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Finals > Neuro > Flashcards

Neuro Flashcards

1
Q

causes of ischaemic stroke?

A

atherosclerosis, thromboembolism (AF, valvular disease. infective endocarditis), vascular (migraine, dissection. vasculitis), haematological (PCV, thombophilia, sick cell)

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2
Q

causes of hameorrhagic stroke?

A

hypertension, vascular (AVM, sacular anyeursms), brain tumours, haemostatic disorders (thrombolyic therapy, oral anticoagulation)

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3
Q

symptoms of ACA stroke?

A

paralysis and sensory loss of foot / leg, gait aprazia, frontal cortical release reflex (grasp / sucking reflex)

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4
Q

symptoms of a left MCA stroke?

A

right motor and sensory loss more profound in R face and arm than R leg; usually dysphasia

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5
Q

symptoms of a right MCA stroke?

A

weakness and sensory loss greater in L arm and face than L leg; visual and sensory neglect, denial of disability.

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6
Q

symptoms of PCA stroke?

A

homonymous hemianopia

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7
Q

internal capsule stroke?

A

face, arm and left affected equally

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8
Q

what does a posterior inferior cerebellar artery stroke cause?

A

Lateral medullary aka “wallenburg syndrome” - consisting of ipsilateral horner’s syndrome, facial sensory loss, vagal palsy, limb ataxia with contralateral spinothalamic loss, vertiginous, failed laryngeal closure and ineffective cough. can also be caused by vertebral artery stroke.

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9
Q

a stroke in which region of the brain causes locked-in syndrome?

A

upper brainstem

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10
Q

a stroke where results in a coma?

A

reticular activating system

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11
Q

4 Imaging investigations to get in a stroke?

A

urgent CT, CXR for aspiration pneumonia, duplex scan of carotid arteries, TTE is ?intracardiac thrombus / valvular disease

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12
Q

Tx of stroke >4.5h from onset?

A

300mg of aspirin, swallow assessment, management in hyper acute unit, maintain hydration and monitor.

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13
Q

how do you classify stroke?

A

the oxford / bamford classification. looks at symptoms to stay whether is total / partial anterior circulation stroke, posterior circulation stroke or lacunar infarct.

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14
Q

what proportion of TIA patients go on to have a stroke or an MI?

A

30% have stroke in first 5 years, 15% have MI.

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15
Q

what score is used in TIA to assess prognosis?

A

ABCD2 score looks at age (>60), BP (>140/90), Clinical features (2p for unilat weakness, 1p for speech issues w/o weakness), Duration of symptoms (2p for>1h, 1p for 10-59m), Diabetes. A score >7 indicates high risk of stroke within 7d of TIA.

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16
Q

when is it appropriate to perform a carotid endarterectomy?

A

> 50% stenosis and symptomatic (best evidence for >70%, do if 50-70% and can be done in first 2 weeks)

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17
Q

3 causes of SAH?

A

saccular aneurysms (80%), AVMs, vertebral artery dissection

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18
Q

management for SAH?

A

fluids (SBP>160), nimodipine (presvent s cerebral artery vasospasm), immediate neurosurgical opinion (embolisation or clipping)

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19
Q

management for SDH?

A

decompression: irrigation and evacuation

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20
Q

which bones meet at the pterion?

A

frontal, temporal, parietal and sphenoid

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21
Q

what is Cushing’s reflex?

A

bradycardia and hypertension, it occurs as a late sign of raised ICP

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22
Q

management of EDH?

A

transfer to neurosurgical unit, give mannitol, intubate and hyperventilate and urgent clot evacuation +/- bleeding vessel ligation, decompression is necessary, burr holes if neurosurgeon not available.

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23
Q

management for migraine?

A

rescue treatment - triptan (sumatriptan) + NSAID/paracetamol + anti-emetic (prochlorperazine)
prophylactic - avoid triggers, headache diary, Topiramate in adults, propranolol in children.

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24
Q

signs of raised ICP?

A

morning headaches, N&V, false localising signs, papilloedema, loss of venous pulsations, loss of retinal vein pulsations, cushion’s reflex.

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25
Q

causes of syncope?

A

vasovagal, cariogenic (rhythm; left outflow obstruction - HOCM or AS; right outflow obstruction - massive PE), Postural hypotension (dehydration, vertebral basilar insufficiency, AN neuropathy, antihypertensives)

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26
Q

what is a seizure?

A

a sudden, synchronous discharge of cerebral neutrons which is either apparent to external observer or as an abnormal perceptual experience to patient.

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27
Q

what is epilepsy?

A

the recurring tendency to have seizures

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28
Q

what is a partial seizure?

A

sometimes called a focal seizure, this is a seizure in which electrical discharge is restricted to a limited part of the cortex.

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29
Q

what is the difference between a simple and complex seizure?

A

in simple seizures, consciousness is retained; in complex seizures, it is not - often accompanied with loss of speech or automatisms and epigastric sensation / nausea auras.

30
Q

what is first-line drug for focal seizures?

A

carbamazepine

31
Q

which seizures can be treated first line with valproate?

A

tonic-clonic, absence, myoclonic, tonic / atonic

32
Q

what are the side effects of valproate?

A

it is the most teratogenic of all AEDs, and is also associated with weight gain, hair loss, tremor and osteoporosis

33
Q

what are the side effects of carbamazepine?

A

neutropenia, hypernatraemia, ataxia, rash, liver enzyme induction

34
Q

which is the least teratogenic AED?

A

lamotragine - suitable for 1st line use in focal, absence and tonic-clonic seizures,

35
Q

what are the side effects of phenytoin?

A

gingival hypertrophy, peripheral neuropathy, hepatotoxicity, strong liver enzyme inducer, osteoporosis . saturation kinetics means there is a narrow therapeutic range - monitor carefully.

36
Q

What is the triad of parkinsonism?

A

rigidity, tremor, bradykinesia

37
Q

what is cogwheel rigidity?

A

tremor superimposed on increased tone

38
Q

symptoms of bradykinesia?

A

expressionless face, micrographic, reduced blink rate, short suffering gate with stooped posture, freezing at objects / doors.

39
Q

symptoms of PSP?

A

symptoms occur at the core of the person - early onset postural instability (falls), speech and swelling problems, vertical saccades. tremor is unusual.

40
Q

symptoms of MSA?

A

cerebellar ataxia, autonomic features, symmetrical onset parkinsonism

41
Q

symptoms of CBD?

A

unilateral kinetic rigidity, cortical sensory loss, apraxia

42
Q

what is Parkinson’s disease?

A

It is a degenerative disorder of movement (triad), involving the degeneration of dopaminergic neurones in the substantia nigra pars compacta associated with intraneuronal Lewy bodies

43
Q

what protein causes PD?

A

alpha synuclein

44
Q

what are the non-motor features of parkinson’s disease?

A

sensory (anosmia), autonomic (postural hypotension, erectile dysfunction, sweating dysfunction), sleep (REM sleep disorders, acting out dreams), cognitive (mild cognitive impairment, dementia, depression)

45
Q

what is the management for parksinon’s disease?

A

conservative - psychoeducation, MDT, support groups
meds - if young then give non-ergot derived dopamine agonists (such as ropinirole) or MAOI (such as rasagiline); if older, give L-DOPA and peripheral decarboxylase inhibitors (such as co-carledopa - containing carbidopa and L-DOPA)
surgical - deep brain stimulation (electrode at stn delivers high frequency stimulation)

46
Q

How does optic neuritis present?

A

partial or total loss of vision over days, retrooribtal pain, reduced colour intensity. patients will have RAPD in affected eye.

47
Q

in MS, patient’s symptoms get worse when body is overheated, what is this called?

A

Uthoff’s phenomenon

48
Q

four common presentation of MS relapse?

A

optic neuritis, traverse myelitis, cerebellar syndromes, brain stem syndromes.

49
Q

bilateral internuclear opthalmoplegia is pathognomic of which condition?

A

MS - lesion in the medial longitudinal fasiculus (which conjugates gaze).

50
Q

what is Lhermitte’s phenomena?

A

shock sensation radiating down spine on neck flexion - seen in MS

51
Q

what is the treatment for MS?

A

conservative - support, education
medical - steroids in acute flare, variety of agents in long term (natalizumab, IFNbeta, fingolimod), variety for symptoms (amitriptyline for pain, SSRI for depression, baclofen for spasticity)

52
Q

what condition is MG associated with?

A

<50 - thymic hyperplasia (70%), thymoma (10%) - do CXR

>50 - thymic atrophy, RA, SLE,

53
Q

what autoantibodies are the most common in MG?

A

anti-AChR

54
Q

what are the common symptoms of MG?

A

eye symptoms (ptosis, diplopia, etraoccular muscle weakness following no specific pattern)
bulbar symptoms (dysarthria, dysphagia, fatiguable chewing)
limb symptoms (proximal extremities)
all symptoms are fatugable (i.e. get worse after activity)
reflexes are normal

55
Q

special tests for MG?

A

CXR (?thymoma), repetitive nerve stimulation (should show fatiguability), tension test (should improve with anti-cholinesterase activity, beware bradycardia)

56
Q

Treatment for MG?

A

conservative - PT, OT, support, vocational counselling
medical - pyridostigmine (anti-cholinesterase inhibitors) +/- steroids; azathioprine as immunosuppressant.
surgical - thymectomy

57
Q

what are the symptoms of an uncal herniation?

A

this is a transtentorial herniation which compresses the upper brainstem and CN3. This causes dilated ipsilateral pupil, ophthalmoplegia, then contralateral hemiparesis and coma.

58
Q

what herniates where in a tonsillar herniation? what symptoms does this cause?

A

The cerebellar tonsils herniate through the foramen magnum leading to, at first, ataxia, CN6th palsy, upping plantar, then causing LOC, irregular breathing and apnoea.

59
Q

in a subfalcine herniation, what herniates where? and what is the major complication and why?

A

The cingulate gyrus herniates underneath the falx cerebri which can compress the anterior cerebral artery, causing a stroke.

60
Q

over which bone is CN6 usually compressed in raised ICP?

A

petrous temporal bone

61
Q

what are the complications of neurofibromatosis?

A

renal artery stenosis, hypertension and pulmonary hypertension

62
Q

Features of NF1?

A

cafe au last spots, neurofibromas (nodular or dermal), fracking in axilla / inguinal region, lisch nodules, skeletal malformations such as sphenoid dysplasia.

63
Q

Features of NF2?

A

fewercutaenous symptoms than NF1 - patients still have cafe au last spots. intracranial tumours - bilateral vestibular schwannomas (acoustic neuromas leading to sensorineural hearing loss and tinnitus / dizziness; also gliomas, meningiomas etc)

64
Q

how does Wernicke’s encephalopathy present?

A

2 of the following 4: ataxia, nystagmus, ophthalmoplegia, acute confusional state

65
Q

how does Korsakoff’s syndrome present?

A

anterograde amnesia, variable retrograde amnesia, confabulation. NB: working, procedural and emotional memory remains intact.

66
Q

how does myotonic dystrophy present?

A

frontal baldness, cataracts, distal muscle wasting and weakness

67
Q

what is brown-sequard syndrome?

A

unilateral transection of spinal cord (hemisection)

68
Q

what is Von Hippel Laundau syndrome characterised by?

A

intracranial and retinal haemoangioblastomas and haemangiomas, renal cysts and RCC, pancreatic tumours and phaechromocytomas.

69
Q

what are the 4 main clinical patterns of MND?

A

ALS (classical), progressive muscle atrophy (LMN signs only), progressive bulbar and pseudo bulbar palsy (only affects CN9-12), primary lateral sclerosis (UMN)

70
Q

what medication is of prognostic benefit in MND?

A

riluzole

71
Q

what medication is used to treat cramp in MND?

A

quinine sulphate

Finals (12 decks)

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