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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

SENSORINEURAL LOSS
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 - how long can this phase last?

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) 1st line
b) 2nd line
c) for kids
d) last line

how to remember this?

A

I Love to ProD BuMs

1st = IV lorazepam
2nd = PR diazepam
kids = Buccal Medazepam
last = IV phenytoin/levetiracetam

can give 2 doses 5 mins apart

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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)

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56
Q

main complication of GCA

A

permanent vision loss

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57
Q

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

A

carotid artery - TEMPORAL, OPTHALMIC, FACIAL

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58
Q

patients of what age are typically affected by GCA?

A

> 60 years old

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59
Q

typical presentation of GCA

A

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

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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
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61
Q

general nonspecific symptoms of vasculitis (GCA)

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

investigations and findings for GCA

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

when should tx for GCA be started?

A

urgently if suspected - before temporal artery biopsy

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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)
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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

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66
Q

what is a stroke?

A

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

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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
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68
Q

general features of a stroke

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

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70
Q

presentation of an anterior cerebral artery stroke

A

LOWER LIMB contralateral hemiparesis and sensory loss

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71
Q

presentation of a middle cerebral artery stroke

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

presentation of a posterior cerebral artery stroke

A
  • contralateral homonymous hemianopia (e.g. cant see out of left of left eye or left of right eye)
  • visual agnosia (inability to process sensory info and recognise objects/people/sounds/smells)
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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
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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
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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

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76
Q

presentation of a retinal/ophthalmic artery stroke

A

amaurosis fugax

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77
Q

presentation of a basilar artery stroke

A

‘locked in’ syndrome

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78
Q

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

A

non contrast CT (rule out haemorrhage)

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79
Q

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

A

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

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80
Q

treatment for thrombotic 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

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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. HbA1c - improve diabetic control
  4. stop smoking and drinking
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82
Q

other than aspirin, what medical tx is given following a thrombotic stroke for preventative measures?

A
  1. statins (atorvastatin) - leading cause of thrombotic stroke is atherosclerosis
  2. clopidogrel 75mg daily
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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)

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84
Q

presentation and timeframe of a TIA

A

same symptoms as stroke but typically lasts <24 hours

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85
Q

what investigation can be used for a TIA?

A

diffusion weighted MRI (but may not show evidence)

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86
Q

immediate management of a TIA if patient is NOT currently taking an anticoagulant - 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)
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87
Q

management of a TIA if patient is currently taking an anticoagulant

A
  1. urgent non contrast CT head - exclude haemorrhage!
  2. once ruled out haemorrhage, specialist review within 24 hours
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88
Q

further management of a TIA
a) once reviewed by specialist, for 21 days
b) long-term secondary prevention after 21 days

A

(after initial 300mg aspirin)

a) aspirin + clopidogrel
b) clopidogrel

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89
Q

3 causes of an SAH. which is most common?

A
  1. trauma
  2. ruptured berry aneurysm (more common)
  3. AV malformation
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90
Q

what condition is strongly associated with berry anuerysms?

A

autosomal dominant polycystic kidney disease

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91
Q

RFs for an SAH

A
  1. smoking
  2. HTN
  3. family hx
  4. alcohol
  5. cocaine
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92
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
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93
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

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94
Q

2 investigation options for an SAH

A
  1. CT no contrast head (first line!)
  2. lumbar puncture
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95
Q

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

A
  1. opening pressure normal/elevated
  2. blood-tinged CSF (if early on)
  3. xanthochromia (yellowish CSF)
  4. normal glucose and protein
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96
Q

medical management for a SAH (5)

A
  1. anticoagulant reversal e.g. if on DOAC, apixaban
  2. manage BP
  3. pain management
  4. anti-emetics
  5. oral nimodipine - prevent vasospasm
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97
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
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98
Q

what is the most common electrolyte abnormality following SAH?

A

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

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99
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

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100
Q

most common bacterial cause of brain abscesses in adults

A

streptococcus family

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101
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
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102
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
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103
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
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104
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
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105
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

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106
Q

what is Huntington’s disease?

A

an autosomal dominant neurodegenerative trinucleotide repeat disorder

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107
Q

what age does Huntington’s typically present?

A

35-45

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108
Q

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

A

huntingtin protein on chromosome 4

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109
Q

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

A

50%

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110
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
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111
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

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112
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
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113
Q

how is Huntington’s diagnosed?

A

clinical diagnosis but can do MRI/CT to confirm

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114
Q

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

A

cerebral atrophy

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115
Q

initial management for Huntington’s

A

counselling for patient and family, carer support

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116
Q

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

A

18

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117
Q

management options for Huntington’s

A
  1. MDT - physio, SLT
  2. chorea - tetrabenazine/sulpiride
  3. mood - SSRIs
  4. psychosis sx/aggression - risperidone
  5. advanced directives for disease progression
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118
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
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119
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)
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120
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
121
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
122
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
123
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

124
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
125
Q

progressive bulbar palsy epidemiology

A

typically late middle-aged man with an affected relative

126
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
127
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

128
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
129
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
130
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

131
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

132
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
133
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

134
Q

investigations for cerebellar disease

A
  1. full neurological examination
  2. MRI head
135
Q

differential diagnosis for cerebellar disease

A

acoustic neuroma

136
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
137
Q

what is guillain-barre syndrome?

A

an acute inflammatory polyneuropathy

138
Q

which organism is Guillain-Barre syndrome typically caused by?

A

campylobacter jejuni

139
Q

presentation of Guillain-Barré syndrome

A
  1. 1-4 weeks post infection e.g. GI/resp
  2. symmetrical ascending muscle weakness/flaccid paralysis

other =
3. absent tendon reflexes
4. paraesthesia distally

140
Q

3 investigations for Guillain-Barre syndrome

A
  1. nerve conduction studies - lack of conduction down bum
  2. lumbar puncture
  3. serology - for antibodies against infective pathogen OR anti-ganglioside antibodies
141
Q

cross reactive antibodies react with which protein in Guillain-Barre syndrome? where?

A

glycoprotein in neuronal tissue

142
Q

lumbar puncture result in Guillain-Barre syndrome

A

isolated elevated protein, normal WCC

143
Q

1st and 2nd line tx for Guillain-Barre syndrome

A

1st line = IV immunoglobulins for 5 days

2nd line = plasmapheresis

144
Q

what is syringomyelia? what congenital malformation is it strongly associated with?

A
  • a collection of CSF within the spinal cord
  • strongly associated with congenital Chiari malformation
145
Q

presentation of syringomyelia

A
  • ‘cape-like’ (neck, shoulders and arms) distribution of loss of sensation to temperature
  • spastic weakness (normally lower limbs)
  • neuropathic pain
  • upgoing plantars
  • muscle wasting
  • reduced reflexes in upper and lower limbs
146
Q

what is the most common form of brain tumour in adults?

A

metastatic brain cancer

147
Q

which tumours most commonly spread to the brain? which is MOST common?

A
  1. lung (most common)
  2. breast
  3. skin
  4. kidney
  5. bowel
148
Q

what is Multiple System Atrophy?

A

a cause of parkinsonism - presents with parkinsonism + unilateral symptoms and severe/early onset autonomic disturbance e.g. postural hypotension, erectile dysfunction

149
Q

what is the most common complication following meningitis?

A

sensorineural hearing loss

150
Q

common reflexes and their nerve roots:
a) ankle
b) knee
c) biceps
d) triceps

A

a) S1-S2
b) L3-L4
c) C5-C6
d) C7-C8

151
Q

presentation of a posterior communicating artery aneurysm

A
  • third nerve palsy (down and out)
  • headache
152
Q

what is the most common cause of peripheral neuropathy?

A

diabetes

153
Q

risk factors for diabetic neuropathy/peripheral neuropathy (5)

A
  1. poor glucose control
  2. diabetic hx
  3. renal disease
  4. obesity
  5. smoking
154
Q

pathophysiology of diabetic neuropathy - which part of the neuron is affected?

A

axonal degeneration - primary damage in the nerve fibres (axon), nerve fibres then die back from periphery

155
Q

diabetic neuropathy - presentation of peripheral neuropathy (most common type)

A
  1. sensory loss in ‘glove and stocking’ distribution
  2. lower legs affected first
  3. pain, numbness, tingling
156
Q

diabetic neuropathy - presentation of autonomic neuropathy

A
  1. hypoglycemia unawareness (erratic sugar control)
  2. orthostatic hypotension
  3. GI - N&V, fullness, loss of appetite, GORD
  4. vision changes
  5. sweating
  6. sexual response probs
157
Q

diabetic neuropathy - presentation of proximal neuropathy

A
  1. thighs, hips, buttocks and legs
  2. severe pain
  3. weak muscles
  4. difficulty rising from sitting
  5. chest wall/abdo pain
158
Q

diabetic neuropathy - presentation of focal neuropathy

A

may be…
- foot drop
- numb/tingling hand
- hand weakness e.g. dropping things
- difficulty focussing/diplopia
- unilateral facial paralysis

159
Q

investigations for diabetic neuropathy

A
  1. neurological exam
  2. bloods
    - rule out other causes e.g. B12/thiamine deficiency
    - check glucose
  3. consider US, electromyography, nerve conduction studies
160
Q

diabetic neuropathy management
a) 1st line
b) 2nd line
c) ‘rescue therapy’ for exacerbations
d) for localised pain

A

a) amitriptyline
b) duloxetine/gabapentin/pregabalin
c) tramadol
d) topical capsaicin

161
Q

how long must a tension headache be going on for a diagnosis to be made?

A

> 15 days in one month

162
Q

exacerbations of a tension headache (6)

A
  • fatigue
  • lack of sleep
  • poor posture
  • anxiety
  • stress
  • depression
163
Q

presentation of a tension headache

A
  1. episodic
  2. bilateral
  3. “band” dull/pressing/non pulsating
  4. no N&V
164
Q

how is a tension headache diagnosed?

A

clinically

165
Q

exacerbations/causes of a migraine (CHOCOLATE)

A

Chocolate
Hydration status (dehydrated) and Hormones (menstruation
Orgasm
Caffeine/COCP
Lights
Alcohol
Trauma
Exercise

166
Q

features of a migraine

A
  1. severe, throbbing
  2. unilateral
  3. lasting up to 72h
  4. photophobia/phonophobia
167
Q

what is a hemiplegic migraine?

A

rare migraine complication, can get unilateral motor weakness alongside aura

168
Q

how is a migraine diagnosed?

A

usually clinically if sx are classical

169
Q

management of migraines:
a) for pain
b) to take at START of headache
c) antiemetic
d) prevention

A

a) ibuprofen/aspirin/paracetemol

b) oral triptans e.g. sumatriptan

c) metoclopramide

d) topiramate/propanolol

170
Q

what advice must women of child-bearing age taking topiramate for a migraine be given?

A

need to be on v good contraception - topiramate is teratogenic

171
Q

features of a cluster headache
a) when
b) where
c) type of pain
d) how long for
e) associated sx

A

a) CYCLICAL e.g. every 6 months have X amount of headaches within X space of time, happens at same time every year

b) unilateral, periorbital or temproral

c) severe, pulsating

d) short attacks

e) autonomic e.g. runny nose, runny eye, partial Horner’s (without anihidrosis)

172
Q

diagnostic criteria for cluster headaches

A

5 attacks of severe unilateral orbital/periorbital pain lasting >15 minutes and EITHER/BOTH of…
- autonomic sx
- sensation of restlessness/agitation

173
Q

management for cluster headaches
a) acute tx
b) prophylaxis

A

a) intranasal sumatriptan, 100% high flow O2

b) verapamil

174
Q

a medication headache should be present for > X days or more per month

A

15 days or more

175
Q

management for medication overuse headaches

A
  • simple analgesics and triptans withdrawn abruptly
  • opioid analgesics withdrawn slowly
176
Q

what is MS? what is it characterised by?

A

a chronic degenerative disease of the CNS, characterised by demyelination and axonal degeneration in the brain and spinal cord

177
Q

what causes MS?

A

immune-mediated inflammation

178
Q

epidemiology of MS - age and gender

A

20-40
more common in females

179
Q

McDonald Criteria for MS

A

there must be dissemination in time and space:
- DIT: appearance of new CNS lesions over time
- DIS: presence of lesions in different regions of CNS

180
Q

investigations for MS

A
  1. MRI with contrast
  2. LP CSF
181
Q

what will be found in MS on:
a) MRI with contrast
b) CSF analysis

A

a)
- MS plaques in white matter, finger-like extensions (Dawson fingers) related to demyelination
- plaques also seen in optic nerve, brainstem and spinal cord

b) oligoclonal bands

182
Q

types of MS (4)

A
  1. relapsing-remitting (MOST COMMON)
  2. secondary progressive
  3. primary progressive
  4. progressive-relapsing
183
Q

describe relapsing-remitting MS

A
  • episodic flare-ups separated by periods of remission
  • not fully recovering between flares
  • so disability increases over time
184
Q

what type of MS do 60% of patients with relapsing-remitting develop within 15 years?

A

secondary progressive - disability becomes constant over time (straight line)

185
Q

what is often the first presentation of MS?

A

optic neuritis - unilateral painful eye with impaired vision and colour blindness

186
Q

MS presentation
a) eyes
b) spinal cord
c) cerebellum
d) CN palsies
e) autonomic dysfunction
f) mental state

A

FATIGUE, HEADACHE

a) optic neuritis
internuclear ophthalmoplegia - problematic eye cannot look inwards, if the pt tries the contralateral eye will experience nystagmus

b) Lhermitte sign (shooting sensation down spine with neck flexion)
pyramidal tract: UMN weakness, spasticity, hyperreflexia, positive Babinski
DC lesion: loss of vibration, touch, numbness, paraesthesia, sensory ataxia
neuropathic pain
absent abdominal reflex

c) poor postural control, imbalance, gait dysfunction, scanning speech, nystagmus

e) diplopia, trigeminal neuralgia, facial palsy

d) bowel and bladder disorders, impaired sexual function

f) impaired conc and memory, emotional change

187
Q

MS: what is Uhtoff phenomenon?

A

worsening of symptoms following increased body temp e.g. in hot shower

188
Q

MS: acute relapse management

A

high dose oral/IV methylprednisolone for 5 days

189
Q

MS: relapse prevention management

A
  • IV natalizumab
  • ocrelizumab
  • fingolimod
  • for fatigue: amantadine
  • for spasticity: baclofen and gabapentin
190
Q

MS vs MND signs

A

MND - mix of UMN and LMN. steady progression.

MS - only UMN signs, often relapsing-remitting

191
Q

drugs exacerbating myasthenia gravis (myasthenia crisis) (6)

A
  1. penicillamine
  2. quinidine
  3. b-blockers e.g. bisoprolol
  4. lithium
  5. phenytoin
  6. abx
192
Q

which condition is Lambert-Eaton syndrome most commonly associated with?

A

small cell lung cancer

193
Q

GCS - what are the 3 components?

A

motor
verbal response
eye opening

194
Q

GCS - motor response scoring (6)

A
  1. none
  2. extends to pain
  3. abnormal flexion to pain
  4. withdraws from pain
  5. localises to pain
  6. obeys command
195
Q

GCS - verbal response scoring (5)

A
  1. none
  2. sounds
  3. words
  4. confused
  5. orientated
196
Q

GCS - eye opening scoring (4)

A
  1. none
  2. to pain
  3. to speech
  4. spontaneous
197
Q

what is Lambert-Eaton syndrome?

A

a rare autoimmune disorder characterised by muscle weakness of the limbs

198
Q

cause and pathophys of Lambert-Eaton syndrome

A

autoantibodies against presynaptic voltage gated C-channels > calcium can’t bind to vesicles that release Ach

impaired release of Ach at the NMJ

199
Q

features of Lambert-Eaton syndrome

A
  1. proximal muscle weakness that improves with muscle use (affects lower limbs first)
  2. waddling gait
  3. reduced/absent reflexes
  4. autonomic sx - dry mouth, impotence, difficulty micturating
200
Q

what sx occurs in MG but not lambert-eaton syndrome?

A

opthalmoplegia and ptosis

201
Q

investigations and results for lambert-eaton syndrome

A
  1. electrical nerve conduction - increased response to electrical stimulation with muscle use
  2. bloods - serum anti-VGCC antibodies

consider investigating for underlying malignancy (CXR)

202
Q

management of lambert-eaton syndrome

A
  1. tx underlying cancer
  2. prednisolone and/or azathioprine (immunosuppression)
  3. consider IV immunoglobulin therapy and plasma exchange
203
Q

what is encephalitis?

A

inflammation of brain

204
Q

who is most commonly affected by encephalitis?

A

young children and elderly

205
Q

non-infective cause of encephalitis

A

autoimmune

206
Q

infective causes of encephalitis

what’s most common in:
a) adults and children
b) neonates

A

mostly VIRAL

a) HSV-1
b) HSV-2

other = ticks, west nile virus, VZV, EBV, mumps, polio, rubella and measles

207
Q

RFs for encephalitis

A
  1. young/old
  2. travel to certain countries e.g. Asia
  3. autoimmune conditions
  4. unvaccinated for polio, mumps, rubella, measles
208
Q

which lobes are most commonly inflamed in encephalitis?

A

temporal, inferior frontal

209
Q

signs and symptoms of encephalitis

A
  • fever
  • headache
  • altered consciousness
  • unusual behaviour
  • vomiting
  • acute onset focal neuro sx e.g. aphasia
  • acute onset seizures
210
Q

investigations for encephalitis

A
  1. LP - PCR testing of CSF
  2. MRI (after LP)
  3. EEG
211
Q

CSF findings in encephalitis

A
  • lymphocytosis
  • elevated proteins
212
Q

when is LP contraindicated? what should be done instead if suspecting encephalitis?

A

if GCS <9, haemodynamically unstable, active seizures, postictal

CT scan

213
Q

MRI findings in encephalitis

A

medial temporal and inferior frontal lobes - petechial haemorrhages

214
Q

ddx for encephalitis

A
  1. meningitis
  2. stroke
215
Q

management of encephalitis

A
  1. IV aciclovir in ALL pts suspected (treats HSV and VZV)
  2. repeat LP to ensure successful tx
  3. FU, support and rehabilitation
216
Q

which antivirals should be given if CMV is the cause of encephalitis?

A

IV ganciclovir

217
Q

what is meniere’s disease?

A

a progressive disorder of the inner ear of unknown cause

218
Q

pathophysiology of meniere’s disease

A
  1. excessive pressure and progressive dilation of the endolymphatic system (endolymph = fluid in inner ear)
  2. distorted info travels to brain
  3. affects balance/sound
219
Q

epidemiology of Meniere’s disease

A

mostly affects middle-aged adults

220
Q

what is the classic triad of meniere’s disease?

A
  1. vertigo
  2. tinnitus
  3. sensorineural hearing loss
221
Q

what pattern of symptoms is exhibited in meniere’s disease?

A
  • episodic
  • sx all happen at same time
  • lasts for minutes/hours then resolves
222
Q

other sx (besides the classical triad) of meniere’s disease

A
  • sensation of aural fullness/pressure
  • nystagmus
223
Q

what test will be positive in meniere’s disease?

A

romberg’s test

224
Q

how is meniere’s disease diagnosed?

A

ENT assessment

225
Q

management of meniere’s disease
a) for acute attacks
b) prophylaxis

A

a) buccal/IM prochlorperazine

b) betahistine (increases blood flow to try and reduce fluid build-up)

226
Q

driving advice for patients with meniere’s disease

A
  • inform DVLA
  • cease driving until control of sx achieved
227
Q

most common type of MND

A

amyotrophic lateral sclerosis (ALS)

228
Q

presentation of MND

A

MIX OF UMN AND LMN
NO SENSORY

  • asymmetric limb weakness
  • UMN: increased tone, hyperreflexia, clonus, babinski +ve, muscle atrophy
  • LMN: flaccidity, fasciculations, babinski -ve
229
Q

what is NOT affected in MND?

A
  • external ocular muscles
  • cerebellum
230
Q

how is MND diagnosed?

A
  • by a specialist
  • clinical
  • nerve conduction studies exclude neuropathy (normal motor conduction)
  • MRI to exclude cervical cord compression and myelopathy
231
Q

management of MND

A
  1. RILUZOLE - prolongs life by ab 3 months, mainly for ALS
  2. resp care - non-invasive (BPAP) at night
  3. PEG tube
232
Q

pathophys of MG

A

autoantibodies against postsynaptic Ach receptors

233
Q

what disease is MG strongly associated with? what are some other ones?

A

THYMOMA

other - thymic hyperplasia, autoimmune e.g. RA, SLE, autoimmune thyroid

234
Q

which gender is myasthenia gravis more common in?

A

females (2:1)

235
Q

features of MG

A

key = muscle FATIGABILITY

  • weakness worse throughout day, if you ask to raised arms up they’ll slowly fall down
  • improves with rest
  • extraocular muscles > diplopia
  • ptosis
  • face, neck, limb, girdle e.g. raising from chair, dysphagia
236
Q

which muscles are commonly affected in MG? how does this present?

A
  • extraocular muscles > diplopia, ptsosis
  • prox muscles (face, neck, limb girdle) > dysphagia
237
Q

what clinical test can be used to test for MG?

A

simpson test - ask pt to look up for 1 minute, eyes will slowly drop down

238
Q

MG investigations and results (3)

A
  1. serum Ach receptors antibody test
  2. electrical nerve conduction - decreasing response with each stimulation
  3. chest CT - rule out thymoma
239
Q

what antibodies may be positive in patients with MG? (2)

A
  1. Ach receptor antibodies
  2. anti-muscle-specific tyrosine kinase antibodies
240
Q

management of MG (3) - what is 1st line?

A
  1. acetylcholinesterase inhibitors - 1st line = pyridostigmine
  2. immunosuppression - prednisolone initially then azathioprine
  3. may need thymectomy
241
Q

what is myasthenic crisis? how does it present?

A

if myasthenic patient ill/has surgery/gets pregnant/has a certain drug then all sx are exacerbated

muscle weakness, dyspnoea, sweating, urinary/faecal urgency, tachycardia > resp failure

242
Q

management of myasthenic crisis

A
  • plasmapheresis
  • IV immunoglobulins
243
Q

how to differentiate between idiopathic vs drug-induced parkinson’s

A
  • idiopathic normally asymmetrical sx
  • drug-induced normally symmetrical sx
244
Q

blood test to differentiate between a true epileptic seizure and a psychogenic non-epileptic seizure

A

serum prolactin - will be raised in true epileptic seizure

245
Q

which B vitamin is thiamine?

A

B1

246
Q

1st line tx for trigeminal neuralgia

A

carbamazepine

247
Q

symptoms of trigeminal neuralgia

A
  • severe unilateral pain
  • brief, electric-shock like pains
  • abrupt in onset and termination
  • limited to one/more divisions of trigeminal nerve
  • evoked by light touch e.g. washing, shaving, smoking, talking, brushing teeth
248
Q

what is cerebral palsy?

A

the permanent neurological problems (disorder of movement and posture) resulting from damage to the brain around the time of birth

249
Q

what are the 4 types of CP?

A
  1. spastic/pyramidal
  2. dyskinetic
  3. ataxic
  4. mixed
250
Q

spastic/pyramidal CP
a) features
b) damage to where
c) subcategories

A

a) HYPERTONIA, reduced function

b) resulting from damage to UMNs

c) monoplegia (one limb), hemiplegia (one side of body e.g. one arm, leg), diplegia (symmetrical parts of body e.g. both legs/both arms), quadriplegia (all four limbs)

251
Q

dyskinetic and ataxic CP
a) features
b) where is the damage?

A

a) dyskinetic - problems controlling muscle tone > hypertonia and hypotonia

ataxic - problems with coordinated movement

b) dyskinetic - damage to basal ganglia

ataxic - damage to cerebellum

252
Q

most common cause of major motor impairment in children

A

cerebral palsy

253
Q

aetiology of cerebral palsy…
a) antenatal causes
b) intrapartum causes
c) postnatal causes

A

non-progressive lesion of the motor pathways in the developing brain due to…

a) cerebral malformation, congenital infection e.g. rubella, toxo, CMV

b) birth asphyxia/trauma, preterm

c) intraventricular haemorrhage, meningitis, head trauma

254
Q

risk factors for CP

A
  1. birth problems/trauma
  2. maternal infection
255
Q

GENERAL features of CP (6)

A
  1. failure to meet milestones
  2. increased/decreased tone
  3. hand preference below 18m
  4. probs with coordination, speech, walking
  5. feeding/swallowing problems
  6. learning difficulties
256
Q

what signs may show in a neurological exam with someone with CP? (gait, UMN, movement, cerebellar exam)

A
  1. gait
    - hemiplegic/diplegic
    - leg extension with plantar flexion of feet/toes (swinging leg in large semi circle when moving leg in front)
  2. UMN signs - increased tone, brisk reflexes
  3. athetoid movements - involuntary writhing
  4. poor coordination on cerebellar exam
257
Q

MDT approach to CP (6)

A
  1. physio
  2. OT for ADLs
  3. SLT - may need NG/PEG
  4. dietician
  5. orthopaedic surgeons - release contractures/lengthen tendons (tenotomy)
  6. regular FU with paediatrician
258
Q

medication options for CP (4)

A
  1. muscle relaxants - baclofen, diazepam
  2. antiepileptic drugs
  3. glycopyyronium bromide (drooling)
  4. analgesia if required
259
Q

complications of cerebral palsy (6)

A
  1. learning disability
  2. epilepsy
  3. kyphoscoliosis
  4. muscle contractures
  5. hearing/visual impairment
  6. GORD
260
Q

what is parkinsons?

A

chronic progressive neurological disorder characterised by motor symptoms

261
Q

epidemiology of parkinsons

A
  • more common in males
  • peak onset 55-65
262
Q

causes of parkinsons (4)

A
  1. IDIOPATHIC (most common)
  2. vascular parkinsonism
  3. infection e.g. encephalitis, Creutzfeldt-Jacob disease
  4. toxin/drug-induced
263
Q

causes of drug-induced parkinsonism

A

any drugs that block action of dopamine!!

  1. antipsychotics e.g. haloperidol
  2. lithium
  3. anti-emetics e.g. metoclopramide, prochlorperazine
264
Q

brief pathophy of parkinsons

A
  1. neurodegenerative loss of dopamine secreting cells from substantia nigra
  2. thalamus (relays motor info) inhibited
  3. decrease in movement, eventually dementia
  4. ALSO depletion of serotonin and noradrenaline > depression
265
Q

classic triad of parkinsons

A
  1. resting tremor
  2. bradykinesia
  3. rigidity
266
Q

are the symptoms of parkinsons classically asymmetrical or symmetrical?

A

ASYMMETRICAL

267
Q

how to differentiate between drug-induced parkinsonism and parkinson’s disease

A
  • motor sx rapid onset and BILATERAL
  • rigidity and rest tremor less common
268
Q

describe how the characteristics of bradykinesia, tremor and rigidity featured in parkinsons

A

BRADYKINESIA
- poverty of movement
- short, shuffling steps
- reduced arm swinging

TREMOR
- mostly at rest
- improves with voluntary movement
- typically ‘pill-rolling’

RIGIDITY
- lead pipe (constant resistance to movement through whole range of movement)
- cogwheel (jerking resistance to movement, resistance stops and starts)

269
Q

other signs and symptoms of parkinsons (8)

A
  1. mask-like facies
  2. micrographia
  3. drooling
  4. depression, dementia, psychosis, sleep disturbance
  5. fatigue
  6. autonomic dysfunction e.g. postural hypotension
  7. stooped posture
  8. hypophonia
270
Q

how is parkinsons diagnosed?

A

clinically by a specialist (would need referral from primary care)

271
Q

NICE recommended investigation for parkinsons if clinically unclear

A

dopamine transporter scan (DaTscan) with SPECT - visualises dopamine in brain

272
Q

parkinsons medical management options and examples

A
  1. L-DOPA
    - levodopa
    - often combined so co-beneldopa or co-careldopa
  2. DOPAMINE AGONISTS
    - cabergoline
    - ropinirole
    - pramipexole
    - rotigotine
    - bromocriptine
  3. MAO-B INHIBITORS
    - selegiline
  4. COMT INHIBITORS
    - rasagiline
    - entacapone
273
Q

1st line tx of parkinsons if…

a) motor sx are affecting QOL
b) motor sx are not affecting QOL

A

a) levodopa

b) dopamine agonist, levodopa or monoamine oxidase B (MAO-B) inhibitor

274
Q

management of parkinsons if pt continues to have sx despite optimal levodopa tx

A

add dopamine agonist/MAO-B inhibitor or catechol-methyl transferase (COMT) inhibitor as an adjunct

275
Q

when are l-dopas used in parkinsons? what with usually?

what are some SEs and how are these dealt with?

A

most effective but becomes less effective over time so often reserved for when other drugs aren’t working

BUT also used in newly diagnosed pts who’s motor sx are ruining QOL

nearly always combined with carbidopa/benserazide (reduces SEs)

SEs = dyskinesia (excessive motor activity e.g. dystonia, chorea, athetosis), dry mouth, anorexia, palpitations, postural hypotension, psychosis

manage SEs with amantadine

276
Q

describe these adverse effects which may occur in pts on levodopa:

a) end-of-dose wearing off
b) on-off phenomenon

A

a) sx worsen towards end of dosage interval. results in decline of motor activity

b) large variations in motor performance - normal function during ‘on’ period and weakness/restricted mobility during ‘off’ period

277
Q

when are dopamine agonists typically used in the tx of parkinsons? what are the main SEs?

A

typically used to delay use of levodopa, then used in combo

main SEs = pulmonary fibrosis, impulse control issues, daytime sleepiness

278
Q

presentation of brown-sequard syndrome

A

CONTRALATERAL paralysis, loss of pain and temp sensation

IPSILATERAL loss of proprioception, vibration and fine touch

279
Q

what is cauda equina? at which spinal segment?

A

lumbrosacral nerve roots extending below the spinal cord are compressed (L4/L5 or L5/S1)

280
Q

most common cause of cauda equina

A

central disc prolapse at L4/L5 or L5/S1

281
Q

other causes of cauda equina (4)

A
  • tumour
  • infection (abscess, discitis)
  • trauma
  • haematoma
282
Q

presentation of cauda equina

A
  1. lower back pain
  2. bilateral sciatica
  3. reduced sensation/pins & needles in perianal area
  4. decreased anal tone
  5. urinary dysfunction
283
Q

investigation for cauda equina

A

urgent MRI

284
Q

where in the spinal cord is a lesion likely to be if…
a) all four limbs affected (quad)
b) only lower limbs affected (di)
c) resp difficulties/diaphragm

A

a) cervical level

b) thoracic level

c) above C3

284
Q

management of cauda equina

A

spinal decompression

285
Q

what is trigeminal neuralgia?

A

severe, episodic headache caused by vascular compression of the trigeminal nerve root

286
Q

which trigeminal branches are typically affected in trigeminal neuralgia?

A

maxillary and mandibular

287
Q

describe the headache and triggers in trigeminal neuralgia

A

SEVERE, EPISODIC FACIAL PAIN
- electric-shock like
- short, up to 2 mins
- unilateral
- recurrent

TRIGGERS
- touching face
- talking
- cold wind
- vibration
- cleaning teeth/brushing hair

288
Q

investigations for trigeminal neuralgia

A

clinical diagnosis

289
Q

management of trigeminal neuralgia

A

1st line = carbamazepine

290
Q

what should prompt a referral to neurology for a pt with trigeminal neuralgia?

A
  • failing to respond to tx
  • atypical features e.g. <50 years old
291
Q

red flag symptoms of trigeminal neuralgia (7)

A
  1. sensory changes
  2. deafness
  3. hx of skin or oral lesions that could spread perineurally
  4. pain only in opthalmic division (eye socket, forehead and nose) or bilaterally
  5. optic neuritis
  6. fam hx of MS
  7. age onset <40
292
Q

what causes neuroleptic malignant syndrome?

A

antipsychotics and dopaminergic drugs e.g. levodopa

293
Q

when does neuroleptic malignant syndrome happen?

A

within hours-days of starting antipsychotics

294
Q

features of neuroleptic malignant syndrome (5)

A
  1. pyrexia (fever)
  2. muscle rigidity
  3. agitated delirium
  4. confusion
  5. HTN, tachycardia, tachypnoea
295
Q

neuroleptic malignant syndrome
a) creatinine kinase
b) WCC
c) LFTs
d) U&Es
e) metabolic…

A

a) raised
b) raised
c) deranged
d) deranged
e) metabolic acidosis

296
Q

management of neuroleptic malignant syndrome (4)

A
  1. STOP ANTIPSYCHOTIC
  2. IV fluids (prevent renal failure)
  3. if severe - dantrolene
  4. can use dopamine agonist e.g. bromocriptine (reverses dopamine blockade)
297
Q

CT results for
a) SDH
b) EDH
c) SAH

A

a) crescent-shaped haematoma

b) biconvex-shaped haematoma

c) blood mixed in with CSF in basal cisterns and ventricles

PHASE 3A (18 decks)

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