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

Vitamins contain reactive functional groups necessary to their established roles as coenzymes and reducing agents. Their reactive potential may produce injury if vitamin concentration, distribution, or metabolism is altered. However, identification of vitamin toxicity has been difficult. The only well-established human vitamin neurotoxic effects are those due to hypervitaminosis A (pseudotumor cerebri) and pyridoxine (sensory neuropathy). In each case, the neurological effects of vitamin deficiency and vitamin excess are similar. Closely related to the neurological symptoms of hypervitaminosis A are symptoms including headache, pseudotumor cerebri, and embryotoxic effects reported in patients given vitamin A analogs or retinoids. Most tissues contain retinoic acid (RA) and vitamin D receptors, members of a steroid receptor superfamily known to regulate development and gene expression. Vitamin D3 effects on central nervous system (CNS) gene expression are predictable, in addition to the indirect effects owing to its influence on calcium and phosphorus homeostasis. Folates and thiamine cause seizures and excitation when administered in high dosage directly into the brain or cerebrospinal fluid (CSF) of experimental animals but have rarely been reported to cause human neurotoxicity, although fatal reactions to i.v. thiamine are well known. Ascorbic acid influences CNS function after peripheral administration and influences brain cell differentiation and 2-deoxyglucose accumulation by cultured glial cells. Biotin influences gene expression in animals that are not vitamin-deficient and alters astrocyte glucose utilization. The multiple enzymes and binding proteins involved in regeneration of retinal vitamin A illustrate the complexity of vitamin processing in the body. Vitamin A toxicity is also a good general model of vitamin neurotoxicity, because it shows the importance of the ratio of vitamin and vitamin-binding proteins in producing vitamin toxicity and of CNS permeability barriers. Because vitamin A and analogs enter the CNS better than most vitamins, and because retinoids have many effects on enzyme activity and gene expression, Vitamin A neurotoxicity is more likely than that of most, perhaps all other vitamins. Megadose vitamin therapy may cause injury that is confused with disease symptoms. High vitamin intake is more hazardous to peripheral organs than to the nervous system, because CNS vitamin entry is restricted. Vitamin administration into the brain or CSF, recommended in certain disease states, is hazardous and best avoided. The lack of controlled trials prevents us from defining the lowest human neurotoxic dose of any vitamin. Large differences in individual susceptibility to vitamin neurotoxicity probably exist, and ordinary vitamin doses may harm occasional patients with genetic disorders.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Vitamin neurotoxicity. 146 88

A literature review and an own case observation of neurological and psychiatrical disturbances in vinyl chloride disease are presented. In acute vinyl chloride intoxication, patients complain of vertigo, nausea and headache. At higher concentrations, vinyl chloride exerts a narcotic effect. In patients with chronic occupational exposure, neurological disturbances include sensory-motor polyneuropathy, trigeminal sensory neuropathy, slight pyramidal signs and cerebellar and extrapyramidal motor disorders. Psychiatric disturbances present as neurasthenic or depressive syndromes. Sleep disorders and disorders of sexual functions are frequently encountered. Pathological EEG alterations can be found in a high proportion of patients. The long term course and prognosis of the neurological and psychiatrical disorders in vinyl chloride disease are obscure. In an own case, a slight sensory polyneuropathy, bilateral hyposmia, a marked neurasthenic syndrome, typical EEG changes and computed tomography signs of cerebral atrophy were found in a 56-years-old patient as late as 16 years after the exposure to vinyl chloride.
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PMID:[Neurologic and psychiatric disorders in vinyl chloride disease]. 227 28

Neurological examination of 28 patients, 4 years after serious poisoning by polychlorinated biphenyl contaminated cooking oil, are compared with similar examinations of the same patients two years earlier (in 1980). Clinical peripheral sensory neuropathy was found in 54%, headache in 36% and dizziness in 46% of the patients; these findings did not differ (p greater than 0.1) from those in 1980. Although the mean blood polychlorinated biphenyl concentration (19.2 ppb) in the patients was lower (p less than 0.001) than that in 1980 (35.9 ppb), it was still higher than the normal value (less than 4 ppb). There was no difference in the blood polychlorinated biphenyl concentration of patients with neurological manifestation from those without. Although the mean motor and sensory nerve conduction velocities (MNCV and SNCV) were still slower (p less than 0.06) than the mean normal NCV, the mean MNCV of tibial nerve and SNCV of sural nerve were improved (p less than 0.06) as compared with those in 1980. EEGs were normal except in two cases showing nonspecific slow wave changes. In addition, evoked potentials (somatosensory, visual and brain-stem auditory) were measured in this study and found to be normal in all 12 cases examined.
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PMID:A clinical and electrophysiological study of patients with polychlorinated biphenyl poisoning. 299 92

Thirty-five patients out of the 2,000 PCB-poisoned cases that occurred in central Taiwan in 1978 were neurologically studied in 1980. Neurological manifestation included clinical peripheral sensory neuropathy in about two thirds of the cases, headache in two-fifths and dizziness in one-third. There was no relationship between the blood PCB concentration in patients with neurological manifestation and those without. Sensory nerve conduction velocity was reduced in about half of the cases and motor nerve conduction was delayed in about one-third of the cases, which suggested that PCB poisoning apparently affected not only sensory nerve conduction but also motor nerve conduction. Normal CSF PCB concentrations (0.5-2.3 ppb) indicated that PCB had difficulty penetrating the blood-brain barrier. A mildly abnormal EEG pattern was found in one fifth of twenty-seven cases.
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PMID:Neurological studies on polychlorinated biphenyl (PCB)-poisoned patients. 642 42

Thirty-five patients out of the 2,000 PCB-poisoned cases that occurred in central Taiwan in 1978 were neurologically studied in 1980. Neurological manifestation included clinical peripheral sensory neuropathy in about two thirds of the cases, headache in two-fifths and dizziness in one-third. There was no relationship between the blood PCB concentration in patients with neurological manifestation and those without. Sensory nerve conduction velocity was reduced in about half of the case and motor nerve conduction was delayed in about one-third of the cases, which suggested that PCB poisoning apparently affected not only sensory nerve conduction but also motor nerve conduction. Normal CSF PCB concentrations (0.5-2.3 ppb) indicated that PCB had difficulty penetrating the blood-brain barrier. A mildly abnormal EEG pattern was found in one fifth of twenty-seven cases.
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PMID:Neurological studies on polychlorinated biphenyl (PCB)-poisoned patients. 642 46

(1) We evaluated efficacy of several treatments for HTLV-I-associated myelopathy (HAM) on the basis of our study on 254 HAM patients and of literature review. Improvement of motor disability more than fair response was obtained as follows: 82% in prednisolone, 69% in interferon-alpha, 92% in fosfomycin, 82% in high-dose vitamin C, 72% in blood purification therapy, 70% in heparin, 59% in salazosulfapyridine, 56% in thyrotropin-releasing hormone, 55% in erythromycin, 50% in mizoribine. (2) In the absence of clear guideline, the efficacy of zidovudine in the AIDS dementia complex has been demonstrated. There are also efficacy of amytriptylinein controlling HIV headache, corticosteroid in mononeuritis multiple and inflammatory myositis, hydrocortisone in autonomic neuropathy and plasmapheresis in distal sensory neuropathy respectively. Otherwise, it is emphasized that ddI, ddC and d4T have peripheral neuropathy as major, dose related side effect.
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PMID:[Therapy for HAM/TSP and AIDS]. 799 4

After liver transplantation, long-term cyclosporin A (CsA) administration is commonly complicated by renal insufficiency and other side effects. To manage these problems, 1.5 to 2.0 mg x kg(-1) x day(-1) of azathioprine for at least 6 weeks was prescribed; CsA was then discontinued or reduced to < or = 2.5 mg x kg(-1) x day(-1) for several months. The dose of prednisone was kept constant. CsA was discontinued in 14 patients because of nephrotoxicity (three or more serum creatinine levels of > or = 1.5 mg/dL), in 1 patient because of headaches and in 1 patient because of a generalized sensory neuropathy; 1 patient refused to continue taking the drug. The CsA dose was reduced in 13 patients, 12 because of nephrotoxicity and 1 because of headaches. One patient in whom administration of CsA was stopped developed azathioprine hepatotoxicity, whereas 1 patient whose dose was reduced developed acute cellular rejection. These complications were controlled by discontinuing azathioprine and reinitiating CsA. In the patients in whom CsA was discontinued, the mean serum creatinine level decreased from 2.42 +/- 0.48 to 1.72 +/- 0.39 mg/dL (P = .00004); in the patients in whom CsA was reduced, the mean serum creatinine level decreased less markedly. This report suggests that discontinuation of CsA along with increased doses of azathioprine is safe for some patients and may be effective in managing CsA-related nephrotoxicity and other side effects after liver transplantation. Additional studies are needed to determine whether this approach is safe and effective for the growing number of post-transplantation patients who may be candidates for such therapy.
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PMID:Cyclosporin A: drug discontinuation for the management of long-term toxicity after liver transplantation. 890 80

To describe three patients with recurrent severe paroxysmal headache precipitated by yawning. Pain elicited by yawning is a well-recognized clinical phenomenon in patients with cranial neuralgia, temporomandibular joint dysfunction syndrome and Eagle syndrome. Clinical history, neurological and oral examinations, brain magnetic resonance imaging (MRI), cranial nerve electrophysiological testing and skull X-rays are reported. In all the patients pain was induced by yawning; in the third patient pain was also triggered by eructation. None had history of migraine. Facial gestures and forceful opening of the mouth did not reproduce the pain. The first patient had retroauricular pain, simvastatin-induced myopathy and subclinical axonal peripheral neuropathy; the second patient had a post-viral benign sensory neuropathy; and the third had retroauricular and facial pain and no underlying neurological illness. Cranial nerve testing and MRI of the brain were normal except for a coincidentally found pituitary adenoma on the first patient. Headache or cranial pain with yawning may occur in patients with no apparent cause (primary yawning headache). It is a chronic, benign condition that requires no specific treatment but needs to be distinguished from secondary yawning headache, of greater clinical relevance.
Cephalalgia 2001 Jul
PMID:Primary yawning headache. 1153 3

Chronic inflammatory demyelinating polyneuropathy is a disorder typified clinically by motor and sensory neuropathy of at least 2 months' duration and pathologically by multifocal inflammatory demyelination. Its usual presentation is with features reflecting the polyneuropathy, namely limb weakness with hyporeflexia or areflexia and sensory symptoms of glove and stocking distribution. In this report, we detail the course of a 53-year-old man who presented to our neurological service with a severe headache in association with papilledema. The initial diagnosis considered was of possible primary intracranial pathology. Two months later, he developed limb weakness and sensory symptoms typical of chronic inflammatory demyelinating polyneuropathy. His headache, papilledema, and limb symptoms responded to oral corticosteroid therapy, the standard treatment for this type of neuropathy. We hypothesize that his headache and papilledema were due to the elevated cerebrospinal fluid protein level as a result of the polyneuropathy. To our knowledge, this is the first report of headache being a prominent and early symptom of this disorder.
Headache 1999 Apr
PMID:Chronic inflammatory demyelinating polyneuropathy presenting with headache and papilledema. 1561 28

Multiple myeloma is a disease in which angiogenesis is postulated to be a target for therapy. Based on this hypothesis, we conducted a phase II trial of ZD6474 (Zactima; a VEGFR inhibitor) 100 mg p.o. daily in patients with relapsed multiple myeloma. The primary efficacy endpoint was objective response as assessed by reduction in M protein. There were 18 patients with a mean age of 64 years. One patient was ineligible and one was not evaluable. Overall, ZD6474 was well tolerated and pharmacokinetic testing demonstrated that adequate drug levels were achieved. The most common drug-related adverse events were nausea, vomiting, fatigue, rash, pruritus, headache, diarrhea, dizziness, and sensory neuropathy, all of which were Grade I-II in severity. There were no drug-related serious adverse events. Laboratory adverse events were infrequent: one patient had Grade III anemia, and there were no Grade III changes in biochemistry. No significant QTc interval changes were seen. There were no responses in M protein levels. In conclusion, ZD6474 was well tolerated at a dose of 100 mg per day and achieved plasma levels predicted to inhibit VEGF signaling. However, this was not reflected in clinical benefit since none of the patients had a reduction in M protein.
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PMID:A phase II study of ZD6474 (Zactima, a selective inhibitor of VEGFR and EGFR tyrosine kinase in patients with relapsed multiple myeloma--NCIC CTG IND.145. 1679 11


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