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)

38 cases of Takayasu's arteritis were reported. The mean age of onset was 23.3 years with a female: male ratio of 1:1.7. The median delay between first symptom and time of diagnosis was 12.2 years. Headache was the most common symptom of neurologic manifestations (55%). Major neurologic events occurred in 52.7% patients in this group, including TIA, cerebral infarction, hypertensive encephalopathy, lacunar infarct, seizure, paraplegia, watershed infarct, cerebral hemorrhage, Moyamoya phenomenon, and confusion in the order of frequency. A variety of mechanisms that must be taken into account in explaining this neurologic events were proposed. The secondary hypertension and cardiac complications play an important role in causing neurologic symptoms. The formation of anastomotic networks has "Jekyll and Hyde" effect on brain both in preventing or limiting the ischemic injury and in producing some special symptoms and signs, that further widen the clinical spectrum of brain involvement.
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PMID:[Neurological manifestation of Takayasu's arteritis]. 136 36

The safety of ondansetron has been carefully evaluated through laboratory studies and clinical trials. Preclinical studies demonstrated that there is no end-organ toxicity in rats and dogs administered ondansetron doses 30 to 100 times those used in humans. At near-lethal doses of ondansetron, animals developed subdued activity, ataxia, and convulsions. Modest transient increases in serum transaminase values were observed. Concurrent administration of ondansetron with chemotherapy had no effect on tumor response in animals. The clinical safety of ondansetron has been evaluated in more than 2,500 cancer patients who received intravenous doses as large as 1.5 mg/kg. In adult patients receiving single-day chemotherapy, the incidence of adverse events was 36% with ondansetron (n = 647) and 50% with metoclopramide (n = 498). Diarrhea occurred in 9% of ondansetron patients and 19% of metoclopramide patients. Headache occurred in 14% of ondansetron patients and 8% of metoclopramide patients. Extra-pyramidal symptoms were reported in none of the ondansetron patients and 5% of the metoclopramide patients. The incidence of vascular occlusive events and seizure disorders was nearly identical with ondansetron and metoclopramide and similar to the cancer population in general. In a group of 209 pediatric patients receiving chemotherapy, the incidence of adverse events was 19% with ondansetron. Serum transaminase values increased significantly in 6% to 8% of ondansetron patients and 2% of metoclopramide patients. There was no apparent relationship between the cumulative dose of ondansetron administered and the incidence of increased transaminase values. However, there was an apparent relationship between the cumulative dose of cisplatin administered and the incidence of transaminase abnormalities. These data demonstrate that ondansetron is better tolerated than metoclopramide and is safe for intravenous administration to pediatric and adult patients receiving chemotherapy.
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PMID:Toxicity and side effects of ondansetron. 138 51

We report a 32-year-old man with a 4-year history of headaches, seizures, and dementia secondary to multifocal amyloidomas in the white matter. Immunohistochemical and electron microscopic analyses suggest that the amyloidomas resulted from processing of plasma-cell-derived amyloidogenic protein by microglial cells.
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PMID:Amyloidoma of the CNS. I. Clinical and pathologic study. 140 86

This study examined the early and late outcome in head injury patients with focal or multifocal (unilateral or bilateral) brain contusions revealed by computerized tomography (CT) scanning. The outcome was also evaluated in patients hospitalized due to brain concussion. Three months after the injury (the early outcome) 43% of the 86 cases with multifocal contusions on the CT scan were dead. As evaluated by the Glasgow Outcome Scale, all the 57 patients with a focal brain contusion, as well as the 117 cases with brain concussion, made a good recovery or were moderately disabled. The late outcome (1 to 5 years after injury) was evaluated in 78 cases with brain contusion and in 85 cases with brain concussion, and revealed that complaints and impaired adaptive functioning were frequent in both the contusion and concussion group. The occurrence of headache, dizziness and sleep problems did not significantly differ among the various head injury groups. However, focal or multifocal brain contusions on the CT scan increased the frequency of impaired memory, impaired concentration, speech problems, weakness in arms or legs and seizures with loss of consciousness. Cognitive deficits and speech problems were particularly common in patients with a focal contusion in the temporal lobe. The late adaptive and social functioning were most markedly impaired in cases with multifocal bilateral contusions.
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PMID:Early and late outcome in head injury patients with radiological evidence of brain damage. 141 31

Waking and sleep EEGs were recorded in 69 siblings of 43 patients with rolandic spikes. 36 suffered from rolandic epilepsy, 7 from other diseases or symptoms (headaches, migraine, learning problems). At least one sibling with epileptic activity was found in 51.16% of the patients. Taking the 69 siblings as a basis, in 26 (37.68%) epileptic activity was recorded. Benign spike foci were recorded in only 4 siblings, generalized spike-wave complexes were seen in 22. Most epileptic activity was recorded in the age group of 5-12 years (54.3%). Nearly one-half (17.4%) was recorded exclusively in sleep, predominantly in sleep stage C (88%). Siblings of patients with (40%) and without seizures (37.5%) showed approximately the same rate, likewise siblings with (40%) and without seizures (34.8%). An autosomal-dominant mode of inheritance is assumed, but a multifactorial mode is also discussed.
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PMID:Contribution to the genetics of rolandic epilepsy: waking and sleep EEGs in siblings. 141 91

We describe the full history and postmortem findings in one of the first identified cases of mitochondrial encephalomyopathy with stroke-like episodes (MELAS). To clarify diagnostic criteria, we analyzed 69 reported cases. The syndrome should be suspected by the following three invariant criteria: (1) stroke-like episode before age 40 yr; (2) encephalopathy characterized by seizures, dementia, or both; and (3) lactic acidosis, ragged-red fibers (RRF), or both. The diagnosis may be considered secure if there are also at least two of the following: normal early development, recurrent headache, or recurrent vomiting. There are incomplete syndromes in relatives of patients with the full syndrome and incomplete syndromes might also be encountered in sporadic cases. Some MELAS patients have features of the Kearns-Sayre syndrome (KSS) or myoclonic epilepsy with ragged-red fibers (MERRF), but none had the full KSS syndrome. In partial or confusing cases, analysis of mitochondrial DNA (mtDNA) may point to the correct diagnosis; however, not all patients with clinical MELAS have had the typical mtDNA point mutation and some patients with the mutation have clinical syndromes other than MELAS.
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PMID:Melas: an original case and clinical criteria for diagnosis. 142

Nineteen patients with advanced cancer were entered into a phase I clinical trial of Tumor Necrosis Factor (TNF) which was designed to determine the pharmacokinetic profile, safety, and maximal tolerated dose (MTD) of the recombinant human cytokine in vivo. TNF was administered by continuous infusion for 24 hours followed by pharmacokinetics and a 120-hour infusion repeated every 3 weeks. The initial dose was 40 micrograms/m2 and was ultimately escalated to 200 micrograms/m2. A total of forty 5-day cycles were administered to 18 of these patients; and all were evaluable for toxicity. Toxicities in this trial included fever, chills, rigors, hypotension, headaches, seizures, lethargy, weight loss, and malaise. At all dose levels, but more significantly at the highest doses, hematological toxicities were observed and grade 3 neurotoxicity (headache and confusion), and hypotension were noted. Two patients expired during the study, and this was felt to be related to septic episodes. Because of these severe toxicities, 160 micrograms/m2 was defined as the MTD. At 160 micrograms/m2 peak serum levels occurred within 5-20 minutes of initiation and were not detectable 1 hour later. No anti-tumor responses were observed. No measurable plasma levels of TNF were observed with the administration of doses of 80 micrograms/m2. This dose level could be further studied in phase II studies alone and in combination with other agents, utilizing a continuous infusion schedule.
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PMID:A phase I pharmacokinetic study of recombinant human tumor necrosis factor administered by a 5-day continuous infusion. 142 28

We report a 15-year-old boy diagnosed with acute lymphoblastic leukemia (ALL) in 1983. Induction therapy included L-asparaginase. After the second dose of L-asparaginase, he had a left sided focal seizure and computed tomography (CT) scan of the head showed a right frontal infarct. No further L-asparaginase was given. Complete remission was achieved and he successfully completed therapy in 1986. Eight months later he had an isolated bone marrow relapse. Reinduction therapy included L-asparaginase. After the fourth dose of L-asparaginase, he presented with severe headache and a CT scan showed a right temporal infarct. Repeat infarction on rechallenge with L-asparaginase has not been previously reported. Prophylactic therapy, such as fresh frozen plasma, should be considered before patients, with a previous cerebral insult, are rechallenged with L-asparaginase. However the effectiveness of such therapy has not been established.
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PMID:Recurrent cerebrovascular accident with L-asparaginase rechallenge. 143 23

The postconcussion syndrome refers to a large number of symptoms and signs that may occur alone or in combination following usually mild head injury. The most common complaints are headaches, dizziness, fatigue, irritability, anxiety, insomnia, loss of consciousness and memory, and noise sensitivity. Mild head injury is a major public health concern because the annual incidence is about 150 per 100,000 population, accounting for 75% or more of all head injuries. The postconcussion syndrome has been recognized for at least the last few hundred years and has been the subject of intense controversy for more than 100 years. The Hollywood head injury myth has been an important contributor to persisting skepticism and might be countered by educational efforts and counter-examples from boxing. The organicity of the postconcussion syndrome has now become well documented. Abnormalities following mild head injury have been reported in neuropathologic, neurophysiologic, neuroimaging, and neuropsychologic studies. There are multiple sequelae of mild head injury, including headaches of multiple types, cranial nerve symptoms and signs, psychologic and somatic complaints, and cognitive impairment. Rare sequelae include hematomas, seizures, transient global amnesia, tremor, and dystonia. Neuroimaging and physiologic and psychologic testing should be used judiciously based on the problems of the particular patient rather than in a cookbook fashion. Prognostic studies clearly substantiate the existence of a postconcussion syndrome. Manifestations of the postconcussion syndrome are common, with resolution in most patients by 3 to 6 months after the injury. Persistent symptoms and cognitive deficits are present in a distinct minority of patients for additional months or years. Risk factors for persisting sequelae include age over 40 years; lower educational, intellectual, and socioeconomic level; female gender; alcohol abuse; prior head injury; and multiple trauma. Although a small minority are malingerers, frauds, or have compensation neurosis, most patients have genuine complaints. Contrary to a popular perception, most patients with litigation or compensation claims are not cured by a verdict. Treatment is individualized depending on the specific complaints of the patient. Although a variety of medication and psychologic treatments are currently available, ongoing basic and clinical research of all aspects of mild head injury are crucial to provide more efficacious treatment in the future.
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PMID:The postconcussion syndrome and the sequelae of mild head injury. 143 59

In a review of our series of patients with arteriovenous malformations (AVMs), a group with atypical angiographic and histopathological characteristics was discovered. Unlike the typical AVM, these lesions contained normal cerebral tissue between the abnormal vessels. We call these lesions diffuse AVMs, and think that this AVM represents one end of the AVM spectrum from a tight nidus to a diffuse lesion. The mean age of these patients was 18.1 years. Eight patients presented with an intracerebral hemorrhage, two with seizures, one with headache without hemorrhage, and one with ischemic symptoms compatible with vascular steal. Cerebral angiography revealed three AVMs to be 2 to 4 cm in diameter, four were 4 to 6 cm in diameter, and five were > 6 cm in diameter. Characteristic angiographic features included multiple small arterial feeders, small ectatic vessels in the malformation itself, multiple small draining veins, and a diffuse, puddling appearance of the contrast dye. Despite 16 operations in 11 patients, complete resection of the AVM was accomplished in only 8. The four patients with residual disease have received radiation therapy. Histopathology of the surgical specimens found AVM vessels interspersed among normal appearing neurons and white matter. Leptomeningeal angiodysplasia was noted when the cerebral cortex was involved. Gliosis was noted in some cases. Diffuse AVMs represent a difficult surgical challenge and recognition of the lesion aids in surgical planning.
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PMID:Diffuse arteriovenous malformations: a clinical, radiological, and pathological description. 143 9


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