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)

In 1987, a 69-year-old female suffering from epilepsy and right hemiparesis was admitted to the hospital and given conservative therapy. During the next three weeks she became a stuporous state. Steroids were then prescribed, and she made a complete recovery. Following hormonal and immunological investigations, a diagnosis of Hashimoto's disease with hypothyroidism was made. Following her discharge, thyroxin and anticonvulsant treatments continued. On May 30, 1989, at the age of seventy-one, the patient was found lying unconscious at home, and taken to our hospital. She had signs of a confused state, and seizures of her right arm on admission. Cranial computed tomography (CT) revealed a low density area in the left parieto-occipital lobe, which was heterogeneously enhanced by contrast medium. Magnetic resonance imaging (MRI) showed a lesion of low signal intensity in T1-weighted images and high signal intensity in T2-weighted images, which was homogeneously enhanced by Gd DTPA. Cerebral angiography disclosed no abnormality. Two weeks later, follow-up CT showed that the lesion had become larger and markedly enhanced. A brain tumor, probably malignant lymphoma, was suspected. On June 14, stereotaxic biopsy of the enhanced lesion was performed. Histopathological examination disclosed dense infiltration of the entire walls of many small parenchymal vessels, both arterioles and venules, by lymphocytes. Treatment for angiitis (betamethasone 16 mg daily) was started on June 20, then gradually tapered, and the lesion diminished on CT. Our case has some features of both isolated angiitis of the central nervous system and encephalopathy in compensated Hashimoto's disease. It is suggested that some common base of the autoimmune diseases exists in this case.
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PMID:[Isolated angiitis of the CNS associated with Hashimoto's disease]. 161 79

Treatment of tuberculous meningitis should begin with an anti-tuberculous regimen of at least three drugs: isoniazid, pyrazinamide, and rifampin. Early in the course of therapy, ethambutol or streptomycin may be of some added benefit. If the local incidence of drug resistance to Mycobacterium tuberculosis is greater than 4%, or is unknown, then a fourth drug (ethambutol or streptomycin) should be added. If the patient is from an area with organisms resistant to multiple drugs, or is likely to be infected with a multiply resistant organism for any reason, then the patient should be on enough drugs to insure that at least two active anti-tubercular drugs are included in the therapy. An expert should be consulted Length of therapy is not standardized. For sensitive organisms, a regimen of three drugs daily for 2 months, followed by two-drug therapy (isoniazid and rifampin) has been recommended. The American Thoracic Society (ATS) and the Centers for Disease Control (CDC) have recommended a minimum of 12 months of therapy for tuberculous meningitis. If cultures remain positive for extended periods, or signs or symptoms respond slowly, therapy should be extended to 18 months. Patients with HIV also may need longer courses of therapy. The severity of tuberculous meningitis can be classified based on a system devised by the British Medical Research Council. Stage I patients are fully conscious, rational, and do not have neurologic signs. Stage II patients are confused or have neurologic signs such as cranial nerve palsy or hemiparesis. Stage III patients are comatose or stuporous with more severe neurologic signs. Corticosteroids are recommended if the patient is mentally confused, has neurologic signs, or is comatose (Stages II and III). In patients with moderate disease (Stage II), corticosteroids appear to improve neurologic sequelae and survival. Dexamethasone 6 to 12 mg per day and prednisone 60 to 80 mg per day tapered over 4 to 8 weeks has been used. Symptoms of central nervous system (CNS) inflammation may recur if the corticosteroid taper is implemented too soon or too fast. Steroids and diuretics such as furosemide and acetazolamide are sometimes used to treat hydrocephalus. Ventriculoperitoneal or ventriculoatrial shunting may be required to relieve signs and symptoms of hydrocephalus.
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PMID:Tuberculosis Meningitis. 1148 56

A 6-year-old, previously healthy male presented with fever and lethargy. Tuberculous meningitis was suspected after cerebrospinal fluid examination. Antituberculous drugs were administered, and an initial computed tomographic scan of brain revealed mild ventriculomegaly only. Steroids were instituted on day 16 and gradually withdrawn 1 month later. Nine weeks after the initiation of antituberculous therapy, markedly impaired visual acuity and bitemporal hemianopsia were observed. Magnetic resonance imaging of brain revealed multiple tuberculomas, including involvement of the optic chiasm. Hydrocephalus was present. A ventriculoperitoneal shunt was inserted, and steroids were reinstituted. Visual acuity improved 9 weeks after the onset of visual acuity impairment and returned to normal 24 weeks later.Follow-up computed tomographic scan of brain 1 year later demonstrated complete resolution of tuberculomas. Development of intracranial tuberculoma during antituberculous therapy, although rare, dose not represent treatment failure, and continuation of antituberculous drugs, with or without the addition of steroids, will usually resolve the lesions.
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PMID:Development of tuberculoma during therapy presenting as hemianopsia. 1551 20

55-year male of Asian descent presented with weight loss, lethargy, drowsiness and low grade fever without cough. Examination revealed crackles in the chest but no focal neurological deficit. Chest X ray revealed an infiltrate consistent with tuberculosis. Biopsy of infiltrate was negative for malignancy. Corrected calcium level revealed parathyroid independent hypercalcemia. Further diagnostic work up for drowsiness and hypercalcemia was normal. Despite receiving hydration and pharmacotherapy for his hypercalcemia, his condition failed to improve. When steroids were started, the patient's calcium levels and symptomatology resolved. Tuberculosis causing hypercalcemia is uncommon. Steroids are useful agents, particularly in refractory cases.
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PMID:Middle aged male with pulmonary tuberculosis and refractory hypercalcemia at a tertiary care centre in South East Asia: a case report. 1982 85