Neuro 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.
What main symptoms would make you suspect stroke in any patient?
- unilateral weakness or paralysis in the face, arm of leg
- dysarthria or expressive or receptive dysphasia
- vision problems
- headache (sudden severe)
- difficulty with coordination and gain
- vertigo or loss of balance
- symptom onset after awakening from sleep
how would an ischaemic stroke of the anterior cerebral artery present?
- limb and/or facial weakness
- expressive and/or receptive dysphasia
- Sensory loss in face and upper and/or lower extremities
- vision loss in one eye or visual field deficit
- gaze paresis (often horizontal and unidirectional)
- homonymous quadrantanopia
What are the clinical features of a posterior circulation stroke?
- double vision
- Motor and/or sensory deficit
- motor: weakness, clumsiness, paralysis of any combination of arms and legs, up to quadriplegia
- Sensory: numbness, sometimes including all four limbs or both side of the face
- Vertigo, with possible nausea and vomiting
- ataxia - loss of full control of bodily movements
- dysarthria
- dysphagia
- homonymous hemianopia
- altered level of consciousness and coma
What are the 4 classifications of stroke?
- Total anterior circulation stroke
- Partial anterior circulation stroke
- Posterior circulation stroke
- Lacunar Syndrome
at what point do symptoms become a stroke, rather than a TIA?
if they last over 24h.
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, combined oral contraceptive pill, hyperlipidaemia, haematology disorders
90% of TIAS affect the anterior circulation, what are the symptoms of this?
- symptoms are usually unilateral and affect the motor area, causing unilateral weakness
- hemiparesis
- may be sensory problems in the same areas
- Broca’s dysphasia
- Amaurosis Fugax
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, focal epilepsy, retinal bleeds, syncope, intracranial lesion
what is the ABCD2 score and what is it used for?
used to predict progression to full stroke after TIA:
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?
300mg Aspirin STAT once haemorrhage ruled out
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
Older age, family history of stroke, hypertension, smoking, diabetes, AF, cardiac/haem conditions, ethnicity (asian, black and/or Hispanic), alcohol
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?
In haemorrhagic:
- more likely to lose consciousness
- more likely to have headache (sudden onset)
- neurological defects are usually sudden (like embolic stroke) but are more likely to be progressive
- patients on oral anticoagulants should be assumed to have haemorrhage unless it is proved otherwise
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?
- pure motor loss
- pure sensory loss
- sensorimotor disturbance
- ataxic hemiparesis (cerebellar and motor symptoms)
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 lesion, migraine, epilepsy, drug overdose
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))
What is the maximum amount of time thrombolysis can be given after a stroke
4.5hrs post onset of symptoms
What is the treatment for a Haemorrhagic stroke
- Any anticoagulants should be reversed
- Control hypertension if possibility of severe hypertensive crisis
- Manual decompression of raised ICP or by giving Mannitol
What are the factors in CHA2DS2-VASc and what is it used for
To calculate stroke risk with AF:
Congestive heart failure = 1
Hypertension: consistently above 140/90 = 1
Age 65-74 = 1
>74 = 2
Diabetes = 1
Stroke/TIA/thromboembolism previously =2
Vascular disease = 1
Sex category = 1 if female
Offer anticoagulation in patients with a score of 2 or above
give 2 examples of primary prevention of stroke
Antiplatelet therapy, treat hypertension, control DM, statins for hyperlipidaemia, regular physical exercise, smoking cessation, anticoagulation after stroke from AF
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, diseases that predispose to aneurysms: polycystic kidney, Ehlers Danlos, coarctation of aorta
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.
describe the symptoms & signs of subarachnoid headache
THUNDERCLAP HEADACHE. sudden, devastating occipital headache (I thought I’d been kicked in the head). vomiting, collapse, seizures, coma, neck stiffness, retinal bleeds/papilloedema
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, personality change, unsteadiness. raised ICP (headache, nausea, vomiting & raised BP), 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 (no loss of consciousness), 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 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 is the status epilepticus management pathway
- open and secure airway and give 100% oxygen
- IV access and take blood: U&E, LFT, FBC, GLUCOSE, Ca2+, toxicology screen if indicated
- IV bolus to stop seizures - Lorazepam 4mg (or suppository Diazepam), give 2nd dose if no response after 10-20mins
- correct hypotension with fluids
- If seizures continue - start Phenytoin
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 are the features of an Aura
Strange feeling in gut, deja vu or strange smells or flashing lights
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,
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
What are the differences with a non-epileptic seizure compared to an epileptic seizure
- non-epileptic seizures are situational
- non-epileptic is longer, closed mouth/eyes during tonic/clonic movements, no incontinence or tongue biting
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 if 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 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 or lamotrigine - 1st line. Sodium Valproate 2nd line
what is the cardinal Parkinsonism triad comprised of?
bradykinesia (Parkinsonian gait), cogwheel rigidity, resting 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 (reduced sense of smell), 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. Reduced arm swing. 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)
MAO-B inhibitor (rasagiline, selegiline)
COMT inhibitors (Entacapone, Tolcapone)
These allow 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 in a combined formation such as Co-careldopa or Co-deneldopa
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.
what is the underlying pathology of Huntington’s chorea?
Caused by increased CAG repeats on chromosome 4. Leads to cerebral atrophy with loss of GABA and Cholinergic neurones. Results in decreased ACh & GABA synthesis in the striatum. Loss of GABA means decreased inhibition of dopamine release and therefore result in excessive thalamic stimulation and thus excessive movements.
How would you diagnose huntington’s
Genetic testings shows many CAG repeats
MRI might show caudate nucleus atrophy & increased sized of the frontal horns of the lateral ventricles (signs of brain matter destruction)
how would you treat Huntington’s chorea?
nothing will stop progression - symptomatic treatment only. - sulpiride or haloperidol - antipsychotic drug
Benzodiazepines e.g. diazepam - sedative drug
Tetrabenazine - a dopamine depleting agent - considered best antichoreic drug
Antidepressants such as SSRIs
name 3 precipitating factors of a tension headache
stress, sleep deprivation, hunger, eyestrain, anxiety, noise
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 are the clinical features that affect the eye in cluster headaches?
lacrimation, transient ipsilateral Horner’s (pupil constriction), lid swelling ± ptosis, 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.
Often nocturnal/early morning - might wake patient from sleep
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?
Verapamil (CCB), avoid alcohol, and possibly prednisolone
give 4 migraine triggers
Chocolate:
- chocolate, hangovers, orgasms, cheese, oral contraceptives, lie-ins, alcohol, tumult (loud noise), exercise
give 3 possible features of a migraine aura
flashing lights and visual phenomena, 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, moderate/severe pain, impairs (or worsened by) routine activity.
how might you pharmacologically treat a migraine?
NSAIDs - ketoprofen, aspirin, naproxen.
Triptans (5HT agonists) - riztriptan, sumatriptan.
Anti-emetic - Prochlorperazine or cyclizine
what drugs might be used to prevent migraines?
1st line - propranolol, amitriptyline, topiramate, CCBs.
what is giant cell arteritis?
systemic immune mediated vasculitis affecting medium and large sized arteries
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 unilateral painless visual loss (amaurosis fugax).
± malaise, lethargy, fever, weight loss, morning stiffness
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 + GI and bone protection
Methylprednisolone for visual symptoms
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?
Anticonvulsants - carbamazepine, lamotrigine, phenytoin
Neuropathic pain - gabapentin.
some surgical options e.g. microvascular decompression or gamma knife surgery
give 3 causes of spinal cord compression
secondary malignancy - breast, lung, prostate, thyroid, kidney. Prolapsed disc or disc herniation. Haematoma. Infection. Primary spinal cord tumour (myeloma)
What is the clinical presentation of myelopathy (spinal cord compression)
progressive weakness with UMN signs ± pain
Sensory loss below the level of the lesion
possibility of bladder and anal sphincter involvement - this involvement is late and manifests as hesitancy, frequency and painless retention
where do the corticospinal tracts decussate? what do they control?
Decussate at the medulla. Are motor tracts so control muscles of arms and legs
which tract controls pain and temperature? where does it decussate?
spinothalamic - goes up 2-3 levels, then decussates
what tract controls proprioception, vibration and 2 point discrimination. where does it decussate?
dorsal columns -
gracile fasciculus - lower body
cuneatus fasciculus - upper body
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.
how would you treat spinal cord compression
If malignant = dexamethasone IV ± radio/chemotherapy
For disc pathology = surgical decompression of the cord (laminectomy or microdiscectomy)
What is Radiculopathy and what does it cause
Pathology of the nerve root
most patients have radiating limb pain, often in the pattern of the dermatome
gives LMN signs and weakness in the myotome
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 e.g. herniation of lumbar disc, tumours, trauma, infection, spondylolisthesis
what are the clinical features of cauda equina syndrome?
flaccid leg weakness and areflexic (LMN) paralysis of legs. Pain, numbness and a tingling sensation that radiates from lower back and travels down one of the legs to the foot and toes. Bladder/bowel dysfunction. Erectile dysfunction.
how would you manage cauda equina syndrome?
surgical decompression (microdiscectomy) within 48h
might also consider epidural steroid injection for leg pain
explain the pathogenesis of multiple sclerosis
inflammatory process in the white matter of the brain (oligodendrocytes) 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 3 possible disease courses in MS. what are the clinical features of each?
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 gradually worsening symptoms with fewer remissions
describe the epidemiology of MS
prevalence increases with distance from equator - possible role of low vitamin D? more common in women, mean age of onset 30yrs. Also possible role of exposure to Epstien-barr virus as a child
give some clinical features of MS
Sensory:
Usually monosymptomatic - 20% present with unilateral optic neuritis: pain in one eye on eye movement & reduced central vision
numbness or tingling in the limbs
Trigeminal neuralgia
GI: Swallowing disorders and constipation
Eye: diplopia, hemianopia, visual phenomena, eye paralysis (ophthalmoplegia)
Amnesia
Motor:
Spastic weakness
Myelitis (inflammation of spinal cord)
Cerebellum: trunk and limb ataxia, intention tremor, monotonous speech, falls
Sexual/GU:
Impotence
Inability to achieve orgasm
Urine retention
Incontinence
what commonly makes symptoms of MS worse?
raised body temp - hot baths & exercise - known as Uhtoff’s phenomenon
what criteria is used for diagnosing MS
McDonald criteria
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 using disease modifying agents:
Alemtuzumab, Natalizumab, Dimethyl fumarate
Also Interferon beta and Glatiramer (but these are not recommended by NICE)
what 3 clinical features make up Cushing’s triad of signs of raised ICP?
irregular resps. bradycardia. hypertension.
What conditions in men and women are associated with myasthenia gravis
Women = pernicious anaemia, SLE and rheumatoid arthritis
Men = thymic atrophy or thymic tumour, RA and SLE
what is the main clinical feature of myasthenia gravis?
increasing muscular fatigue - weakness on sustained/repeated activity, that improves after rest
which muscle groups are affected by mysathenia gravis, in order of most affected
extra-ocular, bulbar (swallowing, chewing), face, neck, limbs, trunk
give some examples of things you can look for to assess mysathenia gravis
ptosis (eyelid droop), diplopia, mysathenic snarl on smiling. voice fades when asked to count to 50 (rare)
what might you seen on serology of a patient with myasthenia gravis?
anti-AChR and anti-MUSK antibodies
what eye test might you perform to aid a diagnosis of myasthenia gravis?
see if ptosis improves by >2mm after ice applied to affected lid for >2 mins
how would you treat myasthenia gravis?
symptom control - anticholinesterase (pyridostigmine). immunosuppression - prednisolone for relapses ± azathioprine/methotrexate. thymectomy may be considered.
What is Lambert-Eaton myasthenic syndrome and what’s its main difference from myasthenia gravis
paraneoplastic syndrome, most often seen with small lung cancer. Weakness tends to improve after repetition e.g. improves after exercise.
name a gene that causes MND. is this the usual cause?
SOD1. causes rare familiar MND - most cases are sporadic.
what distinguishes motor neurone disease from MS/polyneuropathies?
NO sensory loss or sphincter disturbance in MND. affects upper and motor neurones.
MND also never affects eye movements
what happens to the nervous system in MND? what is the prognosis?
selective loss of neurones in motor cortex, cranial nerve nuclei and anterior horn cells. relentless and unexplained destruction of these neurones. most die in 3yrs from respiratory failure due to bulbar palsy and pneumonia.
name the 4 clinical patterns of MND in order of how common they are
ALS (amyotrophic lateral sclerosis).
progressive bulbar palsy.
progressive muscular atrophy.
primary lateral sclerosis. - causes UMN symptoms only (but is rare)
describe the features of progressive muscular atrophy and what it affects
Anterior horn cell lesion
Causes LMN symptoms only
Affects distal muscle group before proximal
who should you suspect MND in?
>40yrs. stumbling spastic gait, foot drop ± proximal myopathy. weak grip and shoulder abduction, or aspiration pneumonia
How is MND diagnosed
El Escorial diagnostic criteria: is to do with if UMN + LMN are present and in how many limbs
nerve conduction studies to show denervation of muscle
Brain/cord MRI, LP for exclusion
how would you treat a patient with MND?
antiglutamatergic drugs - riluzole - only drug that slows progression. for drooling - Propantheline. muscle spasticity - bacolfen or diazepam. Dysphagia - blend food, nasogastric tube
give 3 organisms that can trigger Guillain-Barre syndrome
Campylobacter jejuni, CMV, mycoplasma zoster, HIV, EBV
describe the clinical features seen in Guillain-Barre
After history of recent infection you may see symmetrical ascending muscle weakness. proximal muscles more affected e.g. trunk, respiratory, cranial nerves. pain common (e.g. back limb), but no sensory signs.
autonomic dysfunction - sweating, raised pulse, BP changes, arrhythmias.
if you were to perform lumbar puncture on a patient with Guillain-Barre syndrome, what might you see?
And what other diagnostic test could you do?
increased protein
Nerve conduction studies - shows slowing of conduction
how would you treat a patient with Guillain-Barre syndrome?
IV immunoglobulin/plasmapharesis. heparin to prevent DVT.
What is the main clinical difference in vascular dementia compared to other types
Stepwise deterioration with declines followed by short periods of stability
list the types of dementia
alzheimer’s. vascular dementia. Lewy body dementia. Fronto-temporal dementia.
explain how vascular dementia arises
cumulative effects of many small strokes. sudden onset, with stepwise deterioration.
what are the features of Lewy body dementia?
fluctuating cognitive impairment, detailed visual hallucinations, Parkinsonism. histology = Lewy bodies in brainstem and neocortex.
what are the features of fronto-temporal (Pick’s) dementia and what diagnoses it?
Pick’s bodies are seen histologically. executive impairment, behavioural/personality change, disinhibition, hyperorality, emotional unconcern
how would you diagnose dementia?
clinical history + timeline of progression - ask relatives/spouse! cognitive testing - AMTS (dementia screens), mental state examinations. CT/MRI.
how would you manage dementia?
develop routines early on - retained until later, prolongs independence. Physical activity, low alcohol, stop smoking, leisure activities, being socially active.
Blood pressure control in vascular dementia
describe the pathology behind Alzheimer’s disease
accumulation of beta-amyloid peptide (a degradation product of amyloid precursor protein) results in progressive neuronal damage, neurofibrillary tangles, raised numbers of amyloid plaques and loss of ACh.
give 3 risk factors for Alzheimers disease
1st degree relative with AD. Down’s syndrome. homozygous for apolipoprotein e (ApoE) 4 allele, vascular risk factors, decreased physical/cognitive activity, depression, loneliness
give some clinical features of Alzheimers disease
general dementia features. plus - enduring, progressive and global cognitive impairment, loss of visuo-spatial skill. memory, verbal abilities and executive function affected. late features - irritability, mood changes, behavioural change, psychosis, agnosia. anosognosia - lack of understanding of the problems caused by the disease.
how might you treat Alzheimer’s disease dementia?
acetylcholinesterase inhibitors (rivastagmine, donezepil, galantamine). antiglutamatergic treatment (memantine) in late stage
give 2 mechanisms by which you can develop neuropathy
demyelination - Schwann cell damage.
Axonal degeneration - axon damage, conduction remain intact.
Wallerian degeneration - follows nerve section.
Compression - disruption of myelin sheath.
Infarction - microinfarction of vasa nervorum.
Infiltration - by inflammatory cells, granulomas and neoplastic cells.
what nerve controls the ankle jerk reflex?
S1
a slim female yoga instructor comes to see her doctor complaining that her left foot keeps dragging on the floor, what do you think could be causing her problem?
common peroneal palsy - her symptoms are due to weakness of ankle eversion and extension, she probably also has numbness over anterolateral border of dorsum of foot and lower shin
a patient comes in having had an accident on the rugby pitch with a suspect elbow fracture, he’s now complaining of sensory loss over his little finger and medial side of his hand, what do you think could be causing his symptoms and if left untreated, what could he go on to develop?
ulnar nerve compression, could go on to develop weakness/wasting of medial wrist flexors, interossei, medial 2 lumbricals and hypothenar eminence
what changes in the spine could there be in cervical/lumbar degeneration?
osteophytes, thickening of spinal ligaments, narrowing of spinal canal, disc degeneration and protrusion, vertebral collapse, ischaemic changes
what would be felt in the myotome and dermatome affected by a spinal nerve root lesion?
myotome - pain of root compression. dermatome - tingling discomfort.
give 2 causes of anosmia caused by an olfactory nerve palsy
respiratory tract infection, olfactory groove tumour, meningitis
if someone is referred to you with suspected Horner’s syndrome, what do you expect to find on examination?
unilateral pupillary constriction with slight ptosis, loss of sweating on same side
a patient comes to see you complaining of visual loss at the ‘sides of his eyes’ on both sides and has some vague endocrine symptoms, what are you thinking is the cause, what kind of visual loss does he have and where is the lesion?
pituitary neoplasm pressing on the optic chiasm causing homonymous hemianopia.
you are performing a cranial nerve examination on a patient who has an oculomotor nerve lesion (CN3), what would you see?
ptosis, fixed dilated pupil, eye down and out.
what kind of visual symptoms would you get with a trochlear nerve lesion?
Innervates the superior oblique so would get diplopia on looking down and in
what would you see if trigeminal palsy
loss of corneal reflex and jaw deviates to the side of the lesion
name a drug that can cause sensorineural deafness?
gentamicin, furosemide
what symptoms are caused by vestibular nerve palsy?
hearing impairment, vertigo, loss of balance and nystagmus
why do lesions of the glossopharyngeal and vagus appear together and what symptoms would you see?
they both leave the skull through the jugular foramen
gag reflex issues, vocal issues, swallowing issues
a patient is struggling to turn their head to the right - they think the’ve slept on it in a weird position. what nerve could have been damaged?
left hand side acessory nerve
you ask a patient to stick their tongue out and it immediately deviates to the right and is very stiff to move, what do you suspect?
UMN lesion affecting the right hypoglossal nerve
what is mononeuritis multiplex? give 3 examples of causes
2+ peripheral nerves affected, Amyloid, Rheumatoid Diabetes mellitus, Sarcoidosis
list the muscles involved in precision grip. what nerve controls us, and what are its spinal roots?
median nerve - C6-T1. LOAD: 2 Lumbricals Opponens pollicis. Abductor pollicis brevis Flexor pollicis brevis
describe the patterns of sensory loss seen in median nerve damage and ulnar nerve damage
median nerve damage - loss of radial 3.5 fingers and palm.
ulnar - medial/ulnar 1.5 fingers.
give a sign of radial nerve damage and an example of how this may occur
wrist and finger drop - compression against humerus
give a sign of ulnar nerve damage and how it may occur
weakness/wasting of ulnar side wrist flexors, interossei (can’t cross fingers) and medial two lumbricals (claw hand). hypothenar eminence wasting.
Tends to occur from elbow trauma
how would phrenic nerve (C3-5) damage present?
orthopnoea with raised hemidiaphragm on CXR.
how might damage to the lateral cutaneous nerve of the thigh present (L2-L3)?
meralgia paraesthetica - anterolateral burning thigh pain from entrapment under inguinal ligament
how would sciatic nerve damage present (L4-L5)?
affects hamstrings and all muscles below the knee - foot drop. loss of sensation below the knee laterally.
give 2 signs of damage to the common peroneal nerve (L4-S1)
foot drop, weak ankle dorsiflexion/eversion, sensory loss over dorsum of foot
how would tibial nerve damage present (L4-S3)?
unable to stand on tiptoe, invert foot or flex toes. Sensory loss over the sole
describe the clinical features of carpal tunnel syndrome
aching pain in hand and arm, esp at night. paraesthesiae in thumb, index, middle finger and palm. relieved by dangling hand over edge of bed and shaking it - wake and shake.
Also weakness of abductor pollicis brevis - patient might say they struggle opening jars in the kitchen
list 3 causes of carpal tunnel syndrome
Hypothyroid Myxoedema. Diabetic neuropathy. Obesity. Acromegaly. Rheumatoid arthritis. Amyloidosis. Pregnancy/premenstrual oedema. Sarcoidosis.
how might you manage carpal tunnel syndrome?
splinting, local steroid injection (Methylprednisolone), decompression surgery.
describe the features of a UMN lesion
pyramidal weakness - arm extensors and lower limb flexors. no muscle wasting. spasticity in stronger muscles. hyperreflexia.
Long tract signs = babinski, clonus, cross abductor reflex and hoffman’s
describe the features of a LMN lesion
damage to anterior horn cells, nerve roots, plexi or peripheral nerves.
distribution of weakness corresponds to those muscles supplied by the involved cord segment etc. muscles show wasting ± fasciculation. hypotonia/flaccidity - limb feels soft and floppy. reduced/absent reflexes.
What is the most common and most malignant form of astrocytoma
Glioblastoma Multiforme
name 2 types of benign brain tumour
meningioma, neurofibroma (e.g. from Schann cells)
what is the most common cause of brain tumours?
metastases: Lung, breast, stomach, prostate, thyroid, kidney.
what are the 4 main classes of symptoms you can get from a brain tumours?
raised ICP, seizures, focal neurology, personality change
what investigation would you use to stage a brain tumour?
CT/MRI + CXR etc to look for primary
how would you manage a brain tumour?
surgical removal if possible. IV/PO dexamethasone to reduce cerebral oedema. phenytoin to treat epileptic seizures. Chemotherapy.
Give some risk factors for meningitis
Spinal canal drug administration, immunocompromised, diabetes, malignancy, IV drug abuse, other infections e.g. bacterial endocarditis
list some clinical features of meningitis
neck stiffness (Brudzinski’s neck sign), headache, fever.
cold hands and feet. photophobia, Kernig’s sign (pain + resistance on passive knee extension when hip fully flexed). non-blanching petechial rash (if non-blanching rash, give IV/IM pencillin STAT). vomiting, rigors, irritability, papilloedema. severe headache. Seizures and focal CNS signs
what treatment would you give to a patient presenting with meningitis?
IV Ceftriaxone or IV Cefotaxime (can be used as an alternative in adults)
Add IV Amoxicillin if >60 or immunocompromised
Oral Dexamethasone to reduce cerebral oedema (if evidence of this)
what would you need to do, apart from treat them, if you were presented with a patient with meningitis?
contact tracing for prophylaxis (oral ciprofloxacin). inform local officer/PHE.
give 2 viral causes of encephalitis
(viral is more common than bacterial) herpes simplex, Epstein Barr virus (EBV), mumps, Cytomegalovirus (CMV), Varicella zoster virus (VZV), measles, rabies
give 2 non-viral causes of encephalitis
bacterial meningitis, TB, malaria, listeria, lyme disease, Legionella, leptospirosis, aspergillosis, typhus
what is encephalitis?
inflammation of brain parenchyma
what clinical features would make you suspect encephalitis?
(can be mild, self-limiting - fever/headache/drowsiness) odd behaviour, decreasing consciousness, seizures, focal neurology, headache, fever, history of travel/animal bite
if you performed a lumbar puncture on a patient with encephalitis, what would you expect to see?
increased lymphocyte, increased protein
how would you treat a patient with viral encephalitis?
IV Aciclovir, phenytoin for seizures
what is the primary infection in shingles?
chicken pox - reactivation of herpes zoster/varicella zoster virus
what are the clinical features of shingles?
dermatome distribution of rash (papules and vesicles), pain and tingling. most common in lower thoracic dermatomes and ophthlamic division of trigeminal nerve.
how would you treat shingles?
oral aciclovir or valaciclovir as early as possible
what is the main complication of shingles and how would you treat it? how is it prevented?
post-herpetic neuraligia - pain in distribution of affected nerves. treat with carbamazepine or phenytoin. prevented by prompt antiviral treatment.
how do anti-epileptic drugs work?
they work on sodium channels to inhibit action potentials to stop continuous firing of neurones
pyridostigmine is used in a neurotransmitter disease, which one and how does it relieve symptoms?
myasthenia gravis - acetylcholinesterase inhibitor, which means ACh is around longer to attach to the post-synaptic membranes
ceftriaxone is prescribed in bacterial meningitis, what class of antibiotic is it?
3rd generation cephalosporin
give 2 examples of benzodiazepines. what are they used for?
diazepam, lorazepam, chlordiazepam - first line management of seziures and status epilepticus, management of alcohol withdrawal rections.
how do dopaminergic drugs work to treat Parkinson’s?
there’s a dopamine deficiency in Parkinson’s - treatment increases dopaminergic stimulation to the basal ganglia. levodopa = dopamine precursor that is able to cross the BBB. ropinirole and pramexipol = selective agonists for the D2 receptor, which predominates in the basal ganglia - used to delay starting levodopa.
what is levodopa always given with? why?
a peripheral dopa-decarboxylase inhibitor e.g. carbidopa - combined preparations (co-careldopa, co-beneldopa). this is to reduce conversion to dopamine outside the brain, reducing SE of nausea, and lowering the dose.
how do triptans work?
agonist effects on serotonin 5-HT-1b and d receptors in cranial blood vessels - causes their constriction, and subsequent inhibition of pro inflammatory neuropeptide release. may also work on serotonin receptors in nerve endings to relieve pain through decrease in levels of substance P.
what class of drug do rivastigmine and neostigmine belong to? what are they used to treat?
acetylcholinesterase inhibitors. Alzheimer’s disease, Lewy body dementia and Parkinson’s disease. also myasthenia gravis.
how do acetylcholinesterase inhibitors work as neurological drugs?
inhibit ACh break down. in neurodegenerative disorders they are used to treat memory and learning deficit symptoms - improve due to role of ACh in cognition. in myasthenia gravis there are too few ACh receptors, so with greater ACh availability, symptoms improve.
what might patients complain of in mysathenia gravis?
“stairs, chairs and hair” can’t get up out of chairs, can’t walk up the full flight of stairs, can’t brush their hair.
What is the definition of Delirium
Medical emergency that is transient, acute syndrome, characterised by disturbance of consciousness, perception, sleep-wake cycle, emotion and cognition
Name some causes of Delirium
Pain, infection, alcohol/substance, medication, dementia, environment
What are some symptoms of Delirium
Fluctuating course, impaired cognition, disturbance of consciousness, memory loss, agitation, abnormalities of perception
What assessments would you do in Delirium
General inspection and examination and Confusion Assessment Method and The Abbreviated Mental Test
describe the features of ALS MND and what part of the CNS it affects.
disease of lateral cortiospinal tracts. causes weakness with UMN signs and LMN wasting. progressive spastic tetraparesis with LMN signs and fasciculation.
describe the features of progressive bulbar palsy and what it affects
Affects CN9,10,11,12
LMN lesion of cranial nerves for the tongue and muscle of talking and swallowing
Causes dysarthria, dysphagia, nasal regurg of fluid and choking
give some UMN and LMN signs that may feature in MND
UMN - spasticity, brisk reflexes, upgoing plantars. LMN - wasting, reduced tone, fasciculation of tongue, abdomen, back, thigh
What would you see in a LP for bacterial meningitis compared to other types
Bacterial has polymorphs. Chronic and viral has lymphocytes
In bacteria and chronic, protein is also raised. In Viral it is not
name 3 organisms that commonly cause meningitis
Neisseria meningitides, Streptococcus pneumoniae, H influenzae,
immunocompromised - CMV, cryptococcus, TB, HIV, herpes
give the 2 subtypes of gliomas
astrocytoma and oligodendroglioma
how does pyridostigmine help treat symptoms of myasthenia gravis? name a possible side effect and how you would treat it.
inhibits acetylcholinesterase enzyme from breaking down ACh - thereby increasing level and duration of action of ACh. colic, diarrhoea - atropine.
What is a Myasthenic Crisis and how is it managed
Weakness of the respiratory muscles during a relapse. Ventilatory support and plasmapheresis (antibody removal) + IV immunoglobulin
explain the pathophysiology of myasthenia gravis
an autoimmune disease, producing antibodies to nicotinic ACh receptors, which interfere with neuromuscular transmission by depleting receptor sites. immune complexes of anti-ACh receptor IgG and complement are deposited at the post-synaptic membranes.
What is the emergency management pathway for head injury
- ABC
- intubate and hyperventilate if O2 <92% or hypoxic on ABG
- Immobilise neck until injury to cervical spine excluded
- Stop blood loss and support circulation
- Treat seizures with lorazepam ± phenytoin
- Assess level of consciousness (GCS) - iF GCS ≤8 involve ICU
- Investigations: U&Es, glucose, FBC, blood alcohol, toxicology screen, ABGs, and clotting
- Neurological exam
- Check for CSF leak, from nose or ear. Any blood behind eardrum?
- Palpate the neck posteriorly for tenderness and deformity
- Radiology: if GCS <13 on initial assessment or <15 at 2h following injury then a CT needs to be done <1h, or if there is:
- focal neurological deficit
- severe headache
- skull fracture
- post-traumatic seizure
What are the 7 main causes of blackouts
- Vasovagal syncope - reflex bradycardia ± peripheral vasodilation provoked by emotion, pain or standing too long
- Reflex syncope - has clear precipitant e.g. cough, exercise
- Carotid sinus hypersensitivity
- Orthostatic syncope
- Strokes-Adams attacks - transient arrhythmias
- Epilepsy
- Non-epileptic attack
