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PHASE 3A > NEUROLOGY > Flashcards

NEUROLOGY Flashcards

1
Q

what is Bell’s palsy?

A

unilateral LOWER motor neuron facial nerve palsy of rapid onset

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2
Q

is the forehead affected in Bell’s palsy? what does this help differentiate it from?

A

YES

stroke commonly leaves the forehead spared (UMN lesion rather than LMN)

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3
Q

what causes Bell’s palsy?

A

unknown - could be from inflammation/infection of facial nerve

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4
Q

RFs for Bell’s palsy

A
  • age 15-45
  • diabetes
  • immunocompromise
  • obese
  • HTN
  • pregnancy
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5
Q

how does Bell’s palsy present?

A
  • rapid onset (<72h)
  • unilateral facial weakness/paralysis e.g. loss of forehead and brow movement, inability to close eyes/drooping eyelids, loss of nasolabial folds and drooping lip
  • eye probs e.g. dry, painful, excessive tearing
  • numbness/tingling of cheek and mouth
  • may have ear pain on affected side

will have no other involvement of the body!!! otherwise healthy

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6
Q

investigations for Bell’s palsy. how is it diagnosed?

A

physical exam - cranial nerves, parotid gland, skin of head and neck, eyes

routine lab tests/imaging not required in primary care for new-onset Bell’s palsy

diagnosis made when no other condition is found to be causing the sx

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7
Q

management of Bell’s palsy

A
  1. IF presenting within 72h, can give prednisolone 50mg OD
  2. self-limiting, will recover within 2-3w
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8
Q

what is an acoustic neuroma?
which cells/nerve is it associated with?

A

a benign tumour of the Schwann cells arising from the vestibulocochlear nerve innervating the inner ear

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9
Q

what age patients are normally affected by an acoustic neuroma?
what are 3 risk factors?

A

40-60 years old

RFs
- ionising radiation to head/neck
- neurofibromatosis type 2 (genetic condition)
- family hx

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10
Q

what type of tumour is an acoustic neuroma?

A

a cerebellopontine angle tumour (occurs in the posterior fossa)

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11
Q

which nerve can get compressed if an acoustic neuroma grows large enough?

A

facial nerve

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12
Q

signs and symptoms of an acoustic neuroma

A

GRADUAL ONSET OF…
1. unilateral sensorineural hearing loss
2. unilateral tinnitus
3. dizziness/imbalance
4. sensation of fullness in ear

IF compresses facial nerve > facial nerve palsy (forehead not spared)

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13
Q

clinical hearing tests for an acoustic neuroma and their results

A
  1. Rinne’s - air conduction greater than bone conduction bilaterally
  2. Weber’s - sound lateralises to unaffected ear
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14
Q

1st line and gold standard investigations for an acoustic neuroma

A

1st line = audiometry with audiogram

Gold std = MRI head

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15
Q

treatment options for an acoustic neuroma (3)

A
  1. conservative + monitoring (if v small, no sx)
  2. surgery - partial or total removal
  3. radiotherapy
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16
Q

what pattern of hearing loss will an acoustic neuroma show on an audiogram?

A

sensorineural hearing loss

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17
Q

what is anterior cord syndrome?

A

an incomplete spinal cord lesion affecting the anterior 2/3rds of the spine

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18
Q

what can cause ischaemia of the anterior spinal artery, leading to anterior cord syndrome? (think iatrogenic, direct, indirect)

A
  1. iatrogenic e.g. cross-clamping of aorta during thoracic/AAA repair
  2. direct injury/trauma
    - crush injury
    - burst fracture
    - gunshot/knife injury
  3. indirect injury (occlusion/hypoperfrusion of ASA)
    - severe hypotension
    - atherothrombotic disease
    - vasculitis
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19
Q

what causes anterior cord syndrome?

A

ischaemia within the anterior spinal artery

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20
Q

pathophysiology of anterior cord syndrome…

what tracts are supplied by the ASA?
so what is characteristic of anterior cord syndrome?

A
  1. ischaemia within ASA
  2. ASA supplies blood to anterior 2/3 of spinal cord and to the bilateral SPINOTHALAMIC and CORTICOSPINAL tracts
  3. these tracts are responsible for pain and temp (spinothalamic) and voluntary movement (corticospinal)
  4. the dorsal column (fine touch, proprioception, vibration) is spared

so ACS is characterised by a loss of pain and temperature sensation, and loss of motor function

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21
Q

signs and symptoms of anterior cord syndrome

A

BELOW THE LEVEL OF THE LESION…
1. bilateral loss of pain and temp sensation
2. bilateral loss of motor movement (paralysis)
3. preservation of fine touch, proprioception and vibration

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22
Q

initial and gold std investigations for anterior cord syndrome

A

initial…
1. bloods - FBC, U&E, clotting, cultures, inflamm markers

  1. LP and CSF analysis
    (to rule out MS, infection or inflamm disease)
  2. echo
    (to rule out source of embolism e.g. IE)

GOLD STD…
= MRI

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23
Q

what will be seen on MRI in anterior cord syndrome?

A

thin, pencil-like hyperintensities of the anterior cord (= ischaemia)

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24
Q

management for anterior cord syndrome

A
  • depends on cause, may need surgery if direct damage or blood thinners e.g. apixaban if atherosclerosis
  • MDT including physio
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25
Q

possible causes of secondary epilepsy

A
  1. underlying structural lesions - trauma, neoplasms, malformations, stroke
  2. metabolic - alcohol, electrolyte disorders
  3. infection e.g. encephalitis
  4. rare genetic diseases e.g. ion channel mutations
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26
Q

a) what is a partial/focal seizure?
b) what are the two types?

A

a) a seizure occurring in only one hemisphere/lobe

b) simple partial - pt remains conscious and often remembers
complex partial - pt has impaired/loses consciousness

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27
Q

how does the ICTAL phase of a partial/focal seizure present if the lobe is…
a) temporal
b) frontal
c) parietal
d) occipital

A

a) think memory, emotion and receptive speech…
auras e.g. deja vu, auditory hallucinations, funny smell
out of body experience e.g. lip smacking, chewing, fiddling

b) think motor and thought processing…
Jacksonian march - seizure marches up/down homonculus starting in face or thumb

c) sensory disturbance e.g. tingling, numbness

d) visual phenomena e.g. spots, lines, flashes

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28
Q

what is a generalised seizure? who does it more commonly affect and what is ALWAYS impaired?

A

a seizure affecting BOTH hemispheres of the brain, no localising features
more common in children
consciousness always impaired

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29
Q

what are the 6 seizure types?

A
  1. tonic - muscles stiff and flexed, often causes fall (back)
  2. atonic - muscles relaxed and floppy, loss of tone, often causes fall (forwards)
  3. clonic - violent muscle contractions/convulsions
  4. tonic-clonic (gran mal) - tonic phase followed by convulsions
  5. myoclonic - short muscle twitches
  6. absence - brief, lost and regain conscious temporarily e.g. stopping mid-sentence, zone out then continue
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30
Q

possible preictal signs/symptoms

A
  • lasting hours/days
  • may be change in mood/behaviour
  • aura e.g. feeling in gut, flashing lights (implies focal e.g. temporal)
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31
Q

general postictal signs/symptoms

A
  • headache
  • confusion
  • myalgia/sore tongue
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32
Q

focal lobe specific postictal symptoms
a) temporal
b) frontal
c) parietal
d) occipital

A

a) emotional disturbance, dysphasia, bizarre associations, hallucinations

b) motor features e.g. pedalling legs, motor arrest, dysphasia, speech arrest, postictal Todd’s palsy (paralysis)

c) sensory disturbance e.g. tingling, numbness, pain

d) visual e.g. spots, lines, flashes

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33
Q

investigations following a seizure

A
  1. bloods (FBC, U&Es, LFTs, gluocse) - rule out infection, anaemia, electrolyte abnormalities, metabolic probs, hypoglycaemia
  2. EEG
  3. MRI
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34
Q

which antiepileptic drug is contraindicated in pregnancy?

A

sodium valproate

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35
Q

first-line tx for generalised tonic-clonic seizures in:
a) males
b) females

A

a) sodium valproate
b) lamotrigine or levetiracetam (if not child-bearing age and not likely to need tx when older, consider SV)

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36
Q

first and second line tx for focal seizures

A

first = lamotrigine or levetiracetam

second = carbamazepine, oxcarbazepine

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37
Q

first line tx for absence seizures

A

ethosuximide

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38
Q

how is status epilepticus treated?

A

IV lorazepam

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39
Q

what is an essential tremor? what is it’s heritability pattern?

A

an autosomal dominant condition affecting both upper limbs

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40
Q

intention vs essential tremor

A

intention = slower, zig-zag movements evident when intentially moving towards a target e.g. reaching for a mug

essential = bilateral fine tremor without necessarily intentional movement

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41
Q

RFs for an essential tremor (3)

A
  1. advancing age
  2. family hx
  3. exposure to toxins
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42
Q

signs and symptoms of an essential tremor
a) when does it happen
b) where
c) improves/worsens with what

A

BILATERAL FINE TREMOR
a) more prominent with voluntary movement e.g. tying shoelaces, but can occur at rest
b) bilaterally in the hands, can also affect head, jaw and vocals
c) improves with alcohol and rest
worsens with stress, fatigue, caffeine and extreme temps

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43
Q

what movement can you ask a pt with an essential tremor to do that will exaggerate their tremor?

A

worse when patient outstretches arms (called postural tremor)

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44
Q

1st line tx for an essential tremor
what else can you give?

A

1st line = propranolol

can also give antiepileptic drugs e.g. primidone

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45
Q

where does blood often collect in an EDH? from which artery?

A
  • temporal region
  • middle meningeal artery
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46
Q

what is the most common cause of an EDH? who are they common in?

A

almost always trauma, can be “low-impact” e.g. blow to head or fall

commonly seen in adolescents

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47
Q

what is the classic presentation of a patient with an EDH?

A

loses consciousness, gains it again and has a LUCID PERIOD, then a second loss of consciousness

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48
Q

signs and symptoms of an EDH

A
  • acute
  • headache
  • N&V
  • drowsy
  • rapid neuro deterioration
  • hemiparesis
  • FIXED DILATED PUPIL
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49
Q

gold std investigation for any haemorrhage

A

CT head

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50
Q

how will an EDH appear on CT?

A
  1. biconvex (lentiform/lemon) hyperdense collection around surface of brain
  2. limited by suture lines of skull
  3. may have skull fracture if trauma
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51
Q

definitive tx for an EDH

A

craniotomy and evacuation of haematoma

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52
Q

other than surgery, how may you manage an EDH?

A
  • IV fluids to maintain circulation/preserve cerebral perfusion
  • if raised ICP give IV MANNITOL (osmotic diuretics, reduces cerebral oedema)
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53
Q

what is vasculitis?

A

inflammation and necrosis of blood vessel walls with subsequent impaired blood flow to end-organs

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54
Q

what is giant cell arteritis (GCA)?

A

a type of vasculitis affecting medium and large-sized vessel arteries

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55
Q

which disease does GCA commonly overlap with?

A

polymyalgia rheumatica (50% of pts with GCA will have features of PMR)

56
Q

main complication of GCA

A

permanent vision loss

57
Q

which main artery is often affected by GCA? which branches?

A

carotid artery - TEMPORAL, OPTHALMIC, FACIAL

58
Q

patients of what age are typically affected by GCA?

A

> 60 years old

59
Q

typical presentation of GCA

A

rapid onset (< 1 month)…
- headache
- jaw claudication (pain while chewing)
- visual disturbances
- tender, palpable temporal artery

60
Q

what features of PMR may a patient with GCA present with (alongside typical headache, visual disturbance and jaw claudication)

A
  • aching
  • morning stiffness in proximal limb muscles
61
Q

general nonspecific symptoms of vasculitis (GCA)

A
  • lethargy
  • depression
  • low grade fever
  • night sweats
62
Q

investigations and findings for GCA

A
  1. bloods - inflammatory markers (ESR and CRP) raised
  2. temporal artery biopsy - may show skip lesions
63
Q

when should tx for GCA be started?

A

urgently if suspected - before temporal artery biopsy

64
Q

management for GCA

A
  1. urgent high dose glucocorticoids
    - if no visual loss then prednisolone
    - if evolving visual loss then IV methylprednisolone before pred
  2. urgent ophthalmology review
  3. other - bisphosphonates (due to long-term steroids)
65
Q

define:
a) thrombus
b) embolus

A

a) a blood clot in a blood vessel aka atherosclerosis
b) clot/fat/air which travels through the blood and lodges elsewhere

66
Q

what is a stroke?

A

sudden onset new focal neurological symptoms due to sudden interruption in the vascular supply of the brain

67
Q

what are the 2 types of stroke? what is their pathophysio? which is most common?

A
  1. ischaemic - most common, vascular occlusion/stenosis stops flow
  2. haemorrhagic - vascular rupture leading to reduction in blood flow
68
Q

general features of a stroke

A
  • motor weakness
  • dysphasia
  • swallowing probs
  • visual field defects (homonymous hemianopia)
  • balance problems
69
Q

RFs for a stroke

A

both ischaemic and haemorrhagic:
- age >55
- family hx
- HTN
- T2DM
- smoking

ischaemic:
- Afib
- history of TIA/stroke
- sickle cell disease

Haemorrhagic:
- male
- asian/black
- alcohol
- anticoagulant use

70
Q

presentation of an anterior cerebral artery stroke

A

LOWER LIMB contralateral hemiparesis and sensory loss

71
Q

presentation of a middle cerebral artery stroke

A
  • UPPER LIMB and FACE contralateral sensory loss and paralysis
  • contralateral homonymous hemianopia
  • aphasia
72
Q

presentation of a posterior cerebral artery stroke

A
  • contralateral homonymous hemianopia
  • visual agnosia (inability to process sensory info and recognise objects/people/sounds/smells)
73
Q

presentation of a Weber’s syndrome stroke (branches of posterior artery supplying the midbrain)

A
  • ipsilateral CN III palsy (eye drifting outwards)
  • contralateral weakness in upper AND lower body
74
Q

presentation of a posterior inferior cerebellar artery stroke (Wallenberg syndrome)

A
  • ipsilateral facial pain and temperature loss
  • contralateral limb/torso pain and temp loss
  • ataxia, nystagmus
75
Q

presentation of an anterior inferior cerebellar artery stroke (lateral pontine syndrome)

A

v similar to Wallenberg’s presentation but ipsilateral facial paralysis and deafness

76
Q

presentation of a retinal/ophthalmic artery stroke

A

amaurosis fugax

77
Q

presentation of a basilar artery stroke

A

‘locked in’ syndrome

78
Q

investigation for suspected stroke - what needs to be ruled out?

A

non contrast CT (rule out haemorrhage)

79
Q

what medication is given following a stroke? which type is it for?

A

(for THROMBOTIC) - ASPIRIN 300mg daily for 2 weeks

80
Q

treatment for stroke if:
a) presenting within 4.5 hours of onset
b) presenting within 6-24 hours of onset

A

a) thrombolysis with alteplase
b) thrombectomy

81
Q

how are the potential causes of a stroke investigated/managed?

A
  1. AF - check with ECG
  2. carotid artery USS - stent if stenosed >50%
  3. improve diabetic control
  4. stop smoking and drinking
82
Q

other than aspirin, what medical tx is given following a thrombotic stroke? why?

A

statins - leading cause of thrombotic stroke is atherosclerosis

83
Q

define ischaemia and infarction and use this to explain what a TIA is

A

ischaemia = lack of blood supply
infarction = tissue damage caused by ischaemia

in a TIA, there is ischaemia to the brain tissue but no infarction (unlike in a stroke)

84
Q

presentation and timeframe of a TIA

A

same symptoms as stroke but typically lasts <24 hours

85
Q

what investigation can be used for a TIA?

A

diffusion weighted MRI (but may not show evidence)

86
Q

management of a TIA - when should the pt be referred to a specialist?

A
  1. ASPIRIN 300mg
  2. referral to specialist within 24 hours (OR within 7 days if symptoms were over 7 days ago)
87
Q

3 causes of an SAH. which is most common?

A
  1. trauma
  2. ruptured berry aneurysm (more common)
  3. AV malformation
88
Q

what condition is strongly associated with berry anuerysms?

A

autosomal dominant polycystic kidney disease

89
Q

RFs for an SAH

A
  1. smoking
  2. HTN
  3. family hx
  4. alcohol
  5. cocaine
90
Q

classical features of an SAH (location, type of pain, other signs)

A
  1. occipital (back of head) thunderclap headache
  2. meningeal signs - neck stiffness, photophobia, N+V
91
Q

what 2 signs may be positive in a patient with SAH? why?

A

Kernig (Knee Extension painful) and Brudzinski (Neck flexion leads to Knee flexion) signs

because SAH sometimes presents with meningism due to bleed pressing on meninges

92
Q

2 investigation options for an SAH

A
  1. CT no contrast head (first line!)
  2. lumbar puncture
93
Q

CSF findings from a LP in a patient with SAH (4)

A
  1. opening pressure elevated
  2. blood-tinged CSF (if early on)
  3. xanthochromia (yellowish CSF)
  4. normal glucose and protein
94
Q

medical management for a SAH

A
  1. anticoagulant reversal e.g. if on DOAC, apixaban
  2. manage BP
  3. pain management
  4. anti-emetics
  5. oral nimodipine - prevent vasospasm
95
Q

surgical management options for SAH and when you would use them (2)

A
  1. endovascular coiling - for aneurysm, less invasive but more risk of rebleed
  2. microsurgical clipping - for big aneurysms in patients suitable for more invasive surgery
96
Q

what is the most common electrolyte abnormality following SAH?

A

hyponatraemia (most often due to SIADH -syndrome of inappropriate anti-diuretic hormone)

97
Q
A
98
Q

what is a brain abscess?

A

a suppurative collection of microbes (bacterial, fungal, parasitic) within a capsule, occurring in the brain parenchyma

can be single or mulitfocal

99
Q

most common bacterial cause of brain abscesses in adults

A

streptococcus family

100
Q

common causes/precipitating events of a brain abscess (4)

A
  1. extension of sepsis from middle ear (otitis) or sinuses (sinusitis)
  2. scalp trauma/surgery
  3. penetrating head injury
  4. emboli event from endocarditis
101
Q

RFs for a brain abscess (there are lots)

A
  • sinusitis, otitis media
  • dental procedure/infection
  • meningitis
  • recent head/neck/neurosurgery
  • congenital heart disease
  • endocarditis
  • diabetes
  • HIV/immunocompromise
  • IV drug use
  • birth prematurity
  • haemodialysis
102
Q

presentation of a brain abscess

A

similar to tumour!!

  1. meningism - nuchal rigidity, photophobia, headache
  2. persistent headache
  3. cranial nerve palsy e.g. oculomotor or abducens
  4. +ve Kernig/Brudzinski sign
  5. fever
  6. neuro deficit
  7. raised ICP - papilloedema, nausea, seizures
  8. in infants - increased head circumference, bulging fontanelle
103
Q

investigations for a brain abscess - what test helps distinguish it from a tumour?

A
  1. BLOODS
    - FBC: high WBC (helps rule out tumour)
    - ESR and CRP: high (same as above)
    - could do cultures
  2. first line imaging = CT scan
104
Q

management for a brain abscess:
a) what is given before surgery
b) type of surgery
c) medication options

A

a) give antibiotics
b) craniotomy - abscess cavity debrided
c) IV abx - IV vancomycin + metronidazole + ceftriaxone
if raised ICP - dexamethasone
if seizure - levetiracetam

105
Q

what is Huntington’s disease?

A

an autosomal dominant neurodegenerative trinucleotide repeat disorder

106
Q

what age does Huntington’s typically present?

A

35-45

107
Q

what protein is implicated in Huntington’s? on which chromosome?

A

huntingtin protein on chromosome 4

108
Q

if one parent has Huntington’s and the other doesn’t, what is the chance of their child having it?

A

50%

109
Q

brief pathophysiology of Huntington’s
a) which trinucleotide is involved?
b) how many repeats in a normal human vs Huntington’s?
c) what NT is there too much of?
d) what change occurs in the brain?

A
  • expanded CAG repeat coding for huntingtin protein
  • huntingtin gene normally has 10-35 CAG repeats, in HD there are >36
  • more repeats = greater risk of disease
  • clusters of mutated huntingtin proteins stick in neurons > toxic, neurodegeneration
  • too much dopamine and cerebral atrophy
110
Q

what phenomenon is displayed in Huntington’s? what does this mean?

A

= anticipation
successive generations have more repeats in the gene, leading to:
- earlier age of onset
- increased disease severity

111
Q

typical presentation of Huntington’s

A
  • 35yo with fam hx
  • non motor = irritability, impulsivity, personality changes
  • motor = chorea, twitching, loss of coordination, hyperkinesia, dystonia, saccadic eye movements
112
Q

how is Huntington’s diagnosed?

A

clinical diagnosis but can do MRI/CT to confirm

113
Q

what would be seen on MRI/CT in Huntington’s?

A

cerebral atrophy

114
Q

initial management for Huntington’s

A

counselling for patient and family, carer support

115
Q

at what age can a child of someone with Huntington’s be tested?

A

18

116
Q

management options for Huntington’s

A
  1. MDT - physio, SLT
  2. chorea - tetrabenazine
  3. mood - SSRIs
  4. psychosis sx - antipsychotics
  5. advanced directives for disease progression
117
Q

what are the most common primary tumours that metastasise to the brain? (5)

A
  1. lung
  2. renal cell carcinoma
  3. melanoma (skin)
  4. breast
  5. colorectal
118
Q

how do primary tumours metastasise to the brain? where do they usually become lodged?

A
  • haematogenous spread via blood vessels
  • often lodge at grey matter/white matter junction (where vessels decrease in size)
119
Q

presentation of brain metastases (7)

A

may be asymptomatic! (1/3)

  1. increased ICP
  2. headache - associated N&V, worse on bending/coughing, worse in morning on awakening
  3. focal weakness
  4. altered mental status
  5. seizures
  6. ataxia
  7. stroke
120
Q

investigations for brain metastases (2)

A
  1. neuro exam inc fundoscopy for papilledema
  2. imaging - CT first-line but contrast-enhanced MRI more sensitive
121
Q

initial management for a patient presenting with acute brain metastases symptoms (3)

A
  1. airway, breathing, circulation
  2. dexamethasone (manage oedema)
  3. anti-seizure medication
122
Q

management options for brain metastases if…
a) large number of mets
b) fewer mets, <3cm
c) simple, easily resectable
d) chemo-sensitive tumour

A

a) whole-brain radiation therapy
b) stereotactic radiosurgery (precisely focussed beams)
c) surgical resection
d) systemic therapy

123
Q

what is bulbar palsy? what are the 2 types?

A

result of disease affecting the lower cranial nerves (VII-XII)

  1. non-progressive - uncommon, uncertain aetiology
  2. progressive - more common, type of MN disease
124
Q

progressive bulbar palsy epidemiology

A

typically late middle-aged man with an affected relative

125
Q

causes of bulbar palsy (6)

A
  1. MOTOR NEURONE DISEASE
  2. infection e.g. diphtheria, poliomyelitis
  3. cerebrovascular event of brainstem
  4. brainstem tumour
  5. surgery for acoustic neuroma
  6. Guillain-Barre syndrome
126
Q

general signs and symptoms of a bulbar palsy (5)

A

think LMN signs
1. lips - tremulous
2. tongue - flaccid, fasciculations
3. drooling (dysphagia)
4. dysphonia - quiet, nasal, hoarse speech
5. dysarthria - poor articulation

speech slurred and then indistinct in late stages

127
Q

specific signs of bulbar palsy if caused by MND (progressive bulbar palsy)

A
  1. neuro deficit in limbs e.g. flaccid tone, reduced reflexes, weakness with fasciculations
  2. clumsiness/dropping things
128
Q

investigations for bulbar palsy (4)

A
  1. assess speech function e.g. with electromagnetic articulography (EMA)
  2. bloods - rule out other causes
  3. CT/MRI of brain
  4. electromyography
129
Q

how are the symptoms of bulbar palsy managed? (2)
what about specific managements in MN disease?

A
  1. for drooling - anticholinergics e.g. oral amitriptyline
  2. for dysphagia - PEG tube

in MN disease, consider riluzole and resp care e.g. BIPAP at night

130
Q

what is cerebellar disease? what are some examples?

A

a group of disorders affecting the cerebellum (controls muscle functions and balance)

e.g. cerebellar degeneration, stroke

131
Q

causes of cerebellar disease (7)

A
  1. neoplastic e.g. cerebellar haemangioma or paraneoplastic e.g. 2nd to lung
  2. stroke
  3. alcohol
  4. MS
  5. hypothyroidism
  6. drugs e.g. phenytoin, lead poisoning
  7. genetic disorders
132
Q

signs and symptoms of cerebellar disease and the mnemonic for remembering them

A

DANISH

D - dysdiadochokinesia, dysmetria (past-pointing), appearing Drunk
A - ataxia (loss of muscle control e.g. lack of balance, coordination, slurred, stumbling)
N - nystagmus
I - intention tremor
S - slurred staccato speech, scanning dysarthria
H - hypotonia

133
Q

investigations for cerebellar disease

A
  1. full neurological examination
  2. MRI head
134
Q

differential diagnosis for cerebellar disease

A

acoustic neuroma

135
Q

examples of managing the various underlying causes of cerebellar disease

A
  • if tumour, surgery/chemo
  • if stroke, tx e.g. with aspirin
  • if certain meds, stop them
  • if MS, optimise tx

PHASE 3A (11 decks)

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