Sleep Breath 2002; 06(3): 151
DOI: 10.1055/s-2002-34316
LETTER TO THE EDITOR

Copyright © 2002 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA. Tel.: +1(212) 584-4662

On "Misinterpretation of Sleep-Breathing Disorder by Periodic Limb Movement Disorder" (Sleep Breath 2001;5:131-138)

Arn H. Eliasson, Teotimo Andrada, Yvonne  Taylor
  • Sleep Disorders Center, Walter Reed Army Medical Center, Washington, DC
Further Information

Publication History

Publication Date:
02 June 2004 (online)

In the case report by Dr. Stoohs and colleagues,[1] the authors make the main point that recording and scoring of leg movements must be an integral part of polysomnogram evaluations. They reason that arousals and sleep fragmentation may be improperly assigned to respiratory events and periodic limb movement (PLM) would be missed all together. However, in Figure [2], their representative example appears to be in error. The authors denote central hypopnea following PLM associated with electroencephalogram (EEG) arousal, but there is no decrease in respiratory effort during the periods of hypopnea. The portions of two events recorded in Figure [2] are most appropriately interpreted as obstructive hypopneas followed by PLM and arousals. This is a pattern of sleep-disordered breathing commonly seen in our sleep center. We also see PLM caused by the sleep-disordered breathing termed upper airway resistance syndrome (UARS).[2] We have discovered patients previously diagnosed with periodic limb movement disorder (PLMD), and ineffectively treated with medication for PLMD, who in fact have UARS verified by esophageal catheter manometry during overnight polysomnogram. Arousals, PLM, and sleep fragmentation have been clearly associated with UARS events.[3] As shown in Figure [2] of Dr. Stoohs et al, some hypopneas do not produce desaturations as is also the case with respiratory events in UARS.[4] Either Figure [2] is confirmatory of sleep-disordered breathing in Mr. M. W. or this recording was not a representative choice for demonstrating primary PLMD.

A second issue in the case report involves the extensive neurological evaluation afforded this patient, including physical examination, daytime EEG, computed tomographic scan of the head, and nerve conduction studies. It is unclear why these studies followed an unrevealing neurologic exam in a man whose chief complaints were snoring, witnessed apneas, and intolerance to CPAP.

We agree with the decision to discontinue both drug treatment and nasal CPAP. Dr. Stoohs and associates summarize their rationale very effectively by noting the patient's lack of cardiovascular risk factors and normal subjective alertness. Is it possible that Mr. M. W. does have mild sleep-disordered breathing and UARS events that cause his PLM?

Figure 2 Flow limitation is alleviated by EEG (electroencephalographic) central activation as commonly seen in UARS (upper airway resistance syndrome).

REFERENCES

  • 1 Stoohs R A, Blum H, Suh B Y, Guilleminault C. Misinterpretation of Sleep-Breathing Disorder by Periodic Limb Movement Disorder.  Sleep Breath . 2001;  5 131-138
  • 2 Guilleminault C, Stoohs R, Clerk A, Cetel M, Maistros P. A cause of excessive daytime sleepiness. The upper airway resistance syndrome.  Chest . 1993;  104 781-787
  • 3 Exar E N, Collop N A. The association of upper airway resistance with periodic limb movements.  Sleep . 2001;  24 188-192
  • 4 Netzer N C, Eliasson A H, Netzer C M, Kristo D A. Overnight pulse oximetry for sleep-disordered breathing in adults-a review.  Chest . 2001;  120 625-633