The present study was conducted on 30 non-obese type 2 diabetic patients attending the neurology and internal medicine diabetes clinics, Tanta University Hospitals, in the period between 1st of April and 1st of December 2015. Patients were divided into two groups; group I included 20 clinically evident sensori-motor DPN patients with or without autonomic manifestations and group II included 10 diabetic neuropathies free (DNF) patients. The study also included 10 healthy control subjects (group III) matching the patients’ age, sex, and body mass index (BMI).
Exclusion criteria invloved patients with respiratory or cardiac problems, chronic pain, and advanced metabolic, neuropsychiatric or endocrinal disorders affecting sleep and patients with BMI > 28 and history of medications intake affecting sleep and who are heavy smokers or drug abusers.
The protocol of the study was approved by The Research Ethics Committee and Quality Assurance Unit, Faculty of Medicine, Tanta University. Participation was voluntary, all participants received detailed information concerning the aims of the study and the possible risks, and an informed consent was obtained from all prior to the commencement in the study.
Diabetes mellitus was diagnosed according to American Diabetes Association 2015 (Polonsky and Burant 2016). Patients and controls were submitted to history taking, neurological examination, and routine laboratory investigations. Clinical diagnosis of DPN and grading of its severity was done using the neuropathy symptom score (NSS) and neuropathy disability score (NDS). A total NSS of 3–4 considered mild, 5–6 moderate, and 7–9 severe symptoms. A total NDS of 3–5 considered mild, 6–8 moderate, and 9–10 severe disability. Neuropathy was diagnosed in patients with moderate disability with or without symptoms, or mild disability with moderate symptoms. Mild disability and/or mild symptoms were not considered adequate to diagnose clinical evident DPN (Kisozi et al. 2017; Cabezas-Cerrato 1998). Dysautonomia was clinically assessed by measuring systolic blood pressure response to standing and heart rate response to each of standing, Valsalva, and deep breath.
All subjects were submitted to one-night polysomnogram (PSG) followed in the next day by multiple sleep latency test (MSLT) which is an objective assessment of EDS (Littner et al. 2005). PSG was performed by a Somon Medics Gmbh (Am SonnenstuhL63, D-97236 Rander Sacker, Germany, Type: SOMNO screen™plus, SN: 4259, kw45: 2014). Each PSG included EEG channels montages (O1/A2, C3/A2, C4/A1 and O2/A1), electrooculography (LOC-A1/A2 and ROC-A1/A2), surface tibial and submental EMG, and modified V2 lead ECG. For respiratory sensors, nasal and oral signals by thermal airflow sensors (thermistor) were used, tracheal sounds microphone was applied, and the chest and abdominal effort was measured by dual thoracoabdominal RIP (respiratory inductance plethysmography) belts.
The studied parameters were scored according to The American Academy of Sleep Medicine Scoring Manual, 2012 (Grigg-Damberger 2012). Sleep latency (SL) refers to the length of time taken in transition from wakefulness to sleep, wake after sleep onset (WASO) is the minutes of wake after sleep onset but before the final awakening, sleep efficiency (SE) is the total sleep time (TST) divided by the total in bedtime, sleep fragmentation (SF) is the number of sleep cycles/night, and sleep stage transition index (SSTI) is the number of transition between various sleep stages/hour. The pulse transit time (PTT) is the time taken for the arterial pulse wave to travel from the aortic valve to a peripheral site which reflects the intrathoracic pressure. An arousal refers to abrupt shift of EEG activities which last for ≥ 3 s and are preceded by ≥ 10 s of sleep. An apnea was defined as ≥ 90% drop in the thermistor excursion signal of ≥ 10 s and hypopnea which was defined as a decrease in thermistor signal by > 30% for > 10 s accompanied by a decrease of oxyhemoglobin saturation ≥ 4%. The patient was considered to have sleep apnea syndrome (SAS) if the apnea hypopnea index (AHI) is ≥ 15 or if the AHI ≥ 5 associated with insomnia, cardiovascular comorbidities, or diurnal symptoms mainly EDS, impaired cognition, or mood changes (Sateia 2014).
Statistical analysis was conducted using SPSS version 19 (Statistical Package for Social Studies) created by IBM, Chicago, IL, USA. For numerical values, the range and mean ± standard deviations were calculated. For categorical variable, the number and percentage were calculated and differences between subcategories were tested using the z-score test, ANOVA, Tukey’s tests, and post-hoc tests. Correlation analysis was performed using Pearson’s correlation test. p value < 0.05 was considered statistically significant.