Teotimo Andrada

Successful treatment of upper airway resistance syndrome with an oral appliance.

This case report is the first description of the treatment response to an oral appliance (OA) in a patient with upper airway resistance syndrome (UARS). OAs are devices inserted into the mouth in order to modify the position of the mandible and tongue, thus relieving pharyngeal obstruction during sleep in obstructive sleep apnea (OSA) patients. Findings from this case report suggest that an OA may be a useful treatment option for UARS patients.

Persistence of Apnea in Wakefulness in a Patient with Postradiation Pharyngitis

We report on a patient with the onset of recurrent nocturnal awakenings associated with postawakening stridor with onset a few weeks after receiving radiation therapy to the neck. The onset of nocturnal stridor was also accompanied by complaints of snoring and excessive daytime sleepiness. Stridor did not occur during daytime wakefulness. Nocturnal polysomnography (NPSG) recorded with a calibrated pneumotachometer demonstrated snoring and severe obstructive sleep apnea (OSA) with a apnea/hypopnea index of 51 events/hr. One apneic episode persisted for 17 sec after the onset of wakefulness as evidenced by standard NPSG scoring criteria for arousals. With this event, video monitoring revealed the patient abruptly sitting upright and clutching his throat and auditory recording demonstrated stridorous sounds. During wakefulness endoscopy revealed moderate edema and erythema of the supraglottic region, epiglottis, palatine tonsils, and false and true vocal cords. Vocal cord function appeared normal. This case report represents the observation of two rare findings in a single patient, persistence of apnea in wakefulness, and OSA onset following neck irradiation. We review the literature on the persistence of apnea in wakefulness and discuss possible mechanisms for its occurrence in this patient.

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

151 Sleep and Breathing, volume 6, number 3, 2002. Address for correspondence and reprint requests: Arn H. Eliasson, M.D., Sleep Disorders Center, Walter Reed Army Medical Center, Washington, DC 20307. 1Sleep Disorders Center, Walter Reed Army Medical Center, Washington, DC. Published by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA. Tel: +1(212) 584-4662. 1520-9512,p;2002,06,03,151,151,ftx,en;sbr00214x. 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 sleepdisordered 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?