periodic leg movement

[sheepless]

Damiansd, is that gabapentin?

I'd like to hear more detail if you're willing.

I'm not challenging you, but am curious how you know it's working? like, did they check you with a polysomnogram? how did you learn you have plm in the first place? do you also have restless legs while awake? what symptoms did you have before & not now? have you used audio or video recordings? witness reports? are you experiencing fewer awakenings?

[kappa]

Illorum posted a brief quote from a 2012 paper in another thread which I thought might add to the discussion here:

Eighty-one successively seen patients with PLMs during CPAP titration were investigated. Elimination of AASM-defined hypopnea was not sufficient to eliminate the PLMs observed during the titration; higher CPAP eliminated flow limitation and CAP phases A2 and A3 and persisting PLMs. PLMs were associated with simultaneous EMG bursts in expiratory abdominal muscles.

https://pubmed.ncbi.nlm.nih.gov/22241760/

I've bolded the key message from the paper.

The message here appears to be that flow limitation leads to an expiration burst which also results in leg movements (for reasons unknown... crossed wires? . I expect this aligns with my experience where I see increased flow simultaneously with leg movement.

Has anyone experimented with higher pressures to reduce PLM as seems to be recommended in this paper?

[Damiansd]

Damiansd, is that gabapentin?

I'd like to hear more detail if you're willing.

I'm not challenging you, but am curious how you know it's working?  like, did they check you with a polysomnogram?  how did you learn you have plm in the first place? do you also have restless legs while awake? what symptoms did you have before & not now? have you used audio or video recordings? witness reports? are you experiencing fewer awakenings?

Hey sheepless, sorry for the belated response 

Yes it is Gabapentin and it has been helping. Seeing 6 hours minimum night now which is awesome. Poly was done in January as part of sleep study and it showed pretty clealy. How did I know, just a guess as I have always been a Jiggler. Sit at a table with legs bouncing back and forward the whole time. People tell me to stop it. I try it but after a while I'm at it again. Tried magnesium and other things but no help. 

My wife has seen me twitch as I'm falling asleep and whilst asleep and the bedsheets bear testament to me moving a lot. Since the gabapentin it has settled. Awakenings have lessened but I wouldn't say they have stopped, there is still typically a nature break. My wife visits the toilet a few times during the night so one of her visits typically stirs me enough to prompt to to go. 

Let me know if you have any more  queries. 

D.

[sheepless]

thanks for that info Damian. I have the jiggling problem too; I'm in constant motion, can't sit still or even sit for long. I didn't know enough at the time to check my flow rate to see what effect gabapentin had on my plm. my subjective sense was that it made my before-bed rls worse so I quit. I'm not completely sure yet but ropinirole does seem to ease my waking rls and it for sure has reduced but not eliminated plm. biggest problem with ropinirole is that you have to take it a few hours before bed and as I recall it's half life is just 6 hours so it doesn't last the night. I think there might be a time release version used for parkinson's sufferers; will have to ask my doc about that.

kappa, I saw that too; thanks for re-posting here. I know there's a school of thought that plm is related in some way to apnea or SDB, and I assume it's quite possible that there may be different types, causes, presentations of plm, but that's not been my experience. I thrashed a lot before cpap, struggling to breathe, but I believe my plm is different than that as I really don't thrash about anymore.

I'm interested in learning more about this CAP and would love to find out that pap can help reduce or eliminate plm. however, I've tried apap, asv and vauto at many many different settings, from 10 to 25 cmw, in lots of combinations of min, max, epr, epap, ipap, ps, & have come to the conclusion that only meds help (me).

thanks both for continuing the plm discussion. it doesn't get talked up much but it seems there are a fair number of folks here that have this problem. and my guess: a fair number of folks that don't know they have this problem. many docs, and I would say sleep docs especially, don't seem to want to deal with it.

[Illorum]

Hey guys!
Here's some more information on that study relating to CAP, PLMS, and nasal CPAP

Results
All successively monitored patients during a 7-month period who showed PLMs during nasal CPAP titration and who met the inclusion criteria were included in the study. Eighty-one patients were treated with nasal CPAP; the demographics are presented in Table 1 

PLMs Analyses
The mean peak interval between two EMG leg discharges was 26 s (SD 5 5.1; range, 13-34 s) for the total group. 4 Leg EMG discharges were associated with a sympathetic activation, as indicated by a downward movement of the fi nger plethysmography curve, in 95% 3.1% of the leg movements. An associated change in the sleep EEG was also noted in 95% 3.3% of the EMG bursts. These changes consisted of either a burst of high-amplitude EEG waves in the d frequency range; a mixture of high-amplitude, fasterfrequency, and lower-amplitude waves ( u and a range); or fast-frequency low-amplitude waves ( a and b range). These changes were of variable duration, as short as 1 s 14 and at times longer than 3 s, and were indicative of an AASM arousal. 17


Response to CPAP
Appearance of PLMs: PLMs were present at a pressure of 5 cm H 2 O in 19 of 81 patients. PLMs appeared during sleep while receiving mostly low CPAP, with PLMs noted when pressure was between 5 and 10 cm H 2 O in all subjects; apneas and hypopneas were always present in the recording when PLMs were noted.

Disappearance of PLMs:
PLMs were present in 72 subjects when AASM-defi ned hypopneas 4 were eliminated. These subjects, however, still showed a pattern of “fl ow limitation” and the presence of CAP phases A2 and A3 during NREM sleep. 14,15,17,19 The disappearance of “flow limitation” required higher pressure and was associated with the disappearance of PLMs. Nine subjects had simultaneous disappearance of apnea and hypopnea, fl ow limitation, indication of arousals using the CAP system, and PLMs, and 44 patients needed 2 cm H 2 O of pressure to see the disappearance of fl ow limitation and PLMs. We did not note a difference in the disappearance of flow limitation, CAPs A2 and A3, and PLMs using our scoring criteria requirements of having at least 20 min of stable sleep without the presence of fl ow limitation and CAPs. When comparing the nasal CPAP necessary to eliminate AASM-defi ned “hypopneas” and the pressure necessary to eliminate PLM, we found a mean signifi cant difference of 1.47 1.96 cm H 2 O ( P 5 .02, two tailed). However, there was no significant difference in the pressure that eliminated fl ow limitation or CAPs A2 and A3 and PLMs. In the subjects in whom the disappearance of fl ow limitation and PLMs had already been observed, the drop of pressure with awakening led to a reappearance of PLMs, fl ow limitation, and CAPs A2 and A3. 

Position During Sleep:
Sleep position was monitored continuously, and all patients spent between 92% and 100% (mean 95% 3.5%) of their time during sleep in a supine position because of the CPAP titration protocol. Lateral sleeping, if present, was always short and was seen only in stage 1 NREM sleep

Relationship Between Sleep States and Appearance/ Disappearance of PLMs:
PLMs were always fi rst noted during NREM sleep stages 1 or 2, and rapid eye movement (REM) sleep was never noted during the time spent between sleep onset and the appearance of PLMs, but PLMs were noted during short-lived REM sleep bouts in 59% of cases; long, uninterrupted REM sleep periods were seen only after the disappearance of the PLM because the presence of PLMs was associated with a disruption of REM sleep.

Return to Lower Nasal PAP During the PAP Titration:
Per protocol, PAP drops were performed during an awakening of the patient (bathroom call 78% of the time); 61 of 81 subjects had reached an absence of PLMs at the time of this awakening. Return to lower pressure always led to a reappearance of abnormal breathing and to PLMs. In these 61 subjects, a mean of 58 min was spent increasing the CPAP back to the same level as before the awakening and bathroom trip, and the CPAP that eliminated fl ow limitation and PLMs was found to be the same as the one noted before the pressure decrease. The evaluation showed that at two different times during the night the same CPAP had to be reached to observe a disappearance of PLMs and an absence of fl ow limitation. In summary, titration of CPAP based on elimination of AASM-defined hypopneas4 was not sufficient to eliminate most of the PLMs observed during the PAP titration, and more pressure was needed to eliminate PLMs, fl ow limitation, and EEG disturbances related to abnormal breathing as demonstrated by the persistence of CAP phases A2 and A3. 14,15,17,19 

Recording of Expiratory Abdominal Muscles and Occurrence of PLMs
Respiratory muscles were systematically monitored in all patients. The redundancy of expiratory muscle EMG recordings (right-left and several muscles) allowed continuous investigation of expiratory abdominal muscles; a concomitant increase in abdominal EMG discharge and PLMs was monitored ( Figs 2, 3 ). These abdominal and leg EMG discharges were no longer seen once the nasal CPAP had reached a threshold at which fl ow limitation was not observed. Analysis of both leg and abdominal muscle EMGs showed that both EMG discharges began at the same time; there was a complete temporal concordance at the beginning of the EMG burst. Investigation of the C3/M2 and C4/M1 EEG recordings performed for each EMG burst at an analysis speed of 10 s indicated that there was no preceding arousal pattern before the occurrence of the abdominal-leg EMG burst. Abdominal and leg muscle bursts disappeared at the same time. 

Discussion

PLMs have been noted in patients with different types of SDB, including Cheyne-Stokes breathing. 10,11,20-24 In 1989, Fry et al 10 were the fi rst to show that PLMs could be noted not only during baseline diagnostic recording but also during nasal CPAP titration, emphasizing that the PLM count was higher in the nasal CPAP titration night than during the baseline night and that the PLM count had increased between the initial nasal CPAP titration and the follow-up performed months later, with the persistence of abnormal sleep; this fi nding was confi rmed by others. 23,24 Our study shows that PLMs do not disappear with the elimination of AASM-defi ned hypopnea, but with the elimination of fl ow limitation and the associated instability of NREM sleep. Why do PLMs appear and disappear with nasal CPAP titration? We can only offer suggestions because all necessary data are not available. One may argue that PLM induces “hypopnea” (ie, PLM would increase inspirations secondary leading to a compensatory physiologic pause related to the “hyperbreath” associated with some degree of CO 2 depletion). Clearly, the “hypopnea” induced by such “hyperventilation” may not lead to a drop of oxygen saturation of 4%, and the number of breaths needed to come back to normal breathing may require less than 10 s, particularly if the upper airway is better “opened” by CPAP. PLMs may then be seen without AASM-defi ned hypopnea, with a partially improved air exchange, but the absence of complete resolution of the upper airway narrowing will still lead to EEG disturbances and there will be a discrepancy between the scoring of AASM-defi ned hypopneas and the scoring of more subtle disturbances. There would not be the need to call upon expiratory muscle involvement to explain the fi nding of persistence of abnormal sleep and PLMs after treatment of AASMdefi ned apneas and hypopneas. But no “missed breath” is seen when fl ow limitation is noted and PLM occur, and there is still activation of different muscles, including leg muscles, that reoccurs periodically during the persistence of abnormal breathing. We found that the periodic EMG discharges monitored in the legs are also simultaneously seen in the abdominal muscles, and both EMG bursts disappear with optimal PAP pressure with the absence of fl ow limitation. We believe that this fi nding is relevant to our observation. An increase in both negative esophageal pressure and positive gastric pressure recorded measurements has been noted with CPAP above 8 to 10 cm H 2 O (Jed E. Black, MD, personal communication, January 2011 ); similarly, Lofaso et al, 25 monitoring esophageal pressure and gastric pressure with airfl ow during nasal CPAP titration, and investigating the presence of expiratory abdominal muscle activity, showed that there is a “paradoxical rise” in gastric pressure with a progressive increase in nasal CPAP, with a decrease in abdominal diameter. This abnormal rise in gastric pressure disappeared only when optimum PAP was reached. 25 Also in subjects with untreated OSA, the Wisconsin group has well documented the presence of an expiratory component during hypopnea and apneas, indicating the presence of an expiratory involvement during upper airway obstruction during sleep. 26,27 Such an observation was well confi rmed by Stănescu et al, 28 and both groups showed that such an expiratory component also existed in “heavy snorers,” as had already been suggested by the work of Sanders and Moore. 29 The well-accepted concept of inspiratory upper-airway muscle tone decrease seen in OSA patients can be applied similarly to the pharyngeal constrictor muscles, and this decrease “destabilizes the airway.” One may, thus, suggest the presence of an expiratory muscle component during nasal CPAP titration and, as suggested by Lofaso et al 25 data, this expiratory component disappears only when “optimum CPAP pressure” is reached. Why is such a component not noted more often? Perhaps because nasal CPAP titration is not commonly performed with esophageal pressure and gastric pressure, and even expiratory muscle recordings are not performed systematically; in addition, the patient group was nonobese, a fact that helped in the surface EMG monitoring and visualization of EMG surface signals. Why are PLMs not seen in every OSA patient? First, if a relationship exists between the presence of PLMs and expiratory muscle discharges (as suggested by the temporal relationship of both recorded discharges), there must be a suffi cient expiratory airfl ow limitation to induce active contraction of the expiratory muscles. As mentioned previously, Skatrud and Dempsey, 26 Henke et al, 27 and Stănescu et al 28 demonstrated this involvement in untreated OSA and heavy snorer subjects whom they studied. The importance of this involvement, which is variable, may be related to the degree of expiratory limitation. Some of these subjects had PLMs from the very start of the recording (ie, before any effective treatment) and may have been similar to the OSA subjects reported previously. But some others did not, and the PLMs appeared only after the onset of CPAP treatment. Again, as previously documented, CPAP per se may induce “paradoxical rise in gastric pressure associated with changes in the diaphragmatic diameter” 25 with increasing CPAP. Could the abdominal EMG bursts simply represent a more generalized motor system response with a more generalized EMG response, similar to the arm muscle activity that has been shown to accompany PLMs? Because we did not monitor arm EMGs, we cannot eliminate this possibility, but one may also raise the reverse possibility (ie, that activation of arms with PLMs may be related to the more important activation of the motor system because of the need for greater abdominal response). Further recordings will be needed, and direct intramuscle recording, with simultaneous gastric pressure measurement as used by Henke et al, 27 may be needed

Here's the whole thing: https://sci-hub.tw/10.1378/chest.11-1563

[Sleeprider]

You guys are doing a great job with this thread. Damiansd, you are a wiki editor. Any intereste in putting some of this into a wiki so you can refer to it in the future?

[Damiansd]

The interesting thing with the Gabapentin is that it seems to last for six hours. If I take it too early then I wake early in the morning 3am). When I spoke with my sleep doctor he agreed and suggested taking it as I turn the light off. That has helped.

[sheepless]

"The disappearance of “flow limitation” required higher pressure and was associated with the disappearance of PLMs."

no idea if apples to apples but in my experience the resmed apap will push pressure to the set max and asv will push pressure to the set max ipap and still not resolve my plm induced (or at least plm associated) flow limitations between movements, resulting in runaway pressure, leaks and aerophagia with apap and the same plus disturbing pressure swings with asv.

now that I think about it, while I've had max pressure support as high as it goes at times, I'm not sure I ever set min pressure support above about 5.4 cmw; maybe that would better address flow limitations.

it's not clear from the quoted sections just what the CAP system is, as opposed to AASM.

I can't say on first quick read I get it all but I notice the emphasis on expiratory flow limitations:

"...if a relationship exists between the presence of PLMs and expiratory muscle discharges (as suggested by the temporal relationship of both recorded discharges), there must be a suffi cient expiratory airfl ow limitation to induce active contraction of the expiratory muscles. As mentioned previously, Skatrud and Dempsey, 26 Henke et al, 27 and Stănescu et al 28 demonstrated this involvement in untreated OSA and heavy snorer subjects whom they studied."

as far as I know, we use pressure and pressure support for inspiratory flow limitations. my vague recollection of the occasional references to expiratory flow limitations on this site led me to think there is little pap can do for these. in contrast, if I'm reading it right, the quoted sections seem to suggest higher pressure - higher than necessary for flow limitations (I didn't see 'inspiratory flow limitations' above, just 'flow limitations') - will resolve these expiratory flow limitations and plm too?

I've always interpreted abbreviated below-the-zero-line flow rate as mouth leaks. dark squiggles below zero suggest expiratory snoring. what else would one look for to identify expiratory flow limitations?

I wonder if/how this relates to palatal prolapse, which must be a kind of expiratory flow limitation.

interesting info. gives me hope there's a pap solution in there somewhere.

[sheepless]

"You guys are doing a great job with this thread. Damiansd, you are a wiki editor. Any intereste in putting some of this into a wiki so you can refer to it in the future?" - Sleeprider

great idea. they say the reward for good work is more work, Damian!

[Illorum]

Hi sheepless, I wrote an explanation of CAP here: http://www.apneaboard.com/forums/Thread-...#pid358528

In regards to expiratory flow limitation, my understanding is that it can be hard to detect with traditional means (PAP devices and and nasal cannulas) and the ideal for it is esophageal manometry since you can quantify the effort being put into every exhale. I also remember the discussions relating to palatal prolapse. I believe someone here or on a DME-owned forum put up this website: https://sites.google.com/view/palatal-prolapse and they noted bilevel devices and EPR were worse for their prolapse since the decreased exhale pressure led to less splinting of the airway.

It makes sense, but I personally couldn't tolerate single pressure CPAP very well and that's why I switched to BiPAP... it's a bit of a catch-22.

Also keep in mind the study didn't measure subjective sleep quality outcomes after the increased pressure, we don't know if the higher pressure gave them terrible bloating, etc. It could be that the elimination of PLMS led to the introduction of other consequences when PAP pressure is on the higher side.