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

Many conditions in clinical neurology may be responsive to pyridoxine as a therapeutic agent. The current difficulty is in trying to isolate the conditions that are most likely to respond. Treating seizures is a major part of a neurologic practice. Our current therapeutic agents are only partially successful and limited by multiple side effects. One problem is that patients often have to take these agents for an entire lifetime, further raising the risk of toxicity. If pyridoxine supplementation can improve the efficacy of currently used medications, it will be gladly accepted into our therapeutic arsenal. Headache, chronic pain, and depression all appear to run together in many of our patients. The observations that serotonin deficiency is a common thread between them and that pyridoxine can raise serotonin levels open a wide range of therapeutic options. Small studies have been carried out with mixed success. Comparison with amitriptyline in the treatment of headache appears to show about equal efficacy, although side effects would be expected to be more of a problem with the amitriptyline. Behavioral disorders are relatively common and continue to be a major problem, disrupting the lives of the patients and their families. Current treatments are not acceptable to most people because of the risk of side effects with long-term usage. If, as Dr. Feingold suggests, many of these problems are caused by "toxic" exposures to chemicals that are pyridoxine antagonists, supplementation at early ages may reduce the incidence of hyperactivity and aggressive behavior. This raises the question of safety. Is pyridoxine safe for long-term use in large segments of the population, including children? The studies on children with Down's syndrome and autism, utilizing much higher doses than are used for other therapeutic purposes, seem to indicate relative safety if carefully monitored. Studies involving large population groups with carpal tunnel syndrome, all adults, using 100-150 mg/day have shown minimal or no toxicity in five- to 10-year studies. Women self-medicating for PMS taking 500 to 5000 mg/day have shown peripheral neuropathy within one to three years. It would appear from this retrospective analysis that pyridoxine is safe at doses of 100 mg/day or less in adults. In children there is not enough data to make any sort of suggestion. Because the major neurologic complication is a peripheral neuropathy and the causes of this condition are myriad, pyridoxine may cause neuropathy only in patients with a pre-existing susceptibility to this condition.
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PMID:Vitamin B6 in clinical neurology. 216 44

We reported a case of pure trigeminal motor neuropathy. A 57-year-old man was admitted with the complaints of vague headache and left upper limb numbness. Neurological examination showed mild wasting of the right masseter muscle on chewing. The jaw deviated to the right when he opened his mouth fully. Corneal reflex was intact bilaterally and so was the sensation on the face and taste. Mild hemiparesis including the face was observed on the left. Laboratory data including cerebrospinal fluid analysis were normal except for mild glucose intolerance. Blink reflex, brainstem auditory response and trigeminal sensory evoked potential elicited by electric stimulation of the lower lip were all normal. EMG findings obtained from the left masseter and lateral pterygoid muscles were neurogenic. The CT scan demonstrated a characteristically distributed low density area, which substituted the muscle supplied by the motor branch of he trigeminal nerve, namely, the right masseter, temporalis, lateral and medial pterygoid muscles. With MRI, the lesion was high on T1 and T2 weighted images. In addition, spotty high signal intensities suggestive of small infarction were observed in the bilateral centrum semiovale on T2 weighted images. Judging from the above results, the present case was believed to have pure motor trigeminal neuropathy confirmed by electrophysiological findings and image analyses together with clinical features. The mild left hemiparesis was thought to be incidental complication of vascular origin.
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PMID:[A case of pure trigeminal motor neuropathy]. 225 26

Malignant external otitis (MEO) is a disease of the external auditive channel (EAC) due to Pseudomonas aeruginosa which usually involves individuals with diabetes mellitus. It may result in the invasion of the cranial base with cranial neuropathy and a high mortality rate despite therapy. We report the clinical features, diagnostic procedures, evolution and therapy of 8 patients with MEO, seven of which had cranial neuropathy. All patients have diabetes except one who had acquired immunodeficiency syndrome. All had otalgia, otorrhea and headache lasting for several months. Six patients had homolateral (as related to the MEO) facial palsy. One patient with bilateral MEO developed bilateral facial palsy and lesion of the cranial nerves VI (unilaterally) and IX through XII (bilaterally). In all patients P. aeruginosa was cultured from the EAC exudate scintigraphy with 99Tc showed uptake at medium ear and mastoid level in all 8 patients, suggesting a possible osteomyelitis. Scintigraphy with 67Ga was positive in the 6 cases where it was carried out, showing uptake in the soft tissues of the cranial base. Computed tomography was carried out in 6 patients, and it was useful to define the anatomical extent of the disease. The patients received different therapeutic schedules, particularly the combination of a betalactamic and aminoglucoside antibiotics. Follow up was characterized by common recurrences, and one patient died. The importance of early diagnosis and treatment to prevent the extension and recurrence of MEO are discussed. Cranial neuropathy is considered as a poor prognostic finding.
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PMID:[Otitis externa maligna and cranial neuropathy]. 228 52

2-Phenoxyethanol, used as an anesthetic for handling small fish at a salmon hatchery, caused three women to experience headache and symptoms of intoxication during use, followed by diminished sensation and strength of hands and fingers, worse in the preferred hand. Persistent neuropathy did not develop in any of them. After 1 to 2 years of exposure, the women manifested gradual onset of symptoms of cognitive impairment with an inability to work. Neuropsychologic testing verified that all three had focal cognitive impairments that persisted. One also had documented labyrinthine hypofunction, which originated during this exposure. The immediate and delayed effects of 2-phenoxyethanol on the central nervous system resemble those of the other organic solvents.
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PMID:Occupational phenoxyethanol neurotoxicity: a report of three cases. 232 42

The most common indications for treatment of patients with pseudotumor cerebri are the presence of severe intractable headaches and evidence of optic neuropathy. The role of the ophthalmologist in following patients with pseudotumor cerebri has been to document optic nerve dysfunction in terms of visual field abnormalities or loss of visual acuity. Macular changes have been described in association with papilledema. A case of pseudotumor cerebri and associated macular disease is reviewed to call attention to the need for the ophthalmologist to differentiate between visual loss secondary to optic neuropathy from that of macular disease. The case illustrates how quickly macular disease can develop. The management of patients with pseudotumor cerebri is discussed.
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PMID:Pseudotumor cerebri and macular disease. 247 98

Blood plasma beta-endorphin concentrations were measured in 87 patients with various facial and head pain syndromes: trigeminal neuralgia or neuropathy Horner syndrome and migraine, facial autonomic pains. beta-endorphin concentrations were measured before and after treatment. In the groups under investigation, the neuropeptide showed opposite changes in plasma levels after the therapy depending on the type of the syndrome.
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PMID:[Beta-endorphin levels in patients with pain syndromes in the areas of the face and head]. 253 37

Ocular complications occurring in temporal arteritis are of different severities. These manifestations of the disease occurred in a population of 57 patients with diagnosis of temporal arteritis, in 16 of them (28%). The diagnosis was suggested by finding an inflammatory syndrome (high erythrocyte sedimentation rate) and confirmed by temporal artery biopsy. In making this diagnosis, it was helpful to find a history of characteristic temporal headaches, neckache, jaw claudication, fever and malaise or weight loss in addition to polymyalgia and polyarthralgia. 6 patients presented with diplopia and different ocular muscle or nerve palsies. The 10 others came for sudden loss of vision due to ischemic anterior or posterior neuropathy and in one case, central artery obliteration. Prompt treatment with steroids gave good results on oculomotor troubles and in preventing the risk of involvement of the fellow eye. But loss of vision did not regress with this treatment. That means the importance in making this diagnosis and starting very promptly this treatment.
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PMID:[Eye manifestations of Horton's disease]. 259 Sep 88

A report on 8 patients with idiopathic multiple cranial neuropathy is presented. The syndrome consists of headache, facial pain and diplopia preceding the onset of cranial nerve palsy. The cranial nerves most frequently involved were the third, fifth and seventh. All patients were treated with corticosteroid therapy. The symptoms were self-limiting in their course and corticosteroid therapy appeared to hasten recovery of function. Only in a few cases a noticeable neurological deficiency remained. Differential diagnosis and etiological considerations are discussed.
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PMID:Idiopathic multiple cranial neuropathy. A twenty year experience. 273 41

A 29-year-old woman presented with acute hemicrania, trigeminal neuropathy and posterior fossa dysfunction. The admission differential diagnosis included vertebral artery dissection, posterior circulation aneurysm, vascular malformation and brainstem infarction. However, radiographic and CSF studies indicated demyelination. Acute demyelination should be in the differential diagnosis of vascular hemicrania with signs of posterior fossa dysfunction.
Headache 1989 Jul
PMID:Acute demyelination mimicking vascular hemicrania. 275 50

In a Nigerian town with a stable population of 20,000, a door-to-door survey was conducted, using a questionnaire involving a complete census and a simple neurological evaluation which had previously showed a 95% sensitivity and an 80% specificity for detecting neurological disease. Positive responders were evaluated and categorised, using agreed criteria for diagnoses. Nearly 100% cooperation was obtained. Life prevalence ratio for at least one episode of headache was 51/1000. Crude point prevalence ratio for migrainous headache was 5.3/100, and peak age-specific ratio was in the first decade. Prevalence ratio for epilepsy was 533/100,000 and peak age-specific prevalence ratio occurred in the 5-14 years age groups. The prevalence ratio for peripheral nerve disorders was 268/100,000, and age-specific prevalence ratio for tropical neuropathy increased with age. Prevalence ratio for stroke was rather low at 58/100,000, but was probably due to the people's attitude to the disabled elderly and high mortality of stroke which showed annual mortality rate of 70/100,000 which increased with age to 1519/100,000 per year in the eighth decade. Crude prevalence ratios (cases per 100,000) for others are 112 for neurological complications (including sciatica) of spondylosis, 15 each for poliomyelitis, motor neurone disease, development speech disorders, 10 each for syncope, hereditary neuropathies. Parkinson's disease, benign essential tremor, primary cerebellar degeneration, cerebral palsy, mental retardation, organic psychosis (probable intracranial tumor) and 5 each for muscular dystrophy, pyomyositis, spina bifida occulta, alcohol dependence and cerebral malaria. The implications of the findings are important for development of community neurological services in the developing countries.
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PMID:Neurological disorders in Nigerian Africans: a community-based study. 303 73


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