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Neurology > Neurology: Clinical - MS, headache, epilepsy > Flashcards

Neurology: Clinical - MS, headache, epilepsy Flashcards

1
Q

What is Uthoff’s phenomenon?

A

Heat slowing nerve conduction and so worsening signs of MS on hot days

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2
Q

What is Lehrmitte’s sign?

A

Sudden sensation resembling electric shock that passes down the back of the neck and into spine, may radiate in arms and legs (can be a symptom of MS)

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3
Q

What is the pathology of multiple sclerosis?

A

Demyelination occurring at multiple CNS sites, caused by T-cell mediated immune response

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4
Q

Why does MS often have relapsing and remitting symptoms?

A

Demyelination heals poorly

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5
Q

What does prolonged demyelination in MS cause?

A

Axonal loss and progressive symptoms

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6
Q

How does the demyelination occur in MS?

A

Activated T cels cross the BBB causing demyelination and acute inflammation of the myelin sheath

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7
Q

How does MS present on MRI?

A

Lesions or plaques on MRI = white areas on scan

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8
Q

What are the MS plaques seen on MRI due to?

A

Conduction block/axonal loss

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9
Q

What is benign MS?

A

When people have 1 (or small number of) attacks of the disease

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10
Q

What are the four mains patterns of disease for MS?

A

Progressive-relapsing MS
Secondary progressive MS
Primary progressive MS
Relapsing-remitting MS

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11
Q

What is the most common pattern of disease seen in MS?

A

Relapsing-remitting MS

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12
Q

What is the relapsing-remitting pattern of disease seen in MS?

A

Unpredictable attacks which may or may not leave permanent deficits followed by periods of remission

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13
Q

What is the primary progressive pattern of disease seen in MS?

A

Steady increase in disability without attacks

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14
Q

What is the secondary progressive pattern of disease seen in MS?

A

Initial relapsing-remitting MS, that suddenly begins to have decline without periods of remission

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15
Q

What is the progressive-relapsing pattern of disease seen in MS?

A

Steady decline since onset with super-imposed attacks

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16
Q

What is the aetiology of MS?

A 
Complex genetic inheritance
Association with autoimmune disease
Females more than males
Commoner in temperate climates
?Vitamin D exposure
Young age of onset
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17
Q

What are some of the symptoms of MS?

A

Fatigue, sexual dysfunction (erectile dysfunction), incontinence, constipation, facial numbness/weakness, speech difficulties, dysphagia

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18
Q

What are some of the signs of MS?

A 
Optic neuritis
Sensory symptoms: numbness and paraesthesia (pins and needles)
Limb weakness
Tremor
Diplopia/vertigo/ataxia (brainstem)
Bladder weakness (spinal cord bilateral)
UMN signs: spasticity, weakness, brisk reflexes
Scotoma = dark spot in centre of vision
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19
Q

What are some of the symptoms of optic neuritis?

A

Subacute visual loss in one eye, pain on moving eye, colour vision disturbed, visual field loss, flashing lights

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20
Q

What are some of the signs of optic neuritis?

A

Initial swelling optic disc, optic atrophy seen later, relative afferent pupillary defect

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21
Q

What is internuclear opthalmoplegia (INO)?

A

Disorder of conjugate lateral gaze:

Affected eye shows impairment of adduction

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22
Q

What is internuclear ophthalmoplegia (INO) a disorder of?

A

Brainstem (medial longitudinal fascicles (MLF))

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23
Q

What symptoms might a patient have if the cerebellum is damaged?

A

Vertigo, nystagmus, ataxia

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24
Q

How does myelitis normally present?

A

Muscle weakness or paralysis

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25
Q

What examinations would you perform is you suspect MS?

A 
Afferent pupillary defect
Nystagmus or abnormal eye movements
Cerebellar signs
Sensory signs
Weakness
Spasticity
Hyperreflexia
Plantars extensor
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26
Q

What are lesions or plaques on MRI scan?

A

Areas of demyelination

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27
Q

For 10 lesions, approximately how many relapses will the patient experience?

A

1

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28
Q

What are some differential diagnoses for MS?

A 
Acute disseminated encephalomyelitis (ADEM)
Other auto immune conditions e.g. SLE
Sarcoidosis
Vasculitis
Infection
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29
Q

When does primary progressive MS usually present?

A

5th/6th decade

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30
Q

What are the symptoms for primary progressive MS like?

A

Spinal and bladder symptoms

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31
Q

What is prognosis for primary progressive MS?

A

Poor

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32
Q

What is the other name for Devic’s disease?

A

Neuromyelitis optica

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33
Q

What is the other name for neuromyelitis optica?

A

Devic’s disease

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34
Q

What type of hypersensitivity reaction is MS?

A

Type IV hypersensitivity reaction (cell-mediated)

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35
Q

What is Charcot’s triad in relation to MS?

A

Dysarthria - unclear/difficult speech
Nystagmus
Intention tremor

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36
Q

What are primary headaches?

A

Migraine
Tension type headache
Cluster headache

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37
Q

What are secondary headaches?

A

Caused by structural or biochemical cause e.g tumour, meningitis, vascular disorders, systemic infection, head injury, drug induced

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38
Q

What does ETTH stand for?

A

Episodic tension type headache

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39
Q

What does CTTH stand for?

A

Chronic tension type headache

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40
Q

How many headaches per month for infrequent ETTH?

A

<1 day/month

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41
Q

How many headaches per month for frequent ETTH?

A

1-14days/month

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42
Q

How many headaches per month for CTTH?

A

> 15days/month

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43
Q

What is the treatment for tension type headaches (TTH)?

A

Abortive e.g. aspirin/paracetamol, NSAIDs

Preventative e.g. tricyclic antidepressants (amitriptyline)

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44
Q

What can happen if you have too much abortive treatment for TTH?

A

Develop medication overuse headaches

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45
Q

What should you limit abortive treatment to for TTH?

A

Limit to 10 days/month (2/wk)

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46
Q

What are the triggers for migraine?

A

Diet, dehydration, hunger, stress, sleep disturbances, oestrogen levels in women, environmental stimuli

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47
Q

What are the symptoms of migraine?

A

Headache which is unilateral, pulsating with moderate/severe pain, photophobia, phonophobia, nausea, functional disability (can’t do activities)

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48
Q

What is migraine?

A

Chronic disorder of episodic attacks of complex changes in the brain

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49
Q

What symptoms are there in the premonitory phase of migraine?

A

Mood changes, fatigue, cognitive changes, muscle pain, food craving

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50
Q

What symptoms are there in the early headache phase of migraine?

A

Dull headache, nasal congestion, muscle pain

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51
Q

What percentage of migraineurs experience aura?

A

33%

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52
Q

What can aura symptoms be confused for?

A

TIA

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53
Q

What is the most common aura symptom in migraines?

A

Visual aura - loss of vision, blind spot that progresses or enlarges

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54
Q

What does sensory aura include?

A

Parasthesia in one hand, spreading to arm, elbow, face, lips and tongue

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55
Q

What is aura (migraine)?

A

Transient neurological symptoms resulting from cortical or brainstem dysfunction e.g. visual, sensory, motor or speech symptoms

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56
Q

How does aura typically move from one symptom to the next?

A

Vision -> sensory -> speech

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57
Q

How long can aura last (migraine)?

A

15-60 minutes

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58
Q

What duration is classed as chronic migraine?

A

Headache >15days/month with >8 days as migraine for more than 3 months

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59
Q

What is a transformed migraine?

A

History of episodic migraine and increasing frequency of headaches but migrainous symptoms have become less frequent and less severe
More headaches = less severe

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60
Q

What is duration is classed as a medication overuse headache (MOH)?

A

Headache present on >15days/month which has developed or worsened whilst taking regular symptomatic medication

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61
Q

What is the treatment for migraines?

A

Abortive: aspirin/NSAIDs, triptans
Preventative: propranolol, Cadesartan, anti-epileptics (valproate), tricyclic antidepressants (amitriptyline), venlafaxine

62
Q

What gets better with pregnancy: migraine with aura or migraine without aura?

A

Migraine without aura gets better in pregnancy

63
Q

Which drug is contraindicated in active migraine with aura?

A

Oral contraceptive pill

64
Q

What is the treatment for migraine during pregnancy?

A

Acute attack: paracetamol

Preventative: propanolol or amitriptyline

65
Q

What are trigeminal autonomic cephalalgias (TACs)?

A

A group of headache disorders characterised by attack of moderate to severe unilateral pain in the head/face with associated ipsilateral cranial autonomic features e.g. lacrimation, conjunctival infection, nasal congestion, oedema, ptosis

66
Q

What headaches are included in TACs?

A

Cluster headache
Paroxysmal hemicrania
Short-lasting unilateral neuralgiform headaches with conjunctival injection and tearing (SUNCT)
Short-lasting unilateral neuralgiform headache attacks with cranial autonomic symptoms (SUNA)
Long-lasting autonomic symptoms with hemicranial (LASH)

67
Q

Where is the pain focussed usually for cluster headaches?

A

Oribital and temporal regions

68
Q

Are attacks unilateral or bilateral for cluster headaches?

A

Unilateral

69
Q

What is typical duration of a cluster headache?

A

15 mins - 3 hours

70
Q

Where is the pain focussed usually for paroxysmal hemicrania?

A

Orbital and temporal regions

71
Q

Are attacks unilateral or bilateral for paroxysmal hemicrania?

A

Unilateral

72
Q

What is the typical duration for paroxysmal hemicrania?

A

2-30mins

73
Q

What are 10% of paroxysmal hemicrania attacks precipitated by?

A

Bending or rotating the head

74
Q

Approximately, how many attacks per day for paroxysmal hemicrania?

A

2-40 per day

75
Q

Where is the pain focussed usually for SUNCT?

A

Unilateral orbital, supraorbital or temporal pain

76
Q

What is the character of pain for SUNCT?

A

Stabbing or pulsating

77
Q

What is the duration of an episode of SUNCT?

A

10-240 seconds

78
Q

What are the triggers for SUNCT?

A

Cutaneous triggers - cold, touch, chewing

79
Q

What is the frequency of attacks for SUNCT?

A

3-200/day

80
Q

What is pain accompanied by with SUNCT?

A

Conjunctival inaction and lacrimation

81
Q

What are red flags for headaches?

A

New onset headache
New or change in headache - over 50, cancer, immunosuppresion
Change in freq, characteristics or associated symptoms
Focal neurological symptoms
Non-focal neurological symptoms
Abnormal neurological examination
Neck stiffness/fever
High pressure - worse lying down/wakening patient/precipitated by exercise/valsalva manoeuvre
Low pressure - precipitated by sitting/standing
GCA - jaw claudication/visual disturbance/prominent/beaded temporal arteries

82
Q

What is a thunderclap headache?

A

A high intensity headache reaching maximum intensity in less than 1 minute

83
Q

What are the differential diagnoses for thunderclap headache?

A 
Primary (migraine)
Subarachnoid haemorrhage (SAH)
Intracerebral haemorrhage
TIA/stroke
Carotid/vertebral dissection
Cerebral venous sinus thrombosis
Meningitis/encephalitis
Pituitary apoplexy
Spontaneous intracranial hypotension
84
Q

What percentage of patients with a thunderclap headache will have a SAH?

A

10%

85
Q

What are the investigations for a suspected SAH?

A

CT brain and LP same day

86
Q

What are some symptoms of meningitis?

A

Nausea, vomiting, photo/phono-phobia, stiff neck, headache, fever, rash

87
Q

What CNS infections should be considered with any patient presenting with headache or fever?

A

Meningitis and encephalitis

88
Q

What are the symptoms of encephalitis?

A

Altered mental state/consciousness, focal symptoms/signs, seizures, headache, fever, rash

89
Q

What are some causes of raised intracranial pressure?

A 
Glioblastoma multiforme
Cerebral abscess
Venous infarct with focal area of haemorrhage
Meningioma
Hydrocephalus
Papilloedema
90
Q

What are the features suggestive of a space occupying lesion and/or raised intracranial pressure?

A

Progressive headache with associated symptoms/signs
Headache worse in morning/wakes from sleep
Headache worse lying flat or brought on by Valsalva
Focal symptoms or signs
Non-focal symptoms - cognitive/personality change, drowsiness
Seizures
Visual obscurations and pulsatile tinnitus

91
Q

What are the causes of intracranial hypotension?

A

Dural CSF leak - either spontaneous or iatrogenic (LP)

92
Q

What are the features of a headache of a patient with intracranial hypotension?

A

Headache develops/worsens soon with upright posture and lessens/resolves with lying down

93
Q

What are the investigations for intracranial hypotension?

A

MRI brain and spine

94
Q

What is the treatment for intracranial hypotension?

A

Bed rest, fluids, analgesia, caffeine
IV caffeine
Epidural blood patch

95
Q

What is giant cell arteritis?

A

Arteritis of large arteries

96
Q

Which patient group should giant cell arteritis be considered in?

A

Over 50s with new headache

97
Q

What are the signs and symptoms of giant cell arteritis?

A

Headache: diffuse, persistent, severe
Systemically unwell
Scalp tenderness, jaw claudication, visual disturbance
Prominent, beaded or enlarged temporal arteries

98
Q

What markers support a diagnosis of giant cell arteritis?

A

Elevated ESR

Raised CRP and platelet count

99
Q

What is the treatment is giant cell arteritis is suspected?

A

High dose prednisolone

Temporal artery biopsy

100
Q

When considering epilepsy, what history do you want from the patient?

A

History of preceding events
History of event itself - warning symptoms/level of awareness/recollection
Afterwards - first recollection, seizure markers e.g. prolonged disorientation, tongue biting, incontinence, muscle pains

101
Q

When considering epilepsy, what history do you want from a witness?

A

How were they before?
Description of episode: eyes open/closed, description of abnormal movements, pallor, alteration in breathing pattern, pulses, duration of LOC, time to recovery

102
Q

What are the three categories of syncope?

A

Reflex (neuro-cardiogenic)
Orthostatic
Cardiogenic

103
Q

How is reflex (neuropathy-cardiogenic/vasovagal) syncope caused?

A

Taking blood/medical situations

Cough, micturation

104
Q

How is orthostatic syncope caused?

A

Dehydration
Medication related (antii-hypertensive)
Endocrine
ANS

105
Q

How is cardiogenic syncope caused?

A

Arrhythmia

Aortic stenosis

106
Q

What is the recovery like for normal syncope?

A

Very brief LOC
Fully orientated quickly
Rapid recovery

107
Q

What investigations would you do for syncope?

A

Examination: heart sounds, pulse, postural BPs
ECG: look at QT ratio, for heart block
24hr ECG
Tilt table test

108
Q

What is the usual patient account for signs/symptoms for cardiogenic syncope?

A

On exertion
Chest pain, palpitations, SOB
Came round fairly quickly
Clammy/sweaty

109
Q

What is the usual witness account for signs/symptoms for cardiogenic syncope?

A 
Suddenly went floppy
Looked grey/ashen white
Seemed to stop breathing
Unable to feel pulse
Few brief jerks
Rapid recovery
110
Q

What investigations would you do for cardiogenic syncope?

A 
Family history
Examinations: heart sounds, pulse
ECG: look at QT ratio, for heart block
Refer to cardiology urgently/admission for telemetry
24hr ECG/ECHO/prolonged monitoring
111
Q

What triggers can result in provoked seizures?

A 
Alcohol withdrawal
Drug withdrawal
Within few days of head injury
Within 24hrs of stroke
Within 24hrs neurosurgery
With severe electrolyte disturbance
Eclampsia
112
Q

What are the two main categories of seizure?

A

Generalised seizures

Focal seizures

113
Q

Where do the electrical disturbances occur in generalised seizures?

A

Across whole brain at once

114
Q

Where do the electrical disturbances occur in focal seizures?

A

In one particular part of the brain

115
Q

What types of seizures are included in the classification generalised seizures?

A 
Absence seizures
Generalised tonic-clonic seizures
Myoclonic seizures
Juvenile myoclonic epilepsy
Atonic seizures
116
Q

What types of seizures are included in the classification focal seizures?

A

Simple partial seizures
Complex partial seizures
Secondary generalised
Or by localisation of onset e.g. temporal lobe

117
Q

What are the features of primary generalised epilepsy?

A 
No warning
<25 years
May have history of absences and myoclonic jerks as well as GTCS
Generalised abnormality of EEG
Family history
118
Q

What are the features of focal/partial epilepsy?

A 
May get an 'aura'
Any age
Simple partial and complex partial seizures can become secondary generalised
Focal abnormality on EEG
MRI may show cause
119
Q

What is the usual patient account for a generalised tonic clonic seizure (GTCS)?

A 
Unpredictable - tend to cluster
PMH - trauma, brain injury, meningitis
Irritability before event
May have vague warning
Tongue biting
Incontinence
First recollection a lot later - hospital/ambulance
Muscle pain
120
Q

What is the usual witness account for a generalised tonic clonic seizure (GTCS)?

A 
Groaning sound
Tonic (rigid phase) - generalised jerking in all four limbs
Eyes open - staring/roll upwards
Foaming at mouth
Jerking for few minutes
Groggy for 15-30mins - poor recollection until later
Agitated after
Clusters of episodes
121
Q

Who are prone to getting absence seizures?

A

Children

122
Q

What are absence seizures often provoked by?

A

Hyperventilation

Photic stimulation

123
Q

What happens in an absence seizure?

A

Brief staring
Eye-lid fluttering
Re-start what they were doing

124
Q

Who are prone to getting juvenile myoclonic epilepsy?

A

Adolescents/early adulthood

125
Q

What is juvenile myoclonic epilepsy often provoked by?

A

Alcohol

Sleep deprivation

126
Q

What other seizures can juvenile myoclonic epilepsy get?

A

Absence seizures

GTCS

127
Q

Which type of epilepsy will often have early morning myoclonus, meaning they will drop things and have brief jerks in the limbs?

A

Juvenile myoclonic epilepsy

128
Q

What is the usual patient account for complex partial seizures?

A

Rising feeling in stomach before, funny smell/taste
Deja vu
No recollection of event itself
Disorientated afterwards

129
Q

What is the usual witness account for complex partial seizures?

A

Sudden arrest in activity
Staring blankly into space
Automatisms: lip smacking/repetitive picking at clothes
Disorientated

130
Q

What is the routine clinical assessment for seizures?

A 
Refer to first seizure clinic
ECG, routine bloods (Glc)
CT
Neurology clinic:
MRI for focal lesion
EEG
Discuss anti-epileptic drugs
Discuss driving
131
Q

What investigations would you do for both generalised and focal seizures?

A

Generalised: EEG if hyperventilation/photic stimulation
Focal: MRI/CT
Video-telemetry

132
Q

What are factors influencing seizure risk?

A 
Missed medications (most common)
Sleep disturbance/fatigue
Hormonal changes
Drug/alcohol use, drug interactions
Stress/anxiety
Photosensitivity
133
Q

What is the first line treatment for epilepsy for generalised epilepsies?

A

Sodium valproate
Lamotrigine
Levetiracetam

134
Q

What is the first line treatment for epilepsy for focal and secondary generalised epilepsies?

A

Lamotrigine
Carbamazepine
Levetiracetam

135
Q

What is the first line treatment for epilepsy for absence seizures?

A

Ethosuzimide

136
Q

What is the first line treatment for status epilepticus?

A

Lorazepam/midazolam first line

Valproate or phenytoin second line

137
Q

What are some second line treatment for epilepsy for generalised epilepsies?

A

Topiramate
Zonisamide
Clobazam

138
Q

What are some second line treatment for epilepsy for partial seizures?

A

Sodium valproate
Topiramate
Gabapentin

139
Q

What are the side effects of phenytoin?

A

Arrhythmia
Hepatitis
Medication interactions

140
Q

What are the side effects of sodium valproate?

A 
Tremor
Weight gain
Ataxia
Nausea
Drowsiness
Hepatitis
(Avoid in women of childbearing age)
141
Q

What are the side effects of carbamazepine?

A 
Ataxia
Drowsiness
Nystagmus
Blurred vision
Low serum sodium levels
Skin rash
142
Q

What are the side effects of lamotrigine?

A

Skin rash

Difficulty sleeping

143
Q

What are the side effects of levetiracetam?

A

Irritability

Depression

144
Q

What are the DVLA regulations about epilepsy?

A

After 1 seizure, patient may drive a car after 6 months if investigations are normal and no further events
(HGV after 5 years)
Patients with epilepsy can drive a car once they have been seizure-free for a year or have only have sleep seizures for a year

145
Q

What is status epilepticus?

A

Prolonged or recurrent tonic-clonic seizures persisting for 30mins+ with no recovery period between seizures

146
Q

Who does status epilepticus usually affect?

A

Patients with no previous history of epilepsy e.g. stroke, tumour, alcohol

147
Q

What is non-convulsive status epilepticus?

A

Prolonged unresponsiveness following a seizure

148
Q

What is the first line treatment of status epilepticus?

A

Midazolam
Lorazepam
Diazepam

149
Q

What are the second and third line treatments of status epilepticus?

A

Second: phenytoin, valproate
Third: anaesthesia with propofol or thiopentone

150
Q

What is the usual patient account for a non-epileptic attack/pseudoseizure?

A

Events may occur at time of stress/at rest
Lots of details about other reaction, little of events themselves
May recall what people said during episode
May be prolonged episode
May describe dissociation
Remembers others reactions

151
Q

What is the witness account for a non-epileptic attack/pseudoseizure?

A

May recognise stress as trigger
May report signs of patient retaining awareness
Tracking eye movements, some verbalization
Movements not typical of seizures: pelvic thrusting, asynchronous movements, tremor, episodes waxing and waning

Neurology (9 decks)

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