Headache Flashcards
What are the differences between the trigeminal autonomic cephalalgias? duration of attacks? associated features? preventitive treatment and abortive treatment?
SUNCT: 1 - 240 second attacks.
SUNA without conjunctival injection and or tearing - stabbing headache quality, opthalmic distribution o fpain. Abortive medications often unnecessary. Lamotrigine for preventative.
Paroxysmal hemicrania: 2-30 minutes: high daily attack frequency (>5 per day) absence of agitiation. Abortive medications often unnecessary as good response to indomethacin (use for prevention)
Cluster headache: 15-180 minutes: more prevalent in males: circadian or circannual recurrence, significant associated agitation, triggered by alcohol. Can try subcutaneous sumitriptan, intramuscular DHE, high flow O2 to abort
To prevent- verapamil, lithium, topiramate
Hemicrania continua - 30 mins to 3 days: baseline milder headache for > 3 months attacks with automonic features. Often unnecessary given good response to indomethacin to use abortive but use indomethacin at high doses for preventative treatment.
What is the theorised pathogenesis of migraine?
Activation of hypersensitive “central generator” . →
Disrupted ion homeostasis, release of neurochemicals, and transient neuronal dysfunction (cortical spreading depression). →
Meningeal blood vessel dilation and activation of trigeminovascular system. →
Release of vasoactive neuropeptides (calcitonin gene-related peptide (CGRP), neurokinins, prostaglandins, substance P, etc.) from activated trigeminal sensory nerves leads to sterile neurogenic inflammation. →
Worsening vasodilation, increasing firing of trigeminal afferents and further release of vasoactive neuropeptides causing pain intensification (the vasodilation itself is no longer felt to be the source of pain). →
Trigeminal nociceptive afferents carry pain signals to trigeminal nucleus caudalis (TNC) for processing and ascent through thalamus to cortex. → Continuous ascending pain signals activate more neurons, leading to associated symptoms such as photophobia, phonophobia, nausea, and vomiting. →
8. Continuous TNC firing leads to central sensitization (allodynia) if activated pathways are not stopped (triptans have minimal to no effect at this stage; thus, the importance of early triptan administration).
What associated feature of headache IS considered part of a tension headache according to classification?
The diagnosis of episodic tension-type headache requires 10 headaches, each lasting between 30 minutes and 7 days.
Headache characteristics include bilateral location, pressing/tightening (nonpulsating) quality, mild or moderate pain intensity, and it SHOULD NOT be aggravated by routine physical activity. The diagnosis requires at least two of those four features. Neither nausea nor vomiting is present, and there can be only one of either photophobia or phonophobia (either or neither, not both). Secondary causes or other diagnoses must also be excluded. In essence, the criteria for tension-type headache are the complete opposite for that of migraine headache, and this point can be helpful in differentiating between them.
What is the MOA of triptans?
The triptans work as agonists at the serotonin receptor subtypes 5HT-1B and 5HT-1D. Agonism at 5-HT1B receptors constricts the pain-producing intracranial, extracerebral blood vessels in the meninges. Agonism at 5-HT1D receptors presynaptically inhibits trigeminal peptide release and interferes with central TNC nociceptive transduction and processing, whereas those of the nucleus tractus solitarius in the brainstem are thought to inhibit nausea/vomiting.
Patient can remember exact date a chronic headache started - what is it?
The diagnosis of NDPH requires a distinct and clearly remembered onset of a continuous and unremitting headache, and it must be present for more than 3 months. Secondary causes or other diagnoses must also be excluded. In general, the pain of NDPH lacks characteristic features and may be migraine-like or tension-type-like, or have overlapping features of both.
What is CADASIL? HOw do people present? Where is the mutation and what is it?
This patient’s history and family history are suggestive of CADASIL. This disorder presents with migraine with aura, stroke or stroke-like episodes, progressive dementia, and other neurodegenerative findings. This is an autosomal dominant disorder most often due to a missense mutation in the NOTCH3 gene, on chromosome 19q13.1, although splice site mutations and small in-frame deletions have also been reported. The NOTCH3 gene encodes a transmembrane protein thought to be involved in cell signaling during embryonic development. It can be diagnosed by genetic testing or skin biopsy. Magnetic resonance imaging of
the brain will show confluent deep white matter changes. These deep white matter changes characteristically extend to the anterior temporal lobes/poles.
What is the inheritance of Familial hemiplegic migraine?
There are three types of FHM that are all autosomal dominant with variable penetrance. FHM1 is linked to chromosome 19p13 (CACNA1A gene), resulting in a defect in P/Q calcium-channel subunit. Additional FHM1 symptoms may include cerebellar involvement, such as gaze-evoked nystagmus or ataxia, also attacks of coma, prolonged hemiplegia, or both, but full recovery is the rule. Transient cerebral oedema and cerebral atrophy are less commonly seen. FHM2 is linked to 1q23 (ATP1A2 gene), resulting in a defect in the A1A2 sodium–potassium ATPase channel. Additional FHM2 symptoms may include recurrent coma, frequent and long-lasting hemiplegia, or seizures with mental retardation. Cerebellar ataxia is not associated with FHM2. FHM3 is linked to chromosome 2q24 (SCN1A gene), resulting in defects of presynaptic and postsynaptic voltage-gated sodium channels.
Migraine prophylaxis: what has level A evidence, level B evidence and Level C evidence
Level A (strong) evidence: topiramate, divalproex sodium, sodium valproate, metoprolol, propranolol, timolol, and Petasites (butterbur).
Level B (moderate) evidence: amitriptyline, venlafaxine, atenolol, nadolol, feverfew, riboflavin.
level C (weak) evidence candesartan, lisinopril, carbamazepine, nebivolol, pindolol, clonidine, guanfacine, coenzyme Q10, and cyproheptadine.
level U (insufficient) evidence, verapamil, nicardipine, nifedipine, nimodipine, gabapentin, fluoxetine, fluvoxamine, protriptyline, bisoprolol, and acetazolamide.
What is the definition of chronic migraine?
The diagnosis of chronic migraine requires that the headache is present on 15 or more days per month for more than 3 months. It must occur in a patient who has had at least five attacks fulfilling criteria for either migraine without aura and/or migraine with aura. Also, on 8 or more days per month for more than 3 months, the patient must have migraine with or without aura and/or believed to have migraine at the onset, relieved by a triptan or ergot derivative. Secondary causes must have been excluded.
What is the difference between retinal migraine and migraine with aura?
It can often be difficult to differentiate between migraine with aura and retinal migraine, but if the visual disturbance is truly monocular, then retinal migraine is the diagnosis.
These visual phenomena should be confirmed during an attack by a visual field examination and/or the patient’s drawing of a truly monocular field defect. The attacks must also include at least two of the following features: A headache that occurs with the aura or follows the aura within 60 minutes. The aura spreads over 5 minutes or more. Each aura symptom lasts between 5 and 60 minutes. Secondary causes including other causes of amaurosis fugax must be excluded.
What are the classifications of primary headache disorders:
a. Migraine
i. Migraine without aura ii. Migraine with aura
iii. Childhood periodic syndromes that are commonly precursors to migraine iv. Retinal migraine
v. Complications of migraine vi. Probable migraine
b. Tension-type headache
i. Infrequent episodic tension-type headache
ii. Frequent episodic tension-type headache iii. Chronic tension-type headache
iv. Probable tension-type headache
c. Cluster headache and other trigeminal autonomic cephalgias
i. Cluster headache ii. Paroxysmal headache
iii. Short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT)
iv. Probable trigeminal autonomic cephalgia
d. Other primary headaches
i. Primary stabbing headaches ii. Primary cough headaches
iii. Primary exertional headaches
iv. Primary headache associated with sexual activity
v. Hypnic headache (with sleep) vi. Primary thunderclap headache
vii. Hemicrania continua viii. New daily persistent headaches
What are the diagnostic criteria for migraine without aura?
- At least five attacks fulfilling criteria 2 through 4
- Headache attacks lasting 4 to 72 hours
- Headache has at least two of the following characteristics:
a. Unilateral location
b. Pulsating quality
c. Moderate or severe pain intensity
d. Aggravation by or causing avoidance of routine physical activity - During headache, at least one of the following:
a. Nausea and/or vomiting
b. Photophobia and phonophobia - Not attributed to another disorder
Diagnostic criteria for tension type headache
- At least 10 episodes occurring on 1 or more but less than 15 days per month for at least 3 months and fulfilling criteria 2 through 4
- Headache lasting from 30 minutes to 7 days
- Headache has at least two of the following characteristics:
a. Bilateral location
b. Pressing/tightening (nonpulsating) quality
c. Mild or moderate intensity
d. Not aggravated by routine physical activity such as walking or climbing stairs - Both of the following:
a. No nausea or vomiting (anorexia may occur)
b. No more than one of photophobia or phonophobia - Not attributed to another disorder
Diagnostic criteria for Cluster headache? Acute management and preventative treatment?
E. ICHD-II diagnostic criteria for cluster headache
- At least five attacks fulfilling criteria 2 through 4
- Severe or very severe unilateral orbital, supraorbital, and/or temporal pain lasting 15 to 180 minutes if untreated
- Headache is accompanied by at least one of the following:
a. Ipsilateral conjunctival injection and/or lacrimation
b. Ipsilateral nasal congestion and/or rhinorrhea
c. Ipsilateral eyelid edema
d. Ipsilateral forehead and facial sweating
e. Ipsilateral miosis and/or ptosis
f. A sense of restlessness or agitation - Attacks have a frequency of one every other day to 8 per day.
- Not attributed to another disorder
Acute management: dihydroergotamine or oxygen
Prevention: verampamil, lithium, methysergide
Diagnostic criteria for SUNCT and SUNA
F. ICHD-II diagnostic criteria for SUNCT and short-lasting unilateral neuralgiform headache with cranial autonomic features (SUNA)
- SUNCT
a. At least 20 attacks fulfilling criteria b through d
b. Attacks of unilateral orbital, supraorbital, or temporal stabbing or pulsating pain lasting 5 to 240 seconds
c. Pain is accompanied by ipsilateral conjunctival injection and lacrimation.
d. Attacks occur with a frequency of 3 to 200 per day.
e. Not attributed to another disorder - SUNA
a. At least 20 attacks fulfilling criteria b through e
b. Attacks of unilateral orbital, supraorbital, or temporal stabbing pain lasting 5 seconds to 10 minutes
c. Pain is accompanied by one of the following: i. Conjunctival injection and/or tearing
ii. Nasal congestion and/or rhinorrhea iii. Eyelid edema
d. Attacks occur with a frequency of greater than or equal to one per day for more than half the time.
e. No refractory period follows attacks from trigger areas.
f. Not attributed to another disorder
