Carpal Tunnel Syndrome in Obstructive Sleep Apnea Patients.
Carpal tunnel syndrome (CTS) is the most common compressive neuropathy of the upper extremity with an estimated prevalence of 3%-6% of the general population (1,2,3). CTS is a clinical syndrome most often related to mechanical distortion produced by a compressive force on the median nerve in the carpal tunnel segment (4). Multiple factors including genetic predisposition, injury and workplace biomechanical factors have been blamed for etiology (5,6,7,8). Furthermore, there are consistent and strong associations between CTS and age, gender body mass index (BMI), diabetes mellitus (DM), pregnancy and wrist morphology (2,9,10,11,12). Clinical findings of CTS are pain and dysesthesia in the median nerve distribution, in the region of the thumb, index, middle and the lateral half of the ring finger which may worsen during sleep (13).
Obstructive sleep apnea (OSA) is characterized by recurrent partial and complete airway obstruction episodes during sleep resulting in repetitive apneas and hypopneas (14) with an estimated prevalence of 3%-10% in the adult population (15,16,17). CTS is known to affect almost all systems in the body including the neurological system. Despite a limited number of studies determining axonal damage and peripheral neuropathy in sleep apnea patients (18,19) and those describing sleep disturbances in CTS patients (20,21), no studies have analyzed CTS in OSA. To the best of our knowledge, this is the first study assessing CTS in OSA patients.
In this study we investigated the frequency of CTS in OSA. Because of its relation with waning productivity that causes work disability and high-cost treatments, CTS is an important issue particularly in the workplace (22,23,24). The study also aimed to explore the link between the two syndromes depending on polysomnographic and electrophysiologic data, supported by the use of Boston CTS questionnaire (BCQ), so that early diagnosis, preventive, and/or therapeutic approaches may be possible for OSA patients.
A retrospective review of the polysomnography records of 476 individuals who were admitted to our sleep laboratory between March 2015 and December 2015 was performed. Medical records of 423 subjects (88.9%) who were diagnosed with OSA were reviewed. The severity of OSA was decided by the apnea/hypopnea index (AHI) and total number of respiratory events per hour of sleep, which is supposed to be [greater than or equal to]5 for diagnosis (25). Patients who had HbA1C >6.5%, did regular alcohol consumption, or had a prior diagnoses of DM, hypothyroidism, rheumatic diseases, cervical radiculopathy were excluded. Eighty OSA patients between the age of 28-75 years, meeting the inclusion criteria were included in the study and underwent nerve conduction studies (NCSs). No information about the participants was gathered before NCSs. To provide observer blindness, those who were diagnosed with CTS were then questioned about symptom presence and symptom sides (right, left, or bilateral) and sleeping position (none, right, left, supine) and given the BCQ to investigate the clinical compatibility of electrophysiological findings. The results of the questionnaires have been calculated as the mean values.
Eighty healthy individuals perfectly matching the age, sex, and BMI of OSA patients, without comorbidities like DM, hypothyroidism, cervical radiculopathy, rheumatic diseases and whose HbA1Cs were <6.5% and did not regularly consume alcohol were included in the study as control subjects.
BMI of the patients and the controls was calculated as the weight (kg) divided by the height squared ([m.sup.2]).
All experiments were performed in compliance with the relevant institutional guidelines. The study was approved by the Local Ethics Committee of our Institution and was conducted in accordance with the ethical principles stated in the Declaration of Helsinki. A written informed consent form was obtained from each participant included in the study.
All patients were monitored with a nocturnal PSG that was performed with multichannel monitoring that included neurophysiological electrodes (electroencephalography electrodes), chest wall motion, abdominal motion, arterial oxygen saturation, and electrocardiography electrodes (Grass-Telefactor Cephalo, An Astro-med Inc. Product Group, 2005, USA). Oronasal airflow was measured using a thermistor The oxyhemoglobin saturation was monitored with a finger pulse oximeter with a sampling rate of 1 Hz. The body position was measured by a position sensor attached to the anterior chest wall. Signals recorded in the sleep period were manually analyzed (25). Apneas were scored when the airflow decreased by at least 90% from baseline for at least 10 s and were classified as central, mixed, or obstructive depending on the occurrence of thoracoabdominal movements (25). Hypopneas were scored when airflow decreased by at least 30% for [greater than or equal to]10 s and was associated with an oxygen saturation (Sa[O.sub.2]) fall of [greater than or equal to]3%. AHI was calculated as the average number of apneas and hypopneas per hour of recording in the sleep period. An AHI of [greater than or equal to]5 was used to diagnose OSA (26). Sa[O.sub.2] during the sleep period was automatically analyzed, and after the manual elimination of possible artifacts, mean Sa[O.sub.2] and lowest nocturnal Sa[O.sub.2] values were detected. According to their overall AHIs OSA patients were grouped as mild (5-14.9/h) and moderate to severe (>15/h) (25).
Nerve conduction studies
Eighty patients and eighty healthy control subjects underwent NCSs. Two investigators who were blinded to the patient and control groups assessed all of the electrophysiological studies. All median motor and sensory NCSs were performed using a Medelec Synergy electromyography device (Medelec Synergy EMG, Oxford Instruments Medical, Old Working, UK) and surface bar recording and bipolar surface recording electrodes (Teca Corp.). Median sensory NCSs were performed using the antidromic technique; the recording electrode was placed over the palmar surface of the second digit and the nerve was stimulated from the wrist at 13 cm. The normative value in our laboratory for median motor latency is <4.5 milliseconds and median sensory distal peak latency is <3.5 milliseconds. For motor NCSs, the median motor nerve was stimulated at the wrist 6.5 cm proximal to the active recording electrode. Diagnostic criteria for CTS were accepted as the nerve conduction velocity of the sensory and/or motor median nerves to be <50 m/s.
Filter settings were 5 Hz to 10 kHz for motor NCSs and 20 Hz to 2 kHz for sensory NCSs. During testing procedures the room temperature was maintained at an average of 25[degrees]C, and the skin temperature was maintained above 33[degrees]C in all participants.
Data were analyzed using the Statistical Package for the Social Sciences statistical software version 18.0 (IBM SPSS Statistics, New York, USA). Categorical variables were expressed using percentages. Shapiro--Wilk normality test was used to test the distribution of numerical variables. Categorical variables were compared using the chi-square test. For continuous variables, parametric Student's t-test and non-parametric Mann--Whitney U test were used. Analysis of descriptive variables was presented as mean [+ or -] SD, whereas the analysis of categorical variables was presented as percentile. Statistical significance was set at a p value of <0.05.
Eighty OSA patients and eighty healthy controls were included in the study There were no significant differences between the study groups with respect to age, sex distribution, or BMI. Demographic features of the study participants are presented in Table 1.
CTS was detected in 27.5% (n:22) of the OSA patients. CTS and non-CTS patients revealed no significant difference in sleep statistics (Table 2).
There were no significant differences between the mean AHIs of CTS and non-CTS patients (p=0.730, 27.54/h vs. 29.18/h, consecutively). Comparison of CTS patients with mild vs. moderate to severe OSA revealed no significance difference (p=0.86). Categorization of OSA severity and its relation with CTS presence have been summarized in Table 3. No relation between the side of CTS and the preferred sleeping position was found (p=0.727).
Ten patients (45.5%) with CTS had CTS symptoms, whereas 12 patients (54.5%) were asymptomatic. The mean Boston scaling value of CTS patients was 1.59. However, the scale showed no correlation between the severities of OSA and CTS (p=0. 104).
Occupations of the CTS patients were questioned. Ten patients (45.5%) were manually working, whereas twelve (54.5%) were not manually working.
This study showed that CTS was highly frequent in OSA patients than in the general population. However the presence of CTS in OSA was independent of OSA severity and formerly described factors such as sleeping position and manual working.
Demographic and polysomnographic characteristics of the study group were consistent with the literature (27,28,29,30).
Despite the lack of polysomnographic data, previous studies have reported sleeping problems, mainly insomnia and night-wakings in CTS patients (20,31). Our patients did not complain about insomnia or night-wakings due to CTS symptoms but this may be because of OSA comorbidity of our sample, which already causes repeated awakenings during sleep.
Our aim in this study was to assess the prevalence of CTS in OSA. We found that 27.5% of the OSA patients had CTS. This highly significant finding compared with normal population developed a question regarding the causative relation between the two syndromes. Although CTS is the most common entrapment neuropathy, currently there is no unifying theory that links the multiple known associations of CTS into a common mechanism.
With the increasing interest in sleep and sleep disorders, the possible role of sleeping position in development of CTS has been discussed with supporting results (32,33). McCabe et al. (34) described the association between sleeping on the side and CTS in their prospective study. However the study was based on clinical findings and questionnaires without any electrophysiological data. We wanted to improve this study by adding objective diagnostic tools like PSG and NCS. We gained totally controversial results with McCabe et al. Majority of the patients (54.5%) were asymptomatic and symptom sides of the symptomatic ones had no relation with the CTS side (p=0.43). Similarly, preferred sleeping position had no relation with the CTS side (p=0.73). For this reason, we hypothesized that hypoxia, which is an established cause of peripheral neuropathy (35,36), was the reason for CTS tendency in OSA. Although patients with OSA are already known to have predisposition for several known risk factors for polyneuropathy (37), only a limited number of studies paid attention to the link between OSA and peripheral neuropathy. Smaller amplitudes for sensory and mixed nerve action potentials in patients with OSA have already been described (36). Subsequently, recurrent intermittent hypoxemia in OSA was described as an independent risk factor for axonal damage of the peripheral nerves, which supports our hypothesis (18).
Biomechanical factors had no effect on our CTS patients with OSA. Thus, other explanations for binding the two co-morbidities may be considered. We would propose the inflammation theory OSA is already known to be associated with pro-inflammatory mediators (38,39). The inflammatory cytokine tumor necrosis factor-alpha, which increase ICAM-1 and VCAM-1 synthesis, platelet aggregation and activation that is measured by P-selectin activation, neutrophils' superoxide production, is all known to increase in OSA (40,41,42). CTS can result from any cause that induces compression or irritation of the median nerve, including synovitis, thickening of the tendon or flexor retinaculum, fluid accumulation, or subsynovial connective tissue alterations (43). Hence, primary or secondary inflammation may be expected to cause CTS. Regarding the lack of published evidence supporting this hypothesis, it is necessary to conduct further studies to determine if OSA and CTS share the same of type of inflammatory pathways.
In conclusion, CTS is highly frequent in OSA patients. It is known that CTS amounts to a heavy burden on the national health service to provide care for CTS patients in the form of clinicians' time, diagnosis and treatment. We consider that in OSA patients, intermittent hypoxia is the major reason which facilitates axonal damage in the carpal tunnel. CTS starts earlier than its symptoms in OSA. In other words, OSA patients may have CTS even without any symptoms. Thus, NCSs may be suggested to all OSA patients right after the diagnosis of OSA. Furthermore, we propose that the effective treatment of OSA with positive airway pressure will result in the decrease of the frequency of CTS depending on our hypoxia theory
Ethics Committee Approval: Ethics committee approval was received for this study from the ethics committee of Sureyyapasa Chest Diseases and Chest Surgery Training and Research Hospital.
Informed Consent: Written informed consent was obtained from patients who participated in this study.
Peer-review: Externally peer-reviewed.
Conflict of Interest: No conflict of interest was declared by the authors.
Financial Disclosure: The authors declared that this study has received no financial support.
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Ozgur BILGIN TOPCUOGLU (1,2), Ozlem ORUC (3), Sema SARAC (3), Gulgun CETINTAS AFSAR (3), Kayihan ULUC (2)
(1) Clinic of Neurology, Sureyyapasa Chest Diseases and Thorax Surgery Training and Research Hospital, Istanbul, Turkey
(2) Department of Neurology, Marmara University School of Medicine, Istanbul, Turkey
(3) Clinic of Chest Diseases, Sureyyapasa Chest Diseases and Thorax Surgery Training and Research Hospital, Istanbul, Turkey
Correspondence Address: Ozgur Bilgin Topcuoglu, Sureyyapasa Gogus Hastaliklari ve Cerrahisi Egitim ve Arastirma Hastanesi, Basibuyuk Mahallesi, 34844, Maltepe, Istanbul, Turkiye E-mail: firstname.lastname@example.org
Author Contributions: Concept - O.B.T., K.U.; Design - O.B.T., K.U.; Supervision - K.U.; Resource - O.B.T., G.C.A., S.S.; Materials - O.B.T., G.C.A., S.S., O.O.; Data Collection and/or Processing - O.B.T., G.C.A., O.O.; Analysis and/or Interpretation - O.B.T., S.S., O.O.; Literature Search - O.B.T., G.C.A., S.S., O.O.; Writing - O.B.T., K.U.; Critical Reviews - O.B.T., K.U.
Cite this article as: Bilgin Topcuoglu O, Oruc O, Sarac S, Cetintas Afsar G, Uluc K. Carpal Tunnel Syndrome in Obstructive Sleep Apnea Patients. Arch Neuropsychiatry 2017; 54:307-311.
Received: 23.02.2016 Accepted: 07.04.2016 Available Online Date: 15.04.2016
Table 1. Demographic features of all study participants OSA patients Healthy (n:80) controls (n:80) p Age (years) 49.35 (28-74) 47.63 (35-70) 0.147 9 f (11.25%), 7 f (8.75%), Gender (f/m) 71 m (88.75%) (*) 73 m (91.25%) (*) 0.92 Mean BMI (kg/[m.sup.2]) 30.27 (21.3-40) 29.13 (23-41.4) 0.328 (*) f: female; m: male; BMI: body mass index Table 2. Polysomnographic findings of CTS patients vs. non-CTS patients CTS patients (n:22) Epworth Sleepiness Scale 7.72 ([+ or -]5.04) Sleep latency (min) 10.78 ([+ or -]10.59) Sleep efficiency (%) 82.07 ([+ or -]19.40) NREM1 stage sleep (%) 5.35 ([+ or -]4.64) NREM2 stage sleep (%) 55.29 ([+ or -]15.05) NREM3 stage sleep (%) 17.90 ([+ or -]13.09) REM stage sleep (%) 13.90 ([+ or -]5.04) AHI (/h) 27.54 ([+ or -]22.46) Mean oxygen saturation% 93.18 ([+ or -]2.32) Minimum oxygen saturation% 77.90 ([+ or -]11.36) Non- CTS patients (n:58) p Epworth Sleepiness Scale 9.06 ([+ or -]5.60) 0.305 (**) Sleep latency (min) 14.79 ([+ or -]21.99) 0.457 (**) Sleep efficiency (%) 86.67 ([+ or -]8.09) 0.694 (**) NREM1 stage sleep (%) 5.76 ([+ or -]5.87) 0.966 (**) NREM2 stage sleep (%) 57.15 ([+ or -]12.02) 0.567 (*) NREM3 stage sleep (%) 20.42 ([+ or -]10.27) 0.369 (*) REM stage sleep (%) 13.48 ([+ or -]6.85) 0.769 (*) AHI (/h) 29.18 ([+ or -]19.56) 0.730 (**) Mean oxygen saturation% 93.00 ([+ or -]2.80) 0.926 (**) Minimum oxygen saturation% 76.19 ([+ or -]12.99) 0.726 (**) (*) independent samples t test, (**) Mann--Whitney U. NREM: non rapid eye movement; REM: rapid eye movement; AHI: apne hypopnea index Table 3. Classification of OSA severity in CTS patients vs. non-CTS patients CTS patients Non-CTS (n:22) patients (n:58) p Mild (AHI 5-14.9/h) 27.3% (n:6) 29.3% (n:17) 0.857 Moderate to severe (AHI >15/hour) 72.7% (n:16) 70.7% (n:41) CTS: carpal tunnel syndrome; AHI: apne hypopnea index
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|Author:||Topcuoglu, Ozgur Bilgin; Oruc, Ozlem; Sarac, Sema; Afsar, Gulgun Cetintas; Uluc, Kayihan|
|Publication:||Archives of Neuropsychiatry|
|Article Type:||Clinical report|
|Date:||Dec 1, 2017|
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