Week 14 - Neurological Disease Flashcards

1
Q

What is the difference between primary and secondary headache?

A

Primary = tension-type, migraine, trigeminal autonomic cephalagias (cluster headaches) - a headache that is not caused by a different pathology

Secondary - headache caused by an alternative pathology

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2
Q

What are the red flags for headache?

A
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3
Q

What tests can you order for headaches?

A

Depends on the possible diagnosis - if just tension or migraine and you’re sure, no need to further test.

If worried about underlying pathology…

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4
Q

What are the SNNOOP10 criteria for red flags for headache?

A
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5
Q

How do we manage primary headaches?

A

Classify what type

Determine frequency

If frequent - consider Rx - acute / abortive / preventative

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6
Q

What are the three types of primary headache?

A

Tension-type
Migraine
Cluster

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7
Q

How can you differentiate between different types of headaches?

A
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8
Q

What is another name for trigeminal autonomic cephalgia? What are the Sx?

A

Cluster headache - trigeminal autonomic cephalalgia - excruciating stabbing pain - these Ps cant lie still, agitated, cant get comfortable as the pain so severe (unlike other headaches where the P wants to lie still). Is not related to having headaches in clusters.

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9
Q

How can you calculate whether a tension headache is frequent, infrequent or chronic?

A

Freq = >10 days / month

Infreq = < 10 days / month

Chronic = >15 days / month for at least 3 months

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10
Q

How can you calculate whether migraines are episodic or chronic?

A

15 days

<15 days / per month = episodic

> 15 days / month for at least 3 months

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11
Q

What is it called when a migraine lasts for longer than 72 hours?

A

Status migrainosus

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12
Q

What structure in the neck is thought to be involved with causing headaches?

A

Trigeminocervical complex

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13
Q

Which abortive therapies can be given for tension headaches?

A

Paracetamol
Aspirin

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14
Q

Which abortive therapies can be given for migraine?

A

Paracetamol
Aspirin
NSAIDs
Prochlorperazine (Dopa agonist)
Metoclopramide (Dopa agonist)

Triptains
Monoclonal ABs
Nerve block injection

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15
Q

What abortive therapies can be given for cluster headaches?

A

High flow O2 therapy
Triptans

NeurostimulationWhat

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16
Q

What lifestyle modification can be prescribed for all 3 types of primary headache?

A

Adequate sleep
Hydration
Exercise
Cognitive behavioural therapy

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17
Q

Should you give opioids for headache?

A

No

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18
Q

What is the maximum that analgesics should be used in a month to prevent overuse headaches?

A

<15 days

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19
Q

What preventative medications can be given for tension headaches?

A

Amitryptyline

Acupuncture

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20
Q

What preventative medications can be given for migraine?

A

Propanolol
Amitryptyline

Topiramate
Triptans
CGRP mABs
Botulinum toxins
Nerve block injections
Acupuncture
Neurostimulation

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21
Q

What preventative medications can be given for cluster headaches?

A

Verapamil
Topiramate

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22
Q

What is it called when you get electrical shock-like or stabling pain for anywhere between a few seconds to 2 minutes in the mouth, cheek or gums of the face?

A

Trigeminal neuralgia

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23
Q

What are most cases of trigeminal neuralgia attributed to?

A

Idiopathic cause

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24
Q

What is the first line treatment for trigeminal neuralgia?

A

Carbamazepine

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25
Q

What is second line treatment for trigeminal neuralgia?

A

Gabapentin
Pregabalin
Lamotrigine

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26
Q

What is a seizure?

A

Abnormal firing of the brain

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27
Q

What is the difference between focal and generalised seizures?

A

Focal = positive motor and visual features
Can be aware or have impaired awareness

Generalised = loss of awareness, synchronous movements, eyes are open

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28
Q

Which part of the brain is the most common cause of focal seizures?

A

Temporal lobe (60%)
Then frontal

Rare - parietal or occipital lobes

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29
Q

What is it called when a seizure lasts for longer than 5 minutes?

A

Status epilepticus

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30
Q

In a generalised seizure - which part of the brain is effected?

A

Both hemispheres are affected.

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31
Q

How do seizure symptoms vary by lobe?

A
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32
Q

How is epilepsy defined?

A

2 or more unprovoked seizures separated by 24 hours

or - 1 unprovoked seizure with a high risk of further seizures (>60%) in the next 10 years

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33
Q

How is resolved epilepsy defined?

A

Seizure free for 10 years inc 5 years post medication free

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34
Q

How can you differentiate between non-seizures?

A
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35
Q

What is the commonest cause of seizures occurring in previously well controlled epilepsy?

A

Inconsistency in taking medication

Also - lifestyle changes, new medications which interact with the antiseizure meds, infection, pregnancy

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36
Q

Why does pregnancy affect seizure medication levels?

A

Pregnancy - inc in circulating volume, dilutes amount of protein and renal clearance - can clear medication quicker and can affect protein binding drugs. During pregnancy P needs to be monitored and dose adjusted to prevent seizures in pregnancy

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37
Q

What is SUDEP?

A

Sudden unexplained death of epilepsy

Responsible for 2-18% of deaths of all Ps with epilepsy - 10x inc risk with those who have generalised tonic-clonic seizures.

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38
Q

When is epilepsy deemed to be drug resistant?

A

When two appropriate anti-seizure meds have failed to stop the seizures.

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39
Q

What is an internal sensation of restlessness called?

A

Akathisia

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40
Q

What is asterixis?

A

Negative myoclonus - associated with sudden drop in tone due to metabolic disturbances - hepatic encephalopathy or renal dysfunction.

Myoclonus is a sudden, brief, involuntary muscle jerk. It is caused by abrupt muscle contraction, in the case of positive myoclonus, or by sudden cessation of ongoing muscular activity, in the case of negative myoclonus (NM).

Clonus = hyperreflexia

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41
Q

What are sudden, brief-repetitive, non-rhythmic movements called?

A

Tic

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42
Q

What is involuntary, irregular, non-rhythmic, unpredictable movement flowing between muscles called? Can appear as if Ps are dancing.

A

Chorea

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43
Q

What is the definition of a tremor?

A

Involuntary rhythmic oscillation of one or more body parts

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44
Q

What is myoclonus?

A

Brief, involuntary, regular twitches

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45
Q

What does abrupt or rapid progression of a tremor suggest?

A

A secondary cause - e.g. drug toxicity

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46
Q

What is the difference between pyramidal and extrapyramidal tracts?

A

Pyramidal = voluntary motor control & fine motor control

Extrapyramidal = Modulate motor functions, especially involuntary movement, posture and tone

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47
Q

What are the two main pyramidal tracts?

A

Corticospinal Tract: Controls voluntary movements of the body.

Corticobulbar Tract: Controls voluntary movements of the face, head, and neck.

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48
Q

Which investigations can you do for tremor?

A
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49
Q

Which drugs can commonly cause tremor?

A

Sodium valpoate

Phenytoin

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50
Q

How can you differentiate between an essential tremor and a Parkinsonian tremor?

A

Essential tremor - happens with movement rather than at rest. Also improves with alcohol and worsened by caffeine.

Parkinsons - happens at rest

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51
Q

What is essential tremor plus?

A

Essential tremor with additional signs such as dystonia, ataxia and Parkinsonism.

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52
Q

What scan is 100% specific in determining whether a P has Parkinsons or Essential Tremor?

A

DaTscan

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53
Q

What medications can be given for essential tremor?

A

Propanolol

Also - primidone, topiramate, botulinum

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54
Q

What type of facial paralysis do you get with the following diseases?
- Guillain-Barre
- Lyme
- HIV
- Sarcoid
- MG

A

All cause bilateral LMN facial nerve palsy

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55
Q

How can you determine whether a facial lesion affects an UMN or a LMN?

A

In upper motor neuron - only the lower half of the face is affected

In a LMN - the entire half of the face is affected

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56
Q

What type of lesions (UMN or LMN) are caused by the following?
- stroke
- MS
- Tumour
- Bell’s palsy

A

Stroke, MS & Tumour = UMN

Bell’s palsy = LMN

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57
Q

Which virus is most commonly associated with Bell’s palsy?

A

Herpes simplex virus

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58
Q

What medication can be given in Bell’s palsy?

A

If presenting within 72 hours of first onset - can prescribe prednisolone.

May also prescribe antivirals but seek advice.

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59
Q

What complications can occur during recovery of Bell’s palsy?

A

When the nerve recovers - can be some growth or plasticity of the nerve - may no longer innervate the correct part of the face

Can cause synkinesis (involuntary contraction) or Bogorad syndrome (cry when you eat).

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60
Q

What causes Wernicke’s encephalopathy?

A

Thiamine deficiency

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61
Q

What is the triad of Wernicke’s

A

Mental status changes
Ocular dysfunction
Gait apraxia

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62
Q

What are possible differentials for Wernicke’s?

A
63
Q

What is the biochemical implication of giving glucose to patients who are deficient in thiamine?

A

Thiamine (and magnesium) are needed for co-factors in the breakdown of glucose. Without these - end up down the pyruvate -> lactate pathway = increase of lactate in these patients!

Need to therefore give thiamine before giving glucose in nutritionally deficient patients

64
Q

What would symmetric lesions around the 3rd and 4th ventricles and aqueduct, also affecting mamillary bodies suggest?

A

Wernicke’s encephalopathy

65
Q

What vitamin is thiamine?

A

B1

66
Q

What complications can arise from thiamine deficiency?

A

Wernicke encephalopathy
Korsakoff syndrome
Dry & wet beri beri
GI beri beri
Machiafava Bignami disease - ass with Italian Chianti wine abuse

67
Q

How does Korsakoff’s present?

A

Amnestic disorder - confabulation, personality changes and memory loss

68
Q

What is the management for acute alcohol withdrawal?

A

Correct any metabolic derangements
CXR or CT if concern for head injury

Chlordiazepoxide
Do CIWA
Give IM / IV Pabrinex

69
Q

What factors inc risk of another seizure after a single unprovoked seizure?

A

If it
- occurred in sleep
- if there are MRI brain abnormalities
- If there is concerning EEG
- If there is an underlying genetic disorder

70
Q

Why do focal seizures occur?

A

There is a surrounding loss of inhibition - e.g. decrease in GABA transmission - means that transmission is no longer dampened -> abnormal firing

71
Q

What is the difference between a tonic and clonic phase of seizure?

A

Tonic = stiff phase - due to prolonged depolarisation due to loss of GABA inhibition

Clonic = jerk phase - due to some neuronal repolarisation

72
Q

What is MS?

A

Inflammatory and progressive demyelinating condition - get episodes of inflammation -> demyelination of nerves.

Occurs in CNS.

Causes focal symptoms +/- neurological disability

73
Q

Do we know what causes MS?

A

Not entirely - thought to be a combo of genetic, environmental and other issues. No single gene identified.

Poss link to Vit D deficiency
Inc risk poss with EBV
Smoking inc riskh

74
Q

What questions do we need to ask when taking a seizure Hx?

A
75
Q

What things can present in the post-ictal period?

A

Drowsiness
Confusion
Psychotic
Bitten tongue
Lost continence

76
Q

Does epilepsy occur in provoked seizures?

A

No = epilepsy only occurs in unprovoked seizures

77
Q

What is the term of coordinated involuntary motor activity (almost always accompanied by impaired awareness and amnesia)

A

Automatisms

(e.g. chewing or lip smacking)

78
Q

Are EEGs definitive in diagnosing epilepsy?

A

They can be supportive but are not definitive - can have normal EEGs in frontal lobe seizures

79
Q

Does a normal EEG exclude epilepsy?

A

No! Routine EEG can remain negative in 10% of Ps with epilepsy

80
Q

What things can look like a seizure?

A
81
Q

What is the main treatment for non-epileptic attacks?

A

Psychotherapy

82
Q

How can you differentiate between non-epileptic attack and seizure on exam?

A

Non-epileptic attacks - wax and wane lasting over 2 mins

Have motionless unresponsiveness for over 5 mins

Do not respond to drugs!

If true seizure - on exam - eyes should remain deviated to the ground on turning (check with mirror for visual fixation).

If generalised tonic-clonic seizure, should have positive Babinski and absence of corneal reflexes

83
Q

What is convulsive syncope?

A

Not a seizure or epilepsy

Is cerebral hypoxia that results in myoclonic jerks (usually less than 20)

Usually - there is a lack of BF to brain = cerebral hypoxia = myoclonic jerks.
May see slowing EEG but not epileptiform discharges

84
Q

What percentage of Ps with herpes simplex encephalitis will present with seizures?

A

Up to 50%

85
Q

What is the first imaging done for Ps presenting to A&E with seizures?

A

CT

86
Q

What bleed has a biconvex appearance on CT?

A

Extradural

87
Q

How can you differentiate a subarachnoid bleed from other bleeds on CT?

A

In subarachnoid the blood can leak into the sulci of the brain

88
Q

If the presentation is not acute, which is the best mode of imaging the brain in seizures?

A

MRI

89
Q

Which part of the brain is the most common cause for epilepsy?

A

Temporal lobe

90
Q

What is the most likely cause of mesial temporal sclerosis?

A

Childhood febrile seizures

91
Q

What is limbic encephalitis?

A

AI condition that attacks the limbic system (hippocampus, cingulate gyrus, hypothalamus, frontotemporal lobe and insula)

92
Q

Which nuclear medicine scans can be done for seizure and syncope?

A

FDG PET
SPECT

93
Q

When taking a neurological history - what is the most important thing to ascertain that can help you decipher what is going on?

A

Speed of presentation

Can use it to differentiate between acute and less acute etc.

94
Q
A
95
Q

What does a hyperacute presentation suggest in neurology? (Seconds -> minutes)

A

Vascular pathology

96
Q

What does an acute presentation suggest in neurology? (Hours)

A

Vascular or inflammatory pathology

97
Q

What does a subacute presentation suggest in neurology? (Days-weeks)

A

Inflammatory or metabolic pathology

98
Q

What does an acute on chronic presentation suggest in neurology?

A

Worsening of something preexisting - e.g. metabolic cause

99
Q

What does a chronic presentation suggest in neurology?

A

Neoplastic or degenerative cause

100
Q

Where do UMN and LMN in the motor pathway synapse? (Where the CNS and PNS meet)

A

The anterior horn

101
Q

Which is the descending motor tract?

A

Corticospinal tract
Aka Pyramidal tract

102
Q

What is the path of UMNs in the motor tract?

A

Fibres come from primary motor cortex and amalgamate into the corticospinal tract - through internal capsule and cerebral peduncles, midbrain, through medulla where they decussate to the contralateral side - synapsing in the anterior horn cell.

103
Q

How does UMN damage present in terms of flexors and extensors in the pyramidal pathway?

A

Arm - flexors are stronger

Leg - extensors are stronger

Is increased spasticity (velocity dependent)

Brisk reflexes
Get positive Babinksi (extension of the big toe)

Coordination is not impaired

Sensation - will normally have a hemisensory problem as well

104
Q

What is the difference between spasticity and rigidity?

A

Spasticity = velocity dependant increase in tone. Sign of pyramidal pathology

Rigidity = increased tone that is maintained throughout the movement. Sign of extrapyramidal pathology

105
Q

How do spinal cord lesions present?

A

Depending on the size of the lesion - may get bilateral or unilateral signs.

Can get sensory level involvement

Bowel and bladder involvement is common.

Arms + legs will only be involved if damage is to the cervical spine. If below this impairment will be to legs only.

106
Q

What is the pathway of the LMN?

A

Leaves anterior horn as a ventral root -they then join together to form a plexus - brachial plexus or lumbosacral plexus
Nerves then untangle into individual peripheral nerves. These get to NMJ and communicate with muscles.

107
Q

If damage occurs at the point of the anterior horn - what Sx do you get?

A

Mixed UMN and LMN symptoms

108
Q

What are the signs of LMN pathology?

A

Muscle wasting or fasciculations
Tone is normal or reduced
Reflexes are normal, reduced or absent

109
Q
A
110
Q

Which disease is an example of anterior horn pathology?

A

Motor Neurone Disease

111
Q

How does nerve root pathology present?

A

With myotome and dermatome loss

Also lose the reflex that those roots innervate

112
Q

What things can cause nerve root pathology?

A

Compression of the root (e.g. herniated intervertebral disc)
Inflammation
Infiltrative cause (neoplastic)

113
Q

Is plexus pathology common?

A

No

Consider if there are multiple peripheral nerves involved in a limb.

114
Q

How does peripheral nerve pathology present?

A

With weakness and sensory Sx in the distribution of the single nerve

115
Q

Which nerve is involved?

A
116
Q

Which nerve is involved?

A
117
Q

Which nerve is involved?

A
118
Q

What is the sensory innervation?

A
119
Q

What is generalised polyneuropathy?

A

Weakness that starts distally, moves proximally in a glove and stocking pattern. Sensory and reflexes are also affected.

120
Q

What can cause generalised polyneuropathy?

A

A - Alcohol
B - B12
C - Connective tissue, Cancer
D - Diabetes
E - Everything else (inc Guillain Barre)

121
Q

Name a pathology of the NMJ

A

Myaesthenia Gravis

122
Q

What are the Sx of myaesthenia graves?

A

Fatiguable weakness is the hallmark

Can affect eyes, face, speech, limbs, and SOB.

Is NO SENSORY INVOLVEMENT

123
Q

What is the difference between myopathy and myositis?

A

Myopathy = non-inflammatory process affecting the muscles

Myositis = inflammation of the muscles

124
Q

What is inflammation of the spinal cord called?

A

Myelitis

125
Q

Is there a test for MS?

A

Is no single test - have to come to a clinical diagnosis

126
Q

How can MS affect Ps?

A

Can affect them in different ways depending on which part of the nervous system is affected.

Has a relapsing / remitting presentation

Exam points towards UMN pattern

127
Q

What is the most common cause of cauda equina syndrome?

A

Disc herniation

128
Q

How can cauda equina present?

A

Saddle anaesthesia
Urinary retention
Weakness of ankle dorsiflexion
Absent ankle reflexes

129
Q

Which diagnostic criteria are used for radiological imaging of MS?

A

McDonald Diagnostic Criteria

130
Q

Which MRI sequence was designed for MS?

A

MRI FLAIR

131
Q

How does optic neuritis present?

A

Pain on eye movement
Visual loss

132
Q

If MS attacks the spine - which part is normally affected?

A

The cervical cord

133
Q

How does cerebral small vessel disease present on MRI?

A

Patchy white matter changes - bright on T2 and FLAIR

134
Q

Which MRI finding is common with MS?

A

Dawson fingers

135
Q

What is MS?

A

Inflammatory and progressive demyelinating condition of CNS.

Occurs in attacks or relapses - where areas of demyelination occur - causes focal symptoms +/- neurological disability

136
Q

How does MS differ from other neurological conditions?

A

Their lesions are disseminated in both time and space - no other disease does this.

137
Q

What causes MS?

A

Thought to be a combination of genetic vulnerability + environmental and other insults that lead to the disease forming.

Thought there may be a possible link to Vit D deficiency as the further from the equator you are, the higher the incidence of MS.

Also thought that maybe there is a link between EBV and MS.

138
Q

What are the traditional phenotypes of MS?

A

Relapsing remitting
Secondary progressive
Primary progressive

139
Q

What are the three goals of Rx for Ps?

A

Disease modifying - reduce progression

Symptomatic - reduce symptoms

Acute relapse - manage acute Sx

140
Q

Why do we give amytriptyline in MS?

A

Reduces pain and sensation

141
Q

What is a psuedorelapse / pseudo exacerbation in terms of MS?

A

A pseudoexacerbation is a temporary worsening of symptoms without actual myelin inflammation or damage, brought on by other influences. These can include other illnesses or infection, exercise, a warm environment, depression, exhaustion, and stress.

We’re suspecting that there hasn’t been a new area of inflammation but we’re suspecting that that old area has just made the patient a little bit more vulnerable to re-experiencing those same symptoms when something else happens.

142
Q

What Rx is given for an MS relapse?

A

Methylprednisolone

143
Q

What is myasthenia gravis?

A
144
Q

What is Lambert-Eaton syndrome?

A

ABs against the voltage gated Ca channels in the pres-synaptic membrane.

Similar to MG but MG causes fatigue over time whereas LE may improve with exercise

145
Q

Where can weakness present in MG?

A

Ocular
Bulbar / Facial
Diaphragm
Limbs
Generalised

146
Q

What daily Rx is given for MG?

A

Pyridostigmine (Acetylcholinestease inhibitor)

147
Q

What Rx is given for acute relapse in MG?

A

Prednisolone

148
Q

What do you need to monitor with predinisolone (or any steroids?)

A

If P has diabetes - monitor sugars as can inc risk of hyperglycaemia

149
Q

MG is one of the few situations where long term steroids may be used. Which is most commonly used?

A

Azathioprine

150
Q

How does Azathioprine work?

A

Inhibits purine synthesis

151
Q

What are the potential SE of Azathioprine?

A

Bone marrow suppression
Hepatotoxicity

152
Q

How does Mycophenolate work?

What are its SEs?

A

T & B cell inhibition.

GI side effects are common. Monitor for skin cancer.

153
Q

How does methotrexate work?

What are its SEs?

A

Inhibits DNA synthesis & T cell mediated inflammation

Can cause interstitial lung disease, bone marrow suppression and hepatotoxicity (but quickest to work)

154
Q

What drugs should be avoided in MG?

A

Anything that causes neuromuscular blockade

  • Cardiac drugs
  • Abx
  • APs
  • β blockers
  • Aminoglycosides