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)

Peripheral vestibular disease and lethargy were attributed to an adenocarcinoma in the middle ear of a 10-year-old cat. The tumor was invasive, inducing severe lysis of the tympanic bulla and adjacent temporal bone. Direct invasion to the meninges and brainstem also was observed. Neoplasms of the middle ear are rare in cats, with squamous cell carcinomas reported most commonly, but should be considered as causes of chronic otitis or signs of peripheral vestibular disease.
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PMID:Adenocarcinoma of the middle ear with osteolysis of the tympanic bulla in a cat. 150 54

Hypernatremia resulting in neurologic symptoms ranging from lethargy to coma, and with underlying lesions of cerebral hemorrhage and thrombosis, has been reported in human beings. Herein we report two cases of cerebral infarction with venous thrombosis in cynomolgus monkeys. Both animals were severely hypernatremic because of water deprivation, with serum sodium levels of 185 and 193 meq/liter, respectively. At necropsy, there were bilateral multiple hemorrhagic and malacic areas visible on the surface of the cerebrum and extending into the parenchyma, primarily involving the occipital lobes. These lesions were interpreted microscopically as infarcts because, in addition to hemorrhage and necrosis, multiple thrombi were present in small and medium-sized veins of gray matter and meninges. The pathogenesis of hypernatremia-induced cerebral lesions is believed to involve cellular dehydration that caused shrinkage of the brain. Because the vasculature of the brain is tightly adherent to the skull, this shrinkage results in tearing of blood vessels, with consequent hemorrhage and thrombosis.
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PMID:Cerebral infarction in two cynomolgus macaques (Macaca fascicularis) with hypernatremia. 881 42

A 6-year-old boy with a family history of hemiplegic migraine had a hemiplegic migraine lasting for 6 days complicated by prolonged fever, lethargy, and two brief focal seizures. An acute single photon emission computerized tomogram (SPECT) demonstrated decreased blood flow in the symptomatic cerebral hemisphere as well as crossed cerebellar diaschisis not previously documented in migraine. Another unique finding was the MRI with enhancement of the meninges and pial vessels over the symptomatic cerebral hemisphere. These findings suggest cerebellar and extra-axial involvement as components of hemiplegic migraine.
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PMID:Familial hemiplegic migraine with crossed cerebellar diaschisis and unilateral meningeal enhancement. 938 60

High doses of adenotk were injected into the cerebrospinal fluid of rats and nonhuman primates (Macaca mulatta). Vector administration was followed by ganciclovir administration for 14 days. Despite the absence of clinical symptoms, analysis of the cerebrospinal fluid (CSF) and histopathological examination of the central nervous system (CNS) of the monkeys (3 weeks after vector injection) were consistent with a viral meningitis. Immunohistochemical analysis of the inflammatory infiltrates in the monkeys revealed the presence of T and B lymphocytes, indicating a combined cellular and humoral immune response to the vector. This latter was supported by the finding of intrathecal anti-adenovirus antibody synthesis. Rats receiving high intrathecal adenotk doses showed a transient and dose-dependent clinical toxicity consisting of lethargy, hyperemic eyes and weight loss. Histopathological examination of the meninges showed a shift from polymorphonuclear infiltrates during the first post-injection days to clusters of mononuclear cells after 7 days. Acute toxicity is probably related to the early, innate immune response to the vector. In a separate experiment, high levels of IL-8 and IL-6, were measured during the first 2-3 post-injection days in the CSF of two monkeys which received intrathecal adenoLacZ. Therefore, these cytokines seem to play an important role in initiating the nonspecific immune response. In one monkey which received adenotk, recombinant adenovirus was cultured from serum samples obtained at the 7th post-injection day. At this time-point, no vector could be isolated from CSF samples. Based on these preclinical data, we recommend careful dose finding for clinical studies that aim to treat patients with leptomeningeal metastases.
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PMID:Intra-CSF administered recombinant adenovirus causes an immune response-mediated toxicity. 1098 67

Meningeal melanocytoma is a rare benign primary melanotic tumor of the meninges, most commonly found in the spinal canal and the posterior fossa. The authors report the 19th published case of a supratentorial meningeal melanocytoma and the first reported case in which the tumor arose from the planum sphenoidale. The patient's presenting symptoms were characteristic of a large bifrontal lesion and included headaches, personality change, lethargy, and urinary and fecal incontinence. Computerized tomography and magnetic resonance imaging studies revealed an extraaxial lesion arising from the planum sphenoidale. The patient underwent successful gross total removal of the tumor without neurological sequelae. Based on the findings shown in this case report, meningeal melanocytoma should be included in the differential diagnosis of extraaxial lesions arising from the area of the planum sphenoidale.
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PMID:Meningeal melanocytoma of the planum sphenoidale. Case report and review of the literature. 1135 21

The course of bacterial titers, meningeal inflammation, behavioral abnormalities, and neuronal damage was studied in a mouse model of Streptococcus pneumoniae meningitis. At 24 h after injection of 10(4) colony-forming units (CFU) S. pneumoniae into the right forebrain, infected mice became severely lethargic. Bacterial titers in cerebrospinal fluid and cerebellum rose to 10(9) CFU/ml, with strong granulocyte invasion into the meninges and neuronal necroses in the neocortex, striatum and hippocampal formation. Meningeal inflammation and neuronal damage in intercellular cell adhesion molecule-1- and macrophage colony-stimulating factor-deficient mice was similar to that in wild-type littermates. Untreated, the infection was fatal. Wild-type mice treated earlier than 24 h after infection with ceftriaxone (2 mg every 12 h for 3 days) survived without apparent behavioral abnormalities. Delay of treatment beyond 30 h led to the death of more than 50% of the infected mice. This mouse model is suitable for therapeutic studies and for the investigation of inflammation in knockout mice. The neuronal damage resembles morphological abnormalities observed in humans.
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PMID:A mouse model of Streptococcus pneumoniae meningitis mimicking several features of human disease. 1148 22

Lemierre's syndrome, oropharyngeal infections induced by anaerobic bacteria, leading to fatal septic thrombophlebitis of the internal jugular vein and pulmonary embolic abscesses in humans, was diagnosed in a 6-month-old, male, New Zealand White rabbit. After acute onset of anorexia, lethargy, and depression, the rabbit died suddenly despite emergency clinical care. Necropsy revealed swelling, necrosis, and abscess in the soft tissues around the left caudal mandibular ramus, oral mucosa, and molar teeth, with systemic embolic abscesses and necrosis, especially in the jugular vein, lungs, and brain. Histologic examination revealed necrosis and embolic abscesses with filamentous bacteria in the mandibular soft tissues, salivary gland, jugular veins, alveolar bone and marrow, periodontal tissues and dental pulp, oral and pharyngeal mucosa, lungs, brain, liver, myocardium, meninges, and small intestine. Bacterial culture of the mandibular abscess and heart blood yielded Fusobacterium necrophorum.
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PMID:Oropharyngeal Necrobacillosis with Septic Thrombophlebitis and Pulmonary Embolic Abscesses: Lemierre's Syndrome in a New Zealand White Rabbit. 1208 16

Neurocutaneous melanosis (NM) coexisting with the Dandy-Walker complex (DWC) is a rare condition, with fewer than 15 cases reported in the literature. The authors present a case of an infant with NM and DWC suffering from progressive brainstem compression following ventriculoperitoneal (VP) shunt placement for hydrocephalus. This 1-year-old boy with congenital melanocytic nevi had met normal developmental milestones until the age of 11 months, when he began regressing in ambulation and language function. Intractable vomiting had developed 1 week later. Magnetic resonance (MR) imaging of the brain revealed DWC with hydrocephalus, and spinal MR images demonstrated a proliferative process within the meninges, consistent with NM. The patient underwent right frontal VP shunt placement resulting in immediate symptom relief, but 3 weeks later became irritable, increasingly lethargic, unable to pull to stand, and unable to tolerate solid food without choking. Due to these symptoms and intractable vomiting, the patient presented to the authors' institution. Brain MR imaging revealed a new-onset diffuse cystic process with anterior and posterior brainstem compression, marked kinking of the cervicomedullary junction, melanocyte pigmentation of the left temporal lobe, diffuse leptomeningeal enhancement, and no evidence of hydrocephalus. Consistent with these imaging findings, the degree of brainstem involvement upon gross visualization predictably deterred resection attempts beyond those necessary for biopsy. Pathological examination revealed diffuse melanocytosis, and the family decided not to pursue aggressive measures postoperatively. This report indicates the potential for rapid intracranial manifestation of diffuse melanocytosis in NM patients. Although the prognosis is poor, early neurosurgical involvement in these patients may provide tissue diagnosis and the potential for decompression if the process is caught early in its course.
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PMID:Progressive brainstem compression in an infant with neurocutaneous melanosis and Dandy-Walker complex following ventriculoperitoneal shunt placement for hydrocephalus. Case report. 1815 21

A 13-year-old Standardbred gelding was referred for evaluation of continuous abdominal pain. Rectal examination revealed a dislocated large colon (Dislocatio coli ad dextram). The horse showed muscle fasciculations and appeared lethargic. It was sent to surgery because of persistent colic. In transit the gelding showed an unstable walk and immediately prior to surgery a wide-based stance in the hindlimbs. Laparotomy revealed a retroflexion of the large colon and a secundary mesenterial volvulus. After surgery the horse remained recumbent. Due to the comatose state and poor prognosis the gelding was euthanized after 15 hours of recumbency. Necropsy indicated hyperaemic meninges, edema of gliacells and submeningeal tissue with vacuolization and loss of several cerebellar Purkinjecells as well as multiple conglomerates of Alzheimer type II astrocyte groups within the grey matter. Further findings included marked hepatolipidosis, multiple gastric ulcers, small intestinal hyperaemia with mild mononuclear inflammation, tapeworm-infestation of the caecum and moderate chronic enteritis with eosinophilic component in the large intestine. To the best of our knowledge, this was the first case of a horse with colic and concurrent encephalopathy without primary liver disease described in a German-speaking country.
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PMID:[Encephalopathy and Alzheimer type II astrocytes in a post laparotomy recumbent horse]. 1953 45

We report a case of amebic brain abscess due to Entamoeba histolytica. The patient was a 31-year-old man who presented with amebic liver abscess. His clinical course deteriorated in spite of proper drainage and treatment. He developed delirium, lethargy and then expired. With a history of heroin addiction, withdrawal syndrome from heroin was suspected. At autopsy, amebic abscesses were detected in the liver, large intestine, meninges and brain. A 19 cm amebic liver abscess was found in the right lobe of the liver. A 4 cm amebic brain abscess was found in the right occipital lobe. Microscopically, the tissue sections from the affected organs were confirmed to have degenerated E. histolytica trophozoites. Involvement of the brain in amebic liver abscess should be suspected in patients with neurological signs and symptoms.
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PMID:Undiagnosed amebic brain abscess. 2057 51


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