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

The posterior reversible leukoencephalopathy syndrome (PRES) is a recently proposed cliniconeuroradiologic entity. The most common causes of PRES are hypertensive encephalopathy, eclampsia, cyclosporin A neurotoxicity and the uremic encephalopathies. Most patients are markedly hypertensive at presentation, although some have only mildly elevated or even normal blood pressure. Symptoms may include headache, nausea, vomiting, altered mental status, seizures,stupor, and visual disturbances. On CT and MR studies, edema has been reported in a relatively symmetrical pattern, typically in the subcortical white matter and occasionally in the cortex of the occipital and parietal lobes. These often striking imaging findings usually are resolved on follow-up studies obtained after appropriate therapy. Diffusion-weighted images would not show hyperintense signal because of the presence of interstitial rather than cytotoxic edema. We report a case of PRES due to hypertensive encephalopathy studied by CT and MRI.
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PMID:[Reversible posterior encephalopathy syndrome: case report]. 1224 91

Posterior reversible encephalopathy syndrome (PRES) is a leukoencephalopathy clinically characterized by headache, altered mental status, visual loss and seizures. Neuroimaging demonstrates symmetrical posterior cortical and subcortical lesions. The exact pathophysiology is unknown but there is a strong association with immunosuppressants and hypertension. We report two cases of PRES in normotensive patients with severe hypercalcemia as the only identifiable cause. Possible pathophysiological mechanisms are discussed.
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PMID:Posterior reversible encephalopathy syndrome due to severe hypercalcemia. 1242 98

Glutaric aciduria type I usually presents with an acute metabolic crisis during infancy. The authors report a previously healthy 19-year-old woman who presented with recurrent headaches, oculomotor symptoms, and a severe leukoencephalopathy on MRI. The diagnosis was made by urinary organic acid analysis and confirmed by enzyme studies. Genetic analysis revealed compound heterozygosity with a deletion c.219delC in exon 3 and a novel missense mutation R132G in exon 5 of the glutaryl CoA dehydrogenase (GCDH) gene.
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PMID:Adult onset glutaric aciduria type I presenting with a leukoencephalopathy. 1270 62

We report a case and autopsy findings of posterior leukoencephalopathy (PL) developing during induction chemotherapy for B-cell acute lymphoblastic leukaemia (B-ALL) complicated by tumour lysis syndrome. PL may present with seizures, headache, altered mental status and occipital blindness, associated with transient parieto-occipital abnormalities on neuro-imaging studies. Precipitants include immunosuppressive agents, renal insufficiency, hypertension and fluid retention. It has also been reported in association with pre-eclamptic and eclamptic states, nephrotic syndrome and following liver and bone marrow transplantation. Only rare cases of PL developing during treatment for haematological malignancy have been reported and to our knowledge it has not been previously reported in association with tumour lysis syndrome. Since the condition is generally regarded as being fully reversible few autopsy findings have been reported.
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PMID:Posterior leukoencephalopathy in association with the tumour lysis syndrome in acute lymphoblastic leukaemia--a case with clinicopathological correlation. 1277 51

Dialysis disequilibrium syndrome is a disorder of the central nervous system in patients on dialysis. The underlying etiology is thought to be primarily due to cerebral edema; however, neuroradiologic findings have not been described previously. We describe a patient who presented with new onset headaches and status epilepticus after beginning hemodialysis. Her neuroimaging studies revealed white matter changes in the posterior parietal and occipital lobes similar to those seen in patients with reversible posterior leukoencephalopathy syndrome (RPLS). This case suggests that dialysis disequilibrium syndrome and RPLS may represent a spectrum of disorders in which the underlying mechanism is vasogenic edema.
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PMID:Dialysis disequilibrium: another reversible posterior leukoencephalopathy syndrome? 1295 40

Leukoencephalopathy with severe hypertension is a recently described entity in nephrology, with only a few case reports to date in children. We prospectively studied 18 children with severe hypertension to evaluate the clinical features, severity, reversibility, and prognosis. All were subjected to clinical and biochemical tests, magnetic resonance imaging (MRI), and magnetic resonance angiography (MRA). Headache was reported in 16 children, 13 had confusion and drowsiness, 12 had nausea and vomiting, and 9 had visual disturbances, seizure, and dyspnea. Only 2 had focal neurological deficit (1 with right facial palsy and another with right lateral rectus palsy). Of these 18 children, 14 patients had hypertensive retinopathy and 4 had normal fundus. MRI revealed leukoencephalopathic changes in 16 of 18 patients. These changes were bilateral occipito-parietal in 9 patients, diffuse white/gray matter lesion in 2, brain stem hyperintensity in 2, and hemorrhagic lesion in 3. On MRA, 11 of 18 patients had attenuation of cerebral arteries of different degree. On follow-up, MRI findings resolved in all except 3 patients and all patients had normal MRA, except for 1 with persistent minimal attenuation and another with spasm in all vessels. We conclude that leukoencephalopathy with severe hypertension is reversible both clinically and radiologically in the majority of children after the control of hypertension. However, a few patients may have residual damage and may need psychometric analysis and follow-up for neurodevelopmental sequelae.
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PMID:Is reversible posterior leukoencephalopathy with severe hypertension completely reversible in all patients? 1450 62

Reversible posterior leukoencephalopathy refers to a clinicoradiological syndrome observed in patients presenting with acute or subacute symptoms of various intensity including seizures, headache, vomiting, confusion and visual abnormalities. The radiological features are reversible bilateral white matter abnormalities predominantly located in the posterior regions of the cerebral hemispheres, demonstrated by computed tomography or, better, by magnetic resonance imaging. This syndrome mostly occurs in patients with hypertensive encephalopathy or in immunosuppressed patients. The recognition of this syndrome is critical as delay in the diagnosis or treatment can result in permanent neurological deficit while early prompt control of blood pressure or withdrawal of causative drugs can reverse the syndrome.
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PMID:[Reversible posterior leukoencephalopathy syndrome]. 1457 10

Reversible posterior leukoencephalopathy syndrome is one of the most serious complications of immunosuppressive therapy. The clinical features include headache, altered mental functioning, seizures, cortical blindness and other visual disturbances, with hypertension. The neuroimaging studies reveal predominant posterior leukoencephalopathy. Usually, antihypertensive therapy and reduction or withdrawal of immunosuppressive agents have been reported to resolve the neurological deficits and imaging abnormalities within a few weeks. We discuss here a 51-year-old woman with nephrotic syndrome who developed acute leukoencephalopathy during combination therapy with prednisolone and cyclosporine. She developed severe headache, visual disturbance, consciousness disturbance, and generalized tonic clonic convulsion. A computed tomography scan (CT) revealed low-density areas in the subcortices of the parietal and occipital lobes. Magnetic resonance imaging (MRI) disclosed a high signal intensity area on T2-weighted images and a low signal intensity area on T1-weighted images in the same lesions. Follow-up brain CT and MRI were performed several times. Three weeks after the first study, these lesions had completely resolved, but she had persistent altered consciousness for more than 1 year.
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PMID:Acute posterior leukoencephalopathy in a patient with nephrotic syndrome. 1458 46

Bathing headache is rarely described in literature. We report four middle-aged Taiwanese women who developed severe throbbing headache with maximum intensity of onset during bathing. Diffuse cerebral vasospasm was demonstrated in one of them. All their headaches resolved spontaneously (n = 1) or after nimodipine treatment (n = 3). Except for one patient with vasospasm in whom reversible posterior leukoencephalopathy and an asymptomatic cerebellar infarction developed, the others recovered without any complications. The clinical profile of bathing headache points to idiopathic thunderclap headache. It may not be as benign as previously reported. Nimodipine might be effective in treatment of this special headache syndrome.
Cephalalgia 2003 Nov
PMID:Bathing headache: a variant of idiopathic thunderclap headache. 1461 25

Long-term exposure to carbon disulfide (CS(2)) may induce diffuse encephalopathy with parkinsonism, pyramidal signs, cerebellar ataxia, and cognitive impairments, as well as axonal polyneuropathy. The pathogenic mechanisms of diffuse encephalopathy are unclear, although vasculopathy and toxic demyelination have been proposed. Recently, we have encountered a patient who developed headache, limb tremors, gait disturbance, dysarthria, memory impairment, and emotional lability after long-term exposure to CS(2). The brain magnetic resonance images (MRI) showed diffuse hyperintensity lesions in T(2)-weighted images in the subcortical white matter, basal ganglia, and brain stem. The brain computed tomography perfusion study revealed a diffusely decreased regional cerebral blood flow and prolonged regional mean transit time in the subcortical white matter and basal ganglion. To our knowledge, there have been few reports demonstrating diffuse white matter lesions in chronic CS(2) encephalopathy using brain MRI. In addition, the (99m)Tc-TRODAT-1 single photon emission computed tomography showed a normal uptake of the dopamine transporter, indicating a normal presynaptic dopaminergic pathway. We conclude that diffuse white matter lesions may develop after chronic exposure to CS(2), possibly through microangiopathy. In addition, CS(2) poisoning can be considered as one of the causes of chronic leukoencephalopathy.
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PMID:Diffuse white matter lesions in carbon disulfide intoxication: microangiopathy or demyelination. 1463 66


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