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Phase 2a > Neuro big topics > Flashcards

Neuro big topics Flashcards

1
Q

define TIA

A

transient, reversible neurological phenomenon lasting <24 hours with complete clinical recovery

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2
Q

causes of TIA

A

thromboembolism from carotids
cardioembolism
hyperviscosity

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3
Q

define amaurosis fugax

A

retinal artery embolism, causing sudden transient loss of vision in one eye

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4
Q

DDx TIA

A

hypoglycaemia
migraine aura
focal epilepsy

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5
Q

TIA Ix

A 
carotid doppler
CT brain (existing infarcts)
Echocardiogram (cardiac cause of embolism)
Erythrocyte sedimentation rate
serum glucose
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6
Q

scoring system to estimate risk of stroke following TIA?

A 
ABCD2
1     age >60
1     BP >140/90
clinical features
2    unilateral weakness
1     speech disturbance w/o weakness
duration
1     10-59 mins
2    >60 mins
1     diabetes
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7
Q

treatment of TIA

A

control risk factors:

  • blood pressure (antihypertensive regimen)
  • cholesterol (statins)
  • diabetes
  • stop smoking

antiplatelets
- clopidogrel + aspirin

carotid endarterectomy

driving

  • avoid for 1 month
  • inform DVLA
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8
Q

effects of anterior cerebral artery stroke?

A

front and medial cerebrum superior humunculus thus:

  • leg weakness/sensory disturbance
  • gait apraxia
  • incontinence
  • drowsiness
  • akinetic mutism (damage to cingulate gyrus)
  • face SPARING
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9
Q

effects of middle cerebral artery stroke?

A

most common artery affected

  • contralateral arm and leg weakness/sensory disturbance
  • hemianopia (optic radiation)
  • aphasia - difficulty comprehending (wernicke’s area in dominant temperoparietal lobe) and formulating speech (broca’s area in dominant frontol lobe)
  • facial DROOP
  • visuospatial disturbance
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10
Q

effects of posterior cerebral artery stroke?

A
  • contralateral homonymous hemianopia with macular sparing
  • cortical blindness
  • visual agnosia (cant interpret what seeing)
  • prosopagnosis (cant recognise faces)
  • colour naming and discrimination
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11
Q

effects of poster circulation stroke?

A

supplies brainstem, cerebellum and occipital lobes

  • motor deficits (hemiparesis/facial paresis)
  • dysarthria (slow/slurred speech)
  • vertigo
  • nystagmus
  • dysdiadochokinesia
  • altered consciouness
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12
Q

investigations for stroke?

A
  • urgent CT/MRI brain
    to distinguish ischaemic and haemorrhagic
  • serum glucose
  • coagulation tests
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13
Q

treatment of ischaemic stroke

A

thrombolysis (IV alteplase) if <4.5 hours after onset of symptoms –> alteplase = tissue plasminogen activator

risk management

  • antiplatelets: aspirin + clopidogrel
  • statins
  • AF –> warfarin
  • BP

post-stroke referral:

  • speech and language therapy
  • physio
  • occupational therapy
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14
Q

risk factors for stroke? modifiable and non-modifiable

A

modifiable:

  • HYPERTENSION
  • smoking
  • lack of exercise
  • obesity
  • diabetes
  • hyperlipidaemia

non-modifiable

  • ethnicity (black/asian)
  • age
  • male
  • family history
  • atrial fibrillation
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15
Q

what must always be excluded in DDx for stroke?

A

hypogycaemia

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16
Q

contraindications of thrombolysis in stroke?

A
  • past CNS bleed
  • > 4.5 hours since symptom onset
  • seizures at presentation
  • uncontrolled blood pressure
  • recent lumbar puncture
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17
Q

What might be the cause of crossed signs? ie left arm weakness and right mouth droop

A

BRAINSTEM LESION

  • crossed signs not involving brainstem would require 2 separate cortical lesions on both hemispheres
  • facial involvement suggests lesion abve spinal cord
  • CNs affected on same side as lesion (LMN signs), and corticospinal tract affected before it decussates at medulla (UMN signs)
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18
Q

LMN CN7 palsy (Bell’s palsy) vs UMN CN7 palsy (stroke)?

A

bells palsy = LMN lesion thus NO forehead sparing

stroke = UMN CN7 lesion this FOREHEAD SPARING

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19
Q

primary and secondary causes of haemorrhagic stroke?

A

primary:

  • hypertension (Charcot-Bouchard aneurysm –> affects basal ganglia)
  • lobar (cerebral amyloid angiopathy)

secondary:

  • metastases/tumour
  • arteriovenous malformation
  • anticoagulants (warfarin)
20
Q

treatment of haemorrhagic stroke

A

control BP –> B-blocker

warfarin antidote –> beriplex

21
Q

cause of subarachnoid haemorrhage?

A

rupure of circle of willis due to:

  • saccular/Berry aneurysm rupture
  • arteriovenous malformation
22
Q

risk factors subarachnoid haemorrhage?

A 
smoking
alcohol
hypertension
family history
polycystic kidney disease
23
Q

signs and symptoms of subarachnoid haemorrhage?

A

symptoms:

  • sudden onset thunderclap headache
  • vomiting
  • seizures
  • photophobia
  • drowsiness

signs:

  • kernig’s sign
  • neck stiffness
  • sentinel headache
24
Q

investigations of subarachnoid haemorrhage?

A
  • CT brain –> star-shaped blood pooling, hydrocephalus

- lumbar puncture (wait 12 hours) –> xanthochromia

25
Q

DDx subarachnoid haemorrhage?

A

meningitis

migraine

26
Q

management of subarachnoid haemorrhage?

A

refer all to neurosurgeon
nimodipine (CCB to control BP)
endovascular coiling

27
Q

patho of parkinsons and histological features?

A

degeneration of dopaminergic neurones on substantia nigra pars compacta

associated with lewy bodies

28
Q

features of parkinsons

A

1) pill-rolling tremor, worse at rest, unilateral
2) rigidity
3) bradykinesia (slow to initiate movement, monotonous hypophonic speech, micrographia)
4) postural instability

  • gait (reduced arm swing on one side, shuffling)
29
Q

premotor features of parkinsons

A
  • anosmia (reduced smell sense)
  • depression
  • REM sleep disorders
  • urinary urgency
  • constipation
  • visual hallucinations
30
Q

management of parkinsons

A

early:

  • ropinirole (dopamine-2 agonist)
  • selegiline (monoamine oxidase-B inhibitor)

late:
- co-beneldopa (levodopa with decarboxylase inhibitor)

31
Q

subtypes of motor neurone disease

A
  • amyotrophic lateral sclerosis –> UMN + LMNs affected
  • progressive bulbar palsy –> UMN + LMNs of CN 9-12
  • primary lateral sclerosis –> UMNs affected
  • progressive muscular atrophy –> LMNs affected
32
Q

key features of MND

A
  • muscular atrophy
  • UMNs and LMNs both affected
  • paralysis
  • loss of motor control
  • preservation of mental awareness
  • NO sensory/sphincter disturbance (vs MS and polyneuropathies)
  • NO eye movement involvement (vs MG)
33
Q

pathology of MND

A

degeneration and loss of neurones in motor cortex, CN nuclei and anterior horn cells

34
Q

diagnostic investigations for MND

A

1) electromyography/nerve conduction studies
2) clinical features

  • increased creatinine kinase
  • lumbar puncture
35
Q

diagnostic criteria for MND

A

el escorial

36
Q

treatment of MND

A
  • riluzole (antiglutaminergic)
37
Q

localisation of lesions:

  • cortical lesion
  • internal capsule
  • brainstem
  • spinal cord
A
  • cortical lesion = contralateral weakness over large area
  • internal capsule = complete contalateral hemiparesis
  • brainstem = bilateral weakness, involves CN, bulbar involvement
  • spinal cord
38
Q

what is amyotrophic lateral sclerosis

A

events in the ALS-frontotemperal dementia locus

39
Q

archetypal patient

A
  • over 40
  • stumbling gait
  • foot drop
  • proximal myopathy
  • weak grip
  • weak shoulder abduction (cant wash hair)
  • speech/swallowing –> aspiration pneumonia

UMN signs:

  • spasticity
  • brisk reflexes
  • upgoing plantars

LMN signs:

  • wasting
  • tongue fasciculations
  • hypotonia
40
Q

patho of multiple sclerosis

A

discrete plaques of demyelination at multiple CNS sites due tp CD-4 T-cell mediated immune response, leading to axonal loss and progressive symptoms (relapsing and remitting)

41
Q

key features of MS

A

ALWAYS UMN AFFECTED

optic involvement
- unilateral optic neuritis

brainstem lesions:

  • diplopia
  • vertigo
  • nystagmus
  • facial numbness
  • swallowing difficulty

spinal cord involvement

  • abnormal gait
  • bladder dysfunction
  • numbness/tingling in limbs
  • spastic leg weakness
  • Lhermittes = electric shock feeling down spine/limbs

Uhthoffs = symptoms worsened by heat/exercise

42
Q

risk factors of MS

A

family history
human t-lymphotropic virus-1
decreased vitamin D exposure (temperature climates)

43
Q

investigations of MS

A
  • lumbar puncture = +ve for oligoclonal bands on CSF
  • visual evoked potential = slow signal transmission (due to demyelination)
  • MRI = exclude other causes
  • examination = UMN signs only

Dx = MRI + clinical features

44
Q

diagnostic criteria of MS

A

McDonald Criteria

MRI + clinical features

45
Q

DDx MS

A

cauda equina
prolapsed disc
spinal cord infarct

46
Q

Tx of MS

A

acute (shorten relapse) = methylprednisolone

chronic (prevent relapse):

  • interferon beta-1a
  • azathioprine

spasticity = baclofen (GABAb analogue)

pain = carbamazepine

Phase 2a (5 decks)

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