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Medicine > Neurology > Flashcards

Neurology Flashcards

1
Q

First-line for migraine

A

Oral triptan with NSAID (taken during headache, not aura)

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2
Q

First-line prophylaxis for migraine

A

Propranolol or topiramate [teratogenic]

Second-line: gabapentin

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3
Q

Emergency mx of TIA in primary care

A

Consider 300 mg aspirin (unless known bleeding disorder, anticoagulated, already taking regular low-dose aspirin)

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4
Q

Long-term medical management TIA

A

300 mg aspirin initially (if not contraindicated)
75 mg clopi
80 mg atorvastatin
Control hypertension: ACEi + diuretic

Inform DVLA

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5
Q

Red flags for head injury

A 
High risk mechanism of injury
Reduced GCS
LOC
Retrograde amnesia (>30 mins)
Post-traumatic amnesia (> 5 mins)
post-traumatic seizures
focal neurology
Vomiting (twice or more)
Persistent headache not relieved by simple analgesia
Coagulopathy/ taking anticoags
New or ongoing sx

> 65, alcoholism

Consider NAI

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6
Q

Warning patients about concussion following head injury

A

Dizziness, headaches, poor concentration, visual disturbance

Responsible adult must also be given info (and stay for 24h)

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7
Q

Pain relief for uncomplicated head injury

A

Not opiates in case need to check pupil size

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8
Q

Describe seizure in layman terms

A

A seizure is caused by a disruption of the electrical activity in the brain

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9
Q

Red flags for LOC

A

Focal neurology, first seizure

TIA, HF

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10
Q

When can LOC be diagnosed as faint?

A

No evidence of alternative diagnosis and 3 Ps:
Posture
Provoking factor
Prodromal sxE

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11
Q

Emergency mx temporal arteritis

A

60 mg pred stat

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12
Q

main causes of death due to head trauma

A

traffic collision and alcohol

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13
Q

PRIMARY vs SECONDARY BRAIN INJURY

A

P: direct irreversible damage
S: within hours/ days - hypoxia, ischaemia, infections etc

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14
Q

Head injury and GCS bands

A

13-15: mild injury
9-12: moderate
3-8: severe

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15
Q

COUP vs CONTRECOUP LESIONS

A

at point of impact vs opp side (may be more extensive/ severe)

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16
Q

vessels affected by extradural haemorrhage

A

middle meningeal

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17
Q

presentation of extradural

A

brief LOC, lucid period of minutes/ hours

followed by rapid loss of consciousness

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18
Q

vessels affected in subdural haeorrhage

A

bridging veins passing between cerebral cortex and dural venous sinuses

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19
Q

Cushing’s response

A

Raised ICP, leading to
Arterial HTN
Bradycardia

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20
Q

Buying time when raised ICP

A

Hyperventilation reduces arterial CO2 –> cerebral vasoconstriction –> reduces intracranial blood volume

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21
Q

When is post-traumatic epilepsy considered ‘early’ or ‘late’

A

early within first week

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22
Q

CONCUSSION

A

Head injury sufficient to cause LOC

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23
Q

What is ischaemic penumbra

A

area is damaged but viable if bloodflow restored

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24
Q

Definition TIA

A

Full recovery within 24h

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25
Q

Amaurosis fugax is caused by TIA in which territory

A

carotid territory

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26
Q

what % strokes are ischaemic?

A

85%

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27
Q

Prior to limbs becoming spastic instroke what are they like?

A

Flaccid, fall like dead weights when dropped

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28
Q

Posterior circulation infarcts may cause ‘crossed syndrome’. What is this?

A

Ipsilat cranial nerve deficit

Contralat limb deficit

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29
Q

What are lacunar infarcts?

A

Basal ganglia, internal capsule, thalamus, pons

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30
Q

What is ABCD score for?

A

People with TIA who may go on to have stroke

If +4, give 300 mg aspirin

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31
Q

What usually causes SAH?

A

Bleeding from berry aneurysm in circle of willis

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32
Q

Relevance of family history in SAH

A

x3-7 compared to general population if first-degree relative

Second degree: no link

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33
Q

How relevant is sudden explosive headache in diagnosing SAH?

A

10% will have SAH

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34
Q

When do sentinel bleeds tend to occur?

A

~3 weeks before SAH

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35
Q

What Ix for SAH?

A

CT scanning
CT angio
LP (after 12h)

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36
Q

Why is nimodipine given in SAH?

A

CCB to avoid vasospasm - affects 1/3 pts and can lead to ischaemic brain injury

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37
Q

Triad: normal pressure hydrocephalus

A

dementia, gait disturbance, incontinence

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38
Q

Communicating vs non-communicating hydrocephalus

A

non-comm = obstructive (congenital or acquired blockage)

comm = reduced absorption, increased production etc.

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39
Q

What is hydrocephalus?

A

increased CSF

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40
Q

Causes of focal damage affecting cerebral function

A

vascular events, tumours, trauma, localised inflammatory lesion (abscess, tuberculoma)

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41
Q

Causes of generalised or multi-focal damage

A

degenerative disease, multi-focal infarcts, demyelination, diffuse infection (meningitis, encephalitis)

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42
Q

Definition of dominant side

A

Controls writing and speech

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43
Q

In how many is the L side dominant

A

90% R-handers

60% L-handers

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44
Q

Where is the primary motor cortex? What does it contain?

A

Precentral gyrus in frontal lobe

Umns organised in homonculus - contralateral

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45
Q

Name of cortices co-ordinating and planning complex movements. Location

A

Supplementary motor and premotor cortices (frontal): co-ordinating and planning complex movements

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46
Q

Which part of cortex sorts eye movements?

A

Frontal eye fields (contralateral side)

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47
Q

Where is Broca’s area - what does it control?

A

dominant side frontal lobe

motor/ ‘expressive’ speech

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48
Q

What does the pre-frontal cortex control?

A

personality, emotion, planning

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49
Q

Blood supply of frontal lobe

A

ACA: medial surface, i.e. leg
mca: lateral surface, i.e. face and arm

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50
Q

Which lobe is cortical micturation centre

A

frontal lobe

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51
Q

Pathology of frontal lobe

A 
Frontal seizures
Contralateral weakness/ gait apraxia
Conjugate eye deviation (towards lesion)
Expressive dysphasia (has insight)
Personality change
Primitive reflexes
Incontinence
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52
Q

What is located in the parietal lobe?

A 
Primary somatosensory cortex (postcentral gyrus, contralateral)
Language (dominant side): arcuate fasciculus connecting Broca's + Wernicke's
Calculations (also dominant)
Integration of somatosensory, visual + auditory info (non-dominant)
Visual pathways (pass deep within parietal lobe)
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53
Q

Blood supply of parietal lobe

A

mCA

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54
Q

Name if one limb lost motor control. If half of body.

A

monoparesis/ hemiparesis

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55
Q

Pathology if dominant parietal lobe affected

A

Wernicke’s receptive dysphasia (neologisms, paraphrasia, poor insight)
Dyscalculia, dysgraphia
Inability to distinguish R + L sides of body

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56
Q

Pathology if non-dominant parietal lobe affected

A

Contralateral sensory inattention

problems following sequences etc.

57
Q

Pathology if parietal lobe affected (both lobes affected in these ways)

A

Cortical contralateral sensory loss (doesnt impair sensation, just ability to make sensory judgements)

If deep, contralateral homonymous inferior quadrantanopia

58
Q

Where is Wernicke’s area?

A

Dominant temporal lobe

59
Q

Blood supply of temporal lobe

A

MCA (lateral lobe)

PCA (medial lobe)

60
Q

Where are the auditory and vestibular cortices?

A

temporal
Dominant: comprehension of spoken word
non-dom: sounds/ music

61
Q

A stroke of which vessel may cause global dysphasia

A

L MCA

62
Q

Pathology when temporal lobe affected

A

Wernicke’s dysphasia
Auditory agnosia
Cortical deafness
Memory impairment (hippocampus and parahippocampal gyrus)
Visual disturbance: contralateral superior homonymous quadrantanopia

63
Q

Blood supply of occipital lobe

A

PCA

except occipital poles (serving macular vision - they’re MCA)

64
Q

Triad of Korsakoff’s. Cause. Type of amnesia

A

Memory loss, ataxia, nystagmus
thiamine deficiency secondary to chronic alcoholism
dense retrograde amnesia and confabulations

65
Q

What is syringomyelia? How does it present?

A

Central canal becomes enlarged, compressing adjacent nerves

spinothalamic can be selectively lost, causing temp/ pain loss in upper limbs (cape pattern)

66
Q

what commonly causes subacute combined degeneration of spinal cord? how does it usually present? how treated?
why called combined?

A 
B12 deficiency
falls at night (sensory ataxia with impaired vision)
treated with B12!
Dorsal columns: sensory ataxia and LMN
Corticospinal: UMN
67
Q

Which pathways predominantly affected in tabes dorsalis?

A

Dorsal columns (sensory ataxia/ high-stepping gait)

68
Q

What is Friedrach’s ataxia? how is it inherited?

A

autosomal recessive
degen of many nerve tracts
cerebellar signs
begins in childhood

69
Q

what is clasp-knife rigidity

A

increased tone where there is initial resistance followed by relaxation

70
Q

what is pyramidal weakness

A

UMN sign

weakness of extensors of upper limb, flexors of lower limb

71
Q

parkinsonism triad

A

akinesia
rigidity
dyskinesias

(if unilat lesion these will be contralateral)
[Huntington’s on other side of spectrum where selective death in striatum causes hyperkinesia)

72
Q

which IV disc most commonly affected by sciatica

A

L5/S1

73
Q

which nerve compressed in meralgia paraesthetica

A

lateral cutaneous nerve

74
Q

what causes diabetic ulcers?

A

neuropathy can prevent adequate redistribution of blood to the ulcer, lack of sweating render skin dry/ cracked

75
Q

What causes myaesthenia gravis?

A

Binding of autoantibodies to components of NMJ, most commonly the acetylcholine receptor

76
Q

What is Lambert-Eaton associated with?

A

small cell cancer

77
Q

What is GBS? How is it characterised?

A

disorder causing demyelination and axonal degeneration resulting in acute, ASCENDING, progressive neuropathy

weakness, paraesthesiae, hyporeflexia

usually reaches maximum at 2 weeks, stops progressing after 5 weeks

78
Q

What usually precedes GBS?

A

Infection of respiratory/ GI tract

79
Q

Mx GBS

A

plasma exchange
IV Ig
CS

80
Q

What does normal conscious state depend on (light bulb analogy)

A

Brainstem RAS

both cerebral hemispheres

81
Q

Define syncope.

General causes.

A

Global reduction in blood flow to brain

Vasovagal syncope
Situational syncope
Postural hypotension
Syncope due to cardiac dysfunction
Carotid artery disease
82
Q

Why do people collapse in vasovagal?

A

VASO: peripheral vasodilatation leads to low BP

83
Q

What is convulsive syncope?

A

if persists –> cerebral hypoxia

eyes roll up, brief myoclonic jerks

usually: sphincter control maintained, no postictal state (maybe malaise)

84
Q

What combination of things causes micturition syncope

A

vasodilatation (from emptying bladder)
postural hypotension
bradycardia

85
Q

how to investigate carotid sinus disease

A

carotid sinus massage on ECG

86
Q

Sign of carotid sinus disease

A

carotid bruit

87
Q

DVLA and LOC

A

must inform (unless vaso-vagal with clear precipitant)

cardiovasc causes: 4 weeks after treatment
otherwise: 6 months

88
Q

NARCOLEPSY vs CATAPLEXY

A

excessive sleepiness vs drop attacks (brought on by excitement/ emotion)

89
Q

STATUS EPILEPTICUS

A

continued or recurrent seizures with failure to regain consciousness over 30 mins

90
Q

what causes incidence of grand mal seizures to rise in 50s-60s?

A

subcortical ischaemic changes secondary to HTN

91
Q

New classification of focal-onset seizures

A

focal impaired awareness seizure

focal aware seizure

92
Q

how to tell focal to bilat tonic-clonic vs generalised-onset

A

asymmetry consistent in first

in generalised, lateralisation not consistent from seizure to seizure

93
Q

AEDs for generalised epilepsy

A

sodium valproate

lamotrigine

94
Q

AEDs for focal epilepsy

A

carbamazepine, lamotrigine

95
Q

what elicits lhermitte’s phenomenon

A

neck flexion

cervical cord demyelination

96
Q

Types of MS

A

Relapsing-remitting

Secondary progressive (just get worse, many R-R convert to this)

Primary progressive (declines from beginning)

97
Q

imaging to show MS

A

T2-weighted MRI scan

98
Q

meds for muscular stiffness

A

baclofen

99
Q

what is an intention tremor

A

increases during movement

100
Q

alcohol helps what kind of tremor

A

essential tremor

101
Q

thiamine is which vitamin

A

B1

102
Q

What kind of meningitis may occur in those with splenectomy/ SCD?

A

encapsulated organisms

103
Q

Which microorganism causes outbreaks of meningitis at unis?

A

N.meningitidis

104
Q

What organisms cause meningitis in adults?

A

S.pneumoniae
H.influenzae
N.meningitidis
Staph, strep etc

105
Q

What organisms cause meningitis in HAI or post-trauma?

A

E.coli
Klebsiella
Pseudomonas aeruginosa
Staph aureus

may be multi-drug resistant

106
Q

What causes of meningitis may be seen is immunocompromised?

A

syphilis, TB

107
Q

Causes of aseptic meningitis

A 
Partly-treated bacterial meningitis
Viral
Fungal
Parasites
Kawasaki disease
108
Q

Causes of non-infective meningitis

A

Malignant cells (leukaemia, lymphoma, others)
Sarcoid
SLE
Behcets

109
Q

Ix for meningitis

A 
FBC
CRP
Coagulation screen
Blood culture
Gases
Glucose

Often others like CXR, cultures for urine, nasal swabs, stool etc

110
Q

Rules for giving benzylpenicillin in community

A

If septicaemia

If will take a while to get to hospital

IM or IV

111
Q

What treatment may close contacts of acute bacterial men receive?

A

Prophylactic abx

112
Q

What sort of neurological complaints are seen in coeliac disease?

A

10% have ataxias, neuropathies

113
Q

What sort of neurological complaints are seen in IBD?

A

small % demyelinating peripheral neuropathy

114
Q

Adults needing CT within 1 hour following head injury

A

GCS less than 13 on initial assessment in the emergency department.

GCS less than 15 at 2 hours after the injury on assessment in the emergency department.

Suspected open or depressed skull fracture.

Any sign of basal skull fracture (haemotympanum, ‘panda’ eyes, cerebrospinal fluid leakage from the ear or nose, Battle’s sign).

Post-traumatic seizure.

Focal neurological deficit.

More than 1 episode of vomiting.

115
Q

Holmes-Adie pupil

A

normal varient
young woman
large irreg pupil, slow and incomplete constriction to light
absent ipsilateral deep tendon reflexes

sometimes problem w/ efferent parasympathetic

116
Q

Argyll Robertson pupil

A

neurosyphilis
Dm
ms

miosis, irreg pupil, absent light reflex, intact accommodation

117
Q

where do spinal nerves pass?

A

C1-7 above vertebrae, then below

118
Q

what do the dorsal columns carry?

A

touch, pressure, vibration, proprioception

119
Q

what do the spinothalamic tracts carry?

A

temp, pain - lateral tracts

crude touch, pressure - anterior tracts

120
Q

can there be muscle weakness in umn lesion?

A

pyramidal weakness

121
Q

which cranial nerves carry info on taste?

A

facial - first two-thirds

glossopharyngeal - posterior 1/3

122
Q

how to detect RAPD

A

shine light in unaffected eye: both constrict

in affected eye: constrict to a lesser degree

123
Q

how may posterior communicating artery aneurysm present?

A

third nerve palsy

124
Q

how does third nerve palsy appear?

A

looking down and out

fixed dilated pupil

125
Q

which nerve affected shows trouble down the stairs?

A

CN IV

126
Q

nerve most commonly affected in head injury?

A

abducens

commonly affected by raised ICP too

127
Q

causes of sixth nerve palsy

A

microvascular disease

external compression from acoustic neuroma, raised ICP

128
Q

how to spot sixth nerve palsy

A

drifts towards midline when asked to look forward

129
Q

acute mx cluster headache

A

oxygen + triptan

130
Q

prophylaxis cluster headache

A

verapimil

131
Q

mx trigeminal neuralgia

A

carbamezapine

132
Q

what is encephalitis?

A

inflammation of the brain parenchyma

133
Q

triad of encephalitis

A

fever
headache
altered mental status

134
Q

most common cause of encephalitis

A

HSV-1

135
Q

mx acute relapes ms

A

oral pred or IV methylprednisolone

doesnt alter prognosis

136
Q

spondylosis vs spondylolisthesis

A

spondylosis: age-related degeneration of spinal cord (commonly OA)
spondylolisthesis: anterior pr posterior displacement of vertebra (not disc)

137
Q

triad of parkinsons

A

bradykinesia, resting tremor, rigidity

138
Q

painful third nerve palsy

A

PCA aneurysm rupture

139
Q

3rd nerve palsy with pupillary sparing

A

stroke

Medicine (30 decks)

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