Neuro 1 Flashcards
what area of the brain is involved with comprehension and understanding of speech? where in the brain is this? what is its main blood supply?
Wernicke’s area.
superior temporal gyrus of the dominant hemisphere.
middle cerebral artery.
what area of the brain is involved with the production of speech? where in the brain is this? what is its main blood supply?
Broca’s area.
frontal lobe of the dominant hemisphere.
middle cerebral artery.
how would an ischaemic stroke of the anterior cerebral artery present?
tends to affect feet, legs, up to bowel problems.
leg weakness, sensory disturbance in leg, gait apraxia, truncal ataxia, incontinence, drowsiness, akinetic mutism
what is akinetic mutism?
worst form of ACA stroke - decrease in spontaneous speech, stuporous state, completely mute and don’t move.
a patient presents with leg weakness, incontinence, drowsiness, and some missing sensations in his legs. in what artery is the ischaemic stroke likely to have occurred?
anterior cerebral artery
how would an ischaemic stroke of the middle cerebral artery present?
tends to be more arm and face.
contralateral arm and leg weakness, contralateral sensory loss, aphasia, dysphasia, facial droop.
how would a posterior cerebral artery stroke present?
contralateral homonymous hemianopia, cortical blindness with bilateral involvement of the occipital lobe branches.
visual agnosia (can see, but can’t interpret visual information).
prospagnosia - can’t recognise faces (parietal lobe).
dyslexia, anomic aphasia, colour naming and discrimination problems.
what clinical features might a patient have with a posterior circulation stroke (vertebral/basilar arteries)?
motor deficits e.g. hemiparesis or tetraparesis and facial paresis. dysarthria and speech impairment. vertigo, nausea and vomiting. visual disturbances. altered consciousness.
at what point do symptoms become a stroke, rather than a TIA?
if they last over 24h.
name 2 causes of a TIA, other than atherosclerosis/emboli
vasculitis, sickle cell anaemia, polycythaemia, myeloma - causes of hyperviscosity!
what specific investigation would you carry out if you suspected that atherosclerosis had caused your patient’s TIA? what treatment would you consider?
carotid Doppler and carotid endarterectomy.
name 3 risk factors for a TIA
hypertension, smoking, obesity, diabetes, high alcohol intake
what is amaurosis fugax?
progressive loss of vision in one eye - “like a curtain descending over my field of view” - due to emboli passing into the retinal artery
name 2 differential diagnoses of a TIA
hypoglycaemia, migraine aura, focal epilepsy, hyperventilation, retinal bleeds
what is the ABCD2 score and what is it used for?
used to predict progression to full stroke:
Age >60yo
BP >140/90
Clinical features - unilateral weakness, speech disturbance without weakness.
Duration of symptoms - >1h or 10-59min.
Diabetes.
how would you treat a TIA?
control hypertension/hyperlipidaemia/diabetes.
smoking cessation.
antiplatelet drugs - clopidogrel/aspirin/warfarin.
± carotid endartectomy.
how does warfarin work to reduce platelet aggregation?
inhibits vitamin K dependent synthesis of clotting factors 2, 7, 9 and 10
list 4 risk factors for stroke
hypertension, smoking, diabetes, heart/peripheral vascular disease, past TIA/stroke, hyperlipidaemia, alcohol, increased clotting/clotting disorders, the Pill, syphilis, carotid bruit
what are the 2 main types of stroke?
ischaemic and haemorrhagic
list 5 causes of haemorrhagic stroke
hypertension, trauma, aneurysm rupture, anticoagulation, thrombolysis, carotid artery dissection, subarachnoid haemorrhage
what might be some pointers in the presentation of stroke, to whether it is due to haemorrhage or ischaemia?
haemorrhagic - meningism, severe headache, coma within hours.
ischaemic - carotid bruit, AF, past TIA, IHD.
what would be the clinical features of a brainstem infarct?
quadriplegia, disturbances of gaze and vision, locked-in syndrome
what are the 5 different syndromes produced by lacunar infarcts?
ataxic hemiparesis, pure motor, pure sensory, sensorimotor, dysarthria/clumsy hands
if a patient presented with vertigo, headache, ataxia and vomiting, what structure has been affected and what vessel has caused it?
cerebellar syndrome - due to occlusion of superior, anterior inferior or posterior inferior cerebellar artery
what is the essential investigation to carry out before you start specific stroke treatments?
urgent CT head
give 3 differential diagnoses of stroke
head injury, hypo/hyperglycaemia, subdural haemorrhage, intracranial tumours, hemiplegic migraine, epilepsy, CNS lymphoma, pneumocephalus, Wernicke’s encephalopathy, hepatic encephalopathy, mitochondrial cytopathies, abscesses, mycotic aneurysm
if CT showed that the stroke was caused by an infarct, how would you treat it?
thrombolysis - aspirin and alteplase - recombinant tissue plasminogen activator (tPA)
give 2 examples of primary prevention of stroke
treat hypertension, control DM, statins for hyperlipidaemia, regular physical exercise, smoking cessation, anticoagulation of patients with rheumatic/prosthetic heart valves on left
give 2 examples of secondary prevention of stroke
control risk factors (hypertension, diabetes, hyperlipidaemia).
aspirin or clopidogrel (unless haemorrhagic stroke)
list the causes of subarachnoid haemorrhage
rupture of saccular (Berry) aneurysms - 80%.
AV malformations - 15%.
idiopathic.
list 3 risk factors for subarachnoid haemorrhage
smoking, alcohol misuse, hypertension, bleeding disorders, mycotic aneurysm
what are some common sites for Berry anuerysms?
junction of posterior communicating artery with internal carotid.
junction of anterior communicating artery with anterior cerebral artery.
bifurcation of middle cerebral artery.
what 3 things are Berry aneurysms associated with?
polycystic kidneys, coarctation of the aorta, Ehlers-Danos syndrome
describe the symptoms of subarachnoid headache
THUNDERCLAP HEADACHE.
sudden, devastating occipital headache (I thought I’d been kicked in the head).
vomiting, collapse, seizures, coma.
give some signs of subarachnoid haemorrhage
neck stiffness, Kernig’s sign (inability to straighten knee with flexed hip).
retinal, subhyaloid and vitreous bleeds.
give 2 differential diagnoses of subarachnoid haemorrhage
meningitis, migraine, intracerebral bleeds, cortical vein thrombosis
what would you see on CT head in a subarachnoid haemorrhage?
no clear bleed - blood pools in available spaces, showing up white.
“star sign” - blood pooled in ventricles appears as white star.
what clinical features would indicate you should avoid doing a lumbar puncture and why?
headache, unilateral pupillary dilatation, vomiting, papilloedema, reduced mental state.
these are signs of raised ICP - risk herniation of brain and coning leading to death.
how would the CSF look if you performed a lumbar puncture on a person with subarachnoid haemorrhage?
CSF is bloody early on, then becomes yellow due to bilirubin - finding xanthochromia (yellow CSF) confirms SAH
how would you manage a subarachnoid haemorrhage?
hydrate, aim for systolic BP of 160 in order to maintain cerebral perfusion.
nimodipine - CCB, reduces vasospasm.
endovascular coiling, surgical clipping, intracranial stents, balloon remodelling.
give 2 possible complications of SAH
rebleeding.
cerebral ischaemia due to vasospasm - permanent CNS deficit.
hydrocephalus due to blockage of arachnoid granulations.
explain the process behind subdural haemorrhage
bleeding from bridging veins between cortex and venous sinuses - accumulating haematoma between dura and arachnoid - ICP gradually rises - midline structures shifted away from side of clot - eventual tentorial herniation and coning unless treated
who is at risk of subdural haemorrhage?
(those with small brains) - trauma patients, the elderly.
those prone to falls (epileptics, alcoholics).
those on anticoagulants.
how would a subdural haemorrhage present?
fluctuating consciousness level ± insidious physical/intellectual slowing.
sleepiness, headache, personality change, unsteadiness.
raised ICP, seizures.
what would you see on head CT/MRI of a patient with a subdural haemorrhage?
clot ± midline shift.
crescent shaped collection of blood over one hemisphere.
how would you manage a subdural haemorrhage?
mannitol for ICP.
irrigation/evacuation - burr twist drill/burr hole craniostomy.
craniotomy.
what causes an extradural haemorrhage?
MIDDLE MENINGEAL ARTERY most common.
any tear in dural venous sinus.
fractured temporal or parietal bone - causes laceration of middle meningeal artery and vein, typical after trauma to temple just lateral to eye.
what is a common clinical presentation of extradural haemorrhage?
‘lucid interval’ - walks away from road traffic accident seeming fine, then after a few hours/days, there’s a decrease in GCS from rising ICP.
after a lucid interval, what will be the clinical features of an extradural haemorrhage?
increasingly severe headache, vomiting, confusion, fits ± hemiparesis.
then - ipsilateral pupil dilates, coma deepens, bilateral weakness develops, deep and irregular breathing (brainstem compression)
how would an extradural haematoma appear on head CT?
round shape, rather than the sickle shape seen in subdural haematoma.
how would an extradural haematoma be treated?
mannitol for ICP.
neurosurgery - clot evacuation ± ligation of bleeding vessel
what treatment is contraindicated in all cerebral haemorrhages?
antiplatelets and anticoagulants
what 2 medical treatments can help reduce the risk of complications in intracranial haemorrhages?
dexamethasone (glucocorticoid) - reduces cerebral oedema, stabilises BBB.
nimodipine - CCB, reduces vasospasm
define a seizure, and define epilepsy
seizure = convulsion or transient event caused by a paroxysmal discharge of cerebral neurones.
epilepsy = continued tendency to have seizures.
what do the terms tonic, myoclonic and akinetic mean in terms of seizures?
tonic = intense stiffening of body with no convulsions. myoclonic = isolated muscle jerking (rapid repetitions of this = clonic). akinetic = cessation of movement, falling and loss of consciousness
what may be features of the post-ictal state?
headache, confusion, myalgia, sore tongue.
temporary weakness following focal seizure in motor cortex / dysphasia following seizure in temporal lobe.
list 4 causes of epilepsy
idiopathic/familial - 2/3rds!
cortical scarring, developmental, space-occupying lesion, stroke, hippocampal sclerosis, vascular malformations, tuberous sclerosis, sarcoidosis, SLE, PAN
list 4 non-epileptic causes of seizures
trauma, stroke, haemorrhage, raised ICP, alcohol/benzodiazepine withdrawal, metabolic disturbance, liver disease, fever.
infection - HIV, meningitis, encephalitis, syphilis.
drugs - tricyclics, cocaine, tramdol, theophylline
describe the features of a simple partial seizure
awareness unimpaired.
focal motor, sensory, autonomic or psychic symptoms.
no post-ictal symptoms.
describe the features of a complex partial seizure
impaired awareness.
may have simple partial onset (aura).
arise from temporal lobe.
post-ictal confusion.
what happens in a partial seizure with secondary generalisation?
electrical disturbance that began focally spreads widely causing a secondary generalised seizure - usually convulsive
what occurs in the brain during a primary generalised seizure?
simultaneous onset of electrical discharge throughout cortex with no localised features
describe the features of absence seizures
brief pauses, e.g. stops mid-sentence then carries on - presents in childhood
describe the features of tonic-clonic seizures
loss of consciousness.
limbs stiffen (tonic) then jerk (clonic).
may have one without the other.
post-ictal - confusion, drowsiness.
describe the features of myoclonic seizures
sudden jerk of a limb, face or trunk.
patient may be thrown to the ground suddenly, or have a violently disobedient limb.
describe the features of atonic (akinetic) seizures
sudden loss of muscle tone causing a fall, no loss of consciousness
list some features of a focal seizure that would localise it to the temporal lobe
automatisms - motor phenomena with impaired awareness and no recollection afterwards - lip smacking, chewing, fumbling, fiddling - even complex acts - singing, kissing, driving a car, violence.
abdo rising sensation/pain.
dysphasia.
memory phenomena (deja vu/jamais vu).
hippocampal involvement = emotional disturbance.
uncal involvement = hallucinations of smell or taste.
auditory cortex involvement - auditory hallucinations.
give some features of a focal seizure that would localise it to the frontal lobe
motor - posturing, versive movements of head and eyes, peddling of legs. jacksonian march. motor arrest. subtle behaviour disturbances. dysphasia or speech arrest.
give some features of a focal seizure that would localise it to the parietal lobe
sensory disturbances - tingling, numbness, pain.
motor symptoms - spread to pre-cental gyrus.
give some features of a focal seizure that would localise it to the occipital lobe
visual phenomena - spots, lines, flashes
how would you diagnose an epileptic seizure?
clinically - detailed description of attack from eye witness.
EEG - electroencephalogram and CT/MRI.
how would you treat generalised tonic-clonic seizures?
sodium valproate or lamotrigine.
2nd line - carbamazepine or topiramate.
how would you treat absence seizures?
sodium valproate or lamotrigine or ethosuximide
how would you treat tonic, atonic and myoclonic seizures? what should be avoided?
as for tonic-clonic but avoid carbamazepine.
so, sodium valproate/lamotrigine, with topiramate as 2nd line.
how would you treat partial seizures ± secondary generalisation?
carbamazepine.
give a side effect for each of the main 3 anti-epileptic drugs
sodium valproate - nausea, diarrhoea, weight gain.
lamotrigine - Stevens-Johnsons syndrome, diplopia, blurred vision.
carbamazepine - Stevens-Johnson syndrome, hyponatraemia, impaired balance.
what is the cardinal Parkinsonism triad comprised of?
bradykinesia (Parkinsonian gait), cogwheel rigidity, pill-rolling tremor
explain the pathophysiology of Parkinson’s disease. the presence of what feature in the brain is diagnostic?
degeneration of dopaminergic neurons in the substantia nigra pars compacta, associated with presence of Lewy bodies.
causes decrease in striatal dopamine levels leading to cell loss and akinesia.
give 3 non-motor symptoms of Parkinson’s disease
depression, dementia, dribbling, anosmia, hallucinations, constipation, dysphagia, heartburn, urinary difficulties, micrographia.
what one main risk factor for other diseases, is protective in Parkinson’s disease?
smoking
explain what you are likely to observe if you were to ask a Parkinson’s patient to walk up and down for you
stooping, shuffling gait. struggles to start walking. narrow base making falls common. obstacles, doors etc make them freeze and struggle to restart.
what is the typical age of onset of Parkinson’s disease?
65yrs
describe the medical management of Parkinson’s disease
dopamine agonists (ropinirole, pramipexole) and MAO-B inhibitor (rasagiline, selegiline) allows delay of starting L-Dopa.
start levodopa late - becomes ineffective after several years so start late and at a low dose then increase as needed.
prescribe with a decarboxylase inhibitor (carbidopa, besnerazide) to reduce peripheral side effects (esp. nausea).
why can’t Parkinson’s patient just be treated with dopamine?
it cannot cross the blood-brain barrier - levodopa is a precursor of dopamine and is able to cross the BBB and the be converted to dopamine within the brain.
what non-pharmacological treatment options are available for Parkinson’s?
deep brain stimulation, surgical ablation of overactive basal ganglia circuits.
what is Huntington’s chorea?
autosomal dominant, incurable, progressive, neurodegenerative disease.
define chorea
abnormal involuntary movements - brief, abrupt, irregular, unpredictable, non-stereotyped - may appear purposeful - patient appears fidgety/clumsy
describe the features of the prodromal phase of Huntington’s disease
irritability, depression, incoordination - personality changes, self-neglect (doesn’t wash, doesn’t care about work), fidgeting, tic.
describe the features of Huntington’s chorea
chorea, dementia ± fits and death.
what is the underlying pathology of Huntington’s chorea?
atrophy and neuronal loss of striatum and cortex.
what are the changes in neurotransmitters seen in Huntington’s chorea?
reduced ACh synthesis, depleted GABA and ACE in substantia nigra.
high somatostatin levels in corpus striatum.
dopamine remains normal.
what would an MRI scan of the brain of a patient with Huntington’s chorea show?
caudate nucleus atrophy
how would you treat Huntington’s chorea?
nothing will stop progression - symptomatic treatment only.
phenothiazines - sulpiride - antipsychotic drug, selective dopamine antagonist against receptors D2 and D3.
Tetrabenazine - used in hyperkinetic movement, promotes degradation of dopamine, helps chorea.
name 3 precipitating factors of a tension headache
loud noise, worry, fumes, concentrated efforts
how might a patient describe the pain of a tension headache?
bilateral, ‘tight band’, non-pulsatile, scalp tenderness.
how would you manage a patient with tension headaches?
reassurance. stress relief.
can prescribe NSAIDs, paracetamol or aspirin - watch for analgesic overuse headache
what causes tension headaches?
neurovascular irritation, referred to scalp muscles and soft tissues.
what other symptoms may accompany the pain of a tension headache?
vomiting, sensitivity to head movement
what are the clinical features that affect the eye in cluster headaches?
lacrimation, transient ipsilateral Horner’s, lid swelling, unilateral eye pain
describe the timeline of cluster headaches
recurrent bouts of the headache a couple of times a day, coming on a few times a month, then disappears for a few months and then returns unexpectedly
describe the pain of a cluster headache
rapid onset excrutiating pain around one eye. strictly unilateral - affects same side each time.
how would you treat an acute attack of a cluster headache?
100% O2 for 15min via non-rebreathe mask.
sumatriptan (SC) - 5HT receptor agonist, acts on serotonin receptors.
what preventatives are available to be used for cluster headaches?
suboccipital steroid injections.
intranasal civamide.
both are controversial.
also verapamil (CCB)
give 4 migraine triggers
chocolate, cheese, oral contraceptives, caffeine, alcohol, anxiety, travel, exercise, lie ins, loud noise
give 3 possible features of a migraine aura
flashing lights, tingling and weakness down one side, visual disturbance, ataxia, dysphasia
give 2 possible features of a migraine prodrome
yawning, cravings, mood/sleep change
describe the pain of migraine
severe unilateral throbbing headache, with nausea, vomiting ± photophobia/phonophobia.
what are the diagnostic criteria for migraine without aura?
> 5 headaches lasting 4-72h + nausea/vomiting (or photo/phonophobia) + 2 of:
unilateral, pulsating, impairs (or worsened by) routine activity.
give 3 differential diagnoses of migraine
cluster or tension headache, cervical spondylosis, hypertension, intracranial pathology, sinusitis/otitis media, TIA (may mimic migraine aura)
how might you pharmacologically treat a migraine?
NSAIDs - ketoprofen, aspirin.
triptans (5HT agonists) - riztriptan, sumatriptan.
what drugs might be used to prevent migraines?
1st line - propranolol, amitriptyline, topiramate, CCBs.
2nd line - valproate, pizotifen, gabapentin, pregabalin.
what rheumatological disease is giant cell arteritis associated with?
polymyalgia rheumatica
describe the 3 main clinical features of giant cell arteritis, and what causes them
headache - inflamed superficial temporal/occipital artery that hurts to touch and can become tortuous and thickened (I can’t even comb my hair!)
facial pain - inflammation of facial maxillary and lingual branches of external carotid artery, worse on eating (jaw claudication) - I can’t eat steak anymore!
visual disturbance - arterial inflammation and occlusion causing monocular painless visual loss (amaurosis fugax).
what is the risk if treatment of giant cell arteritis is delayed?
irreversible bilateral visual loss.
how would you diagnose giant cell arteritis? what should be done first?
raised ESR/CRP.
temporal artery biopsy - start steroids first!!
how would you treat giant cell arteritis?
immediate high dose oral prednisolone.
list 3 secondary causes of trigeminal neuralgia
compression of trigeminal root by anomalous/aneurysmal intracranial vessels or a tumour. chronic meningeal inflammation. MS. herpes zoster. skull base malformation.
describe the clinical features of trigeminal neuralgia
paroxysms of intense, stabbing pain, lasting seconds in the trigeminal nerve distribution.
unilateral, affecting mandibular or maxillary divisions.
face screwed up in pain.
give 2 examples of triggers of trigeminal neuralgia
washing affected area, shaving, eating, talking, dental prostheses
how would you treat trigeminal neuralgia?
carbamazepine, lamotrigine, phenytoin or gabapentin.
some surgical options.
give 3 causes of spinal cord compression
secondary malignancy - breast, lung, prostate, thyroid, kidney.
TB - Pott’s disease (destruction of vertebral bodies and disc spaces).
epidural haemorrhage or haematoma
prolapsed disc.
where do the corticospinal tracts decussate? what do they control?
85% - pyramids of medulla - lateral corticospinal tract, muscles of arms and legs.
15% - at the spinal level they leave at - control postural muscles, only present in thoracic levels.
which tract controls pain and temperature? where does it decussate?
spinothalamic - goes up 2-3 levels, then decussates
what tract controls “nice sensations” where does it decussate?
dorsal columns - touch, vibration, proprioception.
gracile fasciculus - legs, cuneatus fasciculus - arms.
decussate in upper medulla.
what imaging would you use to investigate the cause of the symptoms in spinal cord compression?
MRI
in Brown-Sequard syndrome, there is a hemisection of the spinal cord, on what side is there a loss of proprioception, vibration, power, pain and temperature?
contralateral loss of pain and temperature.
ipsilateral loss of proprioception, vibration and power.
what is the T10 dermatome?
umbilical level
what is the L1 dermatome?
inguinal ligament
what is the L2-3 dermatome?
anterior and inner leg
what is the C3-4 dermatome?
clavicles
what is the C6-7 dermatome?
lateral arm/forearm
what is the T1 dermatome?
medial side of the arm
what is the T4 dermatome?
nipple level
how would you treat spinal cord compression due to malignancy?
dexamethasone IV ± radio/chemotherapy
what is the cauda equina?
a bundle of spinal nerves and spinal nerve roots that consists of L2-5 and S1-5, they innervate the lower limbs and pelvic organs.
they also supply the sensory innervation to the perineum and parasympathetic supply to the bladder.
what causes damage to the cauda equina?
damage to spine at or distal to L1
what are the clinical features of cauda equina syndrome?
flaccid leg weakness and areflexic paralysis of legs.
back pain, radicular pain down legs, sensory loss in a root distribution, decreased sphincter tone
how would you manage cauda equina syndrome?
surgical decompression within 48h
explain the pathogenesis of multiple sclerosis
inflammatory process in the white matter of the brain and cord mediated by CD4 T cells.
there are discrete plaques of demyelination at multiple CNS sites.
demyelination leads to axonal damage.
heals incompletely causing relapsing and remitting disease.
describe the 4 possible disease courses in MS. what is necessary for diagnosis?
need lesions disseminated in time and space.
relapsing and remitting - disease relapses followed by full recovery, or at least partial recovery - clear period of time with no disease activity, followed by another relapse.
primary progressive - disease progresses from onset, with occasional plateaus/temporary improvements.
secondary progressive - initially relapsing/remitting, then following progressive phase.
progressive/relapsing - progressive disease from onset, with clear acute relapses that recover then continue to progress.
describe the epidemiology of MS
prevalence increases with distance from equator - possible role of vitamin D?
more common in women, mean age of onset 30yrs.
give some clinical features of MS
unilateral optic neuritis - pain on eye movement, rapid worsening of central vision.
numbness or tingling limbs.
leg weakness.
brainstem/cerebellar symptoms (diplopia, ataxia).
sensory - paraesthesiae, trigminal neuralgia.
motor - spastic weakness, myelitis.
GU - ED, urine retention, incontinence.
GI - swallowing disorders, constipation.
eye - diplopia, hemianopia, visual phenomena, pupil defects.
cognitive decline - amnesia, mood swings, decreased executive functioning.
what commonly makes symptoms of MS worse?
raised body temp - HOT BATHS
what 2 investigations would you carry out in MS and what would you expect to see?
MRI - visible plaques.
CSF - oligoclonal IgG bands on electrophoresis.
lesions disseminated in time and space
how would you treat MS?
acute - IV methylprednisolone (doesn’t affect prognosis, just treats relapse symptoms).
prevention of relapses - beta-interferon, azathioprine.
what is the gold standard investigation for stroke?
CT
why do you get a lucid interval in extradural haematomas?
because the patient is bleeding very slowly - due to how tightly the dura mater is adherent to the skull.
venous bleed.
what is the genetic basis of Huntington’s chorea? how many repeats may a patient have before they develop Huntington’s?
expansion of CAG repeat on chromosome 4 - overexpression of the huntingtin gene.
> 27 repeats is abnormal.
40 almost definitely will get Huntington’s.
the more repeats, the worse the symptoms.
what is giant cell arteritis?
systemic immune mediated vasculitis affecting medium and large sized arteries
what 3 clinical features make up Cushing’s triad of signs of raised ICP?
irregular resps.
bradycardia.
hypertension.
