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

The authors have developed a model of chronic cerebral vasospasm analogous to the clinical situation, by inducing a large subarachnoid hemorrhage (SAH) in monkeys. With this model, the size of the SAH apparent on the first computerized tomography (CT) scan was correlated with the incidence and severity of cerebral vasospasm that developed. Indices monitored for up to 21 days after SAH included cranial CT scan, cerebral blood flow, vessel caliber, and neurological status. The 18 monkeys studied for 48 hours or more were divided into two groups according to the size of the SAH on CT scan. Vasospasm was more common in the group with large SAH. In this group, on Days 0, 7, and 14, the incidence of vasospasm was significantly higher than at other times (p less than 0.001, p less than 0.01, and p less than 0.05, respectively), and the percentage reduction in vessel caliber was significantly greater than in the group with small/medium SAH (Day 7, p less than 0.02; Days 0 and 14, p less than 0.05). Delayed neurological deficit developed in two monkeys with large SHA. Apathy was noted from Day 17 to Day 21 in one, and unsteadiness and drowsiness were noted on Days 4 and 5 in the other. Overall, the incidence, degree, and time course of vasospasm reflected the size of the hemorrhage.
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PMID:Chronic cerebral vasospasm after large subarachnoid hemorrhage in monkeys. 708 15

Akinesia, a common side effect of antipsychotic drugs, often goes unrecognized by physician and patient. Akinetic apathy and lack of spontaneity can be mistaken for the negative symptoms of schizophrenia and add to the well-known social and emotional disability of schizophrenic patients on maintenance therapy. The authors attempted to identify a measure that might distinguish between akinesia and the negative symptoms of schizophrenia but found no relationship between plasma and saliva chlorpromazine levels or prolactin levels and akinesia. The fact that all of the akinetic but only 31% of the nonakinetic patients rated themselves as drowsy 12 hours after their bedtime dose indicates that drowsiness is a fairly accurate correlate of akinesia.
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PMID:Importance of akinesia: plasma chlorpromazine and prolactin levels. 743 84

The first central pharmacodynamic action of chlorpromazine to be described was sedation without narcosis. The antipsychotic action and extrapyramidal symptoms were observed later. Sedation can be separated into nonspecific sedation (drowsiness, somnolence) and specific sedation (psychomotor inhibition and psychic indifference). Both types are parts of the clinical profiles of classical neuroleptics. The sedative properties of neuroleptics may contribute to the overall efficacy in the treatment of psychotic patients, depending on the clinical situation. In most patients, however, sedation is only needed for a short period, or not at all. The drug induced sedation may adversely affect the patients' well-being and functional capabilities. The term neuroleptic-induced deficit syndrome (NIDS) has been coined to focus attention on the adverse mental effects of neuroleptics. NIDS still needs to be properly defined and to be differentiated from the deficit syndrome of schizophrenia and postpsychotic depression. Assessment methods are needed to establish the incidence and prevalence of NIDS, to evaluate the importance of NIDS in the overall treatment outcome in psychoses and to facilitate development of better antipsychotic agents.
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PMID:Neuroleptics and the neuroleptic-induced deficit syndrome. 791 56

We describe the combination of acute bilateral ballism and anterior opercular syndrome in a 75-year-old female hypertensive patient with bilateral multiple small infarcts involving the basal ganglia, the subcortical white matter and the area of the subthalamic nucleus, detected by CT scan and MRI. These clinical manifestations were accompanied by apathy, somnolence and cognitive changes usually observed in cortical involvement. Pathogenetic mechanisms for this unusual clinical picture are discussed on the basis of CT, MRI, and SPECT findings.
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PMID:Paraballism associated with anterior opercular syndrome: a case report. 792 78

Comprehensive data on 30 patients with propionic acidaemia, diagnosed by selective screening for inborn errors of metabolism, are presented. The most valuable diagnostic metabolites found were methylcitric-, 3-hydroxypropionic-, and 2-methyl-3-oxovaleric acids. Hyperlysinaemia and hyperlysinuria are also characteristic findings in this disease. The metabolic pattern found in propionic acidaemia is discussed extensively as are enzymatic findings. Residual activity of propionyl-CoA carboxylase is neither a predictive marker for severity nor for outcome of the disease. Propionate fixation assays were less reliable for confirmation of propionic acidaemia and of no prognostic value. Clinical presentation of the disease is discussed in detail. Besides the well-known unspecific findings (poor appetite, feeding difficulties, vomiting, dehydration, weight loss, muscular hypotonia, dyspnoea, somnolence, apathy, convulsion, coma, severe metabolic acidosis, hyperammonaemia) various skin abnormalities have been detected in about 50% of all patients. In 27% "dermatitis acidemica" was found.
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PMID:Propionic acidaemia: clinical, biochemical and therapeutic aspects. Experience in 30 patients. 795 90

Chronic acquired hepatocerebral degeneration (CAHD) is a heterogeneous disorder that can occur with a primary neurologic, hepatic, or combined presentation. Little has been added to the understanding of this disorder since the detailed, early clinical and pathological descriptions. The spectrum of clinical presentations can be neuropsychiatric (apathy, lethargy, excessive somnolence), a movement disorder (ataxia, tremor, chorea, parkinsonism, myoclonus, dystonia), or both. Cortical laminar necrosis and polymicrocavitation in the cortex and basal ganglia are combined with cerebral and cerebellar atrophy. Microscopically, Alzheimer type II astrocytes and cytoplasmic glycogen granules are characteristic. Recent neuroradiological observations in patients with liver failure have shown a specific magnetic resonance (MR) imaging appearance with a hyperintense T1 signal in the pallidum, putamen, and, rarely, mesencephalon. Using clues from a similar MR appearance in patients receiving total parenteral nutrition as well as animals given parenteral manganese, and the knowledge that manganese is cleared by the hepatobiliary system, deposition of manganese in the brain is postulated in patients with CAHD. In this review we describe three cases of CAHD with detailed clinical and radiological documentation and discuss the aforementioned pathogenetic mechanisms.
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PMID:Chronic acquired hepatocerebral degeneration: case reports and new insights. 886 9

The aim of this study was to determine the acute LD50, clinical symptoms and pathological changes of acute BUREX EKO intoxication in pheasants according to OECD No 205. Medium lethal dose (LD50) of BUREX EKO in pheasant is 3.84 ml/kg body weight with the upper level of reliability 4.50 ml and lower level of reliability 3.27 ml/kg body weight. As far as the calculation to the effective substance is concerned it is 1077 mg of chloridazone per kg body weight with the interval of reliability from 919 to 1263 mg/kg body weight. Calculated the effective substance of chloridazone (3.84 ml is LD50 of BUREX EKO which contains 1077 mg of chloridazone) BUREX EKO can be classified as the moderately toxic substance to pheasants. There were following clinical symptoms of the BUREX EKO intoxication in pheasants: apathy, drowsiness, incapability to move, ruffled feathers, slight diarrhoea, strenuous respiration, tonico-clonical cramps before death, decease with the head expressively bent rearwards. There was a relatively fast beginning of rigor mortis in dead pheasants. Pathologico-anatomical dissection of the pheasants obtained under conditions of acute intoxication did not reveal any changes on the organs of both experimental and control pheasants which would be immediately connected with the effect of the administered substance. Hyperaemia was recorded by histologico-pathological investigation of the liver and kidneys. No changes on the brain and intestine wall were recorded.
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PMID:Acute oral toxicity of the herbicide BUREX EKO in pheasants. 902 51

The chronic fatigue syndrome (CFS) has been intensively studied over the last 40 years, but no conclusions have yet been agreed as to its cause. Most cases nowadays are sporadic. In the established chronic condition there are no consistently abnormal physical signs or abnormalities on laboratory investigation. Many physicians remain convinced that the symptoms are psychological rather than physical in origin. This view is reinforced by the emotional way in which many patients present themselves. The overlap of symptoms between CFS and depression remains a source of confusion and difficulty. But even if all CFS patients were rediagnosed as depressives, this would not negate the possibility of an underlying organic cause for the condition, in view of the growing evidence that depression itself has a physical cause and responds best to physical treatments. There is some evidence both for active viral infection and for an immunological disorder in the CFS. Many observations suggest that the syndrome could derive from residual damage to the reticular activating system (RAS) of the upper brain stem and/or to its cortical projections. Such damage could be produced by a previous viral infection, leaving functional defects unaccompanied by any gross histological changes. In animal experiments activation of the RAS can change sleep state and activate or stimulate cortical functions. RAS lesions can produce somnolence and apathy. Studies by modern imaging techniques have not been entirely consistent, but many magnetic resonance imaging (MRI) studies already suggest that small discrete patchy brain stem and subcortical lesions can often be seen in CFS. Regional blood flow studies by single photon-emission computerized tomography (SPECT) have been more consistent. They have revealed blood flow reductions in many regions, especially in the hind brain. Similar lesions have been reported after poliomyelitis and in multiple sclerosis--in both of which conditions chronic fatigue is characteristically present. In the well-known post-polio fatigue syndrome, lesions predominate in the RAS of the brain stem. If similar underlying lesions in the RAS can eventually be identified in CFS, the therapeutic target for CFS would be better defined than it is at present. A number of logical approaches to treatment can already be envisaged.
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PMID:Chronic fatigue syndrome--aetiological aspects. 946 37

Since 1988, the Netherlands Pharmacovigilance Foundation Lareb and the Inspectorate for Health Care have received 17 reports of patients with neuropsychiatric adverse reactions attributed to the use of oxybutynin hydrochloride. These concerned 6 males and 11 females and 6 out of the 17 patients were children under the age of 13. In all cases patients had been treated according to a normal dosage regimen. Complaints included hallucinations, psychosis, concentration and orientation problems, apathy, listlessness, agitation, drowsiness and sleepiness. Symptoms improved or disappeared in all patients after dose reduction or withdrawal of oxybutynin.
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PMID:[Neuropsychiatric adverse effects attributed to use of oxybutynin]. 962 18

Myotonic dystrophy (m.d.) is an autosomal dominant multisystem disorder involving muscles, brain, heart, eye, endocrine system, alimentary and respiratory systems. M.d. is the most frequent cause of muscle dystrophy. Unstable CTG trinucleotide repeat at 3' untranslated end of the myotonic protein kinase gene on chromosome 19q 13.3 is the molecular basis of the disease. Normal length of CTG trinucleotide repeat is 5-40. Molecular mechanism of the myotonic dystrophy is discussed. Cataract, heart dysfunction, endocrine organs dysfunction, gallbladder stones, impotence are characteristic changes in patient with m.d. Apathy, drowsiness, sometimes dementia point to central nervous system involvement. Clinical course, correlation between CTG expansion and clinical manifestation are described. Nowadays progress in molecular genetic allows to make the diagnosis by DNA examination. Prenatal diagnosis is also possible.
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PMID:[Current problems in myotonic dystrophy]. 986 18


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