Functional morphology of gonads under conditions of antipsychotic therapy

2014 ◽  
Vol 60 (4) ◽  
pp. 30-34
Author(s):  
B P Volkov

Gonadotoxic side effects of antipsychotic agents are known to cause serious disturbances in both germinative and endocrine testicular functions. The hormonal activity of the testes undergo undulating changes whereas the germinative function progressively decreases from the onset of neuroleptic therapy. The morphological and functional disturbances in the testicles are especially well pronounced after 10 years of antipsychotic treatment. The morphofunctional changes in the ovaries become apparent from the very beginning of antipsychotropic therapy; they are indicative of the progressive impairment of reproductive and endocrine functions of the female gonads.

2021 ◽  
Vol 9 (T3) ◽  
pp. 340-344
Author(s):  
Faisal Idrus ◽  
Theodorus Singara ◽  
Dwiwahyu Sunarto ◽  
Saidah Syamsuddin ◽  
Sonny T. Lisal

Background: Schizophrenia is one of the mental disorder with many problematic issues, in both psychologically and socially. This disease requires provision of long-term antipsychotic therapy, hence could rise other potential health problems. Antipsychotic treatment can cause serious glucometabolic side-effects, including type 2 diabetes and hyperglycemic emergency. Recent attention has also been focused on antipsychotic-induced hyperglycemic emergencies experienced by new users of typical and atypical antipsychotic. Patients treated with atypical APDs have ~10 times higher risk in developing hyperglycaemic emergencies. In our pre-eliminary study, hyperglycemia condition in new patients occurs in four  in seven patients who received typical and atypical antipsychotics. This condition is often overlooked and is not routinely evaluated. Moreover, it can develop into diabetes and increase the risk of morbidity and mortality in schizophrenia patients. In this study, we would like to determine the acute effects of metabolic (hyperglycemia) in patients treated with antipsychotic (Risperidone and Haloperidol) Measurement of blood sugar levels was performed in groups treated with haloperidol (N = 15) and treated with risperidone (N = 15). Plasma samples were taken at the beginning of treatment, in week IV, and in week VIII. The measurement of glucose levels was performed after meal and in early morning before breakfast (fasting blood glucose level 8 hours). Results: The blood sugar level after meals was significantly higher in the Risperidone group compared to the Haloperidol group  (p <0.001) after IV and VIII weeks. Meanwhile, the fasting blood sugar level was significantly higher in the Risperidone group compared to the Haloperidol group after VIII weeks of treatment ( p <0.001). Conclusions: Both antipsychotics can cause an increase in blood sugar levels. Treatment with Risperidone significantly increased the blood sugar levels compared to treatment with haloperidol. Measurement of blood sugar level is needed to monitor the metabolic effect of antipsychotic, especially in patients treated with Risperidone. It is necessary to have dietary regulation and physical activities to prevent undesired metabolic side effects.


CNS Spectrums ◽  
2007 ◽  
Vol 12 (S11) ◽  
pp. 1-16 ◽  
Author(s):  
Joseph Battaglia ◽  
Delbert G. Robinson ◽  
Leslie Citrome

AbstractAcute agitation is a nonspecific term applied to an array of syndromes and behaviors. It is frequently defined as an increase in psychomotor activity, aggression, disinhibition/impulsivity, and irritable or labile mood. Etiologies of acute agitation include medical disorders, delirium, substance intoxication or withdrawal, psychiatric disorders, and medication side effects. Treatment of acute agitation requires both environmental and pharmacologic intervention. Patients should be calmed with sedating agents early in the course of treatment, allowing for diagnostic tests to take place. Failure to correctly diagnose causes of agitation may lead to delayed treatment for serious conditions, and can even exacerbate agitation.The most common cause of agitation in patients with schizophrenia is psychotic relapse due to medication nonadherence. Pharmacologic treatment options for these patients include lorazepam and antipsychotic agents. Lorazepam causes nonspecific sedation and treats some substance withdrawal, but has little effect on psychosis. First-generation antipsychotics treat psychosis and, at high enough doses, cause sedation, but may induce extrapyramidal side effects (EPS). Some second-generation antipsychotics have been approved for the treatment of agitation in schizophrenia. These agents treat psychosis with a favorable EPS profile, but are comparatively expensive and cause risks such as hypotension. However, avoiding EPS may reduce patients' resistance to antipsychotic treatment.In this expert roundtable supplement, Joseph Battaglia, MD, provides an overview of the definition of acute agitation. Next, Delbert, G. Robinson, MD, outlines evaluation methods for actue agitation. Finally, Leslie Citrome, MD, MPH, reviews interventions for acute and ongoing management of agitation.


2002 ◽  
Vol 2 (1-2) ◽  
pp. 16-28
Author(s):  
Svjetlana Loga-Zec ◽  
Irfan Zulić ◽  
Nedžad Mulabegović ◽  
Ismet Cerić ◽  
Slobodan Loga ◽  
...  

Antipsychotic drugs produce a wide spectrum of physiological actions. Some of these effects differ among the various classes of antipsychotics. This medications have indications in the treatment of acute psychotic disorders. The main goal of this investigation was to determine the incidence and prevalence of the neuroleptic therapy acute side effects. The reason for this epidemiological investigation performing was the lack of knowledge of the exact neuroleptic therapy side effects incidence. Qualitative study on this problem has not been performed yet. Antipsychotic therapy side effects prevalence rate according to the literature data is ranging from 24% to 74%. Different prevalence rate is a consequence of different antipsychotic drug usage, different drug administration method and different side effects identification. On account of all these facts, we put the hypothesis on the correlation between the antipsychotic therapy and occurred side effects. Our experiment included all patients hospitalised from December 31st 1999 to January 31st 2000 in Intensive Care Unit of Biological Psychiatry Department of Psychiatric Clinic in Sarajevo. All patients were divided in three groups according to the applied therapy. All of them met ICD-10 criteria for schizophrenia (F20-29). During our study the following examinations were performed: psychiatric interview, BRPS, scale of side effects, psychophysiological tests, general clinical impression, scale of appetite, carbon hydrate needs scale. Psychiatric and statistical evaluations were done as well. The evaluation of our examination is showing successful results in all groups of patients. The improvement of psychopathological symptoms was insignificant. Reported side effects were minimal with low incidence rate and relatively high prevalence rate. Statistical tests were calculated from the obtained data after what the null hypothesis was rejected. Consequently, an alternative hypothesis was confirmed and it indicated that the acute side effectsincidence and prevalence were within the range of expectation. Intensity of the recorded side effects was moderate to mild. On the basis of the obtained data, it has been concluded that applied antipsychotic agents did not induce more psychophysiological function impairments in the treated patients. Psychophysiological functions remained in physiological range limits and their changes were not significant. Neuroleptic therapy side effects were minimal, meaning no toxic signs or therapy discontinuations were recorded.


2005 ◽  
Vol 50 (11) ◽  
pp. 703-714 ◽  
Author(s):  
Howard C Margolese ◽  
Guy Chouinard ◽  
Theodore T Kolivakis ◽  
Linda Beauclair ◽  
Robert Miller ◽  
...  

Objective: Tardive dyskinesia (TD), the principal adverse effect of long-term conventional antipsychotic treatment, can be debilitating and, in many cases, persistent. We sought to explore the incidence and management of TD in the era of atypical antipsychotics because it remains an important iatrogenic adverse effect. Methods: We conducted a review of TD incidence and management literature from January 1, 1965, to January 31, 2004, using the terms tardive dyskinesia, management, therapy, neuroleptics, antipsychotics, clozapine, olanzapine, risperidone, quetiapine, ziprasidone, and aripiprazole. Additional articles were obtained by searching the bibliographies of relevant references. We considered articles that contributed to the current understanding of both the incidence of TD with atypical antipsychotics and management strategies for TD. Results: The incidence of TD is significantly lower with atypical, compared with typical, antipsychotics, but cases of de novo TD have been identified. Evidence suggests that atypical antipsychotic therapy ameliorates long-standing TD. This paper outlines management strategies for TD in patients with schizophrenia. Conclusion: The literature supports the recommendation that atypical antipsychotics should be the first antipsychotics used in patients who have experienced TD as a result of treatment with conventional antipsychotic agents. The other management strategies discussed may prove useful in certain patients.


1998 ◽  
Vol 43 (1_suppl) ◽  
pp. 15S-20S ◽  
Author(s):  
Leonardo Cortese ◽  
Emmanuelle Pourcher-Bouchard ◽  
Richard Williams

Objective: To review and discuss the spectrum of adverse events caused by antipsychotic agents that can directly influence the outcome of treatment by interfering with patient acceptance of and adherence to therapy. Method: The adverse effects of traditional and second-generation antipsychotic medications were discussed during a series of clinical workshops attended by psychiatrists from across Canada. The various adverse effects of antipsychotic drugs as well as their assessment and management are reviewed. Results: Simple techniques for assessing adverse effects such as extrapyrimidal symptoms (EPS) are described. In some cases, adverse effects can be managed by dosage reduction and/or the use of adjunctive therapies such as antiparkinsonian agents and benzodiazepines. However, in some patients dose reduction carries the risk of symptom reemergence, while the commonly used adjunctive medications are associated with adverse effects of their own. Conclusions: Treatment-related side effects often require a reduction in dosage or a change in medication. Proper management can help encourage patient compliance and improve the outcome of antipsychotic treatment. The availability of the newer atypical antipsychotics offers another alternative, because they are associated with a much lower incidence of antipsychotic-induced side effects.


Author(s):  
Anggie Rahaya ◽  
Noor Cahaya

Trihexyphenidyl (THP) is used to treat symptoms of Parkinson's disease or involuntary movements due to the side effects of certain psychiatric drugs. It can also decrease other side effects such as muscle stiffness/rigidity (extrapyramidal syndrome or EPS). EPS were an unavoidable consequence of effective antipsychotic therapy. EPS reduce beneficial effects of antipsychotic treatment on the negative, cognitive, and mood symptom domains, while increasing the risk of tardive dyskinesia and reducing compliance. The purpose of this research was to analyze the percentage use of THP and the pattern of THP usage on schizophrenia patient which treated at Sambang Lihum Hospital. This retrospective observational study was conducted at an inpatient Sambang Lihum Hospital. This research were conducted to 264 medical records of patients period January 2013 to December 2013 which receive antipsychotics medication. Data were analyzed by univariate analysis. The result showed 94.32% (n=264) received THP. This research has shown the pattern of THP usage in Sambang Lihum Hospital which was to give THP directly to patients without EPS examination is 96.79% (n=249) and there are 15.66% (n=249) patients evaluated after 14 days after THP administered. Key Words: Schizophrenia, Trihexyphenidyl, EPS


2021 ◽  
pp. 000486742110256
Author(s):  
William Lugg

Objectives: Tardive dyskinesia, psychotic relapse and treatment-refractory psychosis have long been associated. A common underlying mechanism involving antipsychotic-induced ‘supersensitivity’, albeit in different brain pathways, was proposed as early as 1978. This piece seeks to reappraise the concept and potential implications of antipsychotic-induced supersensitivity. Conclusions: Evidence increasingly suggests that chronic antipsychotic exposure induces neuroadaptive physiological changes in dopaminergic, and other, neurotransmitter systems that may render some individuals more vulnerable to psychotic relapse - including those receiving continuous antipsychotic treatment. It is possible that in treating every episode of psychosis with prolonged or indefinite antipsychotic therapy, we paradoxically increase the risk of psychotic relapse in a significant proportion of people. A greater appreciation of supersensitivity may allow us to optimise any potential benefits of antipsychotics while minimising the risk of inadvertent iatrogenic harms. More research is needed to improve our understanding of the underlying neurophysiology of supersensitivity and to better identify which individuals are most vulnerable to its development. It is time we paid more attention to the concept, emerging evidence and potential implications of antipsychotic-induced supersensitivity and, where appropriate, adjusted our practice accordingly.


2021 ◽  
pp. 026988112110264
Author(s):  
Gavin P Reynolds

Guidelines for the treatment of schizophrenia limit the use of antipsychotic agents to clinically-established maximum doses. This acknowledges both the absence of additional efficacy of dopamine D2 receptor antagonists above a receptor occupancy threshold, and the increases in side effects that can occur at higher doses. These limits restrict the dosing of combinations of antipsychotics as they do single agents; drugs sharing the major antipsychotic mechanism of D2 receptor antagonism will act additively in blocking these receptors. Several newer antipsychotic drugs, including aripiprazole and cariprazine, act as partial agonists at the D2 receptor site and avoid action at several other receptors, effects at which are responsible for some non-dopaminergic adverse effects. This pharmacology imparts different characteristics to the drugs resulting often in a more favourable side effect profile. Their partial agonism, along with high affinities for the D2 receptor, also means that these drugs given adjunctively may in part replace, rather than enhance, the D2 antagonism of other antipsychotic agents. This can result in an improvement in certain side effects without loss of antipsychotic efficacy. This article makes the case for distinguishing the D2 partial agonists from antagonists in defining maximum doses of combined treatments, which would increase the options available to the prescriber, emphasising that pharmacological mechanisms need to be understood in identifying optimal treatments for psychotic illness.


2021 ◽  
Vol 35 (3) ◽  
pp. 284-302
Author(s):  
Ilijana Babic ◽  
Dominic Sellers ◽  
Paul L Else ◽  
Jessica Nealon ◽  
Ashleigh L Osborne ◽  
...  

Background: Liraglutide is a glucagon-like peptide-1 (GLP-1) receptor agonist that prevents metabolic side effects of the antipsychotic drugs (APDs) olanzapine and clozapine through unknown mechanisms. Aim: This study aimed to investigate the effect of chronic APD and liraglutide co-treatment on key neural and peripheral metabolic signals, and acute liraglutide co-treatment on clozapine-induced hyperglycaemia. Methods: In study 1, rats were administered olanzapine (2 mg/kg), clozapine (12 mg/kg), liraglutide (0.2 mg/kg), olanzapine + liraglutide co-treatment, clozapine + liraglutide co-treatment or vehicle for six weeks. Feeding efficiency was examined weekly. Examination of brain tissue (dorsal vagal complex (DVC) and mediobasal hypothalamus (MBH)), plasma metabolic hormones and peripheral (liver and kidney) cellular metabolism and oxidative stress was conducted. In study 2, rats were administered a single dose of clozapine (12 mg/kg), liraglutide (0.4 mg/kg), clozapine + liraglutide co-treatment or vehicle. Glucose tolerance and plasma hormone levels were assessed. Results: Liraglutide co-treatment prevented the time-dependent increase in feeding efficiency caused by olanzapine, which plateaued by six weeks. There was no effect of chronic treatment on melanocortinergic, GABAergic, glutamatergic or endocannabionoid markers in the MBH or DVC. Peripheral hormones and cellular metabolic markers were unaltered by chronic APD treatment. Acute liraglutide co-treatment was unable to prevent clozapine-induced hyperglycaemia, but it did alter catecholamine levels. Conclusion: The unexpected lack of change to central and peripheral markers following chronic treatment, despite the presence of weight gain, may reflect adaptive mechanisms. Further studies examining alterations across different time points are required to continue to elucidate the mechanisms underlying the benefits of liraglutide on APD-induced metabolic side effects.


1988 ◽  
Vol 153 (S3) ◽  
pp. 51-58 ◽  
Author(s):  
Malcolm Lader

The tricyclic antidepressants (TCAs) were discovered accidentally by pharmaceutical chemists seeking first, better antihistamines and then antipsychotic agents. Careful clinical assessment revealed the antidepressant properties and suggested that the closer the patient resembled the classical textbook description of ‘endogenous’ depression, the more likely was an adequate clinical response to occur (Kuhn, 1958). However, it was quickly realised that the TCAs possess a plethora of side-effects, particularly sedation and symptoms related to their anticholinergic effects.Despite much research over the past 25 years, it is unclear how TCAs effect clinical improvement. The two main neurotransmitters involved in some way are noradrenaline (Schildkraut, 1965) and 5-hydroxytryptamine (5-HT; serotonin; Van Praag, 1977). It was proposed that TCAs acted by blocking the reuptake of one or other or both of these neurotransmitters, thereby increasing their concentration in the synaptic cleft. However, as well as these acute effects, chronic effects, such as a decrease in the number of central beta-adrenoceptors (‘down-regulation’) occur, and these are probably more relevant to the clinical action.


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