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Query: UMLS:C0085632 (apathy)
 4,089 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sixteen patients with a clinical diagnosis of subcortical arteriosclerotic encephalopathy (Binswanger's disease) were studied. Mild or moderate dementia was found in 14 cases, with characteristic disturbances of concentration, and psychic retardation with apathy. Neuropsychological studies revealed that signs of diffuse lesions in the frontal lobes dominated. Impairment of memory was significant in all cases. Although intellectual impairment in subcortical arteriosclerotic encephalopathy resembled subcortical dementia, some significant differences were found.
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PMID:Evaluation of dementia in subcortical arteriosclerotic encephalopathy (Binswanger's disease). 183 89

Three patients had neurologic signs due to isopropyl alcohol (IPA) intoxication. Over a several-week period, a known alcoholic developed apathy, confusion, ataxia, and hyperreflexia. During this period, there was no ethanol available to him, and he denied use of other intoxicants. He was found stuporous in the hospital after drinking IPA and admitted to IPA abuse during the preceding weeks. Two other men were admitted in a stupor after large ingestions of IPA. Intoxication with IPA has two different presentations: stupor in a known alcoholic and encephalopathy of unknown cause in individuals who hide their addiction. Ethanol, methanol, IPA, and ethylene glycol intoxications are associated with different clinical and laboratory findings.
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PMID:Isopropyl alcohol intoxication. 198 19

Cytostatic long-term treatment for about 36 months was administered to 18 children with acute lymphatic leukaemia who were in long-term remission (43-98 months). Prophylaxis of meningosis involved intrathecal 198Au colloid and methotrexate. Seven recurrences occurred during the long-term remissions: the bone marrow was involved six times, leukaemic meningosis occurred once. Five out of seven recurrences occurred within one year of cessation of treatment. There were no complications induced by intrathecal radio-gold, such as the apathy syndrome or leukoencephalopathy. Intrathecal methotrexate led to side effects before administration of radio-gold: encephalopathy twice, paraplegia once. Symptoms regressed completely in two children, one child with encephalopathy continues to have symptoms. All three children were given 198Au colloid intrathecally thereafter which was tolerated very well. 198Au colloid represents an alternative for prophylaxis of meningosis with 60Co telecobalt irradiation in leukaemias and non-Hodgkin lymphomas in childhood.
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PMID:[Cessation of treatment in childhood acute lymphatic leukemia. Long-term observations after meningosis prevention with intrathecal gold colloid radioisotopes and methotrexate]. 626 99

A 3-year-old girl with left hemiparesis suffered from bilateral paresis, motor rigidity, gait disturbance, axial hypotonia, dysarthria, apathy, and incontinence. After steroid therapy, mild improvement occurred, but muscle weakness, gait disturbance, and rigidity remained. Leigh encephalopathy was excluded on the basis of muscle biopsy and laboratory findings. Computed tomography and serial magnetic resonance imaging at an early stage revealed right-sided dominant lesions in the putamen and caudate nucleus and later bilateral striatal lesions, appearing as hyperintense signals on T2-weighted images and mixtures of hypo- and hyperintense signals on T1-weighted images. This is the first demonstration of serial magnetic resonance imaging findings in infantile bilateral striatal necrosis.
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PMID:Serial MRI in infantile bilateral striatal necrosis. 802 66

Human Immunodeficiency Virus (HIV)-encephalopathy (formerly AIDS Dementia Complex, or ADC) is characterized by global impairment of intellectual and cognitive functions, personality and behavioral disturbances, decreased memory, inability to concentrate, and apathy. Its motor dysfunction is manifested by impaired speech, gait, and coordination, and by psychomotor retardation. Several scientific reports indicate that ADC may be the earliest, and, at times, the only evidence of human immunodeficiency virus infection, and may present a diagnostic challenge, particularly in the aviation context. Several aviation medicine specialists have pointed out the safety questions raised by this condition when it presents in otherwise asymptomatic individuals. Since October 1985, U.S. military pilots have been tested for the presence of HIV antibody and grounded if found positive. In May 1991, the Executive Council of the Aerospace Medical Association approved a position statement that supports testing of pilots for infection by HIV, and maintains that "individuals confirmed to be infected should be found medically disqualified for flying duties." While bureaucrats delay in resolving HIV mandatory screening, HIV-encephalopathy may be precipitously brought to light, with symptoms involving ocular motor disorders such as dissociated nystagmus, gaze-evoked nystagmus, and impaired saccadic function and smooth pursuit, frequent signs of HIV cerebellar and pontomesencephalic dysfunction.
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PMID:HIV-encephalopathy: should we await a catastrophe before screening? 783 42

HIV encephalopathy, which is probably primarily caused by human immunodeficiency virus, is the most common neurological disorder in HIV-infected patients and is more frequent than opportunistic diseases of the central nervous system. It is characterized most often by slowly progressing cognitive impairment, psychomotoric slowing and increasing apathy. The syndrome is found almost exclusively in the late stages of HIV infection; its frequency in patients with full-blown AIDS is estimated as being between 40 and 70%. Although numerous studies have demonstrated alterations in the electrophysiological parameters, cerebral perfusion and cerebrospinal fluid in many asymptomatic patients, there are no reliable parameters that can predict the risk of developing HIV encephalopathy. Also, there is no sufficient correlation between the extent of the frequent but mostly subtle neuropathological changes and the clinical degree of the severity of the encephalopathy. The mechanisms causing cerebral injury are poorly understood. Recent studies indicate that the indirect effects of HIV infection of the brain are the most important pathogenetic factors. In particular, certain viral proteins and cytokines produced by infected macrophages or activated microglia seem to induce neuronal dysfunction and finally loss of nerve cells.
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PMID:[HIV encephalopathy--clinical aspects, neuropathology and pathogenesis]. 845 Aug 99

We report two patients with subacute diffuse encephalopathy characterized by confusion, myoclonic encephalopathy, and mild akineto-rigid extrapyramidal signs in one case and by apathy, memory deficit, and partial complex seizures in the other. Hashimoto's thyroiditis with high titers of anti-thyroglobulin antibodies was diagnosed in both patients, who were unresponsive to anticonvulsant medication, but showed rapid neurological improvement following steroid treatment. On neuropsychological examination, predominant frontotemporal dysfunction was noted. Electroencephalographic activity was remarkable for its rhythmical delta activity, unresponsive to, or even paradoxically increased by, anticonvulsant treatment. On magnetic resonance imaging, atrophy with temporal predominance was found. These observations support the idea that this potentially treatable dementia and movement disorder should be classified as a separate clinical entity.
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PMID:Hashimoto's myoclonic encephalopathy: an underdiagnosed treatable condition? 915 55

HIV-associated neurological manifestations: dementia, myelopathy, and neuropathy, have become one of the commonest causes of neurological disorders in young people. Cognitive impairment develops in about 30 p. 100 of patients with AIDS and frank dementia in 15 to 20 p. 100 with an annual incidence after AIDS of approximatively 7 p. 100. Typically, the onset of dementia is relatively abrupt over a few weeks or months. The clinical manifestations of the encephalopathy now termed "HIV-dementia", suggest predominant subcortical or frontal involvement. Typical presentation includes apathy and inertia, memory loss and cognitive slowing, minor depressive symptoms and withdrawal from usual activities. Neurological examination may show hypertonia of lower limbs, tremor, clonus, frontal release signs and hyperactive reflexes. Terminally, the patient is bedbound, incontinent, abulic or mute with decorticate posturing leading to death over 3 to 6 months. However, a stabilisation and even a regression of the cognitive disorders have been observed following antiretroviral treatment. Radiological features of HIV dementia include both central and cortical atrophy and white matter rarefaction. However they are neither invariable nor specific. Together with CSF examination, they are more important to exclude opportunistic infections. Indeed, although a completely normal CSF profile may reasonably exclude the diagnosis; at present, no single test or combination of tests can reliably diagnose HIV dementia. Although the clinical characteristics of HIV-dementia are now clearly established, its pathogenesis is unclear and its pathological counterpart remains a matter of debate. A number of "HIV-induced" lesions may be found in the brain of AIDS patients and their causative role in HIV-dementia has been considered. They include HIV encephalitis due to productive CNS infection by the virus, diffuse white matter pallor "HIV-leukoencephalopathy" reflecting an abnormality of the blood brain barrier, involvement of the grey matter, "diffuse poliodystrophy", with neuronal loss that results, at least partly, from a process of programmed cell death and axonal damage. These changes are variably associated in patients with HIV dementia, however none of them can be closely related to the cognitive disorders. This suggests that the neuronal dysfunction underlying HIV-dementia results from different mechanisms that are variably associated and may interact mutually. These include production of viral proteins, microglial activation with consequent production of neurotoxic factors such as proinflammatory cytokines, free radicals, derivates of arachidonic acid, or quinoleic acid, and blood borne neurotoxic factors in particular cytokines.
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PMID:[Dementia and human inmmunodeficiency virus infection]. 983 49

Delayed postanoxic encephalopathy is a rare condition in which patients appear to make a complete clinical recovery after an episode of anoxia or hypoxia but then develop a relapse characterized by apathy, confusion, agitation, and/or progressive neurologic deficits. The incidence of delayed postanoxic encephalopathy is unclear but has been reported to range from less than 1 to 28 per 1000 in patients who have suffered hypoxic or anoxic events. The exact pathogenesis remains unknown. We describe a case of an independently living 51-year-old woman admitted to an inpatient rehabilitation unit 11 days after a respiratory arrest. At admission, she exhibited cognitive and visual deficits that were relatively mild but prevented a safe return to independent living. Two days later, she developed the sudden onset and rapid worsening of parkinsonian symptoms and excruciating bilateral lower-extremity pain. The pain was intractable, and over the next 2 days she progressed to being unable to walk or perform her activities of daily living without maximum assistance. A diagnosis of delayed postanoxic encephalopathy was made, and the patient responded to a trial of carbidopa and levodopa as well as redirection of her physical and occupational therapy programs. This case illustrates the unusual presentation of delayed postanoxic encephalopathy during inpatient rehabilitation and suggests that this condition should be considered if patients who have suffered an anoxic or hypoxic event show a sudden neurologic deterioration.
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PMID:Delayed postanoxic encephalopathy: a case report and literature review. 1503 41

Many patients with congestive heart failure develop neurologic dysfunction. This may take the form of a cardiac encephalopathy that shares clinical features with other metabolic encephalopathies. The causes are multiple. There is a particular, previously unreported, syndrome that occasionally develops in some patients with congestive heart failure that resembles the findings in patients with normal pressure hydrocephalus. This syndrome is characterized by apathy and abulia with preserved alertness; it is caused by fluid retention within the cranial cavity. The syndrome may also develop in patients with other conditions that cause anasarca, e.g., severe liver or kidney disease or hypoalbuminemia. Because patients with these conditions are often quite ill, it has been difficult to verify the pathophysiologic aspects of the syndrome so that its mechanism must remain a hypothesis that awaits more definitive study in a series of patients. I have not seen this syndrome discussed in any cardiology or neurology texts or reports, and it seems to be completely unknown to cardiologists and neurologists. I have recognized about one patient per year with this syndrome.
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PMID:Cardiac encephalopathy and congestive heart failure: a hypothesis about the relationship. 1640 54


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