The effect of sleep deprivation on motor impairment and retinal adaptation in Parkinson's disease

Reist, Christopher; Sokolski, Kenneth N.; Chen, Cheng‐Chung; Coskinas, Evagelos; DeMet, Edward M.

doi:10.1016/0278-5846(95)00025-q

Cited by 38 publications

(19 citation statements)

References 18 publications

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“…With the alleviation of secondary depression still being the rationale for testing this patient population with RSD, parameters of its use in PD patients were determined on this basis. When a 24-h period of sleep deprivation was applied, not only was a strong antidepressant effect seen but bradykinesia, rigidity and tremor also improved Reist et al , 1995 ;Demet et al , 1999 ). While the postulated mechanisms responsible for the recovery of function included altered DA receptor sensitivity, reduced acetylcholine transmission and return of circadian rhythmicity, a key factor in its therapeutic effect may well have been the long duration of exposure to ambient light that occurs during RSD.…”

Section: Bright-light Therapy Pd and Underlying Depressionmentioning

confidence: 95%

“…As observed in their rodent counterparts, it could be this aspect rather than the deprivation of REM sleep that was contributing to the therapeutic effect of the treatment. That light exposure contributes to the observed effect is a possibility that has not be ruled out (Reist et al , 1995 ).…”

Section: Bright-light Therapy Pd and Underlying Depressionmentioning

confidence: 97%

“…This is a distinct possibility when you consider the activities undertaken during the 24-h deprivation phase which would require a normal amount of ambient lighting to enable the patients to execute the set tasks. Second, in one study, during the period of assessment it was noted that the neurological assessment was made ' … under a bank of fl uorescent lights … ' (Reist et al , 1995 ). As observed in their rodent counterparts, it could be this aspect rather than the deprivation of REM sleep that was contributing to the therapeutic effect of the treatment.…”

Section: Bright-light Therapy Pd and Underlying Depressionmentioning

confidence: 98%

See 2 more Smart Citations

A historical justification for and retrospective analysis of the systematic application of light therapy in Parkinson’s disease

Willis¹,

Moore²,

Armstrong³

2012

Reviews in the Neurosciences

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For the past 40 years the primary purpose of therapeutics for Parkinson's disease (PD) has been to replace deficient dopamine (DA) in the nigrostriatal dopamine (NSD) system. Even in the presence of limited efficacy, abundant side effects and impoverished quality of life, the involvement of other systems in the aetiology and treatment of this disorder has been sorely neglected and the excessive use of DA replacement therapy (DART) continues on a global basis. Recent scientific work suggests that the retina plays a major role in NSD function and intimates light therapy in the management of PD. After a thorough review of historical evidence supporting this contention, a retrospective, open-label study on 129 PD patients, whereby they were monitored for a period extending for a few months to eight years, was carried out. Primary motor and non-motor symptoms were monitored using an objectified global rating scale and timed motor tests that were assessed at regular intervals for the duration of the study. Thirty-one patients with other neurological disorders (OND) served as controls to determine whether any therapeutic effects seen with light were generalizable across other conditions. Patients were classified as compliant (COM), semi-compliant (SCOM), or early quit (EQUIT; prematurely discontinued treatment). EQUIT patients showed deterioration, while the COM group improved on most parameters. The SCOM patients were not as good as the COM group. The OND group showed significant improvement in depression and insomnia, but exposure to light did not improve motor function. The total drug burden of PD patients maintained on light was less with fewer side effects than SCOM or EQUIT groups. These results confirm the value of the strategic application of light therapy with controlled doses of DART in PD and warrants further controlled investigation. That the symptomatic improvement continued as long patients remained in the program suggests that exposure to light, under a strict daily regimen, combined with controlled DART, actively slows or arrests the progressive degenerative process underlying PD.

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Section: Bright-light Therapy Pd and Underlying Depressionmentioning

confidence: 95%

Section: Bright-light Therapy Pd and Underlying Depressionmentioning

confidence: 97%

Section: Bright-light Therapy Pd and Underlying Depressionmentioning

confidence: 98%

See 1 more Smart Citation

A historical justification for and retrospective analysis of the systematic application of light therapy in Parkinson’s disease

Willis¹,

Moore²,

Armstrong³

2012

Reviews in the Neurosciences

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“…A higher lifetime sleep duration has been associated with a higher risk of developing this disease, while rotating shift work and sleep loss had a protective effect [106] . Probably due to the marked increase in dopaminergic neurotransmission associated with SD, sleep-deprived patients affected by Parkinson's disease temporarily improved their motor scores after total [22,107,108] or partial SD [109] , and the improvement in motor symptoms was associated with a more prolonged amelioration of depression [110] . In subgroups of patients, however, a sleep benefit and a worsening after SD have been reported [111] , and caution should thus be used in administering antidepressant SD to patients with Parkinson's disease.…”

Section: Medical and Neurological Conditionsmentioning

confidence: 99%

Sleep Deprivation in Mood Disorders

2011

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Growing clinical evidence in support of the efficacy and safety of sleep deprivation (SD), and its biological mechanisms of action suggest that this technique can now be included among the first-line antidepressant treatment strategies for mood disorders. SD targets the broadly defined depressive syndrome, and can be administered according to several different treatment schedules: total versus partial, single versus repeated, alone or combined with antidepressant drugs, mood stabilizers, or other chronotherapeutic techniques, such as light therapy and sleep phase advance. The present review focuses on clinical evidence about the place of SD in therapy, its indications, dosage and timing of the therapeutic wake, interactions with other treatments, precautions and contraindications, adverse reactions, mechanism of action, and comparative efficacy, with the aim of providing the clinical psychiatrist with an updated, concise guide to its application.

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“…The same observation can be made during SD. SD improves rigor, akinesia or motor impairment, but not tremor (Bertolucci et al 1987;Reist et al 1995) in Parkinson`s disease. On the other hand, depending on the stage of illness, sleep beneÞt has been reported due to a replenishment of presynaptic dopamine stores (Parkes 1983), and dramatic exacerbations have been reported after SD due to a depletion of brain dopamine (Lauterbach 1994).…”

Section: The Psychostimulant Hypothesis Of Sd Clinical Aspectsmentioning

confidence: 97%

Neurobiological similarities in antidepressant sleep deprivation and psychostimulant use: a psychostimulant theory of antidepressant sleep deprivation

Ebert

Berger

1998

Psychopharmacology

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This paper attempts to summarize the evidence for the hypothesis that psychostimulant-like neurotransmitter processes within certain regions of the limbic system induce the positive effects of antidepressant sleep deprivation (SD). Preclinical and human studies indicate similar neurobiological effects of psychostimulants such as amphetamines, cocaine and SD. In clinical use, SD and psychostimulants have similar characteristics and behavioral effects. Furthermore, acute psychostimulant challenge decreases limbic metabolism in imaging studies, and SD decreases elevated limbic metabolism in SD responders, indicating that psychostimulant-like neurotransmitter release could decrease limbic metabolism in SD responders. Most antidepressant pharmacotherapies change the reactivity of the dopamine system, and a decrease of presynaptic dopamine or postsynaptic availability can induce depression. Sleep is accompanied by a reduction of catecholamine release and those processes which are increased by psychostimulants. It is concluded that a proposed regional postsynaptic deficit in catecholaminergic neurotransmission can be overcome either acutely by enhanced release during SD or psychostimulant use, or chronically by changes in receptor sensitivity or gene expression due to antidepressant therapies. A postsynaptic deficit in these areas becomes evident if presynaptic release is reduced in conditions such as sleep. Therefore, sleep is depressiogenic for predisposed individuals and the reduction of sleep avoids understimulation of subsensitive postsynaptic processes, which are enhanced by psychostimulants.

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The effect of sleep deprivation on motor impairment and retinal adaptation in Parkinson's disease

Cited by 38 publications

References 18 publications

A historical justification for and retrospective analysis of the systematic application of light therapy in Parkinson’s disease

A historical justification for and retrospective analysis of the systematic application of light therapy in Parkinson’s disease

Sleep Deprivation in Mood Disorders

Neurobiological similarities in antidepressant sleep deprivation and psychostimulant use: a psychostimulant theory of antidepressant sleep deprivation

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