, benzodiazepines, gabapentin, botox?
Components of history with a headache?
Aura Location Onset Severity Associated symptoms - nausea, photophobia Exacerbating/relieving factors
Red flag symptoms in headache?
Age <5 or >50 Thunderclap headache Focal/non-focal neuro deficits Worsening with posture or coughing Previous hx of cancer Fever Weight loss Early morning headaches
Thunderclap headache
High intensity headache which reaches maximal intensity in <5 minutes
In most cases of SAH it only takes few seconds
Visual aura
1/3 of px with migraines experience this
Symptoms may be positive (flickering lights, spots) or negative (loss of vision, numbness)
Triggers of migraine
Menstrual period, stress, caffeine, hunger, sleep deprivation
Features to examine for raised intracranial pressure
Papilloedema on fundoscopy
Constriction of visual fields
Enlargement of blind spots
Unilateral or bilateral VIth nerve palsy
Investigations of a migraine?
ESR/CRP may be useful if px has features suggestive of temporal arteritis
Cluster headache other name?
Trigeminal autonomic cephalgias - unilateral and associated with prominent ipsilateral cranial autonomic features
Pathogenesis of migraine
Pain results from interactions between components of the trigeminovascular system
1) pain sensitive cranial blood vessels
2) trigeminal nerves which innervate them
3) cranial parasympathetic outflow
Mx of migraine
Lifestyle - reduce alcohol and caffeine, good sleep pattern and regular meals
Acute tx - anaglesia, triptans (highly selective 5-HT1 agonists), Antiemetics (prochloperazine, metoclopramide)
Prophylaxis - B blockers, tricyclics, anti-epileptic drugs
Differential dx for thunderclap headache?
SAH Intercerbral haemorrhage Arterial dissection Bacterial meningitis Exertional headache
Risk factors for subarachnoid haemorrhage?
Modifiable - smoking, hypertension, alcohol
Non modifiable - previous SAH, polycystic kidney disease, strong family hx
Kernig’s sign
Positive when the hip and knee are flexed to 90 degrees and subsequent extension of knee is painful
Which symptoms suggest meningism?
Headache, photophobia, neck stiffness and a positive kernig;s sign
3rd nerve palsy with dilation of the pupil?
Surgical 3rd nerve palsy
Parasympathetic fibres that supply pupillary constrictor muscles run on outside of 3rd nerve and are subject to compression (e.g. tumour or aneurysm)
Isolated, complete 3rd nerve palsy with dilation of pupil?
Aneurysm of posterior communicating artery until proven otherwise
Isolated, pupil-sparing, complete 3rd nerve palsy?
Small vessel ischaemia
Inv for suspected SAH?
Bloods - FBC, UE, LFT, coag screen, CRP
ECG - ischaemic changes
Imaging - Non contrast CT
Lumbar puncture
What would be seen in a lumbar puncture with SAH?
Xanthochromia - billirubin in CSF as blood breakdown product
Red blood cells
Opening pressure elevated
Pathogenesis of SAH
SAH occurs when blood extravasates into the space between the arachnoid membrane and the pia mater
Most common cause is trauma
Non traumatic are due to saccular or berry aneurysms
Polycystic kidney disease may be a cause
90% of aneurysms develop in the anterior cerebral circulation
Perimesencephalic SAH
Non traumatic SAH in which aneurysms can’t be found
What are berry aneurysms?
Out-pouchings of the intimal layer through the muscular wall of the artery
Can be due to smoking or hypertension
Mx of SAH
Fluid resuscitation
Analgesia
Calcium antagonist (nimodipine) prevents focal cerebral ischaemia
Endovascular coiling
Complications of SAH
Rebleeding
Hydrocephalus
Seizure
Vasospasm
