Chronic Paroxysmal Hemicrania (Sjaastad syndrome)

Chronic Paroxysmal Hemicrania (Sjaastad syndrome)

    * Introduction
    * Signs and symptoms
    * Diagnosis
    * Treatment
Chronic Paroxysmal Hemicrania Sjaastad syndrome is known as a localized headache which normally consists of multiple episodes of severe headache, short. These attacks usually affect only one half of the skull. It is more common in women than in men. Due mostly female, chronic paroxysmal headache was considered a disease of women. Though the disease has been reported growth in men.
Short duration headache syndromes can be divided into activation headaches with autonomous autonomous headache without activation. Contains autonomous activation headaches with chronic and episodic hemicrania, headache and headache nevralgiforma unilateral injection of short duration with the conjunctiva and tearing.
Pain is usually severe oculotemporala area, forehead and behind the ear. Frequency is 10-20 attacks a day and can vary from 2-40 per day. Usually takes 2-25 minutes.
The pain is severe and the attacks are associated with independent features such as tears, conjunctival injection, unilateral nasal congestion, rhinorrhea, and eyelid edema. Tears can occur bilaterally but it is always marked by the symptom.
The disease can be treated with NSAIDs, especially indomethacin, which is totally effective in eliminating symptoms.
Pathogenesis and causes: The mechanism responsible for the pain of this disease remains unknown. Issue of trigeminal and parasympathetic neuropeptides during migraine has been described. Ipilateral trigeminovascular system activation may explain the sudden unilateral headache and may lead to miosis, increased intraocular pressure and other autonomous abnormalities. Increased sweating and decreased salivatiei during attacks and increased intraocular pressure by inhibiting alpha-blocking agents or stellate ganglion blockade suggest sympathetic involvement. Lacrimarii growth, nasal secretion and miosis may be due to parasympathetic stimulation.
Trigeminosimpatica activation during attacks of chronic paroxysmal headache has been suggested, vasoactive intestinal peptide increase was reported. Calcitonin level also increases. Pain and cranial pressure, nociceptive flexion reflex, blinking and corneal reflexes were studied in particular for this disease. Bilateral corneal reflex is low during attacks. Increasing the temperature of the cornea has been reported also nice due to increased corneal blood flow.
The efficacy of indomethacin in chronic paroxysmal headache is due in part to reduce intracranial blood flow and its anti-inflammatory effects. These facts indicate a central control mechanism and a secondary involvement of peripheral factors, affecting both the parasympathetic and sympathetic systems. Recent studies suggest the crucial role of the hypothalamus. Functional neuroimaging studies have shown activation of the hypothalamus in trigeminal cefalalgiilor autonomous case.