neuro Flashcards
How does a cluster headache present?
Severe pain around one eye ± lid swelling, lacrimation, bloodshot, rhinorrhoea, miosis ± ptosis.
Headaches last minutes-hours, occur OD/BD for 4-12 weeks then pain-free for months/years
Rx cluster headache
100% O2
SC sumatriptan at onset
Rx trigeminal neuralgia
Carbamazepine
How does a migraine present?
Aura (commonly visual) lasting 15-30mins, within 1hr get a unilateral throbbing headache; may have assoc N+V, photophobia, phonophobia
Triggers for migraine?
CHOCOLATE Caffeine Hangovers Orgasms Cheese/chocolate Oral contraceptives Lie ins Alcohol Travel Exercise
Rx migraines
Acute = NSAID/paracetamol + PO triptan ± anti-emetic Prevention = propranolol, topiramate
CIs for triptan use
IHD, lithium/SSRI/ergot use, uncontrolled htn, coronary spasm
Cause of rest tremor
Parkinsons
Cause of intention tremor
Cerebellar lesion (e.g. MS, stroke)
Causes of postural tremor (absent at rest, present when maintained posture e.g. arms outstretched)
Benign essential tremor, thyrotoxicosis, anxiety, b-agonists.
How would a subarachnoid haemorrhage present (clinical sx and signs)?
Thunderclap headache (often occipital), vomiting, seizures, collapse, drowsiness, coma. O/E neck stiffness, kernig sign + (>6hr later), retinal/vitreous bleeds, focal neurology at presentation depending on site
How would you investigate a suspected SAH and what would the results be?
CT head - hyper dense areas within cerebral fissures. If negative but still strong clinical suspicion perform an LP at 12h post presentation for xanthochromia
Causes of SAH
Berry aneurysm rupture (85%), arteriovenous malformation, others inc encephalitis, vasculitis, tumours invading BVs
Risk factors for SAH
Hx aneurysmal SAH, family hx Htn Smoking and alcohol misuse Bleeding disorders PCKD Connective tissue disorders e.g. Ehelrs Danlos
Mx of SAH
Neurosurgery for endovascular coiling/surgical clipping.
Continue repeating BP, GCS and pupil observations
Maintain cerebral perfusion with good hydration but SBP <160. Rx nimodipine to reduce cerebral vasospasm
Complications of SAH
Hyponatraemia
Rebleeding
Cerebral ischaemia
Hydrocephalus
Who would you most commonly see a subdural haemorrhage in?
Elderly or those with brain atrophy due to increased shearing forces on bridging veins, minimal or no trauma can result in these breaking and bleeding. Those with recurrent falls or on anticoagulation
Sx of SDH
fluctuating consciousness ± insidious physical or intellectual slowing, sleepiness, headache, changes in personality, unsteadiness. O/E RICP, seizures, later on localising sx
Ddx for ?SDH
Dementia, stroke, CNS mass
Ix findings in SDH
CT head - crescentic collection of blood on one hemisphere not limited by suture lines. Clot ± midline shift
Mx SDH
Asymptomatic/small = conservative management (observe, supportive rx)
Symptomatic/large with mass effect = craniotomy/burr hole to decompress
How does an extradural haematoma usually present?
Result of trauma, causing skull # (commonly pterion -> MMA laceration as source of bleed) - followed by lucid interval in which bleed grows causing RICP -> reduced GCS, severe headache, confusion, vomiting, seizure and coma
Ix EDH and findings
CT head - biconvex (lentiform) collection of blood limited by suture lines
Mx EDH
stabilise and transfer to neurosurgery for craniotomy and evacuation of haematoma
Define epilepsy
Recurrent seizures in the absence of any provoking medical cause/structural abnormality. Seizures = episodes of abnormal uncoordinated neuronal discharge in the brain leading to varied but characteristic patterns of altered behaviour or sensation, LOC or convulsions.
Name 3 conditions associated with epilepsy
CP, tuberous sclerosis, mitochondrial disease
Ddx for seizure
Hypoglycaemia, hyponatraemia, hypocalcaemia; epilepsy; migraine; intracranial SOL or infection (meningitis/encephalitis/abscess); febrile convulsion; alcohol withdrawal; psychogenic non-epileptic seizure
Ix for seizure
EEG only useful during epileptic episode; MRI to exclude structural abnormlaity
What signs and symptoms would make you more suspicious that this was an epileptic seizure than a psychogenic seizure?
Tongue biting
Urinary incontinence
Post-ictal state 15/30mins, may be longer - drowsy, confused, headache, amnesia, myalgia
What localising features would make you suspect a temporal lobe epilepsy?
HEAD
Hallucination (olfactory, auditory, gustatory)
Epigastric rising/emotional
Automatisms (lip smacking, chewing, plucking)
Deja vu, dysphasia post-ictal
What localising features would make you suspect a frontal lobe epilepsy?
Motor sx - head/leg movement, posturing, Jacksonian march, post ictal weakness
What localising features would make you suspect a parietal lobe epilepsy?
sensory alterations eg. paraesthesia
What localising features would make you suspect a occipital lobe epilepsy?
visual sx - flashes and floaters
How does west syndrome present?
Very young child/infant
Salaam attacks lasting a few seconds repeating up to 50 times - flexion head/trunk/legs with extension of the arms; progressive decline in IQ; EEG hypsarrhythmia
How would you manage someone who has had a GENERALISED TONIC CLONIC seizure and you suspect they have epilepsy (assume they are now stable, visiting you in neurology OPD)?
Start AEDs only after 2nd seizure; consider contraceptives/fertility, any P450 drugs, driving - single seizure don’t drive 6m, dx epilepsy seizure free 12m, inform DVLA.
PO sodium valproate or lamotrigine
How would you manage someone who has had a TONIC or ATONIC seizure and you suspect they have epilepsy (assume they are now stable, visiting you in neurology OPD)?
Start AEDs only after 2nd seizure; consider contraceptives/fertility, any P450 drugs, driving - single seizure don’t drive 6m, dx epilepsy seizure free 12m, inform DVLA.
PO sodium valproate or lamotrigine
How would you manage someone who has had a MYOCLONIC seizure and you suspect they have epilepsy (assume they are now stable, visiting you in neurology OPD)?
Start AEDs only after 2nd seizure; consider contraceptives/fertility, any P450 drugs, driving - single seizure don’t drive 6m, dx epilepsy seizure free 12m, inform DVLA.
PO sodium valproate or levetiracetam
How would you manage someone who has had a ABSENCE seizure and you suspect they have epilepsy (assume they are now stable, visiting you in neurology OPD)?
Start AEDs only after 2nd seizure; consider contraceptives/fertility, any P450 drugs, driving - single seizure don’t drive 6m, dx epilepsy seizure free 12m, inform DVLA.
ethosuximide or valproate
How would you manage someone who has had a FOCAL seizure and you suspect they have epilepsy (assume they are now stable, visiting you in neurology OPD)?
Start AEDs only after 2nd seizure; consider contraceptives/fertility, any P450 drugs, driving - single seizure don’t drive 6m, dx epilepsy seizure free 12m, inform DVLA.
Carbamazepine or lamotrigine
Causes of parkinsonism
Parkinsons disease, drug induced Parkinsonism (metoclopramide, antipsychotics), progressive supra nuclear palsy, multiple system atrophy, Wilsons disease, post-encephalitis
How does Parkinsons disease present?
Sx tend to be asymmetrical.
Resting tremor (pill-rolling, low frequency)
hypertonia (cogwheel and leadpipe rigidity)
Bradykinesia (slow to initiate movement, slow shuffling gait with reduced arm swing, actions slow with reduced amplitude with repetition)
Other - reduced facial expression, micrographia, drooling, depression, REM sleep disturbance, fatigue, autonomic dysfunction
How does drug induced Parkinsonism present differently to Parkinsons disease?
Drug induced tends to be bilateral, tremor and rigidity less pronounced, rapid onset.
How is Parkinsons disease managed?
Start rx when sx impact QOL, does not alter course
Motor sx predominate - levodopa
Non-motor sx predominate - non-ergot dopamine agonist, levodopa or MAO-B inhibitor
Side effects of dopamine agonists?
Impulse control disorder, excessive sleepiness, hallucinations.
Non-ergot used as ergot derived can cause cardiac, retroperitoneal, pulmonary fibrosis - baseline and annual U&Es, ESR, ECHO and CXR
A patient on PO co-careldopa for PD is admitted onto the ward but is now unable to swallow; how will you administer his levodopa and why is it important to do this without delay?
Dopamine agonist patch as rescue medicatin
Risk neuroleptic malignant syndrome
How would you manage a patient with PD for whom motor sx are the most distressing?
Levodopa + decarboxylase inhibitor e.g. carbidopa to reduce peripheral metabolism of levodopa to dopamine, more gets to CNS.
Describe the side effects and risks associated with levodopa use
Risk neuroleptic malignant syndrome/acute dystonia if stop suddenly
S/E dyskinesia, dry mouth, anorexia, palpitations, postural hypotension, psychosis, drowsiness.
Warn of ‘on-off effect’ - sx between doses as time dose controls sx for shortens with use; warn of decreased effectiveness with time (usually start noticing around 2yrs)
What is progressive supra nuclear palsy?
Parkinsonism, early postural instability ± falls, vertical gaze palsy (so trouble walking down stairs - gaze and instability). Rigidity of trunk>limbs. Dysarthria. Cognitive impairment. Poor response to levodopa
What is multiple systems atrophy?
Parkinsonism + autonomic disturbance (e.g. postural hypotension, ED, atonic bladder) ± cerebellar signs. Rigidity > tremor. MSA-P or MSA-C on whether Parkinsonism or cerebellar sx predominate
What is multiple sclerosis?
Chronic and progressive demyelination of central nervous system myelinated neurones by inflammatory cell-mediated immune response against myelin. Initially oligodendrocytes re-myelinate neurones but as disease progresses this is performed incompletely and sx become more permanent.
Features of multiple sclerosis?
Lesions are disseminated in time and space - damage has occurred at different times to different parts of CNS. Classically women aged 20-40 + higher latitude, monosymptomatic.
Vision - optic neuritis, internuclear ophthalmoplegia, optic atrophy, Uhthoffs phenomenon (vision worse as body temp increases)
Sensation - paraesthesia, numbness, trigeminal neuralgia, Lhermitte’s sign (flexion of neck causes electrical shooting pains in back and/or upper limbs)
Motor - spastic weakness, usually legs
Cerebellar ataxia/tremor, sexual dysfunction, urinary incontinence, reduced IQ
what is internuclear ophthalmoplegia and in which conditions is it seen?
lesion in MLF causes deconjugate eye movement with impaired adduction of ipsilateral eye, and horizontal nystagmus of contralateral eye. MS and vascular disease.
Subtypes of MS
Relapsing remitting - 85% - acute attacks lasting 1-2m followed by periods of remission without sx.
Primary progressive - 10% - progressive deterioration from onset, more common in older patients
Secondary progressive - relapsing remitting course initially but now getting sx between relapses, gait and bladder disorders seen.
How would you investigate MS?
First exclude other causes of sx - FBC, U+Es, LFTs, calcium, glucose, CRP/ESR, TFT, vitamin B12, HIV.
Then refer to neurology for assessment using McDonalds criteria and MRI brain (high signal T2 lesions, periventricular plaques, Dawson fingers) ± LP (oligoclonal bands and raised IgG)
Mx of MS
Relapse - high dose PO/IV Methylpred for 5/7 to reduce duration of attack (does not alter outcome); select patients for disease modifying drug b-interferon;
mx sx - fatigue (mindfulness, CBT, trial amantidine), spasticity (baclofen, gabapentin), urinary incontinence (intermittent self-catheterisation or anticholinergics)
CN7 palsy differential diagnosis
Forehead sparing (UMN lesion - b/l innervation from motor cortex to sup half facial nucleus) - CVA, SDH, SOL Forehead affecting (LMN lesion) - infective (AOM, HSV1, CMV, EBV), trauma, malignancy (cholesteatoma, parotid), iatrogenic, Bells palsy
How would you manage Bells palsy?
Present within 72h = PO prednisolone; eye-care - lubricants/artificial tears/taping at night. Good prognosis most make full recovery.
What causes Ramsay Hunt Syndrome?
Reactivation of latent VZV in geniculate ganglion of CN7
How does Ramsay hunt syndrome present?
Vesicular rash affecting external ear, auditory canal ± TM; auricular pain, vertigo, tinnitus, deafness, CN7 palsy
How would you manage Ramsay Hunt Syndrome?
PO acyclovir + corticosteroids
What causes Guillain Barre syndrome?
Immune mediated demyelination of peripheral nervous system, often triggered by infection (classically campylobacter jejuni)
How does guillain barre synd present?
Progressive weakness of all 4 limbs (classically ascending weakness), hypo/a-reflexia, very mild sensory signs or symptoms, respiratory muscle weakness, cranial nerve or autonomic involvement. May have hx gastroenteritis
Investigations and treatment for Guillain barre syndrome?
LP - isolated raised protein in CSF, could perform nerve conduction tests.
IV immunoglobulin and/or plasma exchange
What is motor neurone disease?
neurodegenerative disease characterised by selective loss of neurones in the motor cortex, cranial nerve nuclei and anterior horn cells. No sensory loss.
Types of MND
Amyotrophic lateral sclerosis - 85% - UMN and LMN signs
Progressive bulbar palsy - palsy of tongue, muscles of chewing/swallowing + facial muscles
Primary lateral sclerosis - UMN signs only
Progressive muscular atrophy - LMN signs only, affects distal muscles first, best prognosis
How does MND typically present?
Late middle age male (median age onset 60, rare <40); fasciculations, UMN + LMN sx, no sensory sx. Insidious muscle weakness affects trunk, limbs, face, speech - small muscles of hands wasting, clumsiness, tripping, stumbling gait, shoulder abduction to wash hair difficult, quickly fatiguing, aspiration pneumonia. Does not affect EOM, cerebellum, sphincters (until late)
How is MND managed?
Specialist MDT. Only medication shown to improve survival is riluzole - prevents glutamate stimulating NMDA receptors, used mainly in ALS, 3 month survival benefit
Sx’atic - SOB/resp difficulty (BiPAP), drooling (glycopyrronium bromide), specialist equipment for communicating, blending food.
What is the underlying pathophysiology of myasthenia gravis?
Insufficient functioning of nicotinic acetylcholine receptors on the postsynaptic membrane of the NMJ. 80-90% cases are nACh-R antibodies binding and blocking receptors from nACh action.
Features of MG
Muscle fatiguability - progressive weakness with activity, recovery with rest. Causes diplopia (EOM), facial weakness/ptosis/jaw fatigue when chewing/difficulty swallowing/dysarthria (facial muscle)
Associations of MG
thymoma, thymic hyperplasia, autoimmune disorders (hashimotos thyroiditis, RA, SLE)
How would you investigate MG?
Serum autoantibodies - ACh-R, MuSK or LRP4
Single fibre electromyography (v. sensitive)
CT thorax to exclude thymoma
Tensilon test is confirmatory but rarely used due to risk cardiac arrhythmia
How is MG managed?
long-acting acetylcholinesterase inhibitors e.g. pyridostigmine
immunosuppression - 1st line prednisolone
thymectomy
If unsuccessful medical mx consider rituximab
What is a myasthenia crisis and how is it treated?
potentially life-threatening, acute worsening of symptoms in patient with MG usually triggered by infection which can cause respiratory failure (resp muscle weakness). Requires assistance - non-invasive bipap or invasive intubation and ventilation. Mx - plasmapheresis and IVIG
What is Lambert-Eaton Myasthenia syndrome? Pathophysiology, sx, ix and mx
Usually a paraneoplastic syndrome seen in small cell lung ca but can be autoimmune. Antibodies to VGCC on pre-synaptic membrane of NMJ.
Sx - strength improves with repeated contractions (limited), limb-girdle weakness (early gait instability), hyporeflexia, autonomic sx (dry mouth, ED, difficulty micturating). Ix EMG. Mx - immunosuppression with prednisolone, plasmapheresis and IVIG, rx underlying ca.
What is syringomyelia and how does it present?
CSF containing cyst in the spinal cord which causes cape-like distribution of pain and temperature sensation loss, but light touch/proprioception/vibrioception intact. Paraesthesia, neuropathic pain, bowel bladder dysfunction, spastic weakness
What is huntingtons disease and how does it present?
AD trinucleotide repeat CAG expansion (may see genetic anticipation) causing degeneration of GABAergic and cholinergic neurones in the striatum of the basal ganglia. Sx chorea, personality changes (apathy, depression, irritable) and intellectual impairment, dystonia and saccadic eye movement.
What is subacute combined degeneration of the cord and how does it present?
dorsal and lateral column degeneration, usually as a result of vitamin B12 deficiency. Presents as loss of vibrioception and proprioception, progressing to distal paraesthesia and UMN sx in legs.
How is GCS scored (categories)?
Take the best score from either side
motor response - /6
Verbal response - /5
Eye opening - /4
List the scores for motor response on the GCS
6 = obeys motor command 5 = localises to pain 4 = withdraws from pain 3 = abnormal flexion to pain 2 = extension to pain 1 = no response
List the scores for verbal response on the GCS
5 = orientated 4 = confused 3 = words not sentences 2 = sounds/noises only 1 = no response
How is eye opening scores on GCS?
4 = spontaneous 3 = to speech 2 = to pain 1 = no response
define stroke
sudden interruption of blood supply to the brain causing ischaemia and hypoxia of neural tissue, which quickly results in irreversible damage. Can be ischaemic (TIA or ischaemic stroke) or haemorrhagic.
Risk factors for a stroke
ischaemic = cardiovascular risk factors (age, htn, smoking, hyperlipidaemia, diabetes) and AF (cardioembolism) haemorrhagic = age, htn, AVM, anticoagulation therapy
Sx of stroke
Motor weakness, sensory loss, homonymous hemianopia, dysphasia/aphasia, higher cortical dysfunction, swallowing problems, balance problems
How would a TACS present and what vessels are affected?
MCA and ACA
homonymous hemianopia, unilateral hemiparesis/hemisensory loss and higher cognitive dysfunction (e.g. dysphasia)
How would a PACS present and what vessels are affected?
smaller arteries in the anterior circulation e.g. upper or lower divisions of MCA
2 of motor/sensory loss, homonymous hemianopia, higher cognitive dysfunction
How would a lacunar infarct present and what vessels are affected?
perforating arteries around the internal capsule, thalamus and basal ganglia.
purely motor or sensory less or cerebellar ataxia
How would a POCS present and what vessels are affected?
vertebrobasilar arteries
LOC/isolated homonymous hemianopia/cerebellar or brainstem syndrome
What clinical symptoms/signs may indicate haemorrhagic rather than ischaemic stroke?
N+V, LOC, headache, seizures
How would an anterior cerebral artery stroke present?
contralateral hemiparesis lower>upper
minimal sensory loss but in same pattern as motor
apraxia
urinary incontinence
How would a middle cerebral artery stroke present?
contralateral hemiparesis upper>lower (tends to affect both)
contralateral hemisensory loss upper>lower (tends to affect both)
contralateral homonymous hemianopia, deviation conjuguee
dominant (L) - dysphasia/aphasia
non-dominant (R) - perceptual deficit e.g. apraxia, hemispatial neglect, anosognosia
How would a posterior cerebral artery stroke present?
contralateral homonymous hemianopia with macular sparing and visual agnosia
How would a posterior inferior cerebellar artery stroke present?
lateral medullary syndrome with crossed deficits
ipsilateral loss of pain/temp sensation in face
contralateral loss of pain/temp sensation in trunk and limbs
ataxia
nystagmus
How can you assess likelihood of ambiguous sx being stroke in A+E?
rosier score (exclude hypoglycaemia first, score >0 stroke likely)
Ddx stroke
Stroke - ischaemic or haemorrhagic Syncope Seizure hypoglycaemia intracranial SOL
How would you manage a stroke in the acute setting
Immediate CT head to rule out haemorrhagic stroke
Ischaemic - give PO aspirin 300mg
Thrombolysis if present within 4.5h, + thrombectomy if confirmed occlusion of proximal ant circulation and present within 6h (within 24h if limited infarct core volume on CT)
Keep all observations within normal range - BM 4-11, normal temp/O2/HR, only rx BP if hypertensive emergency
CI to thrombolysis
Pregnancy, intracranial SOL, active bleeding, prev intracranial haemorrhage, seizure at onset of stroke, ?SAH, stroke/TBI in last 3/12, LP within last 7d, uncontrolled htn, oesophageal varices.
relative - INR>1.7, trauma/major surgery in last 2 weeks
What would you prescribe for secondary prevention of stroke in someone with AF, and someone without AF?
With AF - 2 weeks of aspirin before discussing anticoagulants
without AF - PO clopidogrel (2nd line aspirin + MR dipyridamole)
Secondary prevention of stroke
Clopidogrel/ if AF - anticoagulant
manage cardiovascular risks, if carotid stroke/TI and carotid stenosis >70% consider endarterectomy, hypercholesterolaemia start on statin.
how would you differentiate a tremor caused by Parkinson’s disease and essential tremor?
ET - family hx, bilateral postural tremor, slowly progressive
PD - no family hx, older patient, usually unilateral (or worse side) postural tremor, other sx of PD present
how would you investigate tremor?
FBC (anaemia), TFT (hyperthyroidism), ?lithium levels, ?GAD-7 questionnaire, ?alcohol misuse questionnaire (could be causative or used to relieve)
mx of essential tremor
reduce caffeine intake, screen for alcohol misuse.
propanolol/primidone for asthmatic
