Dementia with Lewy bodies

More Evidence Links REM Sleep Behavior Disorder and Neurodegenerative Disease.

Posted by

0


Most patients diagnosed with idiopathic REM sleep behavior disorder advance to a neurodegnerative disease associated with alpha synuclein deposition (Lewy body disease) within a decade.

Several longitudinal studies have demonstrated a consistent association between idiopathic rapid eye movement (REM) sleep behavior disorder (IRBD) and the development of neurodegenerative disorders associated with alphasynucleinopathy, including Parkinson disease (PD), dementia with Lewy bodies (DLB), and multiple systems atrophy (MSA). In one previously described cohort of 44 patients with symptomatic IRBD for a median interval of 11 years and followed clinically for a median of 4.5 years, 45% met criteria for a neurodegenerative disorder. Now, the investigators report their findings in this cohort after an additional 7-year interval.

The conversion to a defined neurodegenerative diagnosis was 82% (16 PD, 14 DLB, 1 MSA, and 5 mild cognitive impairment). Four cohort members were lost to follow-up. Three patients in the cohort underwent autopsy during the period of study, which demonstrated characteristic pathological changes confirming diagnoses of PD in 2 and DLB in 1. Compared with healthy controls without IRBD, 4 patients who did not meet criteria for a neurodegenerative disorder demonstrated decreased striatal uptake of dopamine transporter, a biomarker associated with alphasynucleinopathies.

Comment: Although the sample size is relatively small, this report emphasizes the importance of longitudinal observations in slowly progressive neurodegenerative disorders. The findings highlight an opportunity to identify at-risk individuals and potentially intervene as disease-modifying therapies become available. However, clinicians should look carefully for other causes of dream-enactment behavior, such as medications or concomitant sleep disorders. In the absence of such factors, clinicians should confirm the diagnosis with polysomnography. As the authors suggest, idiopathic RBD may be more accurately termedisolated RBD. Patients who have REM sleep behavior disorder but are asymptomatic for parkinsonism or dementia should be made aware of the risk and the need for continued clinical follow-up.

 

Source:Journal Watch Neurology

Idiopathic REM sleep behaviour disorder in the development of Parkinson’s disease.

Posted by

0


Parkinson’s disease is a progressive neurodegenerative disorder associated with Lewy body disease pathology in central and peripheral nervous system structures. Although the cause of Parkinson’s disease is not fully understood, clinicopathological analyses have led to the development of a staging system for Lewy body disease-associated pathological changes. This system posits a predictable topography of progression of Lewy body disease in the CNS, beginning in olfactory structures and the medulla, then progressing rostrally from the medulla to the pons, then to midbrain and substantia nigra, limbic structures, and neocortical structures. If this topography and temporal evolution of Lewy body disease does occur, other manifestations of the disease as a result of degeneration of olfactory and pontomedullary structures could theoretically begin many years before the development of prominent nigral degeneration and the associated parkinsonian features of Parkinson’s disease. One such manifestation of prodromal Parkinson’s disease is rapid eye movement (REM) sleep behaviour disorder, which is a parasomnia manifested by vivid dreams associated with dream enactment behaviour during REM sleep. Findings from animal and human studies have suggested that lesions or dysfunction in REM sleep and motor control circuitry in the pontomedullary structures cause REM sleep behaviour disorder phenomenology, and degeneration of these structures might explain the presence of REM sleep behaviour disorder years or decades before the onset of parkinsonism in people who develop Parkinson’s disease.

Source: Lancet

Sleep and Working Memory in Parkinson Disease.

Posted by

0


Slow-wave sleep may be an important modulator of dopamine-related improvement in working memory among patients with PD.

To investigate whether sleep parameters are associated with improvement in working memory among patients with Parkinson disease (PD) or dementia with Lewy bodies (DLB), researchers conducted overnight polysomnography for 2 nights, followed by cognitive testing, in 53 patients with PD (most without dementia) and 10 patients with DLB. After each night of polysomnography, participants performed digit-span testing four times, beginning 2 hours after awakening and repeated every 2 to 3 hours. The digit-span forward task tested short-term memory, and the digit-span backward task tested working memory.

Sleep parameters did not differ among PD patients who were or were not taking dopaminergic medication and DLB patients. Based on the mean difference in digit-span scores from day 1 and day 2, the PD patients who were taking dopaminergic medications improved significantly on the digit-span backward task; the PD group not taking dopaminergic medications and the DLB patients did not show improvement. On the digit-span forward test, the PD patients did not improve significantly and the DLB patients’ scores declined significantly. In PD patients taking dopaminergic medication, improvement in digit-span backward performance correlated positively with the percentage of sleep that was slow-wave sleep and correlated negatively with duration of time with an oxygen saturation level <90%.

The authors concluded that (1) improvements in working memory based on digit-span backward performance can be seen in PD patients, particularly in those taking dopaminergic medications; (2) slow-wave sleep may be important for these improvements; and (3) nocturnal oxygen desaturation may impede these improvements.

Comment: These findings offer insight into the potential for cognitive improvement in patients with Parkinson disease, particularly those who do not have dementia and who are taking dopaminergic medications. Slow-wave sleep may be an important modulator of this improvement. Increasing slow-wave sleep may improve working memory in people with PD, although the clinical utility of using dopaminergic medications specifically to enhance cognition requires further investigation. Future research should examine the exact mechanisms by which dopamine may enhance working memory, determine whether dopaminergic medications increase slow-wave sleep, and clarify how nocturnal oxygen desaturation can impede this cognitive process.

Source: Journal Watch Neurology