Explicar la fisiopatologia de la migraña, conocerá la clasificación internacional de cefalea.
Entenderá los mecanismos básicos que ocasionan los distintos dolores de cabeza así como dolor facial.
Describir la anatomía de irrigación cerebral y las áreas del sistema nervioso que son irrigadas por cada vaso sanguíneo.
ESTRUCTURAS SENSIBLES AL DOLOR
- piel, tejido subcutáneo, músculos, arterias extracraneales y periostio craneal.
- elementos delicados del ojo. oído, cavidades nasales y senos paranasales.
- senos venosos intracraneales y sus grandes vasos tributarios, en especial las estructuras pericraneales.
- partes de la duramadre en la base del cráneo y arterias dentro de duramadre y piaracnoides, en particular porciones proximales de las arterias cerebral anterior y media y segmento intracraneal de la arteria carotida interna.
- arterias meníngea media y temporal superficial
- nervios óptico, oculootor, trigémino, glosofaríngeo, vago y primeros nervios cervicales.
What are the five phases of a complete migraine attack?
ResponderEliminar1. Prodrome . Premonitory symptoms lasting hours to days may precede 40% to 60% of migraine attacks. The symptoms may include sleepiness, irritability, fatigue, mood changes, yawning, and cravings for sweet or salty foods.
2. Aura . The aura occurs within 1 hour of the headache and is most commonly visual or sensory.
3. Headache . The headache itself is commonly unilateral and may be pulsatile.
4. Headache termination
5. Postdrome . After termination of the headache, the complete migraine attack ends with the postdrome or hangover phase.
A mí me gustó mucho la siguiente explicación de la fisiopatología (solo hay una figura muy buena que esta plataforma no me deja poner, pero si gustan chéquenlo en la liga de abajo):
ResponderEliminarPATHOGENESIS
Intracranial vasoconstriction and extracranial vasodilation were long held to be the respective causes of the aura and headache phases of migraine. This theory received support from the efficacy of vasoconstrictive ergot alkaloids (eg, ergotamine) in aborting the acute migraine attack and of vasodilators such as amyl nitrite in abolishing the migraine aura. Recent studies show a more complicated picture and suggest that a primary disturbance of central neuronal activity may be responsible for both the aura and headache phases.
In many patients, migraine attacks are heralded by prodromal fatigue or cognitive, affective, or gastrointestinal symptoms, which can last for up to 1 day. The basis for this premonitory phase is poorly understood, but it may reflect altered hypothalamic or brainstem functions.
At the onset of the aura phase, a decrease in cerebral blood flow is observed in the occipital cortex and spreads anteriorly across the cortex according to cytoarchitectural rather than vascular boundaries. In this respect, and in its rate of propagation (2-5 mm/min), it resembles the phenomenon of spreading depression, in which a slow wave of neuronal and glial depolarization decreases blood flow and inhibits neuronal activity in its wake. However, the areas of decreased blood flow do not correspond to the cortical regions responsible for a particular aura, the extent of decrease is insufficient to cause ischemic symptoms, and blood flow may remain depressed after aura symptoms have resolved and headache has begun. In addition, inhibiting spreading depression can prevent the migraine aura (but not the subsequent headache). These findings suggest that changes in neuronal activity, rather than ischemia, produce the aura. However, what initiates spreading depression and its relationship, if any, to the premonitory phase are poorly understood.
FIGURE 6-9.
Central and peripheral nervous system sites proposed to be involved in migraine pathogenesis. During the aura phase, a reduction in cortical blood flow spreads anteriorly from the occipital cortex (large arrow), which is thought to be due to spreading depression. During the headache phase, sterile inflammation in the meninges may activate trigeminal (V) nerve sensory fibers that project to the nucleus caudalis, periaqueductal gray, sensory thalamic nuclei, and primary somatosensory cortex (small arrows). Alternatively, this central sensory pathway may convey normal afferent signals that are interpreted as noxious.
Two principal mechanisms have been proposed to explain the headache phase. According to one theory, pain is triggered peripherally in primary sensory trigeminal neurons innervating the meninges and blood vessels, perhaps as a result of sterile inflammation. These neurons project to the nucleus caudalis in the brainstem, and from there to the periaqueductal gray, sensory thalamic nuclei, and somatosensory cortex. Another theory holds that there is a primary disturbance of central pain pathways, so that normally innocuous sensory input is misinterpreted as signaling pain, a phenomenon called allodynia.
Fuente:
Aminoff M.J., Greenberg D.A., Simon R.P. (2015). Headache & Facial Pain. In Aminoff M.J., Greenberg D.A., Simon R.P. (Eds), Clinical Neurology, 9e. Retrieved February 02, 2016 from http://0-accessmedicine.mhmedical.com.millenium.itesm.mx/content.aspx?bookid=1194&Sectionid=78427211.