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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cryptococcosis was diagnosed in an adult male patas monkey (Erythrocebus patas) 9 months after importation. The disease was characterized by an open lesion on the buttock and epileptiform seizures. Diagnosis was confirmed through immunologic identification of the organism in serum and cerebrospinal fluid and by mycologic procedures performed on the cultured organism. The monkey was killed and cryptococcal organisms were found in the lung, brain, subcutaneous lesions, thyroid, pancreas, adrenals, and spinal cord. Retrospective analysis of stored serum indicated that the monkey was infected at the time of importation.
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PMID:Disseminated cryptococcosis in a patas monkey (Erythrocebus patas). 41 1

A case of granulomatous encephalitis in a 42 year old woman is reported. During the course of her illness, she showed over a short period of time a left hemiparesis, epileptic seizures and severe impairment of consciousness. Bilateral carotic angiography showed no evidence of an expansive lesion, while brain-scan presented an hyperactive area in the right parasagittal region. The cerebrospinal fluid examination demonstrated an increasing hyperproteinosis and death occurred 45 days after the first symptoms appeared. At post mortem in addition to brain edema, a soft, grey-brown discoloured area, of the size of hazel nut was found in the right limbic convolution. Histologically the abnormal tissue revealed a granulomatous structure formed by thick masses of lymphocytes, plasmacells and epithelioid cells among which vessel neoformation and hemorrhages were noted. Remarkable perivascular infiltrations were seen in the white matter, in the gray matter and in the leptomeninges also far away from the granulomatous focus. Many round yeast-like elements were observed free in the tissue as well as inglobated in large histiocytes. Although morphologically they resembled Cryptococcus neoformans organisms, the specific staining techniques for the mycoses were negative. The authors, after reviewing the various histopathological pictures of cryptococcosis in the nervous system and the modern diagnostic procedures for this mycotic infection during life, discuss the range of so-called primitive granulomatous encephalites.
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PMID:[Clinical and pathological observations on a case of granulomatous encephalitis (probable criptococcal infection) (author's transl)]. 85 85

A case of cryptococcosis of the brain in a male patient 47 years of age is described. Duration of the disease--about one year. Clincally it was accompanied by epileptic seizures with loss of consciousness. Diagnosis of cryptococcosis was made following the histological investigation of a part of the brain removed in connection with tumour. Morphologically, there was detected an area of necrosis and aggregation of yeast-like fungi with the typical of cryptococcus oval form and felatinous capsule showing intensive colouration when stained by Hochkiss' method. The pathogenic agent was detected in the spinal fluid of the patient and in the tissue culture.
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PMID:[Cryptococcosis of the central nervous system]. 98 41

Involvement of the central nervous system (CNS) is common in patients with advanced disease due to human immunodeficiency virus (HIV). Symptoms range from lethargy and apathy to coma, incoordination and ataxia to hemiparesis, loss of memory to severe dementia, and focal to major motor seizures. Involvement may be closely associated with HIV infection per se, as in the AIDS dementia complex, but is frequently caused by opportunistic pathogens such as Toxoplasma gondii and Cryptococcus neoformans or malignancies such as primary lymphoma of the CNS. The clinical presentations of attendant and direct CNS involvement are remarkably non-specific and overlapping, yet a correct diagnosis is critical to successful intervention. Toxoplasmic encephalitis is one of the most common and most treatable causes of AIDS-associated pathology of the CNS. A great deal has been learned in the last 10 years about its unique presentation in the HIV-infected patient with advanced disease. Drs. Benjamin J. Luft of the State University of New York at Stony Brook and Jack S. Remington of the Stanford University School of Medicine and Palo Alto Medical Foundation's Research Institute have studied T. gondii for many years and are two of the leading experts in the field. This commentary comprises an update of their initial review (J Infect Dis 1988;157:1-6) and a presentation of the current approaches to diagnosing and managing toxoplasmic encephalitis in HIV-infected patients.
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PMID:Toxoplasmic encephalitis in AIDS. 152 Jul 57

In the immunocompromised patient, even mild forms of any combination of headache, meningismus, altered mental status, or focal neurologic signs should initiate an evaluation for possible CNS infection. The limited signs and symptoms of acute CNS infection are not due to specific organisms but to pathologic changes at the neuroanatomic site of infection. The initial clinical history, examination, laboratory, and neuroradiographic data will narrow the problem to one of several groups of agents, although it may not be possible to specify a single causative agent. It should be remembered that several concurrent infections (i.e., CMV and toxoplasmosis, aspergillosis, and bacterial sepsis) may be present. Thus, the clinician should rely on broad antibiotic coverage appropriate to the suspected causative agent or agents at the site of infection. It may be necessary to offer broad-spectrum antibiotic coverage for a CSF presentation that is subsequently found to result from a viral illness or from a noninfectious cause. However, one should avoid undertreating those infections for which specific therapy can be offered, and broad-spectrum treatment usually will not be regretted. Uncertainty in diagnosis following noninvasive procedures should lead to a brain biopsy. Although many of the infections discussed in this article have a poor prognosis, some of the most common pathogens, such as Cryptococcus, Listeria, and Toxoplasma, have effective specific therapies to which the patient should have access as rapidly as possible. The clinician who has successfully treated a patient with CNS infection should remain vigilant for late sequelae or recurrence of infection. Chronic treatment of some infections, such as toxoplasmosis or aspergillosis, may be necessary. The reintroduction of steroids for the treatment of an underlying cancer may reactivate previously treated disease, such as cryptococcosis, and periodic CSF surveillance is appropriate under these circumstances. Recurrence of the symptoms should raise the suspicion of recurrent or new infection, and the patient also should be evaluated with CT or MRI for the development of hydrocephalus or for new metastatic disease. In patients who have had varicella-zoster infection, postherpetic neuralgia and delayed arteritis may develop. Seizures, hearing loss, and neuropsychologic sequelae may follow any meningoencephalitis. The patient should always be reevaluated for the possibility of infection with a different opportunistic organism. CNS infections remain a major cause of morbidity and mortality in immunosuppressed patients with malignancies. In one series, 60% of such patients died as a result of their CNS infection, many at a time when the underlying disease had an otherwise good prognosis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Central nervous system infections in cancer patients. 175 29

A 32-year-old male homosexual presented to the emergency department (ED) with the clinical picture of a nonspecific illness. While in the ED, he experienced a first-time seizure. Computed tomography (CT) showed an enhancing mass lesion. Antibacterial therapy was started and continued until a second lumbar puncture (LP), 36 hours after admission, showed distinct yeast forms. Subsequent institution of appropriate therapy did not prevent the patient's death. The cause of death was disseminated cryptococcosis secondary to acquired immunodeficiency syndrome (AIDS).
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PMID:Acquired immunodeficiency syndrome manifested as disseminated cryptococcosis. 300 87

A case of long-term acetaminophen overdosage in a six-year-old child, which contributed to her death despite optimal medical management including oral acetylcysteine therapy, is reported. Acetaminophen 325 mg every six hours was prescribed for fever associated with measles. Believing that acetaminophen was nontoxic, the child's mother progressively increased the dose over three days, first in response to fever and subsequently for abdominal pain probably secondary to unrecognized acetaminophen toxicity. On admission to the hospital, the patient's serum acetaminophen concentration was 163 micrograms/mL (11 hours after the last dose); subsequently, the acetaminophen half-life was determined to be 15 hours. A course of oral acetylcysteine therapy (a loading dose of 140 mg/kg as the sodium salt followed by 70 mg/kg every four hours for 17 doses) was begun. Hepatic and renal failure developed within two days, followed by the onset of seizures, and brain death occurred on the 11th day. Autopsy findings consistent with acetaminophen toxicity included centrilobular hepatic and renal tubular necrosis. Aspergillis fumigatus and Cryptococcus neoformans isolates from pulmonary abscesses and bronchopulmonary lymph nodes, respectively, were an unexpected finding. However, in the absence of acetaminophen overdosage, death would have been unlikely. Cryptococcal lymphadenitis was believed to have been the initial febrile illness that was treated with supratherapeutic doses of acetaminophen. Fatalities in children from a single overdose of acetaminophen have been rare, and there is only one previous report of a fatality after long-term administration of multiple excessive doses. The lethal outcome in this case illustrates the need to educate the public on the potential toxicity of nonprescription medications.
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PMID:Death of a child associated with multiple overdoses of acetaminophen. 338 45

Cryptococcus neoformans meningoencephalitis was diagnosed as the cause of stupor and generalized seizures in a 2-year-old Cocker Spaniel. Unilateral granulomatous chorioretinitis was observed ophthalmoscopically, and isolation of C neoformans from CSF confirmed the antemortem diagnosis. The dog was euthanatized and necropsied. Multifocal lesions were seen throughout the lungs, nasal turbinates, cerebral cortex, and the optic nerve of each eye. Microscopically, the multifocal lesions were granulomas consisting of lymphocytes, macrophages, plasma cells, and cryptococcal organisms. Infection may have originated in the nasal passages and extended directly through the ethmoid plate into the meninges of the CNS and optic nerves. Although the prognosis is poor in dogs with CNS involvement, various chemotherapeutic agents are available for use by clinicians.
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PMID:Cryptococcosis involving the eye and central nervous system of a dog. 352

The hospital records of 78 patients who underwent surgical therapy for fungal infections of the central nervous system (CNS) between 1964 and 1984 are summarized. Nine different fungal types were identified, but Coccidioides immitis and Cryptococcus neoformans accounted for most (67.1%) of the infections. A variety of clinical syndromes were seen, including chronic basal meningitis (45 patients), intracranial mass lesions (12 patients), and communicating hydrocephalus (six patients). Thirteen patients had rhinocerebral forms of fungal infection, and two presented with spinal involvement. Delays in diagnosis were frequent and ranged from 2 months to 11 years. In 31 patients the CNS lesion was the first indication of a fungal infection, and lesion biopsy or cerebrospinal fluid (CSF) examination confirmed the diagnosis. A total of 144 surgical procedures were carried out, including lesion biopsy or excision in 13 patients, primary CSF shunting in 22, and placement of an Ommaya reservoir for administration of intraventricular or intracisternal antifungal agents in 48. All patients received parenteral and, in some cases, intrathecal or oral antifungal chemotherapy in addition to surgical therapy. Overall mortality was 43.6% (34 deaths). With prompt diagnosis and treatment, the mortality rate was 39% whereas, when appropriate treatment was delayed, the mortality rate was 64%. An additional 14 surviving patients (17.9%) exhibited permanent morbidity due to neurological deficits, seizure disorders, or renal toxicity following treatment with amphotericin B. The combined mortality and morbidity rate was 62.8%. Clinical symptoms were resolved completely in 29 patients, although in 10 evidence of disease persisted and chemotherapy was continued. Fungal infections of the CNS are being recognized with increased frequency. It is suggested that a high index of suspicion, aggressive attempts to obtain a diagnosis, and early and vigorous therapy may reduce the unfortunate outcome seen in a relatively high proportion of patients with CNS fungal infections.
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PMID:Surgical treatment for fungal infections in the central nervous system. 402 Apr 64

Inflammatory diseases of the central nervous system (CNS) are important causes of seizures in dogs. Specific diseases include canine distemper, rabies, cryptococcosis, coccidioidomycosis, toxoplasmosis, neosporosis, Rocky Mountain spotted fever, ehrlichiosis, granulomatous meningoencephalomyelitis, and pug dog encephalitis. Inflammatory disorders should be considered when a dog with seizures has persistent neurological deficits, suffers an onset of seizures at less than 1 or greater than 5 years of age, or exhibits signs of systemic illness. A thorough history, examination, and analysis of cerebrospinal fluid are important in the diagnosis of inflammatory diseases. However, even with extensive diagnostic testing, a specific etiology is identified in less than two thirds of dogs with inflammatory diseases of the CNS.
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PMID:Inflammatory diseases of the central nervous system in dogs. 977 7


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