Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

First symptoms and initial clinical, ultrasonographic and neuroradiological findings ascertained a mean of 5.6 days (SD = 5.6 days), 7.7 days (7.0), and 11.2 days (8.0) after symptom onset were analysed in 44 patients who suffered a spontaneous internal carotid artery dissection (ICD) verified by magnetic resonance imaging, angiography, or both. Common symptoms signalling dissection were unilateral headache in 68%, transient ischaemic attack in 20%, and cerebral infarction in 9%. Severe pain preceded cerebral ischaemia by more than 3 days in 60% of those patients who eventually suffered a stroke. However, only 2 were admitted because of pain alone and 33 for evolving neurological deficits. During the first month, ipsilateral severe headache occurred in 89%, neck pain in 36%, ipsilateral cerebral ischaemia in 82%, ocular ischaemia in 16%, oculosympathetic palsy in 48%, and cranial nerve palsy in 5%. Recent "trivial" head or neck trauma was elicited in 41%. Doppler and duplex sonography confirmed the clinical suspicion of ICD in 91.5% and in 96% of those with a significant stenosis or occlusion. MRI demonstrated a thickened vessel wall in all 33 imaged carotid dissections and a mural haematoma in 30. None of the 32 patients who received anticoagulant treatment subsequently deteriorated. Monitoring anticoagulant treatment with ultrasonographic follow-up studies demonstrated recanalization in 70% and persistent occlusion in 30%. The results demonstrate that familiarity with the initial symptoms, especially headache, and performance of an ultrasonographic study without delay are the cornerstones of an early diagnosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Spontaneous internal carotid artery dissection: early diagnosis and management in 44 patients. 779 22

Stroke was the leading cause of death in Taiwan for 19 years (1963-1981). About 60% of the hospitalized patients dying of stroke suffered from cerebral hemorrhage (CH). This fact denotes an important role of CH in causing fatal stroke. The widely use of computed tomography (CT) in Taiwan in the past decade enables clear differentiation between CH and cerebral infarction (CI). In Taiwan, the ratio of CH: CI is 1:1.5, which is 3.5 times higher than that of the Western countries. CH is most prevalent between aged 55 and 65 years; the male to female ratio after adjusted to that of general population is around 1.1:1. Hypertension is the most important risk factor (86.7%) and spontaneous CH is, therefore, often referred to as "hypertensive CH". CH has a predilection to occur in the putamen (41%), thalamus (23%), putaminothalamus (9.7%), subcortical white mater (9.3%), brainstem (6.5%), and cerebellum (5.9%). Motor dysfunction (80%) is the most frequent clinical manifestation, followed by disturbance of consciousness (50%), and language problems (31.1%). In addition to motor and consciousness disturbance, vomiting (30.8%) and headache (27%) are among important initial presentations, especially for cerebellar and intraventricular hemorrhage. For patients with stable condition after CH, medical treatment is the mainstay of therapy. If condition deteriorates during medical treatment, surgical intervention may be considered for patients with cerebellar, lobar, or putaminal hemorrhage. In Taiwan, 11.6% of patients with CH receive surgical treatment. The mortality rate one month after CH was 53.7% before the CT era; it has decreased to 23.3% in recent years.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cerebral hemorrhage in Taiwan]. 791 73

A 45-year-old man developed generalized convulsion and consciousness disturbance at age 43. An X-ray CT revealed hemorrhagic infarction in the left fronto-parieto-temporal area. A conventional angiography disclosed complete occlusion of the left cortical vein. In the chronic stage of the stroke, he had incomplete right quadrantopsia, a mild right hemiparesis and sensory aphasia. The patient has had partial somatosensory seizures since February 1990. Ictal EEG recordings showed epileptogenic discharges in the left parietal region. The seizures were adequately controlled with clonazepam. Since July 27, 1993, he has become aware of blurred vision in both eyes accompanied with headache and dizziness. On August 6, he was admitted to the hospital with right homonymons hemianopsia, sensory aphsia and tonic seizures in the right hand. Ictal EEG recordings demonstrated theta waves of the left parieto-occipital region and epileptogenic discharges in the left occipital region which consisted of spikes, sharp waves and spike-wave complexes. Single photon emission computed tomography (SEPCT) images obtained during seizures showed considerable hyperperfusion in the left occipital temporal lobes, while there was hypoperfusion in the left temporo-parietal area corresponding to the lesion of the old cerebral infarction. A T2-weighted MRI scan showed an abnormal high-intensity area in the left occipital lobe that suggested brain edema. After the admission, the patient was treated with additional anticonvulsant drugs. The tonic seizures in the right hand disappeared and right homonymous hemianopsia and sensory aphasia showed gradual improvement in the next four weeks.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[An unusual case of status epilepticus of simple partial seizure with an occipital lobe focus]. 799 93

A 26-year old woman, who was diagnosed as having systemic lupus erythematosus at the age of 23 year old, presented diarrhea and headache. She showed severe hypoproteinemia (serum total protein 3.7 g/dl, serum albumin 1.4 g/dl) and hyperlipidemia. She revealed to have protein-losing enteropathy with the result of alpha-1-antitrypsin clearance test using stool. Increase of prednisolone improved the loss of albumin into the bowel and abnormal laboratory findings. She also showed watershed infarction in the area of middle cerebral artery and posterior cerebral artery. Protein-losing enteropathy is a rare complication of SLE, only 18 cases are available on literature. No case is found to have cerebral infarction in patients with protein-losing enteropathy associated with SLE. It is known that blood levels of anticoagulation factors decrease in protein-losing enteropathy due to the leakage of plasma protein into intestinal lumen. Serum antithrombin III was decreased in this case. Hyperlipidemia found in this case seems to be caused by same mechanism in nephrotic syndrome. Lupus anticoagulant was also positive in this patient. These factors seems to be related to the occurrence of cerebral infarction. This case suggests the possibility of cerebral infarction in patients with protein-losing enteropathy in SLE.
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PMID:[Protein-losing enteropathy and cerebral infarction associated with systemic lupus erythematosus]. 814 30

A 9-year-old girl was admitted to our hospital because of fever, headache, vomiting, and convulsive seizures. On admission, she was proved to have homonymous hemianopsia as well as elevated lactate and pyruvate levels in both serum and cerebrospinal fluid. Muscle biopsy study showed scattered ragged-red fibers and strongly succinatedehydrogenase-reactive blood vessels (SSV), suggesting systemic vascular involvement. She had a point mutation at nucleotide pair 3,243 in mitochondrial DNA extracted from muscle and blood samples. Brain CT and MRI showed a large abnormal area mimicking cerebral infarction in the region of the occipital cerebral artery. The cerebral lesion was assumed to be caused by vascular abnormality because of delayed and decreased cerebral blood flow together with vascular changes in her muscle biopsy.
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PMID:[Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes with delayed and decreased cerebral blood flow on cerebral angiography--a case report]. 819 71

We report on a 47-year-old white female with a long history of recurrent episodes of migraine with aura, who progressed to develop a continuous intractable headache during the course of which cortical blindness and quadriparesis occurred due to extensive and bilateral hemispheric cerebral infarction. Severe diffuse intracranial major arterial vasospasm was demonstrated by arteriogram. All studies were negative for CNS vasculitis, including cerebral biopsy. The arterial spasm reversed itself, but the patient did not improve. Smoking was the only additional risk factor. Vasospasm is an important cause to be considered in migrainous infarctions. The use of vasoconstrictor agents such as DHE in patients with migraine with prolonged aura has to be carefully re-evaluated.
Cephalalgia 1993 Aug
PMID:Severe diffuse intracranial vasospasm as a cause of extensive migrainous cerebral infarction. 837 36

A 27-year-old woman suffered from a sudden onset of slight paralysis of the right side of her body and the inability to express herself by speech, writing, or signs. She was admitted to the National Rehabilitation Hospital in Washington, D.C., in the US. 6 months prior to these events, she had been in a motor vehicle accident and had since experienced headaches and generalized musculoskeletal pain. The only drug she took was an oral contraceptive (OC), which she took irregularly. Health workers could not arouse her upon admission. Clinical examination revealed symptoms consistent with a left hemispheric stroke. Cerebral computed tomography and magnetic resonance imaging revealed a left temporoparietal infarct. Her free protein S was only 27% on admission and 14% 11 days after admission (normal range, 55-125%). Over the next 72 hours, her physical condition deteriorated, entailing focal motor seizures, right Babinski's sign, loss of pain reflex response on her right side, and complete paralysis of the right side of her body. The left middle cerebral artery appeared to be constricted, which physicians first believed was caused by vasculitis but later found was the result of emboli. The patient developed right femoral vein deep thrombosis. The physicians treated her initially with heparin and followed with warfarin therapy. Nevertheless, embolus. Health workers placed a filter in her inferior vena cava and continued warfarin therapy. She did not experience any more thrombotic or embolic episodes during the rest of her hospital stay. OCs reduce circulating levels of free protein S which, along with activated protein C, inhibits clotting. OCs likely reduced her already existing low levels of free protein S. Deficiency of free protein S was likely responsible for the cerebral infarction and her thrombotic and embolic episodes.
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PMID:A case of cerebral infarction in association with free protein S deficiency and oral contraceptive use. 823 70

The prevalence and clinical picture of hypertensive urgencies and emergencies in an emergency department are poorly known. The aim of the present study was to evaluate the prevalence of hypertensive crises (urgencies and emergencies) in an emergency department during 12 months of observation and the frequency of end-organ damage with related clinical pictures during the first 24 hours after presentation. Hypertensive crises (76% urgencies, 24% emergencies) represented more than one fourth of all medical urgencies-emergencies. The most frequent signs of presentation were headache (22%), epistaxis (17%), faintness, and psychomotor agitation (10%) in hypertensive urgencies and chest pain (27%), dyspnea (22%), and neurological deficit (21%) in hypertensive emergencies. Types of end-organ damage associated with hypertensive emergencies included cerebral infarction (24%), acute pulmonary edema (23%), and hypertensive encephalopathy (16%) as well as cerebral hemorrhage, which accounted for only 4.5%. Age (67 +/- 16 versus 60 +/- 14 years [mean +/- SD], P < .001) and diastolic blood pressure (130 +/- 15 versus 126 +/- 10 mm Hg, P < .002) were higher in hypertensive emergencies than urgencies. Hypertension that was unknown at presentation was present in 8% of hypertensive emergencies and 28% of hypertensive urgencies. In conclusion hypertensive urgencies and emergencies are common events in the emergency department and differ in their clinical patterns of presentation. Cerebral infarction and acute pulmonary edema are the most frequent types of end-organ damage in hypertensive emergencies.
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PMID:Hypertensive urgencies and emergencies. Prevalence and clinical presentation. 859 78

Cocaine use is associated with a variety of serious neurological complications, including cerebral infarction, intracerebral and subarachnoid hemorrhage, transient ischemic attacks, migraines, and seizures. We report two cases of intracerebral hemorrhage with biopsy-proven cerebral vasculitis associated with the use of cocaine. The first case involved a 32-year-old man who presented with headache, left-sided hemiparesis, and severe hypertension and who was found to have a large right putaminal hemorrhage on cranial tomographic (CT) scan. Cerebral angiography did not show vasculitic changes, but brain tissue obtained during hematoma evacuation revealed a nonnecrotizing leukocytoclastic angiitis of the small vessels. The second case involved a 20-year-old man who presented with headache, agitation, and speech difficulty that progressed to disorientation and dysphasia. He had a large left temporoparietal hematoma seen on CT scan. Cerebral angiography was consistent with vasculitis, and brain tissue obtained during hematoma evacuation revealed a small vessel vasculitis. In both cases, thorough clinical and laboratory investigations found no evidence of systemic vasculitis or an etiologic agent other than cocaine. We also critically reviewed the previously reported cases of cocaine-associated cerebral vasculitis and the relevant medical literature to discuss the "cocaine-associated vasculitis syndrome" in the context of more established vasculitidies, including hypersensitivity vasculitis. In addition, we outline a diagnostic and therapeutic approach to patients with possible cocaine-associated vasculitis.
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PMID:Cocaine-associated cerebral vasculitis. 865 May 87

We investigated 5 patients with intracranial lesions. The initial complaint was tinnitus with normal hearing or sight sensorineural hearing loss. The lesions were 2 cerebello-pontine angle meningiomas, 1 cerebello-pontine angle epidermoid cyst, 1 supratentorial falx meningioma and 1 dural arteriovenous malformation at the temporal bone. Because of pulsatile or severe persistent tinnitus, we performed CT and MRI to determine the presence of intracranial lesions. Some patients had an episode of cerebral infarction and the complaint of headache or head heaviness. Quantitative measurement of tinnitus showed a low-frequency character in a pitch-match examination and moderate loudness in loudness balance. In the patients with falx meningioma and dural arteriovenous malformation, the tinnitus character was pulsatile and abnormal blood flow might have affected the peripheral auditory system. On the other hand, in the patients with a cerebello-pontine angle tumor, the tinnitus character was non-pulsatile and compression on the central auditory system by the tumor might have caused the tinnitus.
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PMID:[Clinical investigations of five patients with intracranial lesions presenting tinnitus]. 869 6


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