Headache and Vertigo Flashcards
Pathophysiology of migraine
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
What is a significant risk factor for migraine WITHOUT aura
Menstruation
Migraine WITHOUT aura improves post menopause
What increases the risk of stroke in a patient with migraine and on OCP
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.
Treatment of migraines in pregnancy
Medications for migraine can be teratogenic
Avoid triptans and ergots - teratogenic
Non pharmacological medications
Acute migraine Mx
- 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
Analgesic overuse headache
Secondary to overuse of analgesica
- triptans and opioids (codeine) > 10 days/month
- simple anlgesics >15 days/month
Migraine prophylaxis
- 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
Features of trigeminal autonomic cephalgias
- 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
Cluster headache
- 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.
Paroxysmal Hemicrania
- Similar to cluster headache but FEMALE
- Occurs 5-10 times/day lasting for 2-20 minues
- Fewer nocturnal events and chronic
- Respond to INDOMETHACIN
Hemicrania continua
- Constant, unilateral, side locked headache
- Indomethacin
SUNCT/SUNA
- 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
Trigeminal Neuralgia
- 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
Features of secondary headaches
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
Features of idiopathic intracranial hypertension
- 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
Secondary causes of IIH
- Venous sinus thrombosis
- Tetracyclines, eg: doxycycline
- Fluroquinolones, eg: ciprofloxacin
- Vitamin A
- Iron deficiency anaemia
- OSA
- Raised CSF protein
Diagnostic criteria of IIH
- PAPILLOEDEMA
- Normal neurological exam except for cranial nerve abnormalities
- Normal MRI
- Normal CSF composition
- Elevated CSF opening pressure > 25
Tx for IIH
- 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
Intracranial hypotension
- 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
Temporal arteritis
- 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
What is the function of the utricle, saccule and semicircular canal
- 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
How can vertigo be split?
- Acute Vestibular Syndrome
- Vestibular neuritis
- Stroke
- Central lesions - Episodic Vestibular Syndrome
(a) Spontaneous -
- Vestibular migraine
- Recurrent posterior circulation TIA
- Meniere’s disease
(b) Triggered
- BPPPV
- CPPV
- Orthostatic hypotension
Features of acute vestibular syndrome
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
Features of vestibular neuritis
- 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.
HINTs exam in peripheral vs central
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
What can cause vertigo and hearing loss
AVS + hearing loss - labyrinthitis
Can be stroke of AICA branch leading to infarction of labyrinth
Treatment of vestibular neuritis
- 1 week of Pred
- Symptomatic treatment
- If concerns for VZV then treat with anti-virals
- Vestibular rehab after acute period
Features of spontaneous episodic vestibular syndrome
- 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
Features of vestibular migraines
- 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
Features of meniere’s disease
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
Features of triggered episodic vestibular syndrome
- 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
Features of BPPV
- 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
Central paroxysmal positional vertigo (CPPV)
- Central cause that mimics BPPV
- Rare
- Causes: posterior fossa tumour, stroke, demyelination
- Distinguished from BPPV based on nystagmus characteristics on hallpike
Nystagmus on dix hallpike for BPPV and CPPV
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
Features of SAH
Causes
- 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
Treatment of carotid and vertebral artery dissections and prevention of stroke
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
Subdural haemorrhage
- 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
Epidural haemorrhage
- 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.
Cavernous sinus thrombosis
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
Treatment for Meniere’s Disease
- 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
