Etiologies of insomnia in Parkinson's disease – Lessons from human studies and animal models

Aviv D. Mizrahi-Kliger*, Lucia K. Feldmann, Andrea A. Kühn, Hagai Bergman

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

16 Scopus citations


Sleep disorders are integral to Parkinson's disease (PD). Insomnia, an inability to maintain stable sleep, affects most patients and is widely rated as one of the most debilitating facets of this disease. PD insomnia is often perceived as a multifactorial entity – a consequence of several of the disease symptoms, comorbidities and therapeutic strategies. Yet, this view evolved against a backdrop of a relative scarcity of works trying to directly dissect the underlying neural correlates and mechanisms in animal models. The last years have seen the emergence of a wealth of new evidence regarding the neural underpinnings of insomnia in PD. Here, we review early and recent reports from patients and animal models evaluating the etiology of PD insomnia. We start by outlining the phenomenology of PD insomnia and continue to analyze the evidence supporting insomnia as emanating from four distinct subdivisions of etiologies – the symptoms and comorbidities of the disease, the medical therapy, the degeneration of non-dopaminergic cell groups and subsequent alterations in circadian rhythms, and the degeneration of dopaminergic neurons in the brainstem and its resulting effect on the basal ganglia. Finally, we review emerging neuromodulation-based therapeutic avenues for PD insomnia.

Original languageAmerican English
Article number113976
JournalExperimental Neurology
StatePublished - Apr 2022

Bibliographical note

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  • Basal ganglia
  • Brainstem
  • Cortex
  • Insomnia
  • Neuromodulation
  • Parkinson's disease
  • Sleep


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