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April2013 Vol.50 Issue:      2 Table of Contents
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Sleep Apnea in Patients with Diabetic Neuropathy

Yossri Ashour1, Ahmed Abou-Hagar1, Nihal  El-Shazly2, Waleed  Al-Deeb1,

Reda Ahmed1, Saly El-Kholy2, Ahmed Osama1

Departments of Neuropsychiatry1, Suez Canal University; Clinical Neurophysiology2, Cairo University; Egypt

 



ABSTRACT

Background: Diabetes mellitus (DM) is a major chronic disease with high morbidity, mortality and economic burden. Sleep apnea is an increasingly recognized medical problem with its important role in metabolic, vascular and behavioral aspects. Association between sleep apnea and DM is likely to be complex. Objective: To detect prevalence, type and severity of sleep apnea in diabetic patients, and to detect any relation between sleep apnea and diabetic state, diabetic peripheral and autonomic neuropathy and phrenic nerve affection. Methods: Forty four diabetic patients were included in the study. Another 44 age and sex matched healthy subjects representing the control group were included. All the subjects were evaluated for diabetic state, peripheral neuropathy, autonomic neuropathy, phrenic nerve affection and sleep disorders. Results: High scores of the Epworth Sleepiness scale (≥10) and sleep apnea were significantly more frequent in diabetic patients (63.6% and 84.1% respectively). Obstructive sleep apnea was the most frequent type (65.9%) followed by mixed type (13.7%) and lastly central sleep apnea (4.5%). All the grades of sleep apneas (mild, moderate and sever) were highly significantly more frequent in diabetics than in non diabetics (P<0.01). There was significant relation between sleep apnea and age of the patient, male sex, uncontrolled DM, duration of DM, diabetic autonomic neuropathy and phrenic nerve affection. There was no relation detected between sleep apnea and diabetic peripheral neuropathy. Conclusion:  Sleep apneas as well as changes in sleep architecture were more frequent in diabetic patients with autonomic neuropathy and phrenic nerve affection. [Egypt J Neurol Psychiat Neurosurg.  2013; 50(2): 187-193]

 Key Words: Sleep apnea, diabetes mellitus, neuropathy, phrenic nerve, polysomnography.

Correspondence  to  Yossri  Ashour, Neurology Unit, Suez Canal University, Ismailia, Egypt.Tel.: +201143541776      e-mail: yossri_a@hotmail.com





INTRODUCTION

 

Sleep apnea is an increasingly recognized medical problem. The attention to its frequency in the general population and its important role in metabolic, vascular and behavioral aspects have sharply increased the number and nature of investigations.1 Sleep apnea has been linked to several medical disorders including: hypertension, heart failure, angina, myocardial infarction and stroke.2

Diabetes Mellitus (DM) is a major chronic disease with high morbidity, mortality and economic burden.3 It is one of the most common diseases that affect the peripheral and autonomic nervous system. Previous studies proved that diabetic individuals had more sleep apnea than non-diabetics.4  DM may be a cause or a consequence of sleep apnea, or possibly both.5 The association between sleep apnea and DM is likely to be complex. This association needs more investigations.

Therefore, this study was done to detect the prevalence, type and severity of sleep apnea in diabetic patients, and to clarify the relation between sleep apnea and diabetic state, diabetic peripheral and autonomic neuropathy and phrenic nerve affection.

 

PATIENTS AND METHODS

 

Forty four diabetic patients were included in the study (6 with type 1 and 38 with type 2 DM). They were recruited from the DM and Neurology outpatient clinics, Suez Canal University Hospital. Age and sex matched 44 healthy subjects, representing the control group, were included.  Subjects with concurrent disease affecting the central or the peripheral nervous system, airway obstruction, medications interfering with the function of the nervous system or body mass index (>25 kg/m2)6 were excluded.

All the subjects went through complete medical history (including duration and treatment of DM). Physical, neurological and Otolaryngology examination were done. Body mass index was measured. Laboratory investigations included fasting and 2-hours postprandial blood sugar and glycosylated hemoglobinA1c (HbA1c).

Patients were considered diabetics if the fasting blood sugar was >126 mg% and the 2-hours post prandial blood sugar was >200 mg%.7 Peripheral neuropathy was assessed according to the Michigan Diabetic Neuropathy Score (MDNS).8 It is a two-stage scheme assessing the clinical and neurophysiological chosen nerves and accordingly, mild, moderate, severe or no neuropathy was estimated. Autonomic neuropathy was assessed through clinical assessment by the translated Arabic form of Composite Autonomic Symptom Scale (COMPASS).9 A score above 43.8 was considered indicative of autonomic neuropathy. Postural hypotension was diagnosed by measuring blood pressure at recumbent and on standing upright for at least 3 minutes. A drop in systolic pressure >20 mmHg or drop of diastolic pressure ≥10mmHg was considered pathognomonic.10 Neuro-physiological assessment was done by the sympathetic skin response test (SSR).11 Sympathetic autonomic neuropathy was considered when one or both parameters (Latency/Amplitude) of SSR of the upper limbs and one or both parameters of the lower limbs were affected.

The phrenic nerve conduction studies were performed.12 The parameters of compound motor action potential of right and left sides (Amplitude in µv and Latency in msec) were evaluated. Phrenic nerve affection was considered if one or more of the parameters of the right and left phrenic nerves were affected.

Sleep was assessed by using the translated Arabic form of Epworth sleepiness scale (ESS) for daytime sleepiness.13 The total score ranged from 0-24. A score >10 was considered as having excessive daytime sleepiness. Overnight polysomnography was used to assess the total sleep time, sleep onset (minutes), sleep efficiency (%), number of awakenings and sleep stages. Total sleep time and latency to each stage (N1, N2, N3 and REM) was assessed. Attacks of central apnea, obstructive apnea, hypopnea were calculated. Lowest oxygen saturation, Oxygen saturation during REM and Oxygen saturation during N-REM were recorded. Sleep disordered breathings were considered.14 An apnea was defined as a reduction ≥90% in naso-oral airflow lasting 10 seconds. A Hypopnea was defined as a reduction ≥50% in naso-oral airflow lasting 10 seconds and accompanied by an arousal or a fall in SaO2 of ≥3%, or a reduction ≥30% in naso-oral airflow lasting 10 seconds and accompanied by an arousal or a fall in SaO2 of ≥4%. Apnea index was defined as the numbers of apneas per hour sleep. Apnea/hypopnea index (AHI) was defined as the number of apneas and hypopneas per hour sleep. Sleep apnea was considered when AHI is ≥5/hour.

Obstructive sleep apnea (OSA) was defined as absence of naso-oral airflow despite continuing respiratory effort. Central sleep apnea (CSA) was defined as Cessation of naso-oral airflow with cessation of respiratory effort. Mixed sleep apnea (MSA) was defined as presence of both central and obstructive patterns. Mild sleep apnea was diagnosed when AHI ≥5-15/h, moderate sleep apnea when AHI >15-30/hour and sever sleep apnea when AHI >30/hour.

All the neuro-physiological studies were done at the Clinical Neurophysiology Unit, Cairo University Hospital. Nerve conduction studies were done by using Nihon Kohden 4 channel apparatus. The SSR test was done by using Nihon Kohden 2 Channels apparatus. Polysomnography was done by using Schwarzer Epos 32 GmpH medical diagnostic polysomnogram, Germany.

Gathered data were processed using the SPSS version 15. Quantitative data were expressed as means ±SD. Qualitative data were expressed as numbers and percentages. Unpaired t test was used to test significance of difference between 2 means; while Chi square test (χ2) was used to test significance of difference between qualitative data. A probability value (P-value) <0.05 was considered statistically significant; while P-value <0.01 was considered statistically highly significant.15

 

RESULTS

 

Out of the 44 diabetic patients, 24 (54.5%) patients were on insulin, and 20 (45.5%) were on oral hypoglycemic drugs. Eighteen patients (40.9%) had controlled diabetic state (HbA1c ≤6.5), while 26 (59.1%) had uncontrolled diabetic state (HbA1c >6.5) in the last 3 months. The duration of DM ranged from 3-24 years (mean of 9.9±5.22 years)

All non-diabetic subjects had no clinical or neuro-physiological evidence of peripheral neuropathy. Twenty seven (61.4%) diabetic subjects had clinical evidence, and 38 (86.3%) had neuro-physiological evidence of peripheral.

According to the clinical score: 17 patients (38.6%) had no neuropathy, 9 (20.5%) had mild, 10 (22.7%) had moderate and 8 (18.1%) had severe peripheral neuropathy. According to neuro-physiological score: 6 patients (13.7%) had no neuropathy, 14 (31.8%) had mild, 14 (31.8%) had moderate and 10 (22.7%) had severe peripheral neuropathy.

None of the non-diabetic subjects had clinical evidence of autonomic neuropathy. Nineteen diabetic patients (43.2%) had clinical autonomic neuropathy and 16 patients (36.4%) had postural hypotension (P<0.01).

By SSR; 36 (81.8%) diabetic patients had abnormal neuro-physiological responses compared to only 2 (4.5%) non-diabetic subjects (P<0.01). The means of the amplitude of SSR of the upper (1.13±1.06 mV) and lower limbs (0.39±0.4 mV) were highly significantly lower in diabetic patients than in non-diabetic subjects (2.46±0.29 and 0.66±0.55 mV respectively) (P <0.01). Moreover, the mean of the latency of the upper limb was highly significantly delayed in diabetics (1.81±0.61 sec) than in non-diabetics (1.51±0.19 sec) (P<0.01). However, there was no significant difference detected between the mean of the latency of the lower limbs of diabetics (1.72±1.06 sec) and non-diabetics (1.63±0.62 sec) (P>0.05).

Twenty six diabetics (59.1%) showed neurophysiological evidence of phrenic nerve affection, compared to only 2 (4.5%) non-diabetics (P<0.01). The means of the amplitude of the right (222.4±109.5 µV) and left (171.9 ±76.7 µV) phrenic nerves in the diabetics were significantly lower than in non-diabetics (263.7±56.4 and 271.5±54.7 µV) (P<0.05). Latencies of the right and left phrenic nerves were delayed in diabetics (7.8±0.8 and 8.1±1.0 msec) in comparison to non-diabetics (8.03±0.2 and 7.9±0.4 msec). However, the difference was statistically non-significant (P>0.05).

Clinical assessment of excessive daytime sleepiness revealed that 26 diabetics (63.6%) had high scores (≥10) of the Epworth Sleepiness scale (ESS) and none of the non-diabetics had high score (P<0.01)

Sleep architecture (Table 1) showed that the total sleep time was significantly reduced in the diabetics than in non-diabetics (P<0.05). The diabetic patients had highly significant delay of sleep onset, less sleep efficiency and more number of awakenings than the non-diabetics (P<0.01).

Sleep stages (Table 2) revealed that in comparison to the non-diabetics; the latency to N1 was significantly increased among the diabetics (P <0.05). No significant difference was detected between the latencies to N2, N3 and REM between diabetics and non-diabetics (P>0.05). The percentage of N1 in the diabetics was highly significantly increased (P<0.01). The percentage of N2 and N3 in the diabetics were highly significantly reduced (P<0.01). The percentage of REM in the diabetics was non-significantly increased (P>0.05).

Sleep abnormalities (Table 3) showed that obstructive apnea index, the central apnea index, the hypopnea  index, the apnea hypopnea index in non REM stage and the apnea hypopnea index in REM stage were statistically highly significantly increased in the diabetics compared to the non-diabetics (P<0.01). Only the mixed apnea index was not significantly different between them (P >0.05). The average oxygen saturation in REM stage and non REM stage and the lowest oxygen saturation were highly significantly reduced in the diabetics (P<0.01).

Sleep apnea was highly significantly more frequent in diabetics (37 patients, 84.1%) than in non-diabetics (8 subjects 18.2%) (P<0.01). Obstructive sleep apnea was the most frequent type in the diabetics (65.9%) followed by mixed (13.7%) and lastly central type (4.5%). Table (4) shows type and severity of sleep apnea among diabetics and non-diabetics. Obstructive sleep apnea was highly significantly more frequent in diabetics than in non-diabetics (P<0.01). Central sleep apnea was only significantly more frequent in diabetic subjects (P<0.05). No significant difference was detected between the frequency of mixed apnea in the diabetics and non-diabetics (P>0.05). All the grades of sleep apneas (mild, moderate and sever) were highly significantly more frequent in diabetics than in non-diabetics (P<0.01).

There was significant relation between sleep apnea and age of the patient, male sex, uncontrolled DM, duration of DM, diabetic autonomic neuropathy and phrenic nerve affection. There was no relation detected between sleep apnea and diabetic peripheral neuropathy (Table 5).


 

Table 1. Distribution of sleep architecture parameters among diabetics and non-diabetics.

 

 

Diabetics

Non diabetics

P-value

Total sleep time (min.)

348.3±96.9

383.1±39.6

<0.05*

Sleep onset (min.)

22.7±21.1

12.5±12.3

<0.01**

Sleep efficiency (%)

81.2±14.2

88.9±3.4

< 0.01**

Number of awakening

12.1±7.1

4.6±2.7

<0.01**

*Statistically significant  at P <0.05 **Statistically significant  at P <0.01

 

Table 2. Latency to different sleep stages (minutes) and percentage of sleep stages among diabetics and non-diabetics.

 

 

Diabetics

Non diabetics

P-value

Sleep latency to N1

22.7±21.1

12.6±12.5

< 0.05*

Sleep latency to N2

48.5±36.7

50.4±48.2

> 0.05

Sleep latency to N3

81.2±79.7

86.6±60.7

> 0.05

latency to REM sleep

140.9±105.2

134.7±92.3

> 0.05

N1 %

32.4±20.9

13.8±9.7

<0.01**

N2 %

36.9±13.6

49.8±9.2

<0.01**

N3 %

17.1±11.5

25.2±13.1

<0.01**

REM sleep %

14.9±10.8

13.1±6.1

> 0.05

N1 Stage-1 NREM sleep, N2 Stage-2 NREM sleep, N3 Stages-3,4 NREM-sleep

*Statistically significant  at P <0.05 **Statistically significant  at P <0.01

Table 3. Sleep abnormalities among the diabetics and non-diabetics.

 

 

Diabetics

Non diabetics

P-value

Obstructive apnea index

6.18±12.67

0.16±0.48

<0.01*

Central apnea index

3.17±7.22

0.10±0.28

<0.01*

Mixed apnea index

1.70±3.04

2.10±4.39

>0.05

Hypopnea index

9.90±5.88

0.43±0.5

<0.01*

Apnea hypopnea index

20.70±19.97

2.67±4.39

<0.01*

AHI in Non-REM

21.26±29.08

1.06±1.76

<0.01*

AHI in REM

23.19±18.9

0.76±2.31

<0.01*

Lowest O2 sat.

79.45±12.91

91.45±4.72

<0.01*

O2 Sat. in REM

94.67±2.81

96.73±1.82

<0.01*

O2 Sat. in Non-REM

94.69±3.15

97.08±1.65

<0.01*

AHI Apnea/Hypopnea Index, REM Rapid Eye Movement

*Statistically significant  at P <0.01

 

Table 4. Types and severity of sleep apnea among diabetics and non-diabetics.

 

Sleep apnea

Diabetics

(n=44)

Non-diabetics

(n=44)

P-value

 Obstructive Apnea  (OAI >5)

29 (65.9%)

2 (4.5%)

< 0.01**

Central Apnea (CAI >5)

2 (4.5%)

0   (0%)

< 0.05*

Mixed Apnea (MAI  >5)

6 (13.7%)

6 (13.7%)

> 0.05

Mild Apnea (AHI 5 - <15/h)

20 (45.4%)

6 (13.7%)

<0.01**

Moderate Apnea (AHI 15 - <30 /h)

8 (18.2%)

2 (4.5%)

<0.01**

Severe Apnea (AHI >30 /h)

9 (20.5%)

0 (0%)

<0.01**

AHI Apnea hypopnea index, CAI Central apnea index, OAI Obstructive apnea index, MAI Mixed apnea index

*Statistically significant  at P <0.05 **Statistically significant  at P <0.01

 

 

Table 5. Relationship between age, sex, diabetic state, diabetic peripheral neuropathy, diabetic autonomic neuropathy and phrenic nerve affection and sleep apnea among diabetic patients.

 

 

Sleep Apnea

N=37

No sleep apnea

N=7

P-value

Age >40 years

27 (73)

4  (57.1)

< 0.01**

Male sex

25  (67.6)

1  (14.3)

<0.01**

Uncontrolled diabetes

25 (67.6%)

1 (14.3%)

< 0.01**

Duration of DM

12 ±5.87

8.12 ±3.97

< 0.05*

Clinical polyneuropathy

23 (62.2%)

4 (57.1%)

>0.05

Electrophysiological PN

33 (89.2%)

5 (71.4%)

>0.05

Clinical Autonomic neuropathy

19 (51.4%)

0 (0%)

<0.01**

Electrophysiological AN

34 (91.9%)

5 (71.4%)

<0.05*

Postural Hypotension

15 (40.5%)

1 (14.3%)

<0.01**

Phrenic nerve affection

24 (64.9%)

2 (28.6%)

<0.01**

AN Autonomic Neuropathy, DM Diabetes Mellitus, PN Peripheral Neuropathy

*Statistically significant  at P 0.05 **Statistically significant  at P <0.01

 


DISCUSSION

 

Excessive daytime sleepiness was more frequent (63.6%) among diabetics. Feinberg16 alerted sleep specialists to the possibility that untreated diabetes should be considered in patients with severe sleepiness. Vgontzas and colleagues17 also reported that diabetes causally associated with excessive daytime sleepiness, a cardinal symptom of sleep apnea that was frequently thought to be related to sleep fragmentation secondary to intermittent breathing cessation.

Sleep architecture was affected in the diabetics. The patients had delayed sleep onset, decrease in the total sleep time, increased number of awakenings and less Sleep efficiency. Sleep stages were also affected. Diabetics had increased percentage of sleep stage N1, and reduced percentage of stages N2 and N3. Gislason and Almqvist18 reported that diabetes was associated with more frequent complaints of difficulty initiating sleep (21.1%) and difficulty maintaining sleep (21.9%). Sridhar and Madhu19 reported increased prevalence of sleep disturbances in diabetics, primarily difficulty initiating sleep.

Sleep apnea was significantly more frequent in the diabetics (84.1%) than in non-diabetics (18.2%). Obstructive sleep apnea was the most frequent type (65.9%) followed by mixed type (13.7%) and lastly central sleep apnea (4.5%). Guilleminault and colleagues20 found obstructive sleep apneas in two and central sleep apneas in one of four type-1 diabetics. Recently, the Sleep Ahead Study21 from the United States reported an alarming prevalence of OSA of more than 86% among type 2 diabetic adults.

OSA was suggested to be linked to DM through the impairment of glucose tolerance. Tamura and colleagues22 reported a prevalence of DM as high as 30% in adults with OSA, half of whom were of moderate/severe degree, and impaired glucose tolerance (IGT) was found in another 30%.

Central sleep apnea appeared to be increased in insulin-dependent DM. The location of insulin receptors in the brainstem and cerebellum suggests that insulin might be involved in control of breathing. However, observations in diabetic mice do not support a direct effect of insulin on ventillatory control.23

Severity of sleep apnea increased among diabetic patients; (20.5%) of patients had mild sleep apnea, (25.0%) of patients had moderate and (38.6%) of patients had severe sleep apnea. Theorell-Haglöw24 emphasized the role of insulin sensitivity in controlling the severity of apnea. They reported a gradual decrease in insulin sensitivity with increasing AHI. Punjabi and Beamer25 found that severity of sleep disordered breathing (SDB) was associated with the degree of insulin resistance and glucose intolerance. There was a progressive reduction in insulin sensitivity with increasing severity of SDB. Tamura and colleagues23 reported that several studies have shown supportive evidence for a dose-dependent relationship between the severity of OSA and glucose dysmetabolism. And the disposition index, a measure of pancreatic β cell function, was also reduced in those with moderate to severe OSA.

There was significant relation between sleep apnea and age of the patient, male sex, uncontrolled DM and duration of DM. Aging was an important variable in sleep apnea in diabetics. Sleep apnea was more prevalent as the age advances.26 Sleep apnea was 2 folds higher among males than female diabetics. Bixler and colleagues27 explained the reduction of sleep apnea in women to the role of women hormones in decreasing the rate of sleep apnea. Other hypotheses for the gender differences in sleep apnea have included differences in airway caliber, soft tissue structure, genioglossal activity, and regional fat distribution.28 Renko and colleagues29 reported an increase in HbA1c and impaired glucose tolerance as a result of sleep disordered breathing.

Statistically significant relationship between diabetic autonomic neuropathy and phrenic nerve affection and sleep apnea was found. Bottini and colleagues30 explained the high frequency of sleep apnea with diabetic autonomic neuropathy by the reduction in the peripheral chemo-responsiveness to C02 may possibly be ascribed to the damage of the parasympathetic nervous fibers that normally convey afferents from the carotid bodies to the respiratory centers. Chokroverty and colleagues31 explained sleep disordered breathing in diffuse diabetic neuropathy by the involvement of nerves supplying the diaphragm, intercostals and accessory muscles of respiration. Involvement of these nerves leads to weakness of these muscles, giving rise to breathlessness on exertion, hypoxia, and hypercapnia. Furthermore, progressive pharyngeal nerve dysfunction can cause collapse of upper airways in patients with obstructive sleep apnea.32

In conclusion, we must consider that many sleep apneas as well as changes in sleep architecture occur in diabetic patients, especially those with diabetic autonomic neuropathy and with phrenic nerve affection.

 

[Disclosure: Authors report no conflict of interest]

 

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الملخص العربى

 

توقف التنفس أثناء النوم في مرضى الاعتلال العصبي السُكّري

 

تم إجراء هذا البحث بهدف دراسة معدل ونوع وشدة توقف التنفس أثناء النوم في مرضى الاعتلال العصبي السكري. وقد خضع لهذا البحث 44 مريضا بالبول  السكرى بالإضافة الي44 شخصا من الأصحاء يمثلون المجموعة الضابطة. وقد خضعت الحالات الى: تقييم إكلينيكي - تحاليل معملية - تقييم الاعتلال العصبي السكري الطرفي - تقييم الاعتلال العصبي السكري الذاتى - تقييم وظيفة العصب الحجابى - اضطراب النوم.

وقد أظهرت النتائج ما يلى: 63.6% من المرضى يعانون من النوم الزائد أثناء النهار تبعا لمقياس ابورث، 84.1% من المرضى يعانون من توقف التنفس أثناء النوم ،توقف التنفس الانسدادى هو الأكثر شيوعا (65.9%) يتبعه توقف التنفس المركب (13.7%) ثم توقف التنفس المركزى (4.5%)، جميع درجات شدة توقف التنفس أثناء النوم (البسيط, المتوسط و الشديد)  كانت أعلي فى مرضى البول  السكرى.

 وقد أظهرت الدراسة أيضا أن هناك علاقة ذات دلالة إحصائية بين توقف التنفس أثناء النوم والسن، النوع (الذكر)، مدة مرض البول السكرى, التحكم في نسبة السكر فى الدم خلال الثلاثة الأشهر الأخيرة، الاعتلال العصبى الذاتى السكرى واعتلال العصب الحجابى - ولا توجد اي علاقة ذات دلالة إحصائية بين توقف التنفس أثناء النوم والاعتلال العصبى الطرفى السكرى.

 

 



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