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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The toxicities of cocaine are far-ranging. They include sudden death, acute medical and psychiatric illness, infectious complications, reproductive disturbances, trauma, criminal activities and societal disruption, including child neglect and abuse and lost job productivity. This chapter focuses on the medical complications. Medical complications in general reflect the intense sympathomimetic activities of cocaine ('sympathetic neural storm'). Psychiatric complications include acute anxiety or panic and paranoid psychosis. Cardiovascular complications include arrhythmias and sudden death, acute myocardial infarction, myocarditis, dissecting aneurysm and bowel infarction. Neurological complications include seizure, intracerebral haemorrhage and brain injury due to hyperthermia and/or seizures, and headache. The incidence of medical complications has been estimated using two databases collected prospectively in the United States. In 1989 and 1990 cocaine ranked first in total encounters, major medical complications and drug-related deaths. An attempt was made to assess the intrinsic toxicity of cocaine by computing the incidence of adverse health outcomes per population of drug abusers. Rates of emergency department visits and deaths were 15.1 and 0.5 respectively, per 1000 persons using drugs in the past year. The magnitude of the cocaine problem, while considerable, is relatively small compared with that of cigarette smoking or alcohol abuse.
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PMID:How toxic is cocaine? 163 9

A 46-year-old man, presenting with headache, nausea, and lassitude, was diagnosed as having diabetes mellitus and hyponatremia, and admitted to Tohoku University Hospital. Insulin treatment improved the hyperglycemia but aggravated hyponatremia, which was proved to be elicited by the inappropriate secretion of antidiuretic hormone (SIADH). An acute water load failed to suppress ADH release in the supine posture but slightly increased plasma atrial natriuretic peptide (ANP). On the other hand, plasma ADH markedly increased in response to an upright posture, accompanied by a fall in blood pressure and a rise in heart rate. After treatment with droxidopa "a sympathomimetic drug", ambulatory blood pressure gradually increased and hyponatremia disappeared. However, blood pressure and ADH responses to upright posture were not improved by treatment with the drug. Moreover, plasma ADH was still not sufficiently suppressed by acute water loading in the supine position, but plasma ANP markedly increased, thereby resulting in urinary dilution and natriuresis. These results suggest that exaggerated ADH release (SIADH) was brought about by the baroreceptor reflex stimulated by the postural hypotension, and also by the impaired osmoregulation associated with diabetic neuropathy, and that droxidopa improved cardiovascular function and increased ANP release with resultant urinary dilution and natriuresis in spite of slightly increased ADH release.
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PMID:A case of syndrome of inappropriate secretion of antidiuretic hormone associated with diabetes mellitus. 179 39

We present two cases of severe headache associated with the use of bromocriptine for lactation suppression in otherwise healthy women. In each case, the additional use of a therapeutic sympathomimetic agent resulted in extreme worsening of symptoms with development of hypertension and life-threatening complications (ventricular tachycardia and cardiac dysfunction in one case, seizures and cerebral vasospasm in the other). Sympathomimetics in combination with bromocriptine in patients with a bromocriptine-associated headache during the puerperium may be dangerous.
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PMID:Bromocriptine-associated headache: possible life-threatening sympathomimetic interaction. 192 36

The records of 21 patients admitted to hospital from January 1985 to December 1988 for acute headache associated with cocaine intoxication were reviewed. Fifteen patients were identified who experienced headaches with migrainous features in the absence of neurological or systemic complications. None of them had a history of cocaine-unrelated headaches or a family history of migraine, and all had a favourable outcome. Three possible mechanisms of cocaine-related vascular headaches are discussed which depend on the interval between cocaine ingestion and development of the headache. We postulate that acute headaches following cocaine use may relate to the sympathomimetic or vasoconstrictive effects of cocaine, while headaches following cocaine withdrawal or exacerbated during a cocaine "binge" may relate to cocaine-induced alteration of the serotoninergic system.
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PMID:Cocaine-related vascular headaches. 195 99

Fifty-three patients with cluster headache, mean age 42.6 years, were examined by means of pupillometry. Pharmacological stimulation was carried out by the instillation of eye drops; the sympathomimetic agents hydroxyamphetamine (a norepinephrine releaser) and phenylephrine (an agent acting directly on the postsynaptic receptors) were applied. Pupillary dilatation was measured at set time intervals, comparing the responses of the symptomatic and non-symptomatic sides. The material was divided into groups according to the degree of basal anisocoria. The subgroup with the most pronounced basal miosis of the symptomatic side demonstrated a uniform pattern of deficient symptomatic side dilatation after OH-amphetamine and supersensitivity to phenylephrine. The other groups demonstrated the same general pattern, but to a far lesser degree. In cluster headache, the extent of nonresponsiveness to OH-amphetamine and of phenylephrine supersensitivity on the symptomatic side thus, at least partly, seems to be a function of the degree of anisocoria. The response pattern in cluster headache seems to differ from that of 3rd neuron Horner's syndrome with an anisocoria of the same extent.
Cephalalgia 1989 Jun
PMID:Cluster headache: pupillometric patterns as a function of the degree of anisocoria. 274 12

Heroin, cocaine, amphetamines, sympathomimetic drugs can cause cerebral angiopathy. We report 2 patients with cerebrovascular disorders after ingestion of a nasal vasoconstrictor containing phenylpropanolamine (P.P.A.). The first patient had two acute repetitive attacks of severe headache and vomiting, occurring after a daily treatment with 180 mg of P.P.A. during 6 weeks. The second patient had an intracerebral hemorrhage, occurring some hours after taking for the first time 120 mg of P.P.A. In both cases, cerebral angiography, performed in the next week, demonstrated segmental narrowing and dilatations of medium-size intracranial arteries. None of the usual causes of cerebral vasculitis were present. The outcome was favorable and follow-up angiograms showed the disappearance of the beading pattern. P.P.A. is widely used over the counter in diet pills and stimulants. Cerebral vascular complications have been rarely reported, always hemorrhagic and often associated with cerebral vasculitis. They are unrelated to duration or dosage of treatment. The mechanism is unclear but could result from several factors: chronic or paroxystic high blood pressure, immuno-allergic vasculitis, arterial spasm, direct "toxic" effect of the P.P.A. on the arterial wall may be increased by other drugs and caffeine.
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PMID:[Benign cerebral angiopathies and phenylpropanolamine]. 304 37

Thirty-one patients with cluster headache were examined with regard to their forehead sweating pattern, by means of the Evaporimeter. Sweating was stimulated in two different ways: by body heating and by parenterally administered pilocarpine. The resulting increase in evaporation was frequently measured at different positions on both sides of the forehead, and the possibility of variations in the pattern related to the passage of time was specifically scrutinized. Some typical patterns emerged. The previously reported, marked asymmetries of response (deficient heat-induced sweating and pilocarpine supersensitivity of the symptomatic side) at the medial positions in the forehead were confirmed. However, the asymmetries invariably faded to some extent with the passage of time. Patients with cluster headache show gross similarities with, but also some minor differences from, the sweat pattern of patients with brain stem lesions causing a Horner's syndrome. A subdivision of the material into groups in accordance with the pupillometric pattern after sympathomimetic stimulation made it clear that the cases of definite evaporimetric asymmetries ("typical reactions") belonged to the group with a typical pupillometric pattern. These results suggest that from an "autonomic" point of view, subpopulations may exist within the clinical entity of cluster headache.
Cephalalgia 1988 Dec
PMID:Cluster headache: forehead sweating pattern during heating and pilocarpine tests. Variation as a function of time. 321 26

A 51-year-old male cluster headache patient had during five bouts in the course of 11 years always had the headache attacks on the left side. Autonomic abnormalities were, however, present on the right side. Pupillometrically, there was thus a Horner-like syndrome on the right (non-symptomatic) side, with miosis and a relatively more marked dilatation of that eye subsequent to topical application of a directly working sympathomimetic agent (phenylephrine) than after an indirectly working one (hydroxyamphetamine), whereas this was not the case on the symptomatic side. The findings on evaporimetry were not as clear-cut as the pupillometric findings; however, even facial sweating was consistent with a pathologic condition on the right (non-symptomatic) side. A primary dichotomy of pain and autonomic signs (that is, not due to change of side of pain localization) thus seems to be present in this case.
Cephalalgia 1988 Jun
PMID:Cluster headache: further observations on the dissociation of pain and autonomic findings. 340 15

Thirty-two cluster headache patients and healthy controls (n = 16-20 for the various tests) were examined by means of a Whitaker pupillometer during pain-free intervals. Eye drops of the sympathomimetic agents tyramine, hydroxyamphetamine, and phenylephrine were instilled into the conjunctival sacs on separate occasions, and pupillary diameters recorded at standard time intervals. The mydriatic responses of the two pupils were compared. A moderate, but statistically significant, basal relative miosis was found on the pain side in cluster headache. The symptomatic-side pupils were less responsive than their counterparts when stimulated with tyramine and hydroxyamphetamine, the difference being statistically significant for the OH-amphetamine test. With the phenylephrine test, however, the mydriasis on the symptomatic side significantly exceeded that of the contralateral pupil. This pattern of reactions does not quite correspond to those of "ordinary" Horner's syndrome (1st, 2nd, and 3rd neuron lesion). There are, however, gross similarities with the recently reported pattern in central sympathetic neuron dysfunction. In cluster headache there is probably a "Horner-like picture" rather than a proper Horner's syndrome.
Cephalalgia 1987 Dec
PMID:Cluster headache pathogenesis: a pupillometric study. 342 28

A case of intracerebral hemorrhage and characteristic angiographic changes associated with methamphetamine is reported. A 23-year-old woman suddenly complained of headache, nausea, vomiting and gait disturbance several minutes after intravenous injection of 30 mg of methamphetamine. She was admitted with consciousness disturbance, aphasia and right hemiparesis 26 hours after the onset. CT scan revealed subcortical hemorrhage in the left fronto-parietal region. Left carotid angiogram showed irregular segmental arterial narrowing, "beading" of the anterior and middle cerebral arteries. Emergency craniotomy was performed and a left fronto-parietal hematoma was removed totally. Histologically, the surgical specimen showed many vessels in which included thrombi with perivascular hemorrhage. Post-operative course was uneventful. Repeat carotid angiogram 4 months after the operation revealed normal anterior and middle cerebral arteries. We discussed about associations between the abuse of methamphetamine and the occurrence of intracranial hemorrhage and characteristic angiographic changes. As far as we know, there were 23 reports in an extensive review of the literature on intracranial hemorrhage associated with methamphetamine abuse. In the present case "beading" of the intracranial vessels may be related to angiitis induced by methamphetamine. Both the presence of arterial inflammation and increased blood pressure caused by sympathomimetic action of methamphetamine are probably the important factors in the occurrence of intracranial hemorrhage associated with methamphetamine.
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PMID:[Intracerebral hemorrhage and characteristic angiographic changes associated with methamphetamine--a case report]. 379 Mar 61


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