Clinical diagnosis in Karwinskia humboldtiana polyneuropathy.

Intoxication by Karwinskia humboldtiana presents a neurological picture similar to that for Guillain-Barré syndrome or other polyradiculoneuropathies. Clinical diagnosis in poisoned humans may be difficult if no evidence of previous fruit ingestion is available. We present our experience in the clinical diagnosis of Karwinskia humboldtiana polyneuropathy, as confirmed by toxin detection in blood. We designed an open trial at the Pediatric Neurology service and included all cases with acute ascending paralysis that were admitted to our hospital in the last two years. In all cases, we performed hematological, immunological and biochemical profiles, CSF analysis including immunological studies, oligoclonal bands and myelin basic protein determinations. Electrodiagnostic studies were performed, including motor conduction velocities, distal latencies, F-wave latency and compound muscle action potential (CAMP) amplitude. The presence of Karwinskia humboldtiana toxins in blood were determined by thin layer chromatography. In six cases, T-514 Karwinskia humboldtiana toxin was detected. These cases had a symmetric motor polyneuropathy with the absence of tendon reflexes and no sensory signs or cranial nerve involvement. Only one patient required assisted ventilation due to bulbar paralysis. In two of these cases, a sural nerve biopsy revealed a segmental demyelination with swelling and phagocytic chambers in Schwann cells and without lymphocytic infiltration. All six cases survived, with complete recovery in five. We conclude that this intoxication is common in Mexico. The availability of toxin detection in blood samples allows the clinician to establish an accurate diagnosis and should be included in the study of children with polyradiculoneuropathy, especially in countries where this poisonous plant grows.

[9 cases of encephalitis in an epidemic outbreak of exanthematous diseases]. / Nueve casos de encefalitis en un brote epidémico de enfermedades exantemáticas.

We report here nine cases of encephalitis secondary to exanthematous diseases diagnosed from March to June 1990 at the University Hospital in Monterrey, Mexico. Two of the cases were secondary to measles, three to rubella, and four to varicella. One patient with varicella died, and the histopathological study showed findings compatible with viral encephalitis. The sex distribution was four males and five females with ages ranging from two to fourteen years. The most common clinical manifestations were hemiparesia, intracranial hypertension, meningism and altered consciousness. The CSF examination showed lymphocytic pleocytosis (mean = 295 cells), increased protein levels (mean = 118 mg/dL) and a normal glucose value in eight cases. These findings and the presence of an exanthematous disease suggested viral invasion of the CNS. Magnetic resonance imaging showed high intensity signal areas mainly in the frontal and temporal lobes. In this paper we compare the relative incidence of encephalitis secondary to exanthematous diseases in our geographical area during the last four years.