Posterior reversible encephalopathy syndrome is a disorder of reversible subcortical vasogenic brain edema in the context of different diseases or exposure to cytotoxic drugs such as fludarabine. We present the case of a pediatric patient with β-thalassemia who develops a fludarabine-induced posterior reversible encephalopathy while he received an induction regimen to achieve an allogenic hematopoietic cell transplantation. The clinical presentation consists in altered mental state, headache, status epilepticus, visual disturbance, and hypertension. His treatment was carried out with the suspension of the medication and the control of hypertension and status epilepticus; the final outcome was positive without additional complications. There are published reports about fludarabine toxicity in the central nervous system with different doses of the drug in different clinical context. We also made a review of the literature available and conclude that fludarabine is not an extraordinary cause of posterior reversible encephalopathy syndrome.
Introduction The human T-lymphotropic virus has been associated with human disease, affecting CD4 + T, CD8 + T, and B lymphocytes. It can cause T-cell leukemia/lymphoma and HTLV-associated myelopathy. Case presentation A 31-year-old woman was admitted after 2 months of cramps, paraparesis, and fecal/urinary incontinence. She was diagnosed with neurosyphilis according to the cerebrospinal fluid analysis. Despite treatment with crystalline penicillin there was no recovery, and anti-HTLV-1/2 tests were positive; therefore, the diagnosis of HTLV-associated myelopathy was made. The patient rejected glucocorticoid treatment; baclofen and carbamazepine were used to treat spasticity and cramps, respectively. The patient has not had progression. Discussion HTLV-associated myelopathy is generated by an exaggerated inflammatory response in the central nervous system with clonal expansion of CD4 + T and CD8 + T lymphocytes. There is not a specific and useful treatment; glucocorticoids can reduce inflammation, but do not improve clinical functional outcomes. There is a high prevalence of syphilis and human T-lymphotropic virus co-infection in tropical countries; however, myelopathy as the first clinical manifestation is unusual. The treatment of neurosyphilis could reduce the inflammation into the central nervous system and could decrease the progression of sequelae. This is the first case of myelopathy secondary to viral and treponemal co-infection confirmed in Colombia.
RESUMENSe presenta un caso local de la variante de Opalski, del síndrome medular lateral (síndrome de Wallenberg) y se hace una revisión de la literatura sobre los síntomas de este cuadro clínico, así como las posibles razones que explican esta modificación en la expresión clínica. La variante de Opalski fue descrita en 1948, ochenta y nueve años después de la descripción original del síndrome por Adolf Wallenberg, su principal característica es la presencia de hemiparesia o hemiplejía del cuerpo del mismo lado de la lesión del bulbo raquídeo. La etiología es vascular en la mayoría de casos, por obstrucción de la arteria cerebelosa postero-inferior o de los ostium de vasos penetrantes que se originan en la arteria. No hay estudios que reporten la incidencia exacta de este cuadro clínico a nivel mundial, sin embargo, su presentación no es tan infrecuente. Lo más interesante al analizar cada caso, es que los hallazgos semiológicos son una muestra de la profunda organización del sistema nervioso.PALABRAS CLAVES: arteria vertebral, bulbo raquídeo, fosa craneal posterior, infarto cerebral, síndrome medular lateral (DeCS).
ContribuCión de los autoresCristian Navarro, recolección de los datos e información del caso. Diseño y elaboración del artículo. Jaiver Macea, diseño y elaboración del artículo. Revisor de la discusión.
SUMMARYA clinical case of the Opalski variant of the lateral medullary syndrome (Wallenberg's syndrome) is presented and a literature review about the symptoms of this clinical picture is done, as well as the possible reasons explaining this modification in the clinical expression. The Opalski variant was described in 1948, eighty-nine years after the original description of the syndrome by Adolf Wallenberg, its main feature is the presence of hemiparesis or hemiplegia of the ipsilateral side of the injury in the medulla oblongata. In most cases the etiology is vascular when the postero-inferior cerebellar artery is occluded or there is an obstruction of the ostium of penetrating vessels originating in the artery. There are no studies that accurately report the worldwide incidence of this clinical variant, however, its presentation is not uncommon. The most interesting discovery of each case is that semiological findings are a good example of the profound organization of the nervous system.
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