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Y6 Senior Med COPY LaLz > Neuro > Flashcards

Neuro Flashcards

1
Q

Define TIA

A

Rapid onset Neurological deficit of vascular origin that resolves spontaneously within 24 hours

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2
Q

Define stroke

A

Rapid onset Neurological deficit of vascular origin that does not completely resolves within 24 hours

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3
Q

What are signs and symptoms of stroke and TIA

A

Vision loss, vertigo, dizziness
Dysarthria, dysphagia
paralysis
Nausea and vomiting

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4
Q

What are investigations for TIA / stroke

A

Bedside: ECG, capillary glucose
Bloods: FBC, U&E, lipids, venous glucose, clotting, cardiac enzymes, G&S
Imaging: CT Head, carotid doppler
Consider swallow assessment

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5
Q

What score can you use to estimate risk of stroke following TIA

A

ABCD2

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6
Q

How do you manage TIA

A

Immediately: aspirin 300mg (unlesss CI)
Review and assessment by specialist
Ongoing management: clopidogrel 75mg PO OD + statin 80mg
Consider carotid artery endarterectomy

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7
Q

What are the two maain causes of stroke and what is their likelyhood

A

ischaemic 80%
haemorrhagic 20%

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8
Q

What classification is used for stroke

A

Bamford classification

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9
Q

How do you manage a haemorrhagaic stroke

A

SAH: Nimodipine (CCB for 21 days) + coiling or surgical clipping

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10
Q

How do you manage an ischaemic stroke

A

AFTER EXCLUDING HAEMORRHAGE:
- Aspirin 300mg PO (PR if impaired swallow)
- Consider thrombolysis with tPA if:
- Age < 80 yrs and < 4.5 hours from start of symptoms
- Age > 80 yrs and < 3 hours from start of symptoms
-Consider thrombectomy <6 hours from start of symptoms

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11
Q

How do you differentiate between haemorrhagic and ischaemic stroke

A

CT head - look for visible haemorrhage

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12
Q

what causes a SAH

A

spontaneous or traumatic head injury
85% are associated with Berry aneurysm (saccular) - RF HTN, PKD, Connective tissue disease, HTN, smoking

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13
Q

What are sx of SAH

A

thunderclap headache across back
nausea and vomiting
photophobia
neck stiffness
reduced consciousness

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14
Q

Long term mx of ischaemic stroke

A

First 2 weeks: 300 mg Aspirin (PR if impaired swallow)

After 2 weeks: change to 75 mg CLOPIDOGREL + Statin (e.g. atorvastatin 80mg)
— or ASPIRIN 75mg + DIPYRIDAMOLE + STATIN

If AF: warfarin / apixaban + statin

Alongside with:
o BP control
o Feeding assessment (screen for safe swallow withni 24h, otherwise NG tube)
o Anticoagulants (e.g. apixaban or warfarin) if co-existing AF

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15
Q

What are core symptoms of Parkinsons

A

bradykinesia + stooped, shuffling gait
hypertonia (leadpipe rigidity, cogwheeling)
pill-rolling tremor (resting tremor)

+ hypomimic face,

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16
Q

What are ix for suspected PD

A

CT/MRI head to esclude vascular causes
DaTScan (= dopamine transporter scan)

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17
Q

What is the general approach to managing PD

A
  • MDT approach
  • Disability UPDRS (uniified PD rating scale)
  • Physiotherapy (postural exercised)
  • Depression screen
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18
Q

What are medications for PD management

A

LEVODOPA + dopa decarboxylase inhibitor e.g. CO-CARELDOPA

Otherwise: MAO-B inhibitors (e.g. seleginine) , DA agonists (pramipexole, ropinirole)

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19
Q

What is indication for levodopa

A

motor symptoms

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20
Q

What are siide effects of levodopa

A

DOPAMINE

Dyskinesia
On/off phenomena
Psychosis
Arterial BP low
Mouth dry
Insomniia
N&V
EDS

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21
Q

What are Parkinson PLUS syndromes?

A

Multiple Systems Atriiphy
Progressive Supranuclear Palsy
Corticobasilar Degeneration
Dementiia with Lewy Bodiea

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22
Q

Features of Multiple Systems Atrophy

A

Autonomic dysfunction (postural hypotension, bladder dysfunction)
Cerebellar ataxia
Rigidity, tremor

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23
Q

Features of Progressive supranuclear palsy

A

Vertical gaze palsy
postural instability &T falls
Speech disturbance
Dementia (forgetfulness, personality change)

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24
Q

Fts of Corticobasilar degeneration

A

Unilateral parkinsonism
Aphasia
Astereognosis (cortical sensory loss > alien limb phenomenon)

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25
Q

Demenita wiith lewy bodies fts

A

VISUAL HALLUCINATIONS
Fluctuing cognition
Demenita > parkinsonism

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26
Q

How do you differntiate Parkinsonism from PD?

A

Parkinsonism: symmetrical, rapid progression, poor response to levodopa
PD: asymmetrical, pprogressive, good response

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27
Q

What are the criteria for a diagnosis of epilepsy?

A

2 or more epileptic seizures

OR 1 seizure + epileptogenic markers (EEG or brain malformation)

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28
Q

What are signs of a tonic clonic seizure

A
  1. Behavioural arrest (stop writing and stop talking)
  2. Head and eyes turn to one side (the side they turn to is opposite to the side of the lesion)
  3. Stiffeniing (tonic)
  4. Shaking (clonic)
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29
Q

Ix for seizure

A

A>E (incl glucose)
ECG (cardiac cause)
MRI (structural cause)
once stabilised, discharge to first fit clinic

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30
Q

What is Alzheimers diisease

A

Most common form of dementia

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31
Q

WHat part of the brain does AD affect first

A

Hippocamppus

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32
Q

RF for AD

A

BIological:
- Age (1% at 60yo, doubles every 5 years)
- Genetics (although most gene mutations are sporadic)
- Head injury
- Vascular risk factors

Psychosocial:
- low IQ
-poor educational level

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33
Q

Four key pathophysiological elements of AD

A
  • Cortical atropy
  • plaque formation
  • neurofibrillary tangle fpormation
  • cholinerhgic loss
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34
Q

Four As in Alzheimers (features of middle progression of disease)

A

Amnesia
Aphasia (broca’’s - difficultuy finding the correct words)
Agnosia (usually visual - unable to recognie phases sso prosopagnosia)
Apraxia (unable tto complete skilled tasks such as dressing, despite normal motor function

+ mood change, abnormal behaviour, delusions and hallucinations

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35
Q

Management of AD

A

biosychosocial

BIO:
Anticholinesterases: aims to raise the ACh available
- donepezil
- galantamine
- rivastigmine
NMDA partial receptor agonist: Memantine

PSYCHOLOGICAL
structural group cognitive stimulation therapu

SOCIAL
explain diagnosis and signopost support
SINGLE CARE MANAGER
Every 6 month follow up
General: always wear ID, Dosset boxes, change gas to electricity, assistive technology around house.
Carers assessment etc

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36
Q

What must you do before giving anticholinesterases

A

ECG

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37
Q

side effects anticholinesterases

A

GI (N&V, diarrhoea, aanorexiia), fatigue, dizziness, headaches

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38
Q

Migraine tx

A

Acute: oral triptain + NSAID / paracetamol
Prophylaxis: topiramate / propanolol (only is >=2 attacks per month)

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39
Q

Mx cluster headache

A

Acute: 100% oxygen, SC triptain
Prophylaxis: verapamil

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40
Q

What is multiple sclerosis

A

autoimmune demyelinating disorder of CNS characterised by multiple plaques separate in time and place

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41
Q

Pathophys of MS

A

CD4 mediated destruction of oligodendrocytes > demyellination > neuronal death

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42
Q

Four types of MS

A

Relapsing remitting ( occasional flare causing worsening, otherwise stable)
Primary progressive (steady decline with no flares)
Secondary progressive (initial flares, then steady decline)
Progressive relapsing (steady decline with occasional flare)

MAARBURG VARIANT = very severe, very rapid

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43
Q

Symptoms of MS

A

Tingling
Eye (optic neuritis)
Ataxia (and other DANISH cerebellar signs)
Motor (spastic paresis)

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44
Q

What does optic neuritis present as

A

CRAP
Central scotoma
RAPD
Acuity drop
Pain on eye movement

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45
Q

What signs occur with MS

A

Lhemitte’s sgn (neck lflexion > electic shock in trunk and limbs)
Uhthoff0s sign (worsening of MS symptoms in increased temperatures)
Internuclear opthalmopledgia

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46
Q

What Ix are done with MS

A

Contrast MRI (gandolium enhanced, T2)
LP (IgG oligoclonal bands)
Blood antibodies
Evoked potnetials

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47
Q

What is acute and chronic management of MS

A

Acute attach: methylpred 1g IV/PO OD for 3 days
Chronic: DMARD (e.g. INF beta), biological (natalizumab) and SYMPTOMATIC MANAGEMENT

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48
Q

What meds can be given for symptomatic management of MS

A

Modafinil (fatigue)
SSRI (depression)
Amyltriptiline, gabapentine (pain)
Baclofen + gabapentine (spasticity)
oxybutynine ( urgency / freqwuency)
sildenafil (ED)
Clonazepam (tremor)

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49
Q

what blood antibodies would you find in MS

A

anti.MBP (myelin basic protein)
NMO-IgG (neuromyelitis optica)

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50
Q

what are good prognostic indicators in MS

A

female, young, sensory siigns at onsets, long interval in relapses, few MRI lesions

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51
Q

what are bad prognostic indicators in MS

A

male, older, motor signs at onset, short initerval in relapses, many MRI lesions, axonal loss

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52
Q

what is myasthenia graviis

A

autoimmune disorder characterised by insufficient functioning of acetylcoliine receptors

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53
Q

what is the most common antibody seen in MG

A

anti acetylcholine receptor antibody

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54
Q

what groups is MG most seen in

A

women:men=2:1
women typically in 20s, men in 60s

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55
Q

what are diseases associated with MG

A

thymic hyperplasia
thymoma
AI disease (PA. RhA, SLE)

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56
Q

what are signs and symptoms of MG

A

muscle fatiguabiliity - progressively weaker during periods of actvity and improviing after rest
- extraocular muscle weakness > diplopia, ptosis
- proximal myopathy (face, neck, limb girdle)
- dysphagia

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57
Q

what drugs exacerbate MG

A

penicillamines
lithium
phenytoin

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58
Q

What ix can you do for MG

A

single fibre EMG
repetitve nerve stimulation
serial pulmonary function tests
antibodies
TENSILON TEST

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59
Q

what iis management of MG

A

1st line symptomatic: long acting acetylcholinesterase inhibitors (pyridostigmine, neostigmine)

1sr line long term: immunupprssion (prednisolone, then azathioprinie)

final: thymectomy

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60
Q

what causes lambert eaton myasthenic syndrome

A

antibodies against presynaptic voltage gated calcium channel in peripheral nervous system

associated with SCLC, breast and ovarian canceer

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61
Q

what are symptoms of LEMS

A
  • limb girlde weakness (affects lower limbs first)
  • repeated muscle cpontractions may lead to increased muscle strngth
    hyporeflexia
    ANS sx
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62
Q

how do you manage LEMS

A

treat the cancer
immunosuppression with pred +- azathioprine

63
Q

what is MND

A

umbrella term for debilitating chronic progressive diseases affecting MN

64
Q

what are the four types of MND

A

Amylotrophic lateral sclerosis ALS
Primary lateral sclerosis
Progressive muscular atrophy
progressive bulbar palsu

65
Q

what area of neuro system does ALS affect

A

corticospinal tracts

66
Q

what are signs of ALS

A

mixed UMN and LMN
- inspection: wasting and fasciculations (incl tongue)
- tone: spastic
- power: weak
- reflexes: absent, +ve babinski
normal sensation!

67
Q

what is MND management

A

MDT managhement (neurologist, physio, OT; dietician, GP, specialist nurse)

Meds:
- Riluzole (extends life by 3 months)
- SUPPORTIVE MX

68
Q

what supportive MX can you consider for MND

A

Drooling - amyltriptiiiline, glycopyrolate
muscle cramps - quinine
spasticity - baclofen, botulinum
pain mx
NIV for respiratory failuyre
NG tube or PEG for dysphagia

69
Q

HOW MUCH time off do bus drivers need to take followoing a seizure

A

10 years

70
Q

how mych time off do you need to take following first / isolated seizure

A

6 months off if clear brain imaging, otherwise 1 year

71
Q

how much time off if established epilepsy with multiple seizures

A

1 year off

72
Q

left sided nystagmys means lesion is whre?

A

LEFT CEREBELLUM

73
Q

what side do signs of a cerebellar lesiono present?

A

IPSILATERAL

74
Q

is bacterial or viral meningitis moree common?

A

BACTERIAL men is more common!!

75
Q

whaat is internuclear opthamoplegia due to

A

lesion in the medial longitudinal fasciculus in brainstem
whichh conncts CN6 to CN3 and 4

76
Q

how does internuclear opthamoplegia pressent

A

weak adduction of IPSILATERAL eye
nystagmus of contralateral eye

77
Q

what can caus internuclear opthamoplegia

A

MS
stroke

78
Q

what is vertigo

A

sensation of movment between person and enviroonment

79
Q

what is vertigo due to

A

sensory input mismatch (due to failure of vestibular system)

80
Q

what territory is affected in facial weakness with forehead sparing on the left side?

A

Right (contralateral) MIDDLE CEREBRAL ARTERY stroke

81
Q

what is a high stepping gait due to

A

LMN lesion (peripheral nerve lesion causing FOOT DROP)

82
Q

what does high stepping / neuropathic gait look like

A

patient takes HIGH STEPS to bypass their foot drop

83
Q

What is a STOMPING GAIT due to

A

sensory neuropathy (defect in proprioception)

84
Q

what does a STOMPING GAIT look like

A

Patient takes HIGH STOMPING STEPS
to maximise their proprioception

85
Q

What is an antalgic gait due to

A

due to pain on affected side

86
Q

what does an ANTALGIC GAIT look like

A

limping
stance phase is relatively shorter than swing phase

87
Q

what is a HEMIPLEGIC gait due to

A

STROKE or other UMN lesion

88
Q

how does HEMIPLEGIC gait present

A

FLEXION HYPERTONIA in UL (flexed arms and wrist)
EXTENSOR HYPERTONIA in LL (circumduction of leg)

spasticity
distal weakness, central power retained > foot drop

89
Q

why does hemiplegic patient have leg circumduction

A

due to EXTENSOR HYPERTONIA in LL and the foot drop

90
Q

what is a diplegic gait due to

A

Cerebral palsy

91
Q

Describe diplegic gait

A

tiptoe walking
foot adduction

92
Q

what is another name for a waddling gait

A

trendlenburg gait

93
Q

what is a waddling gait due to

A

defective hip abductor medhanisms (superior gluteal nerve damage / muscle abscess or inflammation, radiculopathy)

94
Q

describe waddling gait

A

sound side sags – patient leans away from side of lesion as they walk

95
Q

what is an ataxic gait also known as

A

cerebellar gait

96
Q

what occurs in ataxic / cerebellar gait?

A

broad stance
wide staggering steps
sways at rest (titubatin)
sways towards side of lesion

97
Q

explain the vestibular system

A

Semicircular canals contain endolymph fluid
With movement, the endolymph fluid moves around on the stereocilia (which detect the movement)
the vestibular nerve then takes these inputs into the cerebellum

98
Q

What is the anatomical categories of conditions you can divide vertigo into

A

PERIPHERAL (vestibular system / vestibular nerve)

CENTRAL (cerebellum)

99
Q

what are vestibular system causes of vertigo? list

A
  • BPPV
  • Menieres
  • vestibular neuritis
100
Q

What occurs in BPPV

A

cristals displace into semicircular canals > move with head movement > provoke NYSTAGMUS (accelerating towards affected side) and VERTIGO

101
Q

what is classic BPPV presentation

A

positional vertigo
provoked by head movement
very brief (lasts seconds to minutes)
Hallpike maneuvre confirms it

102
Q

What maneuvre confirms BPPV

A

Hallpike maneuvre

103
Q

what maneuvre resolves BPPV

A

Epley maneuvre

104
Q

What is pathophysiology of menieres

A

excess endolymph in canal

105
Q

whar are 3 key symptoms of menieres

A

recurrent vertigo (starts spontaneously, stops after few hours)
unilateral tintinnus
unilateral sensorineural hearing loss

106
Q

how do you manage meniere’s diease

A

histamines, benzos
intratympanic gentamycin (via grommet) if recurrent

107
Q

what is vestibular neuritis

A

inflammation of vestibular nerve due to viral infection
lasts for weeks

108
Q

how doess vestibular neuritis present

A

spontaneouss onset vertigo
constant
worsened by head movement
balance affected, risk of falls

109
Q

what is illness course of vestibular neuritis

A

self resolves within weks

110
Q

how do you maage vestibular neuritis

A

usually self resolving
may need to give chlorperazinr / cyclizine if nausea

111
Q

what is GBS

A

Ascending polyneuropathy (radiculopathy) caused by demyelination post-infection / vaccine

112
Q

How long before GBS and what infections precede it

A

HHV, HIV, campylobacter
1-3 weeks

113
Q

What are sx of GBS

A

Progressive ASCENDING symmetrical limb weakness (lower then upper)
Progressive ASCENDING parasthesia
for 4 weeks, then recovery
in extreme cases; CN may be involved (dysarthhia, dysphagia, facial weakness)
Resp muscle involvement ( T2RF)

114
Q

signs of GBS

A

LMN ascending signs
flaccid paralysis
areflexia
lack of sensation

115
Q

ix of GBS

A

Bloods (incl anti ganglioside antibodies)
CT > LP (high protein)
MRI spine
NERVE CONDUCTION STUDIES (reduced velocity)
EMG

116
Q

how do you manage GBS

A

admit for surveillance
support body cortical functions and ventilation if necessary

117
Q

what are signs of a cerebellar lesion

A

DANISH D
Dysdiadocokinesia
Ataxia
Nystagmus
Intention tremor
Staccato speech
Hypotonia

Dysmetria

118
Q

How are the cerebellar vs vestibular causes of nystagmus?

A

Cerebellar = Closee
- fast phase towards lesion
- maximal looking towards lesion

Vestibular cause (v= far away)
- fast phase AWAY from lesion
- Maximal looking away froom lesion

119
Q

what are the MOTOR SX CLASS in MS?

A

UPPER MOTOR NEURON ONLY

120
Q

what are the types of stroke according to Bamford

A

TACS - total anterior crc
PACS - partial anterior circ
POCS - poosterior circ stroke
LACS - lacunar anterior circ stroke

121
Q

what is TACS

A

hemiparesis + hemisensory deficit
homonymous hemianopia
hgher cortical dysfunctiono (dysphagia, neglect, apraxia)

122
Q

what is PACS

A

2/3 TACS

123
Q

what is POCS

A

any of:
- cerebellar syndrome
- brainstem stroke
- homonymous hemianopia

124
Q

what is brainstem stroke

A

locked in

125
Q

what is Lacunar stroke

A

pure motor / pure sensory / mixed sensorymotosr / dysarthraia / clumsy hand / ataxic hemiparesis

126
Q

when do you do thrombolysis AND thrombectomy in stroke?

A

when they present <4.5 hours from onset with OCCLUDED PROXIMAL ANTERIOR CIRC

127
Q

what is imaging of choice for MS lesions

A

MRI with CONTRAST

128
Q

How does a frontal lobe seizure present

A

JACKSONIAN march

129
Q

How does a temporal lobe sseizure present

A

aura
lip smacking
clothes pucking

130
Q

How does a occipital lobe seizure present

A

visual changes

131
Q

How does a prietal lobe seizure present

A

sensory defect

132
Q

side effects of valproatw

A

VALPROATE

Vomiting and naussea
Anorexia
Liver failure
Pancreatitis
Retention on weight
Oedema
Alopeca
Teratogenicity and tremors
Enzyme inhib

133
Q

what is the progressison of AD

A

EARLY: failing memory, wandering, irritability
MIDDLE: four As
LATE: fully dependent, incontinent, primitive reflexes, EPSE

134
Q

what is prosopagnosia

A

inabiity to recognise faces
typically occurs in AD

135
Q

How does a tension headache present

A

bilateral headache, like a tight band

136
Q

how do you mx a tension headache

A

aspirin
paracetamol
NSAID

137
Q

How does a migraine present

A

unilateral, throbbing, severe headache
lasts 4-72 hours
may be precded by aura
better in dark and quiet

138
Q

when do you give migraine prophylaxis

A

if 2 or more attacks per month

139
Q

what do you give for migraine prophylaxs

A

Topiramate (NOT if childbearing age)
Propanolol

140
Q

What do you givee for migraine mx

A

oral triptan + NSAID/paracetamol

141
Q

how does a cluster headache present

A

intense pain around the eye
watering eye
occurs repeatedly (e.g. every day for 3 months

142
Q

how do you manage cluster headache acutely

A

0xygen + SC triptan

143
Q

how does temporal arteritiss prsent

A

headache
jaw claudication
tender scalp

144
Q

how do you manage temporal arteitis

A

prednsolone

145
Q

list 4 cause of non-dangerous headachr

A

tension headache
Clusster headache
migrainee
medication overuse

146
Q

what kinds of signs can occur with MS

A

UMN
sensory
cerebellar

NEVER LMN

147
Q

trigger for MS

A

EBV exposure
Northern countries
Low vit D

148
Q

what is RAPD

A

Relative affeerent puipillary defect
pupil is more constricted when light is shone in contralateral eye compared to directly in it

149
Q

where is the lesion in RAPD

A

in the optic nerve

150
Q

what chromosome is NF1

A

chr 17

151
Q

waht chromosome is NF2

A

Ch22

152
Q

susmmarise NF1

A
  • neurofibromas (neurocutaneeous)
  • cafe au lait spots (>5, >15mm)
  • Lisch nodules on iris (hamartomas)

frecking on skin folds
scoliosi s
intellectual disability

153
Q

summarise NF2

A

bilateral vestibular schwannomas
meningioma
glioma

thereby presents with:
- sensorineural hearing loss
- tintinnus
- imbalance
- headache
- facial weakness

Y6 Senior Med COPY LaLz (29 decks)

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