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ABSTRACT: Intoxication by Karwinskia humboldtiana (buckthorn) fruit presents a neurological picture similar to that of Guillain-Barré syndrome. In this report, we describe an experimental animal model of peripheral neuropathy induced by buckthorn fruit. Four groups of Wistar rats received one oral dose of 1.5 g/kg followed by oral doses of 0.5 g/kg at days 3, 7, 10, and 14 of dried and ground buckthorn fruit in aqueous suspension. Rats were sacrificed at 24, 48, 58, and 112 days after initial dose. Treated animals developed progressive paralysis through 58 days, then completely recovered by 112 days. Sciatic nerves showed segmental demyelination and cellular infiltrates until 58 days after exposure and then remyelinating changes at 112 days. This experimental model for peripheral neuropathy is reproducible and easy to handle. Its manipulation is relatively innocuous and allows us to study reversible peripheral nerve damage. This model can be developed in other animal species and may be useful to test new therapies for peripheral neuropathy.
Journal of the Peripheral Nervous System 10/2006; 11(3):253-61. · 2.80 Impact Factor
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ABSTRACT: Abstract Intoxication by Karwinskia humboldtiana (buckthorn) fruit presents a neurological picture similar to that of Guillain-Barré syndrome. In this report, we describe an experimental animal model of peripheral neuropathy induced by buckthorn fruit. Four groups of Wistar rats received one oral dose of 1.5 g/kg followed by oral doses of 0.5 g/kg at days 3, 7, 10, and 14 of dried and ground buckthorn fruit in aqueous suspension. Rats were sacrificed at 24, 48, 58, and 112 days after initial dose. Treated animals developed progressive paralysis through 58 days, then completely recovered by 112 days. Sciatic nerves showed segmental demyelination and cellular infiltrates until 58 days after exposure and then remyelinating changes at 112 days. This experimental model for peripheral neuropathy is reproducible and easy to handle. Its manipulation is relatively innocuous and allows us to study reversible peripheral nerve damage. This model can be developed in other animal species and may be useful to test new therapies for peripheral neuropathy.
Journal of the Peripheral Nervous System 08/2006; 11(3):253 - 261. · 2.80 Impact Factor
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ABSTRACT: 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.
Journal of the Neurological Sciences 01/1998; 154(1):49-54. · 2.35 Impact Factor
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ABSTRACT: To determine the extent of extraneural lesions in buckthorn poisoning, 180 CD1 mice were administered either green or ripe fruit or toxins T-544 or T-514 obtained from the fruit of the plant and were observed over a period of three weeks. Marked weakness, hyporeflexia, hair bristling, ptosis, spinal deformity, weight loss and dypsnea were prominent signs. Mortality in mice given green fruit was 100% at all doses; with toxin T-514 the mortality was 100% at 45 mg/kg. One hundred and sixty-two necropsies were performed and major lesions were found in liver and lung. The pulmonary lesions consisted of progressive vascular congestion and hemorrhage. Alterations in liver consisted of congestion, hemorrhage, hepatocyte degeneration, central zone necrosis and acute diffuse necrosis. Green fruit was more toxic than ripe fruit and T-514 was more active than T-544.
Toxicon 02/1986; 24(11-12):1091-7. · 2.51 Impact Factor
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ABSTRACT: M. V. Bermudez, D. Gonzalez Spencer, M. Guerrero, N. Waksman and A. Piñeyro. Experimental intoxication with fruit and purified toxins of buckthorn (Karwinskia humboldtiana). Toxicon24, 1091 – 1097, 1986. — To determine the extent of extraneural lesions in buckthorn poisoning, 180 CD1 mice were administered either green or ripe fruit or toxins T-544 or T-514 obtained from the fruit of the plant and were observed over a period of three weeks. Marked weakness, hyporeflexia, hair bristling, ptosis, spinal deformity, weight loss and dypsnea were prominent signs. Mortality in mice given green fruit was 100% at all doses; with toxin T-514 the mortality was 100% at 45 mg/kg. One hundred and sixty-two necropsies were performed and major lesions were found in liver and lung. The pulmonary lesions consisted of progressive vascular congestion and hemorrhage. Alterations in liver consisted of congestion, hemorrhage, hepatocyte degeneration, central zone necrosis and acute diffuse necrosis. Green fruit was more toxic than ripe fruit and T-514 was more active than T-544.
Toxicon.
