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

The HIV epidemic probably arose in Africa at about the same time as in the West, and there is a significant seroprevalence of HIV in the central African region. However, the epidemiology and clinical course of AIDS are different in Africa and in the West. In Africa males are infected as often as females, and the commonest means of transmission is heterosexual intercourse. Many HIV-infected people are symptomless, but many others present with or progress to generalized lymphadenopathy, pruritus, herpes zoster, herpes simplex, cellulitis, and oral candidiasis. The World Health Organization developed a clinical case-definition of AIDS in Africa, which was found to have a specificity of 90% and a sensitivity of 59% when tested in Zaire. The Kaposi's sarcoma seen in African AIDS patients is more aggressive than that seen in the West and is often visceral. Gastrointestinal AIDS (the "slim" disease) with weight loss and diarrhea is common in Africa, as are oral and esophageal candidiasis. In Africa Pneumocystis carinii pneumonia is rare, but pulmonary tuberculosis is common. Neurological manifestations include cerebral toxoplasmosis, cytomegalovirus infection, headache, and terminal encephalopathy. About 60% of infants born to seropositive women are infected and die within the 1st year of life. Lack of drugs and diagnostic facilities make both diagnosis and treatment of opportunistic infections difficult.
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PMID:Clinical aspects of HIV infection in developing countries. 305 40

2 cases reports are described of patients with renal artery stenosis who presented with hypertensive encephalopathy, normal blood pressures having been recorded within the previous 6 months while taking oral contraceptives (OCs). A 27-year-old woman, admitted to the hospital following 2 grand mal fits, had suffered from increasing headaches, nausea, and vomiting over the previous month. Her blood pressure had been elevated at 160/110 mmHg 1 week prior to admission but had been normal over previous 11 years while taking OCs (various formulations of combined estrogen and progestogen) which she had stopped taking 2 months previously. She was a nonsmoker. Her blood pressure was controlled with atenolol, nifedipine, and bendrofluazide, and her conscious level returned to normal with no further fits. An intravenous urogram revealed a small left kidney with a delayed nephrogram, and subsequent arteriography showed bilateral medial fibromuscular dysplasia with a narrow stenosis of the left renal artery. Attempted balloon angioplasty was unsuccessful due to arterial spasm. 4 months after presentation she became pregnant. Blood pressure was controlled with methyl dopa during pregnancy which progressed uneventfully to full term. In the 2nd case, a 19-year old girl became confused and suffered a grand mal convulsion. She had complained of headaches over the previous 3 days. Her blood pressure had been normal over the previous 6 months while taking Logynon (phased formulation of ethinylestradiol and levonorgestrel). She was a nonsmoker. On admission to the hospital, she suffered further generalized convulsions. Despite control of her convulsions with intravenous chlormethiazole, her blood pressure rose to 220/140 mmHg, and this was controlled with intravenous hydralazine and propranolol. The following day she was conscious and was changed to oral therapy. A renogram and DMSA scan showed normal sized kidneys, but there was evidence of decreased blood flow to the left kidney with an increased transit time. Renal arteriography showed a stenosis of the left renal artery, typical of intimal fibromuscular dysplasia, which was dilated by balloon angioplasty. Anti-hypertensive medication was withdrawn postoperatively, and her blood pressure has remained well controlled. In both of the cases the onset of hypertension was rapid with encephalopathy being the presenting feature. Hypertensive encephalopathy is well recognized as a presenting feature of renal transplant artery stenosis but not in cases of native renal artery stenosis. 1 of the patients had stopped using OCs 2 months before presentation, suggesting that although there may have been an association between OC use and the development of fibromuscular dysplasia, it could not be implicated in the mode of presentation.
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PMID:Encephalopathy in renovascular hypertension associated with the use of oral contraceptives. 311 27

A seventy-two-year-old man with hypertensive cerebral hemorrhage acutely developed severe headache, nausea, vomiting, agitation, and disorientation with abrupt rise in blood pressure on the sixth day after the onset. At that time, there were no remarkable changes in focal neurologic deficits, and repeated brain CT scans revealed a small hematoma located in the right basal ganglia without further enlargement or herniation. Blood chemistry and arterial gas analysis were within the normal ranges except for a slight rise in blood urea nitrogen. Similar episodes occurred three times within two days, and each time the cerebral symptoms disappeared in accordance with lowering of blood pressure by antihypertensive therapy. Complication of hypertensive encephalopathy was strongly suggested. The authors discuss the pathophysiology of this encephalopathy in relation to cerebral hemorrhage.
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PMID:Transient encephalopathy related to rapidly and markedly elevated blood pressure in acute stage of hypertensive cerebral hemorrhage--relationship to hypertensive encephalopathy--a case report. 317 64

Blunt trauma to the head results in acceleration of the brain within the skull. This takes 2 forms: linear or translational acceleration which produces focal lesions, and rotational acceleration which results in 'sheering stresses' with stretching of nerves and bridging veins. Deceleration of the brain within the skull occurs when the head strikes a stationary object (e.g. floor, ring post). Cerebrovascular events are not infrequently encountered. The most common vascular sequalae is the subdural haematoma, which is also the most frequent cause of death in boxers. Epidural bleeds rare, and are generally due to deceleration of the brain. Subarachnoid bleeds have been rarely reported, but, like intraparenchymal haemorrhages, they do occur. Sudden flexion/extension of the neck is suggested as the mechanism of the occasional brainstem haemorrhage reported in boxing. Thrombosis of the internal carotid artery can occur secondary to direct blows to the neck or stretching of the contralateral carotid artery. The best known sequalae of boxing is traumatic encephalopathy--the 'punch drunk' syndrome. This is most common in second-rate and slugging type fighters. Severity correlates with the length of a boxer's career and total number of bouts, with an incidence of approximately 18%. Three stages of clinical deterioration are seen, the encephalopathy may be progressive or may remain clinically stable at any level. The first stage consists of affective disturbances with psychiatric symptoms being most marked. During the second stage an accentuation of the psychiatric symptoms occurs and signs/symptoms of Parkinsonism develop. The final stage consists of a decrease in general cognitive function together with pyramidal tract disease. Generally 2 to 3 years elapse between the first and final stages. Neuropathological studies reveal abnormalities of the septum pellucidum, scarring of the cerebellar and cerebral cortices, and loss of pyramidal neurons in the substantia nigra with neurofibrillary tangles in the absence of senile plaques. A 'groggy state' can occur in some fighters with confusion, impaired active attention and alteration of consciousness. During this period the boxer is at greater risk to suffer brain injury as defensive reflexes are frequently lost. Other neurological syndromes have been reported in addition to the 'groggy state'. These include a midbrain syndrome, headaches and cervical spinal injuries. Additionally, boxing appears to be a significant risk factor for the development of meningiomas.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Neurological sequelae of boxing. 329 90

Sixty-two patients with chronic toxic encephalopathy diagnosed in 1976-1981 were considered for reexamination in 1983-1984. Thirteen were found to have other diseases that might contribute to brain dysfunction. Seventeen were unwilling or unable to participate. The final group consisted of 32 men 33 to 63 (median 55) years of age who were physically and psychometrically reexamined with the same methods used in the initial investigation. The interval between the first and present examination was 21-88 (median 48) months, and exposure to solvents had ceased. The subjects reported some improvement in their neurasthenic problems. In particular they suffered less from fatigue, headache, and dizziness. When diagnosed they had an average of seven out of ten typical neurasthenic symptoms included in the toxic encephalopathy syndrome. At the time of the follow-up the mean number of symptoms had decreased significantly to five. The psychometric retesting showed significant deterioration in verbal memory, improvement in visual memory, and unchanged results on the other tests. In conclusion, these toxic encephalopathy patients improved subjectively when exposure stopped. Psychometrically they performed very close to the initial testing, which excluded progressive brain disease or subacute pharmacological solvent intoxication.
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PMID:Prospective clinical and psychometric investigation of patients with chronic toxic encephalopathy induced by solvents. 335 95

Lyme disease typically begins with a unique skin lesion, erythema chronicum migrans (ECM) (stage 1). Patients with this lesion may also have headache, meningeal irritation, mild encephalopathy, multiple annular secondary lesions, malar or urticarial rash, generalized lymphadenopathy and splenomegaly, migratory musculoskeletal pain, hepatitis, sore throat, non-productive cough, conjunctivitis, periorbital edema, or testicular swelling. After a few weeks to months (stage 2), about 15% of patients develop frank neurologic abnormalities, including meningitis, encephalitis, cranial neuritis (including bilateral facial palsy), motor or sensory radiculoneuritis, mononeuritis multiplex, or myelitis. At this time, about 8% of patients develop cardiac involvement--AV block, acute myopericarditis, cardiomegaly, or pancarditis. Throughout this stage, many patients continue to experience migratory musculoskeletal pain in joints, tendons, bursae, muscle, or bone. Months to years after disease onset (stage 3), about 60% of patients develop frank arthritis, which may be intermittent or chronic. Recently evidence suggests that Lyme disease may also be associated with chronic neurologic or skin involvement. Thus, Lyme disease occurs in stages with different clinical manifestations at each stage, but the course of the illness in each patient is highly variable.
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PMID:Clinical manifestations of Lyme disease. 355 39

Lumbar myelography was performed with high volumes of iohexol (15-24 ml) at a concentration of 180 mgI/ml (average dose, 20 ml) in 48 patients. In 44 patients receiving more than the currently recommended upper dose limit of 17 ml, the frequency of headache (41%), nausea (14%), and vomiting (9%) was comparable to results for routine-dose lumbar metrizamide myelography. Overall, adverse reactions were more frequent, particularly at the highest dose levels, than reported for conventional-dose iohexol myelography. However, there were no occurrences of neuropsychiatric disorder, encephalopathy, or seizure. High-dose technique allows superior visualization of upper lumbar and conus detail and may be advantageous in patients with large subarachnoid spaces and in multi-level examinations. This study supports the results of previous trials that suggested the relative safety of iohexol as a contrast agent and extends those observations to a higher dose range. Because of the increased rate of adverse reactions at the highest dose levels (despite the absence of major adverse reactions), iohexol should continue to be used conservatively, with doses carefully tailored to each examination.
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PMID:High-dose iohexol myelography. 356 26

Dementias which are either reversible or avoidable are discussed in the light of the literature. The frequency is between 6 and 32%. The most important etiological groups are immunological vasculopathies, hyperlipidemia, some types of encephalitis and, mainly, progressive dementia of the insane, benign tumors and in particular meningioma, low pressure hydrocephalus, intoxications due to drugs, industrial products and alcohol, metabolic disturbances, encephalopathy in dialysed patients, ileo-jejunal-bypass encephalopathy and encephalopathy due to neoplasms. Dementias are also seen in endocrinological disturbances and particularly in hypothyroidism. Vitamin B12 and folate deficiency, as well as epilepsy, may be causes of dementia. Depression may mimic a state of dementia. Some features of reversible dementias are listed, including in particular the somewhat more rapid onset, the younger age of patients, and accompanying neurological symptoms such as headache, gait disturbances, ataxia, polyneuropathy, myoclonus or epileptic fits.
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PMID:[Reversible and preventable dementias]. 361 87

Fourteen patients infected with human immunodeficiency virus (HIV) had a lymphocytic pleocytosis unexplained by secondary pathogens or neoplasms. Three men had prior diagnoses of Kaposi's sarcoma; none had acquired immune deficiency syndrome-defining opportunistic infections. Two patterns of illness were observed. Seven men had an acute, self-limited illness that was often accompanied by meningeal findings. The other seven had chronic headaches without signs of meningeal irritation and had less marked abnormalities of cerebrospinal fluid (CSF) cell count and protein. Encephalopathy was a finding in only one of 14 patients. In four of five CSF specimens studied, HIV was recovered. HIV has been associated with acute meningitis at the time of seroconversion and can apparently also cause sporadic episodes of acute or chronic meningitis in patients with prior infection and relatively preserved immune function. Both the clinical presentation with predominant headache rather than encephalopathy and the presence of CSF inflammation differentiate this syndrome from other HIV-related neurologic complications.
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PMID:Human immunodeficiency virus-associated meningitis. Clinical course and correlations. 367 88

A 14-year-old boy with a tetralogy of Fallot showed a subacute, progressive encephalopathy characterized by headache, stupor and coma. Death occurred three months after the beginning of the illness. Neuropathologic examination revealed diffuse foci of necrosis of the cerebral hemispheres and cerebellum, and the presence of the nematode Lagochilascaris minor in the parenchyma and in the cisterns at the base of the brain. In almost all 28 cases of human lagochilascaris previously reported, the worms were located in the soft tissues of the neck and throat, tonsils, mastoids and paranasal sinuses. This is the first reported case in which Lagochilascaris infected the brain. Since the life cycle of the worm is unknown the pathogenesis of the central nervous system lesions is obscure.
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PMID:Fatal encephalopathy due to Lagochilascaris minor infection. 370 24


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