Martínez H R, Bermudez M V, Rangel-Guerra R A, de Leon Flores L
Neurology Service, School of Medicine and Hospital Universitario UANL, Monterrey, N.L., Mexico.
J Neurol Sci. 1998 Jan 21;154(1):49-54. doi: 10.1016/s0022-510x(97)00212-8.
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.
因 Humboldt 卡罗温斯基树中毒会呈现出与吉兰 - 巴雷综合征或其他多发性神经根神经病相似的神经学症状。如果没有先前摄入该果实的证据,对中毒者进行临床诊断可能会很困难。我们介绍了在 Humboldt 卡罗温斯基树多发性神经病临床诊断方面的经验,血液中的毒素检测证实了这一点。我们在儿科神经科开展了一项开放性试验,纳入了过去两年内我院收治的所有急性上行性麻痹病例。对所有病例进行了血液学、免疫学和生化检查,脑脊液分析包括免疫学研究、寡克隆带和髓鞘碱性蛋白测定。进行了电诊断研究,包括运动传导速度、远端潜伏期、F 波潜伏期和复合肌肉动作电位(CAMP)幅度测定。通过薄层色谱法测定血液中 Humboldt 卡罗温斯基树毒素的存在情况。在 6 例病例中检测到了 T - 514 Humboldt 卡罗温斯基树毒素。这些病例表现为对称性运动性多发性神经病,无腱反射,无感觉体征或颅神经受累。仅 1 例患者因延髓麻痹需要辅助通气。其中 2 例病例的腓肠神经活检显示节段性脱髓鞘,施万细胞肿胀并有吞噬腔,无淋巴细胞浸润。所有 6 例病例均存活,5 例完全康复。我们得出结论,这种中毒在墨西哥很常见。血液样本中可进行毒素检测,这使临床医生能够做出准确诊断,并且在对多发性神经根神经病患儿的研究中应包括此项检测,尤其是在这种有毒植物生长的国家。