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3a > Neuro > Flashcards

Neuro Flashcards

1
Q

1st line treatment for migraines

A

PO triptan + NSAIDS

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2
Q

2nd line treatment for migraines

A

non-oral metoclopramide or prochlorperazine

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3
Q

treatment for migraines for patients ages 12-17yrs

A

nasal triptan

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4
Q

prophylaxis for migraines

A

propranolol or topiramate (teratogenic)

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5
Q

Treatment for tension headaches

A

ibuprofen or aspirin or paracetamol

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6
Q

prophylaxis for tension headaches

A

up to 10 sessions of acupuncture over 5-8w.

amitriptyline commonly used but not recommended by NICE

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7
Q

features of cluster headache (6)

A
  1. pain once/twice a day, each ep lasting 15 mins - 2 hours. Typically last 4-12 weeks
  2. intense sharp, stabbing pain around one eye
  3. restless and agitated during attack
  4. redness, lacrimation, lid swelling
  5. nasal stuffiness
  6. miosis and ptosis in a minority
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8
Q

acute treatment for cluster headache (2)

A
  1. 100% O2 therapy

1. SC triptan

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9
Q

prophylaxis for cluster headache

A

verapamil (CCB)

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10
Q

features of temporal arteritis aka giant cell arteritis (8)

A
  1. > 60yrs
  2. rapid onset (<1 month)
  3. headache
  4. jaw claudication
  5. visual disturbances
  6. tender, palpable temporal artery
  7. polymyalgia rheumatica: aching, morning stiffness in proximal limbs
  8. lethargy, depression, low grade fever, night sweats, anorexia
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11
Q

investigations for temporal arteritis

A
  1. GOLD STANDARD: temporal artery biopsy - skip lesions
  2. ESR > 50mm/hr
  3. elevated CRP
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12
Q

Treatment for temporal arteritis

A
  1. high dose prednisolone
  2. consider PPI (omeprazole) as ^ assc w/ GI toxicity
  3. urgent ophthalmology review
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13
Q

trigeminal neuralgia features (4)

A
  1. unilateral brief electric shock-like pains
  2. abrupt in onset + termination
  3. evoked by light touch: washing, shaving, smoking, talking, brushing teeth
  4. nasolabial fold or chin are esp susceptible
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14
Q

red flags suggesting a serious underlying cause of trigeminal neuralgia (7)

A
  1. sensory changes
  2. deafness/ear problems
  3. skin or oral lesions
  4. pain only in ophthalmic division (eye socket, forehead, nose) or bilaterally
  5. optic neuritis
  6. FH of MS
  7. Ages of onset <40 yrs
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15
Q

pharmaceutical management of trigeminal neuralgia

A
  • 1st line: carbamazepine

- 2nd line: phenytoin, gabapentin (analgesics)

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16
Q

surgical management of trigeminal neuralgia

A
  • microvascular decompression

- stereotactic radiotherapy

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17
Q

what is microvascular decompression

A

relieves pressure on nerve by blood vessels touching the nerve or wrapped around it

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18
Q

what is stereotactic radiotherapy

A

concentrated beam of radiotherapy to damage the nerve when it enters the brainstem

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19
Q

what are the 4 types of MND

A
  1. Amyotrophic lateral sclerosis (50%)
  2. Progressive bulbar palsy
  3. Progressive muscular atrophy
  4. Primary lateral sclerosis ``
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20
Q

MND: features of amyotrophic lateral sclerosis

A
  1. LMN signs in arms
    2, UMN signs in legs
  2. in familial cases: gene responsible is on chromosome 21 + codes for superoxide dismutase
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21
Q

MND: features of progressive bulbar palsy

A
  1. loss of function of brainstem motor nuclei: palsy of tongue, muscles of chewing/swallowing + facial muscles
  2. carries worst prognosis
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22
Q

MND: features of progressive muscular atrophy

A
  1. LMN signs only
  2. affects distal muscles before proximal
  3. carries best prognosis
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23
Q

MND: features of primary lateral sclerosis

A

UMN signs only

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24
Q

what disease is eye sparing?

A

MND

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25
Q

treatment for MND

A
  • Riluzole

- non invasive ventilation at night

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26
Q

MND: how does Riluzole work

A
  • prevents stimulation of glutamate receptors
  • Na channel blocker
  • used mainly in amyotrophic lateral sclerosis
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27
Q

MND diagnostic tips

A
  1. no sensory loss (MS/myelopathy)
  2. eye sparing
  3. no sphincter disturbances (MS)
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28
Q

MS inx

A
  • MRI
  • CSF
  • visual evoked potentials
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29
Q

MRI scan of pt w/ MS (3)

A
  1. high signal T2 lesions
  2. periventricular plaques
  3. Dawson fingers: hyperintense lesions perpendicular to corpus callosum
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30
Q

CSF in pt w/ MS (2)

A
  1. oligoclonal bands (and not in serum)

2. increased intrathecal synthesis of IgG

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31
Q

Visual evoked potentials in pt w/ MS

A

delayed but well preserved waveform

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32
Q

what is the aim of treatment for MS

A

reducing the freq + duration of relapses. There is no cure

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33
Q

treatment for an acute relapse of MS

A

high dose steroids (PO/IV methylprednisolone) for 5 days

to shorten length of an acute relapse

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34
Q

what disease modifying drugs would you use for MS

A

beta interferon

glatiramer acetate
natalizumab
fingolimod

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35
Q

what criteria must be met before beta interferons can be used? (2)

A
  1. relapsing-remitting disease + 2 relapses in past 2 yrs + able to walk 100m unaided
  2. secondary progressive disease + 2 relapses in past 2 yrs + able to walk 10m
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36
Q

visual features of MS (4)

A
  1. optic neuritis (common)
  2. optic atrophy
  3. Uhtoff’s phenomenon - worsening of vision following rise in body temp
  4. internuclear ophthalmoplegia
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37
Q

sensory features of MS (4)

A
  1. pins/needles
  2. numbness
  3. trigeminal neuralgia
  4. Lhermitte’s syndrome - paraesthesia in limbs on neck flexion
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38
Q

motor feature of MS

A

spastic weakness: most commonly seen in legs

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39
Q

cerebellar features in MS (2)

A
  1. ataxia - usually in acute

2. tremor

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40
Q

other features in MS (3)

A
  1. urinary incontinence
  2. sexual dysfunction
  3. intellectual deterioration
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41
Q

pathophysiology of myasthenia gravis

A

Autoimmune disorder

  1. IgG destroy ACh receptors on post synaptic membrane
  2. fewer action potentials fire
  3. muscle weakness + fatigue
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42
Q

features of myasthenia gravis (5)

A
  1. MUSCLE FATIGUE - improves over periods of rest
  2. extraocular muscle weakness: diplopia
  3. proximal muscle weakness: face, neck, limb girdle
  4. ptosis - droopy eyelid
  5. dysphagia
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43
Q

myasthenia gravis is associated with…

A
  1. thymomas (in 15%)
  2. autoimmune disorders: pernicious anaemia, autoimmune thyroid disorders, rheumatoid, SLE
  3. thymic hyperplasia (in 50-70%)
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44
Q

inx of MG

A
  1. serial pulmonary function tests (FVC + NIF)
  2. autoantibodies: serum AChR and anti-muscle-specific tyrosine kinase antibodies
  3. single fibre electromyography: high sensitivity (92-100%)
  4. CT thorax to exclude thymoma

(Tensilon test: IV edrophonium reduces muscle weakness temporarily - not commonly used anymore due to the risk of cardiac arrhythmia)

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45
Q

Management of MG

A

1st line: Pyridostigmine (anticholinesterase)

adjunct: prednisolone initially. Azathioprine, ciclosporin mycophenolate mofetil
adjunct: thymectomy

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46
Q

hallmark feature of MG

A

exacerbating factor: exertion resulting in fatigability

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47
Q

signs + symptoms of myasthenic crisis

A
  1. RESP FAILURE
  2. severe muscle weakness
  3. increased HR + BP
  4. aspiration/no swallow or speak
  5. bladder/bowel incontinence
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48
Q

what is myasthenic crisis

A

a life threatening emergency

breathing muscles get so weak that you can’t get air in and out of your lungs.

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49
Q

1st line treatment for a myasthenic crisis

A 
1. intubation + mechanical ventilation 
if FVC <15 (normal ≥60 mL/kg) 
negative insp force (NIF) <20 (normal ≥70 cm H2O)
2. plasma exchange or IVIG
3. Supportive care 
- DVT prophylaxis
- ulcer prophylaxis
- nutrition and hydration
- avoidance of infections + drugs that may worsen it
adjunct: prednisolone
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50
Q

2nd line treatment for a myasthenic crisis

A
  1. eculizumab or rituximab

2. supportive care

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51
Q

what are the subtypes of an ischaemic stroke?

A
  1. thrombotic - thrombosis from large vessels e.g. carotid

2. embolic - blood clot but fat, air or clumps of bacteria may act as an embolus. AF is an important cause

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52
Q

what are the subtypes of haemorrhagic stroke?

A
  1. intracerebral haemorrhage - bleeding within the brain

2. Subarachnoid haemorrhage - bleeding on the surface of the brain

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53
Q

what is the oxford/bamford stroke classification?

A

classifies strokes based on the initial symptoms

  1. total anterior circulation stroke
  2. partial anterior circulation stroke
  3. lacunar syndrome
  4. posterior circulation syndrome
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54
Q

criteria of a total anterior circulation stroke

A

involves middle and anterior cerebral arteries

  1. unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
  2. homonymous hemianopia
  3. higher cognitive dysfunction e.g. dysphasia, visuospatial disorder
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55
Q

criteria of a partial anterior circulation stroke

A

involves smaller arteries of anterior circulation e.g. upper or lower division of middle cerebral artery
2 of:
1. unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
2. homonymous hemianopia
3. higher cognitive dysfunction e.g. dysphasia, visuospatial disorder

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56
Q

criteria of lacunar syndrome stroke

A

involves perforating arteries around the internal capsule, thalamus and basal ganglia
1 of:
1. unilateral weakness (and/or sensory deficit) of face and arm, arm and leg or all three.
2. pure sensory stroke.
3. ataxic hemiparesis

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57
Q

criteria of posterior circulation infarcts

A 
involves vertebrobasilar arteries
1 of:
1. cerebellar or brainstem syndromes
2. loss of consciousness
3. isolated homonymous hemianopia
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58
Q

investigations for suspected ischaemic stroke

A
  1. non contrast CT head - exclude intracranial haemorrhage
  2. serum glucose - exclude hypo + hyperglycaemia
  3. FBC, U&E’s, creatinine
  4. cardiac enzymes
  5. ECG
  6. Prothrombin time
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59
Q

management for confirmed ischaemic stroke presenting within 4.5 hrs

A
  1. supportive care
  2. IV alteplase immediately (thrombolysis) - only if intracranial haemorrhage excluded
  3. thrombectomy
  4. aspirin/clopidogrel - antiplatelet
  5. high intensity atorvastatin 48hrs after
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60
Q

management for confirmed ischaemic stroke presenting after4.5 hrs OR thrombolysis CI’d

A
  1. supportive + monitoring
  2. aspirin/clopidogrel (antiplatelet) immediately
  3. high intensity atorvastatin
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61
Q

treatment for a subarachnoid haemorrhage

A
  1. coil by interventional neuroradiologists
  2. minority: craniotomy + clipping by neurosurgeon
  3. strict bed rest + BP control
  4. Nimodipine (CCB) for 21 days to prevent cerebral artery spasm
  5. external ventricular drain (CSF diverted into bag) to temporarily treat hydrocephalus
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62
Q

confirmation of SAH

A
  1. CT head - blood in sulci

2. LP - wait at least 12 hrs for xanthochromia (result of RBC breakdown)

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63
Q

CSF findings of SAH

A
  • xanthochromia

- normal or raised opening pressure

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64
Q

what does xanthochromia in CSF show

A

SAH

helps distinguish true SAH from a ‘traumatic tap’ (blood introduced by the LP procedure

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65
Q

CT scan of subdural haemorrhage

A
  1. crescentic collection
  2. hyperdense if acute
  3. hypodense (dark) if chronic
  4. midline shift or herniation
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66
Q

what is an extradural haemorrhage

A
  • medical emergency from trauma
  • fracture of temporal bone
  • tear of middle meningeal artery
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67
Q

features of extradural haemorrhage

A
  • brief period of unconsciousness
  • then lucid interval of improvement
  • condition rapidly decreases as ICP increases
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68
Q

CT scan of extradural

A
  • egg shaped

- biconvex hypodense haematoma

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69
Q

presentation of chronic subdural haematoma

A
  • progressive hx of either confusion, reduced consciousness or neurological deficit
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70
Q

inx for TIA

A
  1. blood glucose
  2. FBC + platelet count
  3. PTT, INR, partial thromboplastin time
  4. fasting lipid profile
  5. U&E’s
  6. ECG - AF?
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71
Q

Treatment for TIA

A
  1. clopidogrel immediately (2nd line: aspirin)

2. high intensity atorvastatin

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72
Q

treatment of Parkinson’s (if motor symptoms are affecting QoL)

A

1st line: Levodopa

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73
Q

treatment of Parkinson’s (if motor symptoms are not affecting QoL)

A
  • dopamine agonist (non-ergot derived)
  • levodopa
  • MAO‑B inhibitor
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74
Q

Parkinson’s: what do you do if a pt continues to have symptoms despite optimal levodopa treatment or has developed dyskinesia

A

add
dopamine agonist or
MAO‑B inhibitor or
catechol‑O‑methyl transferase (COMT) inhibitor

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75
Q

cause of Wernicke’s encephalopathy?

A

alcoholism –> thiamine (vit B1) deficiency

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76
Q

triad features of Wernicke’s encephalopathy

A

1) Nystagmus
/ophthalmoplegia
2) Confusion
3) Ataxia

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77
Q

inx of Wernicke’s encephalopathy

A

serum thiamine

or decreased red cell transketolase

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78
Q

how is Korsakoff syndrome different to Wernicke’s encephalopathy

A

it is untreated WE with added

memory impairment + confabulation

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79
Q

features of Huntington’s disease (4)

A

1) chorea
2) personality changes + intellectual impairment
3) dystonia
4) saccadic eye movements

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80
Q

management of Huntington’s disease

A

no cure

1) counselling
2) physio/occupational therapy

3) antidepressants - citalopram (SSRI)
4) behavioural problems where anxiety/insomnia is prominent - carbamazepine
5) antipsychotics

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81
Q

inx for Huntington’s disease

A

1) >36 CAG repeats

2) evident caudate or striatal atrophy on MRI/CT

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82
Q

what is a coma

A
  • a state of unarousable unresponsiveness

- GCS score less than 8

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83
Q

what may a coma progress to

A

persistent vegetative state

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84
Q

coma: altered consciousness is produced by what 3 types of processes

A
  1. diffuse brain dysfunction: due to severe metabolic, toxic or neuro disorders
  2. brainstem lesions
  3. pressure effect: compresses brainstem
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85
Q

coma: give some examples of diffuse brain dysfunction

A
  • drug overdose
  • alcohol excess
  • CO poisoning
  • anaesthetic gases
  • hypo/hyper gly/calc/natr aemia
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86
Q

coma: give some examples of brainstem lesions

A
  • haemorrhage/infarction
  • tumour
  • demyelination e.g. MS
  • Wernicke-Korsakoff syndrome
  • trauma
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87
Q

coma: give some examples of pressure effect

A
  • tumour
  • haemorrhage/infarction
  • abscess
  • encephalitis
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88
Q

coma inx

A
  • serum + urine for drug analysis
  • U&E, LFTs, Ca
  • blood glucose
  • ABG
  • TFTs, cortisol
  • blood cultures
  • CT head
  • CSF if mass lesion excluded
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89
Q

coma management

A

treat cause

  • opiate poisoning? Naloxone
  • benzo complication? Flumazenil
  • alcoholic or malnourished? thiamine
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90
Q

definition of convulsive status epilepticus

A

convulsive seizure that continues for longer than 5 minutes

or convulsive seizures that occur one after the other with no recovery between

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91
Q

definition of non convulsive status epilepticus aka absence status

A

a change in mental status or behaviour from baseline

associated w/ continuous seizure activity on EEG

which is also seen to be a change from baseline

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92
Q

RFs for status epilepticus

A
  • poor antiepileptic treatment adherence
  • alcohol abuse
  • stroke
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93
Q

1st line inx for status epilepticus

A
  1. blood glucose
  2. ABG
  3. urea + creatinine
  4. LFTs, FBCs
  5. Na, Ca, Mg
  6. anticonvulsant drug levels
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94
Q

inx to consider for status epilepticus

A
  1. CXR - aspiration?
  2. CT head - for ppl w/ no previous epilepsy hx
  3. LP - CNS infection or inflammation?
  4. toxicology screen - substance misuse
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95
Q

convulsive status epilepticus in hospital treatment

A

ABC

1st line: IV Lorazepam 4mg initially. repeat after 10-20 min if required

2nd line (20-40min): phenytoin/sodium valporate/levetiracetam

3rd line: general anaesthesia - propofol

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96
Q

convulsive status epilepticus in community treatment

A

1st line: buccal midazolam. repeat once 10 min later

2nd line: rectal diazepam . Repeat once 15 min later

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97
Q

inx for first seizure

A
  1. EEG
  2. blood glucose
  3. FBC, U&E’s
  4. toxicology screen
  5. MRI
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98
Q

management for generalised tonic clonic seizure?

A

1st line: sodium valproate

2nd line: lamotrigine, carbamazepine

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99
Q

management for acute seizure?

A

IV or rectal lorazepam

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100
Q

SE’s of sodium valporate

A
  1. teratogenic
  2. weight gain
  3. ataxia, tremor
  4. hepatitis, pancreatitis
  5. thrombocytopenia
  6. P450 enzyme inhibitor
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101
Q

mechanism of action of sodium valporate

A

increases GABA activity

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102
Q

mechanism of lamotrigine

A

sodium channel blocker

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103
Q

SE of lamotrigine

A

Stevens-Johnson syndrome

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104
Q

types of generalised seizures

A
  1. tonic-clonic (grand mal)
  2. tonic
  3. clonic
  4. typical absence (petit mal)
  5. atonic
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105
Q

localising features of focal seizures

Temporal lobe (HEAD)

A
  • Hallucinations
  • Epigastric rising/ emotional
  • Automatisms (lip smacking/plucking)
  • Deja vu /dysphasia post-ictal
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106
Q

localising features of focal seizures

frontal lobe (motor)

A
  • head/leg movements
  • posturing
  • post-ictal weakness
  • Jacksonian march
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107
Q

localising features of focal seizures

parietal lobe (sensory)

A

parathesia

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108
Q

localising features of focal seizures

occipital lobe (visual)

A

floaters/flashes

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109
Q

management of focal seziures

A

1st line: carbamazepine or lamotrigine

2nd line: levetiracetam, oxcarbazepine or sodium valproate

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110
Q

mechanism of action for carbamazepine

A

binds to sodium channels increasing their refractory period

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111
Q

SE’s of carbamazepine

A
  1. P450 enzyme inducer
  2. dizziness, ataxia, drowsiness
  3. leucopenia, agranulocytosis
  4. syndrome of inappropriate ADH secretion
  5. visual disturbances (esp diplopia)
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112
Q

what are the predominant causative pathogens in meningitis in adults

A
  1. Streptococcus pneumoniae
  2. Neisseria meningitidis

3, Haemophilus influenzae type b (Hib)

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113
Q

symptoms of meningitis

A
  • headache
  • neck stiffness
  • photophobia
  • non blanching petechial rash –> meningococcal septicaemia ?
  • Kernig’s sign - extends knee when hip flexed at right angle –> pain
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114
Q

inx for meningitis

A

TREAT FIRST

  • blood culture
  • serum pneumococcal + meningococcal PCR
  • blood glucose
  • FBC, U&Es, LFTs
  • coagulation screen
  • CSF
115
Q

management for meningitis

Initial empirical therapy aged < 3 months
aged > 50 years

A

IV cefotaxime + amoxicillin

116
Q

management for meningitis

Initial empirical therapy aged 3 months - 50 years

A

IV cefotaxime

117
Q

management for meningitis

Meningococcal meningitis

A

IV benzylpenicillin or cefotaxime

118
Q

management for meningitis

Pneuomococcal meningitis

A

IV cefotaxime

119
Q

management for meningitis

caused by Haemophilus influenzae

A

IV cefotaxime

120
Q

management for meningitis

caused by Listeria

A

IV amoxicillin + gentamicin

121
Q

management for meningitis

close contact prophylaxis

A

PO ciprofloxacin or rifampicin

122
Q

management of meningitis

abx + ___?

A

IV dexamethasone to reduce risk of neurological sequelae

123
Q

management of meningitis

in the community

A

IM or IV benzylpenicillin/ cefotazime/ ceftriaxone

124
Q

features of Guillain-Barre syndrome

A
  1. ASCENDING MUSCLE WEAKNESS
  2. reduced reflexes
  3. mild sensory symptoms
  4. back/leg pain initially

other features

  • gastroenteritis
  • resp muscle weakness
  • CN involvement e.g. diplopia
  • autonomic involvement e.g. urinary retention, diarrhoea
  • papilledema
125
Q

Inx for GBS

A
  • LP: high protein w/ normal WBC

- nerve conduction studies

126
Q

cause of GBS

A

infection (Camylobacter Jejuni) triggers immune-mediated demyelination of peripheral nervous system

an acute polyneuropathy

127
Q

management for GBS

A

immediate

  • IVIG for 5d
  • ventilation if resp muscles involved
128
Q

what is a radiculopathy

A

compression of a spinal nerve root e.g. sciatica, spinal stenosis

129
Q

sciatica

A

s1 nerve root compression

130
Q

what is spinal stenosis

A

spinal column narrows + compresses spinal cord

131
Q

inx of spinal stenosis

A

MRI - shows compression of spinal canal

132
Q

features of spinal stenosis

A
  1. back + leg pain

2. lower extremity paraesthesia brought on by ambulation + relieved by sitting

133
Q

management of spinal stenosis

A

NSAIDs + physiotherapy

epidural corticosteroid injections may provoke symptomatic relief

134
Q

what is shingles

A

Herpes zoster, caused by reactivation of Varicella-zoster virus

135
Q

features of shingles rash

A
  • erythematous maculopapular rash
  • followed by clear vesicles
  • eruption occurs in segments
  • does not cross midline
  • vesicles eventually pustulate + form crusts
136
Q

RF’s of shingles

A
  • > 50 yrs
  • HIV positive
  • chronic corticosteroid use
  • chemo
  • malignancies
137
Q

features of shingles

A
  • localised pain in a dermatome: stinging, itching or tingling preceding rash by days to weeks
  • erythematous maculopapular rash
  • corneal ulceration: pain in eye + reduced vision if trigeminal nerve
138
Q

inx of shingles

A
  • clinical diagnosis
  • PCR: +ve for varicella DNA
  • HIV test
139
Q

Management of shingles

A

1st line: PO antiviral therapy - famciclovir. Start 48-72hrs of rash onset for 7 days

plus: paracetamol + calamine lotion

140
Q

complication of shingles

A

Postherpetic pain

  • Pain > 3 months after shingles rash has healed
  • Increased sensitivity to touch and temperature changes
  • Burning, itching or numbness
141
Q

what is Narcolepsy

A
  • chronic sleep boundary disorders
  • affects the control of sleep + wakefulness
  • rapid eye movement (REM) sleep intrusion
142
Q

symptoms of narcolepsy (4)

A
  1. excessive daytime sleepiness
  2. cataplexy: generalised muscle weakness –> collapse
  3. hypnagogic/ hypnopompic hallucinations
  4. sleep paralysis: feeling of being awake but not being able to move.
143
Q

RF’s for narcolepsy

A
  1. DQ0602

2. prader-willi syndrome

144
Q

types of narcolepsy

A

both types:

  • daily periods of irrepressible need to sleep or daytime lapses for >3months
  • MSLT: sleep latency <8min + >2 REM

Type 1: w/ hypocretin deficiency
- CSF [hypocretin-1] <110 picograms/mL
or 1/3 of normal patient

Type 2

  • absent cataplexy
  • > 110 or >1/3
  • not better explained
145
Q

Inx of narcolepsy

A
  1. actigraphy + sleep diary
  2. overnight polysomnography
  3. multiple sleep latency test (MSLT)
  4. HLA typing
146
Q

Management of narcolepsy

A

1st line: sleep hygiene + lifestyle changes

+ Modafinil (CNS stimulant)

147
Q

what is cataplexy

A
  • Loss of muscle tone
  • typically lasts 0.5 to 2 minutes, but can last up to 30 minutes.
  • Consciousness is usually intact.
  • Frequently triggered by emotional stimuli such as laughter, excitement, or anger.
148
Q

features of normal pressure hydrocephalus

A
  1. hydrocephalus clinical features
    • L-dopa unresponsive gait apraxia
    • urinary incontinence
    • cognitive impairment
  2. no elevated CSF pressure
149
Q

inx of normal pressure hydrocephalus

A
  1. CT head (without contrast)/MRI head
    - enlarged ventricles
  2. Levodopa challenge
  3. LP: normal pressure CSF
150
Q

Treatment for normal pressure hydrocephalus

A
  1. ventriculoperitoneal shunting or endoscopic 3rd ventriculostomy

not suitable for surgery? repeated large volume CSF taps

  1. control CV RFs
151
Q

what is neurofibromatosis type 1 (NF1)

A

an autosomal dominant disease

tumours grow along nerves

café au lait spots

152
Q

features of neurofibromatosis type 1

A
  • café au lait spots
  • pain anywhere
  • gross motor delay, general incoordination
  • visual compromise
  • ASD
153
Q

RFs for neurofibromatosis type 1

A
  • parent with NF1

- severe crush trauma

154
Q

Inx for neurofibromatosis type 1

A

MRI/CT and PET

  • optic pathway gliomas
  • brain tumours
  • hydrocephalus

Biopsy
- histological features of neurofibroma or malignant peripheral nerve sheath tumours

Genetic testing
- NF1 mutation

155
Q

management for neurofibromatosis type 1

A

surgical removal

156
Q

what is encephalitis

A
  • inflammation of the brain parenchyma

- assc w/ neurological dysfunction

157
Q

symptoms of encephalitis

A
  • fever
  • rash (presentation depends on viral infection)
  • altered mental state
  • focal neurological deficit: aphasia, hemianopia, hemiparesis, ataxia

preceding flu like symptoms then altered GCS

158
Q

RFs for encephalitis

A
  • <1 or >65yrs
  • immunodeficiency
  • post-infection
  • blood/body fluid exposure
  • organ transplantation
  • animal or insect bites
  • location
159
Q

inx for encephalitis

A
  • CSF: elevated lymphocytes + protein. normal glucose
  • FBC, LFTs, U&E’s,
  • blood + sputum culture
  • peripheral blood smear
  • CXR, CT/MRI brain
160
Q

causes of encephalitis

A

generally viral cause:

  • HERPES SIMPLEX VIRUS
  • varicella zoster virus
  • hiv
  • parvoviruses
  • mumps
  • measles
161
Q

management of encephalitis

A

initial
1st line: high dose IV acyclovir for 10-21 days

supportive care

  • endotracheal intubation
  • mechanical ventilation
162
Q

causes of spinal cord compression

A
  • trauma
  • disc disease
  • malignancy
  • osteophytes
  • disc prolapse
163
Q

spinal cord compression acute symptoms commonly associated with ____ + _____

A
  • trauma

- disc herniation

164
Q

spinal cord compression chronic symptoms commonly associated with ____ + _____ + _____

A
  • osteoporosis
  • osteomyelitis
  • malignancy
165
Q

clinical features of spinal cord compression

A
  • back pain
  • paraesthesia
  • weakness
  • bladder/bowel dysfunction
  • hyper- reflexia
  • loss of tone below level of suspected injury
166
Q

inx of spinal cord compression

A
  • MRI spine
167
Q

management of spinal cord compression

acute traumatic spinal cord injury

A
  • immobilisation
  • decompressive/stabilisation surgery
  • high dose IV methylprednisolone
  • enoxaparin + compression stockings
  • maintenance of vol + BP: volume resuscitation +/- dopamine
  • omeprazole
168
Q

management of spinal cord compression

cauda equina syndrome

A
  • decompressive laminectomy
169
Q

management of spinal cord compression

malignant spinal cord compression

A
  • methylprednisolone
  • surgery
  • radiation therapy
170
Q

management of spinal cord compression

epidural abscess

A

most common pathogen in epidural abscess: S. aureus

  • IV vancomycin + metronidazole + cefotaxime
  • surgery
171
Q

cauda equina signs

A
  • bilateral sciatica
  • saddle anaesthesia
  • bladder/bowel dysfunction
  • erectile dysfunction
172
Q

what is cauda equina syndrome

A

spinal compression at or distal to L1 nerve root

173
Q

signs of raised ICP

A
  1. headache- worse in morning
  2. papilledema
  3. vomiting
  4. pupillary changes
174
Q

inx of raised ICP

A
  • head CT
  • ophthalmology review
  • don’t LP - risk of coning!
175
Q

treatment of raised ICP

A
  • IV mannitol
  • shunt/decompression
  • depends on cause
176
Q

Dermatomes

C2

A

posterior 1/2 of skull

177
Q

Dermatomes

C3

A

high turtle neck shirt

178
Q

Dermatomes

C4

A

low collar shirt

179
Q

Dermatomes

C5

A

shoulder tip

180
Q

Dermatomes

C6

A

thumb + index finger

181
Q

Dermatomes

C7

A

middle finger + palm of hand

182
Q

Dermatomes

C8

A

ring + little finger

183
Q

Dermatomes

T3

A

Axilla

184
Q

Dermatomes

T4

A

nipples

T4 at the teat pore

185
Q

Dermatomes

T5

A

inframammary fold

186
Q

Dermatomes

T6

A

xiphoid process

187
Q

Dermatomes

T10

A

belly butTEN

188
Q

Dermatomes

T12

A

pubis

189
Q

Dermatomes

L1

A

1nguinal Ligament

190
Q

Dermatomes

L4

A

knee caps

down on all fours

191
Q

Dermatomes

L5

A

big toe + dorsum of foot

L5 largest toe

192
Q

Dermatomes

S1

A

smallest toe + lateral foot

193
Q

Dermatomes

S2, 3

A

genitalia

194
Q

Dermatomes

S4, 5

A

anus

195
Q

what is a brain abscess

A
  • pus filled swelling in the brain

- usually when microbes enter after infection or severe head injury

196
Q

clinical features of a brain abscess

A
  • increased ICP
  • fever
  • headache
  • focal neurology
  • CN palsy
  • +ve Kernig or Brudzinski sign
  • <30 yrs
  • Infants: blugin fontanelle + increased head circumference
197
Q

Inx for a brain abscess

A
  1. MRI/(CT): ring enhancing lesion
  2. increased WBC + CRP
  3. increased serum erythrocyte sedimentation rate (ESR)
198
Q

management for a presumed brain abscess

A
  1. IV vancomycin, metronidazole + ceftriaxone
  2. Phenytoin (anticonvulsant)

Adjunct: IV dexamethasone initially, then PO
urgent surgical decompression

199
Q

Myotomes

diagphragm

A

C3,4,5 keeps the diaphragm alive

200
Q

Myotomes

biceps

A

C5

201
Q

Myotomes

deltoids + bend wrist back (extensor carpii)

A

C6

202
Q

Myotomes

triceps

A

C7

203
Q

Myotomes

bends fingers (palmar interossei)

A

C8

8 is a bendy number

204
Q

Myotomes

spreads fingers (dorsal interossei)

A

T1

205
Q

Myotomes

bends hip (iliopsoas)

A

L2

206
Q

Myotomes

straightens knee (rectus femoris)

A

L3

207
Q

Myotomes

pulls feet up (tibialis anterior)

A

L4

208
Q

Myotomes

wriggles toes (extensor digitii)

A

L5

209
Q

Myotomes

pulls feet down (gastrocnemius)

A

S1

210
Q

Myotomes

bladder, bowel + sex organs

A

S3-5

211
Q

which nerve innervates

index + middle finger

A

median

212
Q

which nerve innervates

palmar aspect of lateral hand

A

median

213
Q

which nerve innervates

medial aspect of the palm

A

ulnar

214
Q

which nerve innervates

dorsal aspect of hand (thumb, index, middle)

A

radial

215
Q

which nerve innervates

posterior forearm

A

radial

216
Q

A 65-year-old woman: dizziness. precipitated by rolling over in bed onto her right side and occasionally when she tilts her head back to look upwards. No hearing loss, tinnitus, or other neurological symptoms. What is it?

A

Benign paroxysmal positional vertigo

217
Q

how do you diagnosis benign paroxysmal positional vertigo

A

Dix-Hallpike manoeuvre

218
Q

how do you treat benign paroxysmal positional vertigo

A

Epley’s manoeuvre

219
Q

difference between chorea and ballismus

A
  • Ballismus has a larger amplitude
  • faster
    ballistic!
220
Q

features of UMN

A
  • spastic
  • hypertonic
  • increases reflexes
  • +ve Babinski
  • no fasciculations
  • clonus present
221
Q

features of LMN

A
  • decreased reflexes
  • hypotonia
  • flaccid
  • -ve Babinski
  • fasciculations
  • absent clonus
222
Q

is MS UMN or LMN lesion

A

UMN

223
Q

MS

clinical features of optic nerve demyelination

A
  • Optic Neuritis

- relative afferent pupillary defect

224
Q

MS

clinical features of cerebral hemisphere demyelination

A

disturbances of

  • mood and cognition
  • memory
  • decision making
  • depression
225
Q

MS

clinical features of cerebellum demyelination

A
  • ataxia
  • dysarthria (slurred)
  • nystagmus
  • lack of coordination
226
Q

MS

clinical features of brainstem demyelination

A
  • double vision
  • sensory + motor disturbance
  • cranial nerves
227
Q

MS

clinical features of cervical spinal cord demyelination

A

Lhermitte’s sign (neck flex - electric shock)

228
Q

MS

clinical features of lumbrical spinal cord demyelination

A
  • erectile dysfunction
  • urinary retention
  • increased frequency
229
Q

MS

what is Uhtoff’s phenomenon

A

worse neuro symptoms after exercise and heat

230
Q

MS management for painful involuntary contractions of leg muscles (spasticity)

A

Baclofen

231
Q

what is optic neuritis

A

inflammation + demyelination of the optic nerve

232
Q

clinical features of optic neuritis

A
  1. Peri-orbital or retro-ocular pain exacerbated by eye movement
  2. decreased visual acuity - ‘cloudy’
  3. dyschromatopsia (colour blindness)
  4. relative afferent pupillary defect (RAPD)
  5. optic disc swelling
  6. may be the first sign of MS
233
Q

causes of optic neuritis

A
  1. MS
  2. infection: lyme, syphillis, HIV
  3. Autoimmune: SLE, GBS, Sarcoidosis
  4. Diabetes
  5. B12 deficiency
234
Q

inx for optic neuritis

A
  • MRI of the optic nerves: swollen optic nerve, white matter lesions if got MS
  • WBC,CRP: high in infection
  • ESR: high in GCA
  • VDRL: +ve in syphilis
  • uric acid: low in MS
  • serum ACE: high in sarcoidosis
  • ANA: +ve in SLE
235
Q

unilateral loss of vision differentials (painful)

A
  • temporal arteritis
  • migraine
  • acute angle closure glaucoma (red eye, N+V)
  • optic neuritis
236
Q

unilateral loss of vision differentials (painless)

A
  • Amaurosis fugax/central retinal artery occlusion
  • central retinal vein occlusion
  • vitreous haemorrhage: flashes, floaters
  • retinal detachment
  • giant cell arteritis
237
Q

management of optic neuritis

A
  1. pulsed methylprednisolone

IV 1000mg OD for 3 days

238
Q

what is progressive supranuclear palsy

A

brain cells are damaged as a result of a build-up of a protein called tau

239
Q

progressive supranuclear palsy early signs and symptoms

A

very similar to Parkinson’s: tremor

  • sudden loss of balance - falls often backwards
  • muscle stiffness, esp neck
  • extreme tiredness
  • changes in personality: irritability, apathy (lack of interest), mood swings
  • changes in behaviour: recklessness, poor judgement
  • photophobia
  • difficulty controlling eye muscles (esp looking up and down)
  • blurred or double vision
240
Q

progressive supranuclear palsy mid stage signs and symptoms

A
  • wheelchair needed
  • slow, quiet, slurred speech,
  • dysphagia
  • reduced blinking reflex
  • involuntary closing of eye: blepharospasm
  • slowness of thought + memory problems
241
Q

progressive supranuclear palsy advanced stage signs and symptoms

A
  • increasing difficulties controlling the muscles of their mouth, throat and tongue.
  • hard to understand speech
  • bowel + bladder problems
242
Q

how to diagnose progressive supranuclear palsy

A
  • rule out other causes like Parkinsons: gvive levodopa to see if this is affects
  • MRI, PET, DaTscan
243
Q

management of progressive supranuclear palsy

A
  • supportive measures

- no treatment but levodopa may work in early stages

244
Q

what is Pseudobulbar Palsy (aka supranuclear)

A
  • bilateral lesion of corticobulbar tract

- UMN lesion central palsy

245
Q

signs and symptoms of Pseudobulbar palsy (supranuclear)

A
  • increased masseter reflex
  • dysarthria, dysphagia
  • emotional liability: unprovoked crying or laughing
246
Q

causes of pseudobulbar palsy (supranuclear)

A
  • stroke

- atherosclerosis

247
Q

what is bulbar palsy (aka as nuclear)

A
  • CN 9-12 are affected

- LMN lesion peripheral palsy

248
Q

signs and symptoms of bulbar palsy

A
  • absent masseter reflex
  • dysarthria, dysphagia
  • tongue atrophy, fasciculations
249
Q

cause of bulbar palsy

A
  • Gullain Barre Syndrome
  • tumours
  • MND
  • meningoencephalitis
250
Q

what is Bell’s palsy

A
  • weakness or paralysis of the muscles of the face
  • damage to the 7th CN (facial)
  • LMN lesion
251
Q

what is the difference between Bell’s palsy and stroke

A
  • Bell’s Palsy is a LMN lesion
  • entire half of face is effected
  • on same side as affected nerve
  • Stroke is an UMN lesion
  • paralysis of lower 1/2 of face
  • on the contralateral side of lesion
252
Q

key features of Bell’s palsy

A
  • single episode
  • absence of other symptoms
  • dry eye
  • unilateral
  • synkinesis (voluntary movement causes a simultaneous involuntary contraction of other muscles )
253
Q

treatment of Bell’s Palsy

A

prednisolone PO within 72 hrs

254
Q

describe vegetative state in terms of:

  1. arousal + attention
  2. cognition
  3. receptive language
  4. expressive language
  5. visuoperception
  6. motor function
A
  1. intermittent periods of wakefulness*
  2. none
  3. none
  4. none
  5. inconsistent visual startle
  6. involuntary movements only
255
Q

describe minimally conscious state in terms of:

  1. arousal + attention
  2. cognition
  3. receptive language
  4. expressive language
  5. visuoperception
  6. motor function
A
  1. intermittent periods of wakefulness
  2. inconsistent. Self or environmental awareness
  3. inconsistent 1-step command following
  4. spontaneous. Single words or short phrases
  5. visual pursuit. object recognition
  6. localisation to noxious stimuli. object manipulation. automatic movement sequences
256
Q

describe post traumatic confusional state in terms of:

  1. arousal + attention
  2. cognition
  3. receptive language
  4. expressive language
  5. visuoperception
  6. motor function
A
  1. extended periods of wakefulness
  2. confused + disorientated
  3. consistent 1-step language
  4. sentences. confused. yes/no
  5. object recognition
  6. functional use of common objects
257
Q

describe locked-in syndrome in terms of:

  1. arousal + attention
  2. cognition
  3. receptive language
  4. expressive language
  5. visuoperception
  6. motor function
A
  1. normal sleep wake cycle
  2. normal
  3. normal
  4. aphonic
  5. normal
  6. tetraplegia
258
Q

what is the age of onset for dunchenne muscular dystrophy

A

5yrs

259
Q

life expectancy for duchenne muscular dystrophy

A

20s

260
Q

signs and symptoms of duchenne muscular dystrophy

A
  • waddling gait
  • Gower’s sign
  • Calf psuedohypertrophy
  • slow + clumsy
  • learning disabilities
  • cardiomyopathy
  • resp failure
  • scoliosis
261
Q

what is gower’s sign

A

using their arms to ‘walk up’ their body from sitting/lying

262
Q

inx for duchenne muscular dystrophy

A

increased creatine kinase

263
Q

what does the dystrophin protein do?

A

attaches actin to the extracellular matrix to stabilise the sarcolemma

264
Q

pathophysiology of duchenne muscular dystrophy

A

no dystrophin protein –> influx of Ca2+ –> progressive myofibre necrosis –> muscular atrophy

265
Q

what is Becker’s muscular dystrophy

A

milder form of duchenne’s because some dystrophin proteins are made

266
Q

what mutation is present in duchenne muscular dystrophy

A

Xp21

267
Q

what mononeuropathy?

  • repeatedly leaning on elbow
  • clawing of hand
  • wasting of hypothenar
  • weakness of interossei
  • sensory loss in little finger and half of ring
A

ulnar nerve compression

268
Q

what mononeuropathy?

  • saturday night palsy
  • wrist drop: weakness of wrist + finger extensors
A

radial nerve compression

269
Q

what mononeuropathy?

  • prolonged bed rest/squatting
  • foot drop: weakened dorsiflexion + eversion of foot
A

peroneal nerve palsy

270
Q

difference between craniotomy and craniectomy

A

craniotomy - the bone flap is returned

craniectomy - the bone flap is not returned

271
Q

treatment of extradural haemorrhage

A

craniotomy

272
Q

what is mononeuritis multiplex

A

sensory disturbances and weakness in the distribution of > 2 affected peripheral nerves

273
Q

causes of mononeuritis multiplex

A
  • vasculitis
  • SLE, Sjogren’s, RA
  • Sarcoidosis
  • Diabetes
  • Amyloidosis
  • Lyme disease, HIV, Leprosy
274
Q

Diagnosis of mononeuritis multiplex

A

electromyogram

275
Q

treatment of mononeuritis multiplex

A 
- treat underlying aetiology 
most vasculitis neuropathies are treated with:
- IV methylprednisolone 
- PO corticosteroids 
- PO cyclophosphamide
276
Q

name 2 polyneuropathies with mostly motor causes

A
  1. Gullain-Barré syndrome

2. Charcot-Marie-Tooth

277
Q

name 2 polyneuropathies with mostly sensory causes

A
  1. Diabetic neuropathy

2. Renal failure

278
Q

features of polyneuropathy

A
  • symmetrical
  • glove + stocking
  • either sensory or motor deficit
279
Q

what are the 4 main causes of syncope

A
  1. reflex syncope
  2. cardiac syncope
  3. orthostatic HTN
  4. Pyschogenic
280
Q

what is reflex syncope

A
  • vasovagal syncope: fever, severe pain, blood phobia, prolonged standing, hot
  • situation syncope: cough, sneezing, micturition, post exercise
  • carotid sinus hypersensitivity
281
Q

what is cardiac syncope

A
  • arrhythmias: bradycardia, tachycardia

- structural causes: valve disease, MI, hypertrophic cardiomyopathy, atrial myxoma, acute aortic dissection

282
Q

what is orthostatic hypertension (postural)

A
  • drop in BP by 20 within 3 min of standing
  • Autonomic failure: MSA, PD, DM, amyloidosis
  • Hypovolaemia: haemorrhage, dehydration, Addison’s - Drug-induced: anti-hypertensives, diuretics, antidepressants
283
Q

what is psychogenic syncope

A
  • anxiety
  • panic attacks
  • hypoventilation

3a (5 decks)

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