HEADACHES Flashcards
MIGRAINE
Headaches during migraine is caused by sterile neurogenic inflammation of meninges.
intracranial sensitivity is made only by meningeal blood vessels and dura mater, innervated by ophthalmic division of trigeminal nerve).
MIGRAINE 2
The trigeminal nerve afferent cause the release of vasoactive substances that induce vasodilation and degranulation of mast cells. From the trigeminal fibers, the pain is transmitted to adjacent tissues, especially superior segments of spinal cord and to pars caudata of trigeminal nerve (trigeminocervical complex).
From this complex, second neurons transmit the impulse towards encephalic structures involved in perception and modulation of pain (thalamic nuclei, periacqueductal grey matter) + collateral branches that transmit to autonomic nuclei of brain stem and hypothalamus (disautonomic symptoms associated to headaches)
MIGRAINE POSSIBLE CAUSE
A possible cause for migraine is a transitory dysfunction of brain stem nuclei involved in central control of nociception. This in turn could cause the activation of trigeminocervical system
MIGRAINE AURA
Migraine aura is an electric phenomenon of the cortex –> a wave of depolarization involves progressively the cerebral cortex starting from the occipital one. Depending on the affected site we can have visual, sensor or motor area phenomenon.
o Depolarization causes at the beginning a peak of activity followed by a transitory depression.
o Alteration of cerebral blood flow of the affected region accompanies this effect (focal hyperemia at the beginning followed by phase of hypoperfusion)
o These phenomena could be responsible for activation of trigemino-vascular system causing the migraine crisis
MIGRAINE WITHOUT AURA
– High diffuse (more frequent in women), it usually affects younger women, with onset before 30 yo.
- Symptomatology triad pain, neurovegetative symptoms and hypersensitivity to sensorial symptoms
- One half of cases presents with recurrent attacks, very severe, with pulsing unilateral headache that can have a variable duration (from 4 to 72 hours). It can be accompanied by photophobia, phonophobia, nausea, vomit
- The other half present as a bilateral or variable headache, pulsing can be absent.
MIGRAINE WITH AURA
- Symptoms develop gradually within 5-20 minutes up to 60 minutes. They are completely reversible.
- 20% of migraine attacks with an irregular frequency (very long remission period, more irregular than migraine without aura). Still, most of the time the two forms coexist in the same patient
- Aura is usually constituted by visual symptoms such as “shining scotoma”
- Aura is usually constituted by visual symptoms such as “shining scotoma”
Some particular types of aura are:
- Troncoencephalic symptoms originate from brains stem so they are accompanied by at least two other symptoms such as dysarthria, vertigo, diplopia, ataxia, reduced level of consciousness
- Hemiplegic it has visual or sensor or dysfasic symptom and a motor deficit reversible within 72 hours (motor symptoms are completely absent in typical aura)
CHRONIC MIGRAINE
15 days of continuous headache every month (at least 8 of migraine) for 3 consecutive months
COMPLICATIONS OF MIGRAINE
- Completely disabling migraine attack that lasts for more than 72 hours
- Persistent aura
- Migraine infarct (ischemic stroke that presents itself as a migraine attack)
- Epilepsy induced by migraine (epilepsy during aura or within one hour after the aura)
THERAPY
Use of symptomatic drugs that are taken during the attack + prophylactic therapy that the patient has to take every day for a period of time not shorter than 3 months.
- Symptomatic treatment: Analgesic, NSAIDs and specific therapy for migraine (such as triptans)
- Simple analgesic and NSAIDs act by inhibiting prostaglandin synthesis and they reduce the pain and inflammation. They are aspecific for migraine.
*Aspirin
*Naproxen
*Ibuprofen
*Paracetamol
side effects : diarrhea and epigastric pain
Triptans –> specific for migraine, agonist for serotonin receptor.
*Act peripherally and centrally by vasoconstricting the brain and inhibit the sterile inflammation.
Antiemetics
Ergot-derived drugs( ergotamine and dihydroergotamine)
-agonist for alpha adrenergic, serotoninergic and dopaminergic receptors leading to diffuse vasoconstricton
PREVENTIVE THERAPY
They are used when there is an elevated severity and frequency of migraine crisis every month (3 crisis that causes disability for 3 or more days). or when symptomatic therapy is not enough.
It must be taken every day, for at least 3 months and it is defined efficient when it reduces the numbers of monthly crisis of at least 50%.
It is usually organized in cycles that are interrupted by a period of suspension and followed by another period of therapy
PREVENTIVE THERAPY DRUGS
- Antiepileptic valproate and topiramate. They stabilize cortical excitability by GABAergic action on glutamatergic transmission.
- Beta-blockers propranolol, atenolol and metoprolol. They cross the blood-brain barrier and they inhibit beta-adrenergic receptors with consequent release of epinephrine
- Ca-antagonist flunarazine, they modulate vascular tone and inhibit dopaminergic and serotoninergic tone.
- Antidepressive amitriptyline, it blocks the reabsorption of noradrenaline and serotonin increasing they availability, it reduce the density of beta-adrenergic receptors and increase GABAergic receptors.
TENSION-TYPE HEADACHE
- Peripheral factors are involved in episodic headaches.
Some important peripheral factors are the increased sensitivity of pericranial myofascial structures associated to bad posture and ora-mandibular disorders. An increase in the nociceptive input that originate in muscles may be responsible for the headache and can be influenced by emotional factors that temporarily reduce the central control of pain (through the limbic system) - Central factors are responsible for the chronic progression of the pathology.
Chronic development is the result of sensitization of nociceptive neurons (centrally) and gradual inactivation of central control system of pain.
TENSION-TYPE HEADACHE
It is the most common form of primary headache with an incidence of 30-78%
It is subdivided in chronic (more than 15 days every month) and episodic (subdivided in sporadic when less than 1 day/monthly or frequent with 1 to 15 days/monthly). Frequent episodic tension-type headache usually transform into chronic disease.
