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GP ACRRM > Neurology > Flashcards

Neurology Flashcards

1
Q

Following a TIA, in what timeframe is the greatest risk of a stroke occurring

A

Within the first 48 hours

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2
Q

How rapidly should complete work-up and initiation of secondary prevention be completed following a TIA

A

Within 24 hours

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3
Q

What urgent work up is required in patients with TIA

A

Diagnostic confirmation by a stroke specialist
ECG +/- cardiac monitoring ?AF
Brain imaging (CT or MRI at minimum)
- if anterior circulation symptoms are present, carotid imaging (USS, CTA or MRA) also indicated

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4
Q

Which TIA patients required immediate hospital referral

A

Those with:

  • ongoing focal neurological symptoms
  • > 1 TIA in the past 7 days
  • Presence of atrial fibrillation
  • Patient treated with anticoagulation (needs exclusion of haemorrhage)
  • ABCD2 score >3
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5
Q

Risk stratification score for TIA

A 
ABCD2:
Age >60 = 1
BP >140/90 =1
Clinical features:
- Unilateral weakness = 2
- Speech disturbance without weakness = 1
- Other symptoms = 0
Duration of symptoms:
- <10min = 0
- 10-59 min = 1
- >60 min = 2
Diabetes history = 1

Score 0-3 = low risk
4-5 points = moderate
6+ = high risk

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6
Q

Clinical features of lacunar/subcortical stroke syndromes

A

PURE motor hemipareses OR PURE sensory loss affecting contralateral face, arm and leg equally
- note that face may not be affected if infarct is beneath the mid pons

NO associated dysphagia, visual inattention or visual field loss

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7
Q

Clinical features of ACA stroke

A

Leg weakness > arm weakness
Personality change
Occulomotor palsy (eye deviated down and out)
Urinary incontinence

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8
Q

Clinical features of MCA stroke

A 
Arm weakness > leg weakness
Dysphasia
Dyspraxias
Agnosia (unable to recognise things e.g. faces, objects, places
Hemi-neglect
Poor two-point discrimination
Dysgraphaesthesia
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9
Q

Clinical features of PCA stroke

A

Cortical blindness - contralateral homonymous hemianopia with normal fundoscopy and light reflex
(Can also have subcortical signs which will confuse picture)

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10
Q

What is Gerstmann’s syndrome

A 
Syndrome due to infarct in the dominant parietal lobe. Clinical features RAAF pneumonic:
Right-left confusion
Agraphia
Acalculia
Finger agnosia
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11
Q

Clinical features of vertebrobasilar territory ischaemia

A

BILATERAL weakness or sensory disturbance
Diplopia
Vertigo
+/- nausea, vomiting, inability to stand

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12
Q

Differences between migraines in children v adults

A

Children:

  • tend to be shorter duration (<4h)
  • photophobia/phonophobia often don’t develop until >12y
  • usually bilateral (though younger kids have difficulty describing this)
  • tend not to be associated with mental health
  • triptans have no clear evidence for <12y, but are safe from >6y
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13
Q

Indications for imaging paediatric headaches (7)

A
  • abnormal neuro exam
  • change in character or pattern of pre-existing headaches
  • new-onset severe headaches
  • seizures or other signs of neurological dysfucntion
  • history of neurocutaneous syndrome (e.g. neurofibromatoisis, tuberous sclerosis, Sturge-Weber syndrome)
  • age <6y
  • headache location exclusively occipital
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14
Q

Risk of a second seizure after a first unprovoked epileptic seizure

A

40%

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15
Q

Causes of provoked seizures

A

Acute neurological insult (stroke, trauma, infection, inflammation)
Biochemical (hypo/hyper - glycaemia, natraemia, calcaemia, hypomagnesaemia, hypoxia, acid-base disturbance)
Alcohol or other drug intoxication OR withdrawal
Pregnancy (eclampsia

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16
Q

Diagnosis of epilepsy

A

Implies demonstrated tendency for recurrent unprovoked seizures
- often made after 2 unprovoked seizures >24h apart
OR
- after one seizure if EEG or neuroimaging indicates a structural basis for seizure tendence

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17
Q

Features of generalised tonic clonic seizures

A

Initial phase of stiffening and few second LOC (often causes fall and forced scream AKA ictal cry)
Followed by all limbs jerking for up to 2 mins
Cyanosis, tongue-biting, urinary incontinence are common
Post-ictal stertor (heavy breathing/snoring), confusion, amnesia typically for several minutes

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18
Q

Clinical features of generalised absence seizures

A

Frequent (>daily) brief (<30 second) episodes of behavioural arrest without motor features and immediate recovery (no post-ictal phase)

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19
Q

Clinical features of myoclonic seizures

A

Single jerks of muscles, usually generalised
No post-ictal period
Occur during wakefulness, but otherwise are similar to hypnic jerks

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20
Q

Clinical features of focal seizures

A

Myriad of presentations but show high degree of sterotypy in an individual
Can be associated with impairment of consciousness (e.g. temporal lobe epilepsy) - typically these type tend to be less frequent, more prolonged than absence seizures and with post-ictal phase
Can evolve into secondary generalisation

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21
Q

Differential diagnoses of ?epileptic seizures

A 
Cardiac syncope:
- arrhythmias, bradycardia, heart block, tachycardia
- aortic stenosis
- cardiomyopathy
Non-cardiac syncope
- vasovagal
- postural hypotension
Migraine
Narcolepsy-cataplexy
Tremors
Tics
Movement disorders
Pscyhiatric/psychological:
- pseudoseizures
- hyperventilation
- panic attacks
- disassociative reactions
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22
Q

Triggers for epileptic seizures

A 
Sleep deprivation
Overuse of alcohol
Fever
Intercurrent illness
Severe sustained stress
(combination of above)

Despite if trigger is identified or not, if first presentation, need work up for epilepsy syndrome

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23
Q

Investigations to consider in first presentation of seizure

A
  • CBE, CRP ?infection
  • BGL!
  • LFT, EUC, CMP
  • blood alcohol or urine drug screen (if indicated)

CT/MRI if:

  • trauma
  • focal onset of seizure
  • diseases that could lead to seizures (e.g. cancer)
  • fever, meningism or neurological signs
  • EEG!! - for all of them
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24
Q

Preferred neuroimaging for workup of seizures and why

A

MRI more sensitive than CT for small/subtle lesions. Can also better demonstrate the temporal lobe than a CT

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25
Q

How to get maximal yield from an EEG after first seizure presentation

A

Best performed within 24h of all acute cases
If initial EEG non-diagnostic, sleep deprivation EEG should be obtained

Indicated for the diagnosis of epilepsy syndromes, NOT for prognosis

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26
Q

Features of childhood absence epilepsy

A
  • Begins 3-12y (peaks at 6y)
  • Frequent episodes (>20/day)
  • Abrupt onset without warning, rapid offset with resumption of previous activities
  • brief impairment of awareness (<20 seconds)
  • adversely affect school performance
  • can be triggered by stress, fatigue, hyperventilation
    Can be accompanied with GCTC (which tend to occur later in adolescence)
    60% will resolve by mid-adolescence
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27
Q

Prognosis of childhood absence epilepsy

A

60% will resolve by mid adolesence

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28
Q

Paediatric idiopathic generalised epilepsy syndromes

A

Childhood absence epilepsy
Juvenile absence epilepsy
Juvenile myoclonic epilepsy

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29
Q

Triggers of childhood absence epilepsy episodes

A

Stress
Fatigue
Hyperventilation

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30
Q

How does juvenile absence epilepsy differ from childhood absence epilepsy?

A

Later age of onset (10-20y)
Less frequent episodes (e.g. 1/week)
Less severe impairment of awareness may occur
Other seizure types more common

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31
Q

Clinical features of juvenile myoclonic epilepsy

A

Onset 8-20y
Isolated myoclonic seizures, especially after awakening
Other seizure types are common (80% GTCT, 30% absence seizures)
Triggered by sleep deprivation, fatigue, alcohol use

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32
Q

Seizure types associated with juvenile myoclonic epilpesy

A

80% GTCS

30% absence seizures

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33
Q

Triggers for juvenile myoclonic epileptic seizures

A

Sleep deprivation
Fatigue
Alcohol use

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34
Q

Treatment of juvenile myoclonic epilepsy

A

Typically respond well to low doses of valproate or levetiracetam

Other AEDs can control GTCs but can worse then absence or myoclonic seizures

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35
Q

Prognosis of juvenile myoclonic epilepsy

A

Usually require lifelong treatment

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36
Q

General management of idiopathic generalised epilepsies in children

A

Valproate is first line (but ensure adequate contraception in child-bearing age)
Lamotrigine second line, especially in combination with valproate

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37
Q

Definition of symptomatic epiepsy

A

Epilepsy occurring in the setting of a known or suspected abnormality of the CNS

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38
Q

Clinical features of West syndrome

A

Epileptic syndrome developing around 6 months
Often mistaken for infantile colic
Clusters of (often subtle) epileptic spasms, developmental arrest or regression

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39
Q

Treatment of West Syndrome

A

Oral corticosteroids

Should be commenced ASAP

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40
Q

Prognosis of West syndrome

A

20% will evolve to Lennox-Gastaut syndrome

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41
Q

Clinical features of Lennox-Gastaut syndrome

A
  • Begins between 1-8y
  • Generally TONIC seizures (but may also have atonic drop attacks, atypical absence seizures, GTCS and/or myoclonic seizures)
    Commonly associated with intellectual disability, cognition may have been normal prior to development of the syndrome
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42
Q

Treatment of Lennox-Gastaut syndrome

A

Difficult to treat

Most effective treatment is often combination of valproate and lamotrigine

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43
Q

Cause of Lennox-Gastaut syndrome

A 
Symptomatic epilepsy
Multiple aetiologies including
- cortical malformations
- tuberous sclerosis
- trauma
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44
Q

Idiopathic partial epilepsies of childhood

A

Benign epilepsy with centro-temporal spikes (BECS, AKA Rolandic epilepsy, or benign focal epilepsy of childhood)
Benign occipital epilepsies of childhood

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45
Q

Most common childhood epilepsy syndrome

A

Benign epilepsy with centro-temporal spikes

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46
Q

Clinical features of benign epilepsy with centro-temporal spikes

A

Begins at 3-13y, stops by 16y
Nocturnal seizures, occurring shortly after falling asleep, or just before waking
Often experience aura of perioral or gum paraesthesia before:
- speech arrest
- drooling
- tonic OR clonic involvement of upper limb or face
- gurgling or grunting noises (generally if progresses to secondary GTCS)

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47
Q

Prognosis of benign epilepsy with centro-temporal spikes/ benign Rolandic epilepsy

A

Excellent prognosis, even with frequent seizures

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48
Q

Treatment of benign epilepsy with centro-temporal spikes

A

No treatment required for first few seizures

- CBZ or valproate should be considered if seizures are frequent

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49
Q

Time of onset of benign occipital epilepsy of childhod

A

Onset between 3-14y, usually resolve by mid teens
Two distinct syndromes:
Early onset = panayiotopoulous syndrome
Late onset = Gastaut syndrome

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50
Q

Clinical features of Early onset benign occipital epilepsy of childhood (Panayiotopoulous Syndrome)

A

Rare, prolonged nocturnal attacks with eye deviation, vomiting and autonomic features

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51
Q

Clinical features of later onset benign occipital epilepsy of childhood (Gastaut syndrome)

A

Frequent, brief episodes of elementary visual auras, prominent headache and transient visual impairment

52
Q

Investigation of benign occipital epilepsy of childhood

A

EEG - abnormal activity is brought out by eye closure

MRI is indicated as symptomatic occipital epilepsy can present very similarly

53
Q

Clinical features of temporal lobe epilepsy

A

Aurus (olfactory or gusstatory hallucinations, perceptual phenomena e.g. deja vu)
Seizure itself:
- staring spell with psychomotor arrest and loss of awareness
- Automatisms involving perioral region or upper limbs
- lasts 30s to few minutes
-Followed by a postictal phase of confusion, drowsiness and headache

54
Q

How does temporal lobe epilepsy differ from absence seizures (clinically)

A

Temporal lobe epilepsy has an associated aura, longer duration, and postictal changes

55
Q

Treatment of temporal lobe epilepsy

A

Is the most common form of refractory epilepsy in children and in adults
Often requires >1 AED
Surgery can be considered (anterior temporal lobectomy) as most common structural cause is hippocampal sclerosis

56
Q

General first line AED for generalised seizures

A

Valproate

If not tolerated, change to lamotrigine or topiramate

57
Q

General first line AED for partial seizures

A

Carbamazepine (controlled release formulation is preferred)

58
Q

Treatment duration of epilepsy

A

Highly variable depending on particular syndrome and individual, generally a MINIMUM of 2 years complete seizure control

59
Q

Common adverse effects of all AEDs

A

Somnoloence, cognitive impairment, ataxia, other neurotoxic adverse effects

All are dose-dependent (which vary a lot between individuals) and resolve rapidly on discontinuation

60
Q

Enzyme inducing anti-epileptic medications

A

Phenytoin
Carbamazepine
Topiramate (weak inducer)
Oxcarbazepine (weak inducer)

61
Q

Non enzyme-inducing anti-epileptic drugs

A 
Clonazepam
Valproate
Lamotrigine
Gabapentin
Levetiracetam
Pregabalin
62
Q

Typical dose of phenytoin for seizure control

A

200-400mg once daily

63
Q

Typical dose of carbamazepine for seizure controll

A

200-600mg BD

64
Q

Typical dose of topiramate for seizure control

A

50-200mg BD

65
Q

Typical dose of oxcarbazepine for seizure control

A

300-900mg BD (approx 1.5x less potent than CBZ)

66
Q

Typical dose of clonazepam for seizure control

A

0.5-2mg BD

67
Q

Typical dose of valpraote for seizure control

A

400-1000mg BD

68
Q

Typical dose of lamotrigine for seizure control

A

50-200mg BD

Note lower dose requiredment (approx half) if also on valproate

69
Q

Typical dose of gabapentin for seizure control

A

300-800mg RDS

70
Q

Typical dose of levetiracetam for seizure control

A

500-1500mg BD

71
Q

Typical dose of pregabalin for seizure control

A

75-300mg BD

72
Q

Adverse effects of phenytoin

A

Hirsutism, acne, coarse facies
Gum hypertrophy
Rash/SJS

(Cosmetic side effects limit use)

73
Q

Adverse effects of carbamazepine

A

Hyponatraemia

Rash/SJS

74
Q

Adverse effects of topirmate

A 
Anorexia &amp; weight loss
Word-finding difficulty
Nephrolithiasis
Oligohidrosis
Metabolic acidosis
Depression
75
Q

Adverse effects of oxcarbazepine

A

Hyponatraemia (more so than with carbamazepine)

76
Q

Adverse effects of clonazepam

A

Sedation

Ataxia

77
Q

Which benzodiazepine is used for seizure control

A

Clonazepam

78
Q

Adverse effects of valproate

A

Weight gain
Tremor
Alopecia

79
Q

Adverse effects of lamotrigine

A

Rash/SJS (risk reduced with slow titration to target dose over 8 weeks)

80
Q

Adverse effects of gabapentin

A

Weight gain

81
Q

Adverse effects of levetiracetam

A

Agitation

Depression

82
Q

Adverse effects of pregabalin

A

Weight gain

83
Q

When should genetic testing be performed prior to AED commencement

A

Asian patients should all have HLA testing prior to commencing carbamazepine, as patients with HLA-B*1502 allele have a higher risk of SJS

84
Q

When is therapeutic drug monitoring indicated for antiepileptics

A

Monitoring efficacy of AEDs is clinical, not pharmocological.

TDM may be useful in cases when adherence is questioned OR when altered pharmacokinetics is expected:

  • pregnancy
  • drug-drug interactions
  • hepatic or renal impairment
85
Q

Which is the only AED that effective controls absence seizures and myoclonic jerks

A

Valproate

86
Q

Which AEDs can exacerbate absence and myoclonic seizures (or cause them to emerge)

A

Carbamazepine

Phenytoin

87
Q

Restrictions to driving in patients with epilepsy

A

Generally, patients with stable epilepsy on AEDs, and patients after a first epileptic seizure will be judged fit to return to driving after being seizure free for 6 months

Ideally, provide DLA with a concise medical report allowing them to make the decision about a person’s driving

88
Q

Epilepsy and contraception

A

ENZYME-INDUCING AEDs reduce the efficacy of COCP by increasing clearance of oestrogen AND progesterone components

Increasing to high dose oestrogen unlikely to prevent ovulation

Strategies for effective contraception on enzyme-inducing AEDs:

  • double dose (of both oestrogen AND progesterone)
  • continuous use of active pills
  • alternative contraceptive methods
  • changing AEDs
89
Q

Risk of AEDs in pregnancy

A

Double the risk of congenital malformations (to 6%) compared to pregnancies not exposed to AEDs
Only agent with a specific higher risk is valproate at a daily dose >1100mg

preconceptional folate supplementation is recommended (not proven) to mitigate risk

90
Q

AED dose in pregnancy

A

Requirements usually increase after the first trimester

  • especially for lamotrigine and levetiracetam
  • therapeutic drug monitoring can be extremely useful
91
Q

Epilepsy and bone halth

A

Evidence that long-term use of AEDs is associated with reduced BMD, thus general preventative measures should be taken

  • optimise physical activity
  • optimise dietary calcium intake
  • correct vitamin D deficiency
  • smoking cessation
92
Q

Factors that influence seizures during pregnancy in epileptic women

A 
Metabolic changes
Pregnancy symptoms (vomiting, malaise, sleep deprivation)
Pharmacokinetic changes (reduced absorption and protein binding, change to volume of distribution, metabolism and excretion of drugs)
93
Q

Anti-epileptic drugs that have the most significant pharmacokinetic changes during pregnancy

A

Lamotrigine

Oxcarbazepine

94
Q

Predictors of seizure control in pregnancy

A
  • significantly more likely if have had a seizure in the 12 months (particularly 1 month) prior to conception
  • AED polytherapy
  • Oxcarbazepine or lamotrigine monotherapy

Valproate monotherapy has the lowest risk in terms of treatment

95
Q

Most likely timing of seizures in pregnancy

A

Focal seizures: 2nd-3rd month, and 6th month of pregnancy

Generalised: 3rd month of pregnancy

96
Q

Risks to pregnancy of having a seizure during pregnancy

A

SGA
Low birthweight babies
Pre-term delivery

97
Q

Risk of AEDs to foetus/child

A

Teratogenicity

  • especially valproate >1.1g daily dose
  • lowest risk in lamotrigine
  • probably increased with AED polytherapy, therefore aim to avoid polytherapy in the 1st trimester
  • recommend pre-conception folic acid supplementation 400microg/day

Reduced cognition

  • increased in AED polytherapy
  • most associated with valproate exposure (esp >1.1g) - language impairment, 7-10 IQ point loss, verbal and memory abilities
  • evidence of benefit with preconception folate
98
Q

What are OBSTETRIC risks of antiepileptic drugs in pregnancy

A

No conclusive evidence of higher risks of obstetric complications in women on AEDs

99
Q

Suggested management of pregnant women with epilepsy

A

Aim for monotherapy prior to conception (lamotrigine if possible)
Take baseline pre-pregnancy lamotrigine levels, and regular monitoring and dose adjustments during pregnancy to maintain pre-pregnancy levels

Beware risk of toxicity in immediate post-partum period due to rapid reduction in metabolism

100
Q

Definition of multiple sclerosis

A

A MULTIFOCAL central nervous system disease characterised by inflammatory demyelinating lesions affecting both white and grey matter, thought to be medited by autoreactive T cells

101
Q

Epidemiology of MS

A

More common the further south (most common in Tasmania 1/1000), progressively less common further north
F:M = 3:1
Mean age of symptom onset and diagnosis in mid 30s

102
Q

Risk factors associated with MS

A 
Family history
Place of residence in pre-adult years (temperate regions higher risk than tropical)
Later age of exposure to EBV (seronegative individuals very low risk)
Smoking
Dairy and saturated fat consumption
Stress
Lack of omega 3s
Inadequate sun exposure 
Low vitamin D
103
Q

Natural history of MS

A

Clinically isolated syndrome (1st demyelinating event occurs in 85%)
Most commonly develops into relapsing remitting MS
40-45% will transition after 10y to Secondary progressive MS

15-20% will have primary progressive MS from the onset

104
Q

Multiple sclerosis clinically isolated syndrome presentations

A

First demyelinating event, occurs in 85% of MS patients

Episode of neurological disturbance evolving over days or weeks

  • motor or sensory deficits (46%)
  • Clinically isolated optic neuritis (21%)
  • brainstem syndrome (10%)
  • multifocal abnormalities (23%)
105
Q

Pattern of disease in relapsing remitting MS

A

Most common pattern of disease in MS

  • Complete resolution or mild residual symptoms or signs between attacks
  • Relapses occur erratically approx every 2y in untreated patients
  • fatigue in isolation is not a relapse, but termed psuedorelapse
106
Q

Pattern of disease in secondary progressive MS

A

40-45% of patients will transition after 10 years of relapsing remitting MS (80% lifetime risk)
Occasional plateaus and temporary minor improvements may be observed, trend progressively increasing disability

107
Q

Pattern of disease in primary progressive MS

A 
15-20% will have this pattern
Progressive from onset
NO relapses or remissions
Most commonly: slowly progressive spastic paraparesis (cerebellar or hemiplegic syndromes next most common)
Does not respond to current treatments
108
Q

Common sites of disease in MS

A 
Optic nerve
Cerebellum
Spinal cord (usually multifocal and asymmetric) - pyramidal tracts or spinothalamic tract and posterior columns
Brainstem
Bowel/bladder upper motor neurons
109
Q

Signs and symptoms of MS involving the optic nerve

A 
(Optic neuritis)
Pain on eye movements
Blurred vision
Reduced monocular acuity
Colour desaturation
110
Q

Signs and symptoms of MS involving the cerebellum

A

Unsteadiness
Limb or gait ataxia
horizontal or torsional gaze evoked nystagmus

111
Q

Signs and symptoms of MS involving the spinal cord

A

Usually multifocal and asymmetric

  1. Involving the pyramidal tracts:
    - upper or lower limb weakness in pyramidal distribution
  2. Spinothalamic tract and posteriod columns
    - unilateral or bilateral numbness or paraesthesias
    - L’hermitte’s phenomemon (short electric shock-like sensation on neck movement)
112
Q

What is L’hermitte’s phenomenon

A

Short electric shock-like sensations on neck movement

Associated with spinothalamic MS

113
Q

Signs and symptoms of MS involving the brainstem

A

(Internuclear ophthalmoplegia)

  • blurred or double vision
  • affected eye shows impaired adduction, whereas contralateral eye abducts but with nystagmus
114
Q

Signs and symptoms of MS involving the upper motor neurons of bowel and bladder

A

Constipation
Urinary frequency
Urge incotinence
Erectile dysfunction

115
Q

Diagnosis of MS

A

Clinical diagnosis supported by:

  • MRI (demyelinating lesions of multiple ages)
  • CSF findings (oligoclonal bands and raised IgG index)
  • evoked potential studies

Only certain diagnosis is through brain biopsy. Though this is not done in practice.

116
Q

Differential diagnoses of MS

A

Other demyelinating conditions:

  • neuromyelitis optica
  • acute disseminated encephalomyelitis

Others:

  • migraine
  • neoplasms
  • nutritional deficiencies (B12 or copper)
  • compressive lesions of spinal cord
  • Infections (syphilis, HIV)
  • Amyotrophic lateral sclerosis
  • Steroid sensitive relapsing disorders (e.g. SLE, neurosarcoidosis)
  • recurrent infarcts
  • paraneoplastic syndromes
  • psychiatric disease/functional symptoms
117
Q

Management of acute MS relapse

A

If relapse significantly impacting quality of life:
- IV methylprednisolone 1g/day for 3 days
If steroid unresponsive with severe relapse -> Plasma exchange

118
Q

Long-term management of MS

A

Disease modifying treatments are useful for patients with clinically isolated syndromes, and those with relapsing remitting MS, but only on PBS for RRMS
Monitor response by suppression of relapses, and suppression of new lesions on repeat MRI after 6 months

Options on PBS:

  1. Interferon B
  2. Glatiramer acetate
    - natalizumab
    - Fingolimod
    - mitoxantrone
    - cyclophosphamide
119
Q

Common troublesome symptoms of MS

A 
Spasticity
Paroxysmal neuralgias, paraesthesias
Fatigue
Intention tremor
Urinary urgency
Erectile dysfunction
120
Q

Good prognostic features of MS

A

Optic neuritis or isolated SENSORY symptoms as the clinically isolated syndrome
Initial relapsing remitting course
Long interval to second relapse
No disability after 57
Normal initial MRI
Younger age at onset
Complete recovery from the first neurological episode

121
Q

Poor prognostic features in MS

A

Efferent systems affected in the clinically isolated syndrome, or “multifocal” ICS
High relapse rate in the first 2-5y
Substantial disability at 5y
Abnormal initial MRI with large lesion load

122
Q

Effect of pregnancy on MS

A

Pregnancy reduces disease activity, especially in 3rd trimester
High risk of relapse in the first 3 months post partum (however breastfeeding offers some protection)

Only disease modifying treatment suitable is glatiramer (B1), and antalizumab (C), others are classed D - decision of when to stop treatment prior to pregnancy is highly individualised

123
Q

What biochemical markers should be obtained in a patient with suspected MS

A

Vitamin D.

Hypovitaminosis D is more common in patients with MS and is a common trigger for relapse

124
Q

Primary prevention of MS in susceptible individuals

A

I.e. close family members of someone with MS

- Vitamin D supplementation 5000IU daily (for adults, or equivalent for children)

125
Q

Eligibility criteria for commencing a PBS subsidised disease modifying agent for multiple sclerosis

A

Must be clinically diagnosed with MS via MRI OR be contraindicated to have an MRI
+ AT LEAST TWO relapses in the previous 2 years prior to commencing PBS subsidised therapy
+ be ambulatory

126
Q

Typical features of an essential tremor

A

Bilateral, largely symmetrical
Postural or kinetic (usually not present at rest, occurs immediately on new posture)
Usually involves hands and forearms - can spread to neck and voice
Tends to have family history
Typically improves with alcohol

127
Q

Typical features of a Parkinsonian tremor

A 
Typically purely at rest, + with postural component emerging after latent period following adoption of a new posture
Low frequency (coarse tremor)
Improves with activity

GP ACRRM (14 decks)

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