Movement Disorders and Hypertension

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Possible mechanisms underlying sleep-related movement disorders and hypertension. First, sudden increases in BP seen with PLMS, probably due to sympathetic activation and vagal withdrawal, may be responsible for elevated BP seen in subjects with RLS and frequent PLMS [Bertisch Sleep 2016, Sforza Clin Neurophysiol 2005, Guggisberg Sleep 2007, Pennestri Neurology 2007].

As with subjects with OSA, this is thought to be an important mechanism underlying elevated BP in individuals with RLS/PLMS, during the night (although the pattern and time frame may be different than that seen in subjects with OSA), and potentially during the daytime as well [Siddiqui Clin Neurophysiol 2007, Pennestri Sleep Med 2013, Izzi Sleep Med 2014]. Other autonomic disturbances, such as impaired BP and HR reduction in response to the head-up tilt test and Valsalva maneuvers, have been demonstrated in subjects with RLS [Izzi Sleep Med 2014].

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Second, difficulty with sleep initiation and/or maintenance with shortened sleep duration secondary to RLS could conceivably lead to the development of hypertension [Innes SMRV 2012]. Third, sleep deprivation and PLMS have been shown to be associated with aortic stiffness and may serve to elevate cardiovascular risk, including that of hypertension, in patients with RLS and PLMS [Sunbul Sleep Breath 2014, Drakatos JCSM 2016].

Fourth, increased evening cortisol is seen in the context of sleep deprivation and higher nighttime cortisol levels have been noted in subjects with RLS, suggesting involvement of the HPA axis [Leproult Sleep 2010, Schilling Mov Disord 2010]. Increased inflammation has been noted in subjects with RLS and may increase the risk of hypertension but it is unclear whether inflammation is a result or causative factor for RLS [Trotti, Sleep 2011]. Fifth, impaired vascular endothelial function has recently been implicated as a potential pathophysiologic mechanism for elevated BP in subjects with RLS [Koh, J Neurol Sci 2015].

Sixth, metabolic dysfunction in the setting of sleep deprivation in RLS/PLMS could contribute to the risk of hypertension . Last, iron deficiency which is an etiologic factor for RLS, may be a cardiovascular risk factor in itself, and has been shown to be associated with diabetes mellitus type 2 and increased mortality in coronary artery disease; intravenous iron has been shown to improve functional status and quality of life and reduce hospitalizations in patients with heart failure . Central iron deficiency with increased dopaminergic tone in the basal ganglia may contribute to abnormalities in regulation of sympathetic tone in subjects with RLS/PLMS.

A number of epidemiologic studies have shown an association between RLS and hypertension [Ferini-Strambi J Neurol 2014, Gottleib Sleep Med 2017]. Innes et al in their systematic review of 17 studies, most of which were cross-sectional in nature including the large Sleep Heart Health Study and the Wisconsin Sleep Cohort Study, found that in 10 studies there was a positive association between RLS and hypertension after accounting for common confounders such as BP, smoking status and sleep problems.

RLS was positively associated with hypertension when symptom frequency exceeded more than half the days of the month [Winkelman Sleep Med 2006, Shahar AJRCCM 2001]. It should be noted that the studies had significant variability in the definition of RLS, measurement of BP and the use of RLS medications. One recent population-based cohort study did not find a significant association between PLMS and hypertension after accounting for confounders [Haba-Rubio Sleep Med 2018].

Some longitudinal studies that did not demonstrate a link between RLS and increased cardiovascular disease suggested a possible inverse relationship, with a trend toward or a significant increase in the incidence of RLS in those with hypertension [Stentkiralyi J Sleep Res 2013]. It should be noted that two other large longitudinal studies, the Physician’s Health Study and Women’s Health study, failed to show that RLS (based on a 3-question survey) was a risk factor for the development of cardiovascular disease while another study, the Nurses’ Health Study, demonstrated a significant association between self-reported diagnosis of RLS of more than 3 years duration made by a physician and incident as well as fatal myocardial infarction [Li Circulation 2012].

With regard to hypertension, in a large longitudinal study of enrollees in the Kaiser Permanente system, a significant association was noted between “primary” RLS and hypertension, although there was no association with overall cardiovascular disease [Van Den Eeden Sleep 2015].

The literature available thus far suggests that perhaps a relationship between RLS and hypertension exists, but the direction and magnitude of this relationship are unknown at this time. Additionally, the potential modification of this association by other factors including the etiology of RLS and presence of PLMS is unclear. Further cross-sectional studies of cardiovascular markers in subjects with RLS and small randomized controlled trials are required to determine whether treatment of RLS is capable of modifying cardiovascular risk [Gottleib Sleep Medicine 2017].

Individual PLMs are associated with increases of 25-30 mm Hg systolic BP and 10-15 mm Hg diastolic BP, from the start of the PLM until 10-15 seconds after the end of the PLM [Winkelman Sleep 1999]. Increases in HR followed by cortical arousal on EEG appear to precede the PLM and persist through the event [Sasai BMC Neurol 2013, Allena Clin Neurophysiol 2009, Ferri Clin Neurophysiol 2007]. Arousals associated with PLMS appear to increase the risk of hypertension compared to PLMS without arousals, possibly due to increased sympathetic activity associated with arousals [Koo Hypertension 2015, Pennestri Neurology 2007].

In one study, the PLM index was shown to be an independent predictor of cardiovascular and cerebrovascular risk scores in subjects with chronic kidney disease [Lindner J Sleep Res 2012]. In another study of older male subjects without prevalent hypertension at baseline, a PLM index of more than 30 per hour increased the risk of cardiovascular disease at 4 years, however, the risk of developing incident hypertension was not known [Koo Circulation 2011]. Koo et al in their multi-ethnic community study, found that the number of PLMs and PLM associated arousals per hour of sleep were independently associated with prevalent hypertension, particularly in African-American subjects [Koo Hypertension 2015].

Other studies have failed to demonstrate a significant association between PLMS and hypertension. In a study of subjects with RLS, those with a PLM index of greater than 35 per hour did not have a greater prevalence of hypertension but did have left ventricular hypertrophy [Mirza J Am Soc Echocardiogr 2013]. A study of subjects with OSA showed no difference in the prevalence of hypertension in those with and without PLMS (defined as a PLM index of 5 or more per hour)[Al-Alawi JCSM 2006].

In narcolepsy-cataplexy, there is sleep disruption with frequent awakenings [Donadio J Sleep Res 2008, Dauvilliers Lancet 2007]. The disorder results from a decrease in hypocretin or orexin which plays a role in autonomic function [Nunez Curr Neurophramacol 2009, Plazzi SMRV 2011, Portaluppi SMRV 2012, Berteotti Clin Auton Res 2017]. Decreased cardiovagal and sympathetic activity during wakefulness have been reported in subjects with narcolepsy [Ferini-Strambi J Neurol 1997, Donadio Neurology 2014]. Mechanisms underlying elevated BP in subjects with narcolepsy-cataplexy may involve the orexin system and may also include sympathetic dysregulation secondary to sleep disruption seen as part of the disorder itself or secondary to PLMS [Pepin SMRV 2014].

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