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)

This study of a series of 40 mildly head injured (concussed) patients suggests that different physiologic pathways underlying the tests done in a six-part resting EEG, and for the 11 evoked electrical potential shifts occurring in the cerebral terrain, are testable. Further work seems likely in order to ascertain which clinical signs and symptoms may be related to specific individual types of recorded electronic brain imaging (EBI) abnormality. Which of the 11 parameters studied, EEG, VER, AER, and SER, would be more or less likely to be abnormal in their individual patterns (as being deviant from normal controls) also remains to be defined. The relationship of these neurophysiologic abnormalities to certain postconcussive symptoms, i.e., headache, dizziness, blurred vision, etc., at this point in time remains to be evaluated more precisely. The authors suggest that further research is necessary in evaluating the clinical use of somatosensory evoked responses as an additional parameter in electronic brain imaging (EBI) technology.
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PMID:Somatosensory evoked responses via electronic brain imaging (EBI). 158 53

T Cell Modulatory Peptide (TCMP-80), L-lysine-L-serine, is a synthetic dipeptide structurally related to a selected amino acid sequence in human immunoglobulin G. Based on in vitro and preclinical in vivo testing, TCMP-80 has immunomodulatory properties. This report describes the first administration of TCMP-80 to man in a randomized, double-blind, placebo-controlled, single rising-dose tolerability trial. Healthy male volunteers received TCMP-80 or placebo as a 10-minute intravenous infusion. At weekly intervals, two of four subjects were given TCMP-80; the remaining two received placebo. Each subject could receive only one dose during the study. Dosing started at 0.01 mg/kg and was increased to 0.03, 0.1, 0.3, 1, 3, 6.5, and 10 mg/kg. CBCs, blood chemistries, urinalyses, and lymphocyte subset populations were monitored predose and postdose on Days 1, 5, and 14. Three placebo and three TCMP-80 subjects reported adverse events. Adverse events reported after TCMP-80 administration were mild in nature (headache, dizziness, hematoma at injection site), appeared to be independent of dose, and resolved without medical intervention. No clinically significant alterations in vital signs, physical examination parameters, or clinical laboratory values were observed. Based on the results of this study, TCMP-80 is safe and well-tolerated within the dose range studied when administered as single intravenous infusions. Additionally, this study design represents an approach to assess the safety of an investigational immunomodulatory drug.
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PMID:Safety and tolerability of single intravenous doses of T cell modulatory peptide (TCMP-80) in healthy volunteers. 214 Mar 70

As recently demonstrated by our group, polymorphonuclear cells (PMNs) from cluster headache patients have an increased ability to incorporate arachidonic acid (AA) and L-serine into phosphatidylserine (PS). To evaluate whether there is an increased incorporation into PS also from fatty acids not involved in eicosanoid metabolism, PMNs from controls (n = 14) and cluster headache patients (n = 12) were incubated with (1-14C)oleic acid. After 1 h 2.7% +/- 1.1 (mean value +/- SD) of the glycerophospholipid radioactivity was found in PS in controls, whereas 4.2% +/- 1.2 was found in cluster headache patients (p less than 0.005). For phosphatidylcholine (PC) the corresponding figures were 74.2 +/- 5.4 in controls and 66.7 +/- 7.6 in cluster headache patients (p less than 0.01). The results suggest that the de novo biosynthesis of PS is increased and the biosynthesis of PC is decreased in cluster headache. The results may have an effect on the role of PS as an obligate protein kinase C activator.
Cephalalgia 1989 Sep
PMID:Cluster headache: incorporation of (1-14C)oleic acid into phosphatidylserine in polymorphonuclear cells. 250 62

It has recently been demonstrated by our group that polymorphonuclear cells (PMNs) from cluster headache patients incorporate more arachidonic acid (AA) into phosphatidylserine (PS) than PMNs from controls. In the present report, the incorporation of L-(U-14C)serine into PS in PMNs from 14 healthy volunteers and 12 cluster headache patients was studied. PMNs from controls incorporated 1194 +/- 578 (mean +/- SD) cpm of L-(U-14C)serine into PS, 268 +/- 292 cpm into phosphatidylethanolamine, and 57 +/- 71 cpm into sphingomyeline. The corresponding figures in cluster headache patients were 2365 +/- 841 cpm, 291 +/- 207 cpm, and 88 +/- 66 cpm, respectively. Incorporation of L-(U-14C)serine into PS was significantly increased (p less than 0.0004) in PMNs from cluster headache patients, whereas no significant difference was seen in other lipids. The results confirm that patients with cluster headache have an increased incorporation of precursors into PS in isolated PMNs, and they indicate that this is due to an increased de novo synthesis of PS.
Cephalalgia 1989 Sep
PMID:Increased incorporation of L-(U-14C)serine into phosphatidylserine in polymorphonuclear cells from cluster headache patients. 250 64

Twelve patients with advanced malignant disease were entered onto a Phase I study of escalating doses of beta-interferon serine given by 4-h i.v. infusion twice a wk. Three patients each were entered at starting doses of 0.01, 1, 10, and 30 million units (MU)/m2. Doses escalation within individual patients was allowed to a maximum dose of 400 MU/m2. Fever, chills, fatigue, and acral cyanosis were commonly seen and increased in frequency at higher doses. Myalgia, nausea, diarrhea, headache, and confusion were seen at lesser frequencies. Mild leukopenia, paresthesia, infusion site erythema, and hypotension were each seen in one patient. No conventional maximal tolerated dose could be defined, since several patients underwent escalation to the highest allowable dose and seemed to develop tolerance to acute toxicities. However, a maximal starting dose of 10 MU/m2 was identified, such that those begun at this level or below tolerated semiweekly dose escalation, while those begun at 30 MU/m2 could not tolerate continued therapy. Detectable serum interferon levels were noted during treatment at 10 and 30 MU/m2, the levels at which significant toxicity also first appeared. A maximal starting dose of 10 MU/m2, with gradual escalation as tolerance to side effects develops, is suggested if therapy with high-dose beta-interferon serine is given by 4-h infusion.
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PMID:Phase I study of recombinant beta-interferon given by four-hour infusion. 380 98

Amino acid levels in plasma were measured by amino acid autoanalyser in 130 convulsive children. The levels of taurine, serine and tryptophan were significantly lower in convulsive children as compared to normal control; in contrast, isoleucine, homocystine, GABA, histidine, arginine and ammonia were higher. The children with paroxysmal disorders (headache, dizziness and abdominal epilepsy) had the highest levels of isoleucine, histidine and arginine and the lowest levels of glutamate and cystein. Clinical seizure activity within 6 months prior to the test seemed to have no obvious effect on the plasma amino acid pattern, except for the levels of glycine and arginine tended to return to normal, and the level of GABA was significantly increased in patients with the seizure being controlled. The patients treated with carbamazepin as a single anticonvulsant had the highest GABA level compared to those with other anticonvulsants. Hyperglycinemia and hyperammonaemia were also noted in patients who took valproic acid. The levels of serine, isoleucine and phenylalanine in the CSF within 6 hours after convulsion were significantly lower than the normal control; while asparagine, tyrosine, lysine and arginine were significantly higher. The concentration of ammonia in the CSF was also elevated after convulsion as compared to the normal control. Amino acids play an important role in the generation of epilepsy and recently there has been an increasing number of studies to help determine their effects during an epileptic attack. However, there still is much debate and controversy on this topic. Therefore, further studies are needed and researchers should carefully consider factors that might affect the accurate assessment of the results.
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PMID:Alteration of amino acid in plasma and cerebrospinal fluid of children with seizure disorders. 851 Jan 96

Cavernous angiomas are vascular malformations that cause neurodegeneration and symptoms including epileptiform seizures, headache, and motor deficits. Following neurosurgical removal of the angiomas, patients mostly recover well and become seizure-free. This study reports on the levels of certain amino acids in angiomas, obtained from 13 patients. Distinct zones of the angiomas were analyzed, from the thrombotic core, via gliotic, hemosiderin-infiltrated intermediate zones, to a periphery without macroscopic abnormalities. The neurotransmitter amino acids glutamate, aspartate, and GABA as well as phosphoethanolamine displayed decreasing levels from the periphery to the core, reflecting the gradual neuronal loss. Compared with normal brain tissue, there was a marked increase in the levels of serine (fivefold), glycine (10-fold), and ethanolamine (20-fold) in the peripheral zone of the cavernous angiomas. The results are discussed in relation to seizures and NMDA receptor activation, neuron-glia interactions, membrane phospholipids, and blood-brain barrier function.
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PMID:High levels of glycine and serine as a cause of the seizure symptoms of cavernous angiomas? 866

A 32-year-old man of Irish descent presented with severe progressive headache and sensorineural hearing loss. MRI/magnetic resonance angiography head scans were normal. A length-dependent sensorimotor peripheral neuropathy with autonomic dysfunction predated these symptoms. Systemic organ involvement and transthyretin (TTR) amyloid immunostaining of bone marrow and fat aspirate were documented. Direct DNA sequencing revealed both the normal TTT (phenylalanine) and a new variant TCT (serine) at position 44 of the TTR gene. This case expands the genotypic and phenotypic variability within TTR amyloidosis.
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PMID:Transthyretin amyloidosis (serine 44) with headache, hearing loss, and peripheral neuropathy. 981 83

There are a number of hypotheses concerning the pathogenesis of migraine, but they are frequently conflicting. In addition to the vascular hypothesis, clinical data are available that excitatory amino acids may play an important role in the development of the disease. In this study, free amino acid concentrations were measured by RP-HPLC in the saliva of 23 migraineurs without aura, 14 migraineurs with aura, and 20 healthy subjects. Significantly higher concentrations of glutamic acid, serine, glycine, arginine, and tyrosine were found in the saliva samples of both groups of migraineurs relative to the control group. It is suggested that amino acids causing hyperexcitability in the central nervous system may be linked to the pathogenesis of migraine.
Headache 1999 Oct
PMID:Amino acids in the saliva of patients with migraine. 1127 59

Neurological disturbances frequently emerge in antiphospholipid syndrome (APS). One hundred and twenty four patients (100 women, 24 men, mean age 37.5 +/- 11.3 years) with primary APS (PAPS), including 76 patients with Sneddon's syndrome and positive antibodies to phospholipids (aPL), have been studied. A structure of neurological disturbances was as follows: ischemic lesions of cerebral blood flow (LCBF) which comprised stroke and transient LCBF (91%); thrombosis of brain venous sinuses (3%); epileptic seizures (24%); headache (65%); chorea (15%); visual neuropathy (9%); peripheral neuropathy (6%); multiple-sclerosis-like syndrome (10%); myasthenia syndrome (1%); syndrome of parkinsonism of non-vascular genesis (1%) and psychotic disorders (2%). 84% patients had main systemic APS symptoms (fetal loss, thrombosis), which preceded neurological appearances in 78% cases. All the patients had aPL: aPL to cardiolipin (aCL) and/or lupus coagulant (LC) and/or aPL to phosphatidyl serine, phosphatidyl inositol, phosphatidyl ethanolamine. In some patients, aCL titres ranged from positive to negative values and LC was not consistently detected. Thus, the presence of clinical symptoms of PAPS including neurological disturbances demands an investigation of different aPL types as well as a replicate study for immunological confirmation of PAPS.
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PMID:[Neurological appearances of primary antiphospholipid syndrome]. 1598 22


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