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Neurology > Headache and Vertigo > Flashcards

Headache and Vertigo Flashcards

1
Q

Pathophysiology of migraine

A

Involves calcitonin gene related peptide

  • Produced in trigeminal ganglion and released in nerve endings
  • Most potent dilator of cerebral and dura blood vessels
  • Release of inflammatory mediators from mast cells
  • Increased levels during acute migraine
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2
Q

What is a significant risk factor for migraine WITHOUT aura

A

Menstruation

Migraine WITHOUT aura improves post menopause

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3
Q

What increases the risk of stroke in a patient with migraine and on OCP

A

Women < 45 or stroke with migraine, OCP and smoking

Migraine with aura is strong contributor to stroke risk.
Estrogen containing oCP should be avoided due to risk of stroke.

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4
Q

Treatment of migraines in pregnancy

A

Medications for migraine can be teratogenic
Avoid triptans and ergots - teratogenic
Non pharmacological medications

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5
Q

Acute migraine Mx

A
  • Paracetamol
  • NSAIDs
  • Metoclopramide
  • Aspirin
  • Triptans: serotonin 5-HT 1b/d receptor agonist, contraindicated in patients with cardiovascular disease
  • Dihydroergotamine
  • Avoid opioids: can cause analgesia rebound headache

Other new medications
PO calcitonin gene related peptide receptor antagonist
- Ubrogepant
- Rimegepant

Migraine with brainstem aura and hemiplegic migraine - triptan contraindicated

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6
Q

Analgesic overuse headache

A

Secondary to overuse of analgesica

  • triptans and opioids (codeine) > 10 days/month
  • simple anlgesics >15 days/month
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7
Q

Migraine prophylaxis

A
  • Amitriptyline: dry mouth, sedation, weight gain, urinary retention
  • Propanolol; hypotension, exercise intolerance, sexual dysfunction, depression
  • Topiramate: acroparaesthesia, weight loss, cognitive dysfunction, depression/anxeity
  • Pizotifen (sandomigran): sedation, dry mouth, weight gain

CGRP inhibitors prophylaxis
Erenumab
Fremanezumab

Migraine

acute: triptan + NSAID or triptan + paracetamol
prophylaxis: topiramate or propranolol

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8
Q

Features of trigeminal autonomic cephalgias

A
  • Hemicrania continua: continuous lasting for days
  • Cluster headache: few episodes lasting for hours
  • Paroxysmal hemicrania: several episodes lasting minutes
  • SUNCT/SUNA
    Short lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing/short lasting unilateral neuralgiform headache attacks with cranial autonomic features
  • Short lasting, uniform, recurrent, neuropathic headaches
  • Associated with cranial autonomic features ipsilateral to pain: ptosis, conjunctival injection, lacrimation, nasal congestion, rhinorrhoea
  • Share common pathophysiology - hypothalamic activation
  • Everyone with TAC syndrome requires a MRI to assess pituitary and posterior fossa lesions
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9
Q

Cluster headache

A
  • Most common TAC
  • MALE predominant
  • Excruciating severe, stabbing pain
  • Can occur daily lasting for hours
  • Last weeks to months and with pain free periods lasting years - follows strict circadian cycle predominantly occurring at night
  • Ipsilateral autonomic features

Acute Tx:

  • Subcut Triptans
  • High flow o2 with non-rebreather

Bridging Tx

  • Steroids
  • Occipital nerve block

Prevention

  • Verapamil - drug of choice
  • Lithium
  • Valproate
  • Melatonin
  • Galcanezumab (CGRP inhibitor)

Need to do MRI brain to exclude structural lesions mimicking cluster headache.

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10
Q

Paroxysmal Hemicrania

A
  • Similar to cluster headache but FEMALE
  • Occurs 5-10 times/day lasting for 2-20 minues
  • Fewer nocturnal events and chronic
  • Respond to INDOMETHACIN
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11
Q

Hemicrania continua

A
  • Constant, unilateral, side locked headache

- Indomethacin

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12
Q

SUNCT/SUNA

A
  • Rare
  • Stabbing, burning pain, orbital pain, hemicranial head pain
  • Occur up to 100 times a day and very brief (seconds)
  • Tx: Lamotrigine
    O2 and indomethacin do not help
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13
Q

Trigeminal Neuralgia

A
  • F>M
  • Distribution: V2/V3 > V1
  • Lasts second to minutes
  • Trigger zone: nasolabial fold, lip, gum, tongue –> cutaneous trigger
  • Exmination normal, subtle sensory deficit
    If sensory loss consider tumour/infiltrate
  • Main cause of trigeminal neuralgia would be neurovascular compression, eg: tortuous superior cerebellar artery impinging on trigeminal nerve root.
    MRI required
  • If someone has BILATERAL trigeminal neuralgia - think MS

Tx

  • Carbamazepine
  • Others: baclofen, lamotrigine, gabapentin
  • Surgery if not responding to medical therapy
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14
Q

Features of secondary headaches

A

SNOOP
- S: systemic symptoms, secondary risk factors
Fever, weight loss, fatigue, HIV, cancer, immunosuppression
- N: neurology: focal deficits, altered consciousness
- O: Onset - thunderclap, acute onset
- O: Older, new onset > 50yo
- P: positional, prior headache
Change in prior headache characteristics
Positional features

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15
Q

Features of idiopathic intracranial hypertension

A
  • Unclear cause
  • Strongly associated with female gender and obesity

Symptoms
- Headache - early morning headaches, position, worse on cough/sneezing (valsalva), wakes them from sleep
Weight loss improves headache
- Decreased visual acuity
- Visual obscuration, eg: sneeze/cough when you valsalva, the vision is impaired momentarily
- Pulsatile tinnitus - not ringing and but a pulsing sound in the ear
- Diplopia is a 6th nerve palsy

Signs

  • Papilloedema
  • VI nerve palsy
  • Loss of visual fields
  • Decreased visual acuity
  • Loss of colour vision

RF

  • female
  • obese
  • reproductive age

Elevated CSF pressure > 25

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16
Q

Secondary causes of IIH

A
  • Venous sinus thrombosis
  • Tetracyclines, eg: doxycycline
  • Fluroquinolones, eg: ciprofloxacin
  • Vitamin A
  • Iron deficiency anaemia
  • OSA
  • Raised CSF protein
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17
Q

Diagnostic criteria of IIH

A
  • PAPILLOEDEMA
  • Normal neurological exam except for cranial nerve abnormalities
  • Normal MRI
  • Normal CSF composition
  • Elevated CSF opening pressure > 25
18
Q

Tx for IIH

A
  • WEIGHT LOSS
  • Acetazolamide: impedes activity at the choroid plexus reducing CSF secretion
  • Topiramate: has weak carbonic anhydrase effect and also cause weight loss.
  • VP shunt or repeated LP
  • Optic nerve fenestration: for patients with visual symptoms, particularly if there is unilateral visual compromise. They put fenestrations in the optic nerve sheath which causes the CSF to spread out and so the CSF does not compress on the nerves
  • Venous stenting
19
Q

Intracranial hypotension

A
  • Postural headache: worse on standing/sitting but better on lying flat
  • Tinnitus, vertigo, decreased hearing
  • Nausea
  • Diplopia
  • Causes
    LP
    Trauma
    Connective tissue disorders, eg: ehlers danlos
    Hypovolemia
  • CSF < 7
  • MRI: pachymeningeal enhancement
Tx
Bed rest
Analgesia
Fluid restriction 
Blood patch 
Caffeine
20
Q

Temporal arteritis

A
  • Large vessel vasculitis affecting tunica media

Clinical
- Headache
- Jaw claudication - most specific symptom
- Scalp tenderness
- Temporal artery tenderness, thickness, reduced pulsation
- Visual loss (amurosis fugax), ophthalmoplegia, eye pain
Anterior ischaemic optic neuropathy, central retinal artery occlusion
- Associated with PMR

21
Q

What is the function of the utricle, saccule and semicircular canal

A
  • Utricle and saccule regulate horizontal and linear movement and static movement.
    Detect linear motion in vertical (saccule) and horixontal (utricle).
  • Semicircular canal and ampulla regulate rotational movement, detect angular acceleration
22
Q

How can vertigo be split?

A
  1. Acute Vestibular Syndrome
    - Vestibular neuritis
    - Stroke
    - Central lesions
  2. Episodic Vestibular Syndrome
    (a) Spontaneous -
    - Vestibular migraine
    - Recurrent posterior circulation TIA
    - Meniere’s disease

(b) Triggered
- BPPPV
- CPPV
- Orthostatic hypotension

23
Q

Features of acute vestibular syndrome

A

Acute Vestibular Syndrome

  • Acute, continuous dizziness lasting days
  • Associated with nausea, vomiting, nystagmus, head motion intolerance (different to head motion triggering symptoms), gait unsteadiness
  • Can have symptom exacerbation but there is constant baseline symptoms
  • MUST HAVE SPONTANEOUS NYSTAGMUS

Peripheral Causes
- Vestibular neuritis/labyrinthitis

Central Causes

  • Stroke: brainstem or cerebella
  • MS (uncommon cause)
  • Rare causes: autoimmune, infection, metabolic, thiamine deficiency

HINTS can discriminate between peripheral and central
HINTS ONLY used for acute vestibular syndrome

24
Q

Features of vestibular neuritis

A
  • Presumed viral or post infectious condition affecting the vestibular nerve
    eg: Ramsay Hunt Syndrome, VZV of CNVII, can affect VIII as well, vesicles in ear and palate
  • Clinical diagnosis, MRI will be normal
  • Develops acutely to subactuely, resolves slowly over weels
  • If hearing is involved, then called labyrinthitis.
25
Q

HINTs exam in peripheral vs central

A

Peripheral
- Head Impulse: positive
(inability to maintain central fixed gaze during head rotation followed by a corrective shift of the eyes back to target)

  • Nystagmus:
  • horizontal nystagmus with torsional component, unidirectional
  • Fast component beats AWAY from the lesion
  • Intensity increases with gaze toward the fast phase and decreases with gaze toward the slow phase (Alexander Law)
  • Direction of nystagmus DOES NOT CHANGE with gaze change
  • Gaze fixation IMPROVES nystagmus
  • Test of Skew: negative
    (eye remains in fixed central gaze on uncovering it)

Central
- Head Impulse: negative, central fixed gaze is maintained during head rotation
- Nystagmus: vertical nystagmus, torsional
Direction changing
Direction of nystagmus CHANGES with gaze changes
Gaze fixation DOES NOT REDUCE nystagmus
- Test of Skew: positive, re-fixation saccade occurs upon uncovering the eyes

26
Q

What can cause vertigo and hearing loss

A

AVS + hearing loss - labyrinthitis

Can be stroke of AICA branch leading to infarction of labyrinth

27
Q

Treatment of vestibular neuritis

A
  • 1 week of Pred
  • Symptomatic treatment
  • If concerns for VZV then treat with anti-virals
  • Vestibular rehab after acute period
28
Q

Features of spontaneous episodic vestibular syndrome

A
  • Episodic dizziness that occurs spontaneously
  • No triggers
  • Lasts minutes to hours (can be seconds to days)
  • Symptoms cannot be triggered by manoeuvres or examination

Causes

  • Vestibular migraine
  • Recurrent posterior circulation TIA
  • Meniere’s disease
  • Panic attacks
  • Medical causes: Vasovagal syncope, cardiac arrythmias, unstable angina, PE, hypoglycaemia
29
Q

Features of vestibular migraines

A
  • At least 5 episodes with vestibular symptoms of moderate or severe intensity, lasting 5 minutes to 72 hours.
POUND 
- Headache that is PULSATILE 
- ONE day duration (with episode lasting 4-72 hours if untreated)
- UNILATERAL
- Associated with N=V
- Disabling 
>3 criteria = migraine
30
Q

Features of meniere’s disease

A

Triad of:

  • recurrent attacks of spontaneous vertigo
  • Reversible hearing loss and tinnitus
  • Fluctuating aural fullness and headaches during attacks
  • Can last minutes to hours
  • Need to demonstrate documented low to medium sensorineural hearing loss before, during or after episode of vertigo, with subsequent resolution.

Tx:

  • Acute: sympotmatic tx
  • Dietary salt restriction, diuretics, dexamethasone, intratympanic steroids (no strong evidence)
  • Intratympanic gentamicin as an ablative therapy
  • Vestibular rehab
31
Q

Features of triggered episodic vestibular syndrome

A
  • Episodic dizziness brought on by a specific trigger
  • Typically a change in head position/body posture
  • Usually lasts < 1 minute
  • Dizziness should be recreated

Causes

  • Benign paroxysmal positional vertigo (BPPV)
  • Orthostatic hypotension
  • Central paroxysmal positional vertigo
  • Superior canal dehiscence
32
Q

Features of BPPV

A
  • Dislodged otoconia from utricle float into semi-circular canal
  • Positional changes lead to gravitational drift down of otoconia stimulating fluid disruption in semicircular canal and increasing firing from hair cells from ampulla
  • 75-85% cases are posterior > horizontal ? anterior
  • Triggered by turning over in bed
  • The primary symptom of BPPV is episodic vertigo that lasts < 1 minute, triggered by sudden changes in head posture in relation to gravity (e.g., bending forwards, rapidly standing up)

Diagnosis:
- Dix hall pike for posterior canal BPPV
Posterior canal: upbeat nystagmus with torsion
Anterior canal: downbeat nystagmus with torsion
- Head roll test for horizontal canal BPPV

Tx
Epley’s Manoeuvre

33
Q

Central paroxysmal positional vertigo (CPPV)

A
  • Central cause that mimics BPPV
  • Rare
  • Causes: posterior fossa tumour, stroke, demyelination
  • Distinguished from BPPV based on nystagmus characteristics on hallpike
34
Q

Nystagmus on dix hallpike for BPPV and CPPV

A

Posterior Canal BPPV

  • Latency of 1-5 seconds
  • Lasts < 30s
  • Fatigability
  • Habituation
  • Mixed upbeat - torsional
  • Crescendo Decrescendo
Red Flags (Likely CPPV)
- No latency 
- No fatigability 
No habituation 
- Typically downbeat, can be horizontal, no torsional component
35
Q

Features of SAH

Causes

A
  • Thunderclap headache that reaches maximum intensity within 1 minute
  • Occur due to rupture of saccular aneurysms, highest risk if >5mm and located in posterior circulation
  • Can develop warning sentinel leaks - transient headaches in the days/weeks before aneurysmal rupture
  • LP: elevated opening pressure, high protein, xanthochromia (yellowing of CSF due to breakdown of heme into bilirubin) - 100% sensitive for SAH between 12 hours and 8 days but may take 4 hours or mre to develop.

Gold Standard: cerebral angiography
Treating the lesion significantly reduces the chance of rebleed

Causes
- 85% are aneurysms
Coiling has lower death
- Other causes include amyloid angiopathy, reversible cerebral vasoconstriction syndrome
- Structural vascular lesions that can also be treated including AVMs or dural AV fistulas

36
Q

Treatment of carotid and vertebral artery dissections and prevention of stroke

A

No evidence supports the superiority of anticoagulation
over antiplatelet therapy in prevention of stroke after
carotid and vertebral artery dissections, and most
patients are initially managed with aspirin

37
Q

Subdural haemorrhage

A
  • Head Trauma →rupture of bridging veins → accumulation of blood between dura and arachnoid membranes
  • Crescent shaped, concave hyperdensity acutely
  • Subdural hematomas can occur in the absence of significant trauma, particularly among older persons and those taking anticoagulant drugs; observation or surgical evacuation is appropriate treatment, depending on the specific presentation.
  • FLUCTUATING CONSCIOUSNESS
38
Q

Epidural haemorrhage

A
  • Head Trauma → lateral skull fracture →tear of middle meningeal artery →accumulation of blood between skull and dura mater
  • Immediate loss of consciousness followed by a LUCID INTERVAL (minutes to hours)
  • CT Findings: Lens-shaped, biconvex hyperdensity
  • The prognosis of epidural hematomas is often excellent after emergent surgical evacuation because the underlying brain tissue is frequently uninjured; without immediate evacuation, however, death can occur within a matter of hours.
39
Q

Cavernous sinus thrombosis

A

Cavernous sinus thrombosis

  • other causes of cavernous sinus syndrome: local infection (e.g. sinusitis), neoplasia, trauma
  • periorbital oedema
  • ophthalmoplegia: 6th nerve damage typically occurs before 3rd & 4th
  • trigeminal nerve involvement may lead to hyperaesthesia of upper face and eye pain
  • central retinal vein thrombosis
40
Q

Treatment for Meniere’s Disease

A
  • acute attacks: buccal or intramuscular prochlorperazine (dopamine antagonist).
  • prevention: betahistine (histamine analogue) and vestibular rehabilitation exercises may be of benefit
  • intratympanic gentamicin as an ablative therapy

Neurology (11 decks)

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