Posterior Reversible Encephalopathy Syndrome Secondary to Hypertensive Encephalopathy Brought on by a MAO Inhibitor: A Case Report.

An elderly woman was admitted to the Family Medicine inpatient service for altered mental status after being brought to the emergency room by a concerned neighbor, who had come across the patient speaking incoherently. Initial evaluation was notable for elevated blood pressures, but extensive lab testing and head computed tomographic imaging were within normal limits. However, subsequent magnetic resonance imaging showed white matter changes consistent with posterior reversible encephalopathy syndrome (PRES), a neurologic syndrome characterized by headache, altered mental status, loss of vision, and seizures as well as radiographic findings of posterior cerebral white matter edema. Multiple etiologies of PRES have been described and include hypertensive encephalopathy, immunosuppressant medications, and eclampsia. This case describes an episode of PRES secondary to hypertensive encephalopathy brought about by an inappropriate dose of a monoamine oxidase (MAO) inhibitor. The patient had significant improvement in symptoms with removal of the offending agent and control of her blood pressure. While PRES generally has a good prognosis, prompt recognition, and management are important in preventing significant disease morbidity and mortality.

'Khatatonia' - cathinone-induced hypertensive encephalopathy.

Khat consumption is an under-recognised cause of hypertensive encephalopathy and intraparenchymal brain haemorrhage. We report the radiological findings of extensive periventricular, subcortical and brain stem white matter pathology of a patient who had consumed excessive amounts of Khat. The Khat plant contains cathinone, an amphetamine-like alkaloid which has been associated with chronic hypertensive end-organ damage, but is seldom considered a cause of cerebrovascular events in northern Europe.

[Cognitive dysfunctions caused by excessive exposure to manganese compounds. Cognitive disturbances in intravenous users of ephedrone (methcathinone) with manganese compounds]. / Zaburzenia funkcji poznawczych spowodowane nadmierna ekspozycja na zwiazki manganu. Zaburzenia funkcji poznawczych u dozylnych uzytkowników preparatów efedronu (metkatynonu).

Intravenous injection of self-produced ephedrone (metcathinone) using potassium permanganate as an oxidant can lead to severe, fixed encephalopathy. This risk applies mainly to young individuals experimenting with "home-made" drugs and results in an irreversible aggravation of overall functioning. Besides multiple neurological symptoms and movement disorders, affected individuals also experience cognitive dysfunction. No systematic research has been conducted in this field. Single case reports and small group descriptions show that assessment with screening tools such as the Mini-Mental State Examination (MMSE) is ineffective. Neuropsychological assessment conducted with other tests indicates significant dysarthric speech disorders, psychomotor function impairment, attentional disorders of varying intensity as well as dysfunctions of verbal and visual working memory processes. Some studies of this group of subjects also indicate working memory and executive function disorders. These dysfunctions seem to be permanent and do not recede following manganese use discontinuation and an improvement of the neuroradiological picture in MRI assessment. A standard test battery should be developed enabling the assessment of both cognitive and neurological dysfunctions that otherwise render some tests impossible to administer.

Hypertensive crisis due to contrast-enhanced computed tomography in a patient with malignant pheochromocytoma.

A 63-year-old man underwent computed tomography (CT) using intravenous low-osmolar iodine contrast medium (LOCM) 6 days after undergoing high-dose (131)I-MIBG therapy for metastatic pheochromocytoma. Immediately after the CT examination, his blood pressure increased to 260/160 mmHg (from 179/101 mmHg before the examination). Phentolamine mesilate was administered, and the blood pressure rapidly went back to normal. Although hypertensive crisis after administration of LOCM is rare, this case suggests that high-dose (131)IMIBG therapy may be a risk factor for hypertensive crisis after administration of intravenous LOCM.

Posterior reversible encephalopathy syndrome after liver transplantation in children: a rare complication related to calcineurin inhibitor effects.

PRES is a neuroclinical and radiological syndrome that results from treatment with calcineurin inhibitor immunosuppressives. Severe hypertension is commonly present, but some patients may be normotensive. We report herein two children who received liver transplants, as treatment for biliary atresia in the first case and for Alagille's syndrome in the second one. In the early postoperative, both patients presented hypertension and seizures. In both cases, the image findings suggested the diagnosis of PRES. The CT scan showed alterations in the posterior area of the brain, and brain MRI demonstrated parietal and occipital areas of high signal intensity. Both children were treated by switching the immunosuppressive regimen and controlling arterial blood pressure. They displayed full recuperation without any neurologic sequelae. Probably, the pathophysiology of PRES results from sparse sympathetic innervation of the vertebrobasilar circulation, which is responsible for supplying blood to the posterior areas of the brain. In conclusion, all liver-transplanted children who present with neurological symptoms PRES should be considered in the differential diagnosis, although this is a rare complication. As treatment, we recommend rigorous control of arterial blood pressure and switching the immunosuppressive regimen.

Reversible posterior encephalopathy syndrome associated with bortezomib.

Reversible posterior encephalopathy (RPES) is an uncommon neurological syndrome that is being increasingly reported in association with anti-neoplastic therapies. The first case of reversible posterior encephalopathy associated with the proteosome inhibitor bortezomib is described and the reported experience of the occurrence of RPES with other antineoplastic therapies reviewed. Dysregulation of cerebral vasomotor autoregulation is postulated as the underlying pathophysiology in this case of bortezomib associated RPES.

[Posterior reversible encephalopathy syndrome induced by a cough and cold drug containing pseudoephedrine]. / Syndrome d'encéphalopathie postérieure réversible induit par un décongestionnant nasal contenant de la pseudo-éphédrine.

INTRODUCTION: Posterior reversible encephalopathy syndrome is a clinico-radiological entity characterized by neurologic symptoms in association with usually reversible bilateral posterior hemispheric oedema on neuroimaging. Many pathological conditions and treatments have been associated with this syndrome. CASE REPORT: We report a 19-year-old woman, followed-up for hypocomplementemic urticarial vasculitis, who presented with a posterior reversible encephalopathy syndrome induced by the intake of an over-the-counter cold remedy containing pseudoephedrine. Clinical manifestations and radiological abnormalities resolved after anti-hypertensive therapy and withdrawal of sympathomimetic drug. CONCLUSION: The diagnosis of posterior reversible encephalopathy syndrome should be considered in patients with compatible clinical and radiological presentation because of its potential reversibility with an appropriate management. Intake of drugs, including over-the-counter cough and cold drugs, should be looked for in the history as well as autoimmune disorders.

Hypertensive encephalopathy in patients with chronic renal failure caused by stopping antihypertensive agents: a report of two cases.

We herein report two cases of patients with chronic kidney disease who developed hypertensive encephalopathy, which occurred after a sudden discontinuance of antihypertensive agents. Both patients underwent care at our hospital after experiencing neurological abnormalities. In both patients, magnetic resonance imaging (MRI) revealed edema in the cerebral white matter and cortices, basal ganglia, brainstem, and cerebellum. Though recently the number of reports about hypertensive encephalopathy has decreased, we describe two case reports and also review the pertinent literature.

PRES following administration of DHE in a patient with unsuspected pheochromocytoma.

We describe neurological complications which manifested after a patient with unsuspected pheochromocytoma was administered dihydroergotamine. Following administration of dihydroergotamine, the patient developed Balint syndrome, with the appearance of symmetric, bilateral occipital signal change on magnetic resonance imaging suggestive of posterior reversible encephalopathy syndrome.

Lysergic acid amide-induced posterior reversible encephalopathy syndrome with status epilepticus.

INTRODUCTION: Posterior reversible encephalopathy syndrome (PRES) is known to occur in association with several substances. However, lysergic acid amide (LSA) is not among the previously reported causes of PRES. METHODS: We report on a patient with PRES presenting as convulsive status epilepticus associated with hypertensive encephalopathy after LSA ingestion. Magnetic resonance imaging was performed and catecholamine metabolites assayed. RESULTS: The patient achieved a full recovery after aggressive antihypertensive therapy and intravenous anticonvulsivant therapy. The clinical history, blood and urinary catecholamine levels, and response to treatment strongly suggest that PRES was induced by LSA. CONCLUSION: LSA, a hallucinogenic agent chiefly used for recreational purposes, should be added to the list of causes of PRES.

Posterior reversible encephalopathy in a child with Langerhans cell histiocytosis following allogeneic PBSCT treatment with cyclosporine.

Posterior reversible encephalopathy syndrome (PRES) is associated with a specific disorder of cerebrovascular autoregulation of multiple etiologies. This syndrome had been subsequently described in numerous medical conditions, including hypertensive encephalopathy, pre-eclampsia and the use with immunosuppressive drugs. Here, we report a child suffering from Langerhans cell histocytosis developing into PRES following immunosuppressive therapy. Symptoms and neuroimaging abnormalities were complete resolution subsequent to the withdrawal of cyclosporine. Although PRES is rarely seen among children, it should always be considered in the differential diagnosis of acute neurological illness, especially undergoing immunosuppressive therapy.

Linezolid-induced posterior reversible leukoencephalopathy syndrome.

OBJECTIVE: To describe a 71-year-old woman who developed clinical and neuroradiological features of posterior reversible leukoencephalopathy syndrome with a compromised blood-brain barrier after 5 days of intravenous linezolid therapy for an infected hip prosthesis. DESIGN: Case report. SETTING: Academic research. MAIN OUTCOME MEASURES: Posterior reversible leukoencephalopathy syndrome was documented using serial cranial magnetic resonance imaging, and the blood-brain barrier disturbance was demonstrated by contrast enhancement of a lesion and by cerebrospinal fluid analysis. RESULTS: Other causes of posterior reversible leukoencephalopathy syndrome, such as renal failure, severe hypertension, inflammatory syndromes, and infectious diseases of the central nervous system, were excluded during hospitalization. After discontinuation of linezolid therapy, the patient's condition improved rapidly. CONCLUSION: To our knowledge, this is the first report of likely linezolid-induced posterior reversible leukoencephalopathy syndrome with an altered blood-brain barrier after short-term intravenous therapy.

Reversible posterior leukoencephalopathy syndrome after treatment of diffuse large B-cell lymphoma.

BACKGROUND: We report the case of a patient who experienced a severe neurologic complication after treatment of diffuse large B-cell lymphoma. CASE REPORT: A 62-year old patient was diagnosed with a diffuse large B-cell lymphoma and treated with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone under prophylactic G-CSF substitution. After the second cycle she developed severe neurologic complications with generalized seizures and soporous condition. The MRI showed bilateral areas of signal hyperintensity in the subcortical and cortical regions in both hemispheres, consistent with the diagnosis of a reversible posterior leukoencephalopathy syndrome. The patient was under surveillance in intensive care, and a meticulous control of the blood pressure was performed. She fully recovered within a few days, and MRI changes normalized. Antineoplastic treatment had to be continued, and we chose a combination of rituximab, doxorubicin, etoposide, and prednisone. CONCLUSIONS: The reversible posterior leukoencephalopathy syndrome is believed to be the result of altered cerebral autoregulation with impaired blood flow control and resultant endothelial damage caused by different situations and agents. Several chemotherapy agents have been described in association with the syndrome. However, little is known about the prevalence of the syndrome and the follow-up of these patients, especially their further treatment.