Online ISSN : 1687-8329


Quick Search 

October2011 Vol.48 Issue:      4 Table of Contents
Full Text

Correlation between Peripheral Neuropathy and Ocular Surface Disorders in Children and Adolescents with Type 1 Diabetes Mellitus

Ali S. Shalash1, Abeer A. Abdelmaksoud2, Amany A.  El-Shazly3,

Eman M. Abdel-Mohsen2, Mona A. Salem2

Departments of Neurology1, Pediatrics2, Ophthalmology3, Ain Shams University; Egypt


Background: Correlation between diabetic polyneuropathy (DPN), corneal, and tear film disorders in young people with type 1 diabetes mellitus (T1DM) has important clinical implications and needs further research. Objective: The aim of this study is to evaluate the clinical characteristics of DPN in children and adolescents with T1DM, and its relation to ocular surface disorders. Methods: forty patients with T1DM and twenty controls were included. Comprehensive clinical assessment was conducted for all patients. Mean HbA1c and microalbuminuria over one year were estimated. Detailed ophthalmological assessment included Schirmer, rose bengal staining, fluorescein staining, tear break up time (BUT), impression cytology (IC) tests and fundus examination. Neurological examination and nerve conduction study (NCS) were conducted. Patients were subdivided into: group I for patients with DPN and group II for patients without DPN. Results: All tear film tests except rose bengal were significantly affected in patients (p<0.001). 19 patients (47%) were diagnosed to have DPN. Patients with DPN had significantly lower tibial mean conduction velocity (MCV) values (36.15± 7.29 versus 45.85 ± 2.43; p =0.01), longer duration of diabetes (mean 6.6±3.09 versus 4.6±3.51 years; p= 0.03), lower mean values of Schirmer (p= 0.001) and BUT (p = 0.0003) tests, abnormal conjunctival IC and fluorescein staining tests (p= 0.007 and 0.035, respectively), compared with patients without DPN. Conclusion: DPN is a common complication of T1DM, and related to age of patients, duration of diabetes, and other chronic diabetic complications, and correlates with the occurrence of ocular surface disorders. [Egypt J Neurol Psychiat Neurosurg.  2011; 48(4): 337-343]

 Key Words: diabetes mellitus, peripheral neuropathy, ocular surface disorders, tear film dysfunction.


Correspondence to Ali S. Shalash, Department of Neurology, Ain Shams University, Egypt.

Tel.:  +201005623036. Email:



Chronic sensorimotor distal symmetric polyneuropathy is the most common type of neuropathy among diabetic patients and is defined as “the presence of symptoms and/or signs of peripheral nerve dysfunction in people with diabetes, after the exclusion of other causes”.1,2 Diabetic neuropathy represents a major complication of type 1 diabetes mellitus (T1DM) in young people, and is detected in up to 57% of this group, by using complete electrophysiological evaluation.3,4

Clinical neuropathy is defined as an abnormal neurologic examination consistent with peripheral sensorimotor polyneuropathy, plus either abnormal nerve conduction in at least two peripheral nerves or unequivocally abnormal autonomic nerve testing.3,5

In addition to retinopathy, ocular surface disorders, including corneal abnormalities (keratopathy) and tear film dysfunction (dry eye), have been identified as complications of T1DM.6,7 Keratopathy associated with diabetes mellitus comprises superficial punctate keratopathy, recurrent corneal erosion, persistent epithelial defect, and corneal endothelial damage.8

These ocular abnormalities are attributed to damage of the nerve supply and might be correlated to diabetic polyneuropathy (DPN).9-11 The association between various chronic diabetic complications was addressed by numerous studies in type 2 diabetes mellitus (T2DM),7,12 but there has been a lack of research related to the changes of ocular surface and their correlation with DPN in young people with T1DM.10,11,13

The aim of this study is to evaluate the clinical characteristics of clinically and electrophysiologically diagnosed DPN in children and adolescents with T1DM, and its relation to ocular surface complications.




This cross sectional study was conducted at Ain Shams University in the period from April 2008 to December 2009. Forty patients with type 1 diabetes mellitus, including 21 male and 19 females, were recruited from Pediatric Diabetes Clinic at Children's Hospital. Their ages ranged from 5 to 17 years old with mean age of 13.51±2.78 years. Twenty age and sex matched healthy children and adolescents were included as a control group. Written informed consent was taken from all parents, after approval of Local Ethical Committee.  Comprehensive history and physical examination was conducted for all patients.

Mean random blood glucose (RBS) and mean glycated hemoglobin (HbA1c) over the last year follow-up were recorded. HbA1c was calculated by using high purified liquid chromatography (HPLC).14 HbA1c target range of <7.5% was recommended for all age groups.15  To diagnose nephropathy; urinary albumin excretion was performed using immune turbidimetric methods. Persistent microalbuminuria was defined when two of three samples showed an excretion rate of 30-300 ug/mg creatinine.16 

The patients were divided into 2 groups according to the clinical and/or electrophysiological diagnosis of DPN, into; Group I; 19 patients with DPN (mean age =14.1; 11 males (58%) and 8 females (42%)) and Group II; 21 patients without DPN (mean age= 12.9; 13 males (62%) and 8 females (38%)). The two groups were compared regarding age, duration, glycated hemoglobin, microalbuminuria, and different ocular tests.

To assess neuropathy, neurological assessment and nerve conduction studies (NCS) were done at department of neurology. Motor conduction velocities (MCVs), distal motor latencies (DMLs) and compound muscle action potential (CMAPs) amplitudes of the median, tibial, and peroneal nerves of both sides were measured using EVOMATIC 8000 Apparatus (Dantec, Denmark). Additionally, sensory conduction velocities (SCVs) and amplitudes of the sensory nerve action potentials (SNAPs) of the median and sural nerves were studied. These nerves, especially of lower limbs, are the most useful and practical nerves for the electrophysiological study in diabetic patients.17, 18

The diagnosis of peripheral neuropathy was based on the presence of symptoms and signs of diabetic polyneuropathy such as dysesthesias, paresthesias, glove and stocking hypesthesia, abnormal tuning fork vibration perception, abnormal motor functions and abnormal deep tendon reflexes, and/or on abnormal nerve conduction velocity.

Bipolar surface stimulating electrodes were used to stimulate both sensory and motor nerves of the skin, while two types of recording electrodes were used (ring sensory electrodes with an active recording electrode placed at the proximal phalanx and a reference electrode placed at least 2 cms distal to the active electrode, and surface electrodes with an active recording electrode placed over the motor point of the muscle and the reference one placed distally over the tendon (at least 2 cms distal to the active electrode)). If two or more of the nerves had at least one abnormal attribute according to normative values,18-20 it is electrophysiologically considered a diabetic neuropathy.

Detailed ophthalmological examination was done for eighty eyes of the 40 patients including fundus examination to diagnose diabetic retinopathy (DR). Tear film changes were tested by variable techniques. Schirmer test was used to quantitatively evaluate basal tear production. A reading of less than 10 mm was considered to show dry eye. Tear break up time (BUT) test reflected tear stability and composition, using a fluorescein filter paper.21 A BUT of less than 10 seconds was considered abnormal. Keratoepitheliopathy was evaluated by staining the cornea with fluorescein staining test, using slit-lamp biomicroscopy.22 The staining area was graded on a numerical scale of 0 to 3, with 0 representing no punctate staining, 1 representing fine punctate staining, 2 representing coarse punctate staining, and 3 representing diffuse staining. Rose bengal staining was used to detect corneal and conjunctival desiccation associated with insufficient tear flow, using diffuse white light. Staining was graded of 0 to 3 for each of the lateral and medial corneal and conjunctival regions of the exposed intrapalpebral ocular surface. If the total staining score was ≥ 3, it was considered abnormal. Conjunctival impression cytology (IC) was conducted to detect conjunctival metaplasia. Three days after tear function examinations, an impression cytologic specimen for light microscopy was obtained. Scoring of tear film tests was based on criteria of Sood and his colleagues.23 Exclusion were made for patients with contact lenses, eye infection, eye trauma, ocular surgery, any other surgeries within the previous 6 months, severe blepharitis with meibomian gland dysfunction, blinking abnormality, or severe pterygium.

Statistical analysis was done using the statistical package for the social sciences (SPSS version 18, Chicago, IL, USA). Qualitative data was analyzed using Chi-square test, and exact tests such Fisher exact and Monte Carlo was applied to compare any two categories. Non-parametric quantitative data was analyzed using Mann Whitney U test to compare between two categories. p-value <0.05 was considered significant. Comparison of NCS findings was done using independent sample t-test.



Mean duration of T1DM was 5.58±3.43 years and 19 patients (47%) were diagnosed to have DPN, after abnormal nerve conduction studies. The abnormalities in tear film were detected by Schirmer, BUT, impression cytology and fluorescein staining in 17.5, 45, 63.7% and 66.2% of patients’ eyes, respectively, compared to none of the controls (p <0.001), while rose bengal staining abnormalities were detected only in 11.3% of patients’ eyes and none of the controls, but this did not reach a statistical significance (p >0.05) (Table 1).

Abnormalities in Schirmer, rose bengal, fluorescein and impression cytology tests were not significantly related to age, sex, RBS, HbA1c, acute or chronic diabetic complications (p >0.05), while; abnormalities in BUT test were significantly related to age (p= 0.047) , high mean RBS (p=0.01), and high HbA1c (88.9% of abnormal BUT test were among those with HbA1c > 7.5%) (p <0.001). Moreover; 55.6% and 75% of patients with severe hypoglycemia and severe DKA respectively had abnormal BUT test (p=0.015 and 0.007, respectively). 63.2% of patients with neuropathy had abnormal BUT test results (p =0.008).

The two studied groups of patients, with and without neuropathy, were statistically matched with respect to age (p= 0.341), sex (p= 0.752), mean RBS (p=0.295) and HbA1c (p=0.331), while group 1 (T1DM with neuropathy) had significantly tibial MCV values (36.15± 7.29 versus 45.85 ± 2.43; p =0.01), and longer duration (mean 6.6 versus 4.6 years; p= 0.03). 16% (3 patients) had nephropathy, while none in group 2) (T1DM without neuropathy) (Table 2).

Patients with DPN had lower mean values of Schirmer and BUT tests than the group without neuropathy, and statistically there was significant difference (p<0.05). Also, conjunctival impression cytology (Figure 1) test was more significantly abnormal (p= 0.007 and 0.035, respectively) in patients with DPN, compared with patient without DPN. Moreover, more patients with DPN had abnormal rose bengal test, but without significant difference (Table 2).

Within group of patients with neuropathy, Schirmer and BUT tests are significantly related (p <0.005) to duration of diabetes and to each other, while not related to age, or RBS. Also, Schirmer test is significantly correlated with Hb A1C level.



Table 1. Tear film tests among studied patients and controls.






Schirmer test (score) (no of eyes,%)





66 (82.5)




14 (17.5)

0 (0)


Median & range (mm/5 min)

14 (8-20)

16 (14-17)


BUT (score)(no,%):




>10 seconds

44 (55)

40 (100)


6 – 10 seconds

29 (36.3)

0 (0)


3- 6 seconds

7 (8.7)

0 (0)


Median & range (mm/5 min)

11 (5-20)

18 (16-22)


Impression cytology (grade) (no,%)







Median &range

29 (36.3)

45 (56.2)

6 (7.5)

0 (1-3)

40 (100)

0 (0)

0 (0)


<0.001 a



Rose bengal (score) (no,%)






71 (88.7)

9 (11.3)

40 (100)

0 (0)


Fluorescein staining findings (no,%)





Fine punctuate

Coarse punctuate

37 (33.8)

26 (45)

17 (21.2)

40 (100)

0 (0)

0 (0)

p <0.001 a

a Monte Carlo test was used

* Significant at p<0.01

Table 2. Comparison of characteristics between diabetic patients with and without neuropathy.



Patients with DPN

Patients without DPN


No of patients/eyes




Gender (F/M)




Age (yr, mean±SD)




Duration of diabetes (yr, mean±SD)








HBA1C (%, mean±SD)




Microalbuminuria (no)

3 (16%)

0 (0%)


Tibial MCV (mean±SD)

36.15± 7.29



SCH (mean±SD)








Rose Bengal staining (no)

5 (26%)

3 (15%)


Fluorescein staining (grade)

1  (1-2)

0.5 (0-1)


Impression cytology (grade)

1.5 (1-2)

0.5 (0-1)


HB A1C glycosylated hemoglobin, MCV motor conduction velocity, SD standard deviation.

* Significant at p<0.05 ** Significant at p<0.01




Figure 1. Conjunctival impression cytology grades among patients with DPN (pn) and without DPN (nopn).





Recently, establishing a surrogate marker for diabetic neuropathy (DN) is extensively studied, to define progression or response to treatment via repeated assessments. So, the ideal surrogate marker should be easy to use, reliable, sensitive, and noninvasive.24 Various markers have been advocated, including invasive and noninvasive techniques. Invasive procedures (e.g., sural nerve biopsy25 and skin biopsy24,26) proved to be accurate, while clinically noninvasive techniques (e.g., electrophysiology, quantitative sensory testing (QST), and assessment of neurological disability27) showed less accuracy.

Nerve conduction studies are the most sensitive noninvasive technique for identification of PDN, compared with other methods as vibration tactile perception.18 As an alternative noninvasive markers, ocular surface disorders, such as corneal dysfunction assessment or tear film dysfunction using different tests, have been extensively studied on diabetic patients, especially patients with T2DM, searching for their correlation with DN.10,12,24,28

Using the ocular surface parameters as a marker for DPN is more appropriate and applicable in younger patients with T1DM. Invasive (biopsy) and painful (electrophysiology) techniques are difficult to advocate among children and adolescents with T1DM. Also, age–related decline in these ocular functions is absent compared with elder people.6 This was confirmed in the present study by absence of any ocular abnormalities in all tests among age and sex matched healthy controls.

In this study, ocular surface disorders have been significantly detected among patients with T1DM, especially those with neuropathy. Other studies indicated that 47% to 64% of diabetic patients have primary corneal lesions during their life time.6,12 A prevalence of dry eye symptoms of 20.6% in diabetics and 13.8% in non-diabetics was reported in previous studies.7,29

In the present study, 17.5 and 45% of examined diabetic eyes, respectively, had abnormal Schirmer and BUT tests, compared to none in the controls. This agrees with reports of other studies that diabetic patients had a decreased BUT test and lower values of basal Schirmer test.12,30 Moreover; this study proved that diabetic patients showed significantly more frequent and more pronounced signs of conjunctival metaplasia as assessed by impression cytology test. This is consistent with other studies that demonstrated pronounced signs of conjunctival squamous metaplasia in patients with insulin-dependent diabetes30 and loss of mucin-secreting goblet cells, indicating chronic irritation.12

Moreover, using clinical assessment and routine nerve conduction studies of lower extremities in this study, 47% of patients with T1DM had DPN. Karsidage and his colleagues suggested that the most useful and practical nerves for the electrophysiological study in diabetic patients were the motor and sensory nerves of lower extremities.17 Also, previous studies found that the peroneal nerve was the highest31 and most sensitive abnormality in diabetic patients.20

Percentage of neuropathy varied across studies due to different methods of assessment (clinical scores, special tests as vibration perception thresholds (VPT) and tactile perception thresholds (TPT), electrophysiological assessment, or nerve biopsy), duration of diabetes, age of group, and involvement of small fiber or autonomic neuropathy18,28,32.

Similar to previous studies,10,17,18 patients with neuropathy are of older age, longer duration of diabetes, and significantly correlated with other chronic complications. Moreover, patients with neuropathy are more vulnerable to ocular surface disorders compared with patients without neuropathy. This was detected by few reports in T1DM11 and many studies in T2DM patients.10,24,28

In diabetic patients, correlation between DPN severity and corneal keratopathy is attributed to loss of corneal nerve fibers secondary to abnormal glucose metabolism and activated polyol pathway.8,10 Also, the presence of dry eye in the studied diabetic patients, which agrees with other studies, is attributed to the decrease in reflex tearing due to a decreased sensitivity of the conjunctiva resulting from neuropathy. Likewise, the BUT test was decreased, especially in diabetes with peripheral neuropathy, suggesting a neuropathy involving the innervations of the lacrimal glands.11,12,28

The present study detects the percentage of DPN in young patients with T1DM, and confirms its correlation with duration of DM, other chronic diabetic correlation, and ocular surface disorders. It also suggests the usefulness of corneal and tear film parameters as markers for DPN, but more extensive prospective studies are needed to confirm this association, with long term follow-up, repeated assessments, using standard measures for DPN and ocular surface disorders, and correlation to DPN severity.

Confirming the relationship between DPN and ocular surface disorders is of high clinical value. It suggests that corneal keratopathy and tear film dysfunction could be a non-invasive, simple marker or screen for DPN. Also, it recommends regular ophthalmological assessment and ocular care in patients with DPN.


[Disclosure: Authors report no conflict of interest]




1.      Daneman D. Type 1 diabetes. Lancet. 2006 Mar 11; 367(9513): 847-58.

2.      Boulton AJ, Vinik AI, Arezzo JC, Bril V, Feldman EL, Freeman R, et al. Diabetic neuropathies: a statement by the American Diabetes Association. Diabetes Care. 2005 Apr; 28(4): 956-62.

3.      Trotta D, Verrotti A, Salladini C, Chiarelli F. Diabetic neuropathy in children and adolescents. Pediatr Diabetes. 2004 Mar; 5(1): 44-57.

4.      Hyllienmark L, Brismar T, Ludvigsson J. Subclinical nerve dysfunction in children and adolescents with IDDM. Diabetologia. 1995 Jun; 38(6): 685-92.

5.      Karavanaki K, Baum JD. Prevalence of microvascular and neurologic abnormalities in a population of diabetic children. J Pediatr Endocrinol Metab. 1999 May-Jun; 12(3): 411-22.

6.      Murphy PJ, Patel S, Kong N, Ryder RE, Marshall J. Noninvasive assessment of corneal sensitivity in young and elderly diabetic and nondiabetic subjects. Invest Ophthalmol Vis Sci. 2004 Jun; 45(6): 1737-42.

7.      Ozdemir M, Buyukbese MA, Cetinkaya A, Ozdemir G. Risk factors for ocular surface disorders in patients with diabetes mellitus. Diabetes Res Clin Pract. 2003 Mar;59(3):195-9.

8.      Yoon KC, Im SK, Seo MS. Changes of tear film and ocular surface in diabetes mellitus. Korean J Ophthalmol. 2004 Dec; 18(2): 168-74.

9.      Nuho A, Subekti I, Ismail D, Sitompul R. Correlation of neuropathy with corneal sensitivity and lacrimal gland secretion in type 2 diabetes mellitus patient. Acta Med Indones. 2004 Jul-Sep; 36(3): 130-5.

10.    Tavakoli M, Kallinikos PA, Efron N, Boulton AJ, Malik RA. Corneal sensitivity is reduced and relates to the severity of neuropathy in patients with diabetes. Diabetes Care. 2007 Jul; 30(7): 1895-7.

11.    Rosenberg ME, Tervo TM, Immonen IJ, Muller LJ, Gronhagen-Riska C, Vesaluoma MH. Corneal structure and sensitivity in type 1 diabetes mellitus. Invest Ophthalmol Vis Sci. 2000 Sep; 41(10): 2915-21.

12.    Dogru M, Katakami C, Inoue M. Tear function and ocular surface changes in noninsulin-dependent diabetes mellitus. Ophthalmology. 2001 Mar; 108(3): 586-92.

13.    Wiemer NG, Dubbelman M, Kostense PJ, Ringens PJ, Polak BC. The influence of chronic diabetes mellitus on the thickness and the shape of the anterior and posterior surface of the cornea. Cornea. 2007 Dec; 26(10): 1165-70.

14.    Swift PG. Diabetes education in children and adolescents. Pediatr Diabetes. 2009 Sep; 10 Suppl 12:51-7.

15.    Goldstein DE, Little RR, Wiedmeyer HM, England JD, McKenzie EM. Glycated hemoglobin: methodologies and clinical applications. Clin Chem. 1986 Oct; 32(10 Suppl): B64-70.

16.    Viberti GC, Hill RD, Jarrett RJ, Argyropoulos A, Mahmud U, Keen H. Microalbuminuria as a predictor of clinical nephropathy in insulin-dependent diabetes mellitus. Lancet. 1982 Jun 26; 1(8287): 1430-2.

17.    Karsidag S, Morali S, Sargin M, Salman S, Karsidag K, Us O. The electrophysiological findings of subclinical neuropathy in patients with recently diagnosed type 1 diabetes mellitus. Diabetes Res Clin Pract. 2005 Mar; 67(3):211-9.

18.    Nelson D, Mah JK, Adams C, Hui S, Crawford S, Darwish H, et al. Comparison of conventional and non-invasive techniques for the early identification of diabetic neuropathy in children and adolescents with type 1 diabetes. Pediatr Diabetes. 2006 Dec; 7(6): 305-10.

19.    Garcia A, Calleja J, Antolin FM, Berciano J. Peripheral motor and sensory nerve conduction studies in normal infants and children. Clin Neurophysiol. 2000 Mar; 111(3): 513-20.

20.    Meh D, Denislic M. Subclinical neuropathy in type I diabetic children. Electroencephalogr Clin Neurophysiol. 1998 Jun; 109(3): 274-80.

21.    Hamano H, Hori M, Hamano T, Mitsunaga S, Maeshima J, Kojima S, et al. A new method for measuring tears. CLAO J. 1983 Jul-Sep; 9(3): 281-9.

22.    Miyata K, Amano S, Sawa M, Nishida T. A novel grading method for superficial punctate keratopathy magnitude and its correlation with corneal epithelial permeability. Arch Ophthalmol. 2003 Nov; 121(11): 1537-9.

23.    Sood S, Shukla R, Nad M, Khurana AK, Arora B. Comparison of tear film profile, conjunctival impression cytology, and conjunctival biopsy in patients with dry eye. Asian J Ophthalmol. 2006; 8(1): 24-7.

24.    Quattrini C, Tavakoli M, Jeziorska M, Kallinikos P, Tesfaye S, Finnigan J, et al. Surrogate markers of small fiber damage in human diabetic neuropathy. Diabetes. 2007 Aug; 56(8): 2148-54.

25.    Malik RA, Tesfaye S, Newrick PG, Walker D, Rajbhandari SM, Siddique I, et al. Sural nerve pathology in diabetic patients with minimal but progressive neuropathy. Diabetologia. 2005 Mar; 48(3): 578-85.

26.    Smith AG, Howard JR, Kroll R, Ramachandran P, Hauer P, Singleton JR, et al. The reliability of skin biopsy with measurement of intraepidermal nerve fiber density. J Neurol Sci. 2005 Jan 15; 228(1): 65-9.

27.    Mojaddidi M, Quattrini C, Tavakoli M, Malik RA. Recent developments in the assessment of efficacy in clinical trials of diabetic neuropathy. Curr Diab Rep. 2005 Dec; 5(6): 417-22.

28.    Messmer EM, Schmid-Tannwald C, Zapp D, Kampik A. In vivo confocal microscopy of corneal small fiber damage in diabetes mellitus. Graefes Arch Clin Exp Ophthalmol. 2010 Sep; 248(9): 1307-12.

29.    Kaiserman I, Kaiserman N, Nakar S, Vinker S. Dry eye in diabetic patients. Am J Ophthalmol. 2005 Mar; 139(3): 498-503.

30.    Goebbels M. Tear secretion and tear film function in insulin dependent diabetics. Br J Ophthalmol. 2000 Jan; 84(1): 19-21.

31.    Dyck PJ, Karnes JL, Daube J, O'Brien P, Service FJ. Clinical and neuropathological criteria for the diagnosis and staging of diabetic polyneuropathy. Brain. 1985 Dec; 108 ( Pt 4): 861-80.

32.    Rahman M, Griffin SJ, Rathmann W, Wareham NJ. How should peripheral neuropathy be assessed in people with diabetes in primary care? A population-based comparison of four measures. Diabet Med. 2003 May; 20(5): 368-74.

الملخص العربى


العلاقة بين اعتلال الأعصاب الطرفية واضطرابات سطح العين فى الأطفال

والمراهقين المصابين بمرض السكر من النوع 1


مقدمة :

العلاقة بين اعتلال الأعصاب الطرفية، واضطرابات القرنية، وطبقة الدمع في مرضى السكر من النوع 1 لها دلالات إكلينيكية هامة، لذا الهدف من هذه الدراسة هو تقييم الخواص الإكلينيكية لاعتلال الأعصاب الطرفية فى الأطفال والمراهقين المصابين بمرض السكر من النوع الأول وعلاقته باضطرابات سطح العين.


طريقة الدراسة :

اشتملت الدراسة علي أربعين مريض بداء السكر من النوع 1، متوسط أعمارهم 13.5±2.78 سنة، حيث تم أخذ تاريخ كامل للمرض، وإجراء فحص طبي كامل، وقياس مستوي السكر العشوائي بالدم، ومستوي الهيموجلوبين المسكر، وفحص قاع العين، وقياس الألبومين الدقيق بالبول، وعمل رسم الأعصاب، وتم عمل تقييم لأمراض سطح العين الذي يتضمن عمل اختبارات لقياس كمية الدموع، وعمل مسحة خلوية للعين لتشخيص جفاف العين لمجموعة المرضي ومقارنتها بعشرين من الأصحاء، وأيضا تم تقسيم المرضى الى مجموعتين حسب وجود اعتلال الأعصاب الطرفية، مع إجراء مقارنة بينهما.


النتائج :

أظهرت الدراسة شيوع أمراض سطح العين منها اعتلال القرنية وجفاف العين  لدى مرضى السكر من النوع 1 ، كما دل اختلال اختبارات سطح العين المتعددة  بشكل واضح، كما أوضحت الدراسة إصابة 47% من مرضى السكر من النوع 1  باعتلال الأعصاب الطرفية، وأن اضطرابات سطح العين تتواجد لدى مرضى الأعصاب الطرفية أكثر من مرضى السكر الغير مصابين باعتلال الأعصاب الطرفية.



توضح هذه الدراسة أن اعتلال الأعصاب الطرفية يعتبر من المضاعفات الشائعة في الأطفال والمراهقين المصابين بمرض السكر من النوع 1، وتوضح ارتباطه بسن المريض، ومدة داء السكر، والمضاعفات الأخري  لمرض السكر، و أن حدوث اضطرابات سطح العين يرتبط باعتلال الأعصاب الطرفية .

2008 � Copyright The Egyptian Journal of Neurology,
Psychiatry and Neurosurgery. All rights reserved.

Powered By DOT IT