Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018681 (headache)
56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 12 year old girl with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke like episodes (MELAS) is reported. After a normal childhood, at 9 years of age she developed generalized and hemilateralized seizures. Posteriorly, these episodes became more frequent and were accompanied by headache, homonimous hemianopsia, ataxia, vomiting, photophobia, left hemiparesis, slurred speech and even convulsive status. Laboratory tests evidenced lactic acidosis, brain lucencies at CT Scan and ragged skeletal muscle fibers at muscle biopsy.
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PMID:[Mitochondrial encephalomyopathy, lactic acidosis and features of cerebrovascular disorders]. 207 86

Eclampsia is the most serious manifestation of a toxaemic encephalopathy which may also have nonconvulsive manifestations, such as headache, visual disorders or retinal or cortical origin, confusion or disturbances of consciousness. Some authors consider eclampsia as being only one particular aspect of hypertensive encephalopathy. However, recent studies have drawn attention to the importance of angiospasm which might not be a pure reaction to hypertension but might result from a relative deficiency in vascular prostacyclin. These physiopathological factors, to which must sometimes be added disseminated intravascular coagulation, account for computerized tomographic and neuropathological findings showing cerebral oedema and, in complicated cases, ischaemic or haemorrhagic lesions. Medical treatment must rapidly control the convulsive attacks as well as the arterial hypertension. Magnesium sulfate is not much used outside the United States where it is now strongly controverted. The obstetrical management depends on the time when eclampsia occurs and on the efficacy of the medical treatment.
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PMID:[Eclampsia]. 214 84

Neurologic consequences of cocaine use frequently present as medical emergencies in the form of stroke, repeated seizures, encephalopathy, acute headache, and unusual transient neurological deficits. The often fatal or disabling neurologic syndromes have only recently been recognized but are now well documented. Cocaine use is a significant cause of stroke in young adults, and the full, long-term ramifications of maternal cocaine use on the fetus will not be known for years to come. Unfortunately, there is not effective treatment other than abstinence, and our understanding of the pathophysiology of cocaine-associated neurologic illness remains limited.
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PMID:Neurologic consequences of cocaine use. 218 41

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 nervous system is frequently involved in patients with infective endocarditis. When a careful review of presenting complaints is undertaken, neurological symptoms have been found in as high as 29% of patients. Because these manifestations may be so protean in nature, for example, stroke or transient ischaemic attack (the most common), toxic encephalopathy, meningitis, brain abscess, visual loss, seizures, headache, backache, or acute mononeuropathy, the neurologist needs to consider infective endocarditis as a possible diagnosis in many patients. During the past two decades, infective endocarditis has occurred in an ever widening clinical setting. It may often be found in persons unknown to have predisposing cardiac disease. This is particularly true in certain subsets of the population, including the elderly, patients subjected to various invasive procedures leading to nosocomial infection, and drug abusers. New diagnostic studies, including refined bacteriological culture techniques, echocardiography, computed tomography, magnetic resonance imaging, and greater availability of skillful cerebral angiography, make earlier diagnosis of infective endocarditis possible. Despite this, patients with neurological complications continue to have an uncertain prognosis.
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PMID:Neurological manifestations of infective endocarditis. Review of clinical and therapeutic challenges. 267 68

Piracetam was applied to the treatment of 60 patients with initial manifestations of brain circulation failure and stage I circulatory encephalopathy. The drug exerted a beneficial therapeutic effect by reducing high brain vascular resistance (both extra- and intracranial) and by increasing the lowered volume of pulse fluctuations. It made fibrinolytic blood activity and aggregation of formed elements of the blood return to normal. An appreciable antiatherogenic effect was discovered as well. It should be taken into consideration that in patients with a dramatic lowering of pulse fluctuations, the use of piracetam in a dose of 1.6 g/day may enhance headache. In such cases the dose should be reduced.
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PMID:[Significance of subjective symptoms and diagnostic criteria in initial forms of cerebral circulation insufficiency]. 269 40

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

D-Lactate-associated encephalopathy is a rare clinical syndrome characterized by dizziness, ataxia, confusion, headaches, memory loss, lethargy, and aggressiveness which may progress to frank but reversible coma. It occurs in patients with profound dysfunction of the short-bowel syndrome and is believed to result from massive carbohydrate malabsorption with resultant over-production of D-lactate and other organic anions by the colonic flora. Extremely elevated serum levels of D-lactate (but not L-lactate) confirm the diagnosis, but currently D-lactate is not clearly established as the putative neurotoxin. We describe a patient who repeatedly developed D-lactate encephalopathy after surgical removal of nearly the entire jejunum and ileum. Markedly elevated D-lactate serum levels were documented during an encephalopathic episode. Potential pathophysiologic mechanisms and the treatment rationale are discussed.
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PMID:D-lactate-associated encephalopathy after massive small-bowel resection. 276 Apr 34

Eight patients with acquired immune deficiency syndrome (AIDS) presented complications affecting the nervous system. The complaints were headache, seizure, confusion or hallucination. Neurologic manifestations included meningitis, focal deficits, cranial nerve palsy, and dementia. Cerebrospinal fluid exhibited a decrease in the percentage of T helper lymphocytes with an inverted helper-to-suppressor cell ratio. The neurologic manifestations of AIDS may depend on multiple factors, such as HIV infection of the central nervous system, concomitant infections with other agents or meningeal invasion by systemic lymphoma or Kaposi's sarcoma. Many patients develop a diffuse encephalopathy which characteristically begins with impaired concentration and mild memory loss, and progresses to severe global cognitive impairment and dementia. Perivascular infiltrates and scattered microglial nodules, consisting of aggregates of microglia and astrocytes, are the most common findings in these patients.
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PMID:[Neurologic complications accompanying acquired immunodeficiency syndrome (AIDS): study of a group of 8 cases]. 295 8

This paper describes the few case reports of neurological effects of acute (primary) HIV infection. Following a typical primary illness (fever, sore throat, headache, rash, lymphadenopathy, superficial oral ulcers, conjunctivitis, leukopenia and thrombocytopenia) aseptic meningitis, myelopathy, spinal myoclonus, peripheral or cranial neuropathy, neuralgia and ganglioneuronitis may occur, usually within 3 weeks. Encephalopathy with spontaneous recovery also occurs, usually without other features of acute HIV infection. Diagnosis depends on demonstration of seroconversion which may be delayed by weeks. No therapy is yet available.
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PMID:The neurological features of acute HIV infection. 304 55


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