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Headache in young children is frequently a cause of concern to parents and physicians. We have reviewed our experience with 104 children with onset of headaches prior to 7 years of age seen by age 9 years. Headaches could be classified in more than 90% of cases. The most common headache type in this population referred to a child neurologist was migraine that constituted 75% of the cases. Seventy-two of 78 cases were common migraine. Posttraumatic headaches accounted for an additional 12%. Associated symptoms such as autonomic signs, nausea, and vomiting were common, particularly in the migraine group. Neuroimaging studies when performed did not reveal any significant abnormalities. Other laboratory tests were also generally unhelpful. No child has gone on to develop new neurologic abnormalities or evidence of an intracranial tumor. We conclude that even in young children headaches are generally benign. Even in this population, neuroimaging studies have a very low yield in the absence of other symptoms and findings and are not always indicated.
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PMID:Headaches in children younger than 7 years of age. 849 99

Criteria for the diagnosis of migraine have evolved from generalized descriptions to specific rules designed to ensure the selection of homogenous groups of patients for research studies. For clinical practice, the former are insufficiently specific and the latter are too complex. For care of headache patients by primary care physicians, we propose that the diagnosis of migraine without aura (common migraine) is warranted if any two of the following symptoms are present: unilateral site, throbbing quality, nausea, photophobia or phonophobia. These criteria are derived from a study comparing the features of 100 patients with migraine without aura and 100 patients with chronic daily headache. The proposed criteria for the diagnosis of migraine without aura were highly sensitive and adequately specific in discriminating groups. These simple criteria should facilitate the diagnosis of migraine by primary care physicians.
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PMID:Criteria for the diagnosis of migraine in clinical practice. 188 79

According to widely accepted theory, migraine is a self-limited neurogenic sterile inflammation characterized by initial cerebral vasoconstriction, subsequent extracranial and intracranial vasodilation, sterile inflammation, and secondary muscle contraction. It is characterized by recurrent attacks of headache, usually unilateral and accompanied by nausea, vomiting, and, often, other symptoms. Frequency, duration, and intensity of attacks are widely variable. Migraine affects more women than men, and is often related to menses. Patients with classic migraine experience visual or neurologic prodromes, but vague "premonitions" occur in both classic and common migraine. Precipitating factors include foods, alcohol, medications, visual stimuli, changes in routine, and stress. The first-line agent for abortive therapy is ergotamine; corticosteroids are indicated for prolonged headache. Propranolol is recommended for daily prophylactic therapy, and alternatives include calcium channel blockers, nonsteroidal anti-inflammatory agents, and tricyclic antidepressants.
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PMID:Strategies for migraine management. 189 57

Common migraine and cervicogenic headache have many traits in common, so many that they may be mixed up. Both are unilateral headaches with a female preponderance. However, as for a number of variables, they differ. This first and foremost has to do with factors concerning the neck. In cervicogenic headache, the following symptoms and signs are present: a reduced range of motion in the neck; mechanical precipitation of attack, either by neck movements or by external pressure over the greater occipital nerve of the C2 root; ipsilateral shoulder/arm pain; unilaterality without side-shift. Similar findings are usually not made in common migraine. Typical migraine symptoms, such as nausea, vomiting, photophobia, and phonophobia also occur in cervicogenic headache, but less frequently and to a lesser degree. Operative procedures directed to occipital/nuchal structures may afford decisive differentiation between the two disorders. In our estimation, cervicogenic headache and common migraine are two distinct disorders, with their own clinical patterns, pathogenesis, treatment - and, in all probability, also prognosis.
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PMID:Cervicogenic headache. The differentiation from common migraine. An overview. 191 61

The characteristics of common migraine are not unique, they also appear in other forms of benign headaches. As there are no laboratory tests and biological signs enabling the diagnosis of migraine and its differentiation from the headache due to muscle contractrion, clinical criteria which are simplified and easy to comprehend should be used. We compared the symptoms in 29 patients of both sexes, suffering from common migraine, as well as 29 patients with headache due to muscle contraction (chronic daily headaches). In common migraine the following symptoms appear in greater percentage (statistically significant): nausea, vomiting, unilateral localization of pain, pulsating pain, photophobia and phonophobia. Bad headache is more frequent in patients with common migraine than in those suffering from chronic headache. We should accept Solomon's and Cappa's attitude who suggest at least two of the following five criteria: 1. nausea with or without vomiting, 2. unilaterality, 3. pulsating pain, 4. photophobia or phonophobia, and 5. provocation by menstruation or positive family history. Besides the above mentioned criteria the authors also mention and emphasize the existence of free interval in migraine when the patient has no difficulties and feels well.
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PMID:[Common migraine--diagnostic criteria]. 226 10

In a double-blind cross-over study we compared tolfenamic acid with paracetamol in out-patients with common migraine (migraine without aura). Each patient was treated during (at least) 4 attacks with one of the following alternatives: tolfenamic acid 200 mg, tolfenamic acid 400 mg, paracetamol 500 mg or paracetamol 1000 mg in a randomized sequence. The same sequence of treatments was applied to (preferably) 4 more attacks. Dosage was repeated after 2 h if the attack had not abated. Escape medication was allowed after 4 h if the treatment was inefficient. A total of 83 patients were admitted to the study, but 3 dropped out, while 10 completed less than 4 attacks. Seventy completed 4 attacks, and 58 completed all 8. The total number of attacks treated was 545. We found a significant superiority of tolfenamic acid over paracetamol with regard to effect on pain after 2 h (p less than 0.01), patients' global evaluation (p less than 0.001), and use of escape medication (p less than 0.02). The trend was the same for duration of attacks, confinement to bed during attack and nausea, but the results were not statistically significant. There was no significant difference between the smaller and the larger dose of either drug nor between the need for escape medication, although the trend favoured tolfenamic acid. Side effects were few. Tolfenamic acid is evidently valuable in treatment of migraine.
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PMID:Randomized double-blind comparison of tolfenamic acid and paracetamol in migraine. 237 49

The effect of 30 min voluntary toothclenching was studied in 48 patients with common migraine, randomized in two groups. Group 1 performed low-level tension at 5% and group 2, high-level tension at 30% of the individual maximum, as judged by surface EMG from the temporal muscle. Pericranial muscle tenderness was evaluated by manual palpation and a four-point verbal scale. Headache, nausea, and soreness of the chewing muscles were scored on visual analogue scales. Although surface EMG, soreness, blood pressure, heart rate and difficulty in completing the toothclenching session all showed that group 2 patients were subjected to significantly higher levels of muscle tension than group 1 patients, headache developed equally often in both groups (63%). Headache was even more pronounced in group 1 (n.s.). Five patients in group 1 and none in group 2 developed an attack of migraine during the following 24 h. Pericranial muscle tenderness was unaffected by the experimental procedure. There was no significant correlation between headache intensity and pericranial muscle tenderness. Muscle ischemia, muscle "fatigue", and strain on muscle insertions are thus unlikely to cause attacks of common migraine.
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PMID:Experimental toothclenching in common migraine. 408 79

Aspirin 650 mg and metoclopramide 10 mg in an effervescent preparation (Migravess) were compared with effervescent aspirin 650 mg (Alka-Seltzer) and placebo for common migraine attacks with a double-blind cross-over design. One hundred and eighteen patients with common migraine were entered. Eighty-five patients completed all three forms of treatment, eleven completed two, and six completed one. Medicine was taken when patients were sure they had a migraine attack and not just interval headache. After each form of treatment, they mailed a report form to the investigators. Additional medication was allowed after 2 h and was taken for 79/95 placebo treated attacks, 63/92 Migravess treated attacks, and 51/86 aspirin treated attacks (p less than 0.01). Aspirin was significantly better than placebo for pain but not quite significant for nausea. Migravess was significantly better than placebo for pain and for nausea. There was no significant difference between aspirin and Migravess with regard to analgesic effectiveness (p = 0.33) or to antinausea effect (p = 0.18).
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PMID:Effervescent metoclopramide and aspirin (Migravess) versus effervescent aspirin or placebo for migraine attacks: a double-blind study. 637 73

In 7 patients given a standard treatment during spontaneous attacks of common migraine, activity in the temporal and sternocleidomastoid muscles was studied for 140 min. Pain and nausea ratings were taken with 20 min intervals. Baseline recordings were obtained from all patients during a period without headache and from 8 dental students without a history of migraine. During the attack of migraine, activity in the anterior temporal muscles significantly exceeded the patient's own baseline recordings and all muscles were activated more strongly than in the control sample. The increase in per cent of maximal muscle activity was insufficient to account for ischemic pain. Following treatment the activity of the temporal and sternocleidomastoid muscles decreased in 5 patients at the same time as the pain and nausea to the level of the controls. It is suggested that the moderate increase of activity on admission was a residual from stronger contractions earlier in the attack. In addition to cessation of the attack, placement in supine position and intake of diazepam may have contributed to the decline of muscle activity.
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PMID:Electromyography of pericranial muscles during treatment of spontaneous common migraine attacks. 717 78

A worsening of migraine headaches has been associated with estrogens, given for birth control and menopausal syndrome. It is suggested in this case history report that the same may be true in the male migrainous patient, in whom estrogens are rarely used. 1 week following surgery for prostatic carcinoma a 75-year-old white man who was started on stilbestrol 5 mg daily began to experience severe bifrontal, throbbing headaches with nausea and occasional vomiting. The headaches lasted 4-6 hours and appeared 3 or 4 times weekly. Fortification spectra in both visual fields and language disturbances occurred during the headache period. Stilbestrol was discontinued 4 months later, and the headaches improved. After 1 week without headaches, stilbestrol was begun again and similar headaches promptly recurred. Stilbestro was again discontinued, and the headaches immediately improved. 1 month later the patient was free from headache and has since remained so. Between the periods of headache, neurological examination was normal. The patient had a history of moderate common migraine, but following estrogen medication his symptoms became those of a severe clsssic migraine. The case raises the possiblity that the relation between estrogens and migraines is not limited to a fall in estrogen blood levels; steady or rising levels of estrogens possibly produce a similar effect.
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PMID:Estrogens and migraine. 721 75


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