Encefalopatía posterior reversible como primera manifestación del Síndrome de Guillain-Barré
| Autor: | Eduardo Venegas R, Sergio Urrutia L, Cristian Figueroa, Catalina Carrizo C |
|---|---|
| Jazyk: | Spanish; Castilian |
| Rok vydání: | 2012 |
| Předmět: |
Guillain-Barre syndrome
medicine.diagnostic_test business.industry Polyradiculoneuropathy Tetraparesis Magnetic resonance imaging Posterior reversible encephalopathy syndrome General Medicine medicine.disease Guillain-Barré syndrome Hypertensive encephalopathy Dysarthria Posterior leukoencephalopathy syndrome Respiratory failure Anesthesia medicine medicine.symptom business Pure autonomic failure |
| Zdroj: | Revista médica de Chile v.140 n.10 2012 SciELO Chile CONICYT Chile instacron:CONICYT |
| Popis: | BACKGROUND We report a 56 year old male hypertensive, who presented with a posterior reversible encephalopathy syndrome (PRES) as an initial manifestation of Guillain-Barre syndrome (GBS). His first symptoms were right hemiparesis and hemihypoesthesia, followed by headache, dizziness, dysarthria and a general feeling of discomfort. On the third day, flaccid tetraparesis, impairment of consciousness, epileptic seizures and respiratory failure appeared, along with severe hypertension. Cerebral Magnetic Resonance Imaging showed the characteristic PRES lesions. Cerebrospinal fluid analyses revealed albumin-cytological dissociation and nerve conduction studies showed an axonal demyelinating polyradiculoneuropathy, which confirmed the diagnosis of GBS. Treatment with intravenous immunoglobulin was given together with antihypertensive therapy and mechanical ventilation, achieving an important clinical and imaging remission of PRES, but maintaining tetraparesis during the hospitalization. Twelve months after discharge and regular motor rehabilitation, the patient achieved complete autonomy on the activities of daily living. It has been postulated that the autonomic failure and the elevation of circulating pro-inflammatory cytokines in GBS may be the cause of a breach in the blood-brain barrier, thus causing PRES, that can completely remit with an adequate management. |
| Databáze: | OpenAIRE |
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