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Biomedical subjects

J Ananth

Publications and source records attributed to J Ananth.

At least 19 recordsLinked to original sources
PubMed2004

Antipsychotic polypharmacy.

The administration of more than one drug for a single medical condition is considered to be polypharmacy. There are many possible reasons for polypharmacy: (1) psychosis is a chronic disease that cannot be cured; (2) expectations to improve patients' quality of life beyond what drugs can actually do is high; (3) the lack of side effects and interactions can cause physicians to be more daring in terms of potential complications; (4) information from the Internet may cause patients and their families to demand medications; (5) the diluted mental health system allows legal guardians and other mental health professionals to force physicians to provide multiple drugs; (6) many new drugs are available; and (7) physicians are forced to shorten hospitalization days. The 1997 American Psychiatric Association Practice Research Network found that 17% of 146 patients with schizophrenia were treated concurrently with more than one antipsychotic medication. Polypharmacy may increase the risk of adverse effects, drug interactions, noncompliance, and medication errors. It is not wise to use polypharmacy only to prevent side effects and drug and interactions. Our attempts to reduce polypharmacy may fail, as academicians also propagate polypharmacy, and all of the algorithms indicate polypharmacy as an option, putting physicians in a legal and ethical bind. Techniques such as experimental ward, peer review, computer information feedback, and comparing different techniques may temporarily reduce polypharmacy but long-term outcome is not affected. Scientific data on the efficacy of polypharmacy is needed in order to sort out good and bad polypharmacy.

Antipsychotic Agents↗
PubMed2004

Drug therapy in schizophrenia.

Over 40 different antipsychotic medications have been introduced around the world, 21 of which are available in the United States. The conventional antipsychotic drugs introduced in late 50s have two major groups of disadvantages, efficacy and safety. All of the atypical antipsychotic agents have higher 5-HT(2) blocking than D(2) blocking. Atypical antipsychotic agents differ in their receptor action and side effect profile. Among them, clozapine has superior efficacy, and both clozapine and olanzapine have a higher propensity to cause weight gain and possibly diabetes. Quetiapine is difficult to use in acute psychotic states as a result of titration. Ziprasidone and aripiprazole are less sedating, and diabetes as well as weight gain have not been reported with their use. In an acute setting, antipsychotic monotherapy in therapeutic doses is the most useful. AAP drugs are preferred because of the lack of acute EPS symptoms. Intramuscular preparations of haloperidol and ziprasidone are sometimes required to treat acute patients. The goal in acute treatment is to prevent harm to self or others by decreasing excitatory symptoms. Continuing the antipsychotic medication treatment after the acute symptoms are controlled reduces the likelihood of a relapse. The neuroleptic medication should be continued indefinitely. The minimum amount antipsychotic drugs necessary to prevent a relapse should be used, based on clinical decision.

Animals↗
PubMed2004

Side effects of atypical antipsychotic drugs.

Recently there has been increased concern over the side effects of the atypical antipsychotic drugs, including diabetes, hyperlipidemia and obesity. The relationship between diabetes and antipsychotic drugs requires a careful analysis. Patients with schizophrenia are known to suffer from diabetes more often than the general population. In addition, a number of case reports indicate that the conventional antipsychotic as well as atypical antipsychotic drugs produce diabetes. Clozapine and olanzapine, in particular, have been implicated producing diabetes as well as diabetic ketoacidosis. Epidemiological surveys have supplemented the case reports, finding increased incidence of diabetes in patients treated with atypical antipsychotic agents, but these surveys have not yielded consistent results regarding the differential effects of the various atypical antipsychotic drugs. The mechanism by which antipsychotic agents produce diabetes is not elucidated. Weight gain and consequent alteration in triglycerides and cholesterol have been known to occur frequently with olanzapine and clozapine. The ensuing metabolic syndrome itself may cause insulin resistance and diabetes. In the absence of definitive scientific data on the differential effects of antipsychotic drugs in inducing diabetes, clinical prudence and careful monitoring of all patients on atypical antipsychotic drugs is necessary. Aripiprazole and ziprasidone have not been shown to increase weight or produce diabetes, but more information on the diabetogenic effects of ziprasidone and aripiprazole is needed. In order to assess the differential effects of atypical antipsychotic drugs in producing diabetes and the mechanisms by which they produce this reaction, further research is necessary.

Animals↗
PubMed2004

The use of antiparkinsonian agents in the management of drug-induced extrapyramidal symptoms.

Antipsychotic drugs induce extrapyramidal symptoms such as dystonia, akathisia and parkinsonian symptoms early in treatment, and tardive dyskinesia later in treatment. With the advent of atypical antipsychotic drugs, the incidence of extrapyramidal symptoms has decreased, but the danger still exists. There are many reasons that extrapyramidal symptoms are still a problem. Most often, psychiatrists use doses higher than the recommended dose of atypical antipsychotic agents. For example, the use of 8 to 10 mg of risperidone, 30 to 40 mg of olanzapine, or 1200 to 1500 mg of quetiapine daily is not uncommon. In addition, combinations of both conventional and atypical antipsychotic drugs are used together in many instances. Extrapyramidal symptoms produce unnecessary suffering and add to the health burden; therefore, prompt recognition of these symptoms is necessary. If EPS occur, it is of paramount importance to start an antiparkinsonian agent immediately to provide relief to the patient. In high-risk patients, prophylactic antiparkinsonian therapy is indicated but routine prophylaxis with antiparkinsonian agents is harmful. As only a segment of patients may develop EPS, many patients receive prophylactic medication unnecessarily, and the side effects of antiparkinsonian drugs prescribed without clinical indication may add to the health burden of the patient. If prophylactic antiparkinsonian treatment is initiated, it should be discontinued at least two weeks after its initiation. The long term use of antiparkinsonian treatment is not therapeutically beneficial to the patient, and studies indicate that the gradual withdrawal of antiparkinsonian medication will not produce recurrence of EPS.

Animals↗
PubMed2004

Rehabilitation of schizophrenic patients.

Schizophrenia is a maldevelopmental disorder of the brain that manifests in positive, negative, cognitive and affective symptoms. Currently, the mainstay of treatment involves pharmacotherapy. The limitations of antipsychotic treatment are that they can only control symptoms and cannot cure the illness, and 20% of patients do not respond, thus leading to the requirement of maintenance treatment. Patients that do respond continue to have disabling residual symptoms such as amotivation and isolation, maladaptive behavior, and impaired social functioning. These symptoms prevent patients from attaining educational, occupational, and social roles. Psychosocial interventions and models of quality of life in schizophrenia are based on the notion that increases in psychosocial functioning will be related to improvement in subjective experiences, such as self-esteem and satisfaction with life. The comparative effect of specific treatment methods and the additional benefits of multiple treatments need to be explored. Diversified techniques have also been employed, such as shaping, cognitive process therapy, mastery-oriented skill training, motivation and enhancement. Issues in designing psychosocial interventions and the role of various professionals in providing such interventions need to be carefully considered. Predictor variables and the indications for particular therapies in an individual need to be explored. Generalizability of the gains made by rehabilitation/recovery is also an important consideration. Patients in jail, chronic mental hospitals, private facilities, and the Veterans Administration system are all different in their ability to benefit, their motivations, and the severity of their psychopathology. Therefore, it is very difficult to generalize findings from one setting to another.

Humans↗
PubMed2001

How do the atypical antipsychotics work?

Understanding the action of atypical antipsychotics is useful in exploring the pathophysiology of schizophrenia and in synthesizing drugs that improve various domains of psychopathology without unwanted side effects. In animal models, atypical antipsychotic drugs appear to have a preferential action in the limbic dopaminergic system. Regionally specific action has been studied by measuring the amount of Fos protein produced in a particular brain region as a consequence of a drug's effects on the c-fos gene. Evidence suggests that the atypical and typical antipsychotic drug-induced increases in Fos levels in the nucleus accumbens are related to improvements in positive symptoms, whereas Fos increases in the prefrontal cortex, with the atypical antipsychotics only, correlate with negative symptom improvement. The extrapyramidal effects seen with typical antipsychotics are thought to be related to Fos increases in the striatonigral pathway. However, studies of Fos levels in specific brain regions reveal only the site of action, not the mode of action. The finding that atypicality is related to surmountable D2 dopamine receptor blocking provides another venue to define and explore atypical antipsychotic drug action.

Animals↗
PubMed1999

Olanzapine treatment after clozapine-induced granulocytopenia in 3 patients.

BACKGROUND: How to best treat psychotic patients who have had past clozapine-induced agranulocytosis or granulocytopenia remains a problem. CASE REPORTS: We report 3 patients with chronic schizophrenia who had previously stopped clozapine due to hematologic side effects. The patients evidenced improvement with olanzapine that equated to 16- to 31-point decreases in rating scale scores during 1-year follow-up without any hematologic abnormalities. CONCLUSION: The results suggest that olanzapine may be useful in treating patients with clozapine-induced granulocytopenia without the risk of recurrence of hematologic side effects.

Adult↗
PubMed1998

Treatment-resistant depression.

Our ability to treat depression has improved with the availability of receptor-specific and chemically diverse groups of antidepressants. Even now, most of the short-term studies indicate that about 20% of depressed patients remain resistant to treatment. Therefore, it is important to properly assess the treatment-resistant depressed (TRD) patients and to separate the truly refractory patients from those inadequately treated. Undiagnosed medical conditions should be eliminated. TRD is neither a clinically nor a biologically identifiable entity. As there are no established methods for the treatment of TRD, all options should be considered. The clinician can be enriched by the knowledge of the treatment modalities available, and yet, in treating an individual patient, clinical skills, intuitive judgment, family history of response to drugs and side effects, all play a vital role. Several of the approaches described in the paper indicate available methods and their merits in general but there is no way of ascertaining by which particular method a patient should be treated. The three common methods of treatment are substitution of one antidepressant drug for another, combination therapies and augmentation techniques. These are based on clinical experiences and not research findings. Therefore the treatment of TRD patients is more an art than a science. The physician should assess all the psychopathological, phenomenological and psychosocial variables to appropriately treat an individual patient.

Adjuvants, Pharmaceutic↗
PubMed1997

Tardive dyskinesia and ethnicity: review of the literature.

Tardive dyskinesia (TD) is a side effect of long-term neuroleptic administration. The wide variation of 2 to 51% in its reported prevalence can be attributed to the varied definitions of TD, the use of different methods of assessment, and the lack of control of independent variables. Why only certain patients develop this side effect is an intriguing question. The occurrence of TD in family members and in those persons with a family history of Parkinson's disease (PD) is suggestive of genetic vulnerability. Further support for a genetic predisposition comes from the fact that only certain strains of monkeys, such as the Cebus apella strain, have a higher propensity to develop TD than others, such as the Macaca sepciosa strain. If genetic factors play a significant role in the development of TD, then, genetically diverse ethnic groups may have a different propensity for the development of TD. One method of evaluating such a possibility is to compare its prevalence in different countries. The current literature on ethnic differences in the prevalence rates of TD is reviewed. This area of study needs further rigorous investigation.

Animals↗
PubMed1995

Regional 133xenon cerebral blood flow and cerebral 99mTc-HMPAO uptake in patients with obsessive-compulsive disorder before and during treatment.

We previously reported increased regional cerebral cortical uptake and decreased caudate nucleus uptake of 99mTc-HMPAO in patients with obsessive-compulsive disorder(OCD) before treatment compared to matched normal controls. In the present study, we determined whether or not these changes persisted during treatment. Single-photon emission computed tomography was used to measure regional cerebral blood flow (rCBF) by 133Xe inhalation and cerebral uptake of 99mTc-HMPAO in eight adult male OCD patients before and during treatment with chlomipramine, and in eight age-matched normal male controls. With 133Xe, there were no significant differences in rCBF between patients with OCD and their matched controls, and no significant differences in rCBF in the patients before and during treatment. Significantly increased HMPAO uptake in the orbital frontal cortex, posterofrontal cortex, and high dorsal parietal cortex bilaterally occurred in the OCD patients before treatment compared to their matched controls, and there were significant reductions of HMPAO uptake, into the normal range, in all these areas in the patients during treatment. Significantly reduced HMPAO uptake in the caudate nucleus bilaterally occurred in the patients before treatment compared to their matched controls, and these reductions persisted during treatment. This study provides additional support for the involvement of both the orbital frontal cortex and the caudate nuclei in the pathophysiology of OCD.

Adult↗
PubMed1995

Porphyria: reexamination of psychiatric implications.

Acute intermittent porphyria mimics a variety of commonly occurring disorders and thus poses a diagnostic quagmire. Psychiatric manifestations include hysteria, anxiety, depression, phobias, psychosis, organic disorders, agitation, delirium, and altered consciousness ranging from somnolence to coma. Some patients develop psychosis similar to schizophrenia. Psychiatric hospitals have a disproportionate number of patients with this disorder as only difficult and resistant patients accumulate there. Presence of photosensitive porphyrins in the urine is diagnostic. When porphyrins are absent, excess of alpha aminolevulinic acid and porphobilinogen are present in the urine. The definitive test is to measure monopyrrole porphobilinogen deaminase in RBCs. This diagnosis should be entertained in the following situations: (a) unexplained leukocytosis; (b) unexplained neuropathy; (c) etiologically obscure neurosis or psychosis; (d) 'idiopathic' seizure disorder; (e) unexplained abdominal pain; (f) conversion hysteria, and (g) susceptibility to stress. Porphyria is important in psychiatry as it may present with only psychiatric symptoms; it may masquerade as a psychosis and the patient may be treated as a schizophrenic person for years; the only manifestation may be histrionic personality disorder which may not receive much attention. Diagnosis is based on a high index of suspicion and appropriate investigation. Various psychotropic drugs exacerbate acute attacks. While it is important not to use the unsafe drugs in porphyric patients, it is also imperative to look for this diagnosis in cases where these drugs produce unprecedented drug reactions.

Acute Disease↗
PubMed1994

Hepatic disease and psychiatric illness: relationships and treatment.

A relationship between hepatic diseases and psychiatric symptoms has long been speculated. While liver detoxication makes the exogenous substances harmless for the body, there are occasions where the liver may convert a harmless substance into a more toxic substance. With such an important role, the liver protects all the organs of the body. When liver is malfunctioning, toxic metabolites injurious to the brain may be produced. As the brain receives a high blood supply, a large amount of metabolites reach this organ. Hence, the metabolic function of the liver keeps a delicate reciprocal relationship between the two organs. In addition, a number of psychiatric medications affect liver functions. Another perplexing clinical problem is the difficulty in treating psychiatric symptoms in patients with liver disease. For example, benzodiazepines which do not affect the liver function in physically healthy psychiatric patients, may induce hepatic coma in patients with liver disease. Benzodiazepine antagonists produce dramatic and temporary improvement in patients with hepatic coma. Clinically, many psychoactive drugs produce hepatic complications. The very same drugs which produce hepatic side effects are required for the treatment of psychiatric symptoms in patients with hepatic disorders. To appropriately handle these situations, a thorough knowledge of the side effects of these drugs is necessary.

Hepatic Encephalopathy↗