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Neurology Flashcards

1
Q

Types of parkinsonism + and distinguishing features

A

Progressive supranuclear palsy - early speech and swallowing issues, gaze palsy
Multiple system atrophy - autonomic features including incontinance and postural hypotension
Lewy body dementia - dementia and visual hallucinations
Corticobasal degeneration - spreading from one limb
Vascular parkinsonism - cvd risk factors, ataxia

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2
Q

Drugs with high risk of parkinsonism

A

Neuroleptics
Metoclopramide
Prochlorperazine

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3
Q

Three cardianal features of parkinsonism and their characteristics

A

Tremor - worse at rest, pill rolling, slow frequency (4/sec), initially asymptomatic
Rigidity - cogwheeling / lead pipe usually worse on one side
Bradykinesia - slow to initiate movement, freezing

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4
Q

Parkinson features of gait

A

Stooping, shuffling, decreased arm swing, turns on box, loss of balance

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5
Q

Features of parkinsons face and speech

A

Expressionless face

Hypophonic, monotone, slurring speech

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6
Q

What is parkinsons type handwriting

A

Micrographia, small shaky handwriting

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7
Q

Effects of parkinsons on mental health, other neuro, GI, GU systems

A

Dementia, depression, visual hallucinations, insomnia, anosmia
Constipation
Heartburn
Uriary difficulties, frequency, urgency,

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8
Q

Prognosis of idiopathic parkinsons disease. How do drugs alter this?

A

Progressive with no remission (though can ease for seconds to minutes in intense emotion e.g. Fear or excitement)
Life expectancy 10-15 years with death from pneumonia
Medications have very little benefit to natural history but can provide marked relief in symptoms.

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9
Q

Risk factors for idiopathic PD

A

None smokers
Genetics
Age

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10
Q

What is the use of head imaging in suspected idiopathic parkinsons disease?

A

To look for differentials - alzheimers, stroke (vascular parkinsons), repeated head injury sequale,

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11
Q

Classes of drugs used in parkinsons disease

A 
Levodopa
Dopa decarboxilase inhibitors
Dopamine agonists
MAOB inhibitors 
COMT inhibitors 
Anticholinergics
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12
Q

What is levadopa commonly given with in PD? Short and long term side effects?

A 
Dopa decarboxylase inhibitor eg carbidopa 
S/E: short term
N+V
Confusion 
Hallucinations
S/E: long term 
Dyskinesia 
Dystonia
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13
Q

Consequences of long term levodopa therapy

A

Resistance leading to:
End of dose deterioration
On/off freezing

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14
Q

2 examples of a weak dopamine agonist used in PD? Use? Side effects?

A

Ropinirole, bromocriptine,
Can delay need for levodopa
S/E: nausea, hallucinations, compulsive behaviour

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15
Q

What drug is best used in PD for drug induced dyskinesia in late disease? What is it?

A

Amantidine, a glutamate antagonist

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16
Q

What can be used to even out end of dose deterioration in late PD or for off episodes? What class is it? How is it administered for each?

A

Apomorphine
Strong dopamine agonist
Administered by sc infusion for end of dose or as a rescue pen for off

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17
Q

Example of a anticholinergic used in pd. What is it best for? Problems?

A

Benzhexol
Reduces tremor
Associated with confusion, dry mouth, dizzyness, urinary retention

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18
Q

Example and use of a MAOB inhibitor in PD

S/E

A

Selegiline
Alternative to a dopamine agonist in early pd,
Postural hypotension, af

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19
Q

Example and use of a comt inhibitor in pd. S/e

A

Entacapone
Lessen end of dose deterioration
Abdo pain, diarrheoa N+V

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20
Q

Surgical methods of treating PD

A

Deep brain stimulation

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21
Q

Rating scale for PD?

A

Hoehn and Yahr

1) unilateral and functionally normal
2) bilateral, able to balance normally
3) bilateral with impaired reflexes, physically independant
4) severe disease, able to walk and stand unassisted
5) confined to bed or wheelchair unless assisted

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22
Q

Advice for pd patients

A

Cloths - avoid fiddly items e.g. use tshirts and velcro shoes
Chairs - use high and upright
Place rails around the house
Remove trip hazards e.g. rugs

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23
Q

How to test for bradykinesia in suspected parkinsons

A

Ask to tap foot or touch thumb to index finger repeatedly - look for slowing or decreased amplitude.

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24
Q

Distinguish the tremor of benign essential tremor from PD

A

Postural tremor (occurs in a certain position, eg. Grasping something)
No micrographia but shaky writing
Worse when anxious
Occurs at rest and on action

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25
Q

Managment of essentail tremor

A

Usually non but can consider
Propanolol
Mirtazapine

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26
Q

DDx of a tremor

A

Parkinsonism
Benign essential tremor
Functional
Asterixis - hepatic or co2 retention

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27
Q

Things to examine in PD and why.

I would then …

A 
Gait - characteristic
Eye movements - psnp 
Tremor and coordination - removed by movement?
Bradykinesia - characteristic 
Tone - cogwheeling and lead pipe

I would then do:
Postural BP - msa
Handwriting - micrographia

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28
Q

Risk factors for MS

A

Family Hx
Northern or southern lattitudes (ie away from equator)
Female

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29
Q

General age of onset of ms

A

20-45 mean 30

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30
Q

The 4 presentation patterns of MS

A

Relapsing remitting
Primary progressive
Secondary progressive
Fulminating

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31
Q

The three areas of the cns effected by MS that lead to classic presentations

A

Optic nerve
Brainstem
Spinal cord

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32
Q

Effects of optic nerve demylination in ms

A

Optic neuropathy
Symptoms - blurred vision to blindness, mild eye pain, worse when hot
Signs - disc swelling (or not if lesion further back), relative afferent pupillary defect (pupil fixed and no contralateral response)

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33
Q

How long does ms optic neuropathy come on over? How long does it last?

A

Hours to days

Several months

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34
Q

What is a long term sequale of optic neuropathy in ms?

A 
Defects in colour vision or scotomata 
Optic atrophy (pale optic disc)
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35
Q

If a demylinating lesion is futher back on the optic nerve in MS what is the effect on symptoms and examination

A

The patient sees nothing

The doctor sees nothing

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36
Q

S+S of brainstem demyelination in MS

A 
Diplopia, vertigo, facial numbness or weakness, dysarthria, dysphagia
Intranuclear opthalmoplegia (adducting eye lags behind abducting eye), nystagmus,
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37
Q

Differentiate vestibular neuronitis (labrinthitis) from a brainstem demylinating MS lesion

A

VN can cause deafness or tinnitus whereas MS does not
VN often follows URTI
MS causes gaze paresis such as intranuclear opthalmoplegia whilst VN does not

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38
Q

How do spinal cord lesions in ms present?

A

Spastic paraparesis
Numbness
Electric type pain down limb on flexion of neck
Urinary symptoms

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39
Q

How long does spastic paraparesis of spinal cord ms lesions typically come on over?

A

Days to weeks

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40
Q

Diagnostic test in ms? Precondition to diagnosis?

A

Mri

Lesions disseminated in space and time with no other cause. Thus needs multiple episodes

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41
Q

Treatment of acute ms relapses?

A

Steroids

Consider ivig and plasmapheresis

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42
Q

Long term treatment of ms (general)

A

Lifestyle - decrease stress
Beta interferon - expensive not license
Monoclonal antibodies eg alemtuzumab - not licenced
Immunosuppressants - limited evidence

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43
Q

Ms symptom management

A 
Spasticity - baclofen, diazepam 
Tremor - botulinum 
Incontinence - anticholinergics 
Swallowing - fluid thickeners
Depression - ssri
Pain - gabapentin, tcas
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44
Q

Who is typically effected by primary progressive ms. What typical symptoms

A

Middle aged men, bowel and bladder problems and difficulty walking

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45
Q

Term for single episode of suspected ms?

A

CIS - clinically isolated syndrome

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46
Q

If ms like lesions are detected on mri but the patient has never had symptoms what is this called?

A

RIS - radiologically isolated syndrome

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47
Q

Some ddx for ms

A

Lupus
Sarcoidosis
Lymes disease
Brain tumour

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48
Q

Causes of parkinsonism

A 
Idiopathic parkinsons disease
Parkinsonism +
Drug induced
Post encephalopathy 
Post repeated head trauma (e.g. Boxer) 
Wilsons disease
HIV
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52
Q

What is a stroke?

A

A sudden onset focal neurological deficit attributable to a neurovascular cause

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53
Q

Why do some people assume that a stroke on waking occurred at the moment of waking?

A

Surge in hormones raises risk at waking far more than when asleep

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54
Q

What is the typical pattern of stroke paralysis?

A

Hemiparesis effecting all muscles proximal to distal and the face

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55
Q

How does an acute stroke progress in the hours following onset?

A

Persists or improves. Doesnt tend to worsen

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56
Q

risk factors for stroke

A

Age, male, fhx (young)
Htn, af, antiphospholipid syndrome, diabetes
Smoking, obesity, sedentary style, drugs (esp cocaine)
Hiv, hepititis

57
Q

How will tone and reflexes present acutely in a stroke?

A

Reduced. Only become increased later. Planters upgoing throughout though.

58
Q

How can a cve with blockage of the basiler artery present?

A

Cerebellar stroke - ataxia, slurred speech, vertigo, N+V, ipsilateral reduced coordination
Brainstem stroke - usually dead, autonomic instability, crossed neurology (ipsilateral facial weakness with contralateral arm weakness for example), cranial nerve palsy

59
Q

How can a stroke of the pca present?

A

Occipital - homonymous hemianopia

Temporal - hearing, language, memory, quadrantanopia

60
Q

How can strokes of the mca present?

A

Parietal - motor, reading, writing recognition, inattention, quadrantianopias, dressing dyspraxia (non-dominanant hemisphere), sensation

61
Q

What territories of stroke cause weakness in the legs? Why?

A

ACA - frontal lobe - area for leg motor in primary motor cortex
MCA - parietal - neurones for leg motor pass through
Basilar - brainstem - corticospinal tract

62
Q

What area of vision is spared in a pca infarction? Why?

A

Macula - area supplied by branch of the mca

63
Q

Symptoms of an ACA stroke

A

ACA - frontal lobe - hemiparesis, personality, memory problems, continence

64
Q

What would occur with a transient occlusion of the retinal artery? Medical name and description.

A

Amaurosis fugax

Sudden transient monocular blindness

65
Q

Sources of ischemic stroke?

A

Thrombotic - in situ

Emoblitic - carotid artery, AF, arch of the aorta, PFO

66
Q

Subclassifications of haemorrhagic stroke

A

Primary - hypertensive, iatrogenic (e.g anticoagulation)

Secondary - aneurysm, AV malformation, tumour

67
Q

How are types of stroke sub classifed by symptoms (name of scale and description)

A

Bamford scale
TACS - total anterior - all of unilateral weakness, hemianopia, higher dysfunction.
PACS - partial anterior - 2/3 of above OR higher cerebral dysfunction OR monoparesis (e.g. Isolated clumsy hand)
LACS - lacunar anterior - one of unilateral weakness, ataxic hemiparesis pure sensory
POCS - posterior - one of loss of consciousness, cerebellar or brainstem syndromes, isolated homonymous hemianopia

68
Q

What sort of thrombotic event is most likely to have caused each of the bamford scale?

A

TACS - emboli from af or aorta - large vessels
PACS - emboli from carotids
LACS - thrombus - small vessel
POCS - thrombus or emboli

69
Q

How is stroke clinically diagnosed in ED?

A

Rosier scale
+1 each for unilateral arm leg face weakness or visual field defect or speech disturbance
-1 for unconscious or seizure
Stroke unlikely if score =/<0

70
Q

How is severity of stroke assessed?

A

NIHSS score

71
Q

On the bamford scale which subtype of stroke has the best prognosis? Which has the worst?

A

Best LACS

Worst TACS

72
Q

A patient has suffered a TACS and is not independent at 1 month. What proportion will improve to independent by 12 months?

A

Essentially none.

73
Q

Why does the bamford scale rank more deaths from TACS than POCS?

A

Most POCS are dead prior to hospital.

74
Q

How can level of independance/dependance be monitored post stroke?

A

Barthel index

Rankin score

75
Q

A suspected stroke arrives in ED, what immediate investigations are you going to perform/order?

A

BM
ECG
Bloods - FBC, U+E, clotting
CT head

76
Q

Justify a fbc taken in acute stroke

A

Hb prior to aspirin

Plts prior to thrombolysis

77
Q

What bloods would you want to order in a stroke a little later?

A

Lipids, lfts, tfts

78
Q

Timing and symptom severity for stroke thrombolysis

A

<4.5 hrs from onset though can be considered up to 6

Technically any level of disability

79
Q

Contraindications to stroke thrombolysis

A 
Untreated hypoglycaemia 
Seizure at onset
Uncertain time of onset or >4.5 hrs
Arterial puncture in 7 days at non compressible site
NOAC or warfarin with INR >1.7
Intercranial haemorrhage 
Stroke in past 3 months 
Uncontrolled HTN (>185/110) 
Known av malformation or neoplasm in brain 
Known bleeding disorder
Resolving stroke
Surgery or major trauma in last 14 days
Pregnancy
Recent lumbar puncture
80
Q

What medications should a stroke patient be started on if not undergoing thrombolysis? How does this change if they are?

A

Aspirin 300mg for 2 weeks (delay by 24 hrs if thrombolised)
Switch to clopidogrel 75mg lifelong
Atorvastatin 20-80mg lifelong

81
Q

What medication is used to thrombolyse strokes

A

Alteplase

82
Q

What gold standard treatment is emerging for stroke

A

Embolectomy

83
Q

What treatment should be administered to a haemorrhagic stroke?

A

Anticoagulation reversal
Blood pressure control
Neurosurgical review
Supportive care

84
Q

If thrombolysis is administered at <3 hrs what is the NNT and NNH

A

NNT 3

NNH 20

85
Q

Why might you be less agressive with bm management with a stroke than with an mi

A

They are likley to be nbm so more at risk of hypos

86
Q

Complications of stroke

A

Disabity, incontinance, pain, aspiration, infections, seizure, depression, spacticity, contractures, siadh, malnutrition, dvt, death

87
Q

If a patient has a seizure post stroke <24 hrs what is the rule for driving? What if it was 48 hrs

A

<24 hrs follow standard stroke guidance

If >24 hrs follow epilepsy guidance

88
Q

What tias must go straight to hospital?

A

On anticoagulants

Crescendo tias

89
Q

How are tias graded?

A

Abcd2 score
AGE >60 +1
BLOOD PRESSURE >140/90 +1
CLINICAL unilateral weakness +2 speech +1
DURATION 10-60mins +1 >60 mins +2
DIABETIC +1
0-3 low risk, 4-5 mod risk, 6-7 high risk

90
Q

What management for a tia?

A

300mg aspirin +/- statin
Refer to tia clinic
Dont drive

91
Q

Typical pretension of myasthenia gravis?

A

Fatiguable eye signs and bulbar signs

92
Q

Eye signs of myasthenia gravis and how to test for?

A

Ptosis - worsens with 60s upgaze, eases with eyes closed or with ice pack.

93
Q

Bulbar symptoms of myasthenia gravis?

A

Dysphonia, dysarthria, dysphagia

94
Q

Other than bulbar and eye signs and symptoms what else can myasthenia cause?

A

Proximal limb weakness

Respiratory muscle weakness

95
Q

What sort of muscle signs would you find on examination of myasthenia gravis

A

Lmns

96
Q

What ages and sex are at risk of myasthenia gravis?

A

20s-30s mainly female 60s-80s mainly male

97
Q

How can myasthenia gravis be diagnosed?

A

Autoantibodies
Tensilon test (give ACHase inhibitor and monitor change in symptoms)
EMG with fatigability

98
Q

What workup would be needed in a confirmed myasthenia gravis? Why?

A

CT chest to look at thymus

Large number of thymus hyperplasia and risk of thymus tumours

99
Q

What major syndromes complicate myasthenia gravis

A 
Myasthenic crisis
Cholinergic crisis (from treatment)
100
Q

What can trigger myasthenic crisis?

A

Stress, medications, pregnancy, menses, illness, trauma, surgery

101
Q

Problems in a myasthenic crisis?

A

Respiratory compromise
Aspiration pneumonia
DVT

102
Q

How to monitor for respiratory compromise myasthenic crisis?

A

FVC monitor
If not available ask to count seconds in one breath - should be 20s
NOT peak flow or SpO2

103
Q

Symptoms of cholinergic crisis?

A 
Salivation
Sweating
Lacrimation
Urinary incontinance
Deification
Gastric hypermobility
Emesis

Bradycardia, myosis

104
Q

Management of myasthenia gravis

A 
ACHase inhibitor - neostigmine, pyridostigmine
Steroids
Azothioprine
Ivig 
Plasmapheresis
105
Q

How should steroids be administered in myasthenia gravis

A

Start low and build - high dose can trigger crisis

106
Q

Main ddx of myasthenia gravis. Name. Pathology. Big difference.
Other ddx

A

Lambert eaton
Decreased ach secreation presynapticly
Not fatigable -actually strengthens
Botulism

107
Q

Natural history of guillian barre syndrome?

A

Infection followed by rapidly ascending polyneuritis several weeks later peaking at 4 weeks then declining again over months.

108
Q

What infection does GBS typically follow

A

Capylobacter

109
Q

There are different subtypes of GBS. What is the practical significance of one of the rare ones?

A

Leads to autonomic instibility thus gbs patients should be monitored

110
Q

What is the pathological mechanism of gbs?

A

Crossed antigenicity of immune system from infection to myelin sheath resulting in peripheral demylination

111
Q

How should gbs patients be motored for impending respiratory failure

A

Handheld fvc

Counting seconds in one breath

112
Q

Other than limb paralysis what other symptom is typical in gbs?

A

Back painf
Paraesthesia and mild sensory impairment
Bulbar involvment - eg blurred vision or dysphagia

113
Q

Typical features of gbs paralysis

A

Symmetrical lmns with loss of reflexes
Ascending
Proximal to distal

114
Q

What proportion of gbs patients need ventilation? How many are fully recoved by 1 year? How many die?

A

25%
70%
5%

115
Q

Complications of gbs?

A 
Respiratory failure
Dvt
Autonomic instability 
Siadh
Hypercalcaemia
Renal dysfunction due to tx
116
Q

Treatment of gbs?

A

Symptomatic

If severe ivig or plasmapheresis

117
Q

What happens if gbs keeps worsening post 4 weeks?

A

Not gbs, another similar condition, will probably be progressive and only relapse temporarily with treatment

118
Q

What condition causes a bulbar followed by a symmetrical decending weakness of the limbs and resp muscles accompanied by fever, N+V and parasympathetic dysfunction? Treatment?

A

Botulism
Antitoxins
Acetylcholine agonist

119
Q

Long term tia treatments

A

Aspirin and dipyridamole (or clopidogrel if aspirin intolerant)
Consider statin
Control bp
Stop smoking

120
Q

In clinic what are the indications for various investigations

A

Carotid imaging if patient a candidate for intervention

MRI if pathology or vascular territory uncertain

121
Q

A total MCA stroke to which side is more likely to cause dysphasia? What is a complication of a stroke on the opposite side to this?

A

Left

Unilateral neglect of contralateral space

122
Q

What are the effects of an MCA branch occlusion to the areas supplying brocas and wernicks areas?

A

Brocas - expressive dysphasia

Wernicks - receptive dysphasia

123
Q

What is used for blood pressure control in an acute stroke awaiting thrombolysis with bp >185?

A

Labetolol

124
Q

Post thrombolysis or in a stroke not awaiting thrombolysis what is used to control bp in very severe (diastolic >140) cases?

A

Sodium nitroprusside

125
Q

Early signs of acute ischemic stroke on ct scan

A

Insular ribbon sign
Obscuration of lentiform nucleus
Hyperdense artery sign

126
Q

How do you describe a darkening or lightening on a. Ct scan

A

Hypoattenuation

Hyperattenuation

127
Q

What colour does blood appear on a ct?

A

Acute - hyperdense

Old - hypodense

128
Q

How is a sah diagnosed? Pitfalls?

A

Ct - can be negative, especially after 6hrs as blood mixes with csf
Lp - can only do after 12 hours as looking for xanthochromia

129
Q

Initial management of sah

A

Analgesia to decrease stress
Antiemetics
Nimodipine to decrease vasospasm
D/w neurosurgery

130
Q

What is a possible cause of a patient presenting with neck pain and focal neurology post a minor rtc?

A

Carotid or vertebral artery dissecton

131
Q

What predisposes a patient to central venous thrombosis

A

Female

Dehydration (labour!)

132
Q

Presentation of central venous thrombosis

A

Diffuse headache, drowsy, seizure, low visual acuity

133
Q

How would a patient with trigeminal neuralgia present?

A

Electric type pain

Normal neuro exam!

FPE (11 decks)

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