New daily persistent headache (NDPH) is a subtype of chronic daily headache. The literature on NDPH is scant and its true aetiology is unknown. A retrospective chart review was carried out from a computerized database at the Jefferson Headache Centre from August 1997 to May 2000 to identify patients with NDPH using the Silberstein et al. criteria. Forty women and 16 men were identified. Age of onset ranged from 12 to 78 years. The peak age of onset was the second and third decade in women and the fifth decade in men. Eighty-two per cent of patients were able to pinpoint the exact day their headache started. Onset occurred in relation to an infection or flu-like illness in 30%. A prior headache history was found in 38% of patients. A family history of headache was documented in 29%. The duration of daily headache ranged from 1.5 h to 24 h; 79% were continuous. Nausea occurred in 68% of patients, photophobia in 66%, phonophobia in 61%, and lightheadedness in 55%. Laboratory testing and neuroimaging in all patients was normal except for Epstein-Barr virus antibody titres, which were positive in 71% of seven patients tested, representing past infection. NDPH appears to be a female-predominant disorder, marked by a continuous daily headache with associated migrainous symptoms. Over 80% of patients could state the exact date their headache began. One-third of patients developed NDPH with a flu-like illness.
Cluster headache is a stereotypic, primary headache disorder that is marked by repeated short-lasting attacks of severe, unilateral head pain and associated autonomic symptoms. Cluster headache is probably due to an abnormality in the circadian hypothalamic generator with subsequent trigeminovascular activation. We have reviewed the clinical manifestations, pathophysiology, gender differences, and treatment options in cluster headache.
The objective was to assess the efficacy of coenzyme Q10 as a preventive treatment for migraine headaches. Thirty-two patients (26 women, 6 men) with a history of episodic migraine with or without aura were treated with coenzyme Q10 at a dose of 150 mg per day. Thirty-one of 32 patients completed the study; 61.3% of patients had a greater than 50% reduction in number of days with migraine headache. The average number of days with migraine during the baseline period was 7.34 and this decreased to 2.95 after 3 months of therapy, which was a statistically significant response (P < 0.0001). Mean reduction in migraine frequency after 1 month of treatment was 13.1% and this increased to 55.3% by the end of 3 months. Mean migraine attack frequency was 4.85 during the baseline period and this decreased to 2.81 attacks by the end of the study period, which was a statistically significant response (P < 0.001). There were no side-effects noted with coenzyme Q10. From this open label investigation coenzyme Q10 appears to be a good migraine preventive. Placebo-controlled trials are now necessary to determine the true efficacy of coenzyme Q10 in migraine prevention.
The objective of this study was to suggest that joint hypermobility (specifically of the cervical spine) is a predisposing factor for the development of new daily persistent headache (NDPH). Twelve individuals (10 female, 2 male) with primary NDPH were evaluated by one of two physical therapists. Each patient was tested for active cervical range of motion and for the presence of excessive intersegmental vertebral motion in the cervical spine. All patients were screened utilizing the Beighton score, which determines degree of systemic hypermobility. Eleven of the 12 NDPH patients were found to have cervical spine joint hypermobility. Ten of the 12 NDPH patients had evidence of widespread joint hypermobility with the Beighton score. Based on our findings we suggest that joint hypermobility, specifically of the cervical spine, may be a predisposing factor for the development of NDPH.
Many people experience headaches that do not fulfil the International Headache Society's criteria for a specific headache disorder yet behave biologically like that disorder. Others fulfil criteria for one headache disorder and yet have features of another disorder. To explain these observations, we propose that groups of neurones called modules become activated to produce each symptom of a primary headache disorder, and that each module is linked to other modules that together produce an individual's headache. This theory has implications for the classification, research and treatment of primary and secondary headache patients.
Many people experience headaches that do not fulfil the International Headache Society's criteria for a specific headache disorder yet behave biologically like that disorder. Others fulfil criteria for one headache disorder and yet have features of another disorder. To explain these observations, we propose that groups of neurones called modules become activated to produce each symptom of a primary headache disorder, and that each module is linked to other modules that together produce an individual's headache. This theory has implications for the classification, research and treatment of primary and secondary headache patients.
Clusterheadache is characterized by multiple attacks of severe, strictly unilateral periorbital pain. Although in some patients the pain may switch sides between cluster cycles, rarely does the headache side alternate within a cycle. To date, bilateral cluster headache has only rarely been described in the literature (1 -3). Case reportA 41-year-old male had stereotypic headaches that lasted 30 to 45 min each and occurred in the afternoon or evening. In addition, another attack would awaken the patient from sleep between 2 and 3 a.m. and would last one and one-half hours. During the initial week of the headache cycle, the pain was always located in the right eye; after this the pain became bilateral, with both eyes equally affected. The pain was severe and squeezing in nature, with associated bilateral lacrimation and rhinorrhea, as well as blurred vision, photophobia, phonophobia, osmophobia, nausea, and a sore, stiff neck. During an attack, the patient would stand or sit and rock in a dark, quiet room. Sumatriptan tablets provided some relief; injections had not been tried. Alcohol was not a trigger. The patient had experienced two 2-month periods of identical headaches 5 years and 2 years prior to evaluation. These cluster periods were also characterized by initial right-sided headaches for 1 week and then bilateral headaches for the remainder of the cluster period.The patient was examined when he was not having an attack and his general and neurologic examinations were normal. A computed tomographic scan of the brain was normal. He was treated with a 7-day prednisone taper and started on 240 mg of slow-release Verapamil a day. He experienced three mild headaches and then a remission. One day after completing the steroid taper, he had a mild, bilateral, ocular headache with associated ptosis, conjunctival redness, and lacrimation. After 4 h he was seen in our office, where his bilateral pain and associated symptoms were aborted with oxygen.-..
Recent population-based studies have suggested that migraine is a risk factor for the development of infarct-like lesions in the territory of the posterior circulation. These lesions are thought to be true vascular infarcts based on their size, location and magnetic resonance imaging (MRI) characteristics. However, as there are no postmortem studies identifying the pathology of these MRI findings, their true aetiology is unknown. A case patient with migraine is presented, who developed what appeared to be cerebellar infarcts on MRI, but these lesions vanished on repeat imaging 16 days later, questioning their aetiology as vascular ischaemic based infarcts.
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