Neuro Flashcards

1
Q

name some of the symptoms that the term dementia describes

A

memory loss
difficulties with thinking, problem solving or language
change in mood or behaviour

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2
Q

what is the most common cause of dementia?

A

Alzeimer’s disease

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3
Q

name some functions of the frontal lobe

A

voluntary & planned motor behaviours
motor speech area [broca’s]
personality
planning

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4
Q

what is the presentation of a subarachnoid haemorrhage?

A

headache which reaches max intensity within seconds of onset

described as worst ever

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5
Q

what symptoms and signs suggest meningeal irritation?

A

neck stiffness

positive Kernig’s sign

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6
Q

how might giant cell arteritis present & in which epidemiological group?

A

headache with generalized aches and pains

in the elderly

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7
Q

what urgent treatment is required for giant cell arteritis and why?

A

steroids

prevent blindness

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8
Q

indications for brain imaging in patients with headache

A
sudden onset
new headache in patient >50
headache that changes w/posture, coughing [^ICP]
cancer history
HIV history
fever
abnormal neurological signs
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9
Q

causes of acute severe headache [onset in mins/hrs]

A
intracranial haemorrhage
cerebral venous thrombosis
carotid/vertebrobasilar dissection
meningitis
head injury
migraine
drugs
alcohol
infection e.g. malaria
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10
Q

vasovagal syncope occurs as a result of..?

A

reflex bradycardia

peripheral & splanchnic vasodilatation

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11
Q

effort syncope on exercise may occur in patients with..

A

aortic stenosis

hypertrophic cardiomyopathy

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12
Q

where does the upper motor neurone of the corticospinal tract originate and terminate?

A

motor cortex

motor nuclei of cranial nerves & ant. spinal horn cells

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13
Q

where do corticospinal pathways decussate?

A

pyramids of the medulla

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14
Q

an upper motor neurone lesion shows signs on same or opposite side?

A

opposite

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15
Q

a lower motor neurone lesion shows signs on same or opposite side?

A

same side

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16
Q

fasciculation occurs with upper or lower motor neurone lesions?

A

lower

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17
Q

what kinds of motor neurone lesions present with wasting?

A

lower

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18
Q

what kinds of motor neurone lesions present with spasticity +/- clonus?

A

upper motor neurone lesions

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19
Q

what kinds of motor neurone lesions present with hypotonia?

A

lower

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20
Q

how does weakness present in upper motor neurone lesions?

A

weakness in extensors of arms

& flexors of legs

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21
Q

what is fasciculation?

A

visible contraction of single motor units, appears as a twitch

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22
Q

how do upper and lower motor neurone lesions tend to affect tendon reflexes?

A

upper: exaggerated tendon reflexes
lower: loss of tendon reflexes

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23
Q

what is paraparesis?

A

weak legs

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24
Q

what is hemiparesis?

A

weakness of limbs on one side

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25
Q

hemiparesis is usually caused by a lesion where?

A

within the brain or brainstem

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26
Q

paraparesis is most often due to a lesion where?

A

in the spinal cord below T1

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27
Q

what is tetraparesis?

A

weakness of arms and legs

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28
Q

tetraparesis indicates damage where?

A

high cervical cord damage

[most commonly from trauma]

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29
Q

describe the pathway of the lower motor neurone

A

from anterior horn cell or cranial nerve
via peripheral nerve
to motor endplate

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30
Q

what signs are seen below, at the level of, and above a cord lesion?

A

UMN signs below lesion
LMN signs @ level of lesion
unaffected muscles above lesion

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31
Q

how does the presentation of muscle disease differ from a lower motor neurone lesion?

A

in muscle disease, reflexes are usually preserved

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32
Q

LMN lesions are most commonly caused by lesions in which 3 areas?

A

anterior horn cell lesions
spinal root lesions
peripheral nerve lesions

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33
Q

what is the most common disease of the neuromuscular junction?

A

myasthenia gravis

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34
Q

how does myasthenia gravis typically present in terms of weakness & wasting?

A

weakness of skeletal muscle

rarely wasting

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35
Q

give an example of a plasma muscle enzyme which when elevated is highly suggestive of muscle disease

A

creatine kinase

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36
Q

diseases that cause anterior horn cell lesions

A

motor neurone disease

poliomyelitis

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37
Q

diseases that cause spinal root lesions

A

cervical and lumbar disc lesions

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38
Q

causes of peripheral nerve lesions

A

trauma
compression
polyneuropathy

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39
Q

describe the path of sensory peripheral nerves

A
nerve endings
dorsal root ganglia
cord
thalamus
cerebral cortex
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40
Q

posterior columns carry sensory modalities for what?

A

vibration, proprioception, 2-point discrimination, light touch

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41
Q

where does the dorsal column decussate?

A

medulla

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42
Q

the spinothalamic tract conveys which senses?

A

pain
temp
crude touch

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43
Q

where does the spinothalamic tract decussate?

A

anterior white commissure

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44
Q

which fibres of the corticospinal tract decussate [75-90%] at the medullary pyramids and which do not?

A

limb decussate

axial don’t

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45
Q

where do the axial fibres of the corticospinal tract decussate?

A

anterior white commissure in spinal cord

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46
Q

what are the principal symptoms of lesions in the sensory pathways below thalamus level?

A

paraesthesia [pins & needles]
numbness
pain

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47
Q

where are symptoms of a sensory spinal root lesion felt?

A

symptoms are referred to the dermatome supplied by that root

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48
Q

lesion in spinothalamic tract in brainstem or spinal cord results in loss of pain-temp sensation below the lesion contra/ipsilaterally?

A

contralaterally

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49
Q

lesion in dorsal column of spinal cord results in loss of propprioception etc. below the lesion contra/ipsilaterally?

A

ipsilaterally

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50
Q

loss of pain/temp sensation in right leg & loss of proprioception in left leg suggests a lesion where?

A

spinal cord

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51
Q

describe sensory loss following pontine lesion

A

loss of all forms of sensation on opposite side to lesion

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52
Q

drugs that block dopamine receptors and may induce parkinsonian syndrome

A

reserpine [antipsychotic, antihypertensive]
phenothiazines [antipsychotic]
butyrophenones [antipsychotic]

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53
Q

diseases that can cause resting tremor

A

Parkinson’s
parkinsonism
Wilson’s

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54
Q

intention tremor suggests disease of which part of the brain?

A

cerebellum

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55
Q

causes of cerebellar lesions

A
MS
space-occupying [tumour, abscess]
haemorrhage
chronic alcohol use
antiepileptic drugs
paraneoplastic syndrome
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56
Q

causes of papilloedema [optic disc oedema]

A

^ICP
retinal vein obstruction [thrombosis/compression]
optic neuritis
accelerated hypertension

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57
Q

3 branches of the trigeminal nerve

A

opthalmic
maxillary
mandibular

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58
Q

anticonvulsant drug used to suppress attacks of trigeminal neuralgia

A

carbamazepine

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59
Q

damage to the facial nerve in the temporal bone may be associated with what symptoms?

A

undue sensitivity to sounds

loss of taste to ant. 2/3rds of tongue

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60
Q

what structure extending from brainstem to thalamus influences the state of arousal/wakefulness?

A

central reticular formation

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61
Q

what does the AVPU score stand for [rapid assessment of unstable patient

A

Alert
responds to Voice
responds to Pain
Unresponsive

62
Q

brain death means irreversible loss of which 2 capacities?

A

capacity for consciousness

capacity to breathe

63
Q

define stroke

A

rapid onset of neurological deficit
result of vascular lesion
associated w/ infarct of CNS tissue

64
Q

define polycythaemia

A

^ haemoglobin in the blood

[^RBCs or decreased plasma vol]

65
Q

which heart condition increases risk of embolic stroke?

A

AF

66
Q

treatment for TIA

A

aspirin [immediately and continued long term]
dipyridamole
(clopidogrel if aspirin intolerant)

67
Q

what does dipyridamole do?

A

vasodilatation

reduce platelet aggregation

68
Q

Tx for TIA pateints with AF, valvular lesions or DCM

A

long-term warfarin

69
Q

the most common stroke is caused by occlusion of which cerebral artery and infarction of which structure?

A

middle cerebral

internal capsule

70
Q

what are lacunar infarcts

and where do they occur?

A

small infarcts that produce local deficits
e.g. pure motor stroke or pure sensory stroke
deep cerebral white matter, basal ganglia, pons

71
Q

what is locked-in syndrome and what is it caused by?

A

all voluntary muscles are paralysed except those that control eye movement
upper brainstem infarction

72
Q

immediate investigation in stroke patient? and why

A

brain CT
distinguishes ischaemic/haemorrhagic
identifies conditions mimicing stroke e.g. tumour

73
Q

what treatment is used to reverse the effects of anticoagulants in patients with intracerebral haemorrhage?

A

prothrombin complex concentrate

74
Q

what causes subarachnoid haemorrhage in 70% of cases?

A

saccular (Berry) aneurysms

at branching points of circle of willis

75
Q

what is the investigation of choice for subarachnoid haemorrhage which should be undertaken as soon as possible?

A

CT

76
Q

if there is a strong clinical suspicion of subarachnoid haemorrhage but CT scan is normal, what test would you carry out?
and what findings would support SAH diagnosis?

A

lumbar puncture

^ in RBC lysis/phagocytosis pigments (bilirubin, oxyhaemoglobin)

77
Q

what drug is given to subarachnoid haemorrhage patients to prevent cerebral artery spasm? [>ischaemia & further neurological damage]

A

nimodipine [calcium-channel blocker]

78
Q

what causes subdural haematoma?

A

rupture of a vein running from the hemisphere to the sagittal sinus
almost always due to head injury [often minor]

79
Q

which groups are particularly susceptible to subdural haematoma & why?

A

elderly & alcoholics.

accident prone & atrophic brains make connecting veins more susceptible to rupture

80
Q

what causes extradural haematomas?

A

injuries that fracture temporal bone

& rupture underlying middle meningeal artery

81
Q

what is the clinical picture of an extradural haematoma?

A

head injury with brief period of unconsciousness
followed by lucid interval of recovery
then rapid deterioration

82
Q

define seizure

A

convulsion or transient abnormal event

caused by paroxysmal discharge of cerebral neurones

83
Q

define epilepsy

A

continuing tendency to have seizures

84
Q

define partial seizure

A

involves only a portion of the brain at onset e.g. temporal lobe
[but may become generalized]

85
Q

describe generalized tonic-clonic seizure [grand mal] & how long episode lasts

A

sudden onset of rigid tonic phase
followed by convulsion [clonic phase] - muscles jerk rhythmically
seconds to minutes

86
Q

describe absence seizure [petit mal] & how long it lasts

A

usually children
cease activity, stares, pales
for few seconds only

87
Q

describe myoclonic seizure

A

isolated muscle jerking

88
Q

describe tonic seizure

A

intense stiffening of the body

89
Q

describe akinetic seizure

A

cessation of movement
falling
loss of consciousness

90
Q

describe simple partial seizure

A

epileptic activity in a part of the brain

not affecting consciousness or memory

91
Q

describe complex partial seizure

A

epileptic activity in a part of the brain

affecting awareness or memory before/during or immediately after

92
Q

emergency management of status epilepticus

A
administer O2
IV access [large vein]
cardioresp, pulse oximetry monitoring
vit B & C
lorazepam [or rectal diazepam]
93
Q

which antiepileptic drug is contraindicated in women of child bearing age?

A

sodium valproate

94
Q

give an example of surgical treatment for patients with poorly controlled epilepsy

A

amputation of the anterior temporal lobe

95
Q

the extrapyramidal system is a general term for what structure/s?

A

basal ganglia

& their connections with other brain areas [particularly those concerned w/ movement]

96
Q

describe the akinetic-rigid syndrome type of movement disorder and give an example

A

slowed movement, increased muscle tone

idiopathic Parkinson’s disease

97
Q

describe dyskinesias movement disorders and give an example

A

added uncontrollable movements

essential tremor

98
Q

what causes the clinical features of idiopathic Parkinson’s disease?

A

progressive depletion of dopamine-secreting cells in the substantia nigra

99
Q

what are the main clinical features of Parkinson’s disease?

A
rest tremor
rigidity/ ^tone
akinesia/bradykinesia
stooped posture
poor balance
100
Q

what is the most common cause of death in parkinson’s disease patients?

A

bronchopneumonia

101
Q

other than Parkinson’s disease, what can cause “parkinsonism”?

A

multi-infarct dementia

repeated head injury

102
Q

what is the options for initial therapy in parkinson’s disease?

A
  1. Levodopa [L-dopa]
    with a peripheral dopa-decarboxylase inhibitor
  2. dopamine agonists
  3. monoamine oxidase B inhibitors
103
Q

how do monoamine oxidase B inhibitors work?

A

inhibit catabolism of dopamine in the brain

104
Q

what is “parkinsonism plus”?

A

rare disorders

parkinsonism + evidence of a separate pathology

105
Q

what is the most common parkinsonism plus disorder?

A

progressive supranuclear palsy

106
Q

what drugs improve benign essential tremor?

A

propanolol
primidone [anticonvulsant]
mirtazapine [antidepressant]

107
Q

what are the symptoms of Huntingdon’s disease?

A

relentlessly progressive course
chorea
personality change
dementia

108
Q

what is the genetic cause of huntingdon’s disease?

A

autosomal dominant
expansion of CAG repeats in Huntingdon’s gene on chromosome 4
leads to production of mutant huntingtin protein

109
Q

what causes the symptoms of Huntingdon’s disease?

A

loss of neurones within basal ganglia

depletion of GABA and ACh [SPARES DOPAMINE]

110
Q

management of huntingdon’s

A

no treatment arrests disease
symptomatic treatment of chorea
genetic counselling of family members

111
Q

what is multi infarct dementia?

A

series of small strokes

leads to loss of brain function

112
Q

name a peripheral dopa-decarboxylase inhibitor

A

benserazide

carbidopa

113
Q

name a dopamine agonist

A

ropinirole

114
Q

what causes MS?

A

autoimmune

disseminated plaques of demyelination

115
Q

exposure to which infectious agent in childhood may predispose to later development of MS in a genetically susceptible host?

A

EBV

116
Q

which part of the CNS is never affected by MS?

A

peripheral nerves

117
Q

name the 3 characteristic common presentations of relapsing & remitting MS

A

optic neuropathy
brainstem demyelination
spinal cord lesions

118
Q

name some symptoms caused by brainstem demyelination

A

diplopia (double vision)
vertigo
dysphagia
nystagmus

119
Q

causes of death in MS

A

recurrent UTIs
uraemia
bronchopneumonia

120
Q

what is the definitive investigation in MS?

A

MRI of brain and spinal cord

121
Q

short term management of MS replase

A

short courses of steroids (IV prednisolone)

reduce severity

122
Q

prolonged MS treatment which reduces relapse rate

A

subcutaneous B-interferon

123
Q

downsides of using B-interferon in MS

A
prolonged treatment
expensive
side effects (flu-like symptoms)
124
Q

which 2 bacteria account for most cases of acute bacterial meningitis outside neonatal period?

A

neisseria meningitidis

streptococcus pneumoniae

125
Q

signs of meningococcal septicaemia

[1. skin, 2. systemically]

A

non-blanching petechial & purpuric rash

signs of shock

126
Q

immediate treatment for suspected meningitis [before hospital transfer]

A

benzylpenicillin

127
Q

why should lumbar puncture not be performed in a patient with suspected meningococcal sepsis?

A

coning of the cerebellar tonsils may follow

128
Q

how long is tuberculous meningitis treated for?

A

at least 9 months

129
Q

what is encephalitis?

A

inflammation of the brain parenchyma

130
Q

how does the presentation of encephalitis compare to meningitis in terms of cerebral function?

A

unlike meningitis, cerebral fn. is usually abnormal in encephalitis with altered mental status, motor and sensory deficits

131
Q

common organisms in the UK to cause acute viral encephalitis

A

herpes simplex
echovirus
coxsackie
mumps

132
Q

treatment for suspected herpes simplex encephalitis

A

IV aciclovir

133
Q

why is lumbar puncture not performed to investigate cerebral abscess?

A

danger of coning in the presence of raised intracranial pressure

134
Q

treatment of cerebral abscess

A

IV antibiotics

sometimes surgical decompression

135
Q

treatment for neurosyphilis? [may arrest but not reverse the neurological disease]

A

benzylpenicillin

136
Q

what would you expect to see on neuroimaging and lumbar puncture in a patient with benign/idiopathic intracranial hypertension ?

A

neuroimaging normal

lumbar puncture - raised CSF pressure

137
Q

management of brain tumour

A

surgery
radiotherapy
corticosteroids [cerebral oedema]

138
Q

when is radiotherapy given in brain tumour patients?

A

gliomas

radiosensitive mets

139
Q

what is hydrocephalus? and why does it usually occur

A

excessive CSF in cranium

obstruction to CSF outflow

140
Q

what causes hydrocephalus in children?

A

congenital malformation of the brain
meningitis
haemorrhage

141
Q

treatment for hydrocephalus

A

surgical insertion of shunt between ventricles and right atrium or peritoneum

142
Q

what is normal pressure hydrocephalus?

A

dilatation of cerebral ventricles without signs of raised intracranial pressure

143
Q

clinical features of hydrocephalus

A

headache
vomiting
papilloedema
may be ataxia & bilateral pyramidal signs

144
Q

name some pyramidal signs

A

muscle weakness
Babinski sign
increased deep tendon reflex

145
Q

how does normal-pressure hydrocephalus present and in whom?

A

elderly people

dementia, urinary incontinence, ataxia

146
Q

describe clinical features of migraine

A

unilateral
throbbing
builds over mins/hrs
nausea/vomiting, photophobia

147
Q

differential diagnosis of migraine

A

meningitis
subarachnoid haemorrhage
thromboembolic TIA [headache unusual]

148
Q

Tx of mild migraine attack

A

paracetamol/ NSAIDs w/antiemetic [metoclopramide]

149
Q

Tx of moderate/severe migraine attack

A

triptans [serotonin agonists]

150
Q

how do triptans work in migraine?

A

inhibit vasoactive peptide release
promote vasoconstriction
block pain pathways in brainstem

151
Q

migraine prophylaxis medications

A

pizotifen [serotonin antagonist]
B-blockers
amitryptiline [serotonin/norepi. reuptake inhibitor]