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

Pituitary adenoma apoplexy was considered an acute life-threatening condition until more benign and even asymptomatic courses were found by advanced neuroimaging procedures. Necrosis and hemorrhage in the pituitary adenoma can cause acute enlargement of the tumor. sometimes with rupture of the tumor capsule and bleeding into the subarachnoid space and surrounding parts of the brain. Clinical symptoms include acute or subacute headache in combination with signs of meningeal irritation and neuroophthalmological and cerebral dysfunction. Severe panhypopituitarism may be an additional complication. Acute blindness due to compression of the optic chiasm and symptomatic compression of basal cerebral arteries require immediate transsphenoid tumor resection. If panhypopituitarism is suspected, immediate hormone substitution is necessary.
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PMID:[Adenomatous hypophyseal apoplexy. Clinical, diagnostic and therapeutic aspects of a frequently misdiagnosed emergency state]. 778 16

Five patients: three children, one adolescent, and one young adult, examined in an emergency room setting were diagnosed with post-traumatic transient cortical blindness. This syndrome is characterized by transient visual loss, normal pupillary response and normal funduscopic examination following minor head trauma. In each case, vision returned to normal within minutes to hours following injury, leaving no neurological sequelae. Headache, confusion, irritability, anxiety, nausea and vomiting were the most common related symptoms. While the mechanism responsible for the transient blindness is unknown, most authors propose an abnormal vascular response to trauma with resultant transient hypoxia and cerebral dysfunction. The similarity between the symptoms accompanying this syndrome and those seen during a classic migraine attack has led many investigators to suggest a common underlying pathophysiology. The purpose of this report is to highlight the salient clinical features and diagnostic approaches to this syndrome, thereby providing ophthalmologists and emergency room physicians a heightened awareness of this entity and the means to detect it.
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PMID:Post-traumatic transient cortical blindness. 813 7

Hypoglycaemia is the most frequent acute complication of insulin-dependent diabetes mellitus. The clinical symptoms of insulin-induced hypoglycaemia can be grouped into those attributable to the sympathetic and adrenergic responses, e.g. tremor, pallor, palpitation, sweating, mydriasis ('hypoglycaemia awareness'), and those attributable to brain dysfunction, ranging from headache to convulsions and coma. Hypoglycaemia in diabetic children can occur at any time of the day, but nocturnal hypoglycaemia is a particular fear and worry. The frequency of mild hypoglycaemia is almost impossible to ascertain and the incidence of severe hypoglycaemia varies between 0.07 and 3.6 episodes per patient-year, though most authors report a range of 0.1-0.2 episode per patient-year. The most frequent causes of hypoglycaemia in diabetic children are deviations from treatment routine such as strenuous exercise, omission of snacks or skipped meals, and gross deviations from the prescribed times of insulin injections and recommended doses of insulin. Other predisposing factors include intensified insulin treatment, improved glycaemic control, young age, longer duration of diabetes and defective counterregulation. The available paediatric studies do not seem to support the suggestion that human insulin impairs the perception of hypoglycaemic symptoms ('hypoglycaemia unawareness') and increases the frequency of hypoglycaemic episodes, but further conclusive studies are needed. Prolonged and recurrent severe hypoglycaemia, particularly in younger children, can cause permanent neuropsychological dysfunction (e.g. learning disabilities) and permanent electroencephalographic abnormalities. Mild hypoglycaemia has also been documented to affect cognitive function, and the performance of neuropsychological tasks can remain decreased for some time (up to several hours) after full clinical recovery from hypoglycaemia. An impending hypoglycaemic attack can usually be averted by the ingestion of 20 g of rapidly absorbed carbohydrate. A severe episode can be effectively treated outside hospital with subcutaneous or intramuscular glucagon (0.5-1.0 mg) or in the hospital by an intravenous bolus of 0.2-0.5 g/kg glucose followed by a continuous glucose infusion. Patient and parent education and vigilant application of diabetes self-care principles are perhaps the most effective means of prevention, but in very young children a less strict metabolic control (higher glycosylated haemoglobin levels) may be necessary.
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PMID:Hypoglycaemia in the diabetic child. 837 14

Migraine is caused by intermittent brain dysfunction. Attacks result in severe unilateral headache with nausea, vomiting, photophobia, phonophobia and general weakness. The prevalence of migraine is 12 to 20% in women and 8 to 12% in man. Treatment of an acute attack is done by antiemetics in combination with analgesics. Severe migraine attacks are treated with ergotamine or sumatriptan. Parenteral treatment is performed most efficiently and safely with i.v. ASA. Frequent and severe attacks require prophylaxis. Drugs of first choice are metoprolol, propranolol, flunarizine and cyclandelate. Substances of second choice are valproic acid, DHE, pizotifen, methysergide and magnesium. Homeopathic remedies are not superior to placebo. Nonpharmacological treatment consists of sport therapy and muscle relaxation techniques.
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PMID:[Migraine--diagnosis, differential diagnosis and therapy]. 913 7

It is well known that some patients with neurally mediated syncope have a feeling of aura before the onset of syncope. A case is reported in which cerebral dysfunction recorded by EEG was present before the onset of a vasovagal reaction. The vasovagal reaction, bradycardia and/or asystole, was preceded by abnormal EEG findings when the patient complained of feeling a headache, photophobia, and nausea. These findings suggest that cerebral hypoperfusion, such as with cerebral vasospasms, before the onset of bradycardia might be involved in the mechanism of neurally mediated syncope in patients with an aura.
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PMID:Possible involvement of cerebral hypoperfusion as trigger of neurally-mediated vasovagal syncope. 955 95

Complex developmental venous anomalies (DVAs) represent variations of normal cerebral venous drainage and consist of dilation of the superficial and/or deep venous system. These rare anomalies can occur unilaterally or bilaterally, supratentorially or infratentorially, focally or they can affect the entire hemisphere. Some DVAs are associated with cervicofacial venous malformations or facial lymphatic malformations. Anomalies of this type are generally clinically silent, and cerebral dysfunction is usually absent. Symptoms, when they occur, are most commonly headache or mild seizure disorders. The angiographic findings are striking, with well-formed but enlarged transcerebral medullary and deep and/or superficial cortical veins. Opacification of these venous structures occurs within the same time frame as a normal angiographic venous phase. The authors report the case of a 33-year-old man in whom a large inoperable arteriovenous malformation had been previously diagnosed and who presented with seizures. Repeated magnetic resonance imaging and angiography demonstrated abnormally dilated transcerebral, superficial, and deep venous structures involving the entire right hemisphere with no identifiable nidus. Additionally, multiple bilateral benign facial hemangiomas were present in this patient. It is important to recognize this rare venous appearance as a developmental variant and not mistake it for an arteriovenous malformation or a partially thrombosed vein of Galen malformation. Because these venous anomalies are extreme variants of the normal venous system, hemorrhage rarely, if ever, occurs and the patient can be reassured that no interventional or surgical therapy is necessary or warranted.
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PMID:Complex right hemisphere developmental venous anomaly associated with multiple facial hemangiomas. Case report. 1019 23

In addition to attacks with the well-known pulsating characteristics of migrainous headache, migraine patients may experience a variety of peculiar pain sensations which are phenomenologically similar to the spontaneous sensations occurring in patients with thalamic disturbances and to the cenesthesias described as basic symptoms in functional psychoses. A 36-year-old artist with a history of migraine with typical aura provided impressive illustrations of cenesthetic pain sensations experienced during his migraine attacks, including sensations of pressure and sensations of pulling. It is suggested that cenesthetic pain sensations represent aura symptoms of migraine indicative of focal cerebral dysfunction, probably in the thalamic region. The occurrence of cenesthetic pain sensations as a migraine symptom supports the notion of an organic etiology of cenesthesias, as postulated in Huber's concept of basic symptoms of functional psychoses.
Cephalalgia 1999 Jul
PMID:Cenesthetic pain sensations illustrated by an artist suffering from migraine with typical aura. 1044 39

Preeclampsia is a disorder specific to pregnancy which can affect all maternal organs. Cerebral involvement with the occurrence of convulsions is the defining factor for eclampsia. The most prominent signs of cerebral dysfunction include headache, hyperreflexia, visual disturbances, confusion and/or altered state of consciousness. Patients usually recover completely however some patients remain disabled due to cerebrovascular damage. Intracerebral and subarachnoidal hemorrhage are severe however rare complications of eclampsia. TCD investigations regularly find vasospasm in all great cerebral arteries. Reversible hypodense lesions in the white matter on early CT-scans and increased signal intensities on T2-weighted MRT images indicate local edema. The etiology of preeclampsia and eclampsia remains unknown and its current pathophysiology is still hypothetical. The clinical picture may best be explained by an endothelial dysfunction with increased vascular sensitivity to circulating pressure agents as well as by a structural endothelial lesion with fluid loss from the intravascular compartment.
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PMID:[Neurological spectrum of pre-eclampsia and eclampsia]. 1063 16

Many anecdotal cases and some clinical studies have demonstrated that formaldehyde exposure can cause multiple health-related problems and cerebral dysfunction. The U.S. Consumer Product Safety Commission has documented multiple hazards related to formaldehyde exposure. Some of this research has suggested that low levels of exposure can be very hazardous to one's health and can potentially result in heightened chemical sensitivities, seizures, and cognitive decline. Some research suggests that exposure results in long-term immunological changes, cell neurofilament protein changes, and demyelination. Symptomatically, exposure has been associated with respiratory problems, excessive fatigue, headaches, mood changes, and impaired attention, concentration, and memory functioning. This article outlines the case of a biology teacher whose chronic formaldehyde exposure resulted in heightened sensitivity to formaldehyde, three tonic-clonic seizures, and dramatic amnesia as well as other cognitive dysfunction.
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PMID:A case of claimed persistent neuropsychological sequelae of chronic formaldehyde exposure: clinical, psychometric, and functional findings. 1459 Jan 91

There are conflicting reports in the literature concerning the neuropsychological functioning of migraine headache patients. The finding in some studies that migraineurs performed more poorly than healthy controls led to the hypothesis that chronic migraine may result in subtle but persistent cerebral dysfunction. Reports describing acute and between-headache neurophysiological disturbances in migraineurs lent support to this hypothesis. To elucidate the cognitive status of these patients, we administered a brief neuropsychological battery to 60 individuals with migraine headache (HA), nonheadache chronic pain (PAIN), or mild traumatic brain injury (MTBI). The PAIN group was included to test the hypothesis that cognitive difficulty in migraineurs might result from the discomfort, depression, medications, etc. often associated with chronic pain, rather than from brain dysfunction. The MTBI patients were considered a useful comparison for the migraineurs because their level of impairment was also expected to be mild, at worst. A MANOVA, with three cognitive index scores as the dependent variables, revealed that the three groups differed significantly. Follow-up contrasts demonstrated that the MTBI group was significantly more impaired on the memory index compared to the HA and PAIN groups, which did not differ from each other. The use of two different normative-based cutoffs to identify individuals who were impaired on the test battery revealed that the frequency of impairment within the two groups of pain patients, but not the MTBI patients, was within normal limits. Thus, the results did not support a link between migraine headache and cognitive impairment.
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PMID:Neuropsychological functioning in migraine headache, nonheadache chronic pain, and mild traumatic brain injury patients. 1459 May 92


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