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Year 6 Medicine > Neurology > Flashcards

Neurology Flashcards

1
Q

What is the definition of TIA?

A

a transient episode of neurologic dysfunction caused by focal brain, spinal cord or retinal ischaemia, without acute infarction

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2
Q

TIA investigations?

A

Bedside: BP, ECG, 24 hour hotter, carotid USS
Bloods: cholesterol, lipids, glucose, clotting
Imaging: CT head,CT angiogram

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3
Q

Management of TIA?

A

Antithrombotic:
Initially aspirin 300 mg
ongoing: Clopidogrel 75 mg + statin
2nd line: aspirin + dipyridamole + statin

Surgical:
carotid artery endarterectomy if stenosis >50% and <2w S/S [NASCET criteria]

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4
Q

When do you not give aspirin in TIA?

A

> 7 days since symptoms
bleeding disorder/ on anticoagulant
takes regular low dose aspirin
aspirin CI

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5
Q

What is the definition of stroke?

A

rapid onset neurological deficit of a vascular origin that does not completely resolve within 24 hours

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6
Q

What are the types of ischaemic stroke?

A

thrombotic, embolic

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7
Q

What are the types of haemorrhage stroke?

A

intracerebral haemorrhage, SAH

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8
Q

What signs are seen in anterior cerebral artery stroke?

A

weakness in legs > arms

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9
Q

What signs are seen in an MCA stroke?

A

weakness in arms >legs

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10
Q

What criteria are considered as part of the bamford stroke classification?

A
  1. unilateral hemiparesis and or hemisensory loss
  2. homonymous hemianopia
  3. higher cognitive dysfunction e.g. dysphagia
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11
Q

What features are seen in total anterior circulation stroke?

A
  1. unilateral hemiparesis and or hemisensory loss
  2. homonymous hemianopia
  3. higher cognitive dysfunction e.g. dysphagia, neglect, apraxia

(ALL 3 FEATURES)

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12
Q

Which vessels are affected in TACS?

A

middle/anterior cerebral arteries

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13
Q

What features are seen in partial anterior circulation stroke?

A

2/3 of TACS

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14
Q

Which vessels are affected in PACS?

A

smaller arteries of the anterior circulation e.g. upper lower division of MCA

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15
Q

What features are seen in posterior stroke?

A

cerebellar syndrome
brainstem stroke (locked in)
homonymous hemianopia
LOC

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16
Q

Which vessels are affected in POCS?

A

vertebrobasillar arteries

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17
Q

What is lateral medullary syndrome aka wallenberg?

A

PICA infarct

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18
Q

What features are seen in lateral medullary syndrome?

A

ipsilateral: ataxia, nystagmus, dysphagia, cranial nerve palsy e.g. horners, facial numbness
contralateral: limb sensory loss

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19
Q

What is weber syndrome?

A

ipsilateral CNIII palsy, contralateral weakness

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20
Q

What features are seen in lacunar anterior circulation stroke?

A

pure motor -> posterior limb of internal capsule
pure sensory -> posterior thalamus (VPL)
mixed sensorimotor-> internal capsule
dysarthria/clumsy hand
ataxic hemiparesis -> anterior limb of internal capsule

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21
Q

What investigations do you do for stroke?

A

bedside: exam, obs, ECG
bloods: FBC, U&E, CRP, clotting, lipids, glucose
imaging: non contrast CT, carotid doppler
SPECIAL: swąllow assessment

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22
Q

What scoring systems may be used for stroke?

A

NIHSS - quantifies severity
ROSIER - assess symptoms in acute setting
CT ASPECT - assess early CT changes

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23
Q

what is penumbra?

A

area of hypoxic parenchyma that is still salvageable

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24
Q

What are investigations for SAH?

A

CT head (if -ve do LP for xanthochromia >12 h later)

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25
Q

what is the management of SAH/haemorrhagic stroke?

A
  1. Nimodipine (CCB; 21 days)
  2. coiling (IR)
  3. surgical clipping (requires craniotomy)

may benefit from acutely lowering BP (See trust guidance)

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26
Q

what is the medical management of ischaemic stroke?

A

aspirin 300 mg
no AF -> clopi (life long) + statin (2nd line clopi + dipyradimole + statin)
AF -> apixaban/warfarin + statin

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27
Q

What is the surgical/radiological management of ischaemic stroke?

A

<4.5h -> thrombolysis (alteplase)
<4.5h + occluded proximal anterior circulation -> throbolysis and thrombectomy
<6h ->thrombectomy

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28
Q

What are some absolute contraindications to thrombolysis?

A 
previous/suspected intracranial haemorrhage
seizure at onset of stroke 
intracranial neoplasm
stroke or TBI in last 3m
LP in last 7d
GI haemorrhage in last 3w
Active bleed
pregnancy
oesophageal varices
HTN >200/120
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29
Q

What are some relative contraindications to thrombolysis?

A 
concurrent anticoagulation (INR >1.7)
haemorrhagic diathesis
active diabetic haemorrhagic retinopathy
intracardiac thrombus
major surgery/trauma in last 2w
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30
Q

What is the other/wider management of stroke

A 
fluid -keep balanced
glycemic control
BP control
cholesterol control-statin if cholesterol >3.5
feeding assessment and management - NG?
disability scales - barthel index
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31
Q

When would you use BP medications in stroke management

A 
thrombolysis if BP >185/110
OR
Hypertensive emergency +1 of:
- hypertensive encephalopathy
- hypertensive cardiac failure/MI
- pre-eclampsia/eclampsia
- hypertensive nephropathy
- aortic dissection
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32
Q

Which BP medications would you use in stroke management

A

IV labetalol, nicardipine, clevidpine

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33
Q

What are the key S/S of PD?

A

Bradykiniesia
Tremor
Hypertonia
Stooped shuffling gait

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34
Q

What eye signs might you see in PD?

A

Nystagmus (MSA), vertical gaze palsy (PSP), slow saccades

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35
Q

What autonomic symptoms might be present in PD?

A

Postural hypotension, constipation, frequency, ED, hyper salivation, hyperhidrosis

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36
Q

What are the Parkinson’s plus syndromes

A
  1. multiple system atrophy (shy drager syndrome)
  2. progressive supra nuclear palsy (PSP)
  3. corticobasilar degeneration (CBD)
  4. dementia with lewy bodes (DLB)
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37
Q

What are the features of multiple system atrophy?

A

autonomic dysfunction (postural hypotension, bladder dysfunction)
cerebellar ataxia
rigidity >tremor

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38
Q

What are the features of PSP?

A 
Vertical gaze palsy
Postural instability - falls
speech disturbance 
dementia
cognitive impairment
poor response to L-DOPA
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39
Q

What are the features of corticobasilar degeneration?

A

unilateral parkinsonism, aphasia, astereognosis (alien limb)

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40
Q

What are the features of dementia with lewy bodies?

A

visual hallucinatoins
fluctuating cognition
dementia - parkinsonism

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41
Q

Investigations of Parkinson’s?

A

CT/MRI to rule out vascular causes

DaTScan = dopamine transporter scan

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42
Q

What is the management of PD?

A

GENERAL:
MDT
Physio
Depression screening

MEDICAL:
Levodopa/co-careldopa
MAO-B inhibitors: selegiline
DA agonists: ropinerole

2nd line adjuncts:
COMT inhibitors (entacapone/tolcapone)
amantadine
apomorphine
deep brain stimulation
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43
Q

Which medications should avoided in PD and why?

A

metoclopramide
haloperidol

dopamine antagonists that cross BBB

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44
Q

What can be given for psychosis in PD?

A

Quetiapine

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45
Q

What are the side effects of levodopa?

A 
DOPAMINE
Dyskinesia
On/off phenomena
Psychosis
Arterial BP down
Mouth dryness
Insomnia
N&V
EDS
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46
Q

What is the difference between parkinsonism and PD?

A

Distribution: symmetrical vs not
Progression: rapid vs progressive
Responseto levodopa: poor vs good

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47
Q

What are the causes of parkinsonism?

A 
Vascular: Strokes
Infection: syphilis, CJD, HIV
Trauma
Autoimmune encephalopathy
Metabolic
Iatrogenic (drugs)L: antipsychotics, metoclopramide
Neoplasm
Congenital: Wilsons
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48
Q

What is parkinsons disease?

A

a progressive disease of the nervous system marked by tremor, muscular rigidity, and slow, imprecise movement, chiefly affecting middle-aged and elderly people. It is associated with degeneration of the basal ganglia of the brain and a deficiency of the neurotransmitter dopamine.

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49
Q

What is parkinsons disease?

A

a progressive disease of the nervous system marked by tremor, muscular rigidity, and slow, imprecise movement, It is associated with degeneration of the basal ganglia of the brain and a deficiency of the neurotransmitter dopamine.

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50
Q

What is the aetiology of AD?

A
  1. amyloid- amyloid A
  2. tau - neurofibrillary tangles
  3. inflammation - decreased neuroprotective proteins
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51
Q

RF for AD?

A 
Bio:
age
genetics - APEN, APP, ApoE
 presenilin 1 gene 
 presenilin 2 gene
 APP gene
head injury
vascular RF

Psychosocial:
LOW IQ
Poor educational level

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52
Q

Pathophysiology of AD?

A

Atrophy from neuronal loss
Plaque formation
Neurofibrillary tangle formation
Cholinergic loss

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53
Q

What are the 4 A’s of AD?

A

Amnesia
Aphasia
Agnosia
Apraxia

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54
Q

What are some bad prognostic indicators of AD?

A

MALE, depression, behavioural problems, severe focal cognitive deficit

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55
Q

What are some good prognostic indicators of AD?

A

Female

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56
Q

Management of AD?

A

BIO:
1ST - anti cholinesterase (donepezil, galantamine, rivastgmine)
2nd - NMDA agonist (memantine)

PSYCHO:
Structured group cognitive stimulation sessions
Group reminiscence therapy
Validation therapy
Multisensory therapy
SOCIAL:
Optimise health in other areas
Future wishes - advance directives etc
House changes eg. electric etc, dosset box
Carer assessment
Social support
Tell DVLA AND INSURERS
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57
Q

What should be checked before starting anticholinesterases?

A

ECG
CI: anticholinergics, beta blockers, NSAIDS, muscle relaxants
relative CI: asthma, COPD, GI disease, bradycardia, sick sinus syndrome, AV block

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58
Q

what is MS?

A

an autoimmune demyelinating disorder of the CNS characterised by multiple plaques in separate time and space

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59
Q

Aetiology of MS?

A

HLA-DRB1, environmental, viral

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60
Q

Types of MS?

A

Relapsing remitting (80%)
Primary progressive (10%)
Secondary progressive
Progressive relapsing

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61
Q

What are the signs and symptoms of MS?

A 
TEAM
Tingling
Eye/optic neuritis
Ataxia (and other cerebellar/DNAISH signs)
Motor

Lhermitte’s sign - neck flexion gives electric shocks in trunk
Uhthoff’s sign - worsening of symptoms with raised temperature
Internuclear ophthalmoplegia

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62
Q

What are the symptoms of optic neuritis?

A 
CRAP
Central scotoma
RAPD
Acuity (decreased central and colour vision)
Pain on movement
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63
Q

IX of MS?

A

Contrast MRI
LP (IgG Oligoclonal bands)
Blood Abs: Anti-MBP, NMO-IgG
Evoked potentials: delayed but well preserved waveform
Non contrast MRI: for monitoring therapies

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64
Q

What is Devic’s syndrome?

A

MS + transverse myelitis + optic atrophy

neuromyelitis optica

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65
Q

What is the acute management of MS?

A

Methylprednisolone 1g IV/PO OD for 3 days

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66
Q

What is the chronic management of MS?

A

DMARDs

  • IFN beta
  • Glatiramer

Biologicals
Natalizumab (anti VLA4 AB) reduces relapse by 66%
Alemtuzumab (anti CD52)

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67
Q

What are some good prognostic signs in MS?

A 
Female
<25yo
Sensory signs at onset
Few MRI lesions
Long interval in relapses
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68
Q

What are some bad prognostic signs in MS?

A 
Male
older
motor signs at onset
Many MRI lesions
Axonal loss
Short interval in relapses
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69
Q

What is myaesthenia gravis?

A

An autoimmune disorder characterised by insufficient functioning nicotinic acetylcholine receptors

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70
Q

what antibody is commonly seen in myaesthenia gravis?

A

Anti Ach R (85-90%)

71
Q

What are some associated conditions with MG?

A

thymoma
thymic hyperplasia
Autoimmune disease

72
Q

which drugs exacerbate MG?

A 
Penicillamine
Beta blockers
phenytoin
lithium
procainamide
73
Q

What is a myasthenic crisis?

A

FVC <= 1L, negative inspiratory force <20 cm H20

need for ventilation

74
Q

What are the S/S of a mysaesthenic crisis?

A

Background of MG
Accessory muscle usage
Weak cough

75
Q

What are the investigations of Myasthenic crisis?

A

ABG (hypercapnia before hypoxia)

FVC

76
Q

What is the management of Myasthenic crisis?

A

plasmapheresis
IVIG
intubation

77
Q

What are the investigations for MG?

A 
SINGLE fibre EMG (>92% sensitive)
repetitive nerve stimulation
serial pulmonary function testing
Antibodies - Anti Ach-R, Anti muscle specific receptor TKAB
Tension test
78
Q

What is the management of myaesthenia gravis?

A

1st (symptomatic): long acting AChE inhibitors -> pyridostigmine, neostigmine

1st (long term control) immunosuppression: prednisolone
2nd: azathioprine, cyclosporine, mycophenolate mofetil

surgical: thymectomy

79
Q

what is lambert eaton myasthenic syndrome?

A

LEMS is caused by an antibody directed against presynaptic voltage gated calcium channel in peripheral nervous system

80
Q

What is LEMS commonly seen with/in association with

A

SCLC
Breast Ca
Ovarian Ca

81
Q

What are the S/S of LEMS?

A

Repeated muscle contractions lead increased muscle strength
Limb girdle weakness (lower first)
hyporeflexia
ANS symptoms (dry mouth, impotence)

NB rarely see eye signs

82
Q

What is the management of LEMS?

A

Treat cancer

Immunosuppression (prednisolone +/- azathioprine)

83
Q

What are the Ix for LEMS?

A

EMG

Incremental response to repetitive electrical stimulation

84
Q

What is MND?

A

motor neurone loss from cortex, brainstem, spinal cord and anterior horn cells

85
Q

What are the 4 types of MND and their incidence?

A
  1. amyotrophic lateral sclerosis (50%)
  2. primary lateral sclerosis (30%
  3. progressive muscular atrophy (10%)
  4. progressive bulbar palsy (10%)
86
Q

What are the features of amyotrophic lateral sclerosis?

A

corticospinal tracts

mixed UMN/LMN

87
Q

What are the features of primary lateral sclerosis?

A

loss of betz cells in motor cortex
UMN mainly
spastic leg weakness and pseudo bulbar palsy (CN5,7,9-12), no cognitive decline

88
Q

What are the features of progressive muscular atrophy?

A

anterior horn cell lesions
LMN mainly -> distal to proximal signs
(best prognosis)

89
Q

What are the features of Progressive bulbar palsy?

A

Cranial nerve 9-12
LMN signs
worse prognosis

90
Q

What are some differentials for mixed LMN/UMN signs

A 
MAST
MND
Friedrichs ataxia
SCDC
Taboparesis
91
Q

What signs are seen in bulbar palsy?

A

nasal speech
absent jaw jerk
normal eye movements

92
Q

What signs are seen in pseudobulbar palsy?

A

hot potato speech
brisk jaw jerk
eye movements normal

93
Q

What investigations can be done for MND?

A

Revised El Escorial Criteria
MRI brain/SC -> exclude structural causes
EMG -> reduced APs with increased amplitude
LP -> exclude inflammatory conditions
Normal motor conduction/nerve conduction studies

94
Q

What is the management of MND?

A

MDT approach: neurologist, physio, OT, dietician, specialist nurse
Riluzole (increase life expectancy)

Supportive management:
drooling -> amitriptyline
respiratory failure -> NIV
spasticity -> baclofen, botulinum
dysphagia -> NG/PEG
pain -> analgesia
95
Q

What can cause an UMN lesion in the cortex?

A 
FACT-D
Functional
Abscess
CVA
Tumour
Demyelination
96
Q

What can cause an UMN lesion in the brainstem?

A 
ACT-D
Abscess
CVA
Tumour 
Demyelination
97
Q

What can cause an UMN lesion in the Spinal cord?

A 
CAT-M
Cord compression 
Anterior spinal artery occlusion
Trauma
MS
98
Q

What can cause mixed UMN/LMN lesion in the spinal cord?

A

MND
Syringomyelia
SCDC

99
Q

What can cause mixed UMN/LMN lesion in the anterior horn cell?

A

Spinal muscular atrophy
Polio
MND (ALS)

100
Q

What causes a circumducting gait?

A

unilateral UMN lesion

101
Q

What gait does a bilateral UMN lesion cause?

A

scissoring gait

102
Q

What is rigidity?

A

increased tone independent of velocity
extra pyramidal
lead pipe

103
Q

what is spasticity?

A

increased tone that is velocity dependent
pyramidal
clasp knife

104
Q

What can cause bilateral UMN signs?

A

MS
Cord compression
Cord trauma
Cerebral palsy

105
Q

what can cause unilateral UMN signs?

A

Hemicord:
MS

Hemisphere:
MS
Stroke
SOL
Cerebral palsy
106
Q

What can cause mixed UMN/LMN signs?

A 
MAST
MND (ALS)
Friedrichs ataxia
SCDC (low B12)
Taboparesis
107
Q

What are the investigations for cord compression?

A

FBC (infection, anaemia)
CXR
DRE

108
Q

What are the investigations for SCDC ?

A

B12

ABs (anti IF, anti PC)

109
Q

What signs are seen in CNIII palsy?

A

ptosis, dilated fixed pupil, down and out eye

110
Q

What signs are seen in CNIV palsy?

A

vertical diplopia (cannot look down)
upwards deviation of eyes
limitation of abduction and outward rotation

111
Q

What signs are seen in CNV palsy?

A

trigeminal pain, loss of corneal reflex, loss of facial sensation, paralysis of mastication muscles
deviation of jaw to the weak side

112
Q

What signs are seen in CNVI palsy?

A

defective eye abduction

horizontal diplopia

113
Q

What signs are seen in CNVII palsy?

A

flaccid paralysis of upper and lower face
loss of taste
hyperacusis
loss of corneal reflex

114
Q

what is the afferent and efferent limb of the corneal reflex?

A

A: ophthalmic nerve (V1)
E: Facial nerve (VII)

115
Q

what is the afferent and efferent limb of the jaw jerk reflex?

A

A: mandibular nerve (V3)
E: mandibular nerve (V3)

116
Q

what is the afferent and efferent limb of the gag reflex?

A

A: glossopharyngeal nerve (IX)
E: vagal nerve (X)

117
Q

what is the afferent and efferent limb of the pupillary light reflex?

A

A: optic nerve (II)
E: oculomotor nerve (III)

118
Q

what is the afferent and efferent limb of the lacrimation reflex?

A

A:ophthalmic nerve (v1)
E: facial nerve (VII)

119
Q

What are some causes of a mixed motor and sensory peripheral neuropathy?

A

Alcoholic neuropathy- toxic effects and low B vit absorption
B12 deficiency - SCDC, dorsal columns first
Congenital - HSMN (Charcot marie tooth)

120
Q

What are some causes of a motor predominant peripheral neuropathy?

A

Infection: AIDP (GBS), polio
Metabolic: porphyria, lead poisoning
AI/: chronic inflammatory demyelinating polyneuropathy (CIDP) - Hepatitis/SLE

121
Q

What are some causes of a sensory predominant peripheral neuropathy?

A

infection: leprosy
metabolic: DM, ETOH, amyloidosis, uraemia
AI/metabolic: Vitamin B12
Iatrogenic: isoniazid

122
Q

what are some causes of proximal myopathy?

A 
Autoimmune: MG, polymyositis
Iatrogenic: ETOH, statins, steroids
Neoplastic: paraneoplastic, LEMS
Congenital: muscular dystrophy
Endocrine: Cushing's, hyperthyroid, acromegaly, osteomalacia, diabetic amyotrophy
123
Q

how can peripheral neuropathy be classified

A 
by nerves affected: 
mononeuropathy
polyneuropathy
mononeuritis multiplex
autonomic neuropathy
neuritis

By sensory and motor

124
Q

what is mononeuritis multiplex?

A

painful asymmetrical asynchronous sensory and motor peripheral neuropathy involving isolated damage to >=2 separate nerve areas

125
Q

What can cause mononeuropathy peripheral neuropathy?

A

Infection (VZV)
Compression - carpal tunnel
Radiation injury

126
Q

What can cause polyneuropathy peripheral neuropathy?

A

AIDP (GBS)
CIDP (dm, etoh, HIV)
HSMN (CMT)

127
Q

What can cause mono neuritis multiplex?

A

DM
Infection (Lyme, leprosy)
Sarcoidosis

128
Q

What can cause neuritis?

A

Trauma (sciatica)
Infection (vzv, post GBS)
Corticosteroids

129
Q

What can cause Autonomic neuropathy?

A

DM
ETOH
HIV

130
Q

What Ix for LMN lesion?

A

Bedside: exam, obs, urine (infection), CBG (DM)
Bloods: FBC, U&E (BL), glucose, HbA1c, OGTT, CK, LDDST, AI screen , ESR, B12, folate
Imaging: CXR (paraneoplastic)
Special: EMG, nerve conduction, muscle biopsy (muscular dystrophy), genetic analysis

131
Q

What is charcot marie tooth?

A

Hereditary sensory and motor neuropathy

132
Q

What are the types of CMT?

A

HSMN 1: AD, PMP22 gene, demyelinating, most common

HSMN 2: AD, axonal degeneration

133
Q

What are the S/S of CMT?

A

pes cavus, distal muscle wasting, thickened common peroneal nerve
BL distal LMN (foot drop, high stepping gait, absent ankle jerk)
Stocking loss of sensation

134
Q

What are the Ix for CMT?

A

nerve conduction:
HSMN1: decreased conduction velocity
HSMN2: decreased conduction amplitude

Genetic testing: PMP22 gene for HSMN1

135
Q

What are the signs and symptoms of cerebellar syndrome?

A 
DANISH
Dysarthria, dysdiadochokinesia, dysmetria
Ataxia
Nystagmus
Intention tremor
Speech (staccato)
Hypotonia
136
Q

What are some causes of cerebellar syndrome?

A 
stroke - vertebrobasillar
encephalitis
trauma
MS
ethanol/poisons
posterior fossa tumour
137
Q

What are some causes of nystagmus?

A

Cerebellar - fast phase towards lesion, maximal looking towards lesion
Vestibular - fast phase away from lesion, maximal looking away

HINTS exam +ve = central

138
Q

What investigations would you do for cerebellar syndrome?

A 
Bloods: FBC, U&E, LFT, ETOH, clotting (thrombophilia), Wilsons (low ceruloplasmin)
ECG (arrhythmia)
CSF (oligoclonal bands)
MRI (posterior cranial fossa)
Pure tone audiometry (cpa lesion)
139
Q

What does the spinocerebellum control?

A

movement and posture
truncal ataxia
midline cerebellar lesions
recieives proprioceptive input from proximally

140
Q

What does the neocerebellum control?

A

motor planning
limb coordination, intention, dysdiadochokinesia
lateral cerebellar lesions
connects to corticospinal tracts

141
Q

What does the vestibulocerebellum control?

A

balance and vision
diplopia, nystagmus, vertigo
connects to vestibular system

142
Q

Features of Duchenne Muscular Dystrophy?

A

X linked recessive dystrophin gene on Xp21
progressive proximal muscle weakness from 5 years
calf pseudohypertrophy
Gower’s sign: child uses arms to stand up from a squatted position
30% of patients have intellectual impairment

143
Q

Features of Becker Muscular Dystrophy?

A

X linked recessive dystrophin gene on Xp21
develops after the age of 10 years
intellectual impairment much less common than duchenne
milder than duchenne

144
Q

What is degenerative cervical myelopathy?

A

Degenerative cervical myelopathy leads to loss of fine motor function in both upper limbs.

145
Q

What are the symptoms of DCM?

A

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)
Hoffman’s sign

Commonly misdiagnosed as carpal tunnel

146
Q

Ix DCM

A

An MRI of the cervical spine is the gold standard test

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

147
Q

Mx DCM?

A

physio
urgently referral for assessment by specialist spinal services (neurosurgery or orthopaedic spinal surgery)
decompressive surgery is the only effective treatment

148
Q

Features of venous sinus thrombosis?

A

headache (may be sudden onset)
nausea & vomiting
reduced consciousness
50% of patients have isolated sagittal sinus thromboses - the remainder have coexistent lateral sinus thromboses and cavernous sinus thromboses

149
Q

Ix venous sinus thrombosis?

A

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

150
Q

Mx venous sinus thrombosis?

A

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

151
Q

Features of sagittal sinus thrombosis?

A

may present with seizures and hemiplegia
parasagittal biparietal or bifrontal haemorrhagic infarctions are sometimes seen
‘empty delta sign’ seen on venography

152
Q

Features of cavernous sinus thrombosis?

A

other causes of cavernous sinus syndrome: local infection (e.g. sinusitis), neoplasia, trauma
periorbital oedema
ophthalmoplegia: 6th nerve damage typically occurs before 3rd & 4th
trigeminal nerve involvement may lead to hyperaesthesia of upper face and eye pain
central retinal vein thrombosis

153
Q

Features of lateral sinus thrombosis?

A

6th and 7th cranial nerve palsies

154
Q

Features of vestibular schwannoma?

A

cranial nerve VIII: vertigo, unilateral sensorineural hearing loss, unilateral tinnitus
cranial nerve V: absent corneal reflex
cranial nerve VII: facial palsy

bilateral seen in NF2

155
Q

Ix vestibular schwannoma?

A

MRI of the cerebellopontine angle is the investigation of choice. Audiometry is also important as only 5% of patients will have a normal audiogram.

156
Q

what is thoracic outlet syndrome?

A

disorder involving compression of brachial plexus, subclavian artery or vein at the site of the thoracic outlet. TOS can be neurogenic or vascular;
neurogenic are 90% of the cases.

157
Q

what is the presentation of neurogenic thoracic outlet syndrome?

A

painless muscle wasting of hand muscles,
hand weakness e.g. grasping
sensory symptoms such as numbness and tingling may be present
if autonomic nerves are involved, cold hands, blanching or swelling

158
Q

What is the presentation of vascular thoracic outlet syndrome?

A

subclavian vein compression leads to painful diffuse arm swelling with distended veins
subclavian artery compression leads to painful arm claudication and in severe cases, ulceration and gangrene

159
Q

Ix thoracic outlet syndrome?

A

neuro and musc exam

  • chest and cervical spine plain radiographs: osseous abnormalities e.g. cervical ribs, exclude malignant tumours or other differentials e.g. cervical spine degenerative changes
  • CT or MRI to rule out cervical root lesions
  • venography or angiography may be helpful in vascular TOS
  • an anterior scalene block may be used to confirm neurogenic TOS and check the likelihood of successful surgical treatment
160
Q

Mx thoracic outlet syndrome?

A
  • conservative management with education, rehabilitation, physiotherapy, or taping is typically the first-line management for neurogenic TOS
  • surgical decompression is warranted where conservative management has failed especially if there is a physical anomaly. Early intervention may prevent brachial plexus degeneration
  • in vascular TOS, surgical treatment
  • other: botox injection
161
Q

Features of subacute degeneration of the spinal cord?

A

due to vitamin B12 deficiency
dorsal columns + lateral corticospinal tracts are affected
joint position and vibration sense lost first then distal paraesthesia
upper motor neuron signs typically develop in the legs, classically extensor plantars, brisk knee reflexes, absent ankle jerks
if untreated stiffness and weakness persist

162
Q

What is used for long term prophylaxis of cluster headaches?

A

verapamil

163
Q

what is charcot marie tooth?

A

hereditary motor sensory neuropathy

typically symmetrical slowly progressive distal muscular wasting

164
Q

what are the two most common types of charcot marie tooth?

A

HSMN type I: primarily due to demyelinating pathology

HSMN type II: primarily due to axonal pathology

165
Q

what are the features of CMT HSMN1?

A

autosomal dominant
due to defect in PMP-22 gene (which codes for myelin)
features often start at puberty
motor symptoms predominate
distal muscle wasting, pes cavus, clawed toes
foot drop, leg weakness often first features

166
Q

What is used to treat cerebral oedema in patients with brain tumours?

A

Dexamethasone

167
Q

How do lacunar strokes present?

A

unilateral motor disturbance affecting the face, arm or leg or all 3.
complete one sided sensory loss.
ataxia hemiparesis.

168
Q

what is autonomic dysreflexia?

A

occurs in injuries to spine above T6
commonly triggered by faecal impaction or urinary retention
sympathetic spinal reflex via thoracolumbar outflow
caused by lack of pelvic splanchnic outflow from T6-T12 which usually mediates response

169
Q

Symptoms of autonomic dysreflexia?

A

extreme hypertension, flushing and sweating above the level of the cord lesion, agitation, haemorrhagic stroke

170
Q

Facial nerve supply?

A

‘face, ear, taste, tear’

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

171
Q

Causes of bilateral facial nerve palsy?

A

Causes of bilateral facial nerve palsy:
sarcoidosis
Guillain-Barre syndrome
Lyme disease
bilateral acoustic neuromas (as in neurofibromatosis type 2)
as Bell’s palsy is relatively common it accounts for up to 25% of cases f bilateral palsy, but this represents only 1% of total Bell’s palsy cases

172
Q

Causes of unilateral facial nerve palsy?

A 
Bell's palsy
Ramsay-Hunt syndrome (due to herpes zoster)
acoustic neuroma
parotid tumours
HIV
multiple sclerosis*
diabetes mellitus
173
Q

What causes symmetrical tremor in PD?

A

DRUG INDUCED

ie antipsychotics

Year 6 Medicine (18 decks)

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