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

300 patients with sleeping sickness have been admitted, at the AHT clinic of Daloa, over a time period of 22 months. The sex ratio of the patients is 1.5 males for 1 female; the mean age is 25.5 years. The most frequent signs and symptoms observed by clinical examination are: fever (30%), nodes (86.3%), prurigo (43.3%), splenomegaly (15.3%), hepatomegaly (1%), headache (72.6%), vigilance and sleeping disturbances (68.7%), perioral reflexes (67.6%), cheiro-oral reflexes (64.3%), movement disorders consisting of tremor, choreo-athetosis movements, buccal dyskinesia or seizures (35%), motor palsy and gait disorders (15%), tonus disturbances (12.3%), sensitivity abnormalities (17%), endocrine disorders (16.3%), psychiatric symptoms (6.3%). According to CSF status, 261 patients have been classified in second period (P2). This group, although biologically well defined, is in fact a miscellaneous group of clinical signs and symptoms ranging from apparently normal patients to sleeping comatose and cachectic patients. 93% of the patients in this group have peripheral signs associated with neurological symptoms. They are as frequent in the first period as in the second period, with a statistical significance. This is an argument to think that the CNS is early affected in the course of the disease. The classification of the patients in groups of increasing neurological impairments, is in accordance with this hypothesis. 89% of the patients in the second period have only slight neurological signs. This explain how difficult it is for a physician to use melarsoprol in the treatment of all patients classified in second period.
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PMID:[The different present-day clinical picture of human African trypanosomiasis caused by T. b. gambiense. Analysis of 300 cases from a focus in Daloa, Ivory Coast]. 284 37

A 60-year-old woman received a 3-day course of nine injections of "fresh" cells from fetal lamb ovary, placenta, brain (hypothalamus) and liver. There were no immediate complications, but a few days later she developed headache, fever and hemiparesis. She subsequently fell into a coma and died 3 weeks after her fresh cell therapy and 2 weeks after the onset of her clinical symptoms. Autopsy revealed perivenous leucoencephalopathy with a probably steroid-treatment-induced paucity of perivascular inflammation. Fresh cell therapy, clinical symptomatology and morphological findings suggest, though do not prove, that this patient's monophasic and probably immune-mediated disease is a rare fatal complication of fresh cell therapy.
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PMID:Fresh cell therapy followed by fatal coma. 287 34

The interest in mountain tracking and climbing has increased and there is a need for knowledge of altitude-related diseases. About one million non-acclimatized individuals annually frequent areas around 2,000 to 3,000 m above sea level and incur unpleasant symptoms in the form of acute altitude sickness or potentially fatal conditions such as pulmonary and/or cerebral oedema. Headache is the most prominent sign of acute altitude sickness but fainting fits, loss of appetite, hesitant gait, euphoria, or confusion also occur. Dyspnoea, cyanosis at rest, and a dry cough are signs of pulmonary oedema. Cerebral oedema may be feared when inexperienced climbers are afflicted by severe headaches, vomiting, and hesitant gait. Coma ensues relatively soon. Treatment consisting in descent to lower altitude, administration of oxygen, and possible medicinal therapy is effective if immediately introduced.
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PMID:[Altitude sickness]. 291 57

A 60-year-old woman who for many years had been taking salicylate-containing tablets for headaches, was admitted to hospital, in a somnolent state, because of increasing weakness, tiredness, memory and speech disorders, and tinnitus. Laboratory tests revealed a decompensated metabolic acidosis (pH 7.25), renal insufficiency (creatinine 2.3 mg/dl) and a decreased Quick value (63%). Whole-blood acetylsalicylic acid concentration was markedly elevated to 330 micrograms/ml. After treatment of the acidosis with bicarbonate and forced diuresis she at first regained consciousness, but clouding of consciousness again occurred eight hours later progressing to coma with unequal pupils and seizure potentials in the electroencephalogram. Status epilepticus without motor component was diagnosed, perhaps the result of a dysequilibrium of acid-base balance between blood and cerebrospinal fluid. The signs and symptoms were quickly reversed under treatment with clonazepam.
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PMID:[Cerebral complications in chronic acetylsalicylic acid poisoning]. 291 58

A 24-year-old woman, gravida 1, para 0, experienced recurrent attacks of headaches and bizarre behavior from the sixth week of gestation onward. Three days before confinement, she lapsed into coma and was delivered of a normal child. Plasma glucose, insulin, and C-peptide levels were diagnostic of insulinoma. Subsequently, after she spontaneously regained consciousness, a pancreatic tumor was removed at laparotomy with complete resolution of symptoms. The problems of diagnosing insulinoma during pregnancy are discussed.
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PMID:Insulinoma complicating pregnancy: case report and review of the literature. 301 82

Blood pressure, which ist the product of cardiac output and peripheral vascular resistance is regulated by a complex feedback mechanism involving the sympathetic and parasympathetic systems and hormones. An acute disturbance of regulation may lead to a life-threatening increase in blood pressure. Diagnosis is based upon a careful measurement of blood pressure, which must be performed under internationally standardized conditions. Hypertensive crisis refers to a rapid blood pressure increase greater than 30 mmHg above the age-related 95th percentile. The main causes of hypertension in childhood are renal diseases, which may be aggravated by additional conditions either by the clinician himself (e.g. cyclosporin, steroids) or by the patient (lack of compliance). Crisis affects the brain (hypertensive encephalopathy), the heart (left ventricular insufficiency), the retina (visual disturbances) and the mucous membranes (epistaxis). Hypertensive encephalopathy is induced by a break-through of the autoregulation of brain flow, leading to hyperperfusion and, thus to cerebral oedema. The clinical manifestations are characterized by restlessness, severe and diffuse headache, vomiting, nystagmus, impaired vision, dizziness, paraesthesia, seizures and palsies, which may lead - if untreated - to coma and death. The course is usually prolonged and reversible by adequate treatment. The morphological consequences are purpura cerebri, fresh retinal haemorrhages and papillary oedema, apart from left ventricular dilatation and hypertrophy. The diagnostic procedure rests on the quick realization of essential anamnestic (blood pressure, renal disease, drugs), clinical (oedema, cardiac action, central nervous system, fundus) and laboratory parameters (serum creatinine, electrolytes, glucose, blood count, urine). Treatment should start before the manifestation of clinical signs (hypertensive emergency) with rapidly acting antihypertensive drugs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The hypertensive crisis in childhood]. 305 87

We are reporting a rare case of clivus chordoma with fatal hemorrhage in the posterior fossa. A 38-year-old woman afflicted with sudden onset of severe headache and vomiting. On neurological examination, she was mildly lethargic. She had slight dysarthria and nystagmus, but no cranial nerve abnormalities. Craniogram revealed erosive changes in the right petrous bone. CT scan showed a massive intracerebellar hemorrhage and isodense mass in the sphenoid sinus, which were not enhanced by contrast medium. She became comatose and died 3 days later. No operation was performed. Autopsy revealed massive hemorrhage in the posterior fossa and yellowish, gelatinous tumor extending from the right clivus to the sphenoid sinus. Histological examination showed a chordoma. This case demonstrates that the hemorrhage associated with brain tumor, especially in posterior fossa, produces a significant sudden elevation of intracranial pressure and leads clinically to a rapid loss of consciousness and death soon after the onset.
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PMID:[A case of clivus chordoma showing hemorrhage in the posterior fossa]. 306 8

We measured the concentrations of tissue-type plasminogen activator (t-PA) in 92 patients with chronic subdural hematoma involving 102 sites. The t-PA level in the normal plasma was 4.0 +/- 1.8 ng/mL (mean +/- SD), while that in the hematoma content of these patients was 11.2 +/- 6.2 ng/mL. Patients showing stupor (grade 3) and coma (grade 4) had higher t-PA levels than those showing headache (grade 1) and somnolence (grade 2) or psychiatric disorder (grade 5). Also, those with the layer-type hematoma on computed tomographic images had higher t-PA levels than those with any other types. The t-PA level in the draining fluid decreased after surgery. In three patients showing a gradual increase of t-PA, subdural fluid reaccumulated and the general condition remained unchanged after surgery. Overproduction of t-PA is considered to initiate intermittent hemorrhage by conversion of plasminogen to plasmin and results in persistence or enlargement of chronic subdural hematoma.
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PMID:Tissue-type plasminogen activator in the chronic subdural hematoma. 313 77

The opiate antagonist naloxone was suggested for the amelioration of cerebral ischemia after subarachnoid hemorrhage (SAH) following the 1981 report of clinical improvement of ischemic deficits in 2 patients. The deficit in 1 patient was exacerbated by morphine, suggesting that analgesics acting on opiate receptors should be avoided after SAH, and this would include codeine phosphate and dihydrocodeine, both widely used for post-SAH headache. We studied 21 consecutive patients with aneurysmal SAH whose condition was worse than Grade 1 on the Hunt and Hess scale. A single observer graded them to avoid interobserver error, and they were also given a score on the Glasgow coma scale. Each patient was then given an intravenous injection of 0.9% saline as placebo or 0.4 mg (7 patients) or 2.0 mg (14 patients) of naloxone. Five minutes later, the same observer regraded the patient. After 30 minutes, a second injection of placebo or naloxone was given, and the patient was regraded a third time. Each patient received placebo in one injection and naloxone in the other, but the order was randomized and unknown to the observer. There was no beneficial effect of 0.4 mg of naloxone after aneurysmal SAH, and we did not find an elevated level of the endogenous opiate beta-endorphin in the cerebrospinal fluid in the majority (6 of 8 of the patients in whom it was assayed). Five of the patients given 2.0 mg of naloxone did improve transiently, and none deteriorated after the drug, suggesting that naloxone in a high dose may have a place in the management of some post-SAH deficits.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of naloxone on deficits after aneurysmal subarachnoid hemorrhage. 315 81

A 31-year-old woman was admitted because of severe headache and dysarthria in December 1985. Neurological examination on admission revealed severe impairment of consciousness, anisocoria, absent light reflex on the right side, and evidence of left hemiparesis, but other brainstem reflexes were intact. A CT scan taken shortly after arrival demonstrated a large hematoma in the right temporal lobe and the right cerebellum. Breathing became irregular and intubation was needed. An emergency operation was performed. After the operation the patient remained comatose without any spontaneous respiration or brainstem reflexes. The next day she was still comatose without any spontaneous movement and other neurological finding remained unchanged. An initial EEG obtained at this time showed an 8- to 9-Hz alpha rhythm of about 15-40 microV with preponderance over the posterior and central regions. Some spontaneous variability was noted. The same day, investigations of brainstem auditory evoked potential (BAEP), visual evoked potential (VEP), and somatosensory evoked potential (SEP) were performed. BAEP showed only the first, second and third waves (I-III) bilaterally. VEP was able to elicit the primary response (II-III) without the secondary response. SEP could not be obtained from the early cortical response to left median nerve stimulation, but showed N14 bilaterally and small N20 upon right median nerve stimulation. On the second day of hospitalization, a repeated EEG showed generalized slowing with loss of alpha frequency rhythms and it proved impossible for SEP to elicit N20 bilaterally. At this time, BAEP showed bilateral I-IIIth waves and VEP still showed primary response.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of alpha coma in acute brainstem dysfunction--consecutive electroencephalograms and evoked potentials]. 317 89


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