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Phase 3 > Week 12 > Flashcards

Week 12 Flashcards

1
Q

Where can cranial nerve abnormalities arise from?

A 
communicating pathways to and from the cortex, cerebellum and other parts of brainstem
nerve nucleus
nerve
neuromuscular junction disorders
muscle
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2
Q

What are the mnemonics for cranial nerves?

A

On old olympus towering tops a frenchman and german viewed some hops.
some say marry money but my brother says bug business makes money

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3
Q

What are the 12 cranial nerves?

A 
olfactory
optic
oculomotor
trochlear
trigeminal
abducens
facial
vestibulocochlear 
glossopharyngeal
vagus
spinal accessory
hypoglossal
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4
Q

Describe the olfactory nerve

A

sensory
smell
olfactory cells of nasal muscosa - olfactory bulbs - pyriform cortex

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5
Q

Describe the optic nerve

A

sensory
vision
retinal ganglion cells - optic chiasm - thalamus- primary visual cortex in occipital cortex

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6
Q

How do you examine the optic nerve?

A

optic discs with opthalmascope
pupillary responses
visual acuity
visual fields and blind spot (tested by confrontation)

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7
Q

Describe the oculomotor nerve

A 
motor
midbrain
movement of eyeball, lens accommodation
inferior oblique, superior, middle and inferior recti muscles
levator palpeerde superiores

part 2 - parasympathetic
midbrain *Edinger_westphal)
pupil constriction
ciliary muscle and pupillary constrictor muscles

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8
Q

Describe the appearance of an oculomotor palsy

A

eye turns down and out - superior oblique and lateral rectus are the only muscles active
ptosis
involvement of pupil only if complete palsy

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9
Q

Describe the trochlear nerve

A

motor
moves eyeball
midbrain (inferior colliculus)
superior oblique muscles
depresses the adducted eye and introits the abducted eye
longest intracranial course
II and IV are only nerves to decussate to contralateral side

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10
Q

Describe the abducens nerve

A

motor
eyeball movement
pons
lateral rectus muscles

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11
Q

Describe an abducens nerve palsy

A

most common CN palsy
lateral rectus
double vision when looking to affected side - horizontal diplopia

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12
Q

Describe internuclear opthalmoplegia

A

disorder of conjugate gaze
failure of adduction of affected eye with nystagmus on lateral gaze in contralateral eye
can be unilateral or bilateral
results from lesion of medial longitudinal fasiculus (connects III and iV nerve nuclei)
commonly seen in MS

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13
Q

What does horner’s system consist of?

A

miosis
ptosis
apparent enopthalmos
anhidrosis

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14
Q

What can cause horner’s syndrome?

A 
results from ipsilateral disruption of cervical/thoracic sympathetic chain
congenital
brainstem stroke
cluster headache
apical lung tumour
MS
carotid artery dissection
cervical rib
syringomyelia
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15
Q

Describe the trigeminal nerve

A

1 - sensory input from face
pons and medulla
face (opthalmic, mandibular and maxillary divisors) and anterior 2/3 of tongue

2 - motor
mastication
pons
masseter, temporalis, medial and lateral pterygoids

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16
Q

Describe the facial nerve

A

1 - motor
pons
muscles of expression

2 - sensory
medulla
taste
anterior 2/3 of tonguw

3 - parasympathetic
medula
salivation and lacrimation

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17
Q

Describe the corneal reflex

A 
useful in patients with reduced conscious level
lightly touch cornea with cotton wool 
afferent - V
efferent - VII
test of pontine function
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18
Q

Describe the vestibulocochlear nerve

A

1 - sensory
balance
pons and medulla
nerve endings within semi-circular canals - cerebellum and spinal cord

2 - sensory
hearing
pons and medulla
cochlear - auditory cortex in the temporal lobes

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19
Q

Describe the glossopharangeal nerve

A

1 - sensory
medulla
taste, proprioception for swallowing, blood pressure receptors
posterior 1/3 of tongue, pharyngeal nerve and carotid sinuses

2 - motor
medulla
swallow and gag reflex
pharyngeal muscles and lacrimal glands

3 parasympathetic
saliva production
parotid glands

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20
Q

In a glossopharyngeal palsy, in what direction does the uvula deviate to?

A

away from the side of the lesion

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21
Q

Describe the vagus nerve

A

1 - sensory
medulla
chemorecptors, pain receptors, sensation
blood oxygen concentration, carotid bodies, respiratory and digestive tracts, external ear, larynx and pharynx

2 - motor
medulla
hert rate and stroke volume, peristalsis, air-flow, speech and swallowing
pacemaker and ventricular muscles, smooth muscles of GI tract, smooth muscles of bronchial tube, muscles of larynx and pharynx

3 - parasympathetic
smooth muscles and glands of the same areas innervated by motor component as well as the thoracic and abdominal areas

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22
Q

Describe the spinal accessory nerve

A

motor
head rotation and shoulder shrugging
medulla
sternocleidomastoid and trapezius muscles

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23
Q

Describe the hypoglossal nerve

A

motor
speech and swallowing
medulla
tongue

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24
Q

In what direction does a hypoglossal nerve palsy cause the tongue to deviate?

A

towards the affected side

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25
Q

What cranial nerves would be affected if there was a lesion in the cavernous sinus?

A

III, IV, V (1st and 2nd divisions), VI, horner’s syndrome

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26
Q

What cranial nerves would be affected if there was a lesion in the superior orbital fissure?

A

III, IV, V(1st division), VI

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27
Q

What cranial nerves would be affected if there was a lesion in the cerebellopontine angle?

A

V, VII, VIII

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28
Q

What cranial nerves would be affected if there was a lesion in the jugular foramen?

A

IX, X (and XI)

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29
Q

What cranial nerves would be affected if there was a lesion in the bulbar /pseudobulbar palsy?

A

IX, X, XI (and XII)

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30
Q

Describe a pseudo bulbar palsy?

A

upper motor neurone lesion
spastic dysarthria, slow and limited tongue movements
lesions involving descending corticobulbar pathways cause pseudo bulbar palsy
stroke, MS, space occupying lesion

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31
Q

Describe a bulbar palsy

A

lower motor neurone lesion
nasal dysarthria, dysphagia with nasal regurgitation, wasted tongue with fasciculations
lesions of nuclei, cranial nerves or muscles can cause bulbar palsy
brainstem stroke, guillain barre syndorme, myasthenia gravis

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32
Q

What makes up the basal ganglia?

A

striatum; both dorsal striatum (caudate nucleus and putamen) and ventral striatum (nucleus accumbens and olfactory tubercle), globus pallidus, ventral pallidum, substantia nigra, and subthalamic nucleus.

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33
Q

What are the basal ganglia loops?

A

motor - movement
oculomotor - eye movement control
lateral orbito-frontal - social behaviour
dorsolateral prefrontal loop - executive functions / working memory

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34
Q

Describe the pathology of Parkinson’s disease

A

loss of dopaminergic neurones within the substantia nigra
surviving neurones contain lewy bodies
PD manifests clinically after loss of approximately 50% of dopaminergic neurones

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35
Q

What protein are lewy bodies made from?

A

alpha synuclein

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36
Q

What are the suggested mechanisms of LB formation

A 
oxidative stress
mitochondrial failure
excitotoxicity
protein aggregation
interference with DNA transcription
nitric oxide
inflammation
apoptosis
trephine deficiency 
infection
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37
Q

Describe the pathological progression of PD

A

1-2 = medullary / pons and olfactory nucleus - asymptomatic
3-4 = midbrain - substantially nivea pars compacts - parkinsonism after extensive damage
5-6 - development of PD dementia

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38
Q

What are the features of parkinson’s disease?

A

bradykinesia
muscular rigidity
4-6Hz rest tremor
postural instability

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39
Q

What is the definition of bradykinesia?

A

slowness of initiation of voluntary movement with progressive reduction in speed and amplitude of repetitive actions

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40
Q

What are the non-motor symptoms of parkinson’s disease?

A

neuropsychiatric - dementia, depression, anxiety

sleep - REM sleep behaviour disorder
restless leg syndrome
daytime somnolence

autonomic - constipation
urinary urgency / nocturia
erectile dysfunction
excessive salivation / sweating
postural hypotension

other - reduced olfactory function
fatigue
pain and sensory symptoms

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41
Q

Describe the differential diagnosis of PD>

A 
diagnosis improves with follow up 
other disorders mistaken for PD
benign tremor disorders
dementia with lewy bodies
vascular parkinsonism
parkinson plus disorders 
drug induced tremor
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42
Q

What are the investigations for PD?

A

bloods - if tremor present, TFTs, copper, caeroplasmin
Structural imagine - CT MRI brain normal
functional imaging - presynaptic dopaminergic function using DAT SPECT is abnormal

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43
Q

What drug classes are there in PD?

A

L-DOPA
dopamine agonists
MAO-B inhibitors
COMT inhibitors

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44
Q

Describe L-dopa

A

taken up by dopaminergic neurones and decarboxylated to dopamine within presynaptic terminals
prescribed with dopa-decarboxylase inhibito
half life about 90 minutes

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45
Q

What are the 2 common preparations of L dopa?

A

sinemet - Ldopa and carbidopa

Madopar - Ldopa and benserazide

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46
Q

What are the peripheral side effects of Ldopa?

A

nausea, vomiting, postural hypotension

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47
Q

What are the central effects of Ldopa?

A

confusion and hallucinations

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48
Q

What are the longer term complications after 5 years of Ldopa?

A

fluctuation in motor response

dyskinesia - most commonly chorieform movements at peak dose

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49
Q

Give examples of dopamine agonists

A

ropinirole
pramipexole
rotigotine
amomorphine

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50
Q

Describe Mao-B inhibitors

A

selegiline, rasagiline
prevents dopamine breakdown by binding irreversible to monoamine oxidase
can be prescribed as mono therapy in early disease or as adjunct in later disease
well tolerated

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51
Q

Describe COMT inhibitors

A

entacapone, tolcapome
inihibitng catechol - o-methyltransferase results in longer L-DOpa half life / duration of action
co-prescribe with Ldopa
side effects - dopaminergic and diarrhoea

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52
Q

What are the problems in advanced PD?

A 
motor complications 
on/off fluctuations
L-dopa induced dyskinesia 
poor balance / falls
speech / swallowing disturbances
cognitive -dementia
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53
Q

What are other degenerative causes of parkinosonism?

A

dementia with lewy bodies
progressive supranuclear palsy
multisystem atrophy
corticobasal degeneration

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54
Q

What are secondary causes of parkinsonism?

A

Drug induced - chronic use of dopamine antagonists
cerebrovascular disease
toxins - CO, organophosphates, MPTP
post infectious

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55
Q

Describe the fibre types in peripheral nerves

A

large fibres (myelinated)
motor nerves
proprioception, vibration and light touch

thinly myelinated fibres
light touch, pain, temperature

small fibres (unmyelinated)
light touch, pain, temperature
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56
Q

Describe length dependent axonal nuropathy

A 
diffuse involvement of peripheral nerves
age >50 years 
length dependent; starts in toes/feet
symmetrical
slowly progressive
no significant sensory ataxia
any weakness distal and mild
glove and stocking distribution
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57
Q

What are the causes of length dependent axonal neuropathy?

A

diabetes
alcohol
nutritional (folate, B12, thiamine, B6 deficiency)
immune mediated - RA, SLE, vasculitis, PAN
metabolic - renal failure , hypothyroidism
drugs -isoniazid, cisplatin, amioderone, gold
infectious - HIV, hepatitis
inherited -
neoplastic - myeloma
paraneoplastic
critical illness

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58
Q

Describe guillain_barre syndrome

A

acute inflammatory demyelinating neuropahy
post infectious autoimmune aetiology
progressive ascending weakness over days
flaccid, quadriparxsis with areflexia
respiratory / bulbar/ autonomic involvement
treated with IV immunoglobulin or apheresis
CIDP - chronic h form

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59
Q

What are the symptoms of muscle disease?

A 
proximal limb weakness
facial weakness
eyes 
bulbar - dysarthria, dysphagia
neck and spine
respiratory 
myocardial
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60
Q

What are some causes of muscle disease?

A 
muscular dystrophies
metabolic muscle disorders
mitochondrial siders 
myotonic dystrophies 
inflammatory muscle disorders 
neuromuscular junction disorders
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61
Q

Describe the pathogenesis and presentation of myasthenia gravis

A

autoimmune disorder 0 antibodies to acetylcholine receptor and post synaptic NMJ
association with other AI conditions
may be associatied with thymoma
affects young women and older men
fatiguable weakness of ocular, bulbar, neck, respiratory and/or limb muscles

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62
Q

what is the investigation and management of myasthenia gravis?

A

antibodies to AChR present in 85% of cases
single fibre EMG and repetitive nerve stimulation also abnormal
managed with pyridostigmine (anti-acetylcholine esterase) and immunosuppressive therapies

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63
Q

What is the definition of dementia?

A

progressive cognitive decline
interfere with the ability ti function at work or at squall activiities
a decline from previous levels of functioning and performing
not explained by delirium or major psychiatric disorder
the cognitive or behavioural impairment involves a minimum of 2 of the following domains - memory, executive function, language, apraxia / visuospatial

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64
Q

What is asked about memory in a cognitive assessment?

A

impaired ability to acquire and remember new information - symptoms include: repetitive questions or conversations, misplacing personal belongings, forgetting events or appointments, getting lost on a familiar route

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65
Q

What is asked about executive function in a cognitive history?

A

impaired reasoning and handling of complex tasks, poor judgement -symptoms include: poor understanding of safety risks, inability to manage finances, poor decision making ability, inability to plan complex or sequential activities

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66
Q

What is asked about visuospatial awareness in a cognitive history?

A

impaired visuospatial abiltiies - symptoms include: inability to recognise faces or common objects or to find objects in direct view despite good visual acuity, inability to operate simple implements or orient clothing to body

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67
Q

Describe what is asked about language in a cognitive history

A

impaired language functions (speaking, reading, writing) symptoms include: difficulty thinking of common words while speaking, hesitations: speech, spelling and writing errors

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68
Q

What does the addenbrookes cognitive assessment examine?

A 
memory
attention / concentration 
language
visuospatial
executive function 
purpose - severity, pattern of impairment
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69
Q

Describe attention / concentration / orientation

A

component of consciousness which allows filtering of information to allow one to focus on a particular stimuli
essential for all aspects of cognitions
pathological process - delirium (depression)

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70
Q

How are attention, concentration and orientation assessed?

A

orientation
serial 7s
working memory facet of attention/concentration e.g digit span

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71
Q

Describe executive function

A

facet of frontal lobe function
behaviour, social awareness (orbitofrontal)
working memory, cognitive estimates planning (dorsolateral prefrontal cortex)
motivation (anterior cingulate)

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72
Q

How do you test executive function?

A

proverbs
verbal fluency
estimates
planning

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73
Q

What is the dorsal stream involved in?

A

position of object in space (dyspraxia) picking an object from a scene

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74
Q

What is the ventral stream involved in?

A

object recognition (visual gnosis)
facial recognition
(prosopagnosia)

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75
Q

How do you test visuospatial parietal lobe function?

A 
pentagons
cubes 
3-D letters
dots counting
assess higher motor control, deficits result in impairment of purposeful motor skills
pantomime gestures to command
use of everyday objects
copying of meaningless gestures
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76
Q

How can language be assessed?

A

naming
repetition
3 stage command (comprehension)
reading

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77
Q

what are the 3 patterns of aphasia?

A

semantic variant
logopenic variant
non-fluent aphasia variant

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78
Q

Describe the semantic variant

A

poor confrontation naming
impaired single word comprehension
poor object / person recognition, surface dyslexia, spared repetition
semantic dementia

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79
Q

Describe logopenic varient

A

impaired single word retreival
impaired repetition, speech sound errors
spared object / person recognition, single word recognition
Alzheimer’s dementia

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80
Q

Describe non fluent variant aphasia

A

effortful, halting speech
phenomic errors
spared object / person recognition, single word recognition
progressive non-fluent apahsia

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81
Q

What is the “cut off” score in the addenbrookes cognitive assessment?

A

88

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82
Q

What does a deficit in episodic memory suggest?

A

alzheimers

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83
Q

What does a deficit in semantic memory suggest?

A

semantic dementia

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84
Q

What does a deficit in attention / concentration suggest?

A

delirium

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85
Q

What does a deficit in naming and fluency suggest?

A

progressive non fluent dementia

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86
Q

What does a deficit in visuospatial abilities suggest?

A

PD plus syndrome

or variants of AD

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87
Q

What leads to aneurysm formation?

A

haemodynamic stress
extensive inflammatory and immunological reactions are common in enraptured intracranial aneurysms and may be related to aneurysm formation and rupture

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88
Q

What are the predisposing factors for aneurysmal SAH?

A 
smoking
female
hypertension
positive family history 
ADPCK, Ehlers dan lose, coarctation of the aorta
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89
Q

Describe the history which is common in SAH

A

sudden onset headache
LOC, seizures, visual, speech and limb disturbance
sentinel headache

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90
Q

Describe the clinical examination of SAH

A 
photophobia
meningism
subhyaloid haemorrhages 
vitreous haemorrahges (Terson's syndrome)
speech and limb disturbance 
pulmonary oedema
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91
Q

how is SAH graded?

A 
By GCS 
15 - grade 1 
13-14 - grade II
13-14 with deficit grade III
7-12 - grade IV
3-6 grade V
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92
Q

Describe the use of CT in SAH

A

confirms diagnosis
clues to aetiology
identifies complications: infarction, haematoma, hydrocephalus
prognostic - fisher grade

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93
Q

Describe the investigations in SAH

A 
LP - xanthochromia - bilirubin vs oxygen Hb
CTA
MRA
DSA: stroke, diabetics
hyponatraemia
ECG changes
elevated troponin
echocardiography - tako tsubo cardiomyopathy
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94
Q

Describe the resuscitation in SAH

A 
bed rest
fluids 2.5-3.0 L normal saline
anti-embolic stockings
nimodipine: 60mg 4 hourly oral? NG or 2.5-10ml/hr IV via central line
analgesia 
doppler studies
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95
Q

What are the management options for SAH?

A

surgical clipping
endovascular (coils, stents and glue)
conservative

96
Q

What are the potential complications of SAH?

A 
rehaemorrhage
delayed ischaemia 
hydrocephalus
hyponatraemia
ECG changes, LVF
LRTI, PE, UTI
97
Q

Describe delayed ischaemia

A

day 3-10
progressive deterioration in LOC associated with new deficit
angiographic spans

98
Q

What is the treatment of delayed ischaemia?

A

fluid management
nimodipine
inotropes
angioplasty

99
Q

Describe hyponatraemia in SAH

A

CWS vs SIADH
establish volume status
hypertonic saline
fludrocortisone

100
Q

Describe the cardiopulmonary complications associated with SAH

A 
sympathetic stimulation and catecholamine release can lead to myocardial injury
elevations of troponin can occur
arrhythmia
wall motion abnormality
 sudden death
normally normal within 3 days
101
Q

What factors can affect consciousness?

A 
trauma
elevated ICP
fever
hypothermia
seizure
hypotension
severe hypertension
hypoxia
hypercapnia
sepsis
metabolic
medications 
etc....
102
Q

What are the three sub scales in GCS?

A

eye
verbal
motor

103
Q

Describe eye opening in GCS

A
  1. spontaneous
  2. to verbal command
  3. to pain
  4. none
    N.B cannot be assessed if eyes are swollen
104
Q

Describe verbal response in GCS

A
  1. orientated (T/P/P)
  2. confused
  3. inappropriate
  4. incomprehensible sounds
  5. none
    append T to score if patient is intubated
105
Q

Describe motor in GCS

A
  1. obeys commons
  2. localises pain
  3. normal flexion
  4. abnormal flexion
  5. extension
  6. none
    N.B cannot be assessed if patient has received muscle relaxants
    also spinal injury?
106
Q

What is a coma?

A

inability to obey commands, speak, open eyes to pain

107
Q

How is the best verbal response modified for young children?

A
  1. none
  2. restless, agitated
  3. persistently irritable
  4. consolable crying
  5. appropriate words, smiles, fixes/follows
108
Q

How is head injury classified?

A

GCS
14-15 = minor
9-13 = moderate
severe <8

109
Q

Describe MS

A

idiopathic inflammatory demyelinating disease of the CNS
acute episodes of inflammation are associated with focal neurological deficits
demyelination results in loss of neurological function - weak leg, visual loss, urinary incontinence
deficits usually develop gradually, last more than 24 hours and may gradually improve over days to a week.
Late in untreated disease patients may become progressively more disabled

110
Q

What are the subtypes of MS?

A

relapsing remitting MS
primary progressive MS
secondary progressive MS
benign MS

111
Q

Describe relapsing remitting MS

A

unpredictable attacks which may or may not leave permanent deficits followed by periods of remission

112
Q

Describe primary progressive MS

A

steady increase in disability without attacks

113
Q

Describe secondary progressive MS

A

initial relapsing-remitting MS that suddenly begins to decline without periods of remission

114
Q

What are examples of symptoms that may develop into MS?

A

optic neuritis
clinically isolated syndromes
transverse myelitis
radiologically isolated syndromes

115
Q

Describe optic neuritis

A

painful visual loss that comes on over a few days
may resolve after a few weeks
many will go on to develop MS

116
Q

Describe transverse myelitis

A 
inflammation of the spinal cord
weakness
sensory loss
incontinence may be only symptom
many causes other than MS
117
Q

Describe clinically isolated syndromes in MS

A

single episode of neurological disability due to focal CNS inflammation
can include optic neuritis and transverse myelitis
may be first attack of MS
can happen after infection and not be related to MS

118
Q

When is MS diagnosed?

A

When there is evidence of 2 or more episodes of demyelination disseminated in space and time

119
Q

What are thought to contribute to the development of MS?

A

genetic factors
sunlight / vitamin D exposure
viral trigger - EBV?
multifactorial - smoking

120
Q

When should MS be suspected?

A

neurological symptoms that develop over a few days

a history of transient neurological symptoms that have lasted for more than 24 hours and spontaneously resolved

121
Q

How can relapses of MS be “hidden”

A 
optic neuritis / visual disruption
Bell's palsy
"Labyrinthitis"
sensory symptoms
bladder symptoms in man/woman without children
122
Q

What are the main symptoms of MS?

A 
fatigue
cognitive impairment
depression
unstable mood
nystagmus
optic neuritis 
diplopia
dysarthria
dysphagia
weakness
spasms
ataxia
pain
hypoesthesias
paraesthesias
incontinence
diarrhoea/constipation
frequency or retention of urine
123
Q

When to suspect symptoms may not be caused by MS?

A 
sudden onset
peripheral signs - areflexia, glove and stocking distribution, muscle wasting, fasciculations
major cognitive impairment 
reduced level of consciousness
prominent seizures
pyrexia/ evidence of infection
normal MRI scan
124
Q

Describe MRI scan in diagnosis of MS

A

MRI brain and cervical spine with gadolinium contrast
possible to diagnose with one scan
evidence of demyelination in 2 regions can indicate dissemination in space
If enchanting and non-enchanting areas of demyelination are seen this can indicate dissemination in time

125
Q

What additional investigations can be carried out for MS?

A

lumbar puncture
bloods - exclude other conditions
visual evoked potentials
CXR - exclude sarcoidosis

126
Q

What is examined in a lumbar puncture for MS?

A

CSF oligobands (need matched blood sample)
CSF cell counts - exclude mimics
CSF glucose (matched blood sample)
CSF protein

127
Q

Describe oligoclonal bands in MS LP

A

immunoglobulin bands seen in blood and spinal fluid after protein electrophoresis
presence of bands in CSF but not blood suggests immunoglobulin production in CNS
supports diagnosis of MS but can be seen in other conditions

128
Q

What blood tests should be carried out to exclude other causes of MS?

A 
B12/folate
serum ACE
lyme serology
ESR/CRP
ANA/ANCA/rheumatoid factor
aquaporin-4 antibodies (if transverse myelitis / optic neuritis)
129
Q

Describe visual evoked potentials

A

measure conduction of nerve signals in optic nerve to look for subclinical optic neuritis
conduction will be slower if a patient has had optic neuritis in the past

130
Q

Describe relapse vs pseudo-relapse in MS

A

a relapse usually involved a new neurological deficit that lasts for more than 24 hours in the absence of pyrexia or infection
a pseudo-relapse is the reemergence of previous neurological symptoms or signs related to an old area of demyelination in the context of heat or infection
if evidence of infection this should be treated

131
Q

Describe the steroid regime for a relapse of MS

A

1g of IV methylprednisalone for 3 days
or
500mg of oral methylprednisalone for 5 days
and PPI for gastroprotection
ideally prescribe at 9am to avoid sleep disruption

132
Q

What are 2 powerful drugs that can be used to treat MS?

A

alemtuzumab

natalizumab

133
Q

What are examples of oral treatments of MS?

A

fingolimod

dimethyl fumarate

134
Q

Describe cladribine

A

old chemo drug
two short courses of tablets over two years
targets B cells
may stop MS activity for many years

135
Q

What is the definition of a stroke?

A

central nervous system infarction (which includes brain, spinal cord and retinal cells attributable to ischaemia), based on objective evidence of focal ischaemic injury in a defined vascular distribution or clinical evidence of the form with other aetiologies excluded

136
Q

In what artery is there most likely to be an infarction if there is leg weakness?

A

anterior cerebral arteries

137
Q

In what artery is there most likely to be an infarction if there is weakness of the trunk and hands?

A

middle cerebral artery

138
Q

What blood vessel supplies the main language areas of the brain?

A

middle cerebral artery

139
Q

What is the definition of an ischaemic stroke?

A

an episode of neurological dysfunction caused of focal cerebral, spinal, or retinal infarction

140
Q

Describe TACS

A

total anterior circulation syndrome
hemiparesis and higher cortical dysfunction and hemianopia
proximal MCA or ICA occlusion

141
Q

Describe PACS

A

partial anterior circulation syndrome
isolated higher cortical dysfunction or any 2 of hemiparesis, higher cortical dysfunction or hemianopia
usually branch MCA occlusion

142
Q

Describe POCS

A

posterior circulation syndrome
isolated hemianopia or brainstem syndrome
can include perforating arteries, PCA or cerebellar arteries

143
Q

Describe LACS

A

lacunar syndrome
pure motor stroke or pure sensory stroke or sensiromotor stroke or ataxic hemiparesis or clumsy hand dysarthria
perforating artery / small vessel disease

144
Q

What is the definition of an intracerebral haemorrhage

A

A focal collection of blood within the brain parenchyma or ventricular system not caused by trauma

145
Q

What is the definition of a stroke caused by intracerebral haemorrhage?

A

Rapidly developing clinical signs of neurological dysfunction attributable to a focal collection of blood within the brain parenchyma or ventricular system which is not caused by trauma

146
Q

What can cause an intracerebral bleed?

A 
hypertension
trauma
blood clotting deficiencies 
abnormalities in blood vessels 
haemorrhage transformation of an infarct 
tumours 
drug usage
147
Q

What is the management of an ischaemic stroke?

A 
IV thrombolysis
thrombectomy +/- IV thrombolysis
aspirin
stroke unit
hemicranectomy
148
Q

What is the management of a haemorrhagic stroke?

A

blood pressure control
stroke unit
neurosurgical evacuation

149
Q

What are the cerebrovascular risk factors for stroke?

A 
hypertension
obesity
sedentary lifestyle
high cholesterol
smoking
alcohol
diabetes
heart disease 
poverty
150
Q

Describe secondary prevention in stroke management

A 
smoking cessation
aspirin for first 2 weeks then clopidigrel
antihypertensives 
statins
diabetes control
endarterectomy if stenosed carotids
151
Q

Describe mononeuropathy of the radial nerve

A 
entrapment at spinal groove 
"saturday night palsy"
presenting symptoms 
wrist and finger drop
usually painless
152
Q

Describe the muscles supplied by the radial nerve and what weakness of them effects

A

extensor carpi radialis longus - wrist extension
extensor digitorum communis - finger extension
brachioradialis - elbow flexion in mid-pronation

153
Q

Where would the sensory change occur in radial nerve damage?

A

the dorsal aspect of the hand - thumb, index and half of middle finger

154
Q

Describe palsy of the ulnar nerve

A

entrapment at ulnar groove (medial epicondyle of humerus)
may be history of trauma at elbow
sensory disturbance and weak grip
usually painless

155
Q

Describe the muscles supplied by the ulnar nerve and what weakness of them effects

A

1st dorsal interosseus - index finger abduction
abductor digiti minimi - pinkie abduction
flexor carpi ulnari - wrist flexion
adductor pollicis - thumb adduction

156
Q

Describe the sensory change in ulnar nerve palsies

A

medial aspect of the hand

157
Q

Describe palsy of the median nerve

A

entrapment within carpal tunnel at wrist
history of intermittent nocturnal pain, numbness and tingling - often relieved by shaking hand
patient may complain of weak grip
positive tine’s sign/phalen’s test

158
Q

Describe the muscles supplied by the median nerve and what weakness of them effects

A

lumbricals I+II - flexion at MCP joints
opponens pollicis - thumb opposition
abductor pollicis brevis - thumb abduction
flexor pollicis brevis - thumb flexion

159
Q

Describe the sensory change in a median nerve palsy

A

lateral aspect of the palm

tips of index, middle and half of ring finger

160
Q

Describe mononeuropathy affecting the median nerve II anterior interosseus branch

A

trauma to forearm
history of forearm pain
patient may complain of weak grip of keys
can’t make OK sign

161
Q

Describe the muscles supplied by themedian nerve II anterior interosseus branch and what weakness of them effects

A

pronator quadratura - flexion at MCP joints
flexor pollicis longus - thumb flexion
flexor digitorum - thumb flexion

162
Q

Describe palsy of the femoral nerve

A

haemorrhage or trauma
weakness of quadriceps
weakness of hip flexion
numbness in medial shin - saphenous branch

163
Q

Describe the motor weakness in female nerve palsy

A

quadriceps - knee extension
illiopsoas - hip flexion
adductor magnus - hip adduction

164
Q

Which nerve supplies the back of the lower leg and what muscles are involved?

A

tibial

gastrocnemius, soleus

165
Q

Which nerve supplies the front of the lower leg and what muscles are involved?

A

peroneal

TA, peroneii

166
Q

Describe peroneal nerve palsy

A

entrapment at fibular head
may be history of trauma, surgery or external compression
acute onset of foot drop and sensory disturbance in the lateral aspect of the shin
usually painless

167
Q

What muscles does the perineal nerve supply and what would be the effect of a palsy?

A

tibialis anterior - ankle dorsiflexion

extensor hallicus longs - great toe extensinon

168
Q

How can you distinguish between a common peroneal nerve palsy and L5 distribution?

A

L5 damage would also affect foot inversion

169
Q

What is mono neuritis multiplex?

A

simultaneous or sequential development palsies of 2 or more nerves

170
Q

What are some common causes of mononeuritis multiplex?

A 
diabetes
vasculitic - Churg strauss, polyarteritis nodosa
Rheumatological - RA, SLE etc
infective - hep C, HIV
sarcoidosis
lymphoma
171
Q

What is primary headache?

A

headache and its associated features is the disorder

e.g. migraine, tension-type headache, cluster headache

172
Q

What is a secondary headache?

A

secondary to underlying cause
e.g Subarachnoid haemorrhage, space occupying lesion, meningitis, temporal arteritis, high/low intracranial pressure, drug-induced

173
Q

What is important to ask about in the history of headache

A 
onset
severity and pain quality
location/radiation
presence of aura / prodrome
periodicity 
associated features 
age of onset
triggering / exacerbating / relieving factors 
family history 
social / employment history 
medication history 
co-morbid depression / sleep disturbance
174
Q

What are the red flag features suggesting secondary headache ?

A

age >50 years
thunderclap headache
focal/non-focal neurological deficit
worsening of symptoms with posture, valsalva or physical exertion
early morning headaches
systemic symptoms - fever, weight loss
seizures, meningism
temporal artery tenderness/ jaw claudication
specific situations - cancer, pregnancy, post partum, HIV, immunosuppression

175
Q

Describe the clinical examination of the patient with headache

A 
general
reduced conscious level
BP/pulse
pyrexia
meningism
skin rash
temporal artery tenderness
cranial nerve
pupillary responses
visual fields +/- blind spots
eye movements
fundoscopy
176
Q

What are upper motor neurones signs in a neurological examination?

A

pronator drift
increased tone
brisk reflexes
extensor plantar response

177
Q

What are cerebellar signs in neurological examination?

A

nystagmus
past-pointing
dysdiagochokinesis
broad based ataxic gait

178
Q

Describe the epidemiology of migraine

A 
female > male
12-16% general population
prevalence highest aged 25-55 years
positive family history 
most patients report triggers 
without aura - 70%
179
Q

Describe the pathophysiology of migraine

A

primary dysfunction in brainstem sensory nuclei (V, VII-X)

pain results from pain sensitive cranial blood vessels and their innervating trigeminal fibres

180
Q

Describe migraine prodrome

A

up to 48 hours before headache

variable symptoms - mood disturbance, restlessness, hyperosmia, photophobia, diarrhoea

181
Q

Describe migraine aura

A

recurrent reversible focal neurological symptoms (visual , sensory, motor)
develops over 5-20 minutes and lasts <60 minutes
visual aura is most common
sensory aura often starts in hand and migrates up arm

182
Q

Give examples of visual aura

A

zigzag fortification spectrum
visual field loss
negative scotoma
positive scotoma

183
Q

Describe a migraine headache

A 
character commonly throbbing or pulsatile
moderate - severe
gradual onset, duration 4-72 hours 
unilateral in 60&amp; can radiate
aggravated by routine physical activity
nausea and vomiting
photophobia
phonophobia 
osmophobia
mood disturbance 
diarrhoea 
autonomic disturbance - lacrimation, conjunctival infection, nasal stiffness
184
Q

Describe the investigation of migraine

A

good history and normal clinical examination does not require further investigaion
cranial imagine advised if red flag features present or aura >24 hours

185
Q

Describe the complications of migraine

A

medication overuse headache: headache >15 days per month associated with frequent use of acute relief medications - NSAIDs, paracetamol, opioid medications, triptans
patients advised to take acute treatments more than 2-3 times per week to prevent this

186
Q

Describe the management of migraine

A

lifestyle
avoid triggers
reduce caffeine / alcohol
encourage regular meals and sleep patterns

acute management
simple analgesia
triptans (sumatriptan)
antiemetics (domperidone, metoclopramide)

prophylaxis
beta blockers (propanalol)
tricyclic antdepressants (amitriptyline)
anti-epilepsy drugs (topiramate, sodium valproate)

187
Q

Describe a thunderclap headache

A

definition - abrupt onset of severe headache which reaches maximum intensity <5mins
should be considered as SAH until proven otherwise

188
Q

What are the causes of thunderclap headache?

A

SAH
intracerebral haemorrhage
arterial dissection
bacterial meningitis
rare - spontaneous intracranial hypotension, pituitary apoplexy
primary headaches - diagnosis of exclusion

189
Q

Describe the investigation of thunderclap headache

A

bloods
U&Es, LFT, glucose, full blood count, coagulation screen, CRP, cultures if pyrexial

12 lead ECG

urgent CT brain

LP after 12 hours to look for xanthochromia

190
Q

What is the cerebral perfusion pressure equation?

A

CPP = mean arterial pressure - ICP

191
Q

What types of cerebral herniations are there?

A 
uncal
central (transtentorial)
cingulate
transcalvarial
upward transtentorial 
tonsillar
192
Q

Describe the history in raised pressure headaches

A 
worse on lying flat
worse in the morning 
persistent nausea/vomiting
worse on valsalva
worse with physical exertion
transient visual obscurations with change in posture
193
Q

What are the examination findings in a raised pressure headache?

A 
optic disc swelling
impaired visual acuity/colour vision
restricted visual fields/ enlarge blind spot
III nerve palsy 
VI nerve palsy (false localising sign)
focal neurological signs
194
Q

What are the causes of raised ICP?

A

mass effect - tumour, infarction with oedema, subdural/extradural/intracerebral haematoma, abscess

Increased venous pressure
cerebral venous sinus thrombosis, obstruction of jugular venous system

obstruction to CSF flow / absorption
hydrocephalus, meningitis

idiopathic

195
Q

What are the features of low CSF pressure headache?

A

headache worse on sitting/standing

results from CSF leakage

196
Q

What are the causes of low CSF headache?

A

post LP

spontaneous intracranial hypotension

197
Q

What is a seizure?

A

episode of neuronal hyperactivity

198
Q

What is epilepsy ?

A

at least two unprovoked episodes of seizure

199
Q

Describe focal epilepsy

A

localised, partial onset
area of abnormality in otherwise normal brain
trauma, infection, abscess
more likely in elderly
transient injuries may lead to focal injuries

200
Q

Describe generalised epilepsy

A

where someone is born with a problem in the way they process neurotransmitters, channels, receptors etc
innate responsiveness in CNS that leaves them more prone to seizures
more likely in children

201
Q

What should you do if you see someone having a seizure?

A

keep them out of harm’s way
recovery position
if movements stop, not impairment of ABCS, does not need hospitalisation once recovers awareness

202
Q

Describe the features of focal epilepsy

A 
history of trauma/birth injury 
focal aura / sequelae
post attack confusion/drowsiness
automatisms
nocturnal events
203
Q

Describe GGE features

A 
photosensitivity 
age of onset 8-26
alcohol or sleep deprivation
myoclonus (AM)
lack of aura
seizures within 2 hours of awakening
family history 
EEG abnormal
204
Q

What investigations are needed for epilepsy ?

A

brain imaging
EEG
systemic provocations

205
Q

Describe the EEG

A 
test takes C 1 hour
 observe activity on EEG lying at rest
hyperventilation
drowsiness
photic stimulation
206
Q

What is the differential for epilepsy ?

A

first seizure vs syncope
multiple seizures vs syncope vs NEAD
rarer - migraine, narcolepsy, transient global amnesia, panic attacks

207
Q

What is status epillepticus

A

repetitive or prolonged epileptic seizures
medical emergency
may cause profound systemic/neuronal damage
recognised mortality

208
Q

What is the clinical definition of status epilepticus?

A

> 2 seizures without full recovery or neurological function between seizures
or continuous seizure activity >30 minutes

209
Q

What is the normal treatment of focal epilepsy?

A

lamotrigine, carbamazepine, levetirecetam

210
Q

What is the normal treatment of generalised epilepsy?

A

valproate
levetiracetam
lamotrigine

211
Q

What are the different anatomical classifications of CNS infection?

A

meningitis
(meningo) encephalitis
mass lesion
myelitis

212
Q

What are the main bacteria that cause meningitis and encephalitis?

A

meningococcus, pneumococcus, listeria

213
Q

What are the main viruses that cause meningitis and encephalitis?

A

HSV, VZV, enterovirus, HIV, Mumps

214
Q

What is a common fungal infection that can cause meaning-encephalitis and mass lesions?

A

crytococcosis

215
Q

What is a common protozoal infection that can cause CNS mass lesions and eosinophils-meningitis?

A

toxoplasmosis

216
Q

Describe meningitis

A

inflammation of meninges (and sometimes cerebrum)
acute- bacterial or viral
sub-acute - bacterial (listeria, TB)

217
Q

What are the signs and symptoms of meningitis?

A

95% will have 2 of headache, neck stiffness, reduced GCS or fever
confusion indicative of celebrities/encephaltis
Rash - purpuric or petechial but macular early on

218
Q

What are the risk factors for pneumococcal meningitis?

A 
middle ear injury
head injury
neurosurgery
alcohol
immunuosuppresion
219
Q

What are risk factors for listeria?

A

immunosuppresion

pregnancy

220
Q

What are signs of pneumococcal meningitis?

A

focal neuro signs
seizures
VIII palsy
other signs of pneumococcal infection - CAP, ENT, endocarditis

221
Q

What indicators are associated with adverse outcomes in bacterial meningitis?

A 
pneumococcus
reduced GCS
CNS signs
older than 60
CN palsy
bleeding
222
Q

Describe the investigations for suspected meningitis

A

history and exam - throat and examine for cervical lymph nodes
blood cultures (PCR)
throat culture, viral gargle
FBC, UEs, LFTs, CRO
lumbar puncture 0 cell count, gram stain, culture and PCR
protein and glucose, viral PCR

223
Q

When to do a CT in suspected meningitis?

A 
CT to exclude mass session /effect, gross cerebral oedema
doesn't exclude RICp
CT before LP if 
GCS < 12
CNS signs
papilloedema
immunocompromised
seizure

ANTIBIOTICS PRE CT SCAN

224
Q

When is LP contraindicated in bacterial meningitis investigation?

A

brain shift, rapid GCS reduction, response/cardiac compromise, severe sepsis, rapidly evolving rash, infection at LP site, coagulopathy

225
Q

How should a possible bacterial meningitis be treated?

A

IV ceftriaxone 2 g 12 hourly
Add amoxicillin 2g 4 hourly if suspicion of listeria
Add dexamethasone if bacterial meningitis strongly suspected (10mg 6 hourly for 4 days)

226
Q

Describe the definitive antibiotic therapy for meningococcal meningits

A

IV ceftriaxone or benzyl penicillin

5-7 days

227
Q

Describe the definitive antibiotic therapy for pneumococcal meningitis

A

IV ceftriaxone or benzyl penicillin

14 days

228
Q

Describe the definitive antibiotic therapy for listeria meningitis

A

IV amoxicillin

21 days

229
Q

Describe special cases of bacterial meningitis

A

travel to sub-saharan africa and other high prevalence areas - ACWY recommended
asplenia, complement deficiency, Men boosters with men B and ACWY, HIB and pneumothorax
cochlear impants - pneumococcal booster

230
Q

Describe viral meningits

A 
usually only diagnosed after exclusion of BM
no confusion
enterovirus
HIV
mumps 
unidentifed 
supportive therapy 
aciclovir only in immunocompromised
231
Q

Describe viral encephalitis

A 
confusion, fever and seizures
HSV encephalitis - 
lymphocytic CSF, PCR
EEG - temporal lobe
MRI
that with aciclivir 2-3 weeks
232
Q

Describe intra-cerebral TB

A 
sub acute
often associated with other sites
may be unmasked during TB Rc
CN lesions usual (II,IV, VI, IX)
sample widely 
CSF may be normal
steroid
paradoxical worsening usual 
treat for one year 
steroids
233
Q

Describe HIV brain disease

A

consequence of unrecognised/untreated infection and marked immunodeficiency or life-style
encephalitis
dementia
neuro-syphilis
opportunistic (tuberculosis, cryptococcus, toxoplasmosis, JCV - progressive multi-focal leuco-encephalopayh

234
Q

Describe progressive multifocal leucoencephalopthhy

A 
progressive motor dysfunction
immunocompromsied 
HIV, anti-TNF, transplant
JC virus
no specific Rx
ARVs if HIV
may occur as part of immune reconstitution
235
Q

Describe intra-cerebral toxoplasmosis

A 
toxoplasma gonii
headache, seizures, focal CNS signs
immunocompromised
multiple enhancing ;lesions
IgG and IgM (blood) PCR (CSF)
Rx sulphadiazine + pyramethamine
restore immune function
236
Q

Describe cryptococcal meningits

A 
immunodeficiency 
SOL or meningo-encepahlitis
CSF - india ink, cryptococcal antigen
treatment with amphotericin B and flucytosone and fluconazole
raised IPC (shunt)
paradoxical worsening with ARVs in HIV

Phase 3 (15 decks)

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