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

AVMs are congenital malformations of central nervous system blood vessels. The majority of lesions become symptomatic prior to age 40. Hemorrhage and epilepsy are the most frequent presenting symptoms. Disabling headache, transient, progressive, and permanent neurological deficit, heart failure, hydrocephalus, macrocephaly, and intellectual impairment may also occur. Long-term mortality is approximately 18%, and morbidity leading to disability occurs in 30% of patients. Aggressive management when possible is indicated.
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PMID:Natural history and pathophysiology of arteriovenous malformations. 54 27

A 72-year-old patient had a meningotheliomatous meningioma that invaded through the skull and into temporalis muscle. One year following craniotomy for removal of the neoplasm, he developed headaches, diplopia, and proptosis of the left eye. Biopsy of the orbital contents revealed a malignant supporting tissue neoplasm having a resemblance to the previous meningioma. No curative therapy was possible and the patient died 33 months after diagnosis. Autopsy examination showed extensive residual intracranial neoplasm and a 3-cm metastasis in the liver. The metastatic tumor appeared similar to the meningioma and did not appear malignant histologically. The case illustrates the distinct histologic variations in meningiomas and the difficulties in predicting their biologic activity. Aggressive local behavior may indicate possible malignant areas in the neoplasm. Therefore, examination of the neoplasm should be thorough. Such a correlation may suggest malignant biologic potential.
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PMID:Meningioma with sarcomatous change and hepatic metastasis. 103 80

The neurophysiologic correlates of explosive rage and violence are uncertain and controversial. We recorded 17-channel electroencephalograms (EEGs), brainstem auditory-evoked potentials (BAEPs), and long-latency auditory-event-related potentials (AEPs) in 23 patients with impulsive, aggressive and violent behavior satisfying criteria for episodic-dyscontrol syndrome. Most patients also satisfied criteria for intermittent explosive disorder, although some had had conduct disorders in childhood or had previously used psychoactive substances. Sixteen of 23 patients had normal EEGs, while 7 had diffuse or focal slowing not ascribable to drowsiness or the effects of medication. They differed significantly from 20 age-matched patients with headaches, of whom 1 had an abnormal EEG (chi 2 = 4.68, p < 0.05), and from 24 depressed patients, all of whose EEGs were normal (chi 2 = 4.83, p < 0.05). Patients and normal control subjects did not differ in BAEP latencies. N100 and P160 AEP amplitudes were lower in episodic-dyscontrol patients than in control, but the difference was not significant. These findings suggest that non-specific cerebral dysfunction and EEG changes may be associated with disordered impulse or behavior control. Episodic dyscontrol may be associated with other evidence of minimal brain dysfunction.
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PMID:EEG and evoked potentials in episodic-dyscontrol syndrome. 129 92

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

In 81 depressed children aged 3 to 14 years the nonepileptic attacks could manifest the different psychopathological phenomena: 1, headaches before and after spells, non-systemic++ vertigo with imbalance and oculovestibular events with or without loss of consciousness; 2, orthostatic symptoms, syncope, cataleptoid seizures, Kloos seizures; 3, depersonalization and derealization episodes, deja vu and jamais vu states; 4, attacks with pain in the stomach and other organs, various other autonomic signs; 5, unsteady neurological signs: pareses, sensory, visual and speech disorders; 6, nightmares, oneiroid states, sleep-walking; 7, convulsive states, hyperkinesis; 8, psychomotor excitation and inhibition states; 9, behavioral spells with aggression. These states are differentiated from epileptic and hysterical attacks.
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PMID:[Clinical aspects of paroxysmal states in children with depression]. 258 6

This review of the effects of sex steroids and oral contraceptives (OCs) on neurologic function in health and disease covers the following: sex steroids and their interaction with neural tissues; the human menstrual cycle and OCs; and sex hormones and OCs in human neurologic disease, i.e., stroke (thromboembolic cerebral infarction, subarachnoid hemorrhage, vascular malformations, and cerebral venous thrombosis), migraine, movement disorders, nervous system neoplasm, and the peripheral nerve. The various sex hormones may exert their effects on the nervous system directly or undergo conversion to more active metabolites. Interactions of sex hormones with neural substrates subserve numerous activities essential to both the well-being and perpetuation of the individual and the species. These interactions are key to the sexual differentiation of the brain, control of the brain-pituitary-gonad axis, and to the establishment of normal patterns of sexual and aggressive behavior in both sexes. Additionally, they play a role in temperature regulation (progesterone), caloric homeostasis (estrogen), and possibly sensory discrimination. The potent influences exerted by sex steroids on catecholamine and indoleamine turnover and the colocalization of labeled E2 within catecholamine and luteinizing hormone-releasing hormone (LHRH) positive perikarya suggest that many of the physiologic effects of sex steroids are mediated by modulation of specific monoaminergic and peptidergic pathways. Estrogens and aromatizable androgens also induce irreversible structural alterations in the rodent hypothalamus during the neonatal and peripubertal periods that are predominantly synaptogenic. In adult mammals, estrogens induce pathologic changes in the hypophysiotropic hypothalamus that may contribute to reproductive senescence in some species. Data from a series of retrospective and prospective studies have implicated OC use as an independent risk factor for the development of hemorrhagic and nonhemorrhagic stroke. Hormonal changes accompanying the pregnant state and the estrogen (and possibly progestogen) content of OCs may be predisposing factors in thromboembolic cerebral infarction, subarachnoid hemorrhage, cerebral venous thrombosis, and bleeding from intracranial and spinal vascular malformations. There are well-documented temporal associations of migrainous headache with specific phases of the menstrual cycle and the modifying influences of pregnancy, the menopause, and OC use. Also well established are relationships between endogenous and exogenous sex hormones and chorea. Fluctuating sex steroids also influence neuropsychiatric states, such depression and neuroendocrine disorders.
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PMID:Neurology of sex steroids and oral contraceptives. 302 81

Two psychological defense mechanisms, repression and self aggression, were studied in 23 young female migraine patients who had not been receiving treatment for their complaints and in 23 relatively headache free matched controls. All subjects were psychology students. Each subject was classified as high or low on repression and self aggression using the defense mechanism inventory. During three separate sessions: adaptation, intelligence test and real-life stress (an examination which was part of the psychology curriculum) pulse amplitudes of the temporal and digital arteries, frontal, temporal and corrugator EMGs, forehead temperature, skin conductance, and heart and respiration rate were measured. The migraine patients showed a trend towards more repression of their emotions and significantly more self aggression than the controls. Self aggression appeared to be positively associated with the headache frequency in the migraine group. With regard to the physiological measurements, in both groups repressors showed a modest tendency to enhanced sympathetic activity. Self aggression was not found to be related to any physiological measure of sympathetic activity, but, instead, related to less temporal blood flow. In general, associations were found between psychological defense mechanisms and physiological activity, which is suggestive of the existence of physiological pathways along which emotional inhibition might contribute to an attack of migraine after a stressful situation.
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PMID:Migraine and defense mechanisms: psychophysiological relationships in young females. 334 55

The reports of 8 female patients who, because of recurrent headache, were using analgesic suppositories containing acetylsalicylic acid and paracetamol (Perdolan) for more than two years are analyzed. Symptoms were nonspecific: anal pain, rectal tenesmus or bleeding. The lesions were located within 8 cm from the anal verge and consisted of superficial ulcerations, fibrotic scar tissue and rectal stenosis. Biopsies showed non-specific inflammation, limited to the rectum. Rectal prolapse or intussusception was not associated. By discontinuing the use of suppositories, symptoms usually resolved; rectal stenoses required anorectal dilatations and in 2 cases surgical resection. When solitary rectal lesions are observed in the absence of rectal prolapse, chemical aggression of the rectal mucosa by use of suppositories containing acetylsalicylic acid should be considered.
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PMID:[Solitary lesions of the rectum caused by suppositories combining acetylsalicylic acid and paracetamol]. 358 73

Four patients aged 11, 11, 8 and 18 years, shunted in early childhood for hydrocephalus, were followed in the outpatient clinic for severe headache from 3 months to 2 years. The headache lasted for days and up to a week, was usually severe, and was often followed by screaming attacks or aggressive behavior. In all patients repeated computed tomography disclosed a normal ventricular system or slit ventricles. The intracranial pressure (ICP) was measured in all four patients and showed an increased intracranial steady-state pressure between 20-50 mmHg, plateau waves and, in two of the patients, a very high intracranial pulse-pressure amplitude. At operation all patients had dysfunction of the shunt (most often of the distal end). In three patients ICP monitoring post-operatively showed normal intracranial pressure without any abnormal increments from the normal steady-state pressure. Thus, severe headache can be the only symptom of long-standing shunt dysfunction, even without ventricular dilation. In shunted hydrocephalic children complaining of headaches, ICP measurement is highly recommended.
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PMID:Severe headache as the only symptom of long-standing shunt dysfunction in hydrocephalic children with normal or slit ventricles revealed by computed tomography. 387 15

Brain abscess is a formidable diagnostic and therapeutic problem with mortality ranging from 35% to 65%. It may occur at any age, and there is a male:female ratio of 2:1. Brain abscess arises from a contiguous focus of infection, direct implantation due to trauma, or hematogenous spread from a remote site. The commonest organisms isolated from brain abscess include streptococci, Staphylococcus aureus, Bacteroides species, and Enterobacteriaceae. Brain abscess frequently produces headache, vomiting, focal neurologic signs, and depressed level of consciousness. Fever and leukocytosis often are absent. Diagnosis is suggested by computerized tomography, but most cases require surgical confirmation. Optimal management consists of intensive antibiotic therapy. Aggressive surgical treatment is required in cases not responding to antimicrobial therapy. Long-term neurologic deficit occurs in up to 60% of cases.
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PMID:Brain abscess: recent experience at a community hospital. 400 2


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