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OSCE - Doctor Clarke 2018 > Neuro > Flashcards

Neuro Flashcards

1
Q

Testing tone in upper limb

A

Supinator catch

flexion and extension of elbow (clasp knife, lead pipe)

dorsiflexion and collar flexion at wrist (cogwheel, reinforced by synkinesis)

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2
Q

Pyramidal pattern of weakness

A
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3
Q

Testing movements and their roots, and peripheral nerves

A
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4
Q

How do you test hand function?

A

grip - C8- long flexors

pincer grip

prayer sign

fine movement (play the piano, general pyramidal function)

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5
Q

Positive prayer sign

A

RA

scleroderma

diabetes

ulnar nerve palsy

T1 palsy

Dupuytren’s

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6
Q

What does pincer grip test?

A
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7
Q

Cerebellar signs

A

DANISH

dysdiadokokinesia

ataxia

nystagmus- 20 dog from centre

intention tremor

scanning (staccato) or slurred speech

hypotonia

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8
Q

Test for cerebellar speech

A

west register street, edinburgh

baby hippopotomus

british constitution

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9
Q

Management of acute stroke

A
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10
Q

Contraindications to thrombolysis

A

high BROW

high BP diastolic >140

bleeding tendancy

recent surgery

over 80

woke with sx

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11
Q

Causes of carpal tunnel

A

RAPID TTT

RA

acromegaly

pregnancy

idiopathic

diabetes

trauma

tenosynovitis

thyroid (hypo)

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12
Q

4 signs of ulnar nerve palsy

A

sensory loss over 5th and ulnar 1/2 of 4th finger

wasting and weakness of dorsal interossei

weak pincer grip

partial claw hand (medial lumbricals)

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13
Q

How does a t1 lesion cause claw hand?

A

Affects the fibres to all lumbricals (ulnar and median)

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14
Q

Lower limb nerve roots

A

L2- hip flexion

L3- knee extension

L4- inversion and dorsiflexion of the foot

L5- dorsiflexion of the big toe

S1- eversion of the foot

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15
Q

TACI criteria

A
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16
Q

PACI criteria

A

2/3:

contralateral hemiparesis

contralateral homonyms is hemianopia

higher cortical dysfunction

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17
Q

POCI criteria

A

Any 3:

cerebellar signs

contralateral homonyms is hemianopia

Brain stem signs (horners, cranial nerve lesion)

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18
Q

LACI features

A

No:

contralateral hemiparesis

contralateral homonyms is hemianopia

higher cortical dysfunction

drowsiness

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19
Q

Path of the optic nerve

A
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20
Q

Visual defect vs site of lesion

A
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21
Q

Causes of papilloedema

A

raised ICP due to tumor

essential intercranial hypertension

malignant hypertension

hypercapnoea

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22
Q

How does optic neuritis cause optic atrophy

A
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23
Q

Signs of optic neuropathy

A

pale disc

loss of visual acuity

loss of red colour vision (desaturation or red dyschromatopsia)

central scotoma

afferent pupillary defect

24
Q

Causes of optic neuropathy

A

demyelination (optic neuritis)

trauma

compression (pituitary tumour or meningioma)

ischaemic (diabetes, cranial arteries, temporal arteritis)

toxic (methanol, ethambutol)

secondary to papilloedema (essential Intercranial HTN)

25
Q

Bell’s palsy Mx

A

eye drops

close eyelid at night

high dose steroids if seen <72hrs

consider referral if still weak at 6/12

check BP, sometimes vascular cause

26
Q

Parkinson’s quadrad

A

tremor

rigidity

bradykinesia

loss of postural reflexes

27
Q

Parkinson’s Hx

A

ADLs

handwriting (micrographia)

buttons and shoelaces

turning over in bed at night

getting in and out of car

28
Q

Parkinson’s Ex

A

poverty of facial expression

5Hz tremor

cogwheel rigidity at wrist

thumb finger test

toe tap test

function

exclude Parkinson’s plus

29
Q

Parkinsonism causes

A

parkinsons disease

vascular parkinsonism

parkinsons-plus syndromes

other (antidopaminergics, Wilson’s)

30
Q

Parkinson’s plus syndromes

A

progressive supernuclear palsy : vertical limitation, axial rigidity

multi-system atrophy- cerebellar signs, autonomic problems

corticobulbar degeneration

lewy body dementia

31
Q

Features of Parkinson’s gait

A

loss of arm swing (early)

hesitancy

shuffling

hurrying (festination)

retropulsion (falling backward)

clock face turning

32
Q

Motor complications in Parkinson’s

A

drug induced dyskinesias: choreo-athetoid movements

fluctuations: predictable (end of dose) unpredictable (on-off effect)

all commoner with L dopa and less common with DA agonists

33
Q

Parkinson’s management

A
34
Q

Pathophysiology of unilateral inter nuclear opthalmoplegia

A
35
Q

Causes of bilateral inter nuclear opthalmoplegia

A

wernickes encephalopathy

stroke

demyelinating disease

MS

36
Q

Ix MS

A

clinical exam and hx may be sufficient

2 separate attacks affecting different parts of the CNS

MRI: periventricular and juxtacorticol plaques

visually evoked potentials: delay in EEG response due to optic neuropathy

somatosensory evoked potentials: delay in EEG response after episode of sensory demyelination

CSF- oligoclonal bands (60% after one attack, 90% after 2)

37
Q

Treatment of acute MS

A

may not need treatment if just sensory

IV methylprednisolone for 3 days

reduces length and severity, no impact long term

small risk of psychosis, diabetes, AV necrosis femoral head

high dose oral may be effective, but also increase relapse rate of optic neuritis

38
Q

Oculomotor palsy features

A

partial ptosis

eye abducted and depressed

pupil dilated (loss of parasympathetic fibres)

39
Q

Causes of oculomotor palsy

A

Diabetes (pupil often spared)

PCA aneurysm (often painful)

raised ICP (false localising)

40
Q

Why is the pupil spared in diabetes?

A

parasympathetic fibres have a separate blood supply from the nerve sheath vessels

41
Q

Features of horners syndrome

A

slight ptosis

constricted pupil

reduced sweating on forehead

eye is bloodshot early

loss of alpha vasoconstrictor tone

42
Q

Causes of acquired ptosis

A
43
Q

Causes of 6th nerve palsy

A
44
Q

Course of 6th nerve

A

The nucleus is in the lower pons.
The nerve exits anteriorly and travels up the brainstem on either side of the basilar artery, in the subarchnoid space (here it is susceptible to meningitis and rarely basilar aneurysms)
It passes forward over the base of the skull towards the tip of the petrous temporal bone (here it.can be damaged by severe ear infections associated with bone infections- osteomyelitis- as well as by skull fractures and by nasopharyngeal cancer)
It enters the cavernous sinus and then goes through the superior orbital fissure to reach the eye.

45
Q

Facial nerve palsy assessment algorithms

A
46
Q

Causes of a unilateral facial nerve palsy

A

Brain stem vascular accident (associated contralateral hemiparesis)

acoustic neuroma, within the cerebello-pontine angle

trauma

Ramsay hunt syndrome - Hz affecting geniculate ganglion

bells palsy- in facial canal

pagets disease of bone

parotid trauma, surgery, tumour

mononeuropathy - sarcoid diabetes

47
Q

Assessment of speech

A

Look for signs of CVA (hemiparesis) Parkinson’s disease, scleroderma etc;
Then say
Hello, my name is ….., would you mind if I ask you some questions to check your speech and memory?
Check orientation while listening to quality of voice Can you tell me your name?
How old are you?
Do you know what day of the week it is?
And what year this is?
And where are we at the moment?
If you suspect problems with cognitive function after this, proceed with mini mental state examination including counting backwards from 20 etc
Check for dysphasia
Can you lift your left hand and place it on top of your head? (tests receptive dysphasia- important not to move your arm as patient may copy you- you need to check that spoken instruction is understood without any visual clues).
What is this? (tests for nominal dysphasia using keys or pen or newspaper etc)
Check for dysarthria
If the speech is suggestive of dysarthria, ask patient to say “Baby hippopotamus” or “British constitution” or “West Register Street, Edinburgh”.
May be appropriate to check cerebellar signs; eg ask patient to stretch out their arms looking for ataxia of upper limbs.
If pseudobulbar palsy suspected, look in mouth (for spastic tongue) plus check jaw jerk- increased in pseudobulbar palsy.
Ask about symptoms
If no abnormality demonstrated, proceed to listen to a longer segment of speech and check symptoms:
“What symptoms led to your admission to hospital?”
In general
Be prepared to modify your approach according to what you find eg if patient has Parkinson’s, be prepared to demonstrate the signs once you have listened to the voice.
Remember that the examiners will probably point you in the right direction if you are going down a blind alley. The main thing to demonstrate is that you are aware of simple ways to elicit dysphasia, dysarthria and orientation.

48
Q

Causes of dysarthria

A

difficulty with mechanism of speech

bulbar palsy= flacid

pseudobulbar palsy = spastic

cerebellar = staccato

myasthenic = weak, quiet, fatigable

49
Q

Causes of dysphasia

A

Difficulty with processing of speech

expressive (Broca’s)= knows what they want to say, but can’t say it

Receptive (Wernicke’s)= fluent, effortless, lacks meaning, can’t follow cues written/spoken.

50
Q

What is a DaT scan?

A

Dopamine transporter scan

single photon scan with contrast

normal ‘comma’ appearance of basal ganglia

loss of DA neurones in lentiform nucleus

occurs in Parkinson’s and parkinsonism

not essential tremor

51
Q

Dopamine agonists

A

parkinsons

less effective then LDopa but cause less effects, so used in younger people

used in addition to LDopa in advanced stages

older ones e.g. pergolide cause pulmonary and cardiac fibrosis —> MR

side effects

sleepiness

hallucinations

impulse control

52
Q

Overview of Parkinson’s Tx

A
53
Q

MS possible mechanisms

A

Probably autoimmune once triggered

antigens attack myelin and oligodendrocye glycoprotein

initial attack leaves inflammation of the bbb

allows B and T cells to cross

direct damage to axons and indirect damage (demyelination)

54
Q

Types of MS

A

Relapsing remitting 80%

primary progressive 10%

benigh 10%

secondary progressive (after about 10 years of relapsing remitting)

55
Q

MS main presenting symptoms

A

sensory 40%

optic neuritis 20%

cerebellar/vertigo 20%

internuclear opthalmoplegia 10%

motor (usually spastic paraparesis) 10%

56
Q

Adult onset spastic paresis differentials

A

MS

amyotrophic lateral sclerosis

transverse myelitis

spinal cord compression/trauma

intramedullary structural lesions

cervical myelopathy

spinocerebellar degeneration

B12 deficiency

Luetic disease

57
Q

Indications for DMT in MS

A

ambulant patients with RRMS

>2 relapses in 2 years

one relapse + radiological progression

OSCE - Doctor Clarke 2018 (12 decks)

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