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)

A comparative study of over 4000 case histories of patients admitted to the Kashchenko Moscow psychiatric hospital in 1951 and 1974 demonstrated that the character of natural history of schizophrenia under conditions of polypharmacotherapy has changed. The drug pathomorphosis was studied by comparing the clinical picture of the psychosis in the preneuroleptic period and under conditions of polypharmacotherapy. In polypharmacotherapy the ratio of the form of schizophrenia has changed towards an increase of attack-like forms and a drop in the number of cases with continuous forms of the disease. It was demonstrated as well that irrespective of the character of schizophrenia progress there was a considerable decrease in severe catatonic conditions, delusional excitation, pronounced stuporous states and increased proportion of depressions. Psychopathlike and pseudoneurotic symptoms during polypharmacotherapy did not undergo any serious changes.
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PMID:[Pharmacotherapeutic pathomorphosis of schizophrenia]. 610 36

Impairment in short-term memory and lingering deficit in psychomotor performance are but two of the acute cannabis intoxication components that may have long-term consequences. The former because it affects learning and the latter because it interferes with proper handling of motor vehicles. The most frequently observed complication of cannabis inebriation, however, is a short-lasting acute psychological disturbance with symptoms of panic, paranoid apprehension and personality disorganization. This type of reaction is often not dose-related, and could appropriately be termed "pathological intoxication". In addition to the acute effects of cannabis on mental performance and behaviour, this paper reviews the psychiatric consequences of chronic use and the accumulated evidence on organic toxicity associated with it: residual cognitive deficit, lethargic symptoms, cannabis psychosis, respiratory, gastro-intestinal and cardiovascular complications, as well as effects on immune response and gonadal functions, are discussed. Also included are reviews on the pharmacology and therapeutic potential of cannabinoids.
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PMID:[Effect of cannabis use on health]. 632 49

The adverse psychic effects of antiepileptics embrace all categories of psychiatric symptomatology, including disturbances of consciousness (delirium, confusion), psychotic state (schizophrenia-like psychosis, affective disorder), neurotic state, behavior and character disorder. Antiepileptic intoxication can take the form of a psychotic episode. The lowered level of consciousness due to a high blood level of antiepileptics is expressed as inhibitory symptoms such as a lack of initiative, psychomotor slowing, lowering mood, stuporous state and the like. Another group of manifestation of a high blood level of antiepileptics, by contrast, consists of salient positive symptoms such as irritability, hyperkinetic syndrome, hysterical symptoms, aggravation of character change, delirium and confusion. An elevated blood level of antiepileptics by itself is not sufficient to give rise to a psychiatric symptom, which is rather prone to occur in the presence of some trouble or problems (defect in intelligence or personality, fragility of brain function, organic brain damage, psychogenic factors) in the patient.
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PMID:Antiepileptic drugs and psychiatric disorders: mechanism involved in manifestation of psychic symptoms of high blood level of antiepileptics. 642 78

The adult type of neuronal ceroid lipofuscinosis (NCL) occurred in a 49-year-old man and his 51-year-old sister. They showed episodic stuporous and psychotic states, mental retardation, generalized convulsions, and ichthyosis vulgaris. At autopsy the woman had excessive accumulation of lipofuscin throughout the CNS. The degree of neuronal lipopigment accumulation was very severe in the neurons of the thalamus, substantia nigra, inferior olivary nuclei, motor nuclei of the brain stem, and cerebral cortex. Mental symptoms, such as stupor, excitement, hallucinations, and delusions, were the predominant clinical manifestations and so were misdiagnosed as schizophrenia. Though the clinical diagnosis of the adult type of NCL (Kufs' disease) is difficult because of its wide variety of manifestations, symptoms such as episodic psychotic and stuporous states accompanied by convulsive disorders with mild neurologic signs may be an indication of this disease.
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PMID:Familial occurrence of adult-type neuronal ceroid lipofuscinosis. 647 18

We describe four major and five minor clinical patterns of acute phencyclidine (PCP) intoxication and give the incidence of findings in each pattern. Major patterns were acute brain syndrome (248 cases; 24.8%), toxic psychosis (166 cases; 16.6%), catatonic syndrome (117 cases; 11.7%), and coma (106 cases; 10.6%). Minor patterns included lethargy or stupor (38 cases; 3.8%), and combinations of bizarre behavior, violence, agitation, and euphoria in patients who were alert and oriented (325 cases; 32.5%). Patients with major patterns of PCP toxicity usually required hospitalization and accounted for most complications. In general, patients with minor patterns had mild intoxication and did not require hospitalization except for the treatment of injuries or autonomic effects of PCP. Various types of injuries occurred in 16%, and aspiration pneumonia occurred in 1.0% of all cases. There were 22 cases of rhabdomyolysis (2.2%), with three patients requiring dialysis for renal failure. One patient who had been comatose from PCP died suddenly. A fresh pulmonary embolism was found at autopsy.
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PMID:Acute phencyclidine intoxication: clinical patterns, complications, and treatment. 723 37

The records of 37 patients with systemic lupus erythematosus (SLE) followed at The Children's Hospital of Philadelphia between 1968 and 1978 were reviewed for evidence of central nervous system (CNS) involvement. Criteria for CNS involvement included evidence of organic brain syndrome, electroencephalographic abnormalities with symptoms referable to CNS, or objective neurologic signs. Sixteen of 37 children had CNS involvement (43%). Thirteen patients had CNS involvement at the onset of SLE. Three patients had late onset CNS manifestations 1 to 2 years after the diagnosis of SLE. The most frequently observed symptoms were headache, behavior disorder, lethargy, diplopia, blurred vision, memory alteration, dizziness, and alteration of consciousness. The most frequently observed neurologic signs were seizures, cranial nerve palsy, ataxia, papilledema, nystagmus, meningitis, tremor, rigidity, cortical blindness, and coma. Neuropsychiatric manifestations included organic brain syndrome, functional psychosis, and personality disorder. Laboratory tests showed elevated cerebrospinal fluid opening pressure and protein, negative cultures, and abnormal electroencephalograms and computerized axial tomography scans. Fourteen of 16 children with CNS manifestations are alive. Thirteen had a mean IQ of 89 by the Wechsler Intelligence Tests. Twelve are in educational programs. One required long-term psychiatric care. A residual neurologic abnormality, a seizure disorder, was present in 3. CNS involvement with SLE in children carries a favorable prognosis.
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PMID:Central nervous system involvement in childhood systemic lupus erythematosus. 731 16

Twenty psychotic patients with psychogenic polydipsia had hyponatremia (98 to 124 mEq/L) lasting up to 28 months, with headache, hypertension, dementia, seizures, lethargy, and coma. Two deaths also may be attributed to this syndrome. Patients drank 7 to 43 L of water daily. Urine was dilute during this water load (37 to 95 mOsm/kg), and free water clearance ranged from 12 to 36 L/day, while plasma osmolality was 236 to 244 mOsm/kg. During fluid deprivation in seven such patients, urinary osmolality exceeded plasma osmolality when plasma concentration had risen to between 242 and 272 mOsm/kg, thus suggesting a "reset osmostat" or antidiuretic hormone response to nonosmotic stimuli. This tended to sustain hyponatremia. Polydipsia should be recognized as a cause of hyponatremia, perhaps with reset osmostat. This ultimately may cause dementia or death, possibly secondary to recurrent cerebral edema. This sequence of events is potentially preventable or correctable.
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PMID:Hyponatremia in psychogenic polydipsia. 745 96

A total of 42 patients with atherosclerotic--and 34 with involutional depression were studied by conjunctival biomicroscopy for particular features of lipid peroxidation and state of microcirculation before and after treatment with vasoactive preparations, antioxidants and calcium antagonists. POL were found to be increased in patients with atherosclerotic depression irrespective of the syndrome, and in involutional depression with anxious symptomatology, as well as in those patients in stuporous state, this being accounted by a decreased provision of the organism with antioxidants as well as by an inadequate activity of antioxidant enzymes; high incidence rate of intravascular and vascular changes was also noted in the above patient populations. Tocoferolum acetatum and corinfar potentiated antiaggregational and spasmolytic actions of vasoactive preparations, which fact made for an earlier eradication of microcirculatory disturbances, decrease in the free radical oxidation activity and recovery of those patients getting out of the psychotic state.
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PMID:[The correction of the metabolic and microcirculatory disorders in patients with atherosclerotic and involutional depressions]. 748 52

Prader-Willi syndrome presents behavioural characteristics at the temperamental level which can be described as oppositional, explosive and at times antisocial. These traits may fluctuate and be driven by unknown biological anxiety symptoms are also frequent. Delusional psychotic thinking is manifest in some cases, but may be latent in several such patients. A third set of manifestations is a 'refusal-lethargy' syndrome of akinesis, refusal of food and drink, and soiling, which seems to be triggered by environmental circumstances but resembles the hypersomnic, lethargic depressions. These three sets of phenomena are documented through the clinical observation of nine cases and may be useful in the study of the genotype-phenotype relationship in this and other syndromes, particularly those in which similar manifestations are observed and cyclic changes are seen. The use of drugs in this syndrome can also become more rational if this classification is used to identify clearer targets for treatment. The possibility that most manifestations of the syndrome may be an expression of a hyposerotonergic defect is suggested.
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PMID:Tentative classification of neuropsychiatric disturbances in Prader-Willi syndrome. 788 Dec 33

A retrospective examination of lethargic encephalitis finds many parallels with neuroleptic effects. The encephalitis, like the neuroleptics, produced an acute continuum of cognitive disorders from emotional indifference through apathy and onto a rousable stupor. It also produced similar acute dyskinesias, including akinesia, akathisia, dystonia, oculogyric crises, and tremors. The encephalitis also caused similar chronic effects, including dementia and psychosis, and somewhat different persistent dyskinesias. The chronic motor and cognitive disorders, like those associated with the neuroleptics, were often delayed in onset. An acute, severe episode of lethargic encephalitis also finds a parallel in the neuroleptic malignant syndrome. These parallels are probably due to a common site of action in the basal ganglia. They provide a model for understanding many neuroleptic effects and alert us to the probability of persistent cognitive deficits, including dementia, from neuroleptic treatment.
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PMID:Parallels between neuroleptic effects and lethargic encephalitis: the production of dyskinesias and cognitive disorders. 810 24


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