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
Bell’s palsy Mx
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
Parkinson’s quadrad
tremor rigidity bradykinesia loss of postural reflexes
27
Parkinson’s Hx
ADLs handwriting (micrographia) buttons and shoelaces turning over in bed at night getting in and out of car
28
Parkinson’s Ex
poverty of facial expression 5Hz tremor cogwheel rigidity at wrist thumb finger test toe tap test function exclude Parkinson’s plus
29
Parkinsonism causes
parkinsons disease vascular parkinsonism parkinsons-plus syndromes other (antidopaminergics, Wilson’s)
30
Parkinson’s plus syndromes
progressive supernuclear palsy : vertical limitation, axial rigidity multi-system atrophy- cerebellar signs, autonomic problems corticobulbar degeneration lewy body dementia
31
Features of Parkinson’s gait
loss of arm swing (early) hesitancy shuffling hurrying (festination) retropulsion (falling backward) clock face turning
32
Motor complications in Parkinson’s
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
Parkinson’s management
34
Pathophysiology of unilateral inter nuclear opthalmoplegia
35
Causes of bilateral inter nuclear opthalmoplegia
wernickes encephalopathy stroke demyelinating disease MS
36
Ix MS
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
Treatment of acute MS
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
Oculomotor palsy features
partial ptosis eye abducted and depressed pupil dilated (loss of parasympathetic fibres)
39
Causes of oculomotor palsy
Diabetes (pupil often spared) PCA aneurysm (often painful) raised ICP (false localising)
40
Why is the pupil spared in diabetes?
parasympathetic fibres have a separate blood supply from the nerve sheath vessels
41
Features of horners syndrome
slight ptosis constricted pupil reduced sweating on forehead eye is bloodshot early loss of alpha vasoconstrictor tone
42
Causes of acquired ptosis
43
Causes of 6th nerve palsy
44
Course of 6th nerve
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
Facial nerve palsy assessment algorithms
46
Causes of a unilateral facial nerve palsy
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
Assessment of speech
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
Causes of dysarthria
difficulty with mechanism of speech bulbar palsy= flacid pseudobulbar palsy = spastic cerebellar = staccato myasthenic = weak, quiet, fatigable
49
Causes of dysphasia
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
What is a DaT scan?
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
Dopamine agonists
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
Overview of Parkinson’s Tx
53
MS possible mechanisms
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
Types of MS
Relapsing remitting 80% primary progressive 10% benigh 10% secondary progressive (after about 10 years of relapsing remitting)
55
MS main presenting symptoms
sensory 40% optic neuritis 20% cerebellar/vertigo 20% internuclear opthalmoplegia 10% motor (usually spastic paraparesis) 10%
56
Adult onset spastic paresis differentials
MS amyotrophic lateral sclerosis transverse myelitis spinal cord compression/trauma intramedullary structural lesions cervical myelopathy spinocerebellar degeneration B12 deficiency Luetic disease
57
Indications for DMT in MS
ambulant patients with RRMS \>2 relapses in 2 years one relapse + radiological progression