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Medicine > Neurology > Flashcards

Neurology Flashcards

1
Q

spinal cord anatomy

where does it start and end?

A

foramen magnum to L1

terminates as conus medullaris

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2
Q

what is the cauda equina?

A

bundle of spinal nerves continuing inferiorly to spinal cord

L2 to L5 nerves, Sacral 1 to 5 and the coccygeal nerves

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3
Q

what suspends the spinal cord in the subarachnoid space?

A

denticulate ligaments

longitudinal support via filum terminale

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4
Q

Blood supply to spinal cord?

A
  • 3 longitudinal vessels
  • 2 posterior spinal arteries: dorsal 1/3
  • 1 anterior spinal artery: ventral 2/3
  • reinforced by segmental feeder arteries
    e. g. artery of Adamkiewicz

Longitudinal veins drain into extradural verterbral plexus

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5
Q

what part of the spinal cord is responsible for fine touch, vibration and proprioception?

A

Dorsal Columns

fasciulus gracilis

fasciculus cuneatus

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6
Q

where does decussation of the dorsal columns occur?

A

in medulla forming the medial lemniscus

-> thus, damage below the medial lemniscus means

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7
Q

what part of the spinal cord is responsible for pain and temperature sensation?

A

lateral spinothalamic tract

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8
Q

where do the lateral spinothalamic tracts decussate?

A

in cord, at entry level.

This fact aids in determining whether a lesion is in the brain or the spinal cord. With lesions in the brain stem or higher, deficits of pain perception, touch sensation, and proprioception are all contralateral to the lesion. With spinal cord lesions, however, the deficit in pain perception is contralateral to the lesion, whereas the other deficits are ipsilateral.

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9
Q

what part of the spinal cord is responsible for crude touch and firm pressure?

A

anterior spinothalamic tract

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10
Q

what part of the spinal cord is responsible for motor function?

A

lateral corticospinal tract

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11
Q

where does decussation of the lateral corticospinal tract occur?

A

pyramidal decussation in ventral medulla

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12
Q

brain stem lesion -> what is affected??

in terms of pain/ temp, fine touch, motor

A

in a brain stem or higher lesion,

everything is affected contralateral to the lesion

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13
Q

spinal cord lesion -> what is affected?

in terms of pain/temp, fine touch, motor

A

fine touch and motor are affected ipsilaterally

while pain/temp is affected contralaterally

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14
Q

what part of the brain is involved with regulation of posture, balance, coordination, movement and speech?

A

Cerebellum

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15
Q

what area of white matter carries axonal fibres from motor cortex to the pyramids of medulla?

A

internal capsule

infarcation of the internal capsule -> contralateral hemiparesis

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16
Q

occipital lobe in charge of ?

A

visual cortex

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17
Q

temporal lobes of brain involved in ?

A

memory

receptive language (Wernicke’s) in the dominant hemisphere

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18
Q

what function is the parietal lobe involved with?

A

sensory cortex

body orientation

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19
Q

what functions are the frontal lobe assoc w?

A

executive function

motor cortex

cognition and memory

dominant hemisphere: expressive speech (Broca’s area)

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20
Q

what is the main neurotransmitter acting across the neuromuscular junction?

A

acetylcholine

which binds to nicotinic receptors on post-synaptic terminal

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21
Q

What blocks presynaptic choline uptake?

A

hemicholine

(hemicholinium-3) decreases synthesis of acetylcholine

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22
Q

what blocks acetylcholine vesicle fusion?

A

botulinum

Lambert-Eaton myasthenic syndrome (antibodies against VGCC decrease ACh release)

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23
Q

what blocks nicotinic ACh receptors at the NMJ?

A

non-depolarising: atracurium, vecuronium

depolarising: suxamethonium

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24
Q

Sympathetic NS vs Parasympathetic NS

A

sympathetic: T1-L2
para: CN 3, 7, 9, 10

Sympathetic: preganglionic fibres are myelinated and release ACh whereas postganglionic fibres are unmyelinateed and release NA (except for sweat glands)

Para: both pre and post release ACh

Para has long preganglionic and short postganglionic fibres.

Sympathetic has short preganglionic fibres and long postganglionic fibres

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25
Q

absence of eye movements in caloric tests?

A

brainstem damage on the side being tested

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26
Q

direction of nystagmus when cold water is used?

and warm?

A

cold: opposite direction
warm: same side

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27
Q

what happens when warm water is placed in the ear during caloric testing?

A

warm water increases firing of vestibular nuclei

-> eyes turn to contralateral side with nystagmus to ipsilateral side

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28
Q

UMN vs LMN signs

A

UMN:

increased tone/ spasticity +/- clonus

hyperreflexia

up going plantars

LMN:

wasting

fasciculation

decreased tone

hyporeflexia

down-going plantars

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29
Q

What is Brown sequard syndrome?

A

ipsilateral loss of proprioception/ vibration and weakness

w

contralateral loss of pain

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30
Q

Cerebellar Syndrome

what signs?

A

DANISH
Dysdiadochokinesia + Dysmetria (past-pointing)

Ataxia: limb/ trunkal

Nystagmus: horizontal = ipsilateral hemisphere

Intention tremor

Speech: slurred, staccato, scanning dysarthria

Hypotonia

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31
Q

Common causes of cerebellar syndrome

A

PASTRIES

Paraneoplastic: e.g. from Ca

Alcohol: thiamine and B12 deficiency

Sclerosis (Multiple)

Trauma

Raised ICP

Infection/ iatrogenic: phenytoin

Endo: Hypothyroidism

Stroke: vertebrobasilar

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32
Q

causes of locked in syndrome

A

central pontine myelinolysis: rapid correction of hypoNa

ventral pons infarction: basilar artery

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33
Q

features of subclavian steal syndrome?

A

syncope / presyncope or focal neurology on using the arm

BP difference of > 20mmHg between arms

due to subclavian artery stenosis proximal to origin of verterbral artery -> blood stolen by vertebral artery by retrograde flow

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34
Q

features of Beck’s syndrome/ anterior spinal artery infarct

A

para/ quadriparesis

impaired pain and temp sensation

preserved touch and proprioception

infarction of spinal cord in distribution of anterior spinal artery: ventral 2/3 of cord

e.g. due to aortic aneurysm dissection

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35
Q

causes of mixed UMN and LMN signs?

A

MAST

motor neurone disease

ataxia: friedrich’s

Subacute combined degeneration of cord

Taboparesis (tertiary syphilis)

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36
Q

infectious causes of vertigo

A

ramsay hunt syndrome

labyrinthitis

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37
Q

trauma causing imbalance?

A

trauma to petrous temporal bone

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38
Q

sudden vertigo provoked by head rotation?

A

benign positional vertigo

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39
Q

recurrent vertigo,

fluctuating tinnitus,

increasing deafness

feeling of fullness in ear

A

Meniere’s disease

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40
Q

lesions of nerve causing vertigo?

A

acoustic neuroma,

vestibular schwannoma

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41
Q

Causes of conductive hearing loss

A

WIDENING

wax/ foreign body

infection: otitis media

drum perforation

extra: ossicle discontinuity- otosclerosis, trauma

neoplasia

INjury: e.g. barotrauma

Granulomatous: wegeners, sarcoid

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42
Q

features of resting tremor

A

4-6 Hz, pill-rolling

abolished on voluntary movement

increases with distraction e.g. counting backwards

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43
Q

tx of resting tremor

A

dopamine agonists

antimuscarinic e.g. procyclidine

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44
Q

features of intention tremor

A

>6Hz, irregular, large amplitude

worse at end of movement

e.g. past pointing

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45
Q

causes of intention tremor

A

cerebellar damage

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46
Q

Features of action/ postural tremor

A

6-12 Hz

absent at rest

worse w outstretched hands or movement

equally bad at all stages of movement

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47
Q

causes of postural / action tremor

A

BEATS

benign essential tremor

endocrine: thyrotoxicosis, low glucose, phaeo

alcohol withdrawal

Toxins: B agonists, theophylline

Sympathetic: anxiety

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48
Q

autosomal dominant

tremor that occurs w action and worse w anxiety, emotion, caffeine

affects arm, neck, voice

better w alcohol

A

benign essential tremor

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49
Q

Causes of subarachnoid haemorrhage?

A

Rupture of berry aneurysm (80%)

Arteriovenous malformations (15%)

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50
Q

RFs of subarachnoid haemorrhage

A

Smoking, HTN, Alcohol

Bleeding diathesis

Subacute bacterial endocarditis (infected aneurysms)

FH

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51
Q

Where do berry aneurysms most commonly affect?

A

classically occurs at the point at which a cerebral artery departs from the circle of Willis

e.g. bifurcation of MCA

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52
Q

Berry Aneurysms are assoc w ?

A

PCKD

Coarctation of aorta

Ehlers Danlos

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53
Q

Features of subarachnoid haemorrhage?

A

Sudden, severe occipital headache

Collapse

Meningism

Seizures

Drowsiness -> coma

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54
Q

Signs of subarachnoid haemorrhage?

A

Kernigs

Retinal or subhyaloid haemorrhage

Focal neuro - suggests aneurysm location

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55
Q

Ix of Subarachnoid haemorrhage?

A
  1. CT head

LP after 12h if CT -ve and no contraindications-> may show xanthochromia

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56
Q

Mx of subarachnoid haemorrhage?

A

Frequent neuro obs: GCS, pupils, BP

Maintain Cerebral perfusion pressure: Keep SBP >160

Nimodipine for 3 wks -> decrease cerebral vasospasm

Endovascular coiling

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57
Q

Complications of subarachnoid haemorrhage?

A

Rebleeding (most common cause of mortality)

Cerebral ischaemia from cerebral vasospasm (most common cause of morbidity)

Hydrocephalus

hypoNa

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58
Q

Causes of stroke?

A

Ischaemia (80%)

Haemorrhage (20%)

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59
Q

Causes of ischaemic stroke?

A

Atheroma

Emboli e.g. from AF, endocarditis, MI

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60
Q

Causes of haemorrhagic stroke?

A

High BP

Trauma

Aneurysm rupture

Anticoagulation

Thrombolysis

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61
Q

When to do endarterectomy in carotid artery stenosis?

A

If >70% symptomatic stenosis according to ECST criteria

or >50% according to NASCET criteria

recommend if patient has suffered stroke or TIA in the carotid territory and are not severely disabled

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62
Q

Posterior circulation stroke - what part of the circulation is affected?

A

Vertebrobasilar territory

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63
Q

What would an infarct in the vertebrobasilar territory cause?

A

Cerebellar syndrome

Brainstem syndrome

Contralateral homonymous hemianopia (macular sparing)

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64
Q

What is a total anterior circulation stroke?

A

All 3 of

  1. Contralateral hemiparesis +/- sensory deficit (2 or more in face, arm, leg)
  2. Contralateral homonymous hemianopia
  3. Higher cortical dysfunction
  • dominant (L usually) lobe: dysphasia
  • non dominant: hemispatial neglect
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65
Q

What is a partial anterior circulation stroke?

A

2/3

Usually

  1. Contralateral hemiparesis +/- sensory deficit (2 or more in face, arm, leg)
  2. Higher cortical dysfunction
  • dominant (L usually) lobe: dysphasia
  • non dominant: hemispatial neglect, constructional apraxia
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66
Q

what would an infarct in the subthalamic nucleus usually present with?

A

Hemiballismus

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67
Q

what is a lacunar stroke?

A

most common type of ischaemic stroke

small infarcts around the basal ganglia/ internal capsule/ thalamus / pons

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68
Q

what are the five classical lacunar syndromes?

A
  1. pure motor: commonest. causes a hemiparesis. post limb of internal capsule affected
  2. Pure sensory: affects contralateral side. post thalamus (VPL)
  3. mixed sensorimotor: internal capsule
  4. dysarthria/ clumsy hand
  5. ataxic hemiparesis: cerebellar and motor symptoms on ipsilateral side.
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69
Q

brainstem infarcts in the corticospinal tracts?

presentation

A

hemi/ quadriparesis

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70
Q

brainstem infarcts in the oculomotor system? presentation

A

conjugate gaze palsy

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71
Q

brainstem infarct in the CN7 nucleus?

presentation

A

facial weakness (LMN)

forehead involved

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72
Q

lesion in the CN8 nucleus?

presentation

A

vertigo, nystagmus

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73
Q

brainstem infarct in the CN9/10 nuclei?

presentation

A

dysphagia

dysarthria

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74
Q

brainstem infarct in the cerebellar connections?

presentation

A

ataxia

dysarthria

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75
Q

brainstem infarct in the sympathetic fibres?

presentation

A

Horner’s syndrome

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76
Q

brainstem infarct in the reticular activating system?

presentation

A

reduced GCS

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77
Q

occlusion of what artery could cause wallenberg’s syndrome/ lateral medullary syndrome?

A

Verterbral artery/

posterior inferior cerebellar artery

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78
Q

features of wallenberg’s syndrome/ lateral medullary syndrome?

A

DANVAH

Dysphagia

Ataxia (ipsilateral)

Nystagmus (ipsilateral)

Vertigo

Anaesthesia

  • ipsilateral facial numbness + absent corneal reflex
  • contralateral pain loss

Horner’s syndrome (ipsilateral)

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79
Q

what is Millard-Gubler syndrome?

A

aka ventral pontine syndrome

lesion of the pons

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80
Q

Millard-Gubler syndrome

what parts of the pons are affected?

A

6th and 7th CN nuclei

corticospinal tracts

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81
Q

Millard-Gubler syndrome

what features?

A

dipoplia (paralysis of the abducens CN VI)

LMN facial palsy + loss of corneal reflex

contralateral hemiplegia

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82
Q

what is locked in syndrome?

A

pt aware and cognitively intact but completely paralysed except for the eye muscles

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83
Q

causes of locked in syndrome?

A

ventral pons infarction: basilar artery

central pontine myelinolysis: rapid correction of hypoNa

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84
Q

acute mx of stroke?

A

Resus: ABCDE, stabilize patient airway, NBM until swallowing assessed by SALT

Monitor: Glucose levels, BP, Neuro obs

Imaging: urgent CT/ MRI

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85
Q

what imaging modality is most sensitive for acute infarct?

A

diffusion-weighted MRI

*CT excludes primary haemorrhage

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86
Q

why is CT head used in ix of stroke?

A

to visualize/ exclude haemorrhage

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87
Q

what medical tx is used in acute stroke?

A

consider thrombolysis if 18-80 yrs and < 4.5 h since onset of symptoms

e.g. alteplase

then CT head post-thrombolysis 24h to look for haemorrhage

Aspirin 300mg +/- PPI

? modified release dipyridamole / clopidogrel

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88
Q

when is neurosurgery indicated in stroke?

A

intracranial haemorrhage

decompressive hemicraniectomy for some forms of infarction

coiling of bleeding aneurysms

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89
Q

Primary prevention of stroke?

A

Control RFs: HTN, high lipids, DM, smoking, cardiac disease

Consider life-long anticoagulation in AF

Carotid endarterectomy if symptomatic- 70% stenosis

Exercise

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90
Q

secondary prevention of stroke?

A

Risk factor control: statin

Aspirin / Clopi 300mg for 2 wks after stroke then either:

  • Clopidogrel 75mg OD
  • Aspirin 75 mg OD + dypyridamole MR 200mg BD

*warfarin instead of aspirin/clopi if cardioembolic stroke/ AF. start from 2 wks post-stroke.

Carotid endarterectomy if good recovery + ipsilateral stenosis >70%

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91
Q

Rehab in stroke?

A

MENDS

MDT: physio, SALT, dietician, OT, specialist nurses, neurologist, family

Eating: Swallowing screen - may need NG/ PEG, supplements if malnourished

Neurorehab: physio and speech therapy

DVT prophylaxis

Sores: avoid bed sores

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92
Q

what drug may be useful to help spasticity seen post-stroke?

A

botulinum

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93
Q

What does OT post-stroke aim to do?

A

aims to minimise disability (e.g. can’t write) and abolish handicap (e.g. cant work as accountant)

impairment: e.g. paralysed arm

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94
Q

what is a transient ischaemic attack?

A

sudden onset focal neurology lasting <24h

due to temporary occlusion of part of the cerebral circulation

(~15% of 1st strokes are preceded by TIAs)

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95
Q

signs of TIA?

A

brief symptoms

global events e.g. syncope/ dizziness are not typical

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96
Q

signs of causes of TIA?

A

Carotid bruits

AF

high BP

heart murmur

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97
Q

causes of TIA

A

atherothromboembolism from carotids

cardioembolism: post-MI, AF, valve disease

Hyperviscosity: polycythaemia, myeloma, Sickle cell

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98
Q

IX of TIA

A

aim to find cause and define vascular risk

FBC, U+E, ESR, Glucose, Lipids

CXR

ECG

Echo

Carotid doppler +/- angiography

Consider brain imaging: diffusion weighted MRI

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99
Q

Mx of TIA

A

avoid driving for 1 month

  1. Antiplatelet therapy/ Anticoagulation:

aspirin/ clopidogrel 300mg for 2 wks then 75mg/d

(add dipyridamole to aspirin)

warfarin if cardiac emboli: AF, MI, MS

  1. Control cardiac RFs: smoking, BP, lipids, diet, exercise, DM
  2. Assess risk of subsequent stroke: ABCD2 score
  3. Specialist referral to TIA clinic
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100
Q

what is the ABCD2 score?

A

Age ≥ 60

BP ≥ 140/90

Clinical features

a. unilateral weakness (2 pts)
b. speech distrubance w/o weakness

Duration

a. ≥ 1h (2 points)
b. 10-59 min

DM

7 points max

predicts stroke risk following TIA

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101
Q

What is the ABCD2 score used for?

A

predicts stroke risk following TIA

score ≥ 6 = 8% risk within 2 days. 35% risk within 1 wk

score ≥4 = pt assessment by specialist within 24h

all pts w suspected TIA should be seen by specialist within 7d

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102
Q

What is a subdural haemorrhage?

A

haematoma between dura and arachnoid

bleeding from bridging veins between cortex and sinuses

often due to minor trauma that occured a long time previously

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103
Q

Risk factors of subdural haemorrhage?

A

elderly: brain atrophy
falls: epileptics, alcoholics
anticoagulation: increased bleeding risk

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104
Q

symptoms of subdural haemorrhage?

A

headache

fluctuating GCS, sleepiness

gradual physical/ mental slowing

unsteadiness

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105
Q

signs of subdural haemorrhage?

A

raised ICP

papilloedema

localising signs occur late

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106
Q

ix of subdural haemorrhage?

A

CT/ MRI head

crescentic haematoma over one hemisphere

clot goes from white -> grey over time

midline shift

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107
Q

mx of subdural haemorrhage?

A

1st line: irrigation/ evacuation via burr-hole craniostomy

2nd: craniotomy then suction/ irrigation to remove the clot

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108
Q

extradural haemorrhage usually due to?

A

fracture over pterion

-> laceration of middle meningeal artery and vein

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109
Q

presentation of extradural haemorrhage?

A

after head injury, there may be a lucid interval.

deterioration of GCS after head injury that caused no LOC/ following initial improvment in GCS

increased ICP: headache, vomiting, confusion, fits, ipsilateral blown pupil (3rd n palsy) +/- hemiparesis w upgoing plantars and increased reflexes

Brainstem compression

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110
Q

signs of brainstem compression?

A

deep irregular breathing

cushing response (late): high BP, low HR

death by cardiorespiratory arrest

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111
Q

Ix of extradural haemorrhage?

A

CT head

  • lens shaped haematoma
  • skull fracture
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112
Q

subdural vs extradural haemorrhage?

difference between where the blood is

A

extradural: blood between skull and dura
subdural: blood between dura and arachnoid

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113
Q

mx of extradural haemorrhage?

A

neuroprotective ventilation (Oxygen)

if raised ICP -> IV mannitol or hypertonic saline

Craniectomy for clot evacuation and vessel ligation.

if small haematoma -> may be treated conservatively but must be observed in case of sudden deterioration

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114
Q

if high ICP, IV mannitol or hypertonic saline?

A

Hypertonic saline is increasingly considered a safer and more effective alternative.

In the trauma situation it has the advantage of repleting/preserving intravascular volume rather than increasing fluid loss by diuresis.

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115
Q

what is neuroprotective ventilation?

A

O2>100, CO2 35-40

excessive hypocapnia should be avoided, as it causes cerebral vasoconstriction.

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116
Q

in extradural haemorrhage, what is the cut off for surgical management?

A

all patients with an EDH volume greater than 30 cm3 should have a surgical evacuation regardless of GCS.

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117
Q

cerebral vein thrombosis

risk factors?

A

triggered by infections of the ear, face, or neck

oestrogen use (e.g ocp) and pregnancy

inherited and acquired clotting disorders

drugs e.g. tranexamic acid

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118
Q

Sinus thrombosis symptoms?

A

severe headache (can be of sudden onset/ develops over few days)

nausea, vomiting

blurred vision

serizures, confusion

other neuro symtpoms

symptoms depend on location and extension of clot

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119
Q

sagittal sinus thrombosis symptoms?

A

Headache, vomiting, seizures, ↓ vision, papilloedema

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120
Q

transverse sinus thrombosis symptoms?

A

Headache ± mastoid pain, focal neuro, seizures,

papilloedema

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121
Q

symptoms of sigmoid sinus thrombosis

A

cerebellar signs

lower CN palsies

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122
Q

symptoms of inferior petrosal sinus thrombosis?

A

5th and 6th CN palsies

(gradenigo’s syndrome)

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123
Q

symptoms of cavernous sinus thrombosis?

A

headache +/- tearing

painful opthalmoplegia

eyelid oedema

proptosis

fever

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124
Q

Ix of cortical vein thrombosis?

A

exclude SAH and meningitis

CT/ MRI venography

LP: high pressure, may show RBCs, xanthochromia

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125
Q

Mx of cortical vein thrombosis

A

LMWH -> warfarin (INR 2-3)

Fibrinolytics e.g. streptokinase

Thrombophilia screen

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126
Q

Features of meningitis

A

Headache

neck stiffness

  • kernig’s +ve
  • Brudzinski’s +ve

Photophobia

N+V

reduced GCS

seizures, focal neurology

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127
Q

what is Brudzinski’s sign?

A

+ve in meningitis

lifting head would cause flexion of legs and thighs

due to neck rigidity

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128
Q

What is Kernig’s sign?

A

+ve in meningitis

Severe stiffness of the hamstrings causes an inability to straighten the leg when the hip is flexed to 90 degrees.

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129
Q

signs in meningococcal septicaemia

A

fever

high HR, low BP

high CRT

purpuric non blanching rash

DIC

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130
Q

antibiotic mx of meningitis in the community?

A

benpen 1.2g IM

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131
Q

antibiotic mx of meningitis in under 50s?

A

IV Ceftriaxone 2g

or IM BD

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132
Q

antibiotic mx of meningitis in >50s?

A

Ceftriaxone + Ampicillin

IV

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133
Q

viral meningitis mx?

A

aciclovir

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134
Q

organisms that cause meningitis

A

enteroviruses/ HSV2

Meningococcus

Pneumococcus

Listeria

TB

cryptococcus

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135
Q

why is dexamethasone used in acute bacterial meningitis?

A

Bacterial meningitis is fatal in 5% to 40% of children and 20% to 50% of adults despite treatment with adequate antibiotics.

corticosteroids can reduce the inflammation assoc w infection

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136
Q

CSF findings:

turbid appearance, mainly neutrophils, high WCC, low glucose (<1/2 plasma), high protein

A

Bacterial meningitis

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137
Q

CSF findings:

clear, lymphocytic, normal glucose, normal protein

A

viral meningitis

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138
Q

CSF findings:

fibrin web, lymphocytic, low glucose, high protein

A

TB meningitis

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139
Q

Contraindications to LP?

A

signs of raised ICP:

reduced GCS, bradycardia/hypotension, focal neuro, abnormal posturing, papilloedema, tense bulging fontanelle

shock

DIC

convulsions until stabilised

coagulation abnormalities

superficial infection at LP site

resp insufficiency

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140
Q

why is LP contraindicated in resp insufficiency?

A

lumbar puncture is considered to have a high risk of precipitating respiratory failure in the presence of respiratory insufficiency

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141
Q

CT head of encephalitis caused by HSV

  • most likely finding?
A

focal bilateral temporal involvement

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142
Q

Ix of encephalitis?

A

Bloods: cultures, PCR, malaria film

CT head

LP

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143
Q

mx of encephalitis

A

aciclovir STAT

supportive measures

phenytoin for seizures

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144
Q

risk factors for cerebral abscess

A

infection of ear, sinus, dental

skull #

congenital heart disease

endocarditis

bronchiectasis

immunosuppression

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145
Q

signs of cerebral abscess

A

seizures

fever

signs of raised ICP

localizing signs

signs of infection elsewhere

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146
Q

Ix of Cerebral abscess

A

CT/MRI head: ring enhancing lesion

raised WCC, ESR

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147
Q

Mx of cerebral abscess

A

neurosurgical referral

treat raised ICP (mannitol/ hypertonic saline)

Antibiotics e.g. ceftriaxone

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148
Q

what is epilepsy?

A

recurrent tendency to spontaneous, intermittent, abnormal electrical activity in part of the brain, manifest as seizures

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149
Q

causes of non-epileptic / provoked seizures

A

alcohol/ benzo/ opiate withdrawal

metabolic: Glucose, Na, Ca, urea, NH2

raised ICP: meningitis, encephalitis, HIV, cysticerosis

eclampsia

pseudoseizures

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150
Q

causes of acquired seizures

A

post-stroke

cortical scarring: trauma, infection

SOL

MS

SLE

sarcoidosis

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151
Q

what is the prodrome of a seizure?

A

change in mood/ behaviour lasting hrs- days

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152
Q

simple seizure?

A

awareness intact

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153
Q

complex seizure?

A

impaired awareness

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154
Q

secondary generalised seizure?

A

focal -> generalized

e.g. aura -> tonic clonic

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155
Q

what is an aura?

A

simple partial seizure (usually temporal)

experienced as a strange feeling:

  • deja vu/ jamais vu
  • automatisms
  • smells, lights, sounds
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156
Q

diagnostic features of seizure

A

aura

specific trigger e.g. flashing lights

lateral tongue biting

typical movements e.g. tonic-clonic

cyanosis

post-ictal phase

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157
Q

features of west syndrome/ infantile spasms?

A

clusters of head nodding and arm jerks

EEG shows hypsarrhythmia

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158
Q

atonic seizure?

A

sudden loss of muscle tone -> fall

no LOC

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159
Q

myoclonic seizure?

A

sudden jerk of limb, face/ trunk

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160
Q

absence seizure features?

A

Abrupt onset and offset

Short: <10s

Eyes: Glazed, blank stare

Clonus or automatisms may occur

EEG: 3hz spike and wave

stimulated by hyperventilation

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161
Q

localising features of seizures suggesting involvement of occipital lobe?

A

visual phenomena: spots, lines, flashes

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162
Q

localising features of seizures suggesting involvement of parietal lobe?

A

sensory disturbance: tingling, numbness

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163
Q

localising features of seizures suggesting frontal lobe involvement?

A

motor features: jacksonian march, Tood’s palsy, arrest

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164
Q

what is a jacksonian march?

A

The characteristic features of Jacksonian march are (1) it only occurs on one side of the body; (2) it progresses in a predictable pattern from twitching or a tingling sensation or weakness in a finger, a big toe or the corner of the mouth, then marches over a few seconds to the entire hand, foot or facial muscles.

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165
Q

what is Todd’s paresis?

A

transient weakness of a hand, arm, or leg after focal seizure activity within that limb. The weakness may range in severity from mild to complete paralysis.

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166
Q

localising features of seizures suggesting temporal lobe involvement?

A

automaticisms: lip smacking, chewing, fumbling

deja/ jamais vu

abdominal rising/ N+V

emotional disturbance: terror, panic, anger, elation

tastes, smells

delusional behaviour

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167
Q

Pt had a one off seizure while awake and lost consciousness

what advice regarding DVLA and driving?

A

cannot drive for 6 months (providing no more attacks)

+

DVLA’s medical advisers decide there isnt a high risk pt will have another seizure (ie. normal MRI/ EEG)

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168
Q

If first seizure but abnormal EEG/ MRI

advice regarding DVLA and driving?

A

cannot drive for 12 months

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169
Q

Seizures only when asleep?

what advice regarding DVLA and driving

A

cannot drive until past 12 months since first attack

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170
Q

Pt has had epileptic attacks while awake and lost consciousness.

advice re driving and DVLA?

A

Cannot drive til no attack for at least a year

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171
Q

if a epilepsy pt had a seizure because doctor had changed/ reduced anti-epilepsy medicine

what advice re DVLA and driving?

A

have to stop driving until seizure > 6m ago

or

back on previous medication for 6 months

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172
Q

seizures that dont affect consciousness or driving?

advice re driving and DVLA

A

need to contact DVLA.

You may still qualify for a licence if these are the only type of attack you’ve ever had and the first one was 12 months ago.

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173
Q

Bus, coach or lorry license.

advice if pt has had more than one seizure?

A

cannot drive unless

  • no seizure for 10 years
  • haven’t taken any anti-epileptic mx for 10 yrs
  • <2% risk of another seizure
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174
Q

bus, coach or lorry license.

if pt had a one-off seizure?

A

no epileptic attack for 5 years

no anti-epileptic mx for 5 years

must have been assessed in the past 12 months by a neurologist

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175
Q

general advice about epilepsy and seizures

A

diagnosis made by specialist

dont diagnose epilepsy from one seizure

after any seizure, advise against driving, swimming, bath until Dx established

after dx, cannot drive until seizure-free for >1 yr

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176
Q

indications for MRI after a seizure?

A

developed epilepsy as an adult

any evidence of focal onset

seizures continue despite 1st line tx

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177
Q

1st line tx of absence seizures?

A

ethosuximide

sodium valproate

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178
Q

1st line mx of focal seizures?

A

carbamazepine

or

lamotrigine

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179
Q

1st line mx of generalized tonic-clonic seizures

A

sodium valproate

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180
Q

1st line mx of myoclonic seizures

A

sodium valproate

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181
Q

1st line mx of atonic/ tonic seizures

A

sodium valproate

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182
Q

tx of epilepsy in pregnancy

A

avoid valproate

take lamotrigine/ carbamazepine

5 mg folic acid daily

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183
Q

side effects of lamotrigine?

A

skin rash-> SJS

rash may be assoc w hypersensitivity -> fever, raised LFTs, DIC

diplopia, blurred vision

levels affected by enzyme inhibitors/ inducers

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184
Q

status epilepticus

mx?

A

ABC approach

IV lorazepam 2-4 mg IV bolus over 30s

(or buccal midazolam/ rectal diazepam)

can repeat if no response within 2 min

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185
Q

Mx of status epilepticus

after first line tx?

A

IV Infusion of Phenytoin

monitor ECG and BP

CI: bradycardia or heart block

or IV Diazepam

Call anaesthetic for airway support

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186
Q

mx of cerebral oedema with malignancy?

A

dexamethasone

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187
Q

primary survey of pt w head injury

A

A to E approach

A: immobilize C-spine (Hard collar), stabilize airway-> jaw thrust, ?intubation

B: 100% O2, RR

C: IV access, HR, BP

D: GCS, pupils

E: expose pt, look for obvious injuries

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188
Q

Head injury

secondary survey

what would you look for specifically?

A

lacerations

obvious facial/ skull deformity

CSF leak from nose or ears

Battle’s sign, Racoon eyes

Blood behind Tympanic Membrane

C spine tenderness /deformity

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189
Q

Hx after head injury

A

GCS after injury

?LOC

headache

fits

vomiting

amnesia

alcohol?

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190
Q

mx of head injury?

A

neurosurgical opinion if signs of raised ICP, CT evidence of intracranial bleed, significant skull #

Admit if:

  • abnormalities on imaging
  • CNS signs: vomiting, severe headache
  • GCS not returned to 15
  • difficult to assess: alcohol, post ictal

Neuro obs half hourly until GCS 15:

GCS, pupils, HR/ BP/ RR/ SpO2/ Temp

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191
Q

Guidelines to intubate after head injury

A

GCS ≤ 8

PaO2 < 9kPa on air / <13 kPa on O2

or PCO2 > 6 kPa

Spontaneous hyperventilation: PCO2 < 4 KPa

Respiratory irregularity

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192
Q

GCS

Eyes

what is 1-4?

A

4 - spontaneous eye opening

3 - open to voice

2 - open to pain

1 - no opening

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193
Q

GCS

Verbal

what is 1- 5?

A

5 - Orientated conversation

4 - confused conversation

3 - inappropriate speech

2 - incomprehensible sounds

1 - no speech

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194
Q

GCS

Motor

what is 1-6?

A

6: obeys commands

5 - localises pain

4 - withdraws to pain

3 - decorticate posturing to pain (flexor)

2 - decerebrate posturing to pain (extensor)

1 - no movement

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195
Q

After Head injury,

CT head guidelines?

A

BANGS LOC

Break: open, depressed or base of skull #

Amnesia > 30 min retrograde

Neuro deficit or seizure

GCS: <13 at any time or <15 2h after injury

Sickness: Vomited >1x

LOC or amnesia and any of:
- Age ≥65

  • dangerous mechanism: RTA, fall from great height
  • coagulopathy (inc warfarin)
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196
Q

risk of intracranial haematoma in adults if confused + skull #?

A

1:4

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197
Q

risk of intracranial haematoma in adults if fully conscious + skull #?

A

1:30

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198
Q

risk of intracranial haematoma in adults if confused + no skull #?

A

1:100

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199
Q

risk of intracranial haematoma in adults if fully conscious + no skull #?

A

very low.

<1:1000

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200
Q

symptoms of raised ICP

A

headache: worse on waking, lying down, bending forward, on straining, coughing

Vomiting

reduced consciousness

visual disturbance: transient visual obscurations and visual loss

pulse synchronous tinnitus (pulsatile tinnitus)

(red flag: waking pt up from sleep)

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201
Q

signs of raised ICP

A

papilloedema

diplopia due to sixth cranial nerve palsy (or other)

reduced GCS

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202
Q

Most common brain tumour is?

A

secondary metastases: e.g. from breast, lung, melanoma

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203
Q

most common primary brain tumour in adults?

A

glioblastoma multiforme

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204
Q

presentation of idiopathic intracranial hypertension?

A

typically obese females

signs and symptoms of raised ICP e.g. headache,

visual disturbances

e.g. blurred vision, 6th CN palsy, enlarged blind spot

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205
Q

causes of idiopathic intracranial HTN?

A

usually idiopathic

may be secondary to venous sinus thrombosis or drugs

206
Q

mx of idiopathic intracranial HTN

A

weight loss if overweight

Acetazolamide: reduces CSF production

loop diuretics

prednisolone - to relieve headaches and reduce the risk of vision loss

regular LPs to drain excess CSF

lumbar-peritoneal shunt may be necessary if drugs fail and visual loss deteriorates

207
Q

ix of idiopathic intracranial HTN

A

full neurological examination

assessment of eyes and vision

CT/ MRI head

LP to detect opening pressure

208
Q

prognosis of idiopathic intracranial HTN?

A

usually self limiting

permanent visual loss in 10%

209
Q

types of cerebral oedema

A

Vasogenic (increased capillary permeability): trauma, tumour, ischaemia, infection

Cytotoxic: e.g. from hypoxia

Interstitial: e.g. obstructive hydrocephalus, low Na+

210
Q

what are some causes of raised ICP?

A

haemorrhage

SOL- tumours, abscess

infection

hydrocephalus

cerebral oedema

cerebral venous thrombosis

211
Q

what is Cushing’s Reflex?

A

a physiological nervous system response to increased ICP

results in Cushing’s triad of:

raised BP, bradycardia, irregular breathing

usually seen in terminal stages of acute head injury and may indicate imminent brain herniation

212
Q

what is Cheyne-Stokes respiration?

A

an abnormal pattern of breathing characterized by progressively deeper, and sometimes faster, breathing followed by a gradual decrease then stop.

pattern repeats with each cycle usually taking 30s - 2 min

213
Q

acute mx of raised ICP

A

ABC

Treat seizures and correct hypotension

Elevate bed to 40 degrees

Neuroprotective ventilation:

PaO2>13, PCO2: 4.5, Good sedation +/- NM blockade

Mannitol or hypertonic Saline: may reduce ICP in short-term but may cause rebound raised ICP later

214
Q

what is tonsillar herniation?

A

increased pressure in posterior fossa

leading to displacement of cerebellar tonsils through foramen magnum.

-> compression of brainstem and cardiorespiratory centres in medulla

215
Q

symptoms of tonsillar herniation?

A

CN6 palsy

upgoing plantars

  • > irregular breathing
  • > apnoea

Death

216
Q

what is an uncal hernation?

A

compression of ipsilateral inferomedial temporal lobe (uncus) against free margin of tentorium cerebelli

217
Q

uncal herniation symptoms?

A

ipsilateral CN3 palsy: dilation of pupil then down and out

ipsilateral corticospinal tract: contralateral hemiparesis

may cause compression of contralateral corticospinal tracts -> ipsilateral hemiparesis (Kernohan’s notch)

218
Q

what is the kernohan’s notch?

A

a secondary condition caused by a primary injury on the opposite hemisphere of the brain

due to transtentorial (uncal) herniation

-> causes ipsilateral motor weakness/ paralysis

219
Q

what is a subfalacine herniation?

A

displacement of cingulate gyrus (medial frontal lobe) under falx cerebri

220
Q

Symptoms of subfalcine herniation?

A

compression of ACA -> stroke symptoms

e.g. contralateral motor/sensory loss in legs>arms

abulia (pathological laziness)

221
Q

Postural instability -> falls

+

speech distrubance (+ dementia)

+

vertical gaze palsy

Dx?

A

Progressive supranuclear palsy

222
Q

Autonomic dysfunction: postural hypotension, bladder dysfunction

+

cerebellar + pyramidal signs

+

rigidity > tremor?

A

Multiple systems atrophy

(shy drager)

223
Q

parkinsonism + visual hallucinations + fluctuating cognition?

A

Lewy body dementia

224
Q

parkinsonism + aphasia, dysarthria, apraxia

+

akinetic rigidity in one limb

+

astereognosis (cortical sensory loss)

+ alien limb phenomenon

A

Corticobasilar degeneration

225
Q

what is astereognosis?

A

Astereognosis (or tactile agnosia if only one hand is affected) is the inability to identify an object by active touch of the hands without other sensory input, such as visual or sensory information.

226
Q

what is alien hand syndrome?

A

prevalent in 60% of ppl with corticobasal degeneration

failure of an individual to control the movements of his or her hand, which results from the sensation that the limb is “foreign”

+

The movements of the alien limb are a reaction to external stimuli and do not occur sporadically or without stimulation

227
Q

other causes of parkinsonism

e.g. infection, vascular, drugs, trauma, genetic

A

infection: syphilis, HIV, CJD
vascular: multiple infarcts in substantia nigra
drugs: antipsychotics, metoclopramide
trauma: dementia pugilistica

Genetic: wilson’s disease

228
Q

features of parkinsonism?

A

tremor: worse at rest, exacerbated by distraction, pill rolling
rigidity: increased tone (lead pipe), rigidity + tremor -> cog wheel rigidity

bradykinesia

gait: decreased arm swing, festinance, freezing

229
Q

what produces the cog wheel rigidity in parkinsons?

A

rigidity (increased tone in all muscle groups)

+ tremor

230
Q

features of bradykinesia of parkinsons?

A

slow initiation of movement with reduction of amplitude on repetition

expressionless face

monotonous voice

micrografia

231
Q

how is Parkinson’s disease diagnosed?

A

Clinical diagnosis

DaTSCAN: Ioflupane has a high binding affinity for presynaptic dopamine transporters (DAT)

232
Q

on-off effect of motor fluctuations in parkinsons?

A

refers to a switch between mobility and immobility in levodopa-treated patients, which occurs as an end-of-dose or “wearing off” worsening of motor function or, much less commonly, as sudden and unpredictable motor fluctuations.

Over time: much less ON and more OFF

233
Q

invasive mx of parkinsons?

A

deep brain stimulation

Consider deep brain stimulation for people with advanced Parkinson’s disease whose symptoms are not adequately controlled by best medical therapy

234
Q

Mx of Parkinson’s disease symptoms by MDT?

A

PD specialist nurses:

point of contact for support, including home visits when appropriate + clinical monitoring and medicines adjustment

Physiotherapy

Occupational Therapy:

help w ADLs

SALT:

to improve speech and communication +

improve the safety and efficiency of swallowing to minimise the risk of aspiration

Dietician:

235
Q

mx of drooling of saliva in PD pts when SALT has been ineffective?

A

glycopyrronium bromide

contraindicated (for example, in people with cognitive impairment, hallucinations or delusions, or a history of adverse effects following anticholinergic treatment)

236
Q

mx of Parkinson’s disease dementia?

A

anticholinesterase inhibitor e.g. rivastigmine

237
Q

mx of psychotic symptoms (hallucinations and delusions) in PD pts?

A

Do not treat hallucinations and delusions if they are well tolerated

or

Reduce the dosage of any Parkinson’s disease medicines that might have triggered hallucinations or delusions, taking into account the severity of symptoms and possible withdrawal effects.

or

Quetiapine

238
Q

mx of daytime sleepiness in PD pts

A

advise not to drive

adjust PD medications

consider modafinil

239
Q

mx of rapid eye movement sleep behaviour disorder in PD pts?

A

Consider clonazepam or melatonin

if a medicines review has addressed possible pharmacological causes

240
Q

1st line mx of PD patients whose motor symptoms impact on their quality of life

A

levodopa

e.g. pts who are biologically frail with comorbidities w lower baseline fitness

241
Q

1st line mx of PD patients in early stages where motor symptoms do not impact on their quality of life

A

e.g. pts who are biologically fit

Dopamine agonists e.g. ropinirole, pramipexole

Levodopa

MAO-B inhibitors: rasagiline, selegiline

242
Q

what is multiple sclerosis?

A

A chronic inflammatory condition of the CNS characterised by multiple plaques of demyelination disseminated in time and space.

243
Q

classification of multiple sclerosis?

A

Relapsing-remitting: 80%

Secondary progressive

Primary progressive: 10%

Progressive relapsing

244
Q

pathophysiology of multiple sclerosis?

A

Plaques of demyelination are hallmark

CD4 cell-mediated destruction of oligodendrocytes →demyelination and eventual neuronal death.

245
Q

what is Lhermitte’s sign?

A

seen in MS

neck flexion ->

electric shocks traveling down neck -> trunk -> limbs

246
Q

presentation of MS?

A

TEAM

tingling (sensory disturbance)

eye: optic neuritis (decreased central vision + pain w eye movement)

ataxia + other cerebellar signs

Motor: usually spastic paraparesis

247
Q

clinical features of sensory disturbance in MS patients?

A

paraesthesia

decreased vibration sense

trigeminal neuralgia

248
Q

clinical features of motor disturbance of MS patients?

A

spastic weakness

transverse myelitis (inflammation extends across the entire width of the spinal cord)

249
Q

GI disturbances in MS?

A

swallowing problems

constipation

250
Q

Genitourinary problems in MS?

A

Erectile dysfunction + anorgasmia

urinary retention

incontinence

251
Q

cerebellar disturbances in MS?

A

falls

scanning dysarthria

trunk and limb ataxia

252
Q

eye disturbances in MS?

A

diplopia

visual phenomena

bilateral conjugate gaze palsy

optic neuritis -> atrophy

253
Q

what is Uhthoff’s phenomenon?

A

worsening of neurologic symptoms in multiple sclerosis (or other neurological, demyelinating conditions) when the body gets overheated

e.g. from hot weather, fever, exercise, saunas or hot tubs

254
Q

presenting complaint of optic neuritis in multiple sclerosis patients?

A

pain on eye movement

rapidly worsening central vision

uhthoff’s phenomenon: vision worsens with heat (hot meal, bath, exercise)

255
Q

Findings of optic neuritis on examination?

A

Decreased visual acuity

decreased colour vision (usually red affected first)

central scotoma

RAPD

256
Q

what is internuclear ophthalmoplegia?

A

a disorder of conjugate lateral gaze in which the affected eye shows impairment of adduction

  1. affected (ipsilateral) eye adducts minimally, if at all
  2. contralateral eye abducts, with nystagmus
  3. divergence of the eyes leads to horizontal diplopia

convergence generally preserved

257
Q

what is the pathology causing internuclear ophthalmoplegia?

A

multiple sclerosis is often the cause- may cause bilateral INO

caused by injury/ disruption of medial longitudinal fasciculus that allows conjugate eye movement by connecting contralateral (PPRF-abducens) CN6 to ipsilateral (oculomotor) CN3

258
Q

Ix of Multiple Sclerosis?

A

MRI Brain + Spine: typically hyper intense plaques

LP: IgG oligoclonal bands

Antibiodies: anti-Myelin basic protein

Evoked potentials: delayed auditory, visual and sensory

259
Q

Diagnosis of MS?

A

clinical

demonstration of lesions disseminated in time and space

may use Macdonald Criteria

260
Q

what is Devic’s syndrome?

A

loss of vision and spinal cord function.

optic neuritis + spinal cord dysfunction -> muscle weakness, reduced sensation/ loss of bladder or bowel control

similar to Multiple Sclerosis

261
Q

differentiate between MS and Devic’s syndrome?

A

Neuromyelitis optica (NMO)- IgG: highly specific for Devic’s syndrome

Devic’s = neuromyelitis optica

MS variant w transverse myelitis and optic atrophy

262
Q

mx of multiple sclerosis long-term

A

MDT team: specialist nurse, neurologist, physio, OT

regular follow up in MS clinic

Regular MRI scans (yearly)

263
Q

mx of Multiple Sclerosis during an acute attack?

A

methylprednisolone

  • decreases duration and severity of attacks
  • doesnt influence long-term outcome
    e. g. oral methylprednisolone 0.5 g daily for 5 days
264
Q

what are some disease-modifying agents recommended for use for preventing relapse in MS patients?

A

Natalizumab: anti-alpha 4 integrin Ab

(decreases relapses by 2/3 in RRMS)

Alemtuzumab: anti-CD52 (2nd line in RRMS)

IFNB

Cladiribine, Dimethyl fumarate, fingolimod, ocrelizumab, teriflunomide

265
Q

symptomatic medication for MS patients suffering from fatigue?

A

amantadine

Explain that MS-related fatigue may be precipitated by heat, overexertion and stress or may be related to the time of day.

266
Q

symptomatic medication for MS patients suffering from depression?

A

SSRI e.g. citalopram

267
Q

symptomatic medication for MS patients suffering from pain?

A

if trigeminal neuralgia: carbamazepine

other neuropathic pain: gabapentin, pregabalin, amitriptyline, duloxetine

268
Q

symptomatic medication for MS patients suffering from spasticity?

A

assess and offer treatment for factors that may aggravate spasticity such as constipation, urinary tract or other infections, inappropriately fitted mobility aids, pressure ulcers, posture and pain.

gabapentin/ baclofen

269
Q

symptomatic management of MS patients suffering from oscillopsia?

A

gabapentin

270
Q

symptomatic management of MS patients suffering from urgency/ frequency?

A

oxybutynin/ tolterodine

271
Q

symptomatic management of MS patients suffering from emotional lability?

A

amitriptyline

272
Q

better vs worse prognostic signs of MS?

A

better:

female, <25, sensory signs @ onset, long interval between relapses, few MRI lesions

poor:

older, male, motor signs @ onset, many relapses early on, many MRI lesions, axonal loss

273
Q

The following cranial nerves also carry parasympathetic fibres:

a. oculomotor
b. trigeminal
c. trochlear
d. hypoglossal
e. optic

A

A

Cranial nerves 3, 7, 10 and S3-5 carry parasympathetic fibres.

274
Q

what is horner’s syndrome?

A

lesion of sympathetic supply to the eye

meiosis, ptosis, anhidrosis

275
Q

what is the visual change assoc with swollen optic discs (papilloedema)?

A

enlarged blind spot

visual obscurations starting from periphery

276
Q

features of optic neuritis?

A

painful on eye movement

reduced visual acuity

loss of red green colour vision

central scotoma

277
Q

herniation of uncus of the temporal lobe can cause what type of nerve palsy?

A

third nerve palsy

278
Q

causes of mononeuropathies?

A

vasculitides e.g. polyarteritis nodosa

diabetes - causes microvascular infarcts in individual nerves

entrapment and pressure palsies

e.g. Carpal tunnel

279
Q

homonymous hemianopia

where could the lesion be?

A

optic tract

optic radiation

occipital lobe

280
Q

grasp reflex absent

which lobe has pathology?

A

frontal lobe

281
Q

what is pseudobulbar palsy?

A

characterized by the inability to control facial movements (such as chewing and speaking)

condition is usually caused by the bilateral damage to corticobulbar pathways (UMN lesion)

282
Q

which cranial nerves lie in close proximity to the cerebellopontine angle?

A

V, VII, VIII cranial nerves

283
Q

what type of deafness does otosclerosis produce?

A

conductive deafness

due to reduced compliance in the bony ossicles

284
Q

how does excess prolonged noise lead to deafness?

A

damages the cochlear hair cells

-> sensorineural deafness

285
Q

what is an acoustic neuroma?

A

develops on the vestibular portion of the VIII th nerve

-> progressive unilateral sensorineural deafness

286
Q

tx of physiological/ essential tremors?

A

usually respont to beta blockers

287
Q

commonest cause of small, poorly reactive pupil?

A

old age

288
Q

lesion in midbrain may cause what change to eyes?

A

enlarged pupil

289
Q

what is a sixth nerve palsy?

A

decreased abduction of affected eye

lateral rectus palsy

290
Q

how does third nerve palsy present?

A

pupillary dilatation

(third n carries parasympathetic fibres to the constrictor pupillae)

ptosis

(levater palpebrae superioris)

diplopia in all positions of gaze

291
Q

internuclear ophthalmoplegia

  • where is the lesion?
A

medial longitudinal fasciculus

292
Q

feature of ramsay-hunt syndrome?

A

painful vesicles

hyperacusis (nerve to stapedius affected)

loss of taste to anterior 2/3rd of tongue

293
Q

features of anterior spinal artery occlusion?

A

loss of pain and sensation

dorsal columns (proprioception and vibration) spared

294
Q

what causes painful neuropathies?

A

due to damage of slow unmyelinated fibres in peripheral nerves that carry pain and temp sensation

common causes: alcohol overuse, diabetes

295
Q

what is cervical spondylosis?

A

age-related wear and tear affecting the spinal disks in your neck

296
Q

features of cervical spondylosis?

A

can cause UMN signs due to compression of cervical spinal cord

+/- LMN signs due to compression of cervical roots

pain often worse at night

secondary headaches are common

297
Q

what is temporal arteritis assoc with?

A

polymyalgia rheumatica

298
Q

features of temporal arteritis?

A

headache

jaw claudication and scalp tenderness

(due to ischaemia of scalp/ muscles of mastication)

299
Q

what is the dominant lobe involved with?

A

the dominant cerebral cortex is on the LEFT in majority of R-handed people and is specifically involved in reading, maths (dyscalculia), writing and langugage.

More subtle functions of the dominant parietal lobe include naming fingers (finger agnosia) and left-right discrimination.

300
Q

monocular visual loss associated with pain on eye movement

suggests?

A

Optic neuritis

301
Q

MS typically presents with?

A

optic neuritis

302
Q

what is capgras syndrome seen in?

(patient accusing spouse of being an imposter)

A

Lewy body dementia

303
Q

why is thymoma removed in multiple sclerosis?

A

remove potential risk of malignant transformation and not to improve the underlying disease

304
Q

features of gerstmann syndrome?

A

Dysgraphia/agraphia: deficiency in the ability to write

Dyscalculia/acalculia: difficulty in learning or comprehending mathematics

Finger agnosia: inability to distinguish the fingers on the hand

Left-right disorientation

305
Q

A left homonymous hemianopia may be due to?

A

lesion on right optic tract/ radiation

or

lesion of right occipital lobe

306
Q

where is the lesion?

superior quadrantanopia

A

mnemonic = PITS (Parietal-Inferior, Temporal-Superior)

lesion in temporal lobe

or due to upper optic radiation

307
Q

where is the lesion?

inferior quadrantanopia

A

mnemonic = PITS (Parietal-Inferior, Temporal-Superior)

lesion in parietal lobe

or lower optic radiation

308
Q

what happens when u give folate to a pt with B12 deficiency?

A

giving folate to a patient deficient in B12 can precipitate subacute combined degeneration of the cord

Always ensure vitamin B12 levels are checked (and replenished) before giving folate for a macrocytic anaemia.

309
Q

features of subacute combined degeneration of the cord?

A

Damage to the dorsal columns - loss of proprioception, light touch and vibration sense (sensory ataxia and a positive Romberg’s test).

Damage to lateral columns - spastic weakness and upgoing plantars (UMN signs).

Damage to peripheral nerves - absent ankle and knee jerks (LMN signs).

310
Q

what is mononeuritis multiplex?

A

simultaneous or sequential involvement of individual non-contiguous nerve trunks.

acute or subacute loss of sensory and motor function of individual nerves

as the disease progresses, deficit(s) becomes more confluent and symmetrical, making it difficult to differentiate from polyneuropathy.

311
Q

what psychiatric conditions are common comorbidities of parkinsons?

A

depression is the most common feature (affects about 40%)

dementia

psychosis

sleep disturbances

312
Q

acute mx of migraine?

A

triptan + NSAID or triptan + paracetamol

313
Q

prophylactic mx of migraine?

A

topiramate or propranolol ‘according to the person’s preference, comorbidities and risk of adverse events’.

Propranolol should be used in preference to topiramate in women of child bearing age as it may be teratogenic and it can reduce the effectiveness of hormonal contraceptives

314
Q

what is Hoffman’s sign?

A

Hoffmann sign was elicited by flicking the nail of the middle finger. Any flexion of the ipsilateral thumb and/or index finger was considered positive.

‘finger flexor reflex’

problem in corticospinal tract (CNS)

315
Q

what is degenerative cervical myelopathy?

A

often mistaken for carpal tunnel syndrome

Pain (affecting the neck, upper or lower limbs)

Loss of motor function (loss of digital dexterity, preventing simple tasks such as holding a fork or doing up their shirt buttons, arm or leg weakness/stiffness leading to impaired gait and imbalance

Loss of sensory function causing numbness

Loss of autonomic function (urinary or faecal incontinence and/or impotence) - these can occur and do not necessarily suggest cauda equina syndrome in the absence of other hallmarks of that condition

316
Q

ix of degenerative cervical myelopathy?

A

MRI of cervical spine = gold standard test

It may reveal disc degeneration and ligament hypertrophy, with accompanying cord signal change.

317
Q

mx of degenerative cervical myelopathy?

A

urgently referred for assessment by specialist spinal services (neurosurgery or orthopaedic spinal surgery).

decompressive surgery

timing of surgery is important, as any existing spinal cord damage can be permanent

Early treatment (within 6 months of diagnosis) offers the best chance of a full recovery

318
Q

mx of malignancy causing cord compression?

A

Dexamethasone IV

consider chemo, radiotherapy and decompressive laminectomy

319
Q

mx of abscess causing cord compression?

A

abx and surgical decompression

320
Q

what is the cauda equina?

A

spinal cord itself ends at L1

horse’s tail

a bundle of spinal nerves and spinal nerve rootlets, L2-5, S1-5 and coccygeal n

321
Q

cauda equina syndrome?

A

saddle anaesthesia

back pain

radicular pain down legs

bilateral flaccid arreflexic lower limb weakness

urinary/ faecal incontinence

poor anal tone

neurosurgical emergency

322
Q

Mx of cauda equina syndrome?

A

Neurosurgical emergency!

urgent imaging (MRI spine)

surgical decompression

323
Q

what is the conus medullaris?

A

the tapered, lower end of the spinal cord.

occurs near lumbar vertebral L1, L2, occasionally lower.

324
Q

conus medullaris syndrome?

A

mixed UMN/ LMN weakness

early constipation and retention

back pain

sacral sensory disturbanced

ED

325
Q

Mx of conus medullaris syndrome?

A

neurosurgical emergency

urgent Imaging

surgical decompression

326
Q

What is spondylosis?

A

degeneration of the spinal column from any cause

usually due to trauma or age related wear and tear

commonly affects verterbral bodies and facet joints

may cause -> spinal cord or nerve root compression

327
Q

presentation of cervical spondylosis?

A

usually asympto

neck stiffness +/- crepitus

stabbing/ dull arm pain

upper limb motor and sensory disturbances according to compression level

can -> myelopathy w quadraparesis and sphincter dysfunction

328
Q

Lhermitte’s sign?

A

neck flexion -> tingling down spine

seen in MS/ compression of spinal cord

329
Q

signs of cervical spondylosis?

A

Lhermitte’s sign: neck flexion -> tingling down spine

Hoffmann’s reflex: flick to middle finger pulp → brief pincer flexion of thumb and index finger (suggests hypertonia)

330
Q

ix of cervical spondylosis?

A

MRI c spine

331
Q

mx of cervical spondylosis?

A

conservative: stiff collar, analgesia

Medical: transforaminal steroid injection

Surgical: decompression- laminectomy or laminoplasty

332
Q

presentation of lumbosacral spondylosis?

A

L5 and S1 roots most commonly compressed by prolapse of L4/5, L5/S1 discs

may present as severe pain on sneezing/ coughing

lower back pain

sciatica - shooting radicular pain down buttock and thigh

333
Q

signs of lumbosacral spondylosis?

A

limited spinal flexion

pain on straight leg raise

334
Q

L5 root compression features?

A

weak hallux extension +/- foot drop

(in foot drop due to L5 radiculopathy, weak inversion (tib post) helps distinguish from peroneal n palsy)

decreased sensation on inner dorsum of foot

335
Q

S1 root compression features?

A

Weak foot plantarflexion and eversion

loss of ankle jerk

calf pain

decreased sensation over sole of foot and back of calf

336
Q

mx of lumbar spondylosis?

A

Conservative: rest, analgesia, mobilisation/physio

Medical: transforaminal steroid injection

Surgical: discectomy or laminectomy may be

considered in cauda-equina syndrome, continuing pain or muscle weakness.

337
Q

what is spinal stenosis?

A

Developmental predisposition ± facet joint osteoarthritis→ generalized narrowing of lumbar spinal canal.

most often lower back and neck

338
Q

presentation of spinal stenosis?

A

spinal claudication

aching or heavy buttock and lower limb pain on walking

rapid onset

parasthesiae/ numbness

pain eased by leaning forward

pain on spine extension

negative straight leg raise

339
Q

ix of spinal stenosis?

A

MRI

340
Q

mx of spinal stenosis?

A

corsets

NSAIDs

epidural steroid injection

canal decompression surgery

341
Q

Pathophysiology of bell’s palsy?

A

inflammatory oedema from entrapment of CNVII in narrow facial canal

usually of viral origin (HSV 1)

75% of facial palsy

342
Q

features of Bell’s Palsy?

A

sudden onset e.g. overnight

complete, unilateral facial weakness in 24-72 h

  • failure of eye closure -> dryness
  • bell’s sign: eyeball rolls up on attempted closure
  • drooling, speech difficulty

Numbness or pain around ear

decreased taste

Hyperacusis: stapedius palsy

343
Q

Ix of Bell’s Palsy?

A

Serology: Borrelia or VZV abs

MRI: SOL, stroke, MS

LP

344
Q

Mx of Bell’s Palsy?

A

prednisolone within 72 h

60mg/d PO for 5/7 followed by tapering

valaciclovir if zoster suspected

protect eye: dark glasses, artificial tears, tape eyes closed at night

345
Q

complications of Bell’s palsy?

A

aberrant neural connections

synkinesis: e.g. blinking causes up turning of mouth

crocodile tears: eating stimulates unilateral lacrimation, not salivation

346
Q

pathophysiology of ramsay hunt syndrome?

A

reactivation of VZV in geniculate ganglion of CNVII (Facial N)

347
Q

features of ramsay hunt syndrome?

A

preceding ear pain or stiff neck

vesicular rash in auditory canal +/- tympanic membrane, pinna, tongue, hard palate

ipsilateral facial weakness, ageusia, hyperacusis

may affect CN8 -> vertigo, tinnitus, deafness

348
Q

mx of Ramsay Hunt syndrome?

A

if diagnosis suspected give valaciclovir and prednisolone within first 72h

349
Q

what is mononeuritis multiplex?

A

2 or more peripheral nerves affected

usually systemic cause: DM most commonly

350
Q

median nerve palsy?

A

sensory: radial 3.5 fingers and palm

tinels and phalens +ve

Thenar wasting

most hand muscles of the anterior forearm -> weakness of wrist and finger flexion + thumb abduction/ flexion/ opposition

351
Q

ulnar nerve palsy?

A

sensory loss: ulnar 1.5 fingers

motor: partial claw hand, hypothenar wasting

weakness and wasting of 1st dorsal interosseous

froment’s sign +ve

352
Q

Radial n palsy?

A

sensory: dorsal thumb root (snuff box)

motor:

low lesion: finger drop

high: wrist drop

v high: triceps paralysis, wrist drop

353
Q

tibial n palsy?

A

sensory loss: sole of foot

motor:

cant plantar flex -> cant stand on tiptoe

weak foot inversion

weak toe flexion

354
Q

common peroneal n palsy?

A

sensory loss: below knee laterally

motor: foot drop (cant walk on heels)

weak ankle dorsiflexion, eversion

(inversion intact)

355
Q

sciatic n palsy?

A

sensory loss: below knee laterally and foot

motor:

hamstrings

all muscles below knee

356
Q

phrenic n palsy?

A

C3-5

orthopnoea + raised hemidiaphragm

357
Q

lateral cutaneous n of thigh palsy?

A

meralgia paraesthetica

  • anterolateral burning thigh pain
358
Q

peripheral neuropathy main causes?

A

DM

B12 deficiency

Alcohol

359
Q

features of peripheral neuropathy?

A

glove and stocking distribution

deep tendon reflexes may be decreased/ absent

signs of trauma or joint deformity (charcot’s joints)

diabetic and alcoholic neuropathies are painful

360
Q

B12 deficiency -> SCDC what fibres are lost first?

A

dorsal columns

361
Q

causes of autonomic neuropathy?

A

DM

HIV

SLE

GBS, LEMS

362
Q

features of autonomic neuropathy?

A

postural hypotension

ED, ejaculatory failure

decreased sweating

constipation/ nocturnal diarrhoea

urinary retention

horners

363
Q

Autonomic function tests?

A

BP: postural drop > 20/10 mmHg

ECG: variation > 10 bpm w respiration

364
Q

what is Miller-Fisher syndrome?

A

variant of guillain-barre

opthalmoplegia + ataxia + areflexia

365
Q

causes of guillain- barre?

A

antibodies cross react to gangliosides

may be idiopathic

bacteria: campylobacter jejuni, mycoplasma

Viruses: CMV, EBV, HSV

Vaccines: esp rabies

366
Q

features of guillain barre?

A

symmetrical, ascending flaccid weakness/ paralysis

LMN signs: areflexia, fasciculations

progressive phase lasts ≤ 4wks

autonomic neuropathy

**breathing problems

367
Q

ix of guillain barre syndrome?

A

serology for anti-ganglioside abs

evidence for infection e.g. stool sample

demyelinating nerve conduction studies: slow conduction velocities

Protein in CSF: protein often > 5.5 g/L, normal WCC

368
Q

Mx of Guillain Barre Syndrome?

A

Supportive:

airway/ ventilation: ITU if FVC < 1.5L

analgesia: NSAIDs, gabapentin
autonomic: may need inotropes, catheter

Antithrombotic: TEDS, LMWH

Immunosuppression: IVIG, plasma exchange

Physiotherapy: prevent flexion contractures

369
Q

what is charcot marie tooth syndrome?

A

a type of hereditary motor and sensory neuropathy

HMSN1:

commonest form

demyelinating

AD mutation

HMSN2:

second commonest

axonal degeneration

370
Q

clinical features of charcot marie tooth

A

onset at puberty

thickened, enlarged nerves esp common peroneal

Motor: foot drop -> high stepping gait

weak ankle dorsiflexion and toe extension

absent ankle jerks

symmetrical muscle atrophy: “champagne bottle” legs due to peroneal muscle wasting, claw hands

Pes cavus (high arched feet)

Sensory: variable loss of sensation in a stocking distribution

neuropathic pain in some

371
Q

Mx of Charcot Marie Tooth?

A

Supportive

Physio

Podiatry

Orthoses e.g. ankle braces

372
Q

Ix of Charcot Marie Tooth?

A

Genetic Testing: PMP22 gene mutation

Nerve conduction studies: decreased conduction speed in HMSN1

373
Q

Characteristics of Motor Neuron Disease?

A

Cluster of degenerative disease characterised by axonal degeneration of neurones in the motor cortex, CN nuclei and anterior horn cells.

UMN and LMN signs

NO sensory loss or sphincter disturbance

dont affect eye movements

374
Q

Causes of motor neuron disease?

A

unknown

10% familial: e.g. SOD1 mutation

375
Q

Ix of motor neuron disease?

A

Brain/ Cord MRI: exclude structural cause

LP: exclude inflammatory cause

EMG: shows denervation

376
Q

Diagnosis of motor neuron disease?

A

Use Revised El Escorial Diagnostic criteria

377
Q

Mx of motor neuron disease?

A

MDT: neurologist, physio, OT, specialist nurse, GP, family

Riluzole: antiglutamatergic that prolongs life by ~3 mo

Supportive:

drooling: propantheline or amitriptyline
dysphagia: NG/ PEG feeding

Resp failure: NIV

Pain: analgesia

spasticity: baclofen

378
Q

prognosis of motor neuron disease?

A

most die within 3 years

-> from bronchopneumonia and resp failure

worse prognosis: elderly, female, bulbar involvement

379
Q

types of MND?

A

Amyotrophic Lateral Sclerosis: 50%

loss of motor neurones in cortex and ant horn -> UMN signs and LMN wasting + fasciculation

Progressive Bulbar Palsy: 10%

only affects CN 9-12 -> bulbar palsy

Progressive muscular atrophy: 10%

anterior horn cell lesion -> LMN signs only

Distal to proximal

Primary lateral sclerosis

loss of Betz cells in motor cortex -> mainly UMN signs

Marked spastic leg weakness and pseudobulbar palsy

no cognitive decline

380
Q

which type of Motor neuron disease has LMN signs only?

A

progressive muscular atrophy

-> only anterior horn cell lesions

381
Q

Features of Bulbar Palsy?

A

LMN lesions of tongue, talking and swallowing

flaccid, fasciculating tongue

speech: quiet or nasal

normal/ absent jaw jerk

loss of gag reflex

382
Q

Pseudobulbar Palsy features?

A

Bilateral lesions above mid pons e.g. corticobulbar tracts -> UMN lesions of swallowing and talking

Spastic tongue

slow tongue movements w slow deliberate speech: hot potato speech

Brisk jaw jerk

Emotional incontinence

383
Q

Bulbar vs Pseudobulbar palsy?

A

Bulbar: LMN lesions of tongue, swallowing, speaking

Pseudobulbar: UMN lesions of tongue, swallowing, talking,

384
Q

features of poliomyelitis?

A

asymmetric LMN paralysis

No sensory involvement

may be confined to upper or lower limbs or both

resp muscle paralysis can -> death

+ fever, sore throat, myalgia

poliovirus affects anterior horn cells

385
Q

Pathophysiology of Duchenne’s Muscular Dystrophy?

A

X-linked recessive, 30% spontaneous -> non functional dystrophin

Dystrophin is important to maintain the muscle fiber’s cell membrane

386
Q

Presentation of duchenne’s muscular dystrophy?

A

~4 yo

muscle loss -> weakness

difficulty standing

calf pseudohypertrophy

Gower’s sign +ve

resp failure

387
Q

Ix of Duchenne’s muscular dystrophy?

A

creatine kinase levels extremely high

388
Q

pathophysiology of Becker’s muscular dystrophy?

A

X linked recessive

partially functioning dystrophin

presents later than duchenne’s, is less severe and has better prognosis

389
Q

pathophysiology of fascioscapulohumeral muscular dystrophy (landouzy-dejerine)?

A

autosomal dominant

affects the skeletal muscles of the face (facio), scapula (scapulo) and upper arms (humeral)

390
Q

presentation of fascioscapulohumeral muscular dystrophy?

A

onset @ 12-14 yo

weakness of face, shoulders and upper arms (often asymmetric w deltoids spared)

Winging of scapula

foot drop

bilat sensorineural hearing loss

life expectancy threatened by resp insufficiency

391
Q

pathophysiology of myotonic dystrophy?

A

autosomal dominant

gradually worsening muscle loss and weakness

muscles often contract and are unable to relax (tonic muscle spasm)

392
Q

presentation of myotonic dystrophy?

A

face:

myopathic facies: long, thin, expressionless

wasting of fascial muscles and SCM

bilateral ptosis

dysarthria

hands:

myotonia: slow relaxation
e. g. unable to release hand after shake

wasting and weakness of distal muscles + areflexia -> wrist drop

percussion myotonia: percuss thenar eminance -> involuntary thumb flexion

others:

frontal balding

cataracts

DM

Cardiomyopathy

dysphagia

testicular atrophy

393
Q

mx of Myotonic dystrophy?

A

no mx for weakness

phenytoin may improve myotonia

caution w GA: high risk of anaesthetic complications

394
Q

features of inclusion body myositis?

A

type of inflammatory myopathy

asymmetric weakness affecting distal and prox muscles

  • early involvement of quads, ankle dorsiflexors and wrist/ finger flexors
  • > loss of grip strength and decreased dexterity

dysphagia is v common

myalgia is uncommon

395
Q

what drugs are assoc w idiopathic intracranial HTN?

A

oral contraceptive pill, steroids, tetracycline, vitamin A, lithium

396
Q

what antiplatelet regimens are recommended for secondary prevention following acute ischaemic stroke?

A

Aspirin 300 mg for 2 weeks after stroke then Clopi 75 mg for the long term

397
Q

Indications for thrombolysis?

A

administered within 4.5 hours of onset of stroke symptoms

haemorrhage has been definitively excluded (i.e. Imaging has been performed)

398
Q

what thrombolysis mx is currently recommended?

A

alteplase

399
Q

pathophysiology of NF1 vs NF2?

A

both autosomal dominant

NF1: aka von Recklinghausen’s syndrome. It is caused by a gene mutation on chromosome 17 which encodes neurofibromin

NF2: gene mutation on chromosome 22

400
Q

Features of NF1?

A

Café-au-lait spots (>= 6, 15 mm in diameter)
Axillary/groin freckles
Peripheral neurofibromas
Iris hamartomas (Lisch nodules) in > 90%
Scoliosis
Pheochromocytomas

401
Q

Features of NF2?

A

Bilateral vestibular schwannomas (SNHL first sign)
Multiple intracranial schwannomas, mengiomas and ependymomas

402
Q

cafe au lait spots in NF1?

at least how many? and size?

A

> 6, >15mm across

403
Q

complications of neurofibromas?

A

sarcomatous change

compression:

  • nerve roots: weakness, pain, paraesthesia

GI: bleeds, obstruction

404
Q

What are Lisch nodules?

A

iris hamartomas

seen in NF1

use a slit lamp

405
Q

mx of NF1?

A

MDT

Yearly BP and cutaneous review

Excise some neurofibromas

genetic counselling

406
Q

Juvenile posterior subcapsular lenticular opacity?

A

form of cataract

bilateral

assoc w NF2

occur before other manifestations and may be useful for screening those @ risk

407
Q

Mx of NF2?

A

Hearing tests from puberty in affected families (bilat vestibular schwannomas)

MRI brain if abnormality detected

(look for schwannomas, meningiomas, gliomas)

408
Q

pathophysiology of myasthenia gravis?

A

autoimmune disease mediated by antibodies against nicotinic Ach receptors

interferes with neuromuscular transmission via depletion of working post synaptic receptor sites

409
Q

presentation of myasthenia gravis?

A

increasing muscular fatigue

  • extra-ocular: bilateral ptosis, diplopia
  • bulbar: voice deteriorates on counting to 50
  • face: myastthenic snarl on attempting to smile
  • neck: head droop
  • limb: asymmetric proximal weakness

normal tendon reflexes

weakness worsened by pregnancy, infection, emotion, drugs (BB, gent, opiates, tetracyclines)

410
Q

Ix of myasthenia gravis?

A

Tensilon Test: IV edrophonium, +ve if power improves within 1 min

Anti-AChR abs increased

EMG: decreased response to a train of impulses

Resp function: decreased FVC

Thymus CT (thymoma may be present)

TFTs

411
Q

Pathophysiology of Lambert-Eaton Myasthenic Syndrome?

A

antibodies to VGCC -> decreased influx of calcium during presynaptic excitation -> decreased presynaptic ACh-vesicle fusion

412
Q

causes of lambert eaton myasthenic syndrome?

A

autoimmune

paraneoplastic e.g SCLC

413
Q

presentation of lambert eaton myasthenic syndrome?

A

Muscle fatigue - movement improves symptoms

leg weakness early (before eyes)

autonomic neuropathy and areflexia

small response to edrophonium

414
Q

antibodies found in lambert eaton myasthenic syndrome?

A

Anti-VGCC abs

415
Q

mx of lambert eaton myasthenic syndrome?

A

IVIG

Do regular CXRs as symptoms may precede Cancer by 4 years

416
Q

Myasthenia gravis assoc w ?

A

<50 yrs: more common in women

assoc with other autoimmune disease (DM, RA, Graves)

thymic hyperplasia

417
Q

Treatment of myasthenia gravis?

A

symptom control

  • anticholinesterase e.g. pyridostigmine

Immunosuppression:

  • tx relapses with prednisolone

Thymectomy:

  • consider if young onset and disease not controlled by anticholinesterases
  • remission in 25%, benefit in further 50%
418
Q

Complications of Myasthenia gravis?

A

myasthenic crisis:

  • weakness of respiratory muscles
  • monitor FVC -> ventilation support if < 20ml/kg
  • plasmapheresis or IVIG
  • tx trigger for relapse (e.g. drugs, infection)
419
Q

pathophysiology of botulism?

A

Botulinum toxin prevents ACh vesicle release

420
Q

Presentation of botulism?

A

Descending flaccid paralysis with no sensory signs

Anti-cholinergic effects: mydriasis, cycloplegia, n/v, dry mouth, constipation

421
Q

mx of botulism?

A

benpen + antiserum

422
Q

cerebellar vermis vs cerebellar hemisphere lesions?

A

Cerebellar hemisphere lesions cause peripheral (‘finger-nose ataxia’)

Cerebellar vermis lesions cause gait ataxia (locomotion)

423
Q

Acute vs chronic subdural haematoma on CT?

A

On CT imaging, acute haematomas appear bright (hyperdense) whereas chronic haematomas appear dark (hypodense).

424
Q

who is at risk of chronic subdural haematomas?

A

Elderly and alcoholic patients are particularly at risk of subdural haematomas since they have brain atrophy and therefore fragile or taught bridging veins.

Rupture of the small bridging veins within the subdural space rupture and cause slow bleeding.

Presentation is typically a several week to month progressive history of either confusion, reduced consciousness or neurological deficit.

425
Q

presentation of intrinsic cord disease?

A

Painless

Early sphincter / erectile dysfunction

Bilateral motor and sensory disturbance below

lesion

426
Q

what is brown-sequard syndrome?

A

Hemi-cord lesion

Ipsilateral loss of proprioception and vibration

sense

Ipsilateral UMN weakness

Contralateral loss of pain sensation (since pain fibres decussate at level of entry)

427
Q

bilateral acoustic neuromas assoc w?

A

NF2

428
Q

Ix of vestibular schwannoma / acoustic neuroma?

A

MRI cerebellopontine angle

429
Q

what is syringomyelia?

A

syrinx: fluid filled cavity formed within the spinal cord

commonly in cervical cord

Symptoms may be static for yrs but then worsen fast

 e.g. on coughing, sneezing as ↑ pressure → extension

Syrinx expands ventrally affecting:

  • Decussating spinothalamic neurones
  • Anterior horn cells
  • ant Corticospinal tracts
430
Q

causes of syringomyelia?

A

Blocked CSF circulation w decreased flow from posterior fossa

  • Arnold-Chiari malformation
  • masses

Spina bifida

2o to cord trauma, myelitis, cord tumours, and AVMs

431
Q

signs of syringomyelia?

A

Dissociated sensory loss:

  • absent pain and temp
  • preserved touch, proprioception and vibration
  • root distribution reflects syrinx location (usually cape distribution: upper limbs and chest)

Wasting/ weakness of hands +/- claw hand

Loss of reflexes in upper limb

Charcot joints: shoulder and elbow

Horner’s syndrome

syringobulbia: cerebellar and lower CN signs

UMN weakness in lower limbs w upgoing plantars

432
Q

ix of syringomyelia?

A

MRI spine

433
Q

what is friedrich’s ataxia?

A

auto recessive progressive degeneration of Dorsal root ganglions, spinocerebellar and corticospinal tracts and cerebellar cells

mitochondrial disorder

onset in teenage years

assoc w HOCM and mild dementia

434
Q

Adult T cell leukaemia/ lymphoma

+

Tropical spastic paraplegia

  • slowly progessing spastic paraplegia
  • sensory loss and parasthesia
  • bladder dysfunction
A

HTLV- 1

-> HTLV myelopathy

435
Q

gold standard of venous sinus thrombosis?

A

MR venogram

436
Q

mx of cluster headaches?

A

Acute: 100% Oxygen
triptans e.g. sc sumatriptan

2/52 course of steroids may reduce attack frequency at onset of the cycle

437
Q

what anaesthetic drug is not as effective in myasthenia gravis pts?

A

suxamethonium

438
Q

What kind of diet is an established treatment for children with epilepsy that is hard to control and is generally unresponsive to antiepileptic medications?

A

Ketogenic diet

high in fat, low in carb, controlled protein

439
Q

prophylaxis of migraine?

A

1st line: topiramate or propranolol

440
Q

presentation of lacunar infarct?

A

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
441
Q

presentation of Weber’s syndrome?

A

ipsilateral III palsy

contralateral weakness

442
Q
A

CT head

high density fluid (Blood) in the cerebral sulci, sylvian fissure and basal ganglia

-> subarachnoid haemorrhage

usually due to rupture of berry aneurysm

443
Q

Most common cause of mengitis in adults?

A

neisseria meningitidis

Pneumococcus

444
Q

Complications of Meningitis?

A

deafness (most common)

other neurological: epilepsy, paralysis

infective: sepsis, intracerebral abscess
pressure: brain herniation, hydrocephalus

445
Q

what triggers pain in trigeminal neuralgia?

A

light touch, including washing, shaving, smoking, talking, and brushing the teeth

446
Q

Mx of trigeminal neuralgia?

A

1st line carbamazepine

447
Q

Gold standard Ix for Cervical myelopathy?

A

MRI cervical spine

448
Q

Mx of cervical myelopathy?

A

All should be urgently referred for assessment by specialist spinal services (neurosurgery or orthopaedic spinal surgery)

early tx is essential, as any existing spinal cord damage can be permanent

decompressive surgery only effective treatment.

close observation is an option for mild stable disease.

Beware of physio: only initiated by specialist services, as manipulation can cause more damage

449
Q

Diagnosis of Lewy Body Dementia?

A

usually clinical

SPECT increasingly used - specificity of 100%

450
Q

Mx of Lewy Body dementia?

A

both acetylcholinesterase inhibitors (e.g. donepezil, rivastigmine) and memantine can be used as they are in Alzheimer’s.

451
Q

Mx of Acute ischaemic stroke which develops into haemorrhagic transformation?

A

stop aspirin 300mg & control BP (<140)

452
Q

features of fourth n palsy?

A

Cant depress eye, look medially

vertical diplopia

classically noticed when reading book or going down stairs

453
Q

subungual fibromata?

A

tuberous sclerosis:

ash leaf spots

shagreen patches

adenoma sebaceum

454
Q

1st line ix for suspected vestibular schwannoma?

A

audiogram and gadolinium-enhanced MRI head scan (MRI of cerebellopontine angle)

455
Q

adverse effects of Levodopa?

A

dyskinesia

‘on-off’ effect

postural hypotension

cardiac arrhythmias

nausea & vomiting

psychosis

reddish discolouration of urine upon standing

456
Q

levodopa features?

A

usually combined with a decarboxylase inhibitor (e.g. carbidopa or benserazide) to prevent peripheral metabolism of L-dopa to dopamine

reduced effectiveness with time (usually by 2 years)

no use in neuroleptic induced parkinsonism

457
Q

features of essential tremor?

A

Postural tremor: worse if arms outstretched
Improved by alcohol and rest
Titubation (nodding movement of head or body)
Often strong FH

458
Q

Features of migraine more common in children?

A

attacks may be shorter-lasting

headache is more commonly bilateral

GI disturbance is more prominent.

459
Q

What are some typical auras with migraines?

A

transient hemianopic disturbance or a spreading scintillating scotoma (‘jagged crescent’). Sensory symptoms may also occur

460
Q

Features of Neuroleptic malignant syndrome?

A

more common in young male patients

onset usually in first 10 days of treatment or after increasing dose

pyrexia

rigidity

tachycardia

raised CK and WCC

461
Q

Mx of neuroleptic malignant syndrome?

A

stop antipsychotic

IV fluids to prevent renal failure

dantrolene* may be useful in selected cases

bromocriptine, dopamine agonist, may also be used

462
Q

triggers for neuroleptic malignant syndrome?

A

antipsychotics

dopaminergic drugs (such as levodopa) for Parkinson’s disease, usually when the drug is suddenly stopped or the dose reduced

463
Q

bilateral sensorineural hearing loss + cafe au lait spots?

A

NF II

Neurofibromatosis type 2 is associated with bilateral vestibular schwannomas

464
Q

what cranial nerves pass through the superior orbital fissure?

A

III, IV, V1, VI

465
Q

trigeminal nerve palsy causes?

A

trigeminal neuralgia

loss of corneal reflex (afferent)

loss of facial sensation

paralysis of mastication muscles

deviation of jaw to weak side

466
Q

Facial n palsy causes?

A

flaccid paralysis of upper + lower face

loss of corneal reflex (efferent)

loss of taste

hyperacusis

467
Q

Hypoglossal n palsy?

A

Tongue deviates towards side of lesion

468
Q

Accessory n palsy?

A

Lesions may result in;

weakness turning head to contralateral side

469
Q

Vagus n palsy causes?

A

uvula deviates away from site of lesion

loss of gag reflex (efferent)

470
Q

glossopharyngeal n palsy causes?

A

hypersensitive carotid sinus reflex

loss of gag reflex (afferent)

471
Q

Corneal reflex

afferent and efferent?

A

afferent: V1

Efferent: Facial n

472
Q

Jaw jerk

afferent and efferent?

A

afferent: mandibular nerve V3
efferent: Mandibular nerve

473
Q

gag reflex / carotid sinus

afferent and efferent?

A

afferent: glossopharyngeal (IX)

Efferent: Vagal (X)

474
Q

Lacrimation

afferent and efferent?

A

afferent: ophthalmic V1
efferent: facial n

475
Q

bitemporal hemianopia

upper quadrant defect > lower quadrant defect?

A

inferior chiasmal compression, commonly a pituitary tumour

476
Q

bitemporal hemianopia

lower quadrant defect > upper quadrant defect?

A

superior chiasmal compression, commonly a craniopharyngioma

477
Q

ondansetron MOA?

A

5-HT3 antagonists

used mainly in the management of chemotherapy related nausea

act in the chemoreceptor trigger zone area of the medulla oblongata

SE: constipation is common

478
Q

A 60 year-old male presents with clumsy hands. He has been dropping cups around the house. His wife complains he doesnt answer his mobile as he struggles to use it. His symptoms have been gradually deteriorating over the preceding months.

A

Degenerative cervical myelopathy

loss of fine motor function in both upper limbs

479
Q

in what situation might you consider stopping a pt’s anti epileptic drugs?

A

if seizure free > 2 yrs

AEDs stopped over 2-3 mo

480
Q

ix. of degenerative cervical myelopathy?

A

MRI cspine

may reveal disc degeneration and ligament hypertrophy, with accompanying cord signal change.

481
Q

features of common peroneal n palsy?

A

weakness of foot dorsiflexion

weakness of foot eversion

weakness of extensor hallucis longus

sensory loss over the dorsum of the foot and the lower lateral part of the leg

wasting of the anterior tibial and peroneal muscles

482
Q

prophylaxis of migraine?

A

topiramate or propranolol

riboflavinn may help

menstrual migraine: frovatriptan

483
Q

MRC power grading?

A

Grade 0: No muscle movement

Grade 1: Trace of contraction

Grade 2: Movement at the joint with gravity eliminated

Grade 3: Movement against gravity, but not against added resistance

Grade 4: Movement against an external resistance with reduced strength

Grade 5: Normal strength

484
Q

recommended screening tool to assess for likelihood of stroke?

A

ROSIER is an acronym for ‘Recognition Of Stroke In the Emergency Room’

Exclude hypoglycaemia first, then assess

A stroke is likely if > 0

485
Q

mx of acute cluster headaches?

A

100% oxygen (80% response rate within 15 minutes)

subcutaneous triptan (75% response rate within 15 minutes)

486
Q

prophylaxis of cluster headache?

A

verapamil

some evidence to support a tapering dose of prednisolone

487
Q

blockage of which artery causes aphasia?

A

Dominant hemisphere middle cerebral artery strokes cause aphasia

usually L

488
Q

triad of normal pressure hydrocephalus?

A

urinary incontinence

dementia and bradyphrenia

gait abnormality (may be similar to Parkinson’s disease)

489
Q

what is autonomic dysreflexia?

A

clinical syndrome occurs in patients who have had a spinal cord injury at, or above T6 spinal level

Briefly, afferent signals, most commonly triggered by faecal impaction or urinary retention cause a sympathetic spinal reflex via thoracolumbar outflow. The usual, centrally mediated, parasympathetic response however is prevented by the cord lesion.

-> unbalanced physiological response, characterised by extreme hypertension, flushing and sweating above the level of the cord lesion, agitation, and in untreated cases severe consequences of extreme hypertension have been reported.

490
Q

antiemetic recommended for Parkinsons?

A

Domperidone

Domperidone does not cross the blood-brain barrier and therefore does not cause extra-pyramidal side-effects

491
Q

which type of MND carries the worst prognosis?

A

Progressive bulbar palsy

  • palsy of the tongue, muscles of chewing/swallowing and facial muscles due to loss of function of brainstem motor nuclei
492
Q

mx of fatigue in MS?

A

once other problems (e.g. anaemia, thyroid or depression) have been excluded NICE recommend a trial of amantadine

CBT/ mindfulness

493
Q

mx of spasticity in MS?

A

baclofen and gabapentin are first-line

physio

494
Q

mx of bladder dysfunction in MS?

A

guidelines stress the importance of getting an ultrasound first to assess bladder emptying - anticholinergics may worsen symptoms in some patients

if significant residual volume → intermittent self-catheterisation

if no significant residual volume → anticholinergics may improve urinary frequency

495
Q

Mx of oscillopsia (visual fields appear to oscillate) in MS?

A

gabapentin is first-line

496
Q

what anti-emetics are impt in chemotx related nausea?

A

5-HT3 antagonists

e.g.

ondansetron

granisetron

mainly act in the chemoreceptor trigger zone area of the medulla oblongata.

497
Q

what is a lacunar stroke?

A

most common type of ischaemic stroke, and results from the occlusion of small penetrating arteries that provide blood to the brain’s deep structures

5 classic syndromes

  1. hemiparesis / pure motor
  2. Ataxic hemiparesis
  3. dysarthria/ clumsy hand
  4. Pure sensory
  5. Mixed sensorimotor
498
Q

what to give Parkinsons patients if they are unable to take their levodopa orally?

A

dopamine agonist patch as rescue medication to prevent acute dystonia

499
Q

viral labyrinthitis vs vestibular neuritis?

A

vestibular neuritis = only vestibular nerve is involved -> no hearing impairment

Labyrinthitis = both vestibular nerve and labyrinth involved -> vertigo and hearing impairment

500
Q

symptoms of viral labyrinthitis?

A

vertigo: not triggered by movement but exacerbated by movement

nausea and vomiting

hearing loss: may be unilateral or bilateral, with varying severity

tinnitus

preceding or concurrent symptoms of upper respiratory tract infection

501
Q

signs of labyrinthitis?

A

spontaneous unidirectional horizontal nystagmus towards the unaffected side

sensorineural hearing loss

abnormal head impulse test: signifies an impaired vestibulo-ocular reflex

gait disturbance: the patient may fall towards the affected side

normal skew test

abnormality on inspection of the external ear canal and the tympanic membrane e.g. vesicles in herpes simplex infection

502
Q

What is intranuclear ophthalmoplegia?

A

problem in the communication between CN VI (abducens) of the R eye and CN III (occulomotor) of the L eye or vice versa

  • cant maintain conjugate gaze -> diplopia
  • the side able to abduct will develop compensatory nystagmus
503
Q

mx of recalcitrant psoriasis (not responsive to conventional treatment)?

A

topical retinoids

phototherapy

oral drugs e.g. methotrexate, cyclosporin

504
Q

what hormone can be used to differentiate between true seizure and pseudoseizure?

A

serum prolactin

505
Q

what is Hoover’s sign?

A

differentiates between organic and non-organic lower leg weakness

due to synergistic contraction: examiner would feel the ‘normal’ limb pushing downwards against their hand as the patient tries to lift the ‘weak’ leg.

if -ve: not a true weakness

506
Q

Features of Lambert-Eaton?

A

repeated muscle contractions lead to increased muscle strength*

limb girdle weakness (affects lower limbs first)

hyporeflexia

autonomic symptoms: dry mouth, impotence, difficultly micturating

507
Q

EMG in Lambert Eaton?

A

incremental response to repetitive electrical stimulation

508
Q

Mx of Lambert Eaton syndrome?

A

treatment of underlying cancer (ie. SCLC)

immunosuppression (prednisolone and/or azathioprine)

intravenous immunoglobulin therapy and plasma exchange may be beneficial

509
Q

causes of lambert eaton syndrome?

A

autoimmune

malignancy: SCLC, breast, ovarian ca

510
Q

What blood tests are done to exclude reversible causes of dementia?

A

FBC, U&E, LFTs, calcium, glucose, TFTs, vitamin B12 and folate levels.

511
Q

In secondary care, what ix can be done to exclude reversible causes of dementia?

A

neuroimaging

e.g. subdural, normal pressure hydrocephalus

Medicine (16 decks)

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