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neurology Flashcards

1
Q

first line for muscle spasticity in MS

A

baclofen and gabapentin

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2
Q

how to treat a brain abscess

A

IV 3rd-generation cephalosporin (ceftriaxone) + metronidazole

(+ intercranial pressure mx (dexamethasone) )

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3
Q

what does it show on CT scan w brain abscess

A

ring enhancing lesion

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4
Q

what would you find on a head CT for Alzheimer’s

A

atrophy of cortex + hippocampus

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5
Q

what would you find on a head CT for frontotemporal dementia (pick’s disease)

A

atrophy of the frontal + temporal lobes
knife-blade appearance

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6
Q

what do you find on a head CT for SAH

A

Hyper-attenuating area in the basilar cistern (Circle of Willis)

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7
Q

most common cancers than spread to the brain

A

lung (most common)
breast
bowel
skin (namely melanoma)
kidney

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8
Q

tx for cerebral oedema in context of malignancy

A

dexamethasone

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9
Q

tx increased icp

A

mannitol

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10
Q

what happens if you give folate to someone who is b12 deficient

A

it can precipitate subacute combined degeneration of the cord

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11
Q

features of subacute combined degeneration of the cord

A

dorsal column involvement
- distal tingling/burning/sensory loss is symmetrical and tends to affect the legs more than the arms
- impaired proprioception and vibration sense

lateral corticospinal tract involvement
- muscle weakness, hyperreflexia, and spasticity
- upper motor neuron signs typically develop in the legs first
- brisk knee reflexes
- absent ankle jerks
- extensor plantars

spinocerebellar tract involvement
- sensory ataxia → gait abnormalities
- positive Romberg’s sign

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12
Q

most common site of berry aneurysm

A

anterior communicating artery

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13
Q

what condition is assoc w berry aneurysms

A

AD PKD

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14
Q

presentation of normal pressure hydrocephalus

A

dementia
gait abnormalities
urinary incompetence

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15
Q

neuro-imaging in normal pressure hydrocephalus

A

ventriculomegaly in the absence of sulcal enlargement

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16
Q

tx normal pressure hydrocephalus

A

ventriciuloperitoneal shunting

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17
Q

what is the barthel index

A

scale that measures disability/dependence in ADLs in stroke px

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18
Q

what is the most common cause of brain mets

A

lung tumours

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19
Q

SEs of levodopa

A

on-off effect
cardiac arrhythmias
N&V
psychosis
reddish discol of urine
dyskinesias

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20
Q

parkinson’s presentation

A

cogwheel rigidity
bradykinesia
- small writing
- shuffling gait
- can’t initiate movement/turn
tremor
- asymmetric, AT REST, improves w voluntary activity
mask-like facies
postural instability

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21
Q

describe parkinson’s tremor

A

resting
pin-rolling
4-6 Hz
improves w voluntary movement, worsens when distracted
No change with alcohol
Asymmetrical

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22
Q

what is levodopa usually combined w + why

A

peripheral decarboxylase inhibitors e.g. carbidopa
stops levodopa being broken down in the body before it gets the chance to enter the brain

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23
Q

what is dystonia

A

This is where excessive muscle contraction leads to abnormal postures or exaggerated movements.

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24
Q

what is chorea

A

These are abnormal involuntary movements that can be jerking and random.

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25
Q

what is athetosis

A

These are involuntary twisting or writhing movements usually in the fingers, hands or feet.

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26
Q

what is syringomyelia

A

cape-like loss of pain + temp sensation due to a collection of cerebrospinal fluid within the spinal cord

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27
Q

what is brown-sequard

A

damage to lateral 1/2 of the spinal cord

ipsilateral loss of proprioception + vibration (dorsal column decussates at medulla after leaving spinal cord)

contralateral loss of pain + temp (spinothalamic tract decussates asap)

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28
Q

sx optic neuritis

A

unilateral decrease in visual acuity over hours or days
poor discrimination of colours, ‘red desaturation’
pain worse on eye movement
relative afferent pupillary defect (respond diff to light)
central scotoma (blind spot)

think ms?!

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29
Q

3rd nerve palsy

A

ptosis
dilated pupil
looking down + out

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30
Q

encephalitis sx

A

fever
headache
altered mental status

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31
Q

viral encephalitis tx

A

IV aciclovir

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32
Q

bacterial encephalitis tx

A

IV ceftriaxone

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33
Q

what is Ramsay Hunt syndrome

A

infection of facial nerve by HZV

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34
Q

presentation of Ramsay Hunt syndrome

A

ipsilateral LMN facial palsy (forehead not spared)
ear pain
hearing loss
vertigo
vesicular rash in outer ear

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35
Q

what is bell’s palsy

A

LMN facial nerve lesion

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36
Q

presentation of bell’s palsy

A

ipsilateral facial paralysis (forehead not spared)
post-auricular pain
altered taste
dry eyes
hyperacusis (reduced tolerance to sound)

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37
Q

tx bell’s palsy

A

oral prednisolone 10 days
if no improvement after 3 wks, refer urgently to ENT

eye drops

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38
Q

presentation of acoustic neuroma (vestibular schwannoma)

A

vertigo
hearing loss
tinnitus
absent corneal reflex

fullness in ear

facial nerve palsy if big

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39
Q

ix acoustic neuroma (vestibular schwannoma)

A

MRI of cerebellopontine angle
audiometry

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40
Q

mx acoustic neuroma (vestibular schwannoma)

A

urgent ENT referral

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41
Q

what is acoustic neuroma (vestibular schwannoma) assoc w

A

neurofibromatosis type 2 (AD)

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42
Q

what is charcot-marie-tooth

A

most common hereditary sensory + motor peripheral neuropathy

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43
Q

charcot-marie-tooth presentation

A

Patients can present with lower motor neurone signs in all limbs and reduced sensation (more pronounced distally).

motor loss
distal muscular weakness + atrophy
hyporeflexia
hx of freq sprained ankles
foot drop
high arched feet - pes cavus
hammer toes
stork leg deformity

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44
Q

what is chronic inflammatory demyelinating polyneuropathy

A

chronic version of GBS
progressive weakness + impaired sensory func in legs + arms

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45
Q

tx of chronic inflammatory demyelinating polyneuropathy

A

corticosteroids

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46
Q

what is degenerative cervical myelopathy + presentation

A

spinal cord compression in neck

loss of fine motor func in upper limbs, pain, numbness
Hoffman’s sign

50% of patients were initially incorrectly diagnosed and sometimes treated for carpal tunnel syndrome

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47
Q

dx degenerative cervical myelopathy

A

MRI cervical spine = disc degeneration + ligament hypertrophy
cord signal change

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48
Q

what is autonomic dysreflexia

A

syndrome that occurs in px w spinal cord injury at/> T6.
sympathetic reflex caused by trigger

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49
Q

what commonly triggers autonomic dysreflexia

A

faecal impaction or urinary retention

px cld:
- bed bound/immobile
- meds (opioids)
- anal fissure
- Hirschsprungs
- dementia
- spinal trauma

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50
Q

sx of autonomic dysreflexia

A

extreme HTN
flushing + sweating above lesion level
agitation

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51
Q

where does the spinal cord end

A

L1-2 - splits to cauda equina

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52
Q

what does the dorsal column do

A

ascending tract
carries sensory info to the brain

fine touch
vibration sense
proprioception

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53
Q

where does the dorsal column decussate

A

after leaving the spinal cord at medulla
therefore stays in same lane for ages

therefore if damaged problems are on ipsilateral side

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54
Q

what does the spinothalamic tract do

A

ascending tract
carries sensory info to brain

pain + temperature

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55
Q

where does the spinothalamic tract decussate

A

as soon as in spinal cord so ascends contralaterally
therefore crosses lanes immediately

therefore if damaged problems on opposite side (2 segments below injury)

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56
Q

what is the corticospinal tract

A

descending pyramidal tract sending motor signals to muscles
voluntary muscle control

immediately changes lanes + travels contralaterally

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57
Q

what is the corticobulbular tract

A

descending pyramidal tract
voluntary muscle control of the face, head + neck

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58
Q

what are upper motor neurons

A

originate in cerebral cortex + travel down to brainstem or spinal cord

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59
Q

what are lower motor neurons

A

begin in spinal cord + innervate muscles + glands throughout the body

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60
Q

what are signs of upper motor neuron lesions

A

increased tone
- spasticity
- clonus?

increased reflexes

positive babinski sign
positive hoffman sign

upper limb has weak extensor muscles
lower limb has weak flexor (bend) muscles

pyramidal drift

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61
Q

what are signs of lower motor neuron lesions

A

decreased tone - flaccid

decreased reflexes/none

fasciculations

muscle wasting
- bulbar = speech + swallow
- resp - diaphragm higher up
- hand
- foot drop

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62
Q

what do extrapyramidal tracts do

A

involuntary control i.e. tone + balance

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63
Q

what are manifestations of extrapyramidal injury

A

parkinsonism
- rigidity
- bradykinesia
- tremors
- postural deficits

chorea

athetosis

dystonia

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64
Q

initial dementia blood screen

A

FBC
U&Es
LFTs
Ca
glucose
ESR/CRP
TFTs
vitamin B12
folate levels

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65
Q

what is wernicke’s encephalopathy + how does it present

A

thiamine (v B1) deficiency (in alcoholics)

ophthalmoplegia
ataxia
confusion

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66
Q

wernicke’s encephalopathy tx

A

thaimine replacement -> pabrinex

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67
Q

what do you get if you don’t treat wernicke’s encephalopathy + how does it present

A

Korsakoff syndrome

antero + retrograde amnesia
confabulation (false mems)

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68
Q

presentation of multiple system atrophy

A

parkinsonism
autonomic disturbance
- erectile dysfunction: often an early feature
- postural hypotension
- atonic bladder
cerebellar signs

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69
Q

Posterior inferior cerebellar artery stroke (PICA) (lateral medullary syndrome) (Wallenberg syndrome)

A

Ipsilateral: facial pain and temperature loss
Contralateral: limb/torso pain and temperature loss
Ataxia
Nystagmus
sudden vomiting/vertigo

to differentiate from ANTERIOR….
POSTERIOR has no deafness or facial paralysis

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70
Q

Anterior inferior cerebellar artery stroke (AICA) (lateral pontine syndrome)

A

Ipsilateral: facial paralysis and deafness, facial pain + temp loss
contralateral: body pain + temp loss
pin point pupils

to differentiate from POSTERIOR….
ANTERIOR has deafness and facial paralysis as well as the ipsilateral face sx + contralateral body sx

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71
Q

what does a basilar artery stroke cause

A

locked in syndrome

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72
Q

what does a retinal/ophthalmic artery stroke cause

A

Amaurosis fugax

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73
Q

Anterior cerebral artery stroke

A

Contralateral hemiparesis and sensory loss
Lower extremity more affected (ants have legs)
logical thinking/personality

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74
Q

Middle cerebral artery stroke

A

Contralateral hemiparesis and sensory loss
Upper extremity more affected
Contralateral homonymous hemianopia
Aphasia

Most common

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75
Q

Posterior cerebral artery stroke

A

Contralateral homonymous hemianopia with macular sparing
Visual agnosia (can’t rec faces)

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76
Q

Weber’s syndrome

A

Ipsilateral CN III palsy (down + out)
Contralateral weakness of upper and lower extremity

(branches of the posterior cerebral artery that supply the midbrain)

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77
Q

what do total anterior circulation infarcts have to have

A

involves middle and anterior cerebral arteries

all 3 of the criteria are present:
1. unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
2. homonymous hemianopia
3. higher cognitive dysfunction e.g. dysphasia

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78
Q

what do partial anterior circulation infarcts have to have

A

involves smaller arteries of anterior circulation e.g. upper or lower division of middle cerebral artery

2 of the criteria are present:
1. unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
2. homonymous hemianopia
3. higher cognitive dysfunction e.g. dysphasia

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79
Q

what do lacunar infarcts have to have

A

presents with 1 of the following:
1. unilateral weakness (and/or sensory deficit) of face and arm, arm and leg or all three.
2. pure sensory stroke.
3. ataxic hemiparesis

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80
Q

ix TIA

A

MRI brain w diffusion-weighted imaging

only do to exclude other dx

all patients should have an urgent carotid doppler unless they are not a candidate for carotid endarterectomy (to check as a source of emboli)

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81
Q

immediate tx TIA

A

aspirin 300mg

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82
Q

what to do if px has had more than 1 TIA or has a suspected cardioembolic source or severe carotid stenosis

A

discuss the need for admission or observation urgently with a stroke specialist

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83
Q

what to do if If the patient has had a suspected TIA in the last 7 days

A

arrange urgent assessment (within 24 hours) by a specialist stroke physician

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84
Q

what to do if the patient has had a suspected TIA which occurred more than a week previously

A

refer for specialist assessment as soon as possible within 7 days

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85
Q

driving + TIAs

A

Advise the person not to drive until they have been seen by a specialist.

Can start driving if sx free after 1 month

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86
Q

2ndary prev after TIA

A

antiplatelet therapy after initial aspirin
- clopidogrel

high-intensity statin

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87
Q

when to do a carotid artery endarterectomy in TIA

A

carotid stenosis > 70% + sx

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88
Q

tx ischaemic stroke

A

aspirin 300 mg

< 4.5 hrs of onset = thombolysis w alteplase AND thrombectomy

4.5 - 6 hrs of onset = thrombectomy

or thrombectomy after 6 hrs if there is the potential to salvage brain tissue, as shown by imaging
(but not usually after 24 hrs)

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89
Q

features of acute subdural haemorrhage

A

4-7 wks following high impact trauma

fluctuating conc + sx come on gradually

crescent shaped
hyperdense

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90
Q

features of chronic subdural haemorrhage

A

wks/months
confusion
decreased conc
neuro def

more likely elderly + alcoholic as brain atrophy
or in shaken baby syndrome

hypodense
crescent shaped
slow bleeding

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91
Q

what ruptures in subdural haemorrhage

A

bridging veins

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92
Q

tx acute subdural haemorrhage

A

decompressive craniotomy

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93
Q

tx chronic subdural haemorrhage

A

burr hole evacuation

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94
Q

features of extradural haemorrhage

A

sudden onset soon after injury following brief lucid interval
headache
compression of CN III - fixed + dilated pupil

lemon shaped (biconvex)

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95
Q

what ruptures in extradural haemorrhage

A

middle meningeal artery

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96
Q

tx extradural haemorrhage

A

burr holes
craniotomy

ligation of bleeding artery

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97
Q

ix SAH

A

CT = acute blood (hyperdense/bright on CT) is typically distributed in the basal cisterns, sulci and in severe cases the ventricular system.

if done within 6 hrs of sx onset + normal, no LP needed - consider an alt dx

if CT is done 6+ hrs after sx onset + normal
-> LP (at least 12 hrs after sx) =
xanthochromia (RBC breakdown) + normal/raised opening pressure
-> refer to neurosurgery

98
Q

ix is to identify a causative pathology of SAH

A

CT intracranial angiogram (to identify a vascular lesion)

99
Q

mx SAH

A

coil/clip

IV nimidopine 21 days to prevent vasospasm

100
Q

what signs do you get in GBS

A

LMN

101
Q

features of temporal lobe seizure

A

Hallucinations
Epigastric rising/Emotional
Automatisms (lip smacking)
Deja Vu/Dysphasia post ictal

102
Q

features of a frontal lobe seizure

A

Head/leg movements, posturing
Post ictal Todd’s palsy (weakness)
Jacksonian march (clonic movements travelling proximally)

103
Q

what is an atonic seizure

A

suddenly fall to the ground due to sudden loss of muscle tone
confused after

104
Q

EEG on absence seizure

A

3Hz spike + wave

105
Q

what is status epilepticus

A

seizure > 5 mins / > 2 in 5 mins not returning to normal

106
Q

drug tx for male generalised tonic clonic epilepsy

A

sodium valproate

107
Q

drug tx for female generalised tonic clonic epilepsy

A

lamotrogine/levetiracetam

108
Q

drug tx for males in myoclonic epilepsy

A

sodium valproate

109
Q

drug tx for focal seizures in epilepsy

A

1 = lamotrogine/levetiracetam
2 = carbamazepine

110
Q

drug tx for females in myoclonic epilepsy

A

levetiracetam

111
Q

tx status epilepticus

A

ABC
- airway adjunct
- oxygen
- check blood glucose

Pre-hosp = PR diazepam / buccal midazolam

Hosp = IV lorazepam. Repeat after 5-10 mins

Ongoing = phenytoin

Anaesthesia

112
Q

what are infantile spasms (West syndrome)

A

rare disorder starting in infancy at around 6 months of age

brief spasms of sudden uncontrolled movements including flexion of the head, trunk, limbs, and extension of the arms (Salaam attack)

poor prognosis

usually secondary to serious neurological abnormality (e.g. tuberous sclerosis, encephalitis, birth asphyxia) or may be idiopathic

113
Q

EEG of infantile spasms

A

Hypsarrhythmia

114
Q

drug tx absence seizures

A

ethosuximide

115
Q

drug tx for female tonic / atonic seizures in epilepsy

A

lamotrigine

116
Q

drug tx for male tonic / atonic seizures in epilepsy

A

sodium valproate

117
Q

features of MG

A

Autoimmune autoantibodies at post-synaptic membrane = AChR. These prevent ACh from being able to stim the receptor + trigger muscle contractions

Assoc w thymomas (CT to exc) -> dry cough, breathlessness

Muscle fatiguability
- extraocular
- proximal
- ptosis
- dysphagia

118
Q

ix in MG

A

Acetylcholine receptor (ACh-R) antibodies (85% of patients)
Muscle-specific kinase (MuSK) antibodies (10% of patients)
LRP4 (low-density lipoprotein receptor-related protein 4) antibodies (less than 5%)

EMG (nerve conduction studies)
CT
Edrophonium Test

119
Q

MG tx

A

anticholinesterase inhibitors = PYRIDOSTIGMINE
Prednisolone
Thymectomy

120
Q

tx for myasthenic crisis

A

plasmapheresis
IV immunoglobulin

121
Q

what can make sx of MG worse

A

BBs

gentamicin is CI

122
Q

features of Lambert Eaton syndrome

A

AI antibodies against VG calcium channels in pre-synaptic membrane so ACh cannot be exocytosed

assoc w small cell lung cancer

proximal muscle weakness espesh in lower limbs

strength increases w effort

autonomic features

123
Q

tx Lambert Eaton syndrome

A

Amifampridine

124
Q

features of GBS

A

progressive, symmetrical weakness of all the limbs
- classically ascending
- reduced or absent reflexes

hx viral infection e.g. gastroenteritis

125
Q

ix GBS

A

LP
- rise in protein with a normal WBCS (albuminocytologic dissociation) - found in 66%

nerve condution studies
- decreased motor nerve conduction velocity (due to demyelination)
- prolonged distal motor latency
- increased F wave latency

126
Q

what is GBS

A

an immune-mediated demyelination of the peripheral nervous system often triggered by an infection (classically Campylobacter jejuni)

127
Q

most common causative organism of viral encephalitis

A

herpes simplex virus 1

128
Q

CSF in viral encephalitis

A

high lymphocytes
high protein

129
Q

EEG in viral encephalitis

A

lateralised periodic discharges at 2 Hz

130
Q

causes of bacterial meningitis

A

NEISSERIA MENINGITIDIS
Streptococcus pneumoniae (pneumococcus)
Haemophilus influenzae
Group B streptococcus (GBS) (particularly in neonates as GBS may colonise the vagina)
Listeria monocytogenes (particularly in neonates)

131
Q

causes of viral meningitis

A

Enteroviruses (e.g., coxsackievirus)
Herpes simplex virus (HSV)
Varicella zoster virus (VZV)m

132
Q

meningitis presentation

A

Fever
Neck stiffness
Vomiting
Headache
Photophobia
Altered consciousness
Seizures

meningococcal septicaemia (when it has entered the blood) = non-blanching rash.

133
Q

special to look for meningeal irritation

A

Kernig’s test
Brudzinski’s test

134
Q

LP for bacterial meningitis

A

cloudy
high protein
low glucose (relative to serum)
high neutrophils (polymorphs)

135
Q

LP for viral meningitis

A

clear
mildly raised/normal protein
normal glucose
high lymphocytes

136
Q

features of benign essential tremor

A

fine tremor
6-12 Hz
symmetrical
more prominent w voluntary movement
worse when tired, stressed or after caffeine
improved by alcohol
absent during sleep

137
Q

mx benign essential tremor

A

just to improve sx:
propranolol
primidone (a barbiturate anti-epileptic medication)

138
Q

what is MS

A

chronic + progressive AI condition involving demyelination in the CNS (oligodendrocytes) (multiple sites)

T cell mediated type 4 hypersensitivity reaction

begins early adulthood, more common in F

139
Q

typical presentations of MS

A

LOSS NB
- Lhermitte’s sign - electric shock runs down back + radiates to limbs on neck flexion
- Optic neuritis – impaired vision + eye pain
- Spasticity + other pyramidal signs
- Sensory symptoms + signs - ataxia
- Nystagmus, double vision + vertigo
- Bladder + sexual dysfunction

Exacerbated by heat – showers, hot weather, saunas (Uhthoff’s phenomenon)

140
Q

types of MS

A

relapsing + remitting (80%)
- onset over days recovery over weeks
- periods of gd health in betweeen

secondary progressive
- gradually worsening sx + fewer remissions
- evolves from relapsing + remitting

primary progressive
- gradually worsening disability WITHOUT relapses or remissions

141
Q

diagnosis of MS

A

TWO+ attacks affecting DIFFERENT PARTS of CNS; that is 2 CNS lesions disseminated in time + space

142
Q

ix in MS

A

MRI brain + spinal cord
* 95% have periventricular lesions
* Over 90% show discrete white matter abnormalities
* Multiple scattered plaques are usually seen
- with contrast - active lesions will take up contrast + appear white in colour
= Dawson fingers: often seen on FLAIR images - hyperintense lesions penpendicular to the corpus callosum

LP
* oligoclonal IgG bands in CSF

143
Q

tx for acute relapse MS

A

High-dose steroids (e.g. oral or IV methylprednisolone) may be given for 5 days to shorten duration of relapse

144
Q

First line drug for reducing the risk of relapse in MS

A

natalizumab IV - a recombinant monoclonal antibody

145
Q

drug for fatigue in MS

A

amantadine

(once other probs - anaemia, thyroid, depression - have been excluded)

146
Q

tx for bladder incompetence in MS

A

get US first to assess bladder emptying

if significant residual volume → intermittent self-catheterisation
if no significant residual volume → anticholinergics may improve urinary frequency

147
Q

tx for oscillopsia in MS

A

gabapentin

148
Q

inheritance of huntington’s disease

A

AD

149
Q

what is huntingtons disease (+what is its genetics)

A

genetic condition that causes progressive neurological dysfunction.

trinucleotide repeat (CAG) disorder involving a genetic mutation in the HTT gene on chromosome 4, which codes for the huntingtin (HTT) protein.

150
Q

examples of trinucleotide repeat disorders

A

Huntington’s disease
Fragile X syndrome
Spinocerebellar ataxia
Myotonic dystrophy
Friedrich ataxia

151
Q

what is genetic anticipation

A

a feature of trinucleotide repeat disorders where successive generations have more repeats in the gene, resulting in:
Earlier age of onset
Increased severity of disease

152
Q

Huntington’s disease presentation

A

insidious, progressive worsening of symptoms.

It typically begins with cognitive, psychiatric or mood problems, followed by the development of movement disorders:

Chorea (involuntary, random, irregular and abnormal body movements)
Dystonia (abnormal muscle tone, leading to abnormal postures)
Rigidity (increased resistance to the passive movement of a joint)
Eye movement disorders
Dysarthria (speech difficulties)
Dysphagia (swallowing difficulties)

153
Q

dx huntington’s disease

A

genetic testing

154
Q

med for chorea sx in huntington’s

A

Tetrabenazine

155
Q

prognosis huntington’s

A

Life expectance is around 10-20 years after the onset of symptoms. As the disease progresses, patients become more frail and susceptible to illness (e.g., infections, weight loss, falls and pressure ulcers). Death is often due to aspiration pneumonia. Suicide is also a common cause of death.

156
Q

what is motor neurone disease

A

progressive degeneration of both the upper + lower motor neurones

sensory neurones are spared

157
Q

classic features of MND

A

asymmetric limb weakness is the most common presentation of ALS (usually upper limbs first)
the mixture of lower motor neuron and upper motor neuron signs
wasting of the small hand muscles/tibialis anterior is common
fasciculations
the absence of sensory signs/symptoms
vague sensory symptoms may occur early in the disease (e.g. limb pain) but ‘never’ sensory signs

rarely presents before 40 yrs

does NOT affect
- external occular muscles
- no cerebellar signs
- abdo reflexes preserved

158
Q

types of MND

A

Amyotrophic lateral sclerosis (ALS) - most common - LMN + UMN
Progressive bulbar palsy - tongue , worst prog
Progressive muscular atrophy - LMN
Primary lateral sclerosis - UMN

159
Q

pattern of signs in ALS

A

LMN signs in the arms and UMN signs in the legs

Asymmetric limb weakness

160
Q

MND dx

A

clinical
exclude
done by specialist

161
Q

what drug can slow progression of MND + how does it work

A

Riluzole
- prevents stim of glutamate receptors
- used mainly in ALS
- prolongs life by about 3 months

162
Q

other tx MND

A

Respiratory care
non-invasive ventilation (usually BIPAP) is used at night

Nutrition
percutaneous gastrostomy tube (PEG) is the preferred way to support nutrition and has been associated with prolonged survival

163
Q

causes of peripheral neuropathy

A

ABCDE:

A – Alcohol
B – B12 deficiency
C – Cancer (e.g., myeloma) and Chronic kidney disease
D – Diabetes and Drugs (e.g., isoniazid, amiodarone, leflunomide and cisplatin)
E – Every vasculitis

164
Q

charcot-marie-tooth inheritance

A

AD

165
Q

what is neurofibromatosis

A

genetic condition that causes neuromas to develop throughout the nervous system

benign tumours but cause neuro + structural probs

166
Q

Neurofibromatosis Type 1 Gene

A

found on chromosome 17

codes for neurofibromin (a tumour suppressor protein)

Mutations in this gene are inherited in an autosomal dominant pattern.

167
Q

diagnostic criteria for neurofibromatosis type 1

A

“CRABBING” mnemonic:

C – Café-au-lait spots (more than 15mm diameter is significant in adults)
R – Relative with NF1
A – Axillary or inguinal freckling
BB – Bony dysplasia, such as Bowing of a long bone or sphenoid wing dysplasia
I – Iris hamartomas (Lisch nodules), which are yellow-brown spots on the iris
N – Neurofibromas
G – Glioma of the optic pathway

168
Q

what is a neurofibroma + when are they significant

A

Skin-coloured, raised nodules or papules with a smooth, regular surface.
Two or more are significant.

A plexiform neurofibroma is a larger, irregular, complex neurofibroma containing multiple cell types.
A single plexiform neurofibroma is significant.

169
Q

complications of neurofibromatosis

A

Migraines
Epilepsy
Renal artery stenosis, causing hypertension
Learning disability
Behavioural problems (e.g., ADHD)
Scoliosis of the spine
Vision loss (secondary to optic nerve gliomas)
Malignant peripheral nerve sheath tumours
Gastrointestinal stromal tumour (a type of sarcoma)
Brain tumours
Spinal cord tumours with associated neurology (e.g., paraplegia)
Increased risk of cancer (e.g., breast cancer and leukaemia)

170
Q

Neurofibromatosis Type 2 genetics

A

The gene is found on chromosome 22
It codes for merlin (a tumour suppressor protein important in Schwann cells).
Mutations in this gene lead to schwannomas

Inheritance is also autosomal dominant.

Assoc w acoustic neuromas

171
Q

what is tuberous sclerosis

A

autosomal dominant genetic condition

leads to development of harmartomas (benign tissue growths)
commonly affect:
Skin
Brain
Lungs
Heart
Kidneys
Eyes

172
Q

Tuberous sclerosis is caused by mutations in either:

A

TSC1 gene on chromosome 9, which codes for hamartin
TSC2 gene on chromosome 16, which codes for tuberin

Hamartin and tuberin interact with each other to control the size and growth of cells. Abnormalities in one of these proteins lead to abnormal cell size and growth.

173
Q

Tuberous sclerosis skin features

A

Ash leaf spots (depigmented areas of skin shaped like an ash leaf)
Shagreen patches (thickened, dimpled, pigmented patches of skin)
Angiofibromas (small skin-coloured or pigmented papules that occur over the nose and cheeks)
Ungual fibromas (circular painless lumps that slowly grow from the nail bed and displace the nail)
Cafe-au-lait spots (light brown “coffee and milk” coloured flat pigmented lesions on the skin)
Poliosis (an isolated patch of white hair on the head, eyebrows, eyelashes or beard)

174
Q

Tuberous sclerosis neuro features

A

Epilepsy
Learning disability
Brain tumours

175
Q

systemic features tuberous sclerosis

A

Rhabdomyomas in the heart
Angiomyolipoma in the kidneys
Lymphangioleiomyomatosis in the lungs
Subependymal giant cell astrocytoma in the brain
Retinal hamartomas in the eyes

176
Q

headache red flags

A

Fever, photophobia or neck stiffness (meningitis, encephalitis or brain abscess)

New neurological symptoms (haemorrhage or tumours)

Visual disturbance (giant cell arteritis, glaucoma or tumours)

Sudden-onset occipital headache (subarachnoid haemorrhage)

Worse on coughing or straining (raised intracranial pressure)
Postural, worse on standing, lying or bending over (raised intracranial pressure)

Vomiting (raised intracranial pressure or carbon monoxide poisoning)

History of trauma (intracranial haemorrhage)

History of cancer (brain metastasis)

Pregnancy (pre-eclampsia)

177
Q

why to do fundoscopy in headaches

A

to check for papilloedema - suggests raised ICP

178
Q

first-line for chronic or frequent tension headaches

A

Amitriptyline

179
Q

Tension headaches may be associated with:

A

Stress
Depression
Alcohol
Skipping meals
Dehydration

180
Q

mx tension headaches

A

Reassurance
Simple analgesia (e.g., ibuprofen or paracetamol)

181
Q

first line abx for sinusitis that has lasted > 10 days

A

phenoxymethylpenicillin

182
Q

why do you get hormonal headaches + how do they present

A

low oestrogen

unilateral, pulsatile headache associated with nausea

They may occur:
- Two days before and the first three days of the menstrual period
- In the perimenopausal period
- Early pregnancy (headaches in the second half of pregnancy should prompt investigations for pre-eclampsia)

183
Q

tx hormonal headaches

A

Triptans and NSAIDs (e.g., mefenamic acid)

184
Q

what is trigeminal neuralgia

A

intense facial pain in the distribution of the trigeminal nerve, which has three branches:
Ophthalmic (V1)
Maxillary (V2)
Mandibular (V3)
Can affect any combo of branches

185
Q

presentation trigeminal neuralgia

A

> 90% are unilateral

pain comes on suddenly + can last seconds to hrs
an electricity-like, shooting, stabbing or burning pain
may be triggered by touch, taking, eating, shaving or cold
Attacks may worsen over time.

more common in px w MS

186
Q

first line tx trigeminal neuralgia

A

carbamazepine

187
Q

4 types of migraine

A

Migraine without aura
Migraine with aura
Silent migraine (migraine with aura but without a headache)
Hemiplegic migraine

188
Q

stages of migraine

A

Premonitory or prodromal stage (can begin several days before the headache)

Aura (lasting up to 60 minutes)

Headache stage (lasts 4 to 72 hours)

Resolution stage (the headache may fade away or be relieved abruptly by vomiting or sleeping)

Postdromal or recovery phase

189
Q

sx migraine

A

Usually unilateral
Moderate-severe intensity
Pounding or throbbing in nature
Photophobia (discomfort with lights)
Phonophobia (discomfort with loud noises)
Osmophobia (discomfort with strong smells)
Aura (visual changes)
Nausea and vomiting

190
Q

what is aura + its sx

A

Can affect vision, sensation or language. Visual symptoms are the most common:
Sparks in the vision
Blurred vision
Lines across the vision
Loss of visual fields (e.g., scotoma)

Sensation changes may include tingling or numbness.
Language symptoms include dysphasia (difficulty speaking).

191
Q

what is a hemiplegic migraine

A

rare subtype of migraine with aura that is hemiplegia / ataxia / impaired consciousness

192
Q

inheritance of familial hemiplegic migraine

A

AD

193
Q

migraine triggers

A

Stress
Bright lights
Strong smells
Certain foods (e.g., chocolate, cheese and caffeine)
Dehydration
Menstruation
Disrupted sleep
Trauma

194
Q

medical mx for acute migraine attack

A

NSAIDs (e.g., ibuprofen or naproxen)
Paracetamol
Triptans (e.g., sumatriptan) - taken as soon as it starts to halt the attack, do not take again in same migraine if does not work
Antiemetics if vomiting occurs (e.g., metoclopramide or prochlorperazine)

195
Q

CI for triptans

A

risks associated with vasoconstriction, for example, hypertension, coronary artery disease or previous stroke, TIA or myocardial infarction

196
Q

migraine prophylaxis

A

headache diary to identify triggers

Propranolol (CI asthma)
Topiramate (teratogenic and very effective contraception is needed)
Amitriptyline

197
Q

tx for menstrual migraines

A

Prophylactic triptans (e.g., frovatriptan or zolmitriptan)

Sx tend to occur two days before until three days after the start of menstruation

198
Q

sx cluster headaches

A

Severely painful headache
- unilateral
- centred around the eye

Red, swollen and watering eye
Pupil constriction (miosis)
Eyelid drooping (ptosis)
Nasal discharge
Facial sweating

Comes in clusters of attacks lasting 15mins-3hrs

199
Q

who typically gets cluster headaches

A

A typical patient is a 30-50 year old male smoker. They may have triggers, such as alcohol, strong smells or exercise.

200
Q

acute mx cluster headaches

A

Triptans (e.g., subcutaneous or intranasal sumatriptan)
High-flow 100% oxygen (may be kept at home)

201
Q

cluster headache prophylaxis

A

Verapamil

202
Q

RFs Alzheimer’s

A

age
FHx - 5% of cases are inherited as an AD trait
apoprotein E allele E4 - encodes a cholesterol transport protein
Caucasian ethnicity
Down’s syndrome

203
Q

medical mx mild-moderate Alzheimer’s

A

Acetylcholinesterase inhibitors
- donepezil
- galantamine
- rivastigmine

204
Q

medical mx severe Alzheimer’s / when 1st line not worked/CI

A

memantine - an NMDA receptor antagonist

205
Q

blood screen when ix dementia

A

FBC
U&E
LFTs
calcium
glucose
ESR/CRP
TFTs
vitamin B12 and folate levels

206
Q

characteristic feature Lewy body dementia

A

alpha-synuclein cytoplasmic inclusions (Lewy bodies) in the substantia nigra, paralimbic and neocortical areas

207
Q

presentation of Lewy body dementia

A

progressive cognitive impairment
- BEFORE parkinsonism, but usually both features occur within a year of each other (in Parkinson’s disease, motor sx typically present at least one year before cognitive symptoms)
- cognition may be FLUCTUATING, in contrast to other forms of dementia
- early impairments in attention and executive function rather than just memory loss

parkinsonism

visual hallucinations (other features such as delusions and non-visual hallucinations may also be seen)

208
Q

mx Lewy body dementia

A

same as Alzheimer’s
avoid neuroleptics

209
Q

what is vascular dementia

A

a group of syndromes of cognitive impairment caused by different mechanisms causing ischaemia or haemorrhage secondary to cerebrovascular disease

210
Q

subtypes of vascular dementia

A

Stroke-related VD – multi-infarct or single-infarct dementia
Subcortical VD – caused by small vessel disease
Mixed dementia – the presence of both VD and Alzheimer’s disease

211
Q

RFs vascular dementia

A

History of stroke or TIA
AF
HTN
Diabetes
Hyperlipidaemia
Smoking
Obesity
Coronary heart disease
A family history of stroke or cardiovascular

212
Q

presentation vascular dementia

A

Several months or several years of a history of a sudden or stepwise deterioration of cognitive function.

Sx and the speed of progression vary:
Focal neurological abnormalities e.g. visual disturbance, sensory or motor symptoms
The difficulty with attention and concentration
Seizures
Memory disturbance
Gait disturbance
Speech disturbance
Emotional disturbance

213
Q

dx vascular dementia

A

Presence of cognitive decline that interferes with activities of daily living, not due to secondary effects of the cerebrovascular event
+
Cerebrovascular disease
+
A relationship between the above two disorders inferred by:
- the onset of dementia within three months following a recognised stroke
- an abrupt deterioration in cognitive functions
- fluctuating, stepwise progression of cognitive deficits

214
Q

types of frontotemporal lobar dementias

A

Frontotemporal dementia (Pick’s disease)

Progressive non fluent aphasia (chronic progressive aphasia, CPA)

Semantic dementia

215
Q

Common features of frontotemporal lobar dementias

A

Onset before 65
Insidious onset
Relatively preserved memory and visuospatial skills
Personality change and social conduct problems

216
Q

features of pick’s disease

A

personality change
impaired social conduct
hyperorality (putting things in mouth)
disinhibition
increased appetite
perseveration behaviours (get stuck on idea)

217
Q

microscopic changes in pick’s disease

A

Pick bodies - spherical aggregations of tau protein (silver-staining)
Gliosis
Neurofibrillary tangles
Senile plaques

218
Q

Progressive non fluent aphasia (chronic progressive aphasia, CPA)

A

non-fluent speech

short utterances that are agrammatic
comprehension is relatively preserved.

219
Q

Semantic dementia

A

fluent progressive aphasia

speech is fluent but empty and conveys little meaning

memory is better for recent rather than remote events (unlike alzheimer’s)

220
Q

what spinal tract does neurosyphilis affect and what does that cause

A

dorsal columns
-> Loss of proprioception and vibration sensation

(posterior cord syndrome)

221
Q

presentation of anterior cord syndrome

A

acute onset

loss of pain + temp sensation
loss of movement

bilaterally

Autonomic dysfunction: abnormal blood pressure
Bladder dysfunction: Urinary incontinence

222
Q

what is anterior cord syndrome

A

A clinical syndrome due to damage to the anterior two-thirds of the spinal cord.
Damage to:
1. Lateral corticospinal tracts
2. Lateral spinothalamic tracts

223
Q

causes of anterior cord syndrome

A

ischaemia of the anterior spinal artery:
Thromboembolism
Trauma
Hypotension
Aortic disease

Other pathology:
Disc herniation
Tumour
Trauma
Epidural collection

224
Q

features of Intracranial venous sinus thrombosis

A

headache (may be sudden or gradual onset)
nausea & vomiting
reduced consciousness

225
Q

GS ix for Intracranial venous sinus thrombosis

A

MRI VENOGRAPHY

CT venography is an alternative
non-contrast CT head is normal in around 70% of patients
D-dimer levels may be elevated

226
Q

Mx Intracranial venous sinus thrombosis

A

anticoagulation
- typically with low molecular weight heparin acutely
- warfarin is still generally used for longer term anticoagulation

227
Q

tx degenerative cervical myelopathy

A

decompressive surgery

228
Q

sign of potentially salvageable tissue on CT

A

limited infarct core

229
Q

what does the facial nerve supply

A

‘face, ear, taste, tear’

face: muscles of facial expression
ear: nerve to stapedius
taste: supplies anterior two-thirds of tongue
tear: parasympathetic fibres to lacrimal glands, also salivary glands

230
Q

what is erb’s palsy a result of

A

injury to the C5/C6 nerves in the brachial plexus during birth

associated with shoulder dystocia, traumatic or instrumental delivery and large birth weight

231
Q

what does erb’s palsy lead to

A

weakness of shoulder abduction and external rotation, arm flexion and finger extension. This leads to the affected arm having a “waiters tip” appearance:

Internally rotated shoulder
Extended elbow
Flexed wrist facing backwards (pronated)
Lack of movement in the affected arm

232
Q

Pontine haemorrhage

A

reduced GCS, paralysis (tetraparesis ) and bilateral pin point pupils
may have facial droop

233
Q

Idiopathic intracranial hypertension RFs

A

obesity
female sex
pregnancy
drugs: COCP, steroids, tetracyclines, retinoids (isotretinoin, tretinoin) / vitamin A, lithium

234
Q

Idiopathic intracranial hypertension features

A

headache
blurred vision
papilloedema (usually present)
enlarged blind spot
sixth nerve palsy may be present

235
Q

Idiopathic intracranial hypertension tx

A

weight loss
carbonic anhydrase inhibitors e.g. acetazolamide

topiramate is also used, and has the added benefit of causing weight loss in most patients

repeated lumbar puncture may be used as a temporary measure but is not suitable for longer-term management

surgery: optic nerve sheath decompression and fenestration
lumboperitoneal or ventriculoperitoneal shunt to reduce ICP

236
Q

which are of the brain does herpes simplex encephalitis affect

A

temporal lobes

237
Q

which antiemetic to prescribe in parkinsons

A

Domperidone

238
Q

what to do if not tolerating clopidogrel after stroke

A

aspirin and modified release dipyramidole

239
Q

where is the lesion for
broca’s (expressive) aphasia

A

inferior frontal gyrus

240
Q

where is the lesion for
wernicke’s (receptive) aphasia

A

superior temporal gyrus

241
Q

prev of vasospasm after SAH

A

nimodipine

finals (27 decks)

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