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

Out of the 140 adult patients with chronic subdural haematoma 17% were female. An overall relationship of CSH cases to the total number of subdural haematomas was 27%. In only 78% of the CSH could a history of trauma be traced. Most of the patients were between the ages of 50 and 70. The main symptoms were headache, abnormal psychic behaviour and paresis. Alcoholism and anticoagulant therapy accounted for only 13% and 3% respectively. Recurrent bleeding occurred in 25% of cases not only after craniotomy but also after burr-holes. The total mortality was 15%. With regard to diagnosis and the indications for operation, angiography which was previously used has, since 1977, been superseded by the CT-scan.
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PMID:[Clinical studies on chronic subdural haematomas in 140 adults (author's transl)]. 744 94

This retrospective study from two hospitals is about a hundred patients who have been operated upon a spontaneous cerebral hematoma. By a spontaneous cerebral hematoma we mean a hematoma without a proven tumor, without aneurysm, without arteriovenous malformation, without preceding trauma, without aortical phlebitis and without pathology of the vessel-wall. In this study patients with coagulopathy, arterial hypertension and artherosclerosis are included. In order to comply with these conditions an angiography will have to take place pre-operatively as well as postoperatively. Moreover histological examination of the wall of the hematoma will have to be done. The etiology of the spontaneous cerebral hematoma is not clear in most cases. The indication to operate, the way of operating and the moment in which the operation takes place, vary strongly in medical literature. We operate when there is an aggravation of the clinical picture, persisting severe headache and neurological paresis which does not improve. As a rule we abide for one week before operating, if the clinical picture allows this. After the operation unconscious patients may recover and a hemiparesis may improve. The best way of diagnosing a cerebral hematoma is computerised tomography.
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PMID:[The spontaneous cerebral hematoma (author's transl)]. 744 12

It is well known that thromboembolism is 1 of the most serious side effects of oral contraceptives (OCs). In Japan, however, reports of thromboembolism following use of OCs are rare, since their clinical use in Japan is restricted to treatment of menstrual irregularities. We reported here on 2 patients affected with cerebrovascular occlusive diseases associated with the administration of OCs. The 1st case was that of a 32-year old woman who developed headaches, paresis, and dysesthesia of the right limbs following daily intake for 20 days of OCs (0.15 mg mestranol and 5 mg lynestrenol). Neurological symptoms as well as examinations led to the diagnosis of a kind of thalamic syndrome due to cerebral thrombosis. The 2nd case was that of a 37-year old woman who developed right hemiparesis following daily consumption over a 21 day period of OCs as administered above. Clinical symptoms and neurological examinations led to the diagnosis of right hemiparesis due to cerebral thrombosis. The pathogenesis of cerebral thrombosis caused by taking OCs was discussed mainly in connection with coagulation and fibrinolysis. Certain evidence suggesting that hypercoagulability may play a major role in the pathogenesis of thromboembolism during OC ingestion has been derived from the works of other investigators. It is true that estrogen in this compound may induce a state in which an increase in coagulation factors together with a decrease of antithrombin 3 combine to produce hypercoagulation; laboratory tests with our patients, however, produced nothing compatible with a state of hypercoagulability. (author's modified)
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PMID:[Cerebral thrombosis in woman receiving oral contraceptives: report of two cases (author's transl)]. 746 38

We report a 57-year-old woman with progressive gait disturbance, headache, character change, convulsion and coma. She was well until 55 years of age, when she noted an onset of unsteady gait. At times she experienced transient weakness in her right hand, which was followed some difficulty in articulation. She was admitted to our service for the work up on April 6, 1992. Neurologic examination at that time revealed an alert Japanese lady in no acute distress. She was oriented to all spheres, however, she was somewhat bradyphrenic and had some disturbance in recent memory. Higher cerebral functions appeared intact. The visual acuity and visual fields were normal as were the optic fundi. Pupils were round and isocoric reacting promptly to light. Ocular movement was full, however, horizontal nystagmus was noted upon right lateral gaze. The sensation of the face was intact. She showed right facial paresis of the central type. Hearing was intact. She showed slurred speech and some difficulty in swallowing. The tongue was deviated to the right. Her gait was wide based and unsteady; tandem gait was difficult, however, walking on toes and on heels were performed well. No cerebellar ataxia was noted, but she showed some clumsiness in her right hand. Deep reflexes were symmetric and normally reactive; plantar response was extensor bilaterally. Sensation was intact; no meningeal sign was elicited. Routine laboratory work up was unremarkable; the CSF was under a borderline pressure (180 mmH2O) and contained 39 mg/dl of protein and 59 mg/dl of sugar. Cranial CT scan revealed diffuse low density areas involving bilateral cerebral white matter as well as the brain stem; MRI revealed high signal intensity lesions in those areas; gadolinium enhancement was negative; cortical sulci were effaced and the anterior part of the left lateral ventricle was compressed without deviation of the midline structure. The patient was treated with steroid pulse therapy without effect. She was discharged for out patient follow up, however, she developed a convulsion which was followed by loss of consciousness, and was admitted again to our service. She had never gained consciousness after this episode, and remained in the state of akinetic mutism. Follow-up CT and MRI did not show much change, although the area of high signal density lesions slightly enlarged on June 1, 1993. Her clinical course was complicated by drug induced bone marrow suppression and nephrotic syndrome. She expired on September 8, 1993 after developing sudden drop of blood pressure and bradycardia.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 57-year-old woman with gait disturbance, headache, character change, convulsion, and coma]. 761 89

We discuss four patients with the clinical diagnosis of basilar migraine and suspected coexisting epilepsy who were referred to our epilepsy center. Their symptoms suggested episodic dysfunction in the distribution of the basilar artery, followed by pulsating headache with nausea. Verbal unresponsiveness and sensory symptoms occurred in all four patients; two also had focal paresis or jerking movements. Diagnostic studies excluded other disorders with similar symptoms. None of the patients improved with antimigraine or antiepileptic drugs. Provocation tests with suggestion elicited typical events in three patients and aura and headache in one patient. There were no EEG or ECG abnormalities during spontaneous or provoked episodes. Two patients improved with psychiatric treatment. Conversion disorder or malingering should be considered in patients whose symptoms of basilar migraine are atypical or refractory to treatment.
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PMID:Psychogenic basilar migraine: report of four cases. 871 Jan 6

The interhemispheric subdural hematoma is a rare condition. We present a case of interhemispheric subdural hematoma in a patient aged 65 years. A day prior to admission he was struck with a water-pipe on the head. He went to sleep the same evening complaining of a slight headache. At about two o'clock in the morning the headache increased in intensity. By the morning he lost consciousness. On examination by a neurosurgeon the patient was found to be comatose. The physical examination revealed blue eyelids of the left eye, paraplegia of the right leg, paresis of the left leg and arms. Bilateral Babinski's reflex was present, the abdominal reflexes were absent, the tendon and periosteal reflexes were hyperactive. The pupils were equal in size and slowly reactive to light. The patient exhibited symptoms of meningoradicular irritation. An emergency CT scan revealed high-density area in the interhemispheric sulcus extending frontally to parietally. The patients was operated on in an emergency. At operation, extensive rupture of the sagittal sinus was identified. Later the patient died. The presented case was interesting with the extensive rupture of the sagittal sinus and the relatively long lucid interval until clear manifestation of the clinical picture becomes evident.
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PMID:A case of interhemispheric subdural hematoma. 786 95

We report a 65-year-old woman with progressive multiple cranial neuropathy. She had been suffered from bronchial asthma since 1979 for which prednisolone had been prescribed. She noted an onset of pain around her nose in October, 1989, which extended into the periorbital regions bilaterally. In February, 1990, she was treated with stellate ganglion block and trigeminal nerve block; these treatments partially alleviated her pain. In May of 1991, she noted a difficulty in swallowing solid foods. In November of the same year, she developed right facial paresis; two weeks later, she noted numbness in her left face, and was hospitalized to our service on December 16, 1991. On admission, she was afebrile and general physical examination was unremarkable except for piping rales in her both lung fields. On neurologic examination, she was alert and oriented to all spheres; higher cerebral functions were intact. In the cranial nerves, her olfactory sense was lost bilaterally; her vision was markedly diminished bilaterally only to recognize hand movements; the optic fundi appeared normal; the pupils were isocoric and reacted to light promptly. The extraocular muscles were moderately weak to most of the directions more on the left; no nystagmus was present. Facial sensation was diminished bilaterally; the jaw deviated to right; right facial paresis of peripheral type was present; her hearing was diminished bilaterally more on the right. The movement of the soft palate was diminished on the right side; dysphagia was present; her voice was horse; the gag reflex was diminished. The sternocleidomastoid muscle was weak bilaterally; the tongue appeared normal. Examination of gait was differed because of headache, however, no apparent motor weakness was present. No ataxia or involuntary movement was noted. Deep reflexes were normally elicited and symmetric. Plantar response was flexor. Sensation in the extremities was intact. Kernig's sign was positive at 70 degree leg extension; eyeball tenderness was also present bilaterally, however, no nuchal stiffness was noted. Following abnormalities were present in the laboratory examination: WBC 11,400/microliters, ESR 50 mm/hr, CRP 6.1 mg/dl. The lumbar CSF was under a normal pressure containing 29 WBC/microliters (neutrophils 7, lymphocytes 20, others 2), 67 mg/dl of protein, and 53 mg/dl of sugar; cultures for acid-fast bacilli as well as for other bacteria were negative; no malignant cells were found. A cranial CT scan revealed an isodensity mass in the orbit and ill-defined low density areas in the white matters of the frontal lobes.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 65-year-old woman with headache, facial pain, and progressive multiple cranial neuropathy]. 787 85

Sixteen patients (8 female, 8 male) with primary angiitis of the CNS (PACNS), were followed prospectively in a vasculitis clinic. Diagnosis was by angiography in patients without underlying disease. Median age at diagnosis was 36.5 years, and median duration of follow-up was 28 months. Onset was acute in 14 patients (88%), with 3.5 weeks (median) from onset symptoms to diagnosis. Three women developed symptoms within 3 weeks postpartum. The most frequent symptoms were severe headaches (12, 75%), stroke (6, 30%), transient ischaemic attack (TIA) (4, 28%), seizures (7, 44%), visual aberration (3, 19%), and cognitive impairment (5, 31%). Laboratory data included high ESR (2, 13%), leucocytosis (8, 80%), thrombocytosis (1, 6%), positive antinuclear antibody titre (3, 15%), and high levels of complement (5, 31%). Lumbar puncture was performed in 12 patients (75%). CSF analysis was abnormal in five patients (42%). EEG was abnormal in 5/9 patients. The major CT/MRI scan findings were cerebral haemorrhage (4, 25%), brain infarcts (5, 31%), brain atrophy (2, 13%) and non-specific lesions (2, 13%). Four patients had normal studies. All patients received corticosteroids (CS), and five were treated with oral cyclophosphamide. Two patients relapsed despite CS and cyclophosphamide therapy. All patients are alive, and at the last assessment, eight had a permanent neurological deficit, which included paresis (3, 19%), neurocognitive abnormalities (2, 13%), visual loss (2, 13%) and seizure activity (5, 31%). Our data suggest a non-progressive, non-fatal course in those PACNS patients diagnosed angiographically and treated with CS with or without cyclophosphamide.
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PMID:Primary angiitis of the CNS diagnosed by angiography. 804 67

In a population based register of stroke (n = 536) compiled in Perth, Western Australia during an 18 month period in 1989-90, 60 cases (11%) of primary intracerebral haemorrhage were identified among 56 persons (52% men). The mean age of these patients was 68 (range 23-93) and 46 (77%) events were first ever strokes. The crude annual incidence was 35 per 100,000, with a peak in the eighth decade, and a male predominance. Deep and lobar haemorrhages each accounted for almost one third of all cases. The clinical presentations included sudden coma (12%), headache (8%), seizures (8%), and pure sensory-motor stroke (3%). Primary intracerebral haemorrhage was the first presentation of leukaemia in two cases (both fatal) and it followed an alcoholic binge in four cases. 55% had a history of hypertension. 16 (27%) patients, half of whom had a history of hypertension, were taking antiplatelet agents, and one patient was taking warfarin. There were only two confirmed cases of amyloid angiopathy. The overall 28 day case fatality was 35%, but this varied from 100% for haemorrhages in the brainstem to 22% for those in the basal ganglionic or thalamic region. Other predictors of early death were intraventricular extension of blood, volume of haematoma, mass effect, and coma and severe paresis at onset. Although based on small numbers, these data confirm the heterogeneous nature of primary intracerebral haemorrhage, but they also suggest a different clinical spectrum of this type of stroke in the community compared with the experience of specialist neurological units.
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PMID:Spectrum of primary intracerebral haemorrhage in Perth, Western Australia, 1989-90: incidence and outcome. 805 17

Outbreaks of illnesses of unknown etiology typified by a chronic relapsing course of constitutional symptoms and nervous system involvement have collectively been referred to as chronic fatigue syndrome, epidemic neuromyasthenia, and myalgic encephalomyelitis. To examine heterogeneity of clinical presentation, a comparative review was undertaken for 12 well-documented outbreaks reported since 1934. A systemic syndrome characterized by excessive fatigue, myalgias, headache, low-grade fever, and other constitutional symptoms was common to cases in all outbreaks. However, marked heterogeneity in the range of neurological features was apparent. On the basis of predominant neurological manifestations, outbreaks could be grouped into four levels of increasing neurological involvement: affective neuropsychological changes (level I); prominent cutaneous sensory symptoms with both affective and cognitive neuropsychological changes (level II); marked objective paresis with cutaneous sensory as well as affective and cognitive neuropsychological changes (level III); and cutaneous sensory, affective and cognitive neuropsychological, posterior column, cranial nerve, and mixed upper and lower motor neuron changes (level IV). Groups with the most prominent objective neurological findings (levels III and IV) comprised exclusively outbreaks reported between the 1930s and 1950s. All but one outbreak in groups with less prominent neurological findings (levels I and II) were reported between the 1960s and 1980s; a range of neurological features was observed for these groups. Because a complete neurological examination is not emphasized as part of the diagnostic workup in current outbreaks, it is possible that less obvious neurological findings may be overlooked. Careful evaluation of neurological features in epidemic and endemic cases of what is now called chronic fatigue syndrome may be one approach to distinguishing subtypes of what has been described in the past as a nosological entity.
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PMID:A comparative review of systemic and neurological symptomatology in 12 outbreaks collectively described as chronic fatigue syndrome, epidemic neuromyasthenia, and myalgic encephalomyelitis. 814 51


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