Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 22-year-old man developed unconsciousness, severe quadriplegia and muscle atrophy, and had markedly elevated serum creatine kinase levels after using the high-dose steroid and nondepolarizing neuromuscular blocking agents during the course of sepsis and DIC. On neurological examination, he was lethargic. The patient had generalized muscle weakness and wasting, and diminished deep tendon reflexes. He weakly responsed to painful stimuli on the legs. The motor nerve conduction study demonstrated decreased CMAP (compound muscle action potential) amplitudes. Motor and sensory nerve conduction velocities and their distal latencies were normal. Muscle biopsy revealed marked muscle fiber atrophy predominantly in type 2 fibers and numerous basophilic and a few necrotic fibers. Some atrophic fibers had decreased to absent myosin adenosine triphosphatase activity in their center. Accordingly, he was diagnosed as having acute quadriplegic myopathy (AQM), which has been reported mainly in Western countries. The mechanism of muscle fiber degradation in this myopathy is still unknown. On immunohistochemical analysis to our patient, enzyme activities of various proteases such as calpain, cathepsin B, and proteasomes were increased in the sarcoplasm, especially in the atrophic fibers. We suggest that lysosomal cathepsin, nonlysosomal calpain, and ATP-ubiquitin-proteasome proteolytic pathways participate in muscle fiber degradation in AQM.
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PMID:[A case of acute quadriplegic myopathy]. 1108 98

A 14-year-old female alpaca (Vicugna pacos) was presented with a 1-week history of lethargy and anorexia and a 2-day history of recumbency, trembling, and hypothermia. There were no significant gross findings on postmortem examination. Hematoxylin and eosin-stained sections of brain demonstrated the presence of intracytoplasmic crystalline eosinophilic rod-shaped inclusions, mainly in the hippocampal pyramidal cells. Immunohistochemical staining for synuclein, tau protein, ubiquitin, and smooth muscle actin was negative. All inclusions were positive with phosphotungstic acid hematoxylin. Ultrastructurally, the inclusions were multilamellar and filamentous with longitudinal herringbone pattern and cross-sectional latticelike structure. The combination of hematoxylin and eosin appearance, special stains, immunostaining, and ultrastructural findings was consistent with Hirano-like bodies. The Hirano-like bodies were highly unlikely to be the cause of the neurologic signs experienced by this alpaca. To the authors' knowledge, this is the first report of spontaneous cerebral Hirano-like bodies in an alpaca.
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PMID:Cerebral Hirano-like bodies in an alpaca (Vicugna pacos): histologic and ultrastructural characterization. 2155 25

Ipomoea carnea is a toxic plant that affects goats, with symptoms being characterised by nervous disorders and death. Swainsonine and calystegines are the principal toxic components isolated from I. carnea, which also yields lysergic acid derivatives. The aim of this study was to improve the clinical characterisation of experimental intoxication by I. carnea in guinea pigs through the evaluation of behavioural changes and to perform a thorough histopathological analysis of the affected CNS. Leaves of I. carnea were administered to guinea pigs. Open-field gait analysis and monoamine levels were measured. The poisoned animals exhibited increased vocalisation, lethargy, and a reduction in the locomotion frequency after the fourth week of intoxication, as demonstrated in the open-field test. Significant differences were observed in hind-limb gait width by the last week of intoxication. After 65 days, the guinea pigs were euthanised, necropsied, and examined using light and electron microscopy. At the end of the experiment, plasma serotonin decreased. In contrast, dopamine decreased, and noradrenaline increased in urine. Brain sections were evaluated with conventional histological methods and immunohistochemistry (IHC), as well as by transmission electron microscopy (TEM). Vacuoles were observed throughout the brain, but they were particularly prominent in the brainstem. In addition, there were PAS-negative regions, and the Nissl substance was dispersed or absent, which was confirmed with the Kluver-Barreda stain. Moderate microgliosis was observed by immunohistochemistry. In the medulla oblongata, numerous ubiquitin-positive spheroids together with neuronal degeneration were observed in the nucleus gracilis/cuneatus. Furthermore, vacuoles were observed in astrocytes, oligodendrocytes, and endothelial cells by TEM. Our results showed that the behavioural effects may have been caused by alterations in the brain in conjunction with changes in monoamine levels. This research confirms the utility of this model for studying the pathogenesis of plant-induced lysosomal storage diseases.
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PMID:Experimental intoxication of guinea pigs with Ipomoea carnea: behavioural and neuropathological alterations. 2399 28