Problem 15 Flashcards
Who is most likely to suffer from migraines
women
What does migraine look like
episodic headache with sensitivity to light, sound and movement
accompanied by nausea and vomiting
What is migraine
recurring syndrome of headache with other neurologic symptoms that has triggers
Some examples of sensory and environmental stimuli
The brain of the migraineur is particularly sensitive to environmental and sensory stimuli; migraine-prone patients do not habituate easily to sensory stimuli. This sensitivity is amplified in females during the menstrual cycle. Headache can be initiated or amplified by various triggers, including glare, bright lights, sounds, or other afferent stimulation; hunger; let-down from stress; physical exertion; stormy weather or barometric pressure changes; hormonal fluctuations during menses; lack of or excess sleep; and alcohol or other chemical stimulation, such as with nitrates. Knowledge of a patient’s susceptibility to specific triggers can be useful in management strategies involving lifestyle adjustments.
What is the pathogenesis of migraines
le facteur déclenchant est encore inconnu. La phase céphalalgique est causée par deux phénomènes :
1) Phénomène inflammatoire vasculaire + vasodilatation (dans le territoire de la carotide externe) : Médié par la libération de sérotonine (noyau du raphé) et de NA (locus coeruleus)
- NB : sérotonine : par action sur 5-HT2 -> inflammation et agrégation plaquettaire (+ vasocontriction). 5-HT1 -> vasocontriction. On utilise donc des agonistes 5-HT1 et des antagonistes 5-HT2 pour le TTT de la migraine !
2) Phénomène inflammatoire à médiation neurogène : Par le noyau du V -> libération de NT vasoactifs
- dopamine receptor hypersensitivity
- predisposition genetique pour familial hemiplegic migraine (ion channels, disturbing membrane excitability)
Brainstem pathways that modulate sensory input
The key pathway for pain in migraine is the trigeminovascular input from the meningeal vessels, which passes through the trigeminal ganglion and synapses on second-order neurons in the trigeminocervical complex (TCC). These neurons in turn project in the quintothalamic tract and, after decussating in the brainstem, synapse on neurons in the thalamus. Important modulation of the trigeminovascular nociceptive input comes from the dorsal raphe nucleus, locus coeruleus, and nucleus raphe magnus.
What is the migraine aura
migraine aura, consisting of visual disturbances with flashing lights or zigzag lines moving across the visual field or of other neurologic symptoms
What is acephalic migraine
recurrent neurologic symptoms, often with nausea or vomiting, but with little or no headache. Vertigo can be prominent
basilar migraine = migraine with brainstem aura
What is tension-type headache
chronic head-pain syndrome characterized by bilateral tight, band-like discomfort can be episodic or chronic slowly increases in intensity more or less for many days NO accompanying features
Pathophysiology of tension-type headache
It seems likely that TTH is due to a primary disorder of central nervous system pain modulation alone, unlike migraine, which involves a more generalized disturbance of sensory modulation
What are the trigeminal autonomic cephalalgias (TACs)
describe a grouping of primary headaches including cluster headache, paroxysmal hemicrania, SUNCT (short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing)/SUNA (short-lasting unilateral neuralgiform headache attacks with cranial autonomic symptoms), and hemicrania continua
Characteristics of TACs
TACs are characterized by relatively short-lasting attacks of head pain associated with cranial autonomic symptoms, such as lacrimation, conjunctival injection, or nasal congestion. Pain is usually severe and may occur more than once a day. Because of the associated nasal congestion or rhinorrhea, patients are often misdiagnosed with “sinus headache” and treated with decongestants, which are ineffective.
TACs must be differentiated from short-lasting headaches that do not have prominent cranial autonomic syndromes, notably trigeminal neuralgia, primary stabbing headache, and hypnic headache. The cycling pattern and length, frequency, and timing of attacks are useful in classifying patients. Patients with TACs should undergo pituitary imaging and pituitary function tests because there is an excess of TAC presentations in patients with pituitary tumor–related headache.
What is cluster headache
Cluster headache is a relatively rare form of primary headache with a population frequency of approximately 0.1%. The pain is deep, usually retroorbital, often excruciating in intensity, nonfluctuating, and explosive in quality. A core feature of cluster headache is periodicity. At least one of the daily attacks of pain recurs at about the same hour each day for the duration of a cluster bout. The typical cluster headache patient has daily bouts of one to two attacks of relatively short-duration unilateral pain for 8 to 10 weeks a year; this is usually followed by a pain-free interval that averages a little less than 1 year. Cluster headache is characterized as chronic when there is less than 1 month of sustained remission without treatment. Patients are generally perfectly well between episodes. Onset is nocturnal in about 50% of patients, and men are affected three times more often than women. Patients with cluster headache tend to move about during attacks, pacing, rocking, or rubbing their head for relief; some may even become aggressive during attacks. This is in sharp contrast to patients with migraine, who prefer to remain motionless during attacks.
Cluster headache is associated with ipsilateral symptoms of cranial parasympathetic autonomic activation: conjunctival injection or lacrimation, rhinorrhea or nasal congestion, or cranial sympathetic dysfunction such as ptosis. The sympathetic deficit is peripheral and likely to be due to parasympathetic activation with injury to ascending sympathetic fibers surrounding a dilated carotid artery as it passes into the cranial cavity. When present, photophobia and phonophobia are far more likely to be unilateral and on the same side of the pain, rather than bilateral, as is seen in migraine. This phenomenon of unilateral photophobia/phonophobia is characteristic of TACs. Cluster headache is likely to be a disorder involving central pacemaker neurons in the posterior hypothalamic region
ttt of cluster headaches
oxygen inhalation
pour prevention: prednisone et lithium
neurostimulation therapy
Characteristics of paroxysmal hemicrania
The essential features of PH are unilateral, very severe pain; short-lasting attacks (2–45 min); very frequent attacks (usually more than five a day); marked autonomic features ipsilateral to the pain; rapid course (<72 h); and excellent response to indomethacin. In contrast to cluster headache, which predominantly affects males, the male-to-female ratio in PH is close to 1:1.
What is SUNCT/SUNA
SUNCT (short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing) is a rare primary headache syndrome characterized by severe, unilateral orbital or temporal pain that is stabbing or throbbing in quality. Diagnosis requires at least 20 attacks, lasting for 5–240 s; ipsilateral conjunctival injection and lacrimation should be present. In some patients, conjunctival injection or lacrimation is missing, and the diagnosis of SUNA (short-lasting unilateral neuralgiform headache attacks with cranial autonomic symptoms) can be made.
Diagnosis of SUNCT/SUNA
The pain of SUNCT/SUNA is unilateral and may be located anywhere in the head. Three basic patterns can be seen: single stabs, which are usually short-lived; groups of stabs; or a longer attack comprising many stabs between which the pain does not completely resolve, thus giving a “saw-tooth” phenomenon with attacks lasting many minutes. Each pattern may be seen in the context of an underlying continuous head pain. Characteristics that lead to a suspected diagnosis of SUNCT are the cutaneous (or other) triggers of attacks, a lack of refractory period to triggering between attacks, and the lack of a response to indomethacin. Apart from trigeminal sensory disturbance, the neurologic examination is normal in primary SUNCT.
The diagnosis of SUNCT/SUNA is often confused with trigeminal neuralgia (TN) particularly in first-division TN. Minimal or no cranial autonomic symptoms and a clear refractory period to triggering indicate a diagnosis of TN.
What to do if patient comes with a headache
Approche clinique ciblee en 10 questions red flags ? soulager le patient if red flags -> urgence ou ambulatoire if no red flags -> primary headache (cluster, tension-type, migraine, nevralgie)
Quelles sont les 10 questions a poser dans l’approche ciblee
- 1er épisode ou bien déjà connu ?
- Depuis quand?
- Dans quelles circonstances ?
- Où? (début, point max.)
- Intensité ? (EVA 0-10)
- Qualité ?
- Evolution (time-to-peak, fluctuant) ?
- Phénomènes associés ?
- Soulagée ou aggravée par ?
- Effet des antalgiques ?
Red flags pour l’anamnese
- Céphalées inhabituelles (localisation, durée, évolution, qualité, intensité, mode d’apparition) ou réfractaires au traitement habituel
- Aggravation progressive au cours des derniers jours/semaines
- Céphalées évocatrices de migraine mais toujours latéralisées du même côté
- Céphalées en « coup de tonnerre », « explosives », les pires jamais expérimentées
- Céphalées brutales déclenchées par : Valsalva, effort, changement de position
- Vomissements (sauf si migraine)
- Symptômes neurologiques, crise d’épilepsie
- Céphalées posturales
- Douleurs des ceintures, claudication de la mâchoire, myalgie et/ou sensibilité temporale
- Traumatisme récent, manipulation de la nuque
- Âge >50 ans
- Perte de poids, fatigue, sudations nocturnes
- Situations à risque : immunosuppression, cancer, grossesse, post-partum, anticoagulation
Quelles sont les cephalees primaires
Quatre diagnostics représentent 90% des céphalées primaires: céphalées de tension (prévalence à 1 an :
65%), migraine (environ 15% des céphalées primaires), céphalées en grappe (prévalence à 1 an <1%),
céphalées quotidiennes chroniques.
Cephalees de tension
se classent en types « peu fréquent », « fréquent » et « chronique ». Classiquement, les douleurs peuvent impliquer les muscles frontaux, péricrâniens,
occipitaux et s’accompagnent de tension des muscles para-cervicaux et des trapèzes. Les facteurs
déclenchants sont multiples : stress physique/psychique, conditions météorologiques
Cephalees de tension
se classent en types « peu fréquent », « fréquent » et « chronique ». Classiquement, les douleurs peuvent impliquer les muscles frontaux, péricrâniens,
occipitaux et s’accompagnent de tension des muscles para-cervicaux et des trapèzes. Les facteurs
déclenchants sont multiples : stress physique/psychique, conditions météorologiques…
Classification des cephalees de tension
A. Type « peu fréquent » : au moins 10 épisodes de céphalées survenant en moyenne <1 jour/mois (soit <12
jours/ an), remplissant les critères B à E.
Type « fréquent » : 1 à 14 épisodes par mois, remplissant les critères B à E
Type « chronique » : >15 épisodes par mois, remplissant les critères B à E
B. Durée des céphalées : 30 minutes - 7 jours
C. ≥2 caractéristiques suivantes :
1. Localisation bilatérale
2. Constrictives, pesantes, non pulsatiles
3. Intensité légère à modérée
4. Pas d’aggravation par l’activité physique simple (marcher, monter les escaliers,…)
D. Présence des 2 caractéristiques suivantes :
1. Pas de nausées, pas de vomissements (anorexie possible)
2. Pas de photo-/phonophobie (ou seulement 1 des 2)
E. Non attribuable à une autre affection
Une céphalée de tension épisodique peut être évoquée (avec moins de certitude) si <10 épisodes.
