Detailed insight into the pathophysiology and the behavioral complications associated with the Parkinson's disease and its medications (original) (raw)
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Parkinson's disease severity and use of dopaminergic medications
Parkinsonism & Related Disorders, 2015
Background-The effects of dopaminergic therapy in Parkinson's disease (PD) can vary depending on the class of medication selected. Objective-The aim of this post hoc study was to determine if the class of dopaminergic therapy correlated with disease severity in persons with early, treated PD. Methods-A non-parametric global statistical test (GST) was used to assess the status of participants treated with dopamine agonist (DA) monotherapy, levodopa (LD) monotherapy or combined LD and DA therapy on multiple PD outcomes encompassing motor, cognitive, psychiatric and autonomic function, as well as disability and quality of life. Results-The outcomes measured at the beginning of the study showed lower disease burden for participants on initial DA monotherapy compared to those taking combined LD and DA therapy after controlling for age, education, taking cogmeds and amantadine. Conclusion-This observation suggests that clinicians treating early PD patients favor combined LD and DA therapy in patients with more disabling features over DA monotherapy. As such, studies of PD progression in treated PD patients may be affected by the class of symptomatic dopaminergic therapy.
Parkinson’s disease: A review article
The Pharma Innovation Journal, 2017
Parkinson’s is one of the most horrendous disease affecting 1% of the adult population above the age of 60 and 4% over the age 85 . This disease is chronic and progressive in neurodegeneration causing dopaminergic neurons in Substantia nigra region of the mid brain to die which ultimately leads to decrease in dopamine production in our brain. Though any direct cause of this disease has not been identified yet, but many genetic mutations and environmental factors are found to be related to it. The diagnosis depends on family genetic history and disease symptoms. Dopamine is a neurotransmitter which controls certain notable functions of body including movement, memory, sleep, attention and learning. Due to plummeted production of dopamine, a Parkinson’s patient encounters several symptoms like tremor, bradykinesia, rigidity, postural instability.
Parkinson’s disease between internal medicine and neurology
Journal of Neural Transmission, 2015
General medical problems and complications have a major impact on the quality of life in all stages of Parkinson’s disease. To introduce an effective treatment, a comprehensive analysis of the various clinical symptoms must be undertaken. One must distinguish between (1) diseases which arise independently of Parkinson’s disease, and (2) diseases which are a direct or indirect consequence of Parkinson’s disease. Medical comorbidity may induce additional limitations to physical strength and coping strategies, and may thus restrict the efficacy of the physical therapy which is essential for treating hypokinetic-rigid symptoms. In selecting the appropriate medication for the treatment of any additional medical symptoms, which may arise, its limitations, contraindications and interactions with dopaminergic substances have to be taken into consideration. General medical symptoms and organ manifestations may also arise as a direct consequence of the autonomic dysfunction associated with Pa...
Privação de sono total na doença de Parkinson
Arquivos De Neuro-psiquiatria, 1987
A major problem in the long-term management of Parkinson disease (PD) is the progressive loss of efficacy of L-Dopa, an effect attributed, at least in part to diminished responsiveness of dopaminergic receptors in basal ganglia 14. The restoration of normal responsiveness or the induction of receptors hypersensitivity would be valuable not only in the management of L-Dopa therapy complications, but also as a treatment of PD. It is known, since the work of Ferguson & Dement (1969) that rapid eye movement sleep deprivation (REMSD) enhances the aggressive behavior induced by amphetamine 8. This effect, first attributed to either norepinephrine or serotonin, was later demonstrated to be dopamine dependent, at least in part. Thus, it was shown that REM SD enhances aggressive behavior induced by apomorphine, a powerful agonist of dopaminergic receptor 5,16. Further studies demonstrated the same effect for the stereotyped behavior induced by apomorphine 24. Aggressive behavior was also observed in nomifensine, piribedil and bromocriptine-treated rats after REM SD 6,22 again suggesting dopaminergic system participation. These evidences taken together suggest that an effect of REM SD could be the induction of hyperresponsiveness to dopaminergic agents. In this respect, it is pertinent that in rats with an experimental model of PD obtained by bilateral lesion of nigrostriatal pathway, REM SD improved ambulation and rearing 1. It is well known that in PD there is a dopaminergic deficiency in the nigrostriatal system (for a review of the subject see Hornykiewicz 11 and Rinne 20). A less appreciated point is the role of CNS dopaminergic systems in depression: although data are often conflicting, several investigators reported lowered levels of 5-hydroxyndolacetic acid (5HIAA), homovanilic acid (HVA) and 3-methoxy-4-hydroxyphenilglycol (MHPG), respectively major metabolites of serotonin, dopamine and norepinerphrine, in cerebrospinal fluid of depressed patients 2,7,18. Similar trends were observed with the urinary excretion of cathecolamines and their metabolites 21. Several antidepressant drugs, including nomifensine, exhibit a rather potent inhibition of dopamine uptake in brain 9,19.29. Therapeutic trials of L-Dopa in depressive patients were benefitial, specially in the cases with
Neuropsychiatric effects of Parkinson's disease treatment
Australasian Journal on Ageing, 2012
Advances in the treatment of Parkinson's disease have led to significant improvement in many of the disabling motor symptoms of the disease, but often at the cost of neuropsychiatric side-effects. These include psychosis, dopamine dysregulation syndrome, impulse control disorders, mood disorders and Parkinson's disease drug withdrawal syndromes. Such side-effects can be as disabling and have as much impact on activities of daily living, quality of life, relationships and caregiver burden as motor symptoms. Awareness of these potential side-effects is important both in terms of obtaining informed consent, and to aid early identification and intervention, as patients may not spontaneously report side-effects because of lack of insight, or deny them out of shame or embarrassment. The challenge of treatment can be a trade off between the emergence of such side-effects and the amelioration of parkinsonism, best mastered with an informed dialogue between clinician and patient.
Parkinsonism & Related Disorders, 2014
Background: Drug-induced Parkinsonism is common, causes significant morbidity, and can be clinically indistinguishable from idiopathic Parkinson's disease. Additionally, drug-induced Parkinsonism may, in some cases, represent "unmasking" of incipient Parkinson's disease. Clinical features or tests that distinguish degenerative from pharmacologic Parkinsonism are needed. Methods: We performed a retrospective case-control study of 97 drug-induced Parkinsonism subjects and 97 age-matched patients with Parkinson's disease. We compared the frequency of subjective motor and non-motor complaints, objective motor findings (Unified Parkinson's Disease Rating Scale Part III) and, where available, objective olfactory tests. We also performed a nested case-control study wherein we compared these same features between drug-induced Parkinsonism patients based on whether or not they recovered after changing the offending agent. Results: Non-motor symptoms including constipation and sexual dysfunction were more common in Parkinson's disease than in drug-induced Parkinsonism. While total motor scores were similar between groups, Postural Instability-Gait Difficulty scores were also higher in Parkinson's disease. Features that were significantly different or showed a trend towards significance in both comparisons included subjective loss of facial expression, dream-enactment behavior, autonomic complaints and Postural Instability-Gait Difficulty scores. Hyposmia was more common in Parkinson's disease and was strongly predictive of persistent drug-induced Parkinsonism after therapy change (odds ratio 30.3, 95% confidence interval: 1.5e500, p ¼ 0.03). Conclusions: A constellation of motor and non-motor features may differentiate unmasked Parkinson's disease from drug-induced Parkinsonism. In particular, olfactory testing may offer a simple and inexpensive method to help predict outcomes in drug-induced Parkinsonism and, potentially, identify a cohort of pre-motor Parkinson's disease.
Treatment of Parkinsonian Features in Neurological Disorders Other than Parkinson’s Disease
Handbook of experimental pharmacology, 1989
Parkinsonism is a collection of neurological features, including tremor, rigidity, akinesia and loss of postural reflexes. This syndrome is most commonly due to Parkinson's disease, but may occur with a wide variety of conditions in which parkinsonian features may be found alone or in combination with other neurological, medical and psychiatric deficits. From a therapeutic viewpoint, the conditions causing parkinsonism can be grouped under four headings: 1. Drug-induced parkinsonism, in which management is influenced by a compromise between the desired effect of antipsychotic drug treatment and this unwanted side effect. 2. Conditions in which the primary treatment of parkinsonism is the specific management of the causative disorder rather than palliation. In this category, Wilson's disease will be discussed in detail. 3. The multiple system degenerative diseases of the nervous system in which the therapeutic approach is similar to that in Parkinson's disease, but usually only a partial or temporary response of the parkinsonism is seen and nonparkinsonian features tend to be unchanged. 4. Other types of parkinsonism. B. Drug-Induced Parkinsonism A necessary step in the management of drug-induced parkinsonism is an awareness of which drugs are capable of causing this syndrome. The most important group is the neuroleptic drugs (the phenothiazines, the thioxanthenes and the butyrophenones) which act as dopamine antagonists. Extrapyramidal effects are most likely to occur with fluphenazine, perphenazine, trifluoperazine, triflupromazine and haloperidol, and least likely to occur with thioridazine and molindone. Chlorpromazine, acetophenazine, chlorprothixene and thiothixene are in an intermediate category (BALDESSARINI 1980). Metoclopramide, a centrally active D2 receptor antagonist, is a common cause of drug-induced parkinsonism. Reserpine and its synthetic analogue tetrabenazine cause parkinsonism by depletion of presynaptic stores of dopamine. D. B. Calne (ed.
Pharmacologic safety concerns in Parkinson's disease: facts and insights
The International journal of neuroscience, 2011
Knowledge and insight of pharmacologic safety issues and drug interactions are important for medical management of Parkinson's disease (PD). This review will discuss several topics, including apomorphine safety and interactions, impulsivity and excessive daytime somnolence associated with dopamine agonists (DAs), tolcapone hepatotoxicity, and monoamine oxidase type-B (MAO-B) inhibitor drug interactions. Initiation of apomorphine requires antiemetic prophylaxis to minimize nausea and orthostatic hypotension. Centrally acting antidopaminergic antiemetics will worsen parkinsonism and block the therapeutic effects of apomorphine and should be avoided. Additionally, serotonin 5-HT(3) receptor antagonist antiemetics should be avoided on the basis of limited clinical data suggesting lack of efficacy for apomorphine-induced nausea. Dopamine-agonist-induced impulsivity and daytime somnolence are not uncommon. When severe, these effects can be disabling and unsafe. Tolcapone-induced hepat...