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

Twenty-one patients experienced headache related to sexual activity. Two varieties of headache could be distinguished from the clinical histories. The first, developing as sexual excitement mount, had the characteristics of muscle contraction headache. The second, severe, throbbing or 'explosive' in character, occurring at the time of orgasm, was presumably of vascular origin associated with a hyperdynamic circulatory state. Two of the patients with the latter type of headache had each experienced episodes of cerebral vascular insufficiency on one occasion which subsequently resolved. A third patient in this category had a past history of drop attacks. No evidence of any structural lesion was obtained on clinical examination or investigation, including cerebral angiography in seven patients. Eighteen patients have been followed up for periods of two to seven years without any serious intracranial disorder becoming apparent. While the possibility of intracranial vascular or other lesions must always be borne in mind, there appears to be a syndrome of headache associated with sexual excitement where no organic change can be demonstrated, analogous to benign cough headache and benign exertional headache.
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PMID:Headaches related to sexual activity. 101 Oct 34

Blood pressure and clinical status of 1,736 patients with cerebrovascular disease were observed during 12 months of treatment with nicardipine. The most common diagnoses were chronic cerebral ischemia (53.2%), transient ischemic attacks (TIA; 25.1%), and cerebral infarct (8.7%); 50.1% of patients were classed as hypertensive [systolic blood pressure (SBP) > or = 160 mm Hg or diastolic blood pressure (DBP) > or = 90 mm Hg]. Most patients (91.2%) received a daily dose of 60 mg nicardipine. Additional treatments included diuretics (37%), beta-blockers (11.5%), other antihypertensive drugs (15.8%), platelet antiaggregants (25.1%), and cardiotonic drugs (15.1%). A total of 282 patients (16.2%) were lost to follow-up, 21 (1.2%) patients withdrew due to side effects, 32 (1.8%) died, and 9 (0.5%) patients had treatment interrupted due to concomitant illness. In the hypertensive subgroup, blood pressure (SBP/DBP) was reduced from a mean baseline value of 175 +/- 22/97 +/- 14 mm Hg to 152 +/- 17/85 +/- 11 mm Hg at 3 months and 149 +/- 23/81 +/- 11 mm Hg after 12 months of treatment. The incidence of TIA or stroke among these patients was reduced from 29 cases (3.5%) during the first 3 months to 11 cases (1.54%) during months 4-12 (p < 0.01). In normotensive patients there were 18 (2.15%) cases during months 1-3 and 13 (1.55%) cases during months 4-12 (difference not significant). In the 280 patients treated with nicardipine alone, the most frequent side effects during the first month were facial flushing (6.8%), gastrointestinal problems (5%), dizziness (3.2%), headache (3.2%), drowsiness (3.2%), and hypotension (1.1%). Most of these side effects were transient.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The influence of nicardipine in patients with high risk of stroke. 136 3

We present four cases of cerebral ischemia secondary to dissections of cervicocerebal arteries. The majority of patients presented with transient ischemic attacks and strokes, although one patient presented with headache and focal seizure. In addition to history and physical examination, the diagnostic evaluation of these patients included computed tomography scan, carotid duplex studies, angiogram, and, in some cases, magnetic resonance imaging studies. Initially, the patients were anticoagulated with heparin and then with warfarin for a period of six to eight weeks. The emergency physician must consider such dissections in younger patients with sudden neurologic deficits and no or few risk factors for cerebrovascular disease. In our experience, these are not rare syndromes; with proper workup, prompt diagnosis, and therapy, the prognosis is usually excellent.
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PMID:Dissections of the cervicocerebral arteries. 187 73

Cortical spreading depression (SD) has been implicated in the pathophysiology of classical migraine headache and cerebral ischemia. A reduction in cerebral blood flow (CBF), mimicking that seen during the aura and headache phase of migraine, is typically observed following SD in the rat. This phenomenon may also play a role in potentiating ischemic brain damage. In the present study, brief cortical exposure to 1 M KCl produced a marked suppression of EEG amplitude which persisted 20 min in the rat. Upon normalization of the EEG, cortical blood flow declined 20-30% and remained low for at least 2 h. Treatment with a 1 mg/kg i.v. dose of the 21-aminosteroid antioxidant tirilazad mesylate (U-74006F), 2 min following KCl application, completely blocked the hypoperfusion while leaving the magnitude and duration of the EEG suppression and mean arterial pressure unchanged. Tirilazad mesylate is a potent inhibitor of oxygen radical-mediated lipid peroxidation both in vitro and in vivo. Thus, based on present results, an oxygen radical hypothesis is proposed to account for the SD-induced cerebral hypoperfusion.
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PMID:The 21-aminosteroid antioxidant tirilazad mesylate, U-74006F, blocks cortical hypoperfusion following spreading depression. 193 84

Spontaneous dissection of the internal carotid artery is supposed to be a rare condition, but seems to be increasingly diagnosed. The symptoms are protean from unilateral headache, Horners syndrome, tinnitus, to cerebral ischemia and hemipareses. The condition is of unknown incidence and usually affects previously healthy persons. It is nearly always unilateral. The diagnosis is ascertained by characteristic angiographical findings. The prognosis depends on the exhibited symptoms. Three patients seen during the last year at the Department of Neurology at the National Hospital (Rikshospitalet) are presented, together with a brief survey of symptomatology, diagnosis, prognosis and treatment.
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PMID:[Spontaneous dissection of the internal carotid artery]. 200 Jun 17

Since 1978, the authors have observed 7 cases of dissecting aneurysm in the internal carotid artery. Symptoms were severe headache and subsequent neurologic deficit in young persons (3 women, 4 men; mean age 35 years). The underlying pathology was spontaneous dissection of the cervical internal carotid artery, with surgical confirmation in 3 cases and typical angiographic patterns in all cases. Spontaneous dissection of the cervical internal carotid artery is being increasingly recognized as a cause of cerebral ischemia in young adults. Moreover this clinicopathologic event is more common than had previously been supposed. The etiology remains unclear, except in 15% of cases in which dystrophy of the media (Marfan's syndrome) is in cause. No history of cervical trauma can be found. Typical clinical features consist in ipsilateral headache preceding an abrupt neurologic deficit in a 40-year-old person. An incomplete Horner syndrome (oculosympathetic paresis without facial anhidrosis) associated with facial pain and numbness is pathognomonic, but the majority of dissections are less typical. The typical angiographic pattern is an elongated regular stenosis of the high cervical internal carotid artery, 2 cm above the non-involved bulbus ("string sign"). The dissection may modify to a tapered occlusion above the point of origin of the internal carotid artery. The natural course is spontaneous resolution of the stricture, without relapse. Optimal management is non-operative since medical treatment has proved to be efficient. These cases confirm the benign course and overall good prognosis of spontaneous dissections of the internal carotid artery which are not as rare as the scarcity of reports might indicate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Spontaneous dissection of the internal carotid artery. Apropos of 7 cases and a review of the literature]. 217 45

We studied the patterns of cerebral blood flow (CBF), over time, in patients with systemic lupus erythematosus and varying neurologic manifestations including headache, stroke, psychosis, and encephalopathy. For 20 paired xenon-133 CBF measurements, CBF was normal during CNS remissions, regardless of the symptoms. CBF was significantly depressed during CNS exacerbations. The magnitude of change in CBF varied with the neurologic syndrome. CBF was least affected in patients with nonspecific symptoms such as headache or malaise, whereas patients with encephalopathy or psychosis exhibited the greatest reductions in CBF. In 1 patient with affective psychosis, without clinical or CT evidence of cerebral ischemia, serial SPECT studies showed resolution of multifocal cerebral perfusion defects which paralleled clinical recovery.
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PMID:Cerebral blood flow variations in CNS lupus. 229 89

The pathophysiology and treatment of acute subarachnoid hemorrhage (SAH) are reviewed. SAH occurs when blood is released into the subarachnoid space, which surrounds the brain and spinal cord. Symptoms of SAH include severe headache, nausea, vomiting, neck pain, nuchal rigidity, and photophobia. The initial hemorrhage is fatal in 20-30% of patients. Complications of SAH include rebleeding, hydrocephalus, delayed cerebral ischemia associated with cerebral vasospasm, and seizures. The likelihood of rebleeding is increased by measures that rapidly lower intracranial pressure. The risk of developing hydrocephalus is associated with the volume of blood within the subarachnoid space and ventricular system. Cerebral vasospasm develops in 20-40% of patients, and up to 50% of affected patients die or suffer permanent neurological damage. Seizures occur in 5-15% of patients with SAH. Radiologic procedures form the foundation for the diagnosis of SAH. The most commonly used rating scale classifies the severity of SAH based on the clinical presentation of the patient. Surgery is the definitive treatment for the prevention of rebleeding. Hydrocephalus can only be treated surgically, most commonly by insertion of a drain. The only measures proved to be effective for treatment of delayed cerebral ischemia are volume expansion and the induction of hypertension. The calcium-channel blocker nimodipine was recently approved for treatment of arterial spasm in SAH. Intravenous nicardipine is also being studied for the same indication. These agents may improve clinical outcome substantially by limiting fixed neurological deficits. To prevent seizures, prophylactic antiepileptic therapy with phenytoin sodium is generally accepted. The SAH complications of rebleeding, hydrocephalus, delayed cerebral ischemia, and seizures are managed by surgical, drug, and fluid therapy.
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PMID:Pathophysiology and treatment of subarachnoid hemorrhage. 240 1

The Hemostasis and Thrombosis Laboratory at the Oregon Health Sciences University identified 80 patients with significantly elevated anticardiolipin antibody (ACLA) levels. We reviewed all of their available medical records and found that 25 of these patients had associated neurological symptoms or disorders. These symptoms and disorders could be grouped into four distinct clinical patterns comprising encephalopathy, multiple cerebral infarctions, migraine-like headaches, and visual abnormalities including amaurosis fugax and ischemic optic neuropathy. Cerebral ischemia best explained these neurological dysfunctions. There was no correlation between the presence or absence of neurological disease and ACLA levels, but ACLA levels were higher in patients with encephalopathy than in others with neurological involvement (p less than 0.05). How neurological dysfunction and the presence of these antiphospholipid antibodies are related remains to be clarified. Nevertheless, in patients with unexplained cerebral ischemia, establishing the presence of ACLA may have prognostic and therapeutic importance. In particular, acute immunosuppressive therapy and plasmapheresis may be useful in patients with acute ischemic encephalopathy.
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PMID:Neurological disease associated with antiphospholipid antibodies. 272 12

The opiate antagonist naloxone was suggested for the amelioration of cerebral ischemia after subarachnoid hemorrhage (SAH) following the 1981 report of clinical improvement of ischemic deficits in 2 patients. The deficit in 1 patient was exacerbated by morphine, suggesting that analgesics acting on opiate receptors should be avoided after SAH, and this would include codeine phosphate and dihydrocodeine, both widely used for post-SAH headache. We studied 21 consecutive patients with aneurysmal SAH whose condition was worse than Grade 1 on the Hunt and Hess scale. A single observer graded them to avoid interobserver error, and they were also given a score on the Glasgow coma scale. Each patient was then given an intravenous injection of 0.9% saline as placebo or 0.4 mg (7 patients) or 2.0 mg (14 patients) of naloxone. Five minutes later, the same observer regraded the patient. After 30 minutes, a second injection of placebo or naloxone was given, and the patient was regraded a third time. Each patient received placebo in one injection and naloxone in the other, but the order was randomized and unknown to the observer. There was no beneficial effect of 0.4 mg of naloxone after aneurysmal SAH, and we did not find an elevated level of the endogenous opiate beta-endorphin in the cerebrospinal fluid in the majority (6 of 8 of the patients in whom it was assayed). Five of the patients given 2.0 mg of naloxone did improve transiently, and none deteriorated after the drug, suggesting that naloxone in a high dose may have a place in the management of some post-SAH deficits.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of naloxone on deficits after aneurysmal subarachnoid hemorrhage. 315 81


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