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Neuro Flashcards

1
Q

What is the pathophysiology of multiple sclerosis

A

acquired chronic immune mediated inflammatory condition of the CNS.
autoimmune destruction of oligodendrocytes by T cells
demylination
gliosis - scarring
neuronal damage leading to cell loss

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2
Q

What are the different types of MS

A

relapsing remitting
secondary progressive
primary progressive

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3
Q

Describe the course of relapsing remitting MS

A

symptoms come and go. Periods of good health or remission are followed by sudden symptoms or relapses

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4
Q

Describe the course of secondary progressive MS

A

the onset of MS is of the RRMS pattern. But, at some point later, the disease course changes and neurological function gradually worsens, with or without continued relapses.

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5
Q

Describe the course of primary progressive MS

A

from the beginning, symptoms gradually develop and worsen over time

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6
Q

Define a relapse in MS

A

onset of new or worsening of current symptoms
attributable to demyelinating disease
>24hr onset
absence of infection, fever, metabolic disturbance

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7
Q

What are the most common presentations of MS

A

optic neuritis - partial or total unilateral visual loss, pain on movement, dereased visual acuity, decreased colour sensitivity

transverse myelitis - paresthesia or weakness below level of inflammation

cerebellar problems - ataxia, vertigo, clumsiness, dysmetria

brain stem problems - ataxia, abnormal eye movements, dysphagia

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8
Q

What is Lhermitte’s phenomena

A

shock like sensation radiating down the spine induced by neck flexion

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9
Q

Give some differentials for MS

A 
neuromyelitis optica
low vit B12
Lyme disease
tertiary syphilis
HIV
SLE
sarcoidosis
brain neoplasm
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10
Q

What is the key diagnostic investigation in MS

A

MRI head - periventricular lesions and discrete white matter abnormalities

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11
Q

What is the treatment for a relapse of MS

A

IV or oral steroids - metyhlprednisolone for 5 days

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12
Q

What is the treatment long term for MS

A

DMARDs - eg. interferon beta

management of long term problems of fatigue, pain etc

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13
Q

What causes a seizure

A

neurons synchronously depolarising due to increased excitation or decreased inhibition

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14
Q

What are the main excitatory and inhibitory neurotransmitters in the brain

A

excitatory: NMDA
inhibitory: GABA

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15
Q

Define seizure

A

transient occurrence of signs and symptoms due to abnormal electrical activity in the brain

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16
Q

What is the difference between a partial seizure and a generalised seizure

A

partial - only part of the brain is affected

generalised - both hemispheres affected

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17
Q

What is the difference between a simple partial seizure and a complex partial seizure

A

partial - no loss of consciousness, remember what happened

complex - partial or complete loss of consciousness, may not remember it

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18
Q

What is a secondary generalised seizure

A

started as partial, becomes generalised

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19
Q

What happens in a tonic seizure

A

become stiff, flexed. fall backwards

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20
Q

What happens in an atonic seizure

A

become relaxed, complete loss of tone, fall forwards

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21
Q

What happens in a clonic seizure

A

convulsions

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22
Q

What happens in a tonic-clonic seizure

A

increased tone and convulsions

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23
Q

What happens in a myoclonic seizure

A

short muscle twitches

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24
Q

What happens in an absence seizure

A

lose and regain consciousness, zones out

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25
Q

What is a Jacksonian march

A

seizure starts in small area eg hand, then spread to larger eg arm. Can become generalized

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26
Q

What are some of the signs or symptoms of post-ictal period

A

Drowsiness or amnesia.
Injury, including bites to the sides of the tongue.
Aching limbs or headache.
Focal neurological deficit, that slowly recovers.

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27
Q

What is Todd’s paralysis

A

a focal neurological deficit, most commonly weakness, that occurs after a seizure
fully recovers after 48 hours

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28
Q

How is epilepsy defined

A

At least two unprovoked seizures occurring more than 24 hours apart.

One unprovoked seizure and a probability of further seizures similar to the general recurrence risk after two unprovoked seizures, occurring over the next 10 years.

Diagnosis of an epilepsy syndrome — there are at least 30 different epilepsy syndromes distinguished by their seizure type, age of onset, family history, neurological findings, cerebral imaging (such as CT or MRI scan), electroencephalogram (EEG) pattern, and underlying cause.

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29
Q

What are the causes of epilepsy

A 
idiopathic
cerebrovascular disease
cerebral tumour
post traumatic
fetal hypoxia or trauma
cortical or vascular malformation
cerebral abscess
epilepsy syndromes
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30
Q

What are the differential diagnoses for a seizure

What would help you rule these in/out

A

syncope - postural change, pale. Feel faint/lightheaded beforehand, blurred vision, ringing ears

arrhythmia - prev IHD/SHD, palpitation, breathless, CP

hyperventilation of anxiety - fear, breathless, paresthesia

febrile convulsions - temp >37.8, 6m-5y

alcohol withdrawal - known alcoholic, around 36 hours following cessation of drinking

infantile spasms - flexion of head, trunk and limbs, extension of arms

Psychogenic non-epileptic seizures - history of mental health problems or a personality disorder

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31
Q

What investigations need to be done in a patient presenting with a seizure

A

obs, LSBP, ECG
glucose, U+E
EEG, MRI

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32
Q

What is the definition of status epilepticus

A

continuous seizure for 30 minutes or longer,

or recurrent seizures without regaining consciousness lasting 30 minutes or longer.

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33
Q

What is the emergency treatment for a seizure

A

<5mins
Protect them from injury by:
Cushioning their head with your hands or soft material.
Removing harmful objects from nearby
Do not restrain them or put anything in their mouth.
When the seizure stops, check their airway and place them in the recovery position.
Observe them until they have recovered.
Examine for, and manage, any injuries.
Arrange emergency admission if it is their first seizure.

> 5mins or more than 3 in 1hr
Buccal midazolam as first-line treatment or rectal diazepam
Intravenous lorazepam if intravenous access is already established and resuscitation facilities are available.
Phenytoin after 20 mins

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34
Q

When should an ambulance be called for someone having a seizure

A

if seizures do not respond promptly to treatment.

Seizures were prolonged or recurrent before treatment was given, particularly if seizures had developed into status epilepticus.

There is a high risk of recurrence, such as a history of repeated seizures or status epilepticus.

There are difficulties monitoring the person’s condition.

This is their first seizure.

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35
Q

What is the first line management of generalised seizures

A

sodium valproate

or ethosuximide in absence

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36
Q

What is the second line management for generalised seizures?

A

lamotrigine
myoclonic: levetiracetam or topiramate
tonic/atonic: lamotrigine as adjunctive

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37
Q

What is the first line management of partial seizures

A

lamotrigine or carbemazepine

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38
Q

What is the second line management of partial seizures

A

levetiracetam, carbemazepine or sodium valproate

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39
Q

When can one consider stopping antiepileptic drugs?

A

if seizure free for >2 years

stop gradually over 2-3 months

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40
Q

What are the key side effects of lamotrigine

A

Stevens-Johnson syndrome

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41
Q

What are the indiations for starting AEDs

A

second seizure
the patient has a neurological deficit
brain imaging shows a structural abnormality
the EEG shows unequivocal epileptic activity
the patient or their family or carers consider the risk of having a further seizure unacceptable

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42
Q

What is the pathophysiology behind alcohol withdrawal seizures

A

chronic alcohol consumption enhances GABA mediated inhibition in the CNS (similar to benzodiazepines) and inhibits NMDA-type glutamate receptors.
Alcohol withdrawal is thought to be lead to the opposite (decreased inhibitory GABA and increased NMDA glutamate transmission), therefore leading to over excitation

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43
Q

What are the key side effects of sodium valproate

A 
increased appetite and weight gain
alopecia: regrowth may be curly
P450 enzyme inhibitor
ataxia
tremor
hepatitis
pancreatitis
thrombocytopaenia
teratogenic (neural tube defects)
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44
Q

What are the key side effects of carbemazepine

A

P450 enzyme inducer - decreases effectiveness of contraceptives
dizziness and ataxia
drowsiness
leucopenia and agranulocytosis
SIADH
visual disturbances (especially diplopia)

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45
Q

Which contraceptives are recommended to take whilst on carbemazepine?
Why is this?

A

copper IUD
mirena
depo-provera injection

not metabolised by P-450

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46
Q

What advice is given to patients with epilepsy during pregnancy

A

risks of uncontrolled epilepsy during pregnancy generally outweigh the risks of medication to the fetus.

All women thinking about becoming pregnant should be advised to take folic acid 5mg per day well before pregnancy to minimise the risk of neural tube defects.

lamotrigine
decreased risk of teratogenicity

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47
Q

What advice is given to patients with epilepsy who drive

A

need to inform DVLA
cannot drive for 6 months following a seizure.
must be fit free for 12 months before being able to drive if they have established epilepsy

48
Q

Is breast feeding safe whilst taking AEDs

A

yes

although not with barbiturates

49
Q

What is motor neruone disease

A

group of disordrs characterised by progressive paralysis due to anterior horn cell and motor cranial nuclei damage
leads to LMN and UMN dysfunction

50
Q

What age group is MND most common in

A

43-52 years in familial

58-63 years in sporadic

51
Q

What are the features of MND

A

limbs: dropping objects, fasciculations, NO SENSORY SIGNS, wasting of hand muscles, weakness and cramping
bulbar: slurring, tongue fasciculations and wasting, dysphagia, emotional lability
resp: dyspnoea, orthopnoea, waking from sleep

52
Q

What is a stroke?

A

a sudden interruption of blood supply to the brain

53
Q

What is the difference between an ischaemic and haemorrhagic stroke

A

Ischaemic: obstruction within blood vessels preventing blood flow to the brain,

Haemorrhagic stroke: blood vessel ruptures reducing blood flow to the brain

54
Q

What is the difference between an ischaemic stroke and a TIA

A

stroke: obstruction within blood vessels preventing blood flow to the brain, lasting >24 hours

TIA: obstruction within blood vessels preventing blood flow to the brain, lasting <24 hours

55
Q

What is the difference between a thrombotic and embolic stroke

A

Thrombotic - Thrombus from a large artery e.g. carotid

Embolic - Blood clot, fat, air or bacterial embolus. AF can cause

56
Q

What are the risk factors for stroke (including specific for ischaemic and haemorrhagic)

A 
Non-specific:
•	Age
•	HTN
•	Smoking
•	Hyperlipidaemia
•	Diabetes
•	Alcohol
•	Medications
•	Genetics
•	Obesity
•	Sedentary lifestyle

Ischaemic stroke:
• AF

Haemorrhagic stroke:
• Anticoagulation therapy
• Arteriovenous malformation`

57
Q

What do the parietal lobes do

A
  • Communication with other lobe
  • Perception

Dominant hemisphere

  • Understanding the world
  • Maths
  • Language

Non-dominant hemisphere:
- Visuospatial functions

58
Q

What do the frontal lobes do

A
  • Higher level cognition (executive functioning)
  • Thinking
  • Planning
  • Organising and problem solving
  • Emotions
  • Behaviour control
  • Personality
  • Broca’s area in dominant = Produce speech
59
Q

What do the occipital lobes do

A
  • Visual processing
60
Q

What do the temporal lobes do

A
  • Auditory processing
  • Primary auditory cortex
  • Wernicke’s in Left temporal lobe = Understanding Language
  • Memory
61
Q

What does the cerebellum do

A
  • Balance
  • Movement
  • Coordination
62
Q

What does the brainstem do

A
  • Involuntary actions
  • Heart rate
  • Breathing
  • Blood pressure
  • Swallow
  • Regulates hormones
63
Q

Which parts of the brain do the anterior cerebral arteries supply

A

most midline portions of the frontal lobes

superior medial parietal lobes.

64
Q

Which parts of the brain do the middle cerebral arteries supply

A

lateral surface of the hemisphere;
lateroinferior frontal lobe (location of Broca’s area i.e. language expression)
lateral temporal lobe (location of Wernicke’s area i.e. language comprehension)

65
Q

What parts of the brain do the posterior cerebral arteries supply

A

cerebellum

occipital lobe

66
Q

What are the three signs that the OXFORD (Bamford) STROKE CLASSIFICATION use to classify strokes

A
  1. unilateral contralateral hemiparesis and/or hemisensory loss of the face, arm & leg
  2. contralateral homonymous hemianopia
  3. higher cognitive dysfunction e.g. dysphasia
67
Q

What causes a TACI (total anterior circulation) and what are the symptoms

A
  • Middle and Anterior Cerebral arteries
  • All 3 criteria are present

(1. unilateral contralateral hemiparesis and/or hemisensory loss of the face, arm & leg
2. contralateral homonymous hemianopia
3. higher cognitive dysfunction e.g. dysphasia)

68
Q

What causes a PACI (partial anterior circulation) and what are the symptoms

A
  • Smaller arteries of the Anterior Circulation e.g. Upper or Lower division of Middle Cerebral artery
  • 2 criteria are present

(1. unilateral contralateral hemiparesis and/or hemisensory loss of the face, arm & leg
2. contralateral homonymous hemianopia
3. higher cognitive dysfunction e.g. dysphasia)

69
Q

What causes a POCI (posterior circulation) and what are the symptoms

A

• Vertebrobasilar arteries

Presents with 1 of:
• Cerebellar or brainstem syndromes
• Loss of consciousness
• Isolated homonymous hemianopia

70
Q

What causes a LACI (lacunar circulation) and what are the symptoms

A

• Perforating arteries around internal capsule, thalamus and basal ganglia

Presents with 1 of:
•	Pure unilateral motor dysfunction of face and arm, arm and leg or all 3.
•	Pure sensory stroke
•	Mixed motor and sensory
•	Ataxia: ataxic hemiparesis
71
Q

What causes a LACI (lacunar circulation) and what are the symptoms

A

• Perforating arteries around internal capsule, thalamus and basal ganglia

Presents with 1 of:
•	Pure unilateral motor dysfunction of face and arm, arm and leg or all 3.
•	Pure sensory stroke
•	Mixed motor and sensory
•	Ataxia: ataxic hemiparesis
72
Q

What problems does a lesion in the anterior cerebral artery cause

A

Contralateral hemiparesis and sensory loss,

lower extremity > upper (midline does lower extremities)

73
Q

What problems does a lesion in the middle cerebral artery cause

A

Contralateral hemiparesis and sensory loss, upper extremity > lower
Contralateral homonymous hemianopia
Aphasia

74
Q

What problems does a lesion in the posterior cerebral artery cause

A

Contralateral homonymous hemianopia with macular sparing

Visual agnosia

75
Q

What problems does a lesion in the posterior inferior cerebellar artery cause

A

Ipsilateral: facial pain and temperature loss (sensory)
Contralateral: limb/torso pain and temperature loss
Ataxia, nystagmus

76
Q

What problems does a lesion in the anterior inferior cerebellar artery cause

A

Ipsilateral: facial pain and temperature loss (sensory)
Contralateral: limb/torso pain and temperature loss
Ataxia, nystagmus

also
Ipsilateral: facial paralysis and deafness

77
Q

What problems does a lesion in the basilar artery cause

A

locked in syndrome
paralysis of body and facial muscles
consciousness and some eye movements are preserved

78
Q

What causes Weber’s syndrome? What are the features?

A

lesion in branches of the posterior cerebral artery that supply the midbrain

Ipsilateral CN III palsy - down and out
Contralateral weakness of upper and lower extremity

79
Q

How should an ischaemic stroke be managed immediately?

A
  1. A to E assessment
  2. Ensure the following parameters are normal:
    Blood glucose
    Hydration
    Oxygen saturation
    Temperature
  3. Do not try and lower blood pressure in the acute phase
  4. Aspirin 300mg PO/rectally as soon as haemorrhagic stroke excluded
  5. Statin if cholesterol > 3.4mmol/L (wait for 48 hours)
  6. Thrombolysis with Alteplase if:
    Able to be administered within 4.5 hours of onset of symptoms
    Exclusion of haemorrhagic stroke by imaging
  • Carotid endarterectomy if carotid territory and no severe disability *
80
Q

What drugs are used for long term secondary prevention after an ischaemic stroke

A

first line: clopidogrel

second line: aspirin plus MR dipyridamole if clopidogrel is contraindicated or not tolerated,

third line: MR dipyridamole alone only if aspirin or clopidogrel are contraindicated or not tolerated

81
Q

How should a TIA be managed

A
  1. Aspirin 300mg immediately (unless contraindicated due to bleeding disorder or already taking anticoagulant)
  2. Refer to specialist
82
Q

What are the absolute contraindications to thrombolysis in an ischaemic stroke

A
  • Previous intracranial haemorrhage
  • Seizure at onset of stroke
  • Intracranial neoplasm
  • Suspected subarachnoid haemorrhage
  • Stroke or traumatic brain injury in preceding 3 months
  • Lumbar puncture in preceding 7 days
  • Gastrointestinal haemorrhage in preceding 3 weeks
  • Active bleeding
  • Oesophageal varices
  • Pregnancy
  • Uncontrolled hypertension >200/120mmHg
83
Q

What are the relative contraindications to thrombolysis

A
  • Concurrent anticoagulation (INR >1.7)
  • Haemorrhagic diathesis - unusual susceptibility to bleed (hemorrhage) mostly due to hypocoagulability
  • Active diabetic haemorrhagic retinopathy
  • Suspected intracardiac thrombus
  • Major surgery / trauma in preceding 2 weeks
84
Q

How should a haemorrhagic stroke be treated?

A
  1. Consult neurosurgery
  2. Stop anticoagulants and antithrombotics
  3. Reverse anticoagulation ASAP
    Warfarin: fresh frozen plasma
    Heparin: Protamine Sulfate
  4. Some trials have shown benefit to acutely lowering the BP
85
Q

What is the ROSIER score used for?

A

assess likelihood of stroke

86
Q

How is the ROSIER score calculated

A

Exclude hypoglycaemia first, then assess the following:

Lose a point for each of:
• Loss of consciousness or syncope
• Seizure activity

Gain a point for each of:
•	Asymmetrical facial weakness
•	Asymmetrical arm weakness
•	Asymmetrical leg weakness
•	Speech disturbance
•	Visual field defect
87
Q

What is the advice regarding driving after a Stroke/TIA

A

1 month off driving, may not need to inform DVLA if no residual neurological deficit

88
Q

What is cauda equina syndrome

A

compression of the cauda equina, the nerve roots caudal to the level of spinal cord terimination

89
Q

What can cause cauda equina syndrome

A

Herniation of a lumbar disc - L4/L5 and L5/S1 level.
Tumours: metastases, lymphomas, spinal tumours.
Trauma.
Infection, including epidural abscess.
Congenital - eg, congenital spinal stenosis, kyphoscoliosis and spina bifida.
Spondylolisthesis.
Late-stage ankylosing spondylitis.
Postoperative haematoma.
Following spinal manipulation.
Inferior vena cava thrombosis.
Sarcoidosis.

90
Q

What are the features of cauda equina syndrome

A 
back pain- sudden onset
urinary retention
problems initiating urination or stopping stream
lower limb sensory or motor deficit
loss of reflexes at affected nerve root
saddle/perianal paraesthesia
constipation or incontinence
reduced anal tone
sexual dysfunction
91
Q

What investigaitons need to be done urgently in cauda equina syndrome

A

MRI spine

92
Q

How is cauda equina syndrome managed

A

urgent spinal decompression surgery!!!

Anti-inflammatory agents if inflammatory cause - eg, ankylosing spondylitis.
Infection causes should be treated with appropriate antibiotic therapy.
Spinal neoplasms should be evaluated for chemotherapy and radiation therapy.

93
Q

Explain the difference between paraparesis, hemiparesis, monoparesis and quadraparesis

A

para = partial paralysis of the lower limbs
hemi - partial weakness on one side of the body.
mono = paresis of one limb due to due to a small infarction in the contralateral motor cortex.
quadra = all four limbs, usually as the result of injury to the spine.

94
Q

What sensory level is the umbilicus at

A

T10

95
Q

What sensory level is the nipple at

A

T4

96
Q

What is the function of the corticospinal tract

A

voluntary motor control of body and face

97
Q

Describe the route of the corticospinal tract

A

internal capsule
medulla - decussates here
travels in anterolateral spinal cord

98
Q

State the location in the spinal cord, blood supply and level of decussation of the corticospinal tract

A

anterolateral spinal cord
anterior spinal artery
decussates at the pyramids of the medulla

99
Q

What is the function of the lateral spinothalamic (part of the anterolateral system) tract

A

pain and temperature sensation

100
Q

State the location in the spinal cord, blood supply and level of decussation of the lateral spinothalamic tract

A

anterolateral spinal cord
anterior spinal artery
decussates at or within an few segments of level of entry to the cord

101
Q

What would a lesion to the lateral spinothalamic tract in the cord cause

A

contralateral loss of pain and temperature perception below level of lesion

102
Q

State the location in the spinal cord, blood supply and level of decussation of the dorsal column medial lemniscus tract

A

posterior spinal cord
posterior spinal artery
decussates at medulla oblongata

103
Q

What is the function of the DCML tract

A

sensation of proprioception and fine touch

104
Q

What would a lesion to the DCML tract in the cord cause

A

ipsilateral loss of fine touch and proprioception sensation below level of lesion

105
Q

What is Brown-Sequard syndrome and what does it cause?

A

hemisection (one sided lesion) of the spinal cord.

DCML pathway – ipsilateral loss of touch, vibration and proprioception.
Anterolateral system – contralateral loss of pain and temperature sensation.

It will also involve the descending motor tracts, causing an ipsilateral hemiparesis.

106
Q

What causes Horner’s syndrome

A

disruption of tthe sympathetic nerves anywhere along their course -

107
Q

Describe the course of the sympathetic nerve fibres to the eye

A

First-order sympathetic fibres originate in the hypothalamus and descend through the brainstem to level C8-T2 of the spinal cord where they synapse on preganglionic sympathetic nerve fibres.

Second-order fibres leave the cord at level T1 and ascend in the sympathetic chain over the apex of the lung to synapse in the superior cervical ganglion at the level of the bifurcation of the common carotid artery (C3-C4).

Third-order (postganglionic) fibres pass alongside the internal carotid artery, sending branches to the blood vessels and sweat glands of the face, and pass via the cavernous sinus to enter the eye via the superior orbital fissure. They pass via the long ciliary nerves to supply the iris dilator and Müller’s muscle (superior tarsal muscle)

108
Q

What are the key features of horner’s syndrome

A

partial ptosis
miosis
hemifacial anhidrosis

109
Q

What are the symptoms of horner’s syndrome

A 
asymptomatic!
partial ptosis
miosis
hemifacial anhidrosis
facial flushing - if pre-glanglionic
orbital pain/headache - if post-ganglionic
110
Q

What should be examined in horner’s syndrome

A

Constricted pupil on the affected side -
Shine a torch in the eye to make the pupil constrict.
Remove the torch and watch the pupil dilate - the affected pupil lags behind the other in dilation

Ipsilateral dry skin on the face due to loss of sweating:

Ipsilateral partial ptosis

There is increased amplitude of accommodation - can focus on nearer objects more easily

Heterochromia irides may occur with congenital Horner’s syndrome - the iris on the affected side remains blue whilst the other changes to brown.

Examine for the presence of lymphadenopathy

111
Q

What are the causes of Horner’s syndrome

A

central:
cerebrovascular accident
MS

preganglionic:
Pancoast tumour
lymphoma
TB causing lymphadenopathy
aortic or common carotid artery dissection
trauma

Postganglionic
HSV
internal carotid artery dissection

112
Q

How can the location of the lesion in Horner’s syndrome be determined clinically

A

the extent of the anhidrosis

if central: anhidrosis of face, arm adn trunk
if preganglionic: anhidrosis of face
if post ganglionic: no anhidrosis

113
Q

What investigations should eb done in Horner’s syndrome

A

CXR
CT/MRI head
CT angiogram

114
Q

What are some important questions to ask in a headache history? Why?

A

Site -
• Unilateral headache and eye pain—cluster headache, acute glaucoma
• Unilateral headache and ipsilateral symptoms—migraine, tumour, vascular

Quality -
• First and worst headache—subarachnoid haemorrhage
• Thunderclap headache—subarachnoid haemorrhage

Timing
• Worse in the morning or bending forward—↑icp/venous thrombosis
• Change in the pattern of ‘usual headaches’.
• Where have you been? - Malaria

Aggravating -
• Cough-initiated headache—↑icp/venous thrombosis

Secondary symptoms
• Persisting headache ± scalp tenderness in over-50s—giant cell arteritis
• Headache with fever or neck stiffness—meningitis
• Might you be pregnant? - pre-eclampsia

115
Q

What do teh flexor and extensor response to pain show?

A

Flexion = decorticate posture (arms bent inwards on chest, thumbs tucked in a clenched fist, legs extended) implies damage above the level of the red nucleus in the midbrain.

• Extension = decerebrate posture (adduction and internal rotation of shoulder, pronation of forearm) indicates midbrain damage below the level of the red nucleus.

116
Q

What are the features needed for a diagnosis of migraines

A

5 attacks
• Lasting 4 hours – 3 days
• 2 of unilateral, pulsating, severe affecting life
• 1 of N+V, photophobia, phonophobia

Finals (32 decks)

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