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PubMedDate not supplied

Elevated glycosylated hemoglobin in diabetic neuropathy.

Glycosylated hemoglobin (GHb) levels were measured in 36 patients with established symptomatic neuropathy and in an identical number of matched controls. Strict criteria were employed in the selection of subjects and all had neuropathy of at least 12 months' duration. The diagnosis of neuropathy was supported by estimation of motor conduction velocities and vibration perception threshold. A semi-automated colorimetric technique, employing the reaction between thiobarbituric acid and 5-hydroxy-methyl furfural, was used for the estimation of GHb. Those patients with neuropathy had significantly higher GHb levels (58.2 +/- 11.3 mmol HMF/mol Hb) than the controls (50.0 +/- 8.9 mmol HMF/mol Hb) (p less than 0.01). This suggests that hyperglycemia or related metabolic abnormalities are important factors in established symptomatic neuropathy.

Diabetes Mellitus↗

PubMed1984

Influence of continuous subcutaneous insulin infusion (CSII) treatment on diabetic somatic and autonomic neuropathy.

Near-normal plasma daily glucose profile was induced by Continuous Subcutaneous Insulin Infusion (CSII) treatment in order to evaluate its influence on diabetic somatic and autonomic neuropathy. Twelve insulin-dependent diabetic subjects with somatic neuropathy were studied before and after a short term CSII treatment of 10 days. Four out of these subjects, all affected by autonomic neuropathy, were followed for 1 yr with controls every four months. Metabolic equilibrium was monitored by mean daily plasma glucose (MPDG) profile and by Glycosylated Hemoglobin (GHb) evaluation. Somatic neuropathy was studied assessing conduction velocity at peroneal motor (PMCV) nerve, ulnar motor (UMCV), ulnar sensory (USCV) and sural sensory (SSCV) nerves. Autonomic neuropathy was assessed by means of a battery of five cardiovascular autonomic tests: Valsalva Manoeuvre (VR), Deep Breathing (DB), Lying-to-Standing (LS), Sustained HandGrip (SHG) and Postural Hypotension (PH). Short-term CSII treatment induced a near normalization of metabolic parameters, a significant improvement in VR (p less than 0.05) and DB (p less than 0.01) values, but no changes in NCV. The prolongation of CSII treatment in 4 subjects induced a significant (p less than 0.05) improvement in VR, DB and LS values and in PMCV and UMCV after 4 months. This improvement did not increase with the longer CSII treatment (1 yr).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed2000

Hypoglycaemic neuropathy: occurrence of axon terminals in plantar skin and plantar muscle of diabetic BB/Wor rats treated with insulin implants.

It is generally believed that diabetic neuropathy is due to chronic hyperglycaemia. However, experience from insulinoma patients and experimental studies show that hypoglycaemia may also cause neuropathy. Accordingly, the plantar nerves of diabetic eu-/hypoglycaemic BB/Wor rats treated with insulin implants exhibit a distinct neuropathy. To what extent hypoglycaemic neuropathy affects axon terminals in skin and muscle is unknown. In the present study we examine the occurrence of epidermal axon profiles and the neuropeptide calcitonin gene-related peptide (CGRP) in plantar skin, and of end plate axon terminals in a plantar muscle of diabetic BB/Wor rats subjected to long periods of hypoglycaemia. The number of protein gene product-immunoreactive axon profiles was found to be normal in heel skin biopsy specimens from eu-/hypoglycaemic rats, but many profiles were short and thin. The content of CGRP in the skin biopsy samples was significantly below normal. After staining with antibodies against the vesicular acetylcholine transporter protein, the occurrence of end plate axon terminals was significantly reduced in sections from the flexor hallucis brevis muscle of eu-/hypoglycaemic rats. Moreover, the end plate axon terminals tended to be abnormally small in these rats. We conclude that the hypoglycaemic neuropathy seen in plantar nerve trunks of diabetic BB/Wor rats treated with insulin implants is accompanied by mild alterations in the epidermal innervation of plantar skin and a more obviously abnormal nerve terminal pattern in plantar muscle.

Animals↗

PubMed2005

Sural nerve pathology in diabetic patients with minimal but progressive neuropathy.

AIMS/HYPOTHESIS: The early pathological features of human diabetic neuropathy are not clearly defined. Therefore we quantified nerve fibre and microvascular pathology in sural nerve biopsies from diabetic patients with minimal neuropathy. METHODS: Twelve diabetic patients underwent detailed assessment of neuropathy and fascicular sural nerve biopsy at baseline, with repeat assessment of neuropathy 8.7+/-0.6 years later. RESULTS: At baseline, neuropathic symptoms, neurological deficits, quantitative sensory testing, cardiac autonomic function and peripheral nerve electrophysiology showed minimal abnormality, which deteriorated at follow-up. Myelinated fibre density, fibre and axonal area, and g-ratio were normal but teased fibre studies showed paranodal abnormalities (p<0.001), segmental demyelination (p<0.01) and remyelination (p<0.01) without axonal degeneration. Unassociated Schwann cell profile density (p<0.04) and unmyelinated axon density (p<0.001) were increased and axon diameter was decreased (p<0.007). Endoneurial capillaries demonstrated basement membrane thickening (p<0.006), endothelial cell hyperplasia (p<0.004) and a reduction in luminal area (p<0.007). CONCLUSIONS/INTERPRETATION: The early pathological features of human diabetic neuropathy include an abnormality of the myelinated fibre Schwann cell and unmyelinated fibre degeneration with regeneration. These changes are accompanied by a significant endoneurial microangiopathy.

Axons↗

PubMed1996

Cation binding at the node of Ranvier in biopsied peripheral nerves of patients with Charcot-Marie-Tooth disease type 1A and hereditary neuropathy with liability to pressure palsies.

The node of Ranvier in myelinated fibers is known to have an affinity to bind cations. Demyelination and remyelination due to abnormal expression of a myelin protein may affect cation binding or vice versa under pathological conditions. To study the cation binding at the node of Ranvier in inherited demyelinating neuropathies associated with over- and under-expression of the peripheral myelin protein 22 (PMP-22), the reaction with ferric ion and ferrocyanide was used to visualize the cation binding sites in biopsied nerves of four patients with Charcot-Marie-Tooth disease type 1A (CMT1A) and two patients with hereditary neuropathy with liability to pressure palsies (HNPP), and the results were compared with those of four patients having acquired neuropathies with normal PMP-22 expression. In CMT1A, nodal widening or paranodal demyelination was associated with dense precipitates focally on both sides of the widened node. Although fainter precipitates were present at the node between remyelinated internodes, the percentage of nodes exhibiting the reaction product between normal and remyelinated internodes was not statistically different from that between normal internodes in CMT1A. In acquired neuropathies, on the other hand, the difference was significant between the two (P < 0.05), with reduction between normal and remyelinated internodes. At the nodes neighboring demylinated internodes, the percentage of nodes exhibiting the reaction product was reduced significantly in both CMT1A and acquired neuropathies, but to a lesser degree in CMT1A. Precipitates were clearly seen at the nodes neighboring a tomaculum in HNPP. The results suggest that preserved cation binding at the node may allow nerves to keep the electrical excitability in CMT1A and HNPP where myelin remodeling takes place at high frequency.

Adolescent↗

PubMed1998

Neuropathy in diabetic BB/Wor rats treated with insulin implants.

To elucidate the pathophysiology of diabetic neuropathy many workers have examined nerve specimens from diabetic rats. While most workers found that animals with high blood glucose levels develop neuropathy, some researchers report that the peripheral nerves are normal in hyperglycaemic rats. Hypoglycaemia may also cause neuropathy. Some workers suggest that neuropathy is linked to fluctuations of the blood glucose level. In the present study we examine plantar nerves of diabetic BB/Wor rats maintained on an eu-/hyperglycaemic or an eu-/hypoglycaemic regime with insulin implants. Treatment with implants worked well. Light microscopic examination of nerve fibres in non-diabetic control rats and in eu-/hyperglycaemic diabetic rats showed a normal picture. Preparations from eu-/hypoglycemic rats showed irregular myelin sheaths and signs of Wallerian degeneration. The lengths and diameters of the largest internodes were significantly subnormal. We conclude, that periodic moderate hypoglycaemia, but not periodic moderate hyperglycaemia, elicits neuropathy in diabetic BB/Wor rats treated with insulin implants.

Animals↗

PubMed2003

Diabetic neuropathy in patients with "latent autoimmune diabetes of the adults" (LADA) compared with patients with type 1 and type 2 diabetes.

OBJECTIVE: In previous studies, a lower incidence of diabetes-related complications such as diabetic neuropathy has been reported in patients with early stages of type 1 diabetes compared with type 2 diabetes. The aim of this study was to compare the prevalence of diabetic neuropathy in patients with manifestation of a slow onset type 1 diabetes in adulthood - latent autoimmune diabetes in adults (LADA) - with classical type 1 and type 2 diabetes patients. RESEARCH DESIGN AND METHODS: Altogether, 37 patients (14 LADA, 9 type 1 and 14 type 2 diabetes) with short term diabetes (duration < 5 years) were investigated for diabetic neuropathy on the basis of clinical and neuroelectrophysiological evaluations. The neurological functions were evaluated by a standardized questionnaire and clinical examination. In electrophysiological evaluations the different nerve fibres were investigated using motor and sensory nerve conduction studies, quantitative thermotesting, vibratometry and autonomic function tests (heart rate variability). RESULTS: LADA patients had a significantly lower clinical examination score (p = 0.008), cardiorespiratory reflex index (p = 0.009) and cold perception threshold index (p = 0.004). The neurological symptom score, the indices of motor and sensory nerve conduction, the index of thermotesting (warm perception threshold) and the vibratometry showed a trend to higher values in LADA patients than in type 2 diabetes patients. There were no significant differences between LADA and type 1 diabetes patients. CONCLUSIONS: LADA patients had fewer features of diabetic neuropathy than type 2 diabetes patients in the early stages of disease, thus being more similar to classical type 1 diabetes patients who normally develop diabetic neuropathy rather late.

Adult↗

PubMed2004

Differential diagnosis of Charcot-Marie-Tooth disease and related neuropathies.

The diagnosis of Charcot-Marie-Tooth disease (CMT) and related neuropathies (e. g. Déjèrine-Sottas disease; hereditary neuropathy with liability to pressure palsies) appears to be easy. However, the incredible advances in molecular genetics have greatly complicated the classification of these disorders, and the proper diagnosis of the CMT subtype may be important for correct genetic counselling and prognosis. Moreover, these diseases may be confused with potentially treatable acquired and inherited neuropathies, such as dysimmune neuropathies, familial amyloid polyneuropathy, and Refsum's disease. A number of clinical, laboratory, electrophysiological, morphological and neuroradiological features that may help in the diagnostic process are reviewed in the present paper. DNA investigations are fundamental but need to be properly addressed. Currently, great interest is focused on the role of the immune system in hereditary neuropathies, and surprising findings are coming from research on animal models.

Charcot-Marie-Tooth Disease↗

PubMed1995

Gosha-jinki-gan (herbal medicine) in streptozocin-induced diabetic neuropathy.

Long-established systems of traditional medicine have evolved from systematic recordings of human experience over several millennia. Although not strictly based on concepts of modern science, they nevertheless are founded on a corpus of organised knowledge written in documents, and the evident conclusion is that the alleged "trial and error" methodology has provided useful drugs for humans. Herbal medicine should be investigated as a potential regimen for diabetic neuropathy for the following reasons: (1) diabetic neuropathy remains an important clinical problem affecting a significant proportion of diabetic subjects without satisfactory treatment; (2) there are multiple pathogenetic mechanisms in diabetic neuropathy; and (3) herbal medicine which is a combination prescription has unique synergistic and synthetic effects that result from interactions between individual herbal components, and may induce a wide range of therapeutic potential and utility. Gosha-jinki-gan (GJK), consisting of 10 herbs, has been widely used for a regimen of diabetic complications, including neuropathy, in Japan. However, the effect of GJK on experimental diabetic neuropathy has never been previously evaluated. We examined nerve conduction velocity (NCV) and nerve glucose, sorbitol, fructose and myo-inositol levels in streptozocin (STZ)-induced diabetic rats that were treated with GJK. After 1 week of the STZ injection in 7-9-week-old rats, GJK treatment (100 mg/100 g body weight/day) was started orally. At 16 weeks after the STZ injection, the sciatic NCV of GJK-treated diabetic rats improved significantly when compared to non-treated diabetic rats, although they were not yet normalised.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1996

Sympathetic skin response in diabetic neuropathy: a prospective clinical and neurophysiological trial on 100 patients.

Sympathetic skin response (SSR) can be employed to assess axonal damage of sympathetic sudomotor neurons in neuropathy. We examined a population of 100 patients with diabetic neuropathy, and 100 age- and sex-matched healthy volunteers. SSR was recorded from the skin of the hand and foot by means of surface electrodes. Stimulation was applied with 30 mA over the median nerve at the wrist contralateral to the derivation site. Irregular interstimulus intervals of more than one minute were applied. Peak-to-peak amplitude measurement showed values of 2.91 +/- 1.10 mV on the hand and 1.37 +/- 0.54 mV on the foot. Latencies lasted 1.44 +/- 0.10 s on the hand and 2.12 +/- 0.15 s on the foot. A total of 37% of the diabetics showed loss of SSR, a further 39% showed amplitude reductions or latency prolongations: Altogether, 76% of all diabetics did not show normal test results. The clinical stage of diabetic neuropathy exerted a significant influence: the further developed the clinical picture of the disease was, the more pathologic were the results of SSR testing. However, even at early stages of neuropathy abnormal values of amplitude reduction or latency prolongation could be observed in over 50% of the patients. SSR examinations performed in diabetics with no or only slight clinical signs of neuropathy may be able to detect those subjects with autonomic disturbances at an initial stage.

Adolescent↗

PubMed1995

Implication of insulin-like growth factors in the pathogenesis of diabetic neuropathy.

Neuropathy can be a highly debilitating complication for about 10-15% of diabetic individuals. Unfortunately, the complex syndrome has proven difficult to explain and a consensus as to its cause has not emerged. It has recently come to light that insulin and insulin-like growth factors (IGFs) have neurotrophic actions on sensory, sympathetic and motor neurons. These are the main types of neurons afflicted in this disorder. Moreover, IGF activity is reduced in both clinical and experimental diabetes. The premise that insulin, IGF-I and IGF-II provide redundant neurotrophic support underlies the following new theory for pathogenesis of diabetic neural disturbances: a loss of insulin activity leads to a secondary partial decline in IGF-I activity. Although most of the redundant neurotrophic support is thereby eliminated, IGF-II activity continues to support the nervous system. The final enemy is time and the relentless age- and duration-dependent run-down of IGF activity is suggested to contribute to the age- and duration-dependent neuropathy. Weight loss or anorexia nervosa are independent risk factors that can cause a rapid, painful neuropathy to develop as a result of a rapid loss of IGF activity. A distinguishing feature of this new theory is that hyperglycemia is not considered to be the main culprit. The following critical predictions from the theory were tested in diabetic rats: (i) IGF activity is reduced in diabetic neural tissues; (ii) conduction velocity is impaired in the diabetic spinal cord; (iii) replacement therapy with IGF can prevent neuropathy in diabetic nerves; and (iv) IGFs can prevent diabetic neuropathy, despite hyperglycemia. All of these predictions have been validated. It is hoped that a fresh perspective will stimulate renewed study into the causation of this most unfortunate disorder.

Age Factors↗

PubMed1990

Erythrocytes from diabetics with neuropathy have fewer sodium pumps.

Erythrocytes from diabetics with neuropathy had fewer binding sites for ouabain and, therefore, fewer sodium pumps than did erythrocytes from diabetics without neuropathy or from age-matched controls (P less than 0.001). Diabetics with neuropathy excreted in their urine significantly less C-peptide immunoreactivity (CPR) than those without neuropathy, which is a sign of lower endogenous insulin secretion levels. Significant positive correlations existed between the number of pumps and tibial motor nerve conduction velocity (MNCV) and urinary CPR in diabetics, and between urinary CPR and MNCV. This suggests that there is close correlation between the fall in the number of pumps in diabetics and diabetic neuropathy and insulin deficiency.

Biomarkers↗

PubMed1992

Lower limb arterio-venous shunts, autonomic neuropathy and diabetic foot.

We have quantitatively assessed the percentage of lower limb arterio-venous (a-v) shunting using a radioisotopic technique and correlated it with autonomic neuropathy evaluated by cardiovascular tests. We have studied three groups of diabetic patients: Group A, 12 non-neuropathic subjects without foot lesions; Group B, 12 neuropathic subjects without foot lesions; Group C, 12 neuropathic subjects with recurrent foot ulcers. Shunting was higher in Group C (10.4 +/- 2.7%) than in Group B (6.8 +/- 2.3%, P less than 0.01) and Group A (3.8 +/- 1.2%, P less than 0.001). Shunts in Group B were higher than in Group A (P less than 0.05). All the tests exploring autonomic function were more impaired in Groups B and C than in Group A, with no difference between Groups B and C. A direct correlation was found between a-v shunting and the following cardiovascular tests: postural hypotension (PH) (r = 0.41, P less than 0.02), sustained handgrip (SH) (r = 0.56, P less than 0.001), deep breathing (DB) (r = 0.40, P less than 0.005) and lying to standing (LS) (r = 0.44, P less than 0.01). A positive correlation was also found between a-v shunts and duration of the disease (r = 0.62, P less than 0.001). Arterio-venous shunting was found to be directly related to autonomic neuropathy even if the higher shunting found in the patients with foot ulcers was not related to a higher degree of autonomic involvement; in addition, this group of patients was characterized by having a more advanced sensory and motor neuropathy. In conclusion, autonomic neuropathy, through its influence on a-v shunts, may play a role in the pathogenesis of diabetic foot, but peripheral neuropathy probably plays a key role in conditioning the development of the overt clinical manifestations of diabetic foot.

Albuminuria↗

PubMed1992

Profound vasoconstrictive effect of cigarette smoking in diabetics with autonomic neuropathy.

Changes in leg skin temperature during and after cigarette smoking were examined in 25 diabetics with autonomic neuropathy (au-neuropathy) (mean age 52 +/- 2 years) and 23 without (mean age 49 +/- 2 years), and 15 normal controls (mean age 49 +/- 2 years) using a Thermoviewer JTG 3300. All subjects were habitual smokers. Japanese Seven Star cigarettes (each containing 1.2 mg nicotine) were used for the test. Tender brand cigarettes (0.3 mg) were used additionally to compare the effect of nicotine content on the results. The smoking-stimulated thermographic pattern in the control group was rather flat, with a slight decrease in temperature followed by a slight increase before returning to the baseline level 15-20 min after smoking. The frequency of the typical temperature decreasing pattern, characterized by a profound decrease and gradual return to the baseline level in about 1 h, was significantly higher in the diabetic group than in the control group (33/48 vs 1/15; P less than 0.005). A comparison of the two diabetic subgroups revealed that the frequency was considerably higher in the subgroup with au-neuropathy (23/25 vs 10/23). These results suggest that au-neuropathy affects smoking-induced vasoconstriction in diabetic subjects. The maximum temperature decreases recorded were 1.5 +/- 2.0 and 2.69 +/- 0.24 degrees C in the controls and diabetics with au-neuropathy, respectively. The effect of Tender cigarettes with a low nicotine content was much weaker than that of Seven Star, which further suggests that smoking-induced vasoconstriction was also nicotine-dependent.

Diabetic Angiopathies↗

PubMed1994

Somatosensory evoked potentials in non-insulin-dependent diabetics with different degrees of neuropathy.

Changes in median nerve somatosensory evoked potential (SEP) in diabetic patients have amply been reported. However the relationships between the diabetic polyneuropathy and the abnormalities of SEPs are still a matter of discussion. To elucidate these relationships, we have studied SEPs in 38 non-insulin-dependent diabetics with mild or severe degree of peripheral neuropathy. Our principal findings are as follows. (i) The wrist-Erb point (EP) conduction velocity (WECV) and the EP-N13 interpeak latency are significantly altered in diabetics. The N11-N13, N13-N20 and N13-P22, interpeak latencies are within the normal range. (ii) The WECV is more reduced in patients with severe neuropathy than in those with mild neuropathy, whereas the degrees of neuropathy have no influence on the alterations of EP-N13 interpeak latency. (iii) No significant correlation is found between the WECV and the EP-N13 interpeak latency. (iv) The WE conduction velocity was significantly correlated with both motor and sensory peripheral nerve conduction velocities. On the contrary, no correlation is found between these latter peripheral parameters and the EP-N13 interpeak latency. These findings indicate that the alteration in the tract from brachial plexus to the posterior column could not be a parallel process of distal neuropathy of non-insulin-dependent diabetic patients.

Adult↗

PubMed2006

Medial calcaneal neuropathy is associated with plantar fasciitis.

OBJECTIVE: To demonstrate a method of sensory nerve conduction study (NCS) for the medial calcaneal nerve (MCN) and confirm the medial calcaneal neuropathy in patients with plantar fasciitis (PF). METHODS: Twenty-six patients with clinical and ultrasonographic diagnosis of PF participated in the present study. An antidromic method for sensory NCS of MCN was performed in each patient and in 30 controls. The conduction latency, sensory nerve conduction velocity (SNCV) and amplitude of the sensory nerve action potential (SNAP) were measured and the correlation of the SNCV of MCN with both body weight and body mass index (BMI) was studied. RESULTS: The mean conduction latency obtained in the MCN was greater in the PF patients than in the normal controls. Mean SNCV and SNAP amplitude of the MCN were significantly less in the PF patients than in the normal controls. Body weight and BMI were greater in PF patients than in controls. Six patients were identified as having a medial calcaneal neuropathy by using the criteria of the lowest normal values of the NCS of MCN from the normal controls. CONCLUSIONS: Medial calcaneal neuropathy is associated with PF. The present method of sensory NCS is useful and objective in the diagnosis of the medial calcaneal neuropathy. SIGNIFICANCE: Medial calcaneal neuropathy was confirmed by the sensory NCS of MCN and shown to be associated with PF.

Calcaneus↗

PubMed2004

Can diabetic neuropathy be prevented?

The incidence of diabetes and its complication have rapidly increased. Decreased quality of life and increased mortality are the major problems of people with diabetes. These problems are mainly caused by chronic complications. The incidence of diabetic neuropathy, which is one of these chronic complications, approaches 50% in most diabetic patients. The intensive metabolic management alone cannot completely prevent the development and progression of diabetic complications. Therefore, blocking and management of pathogenic mechanism of complication are required. Pathogenesis of diabetic neuropathy has multifactorial causes. Diabetic neuropathy is thought to occur both from direct hyperglycemia-induced damage to the nerve parenchyma and from neuronal ischemia brought about indirectly by hyperglycemia-induced decreases in neurovascular flow. The effects of hyperglycemia get converted to neuronal dysfunction via at least three secondary biochemical pathways: the polyol pathway, non-enzymatic glycation of proteins, oxidative stress and protein kinase C, and the interactions between them. Because of these interactions, interference with one of these biochemical pathways could either worsen or attenuate the effects of the others. So, the use of therapeutic intervention of these pathways is inevitable and valid to prevent the progression of diabetic neuropathy. As yet, a satisfactory and fundamental, preventive, and therapeutic method is not available with us to prevent progression. So, we will introduce the earlier diagnostic methods of diabetic neuropathy and will discuss the advantages and limitations of each method.

Diabetic Neuropathies↗

PubMed2004

Pupillography refines the diagnosis of diabetic autonomic neuropathy.

Although diabetic autonomic neuropathy involves most organs, diagnosis is largely based on cardiovascular tests. Light reflex pupillography (LRP) non-invasively evaluates pupillary autonomic function. We tested whether LRP demonstrates autonomic pupillary dysfunction in diabetics independently from cardiac autonomic neuropathy (CAN) or peripheral neuropathy (PN). In 36 type-II diabetics (39-84 years) and 36 controls (35-78 years), we performed LRP. We determined diameter (PD), early and late re-dilation velocities (DV) as sympathetic parameters and reflex amplitude (RA) and constriction velocity (CV) as parasympathetic pupillary indices. We assessed the frequency of CAN using heart rate variability tests and evaluated the frequency of PN using neurological examination, nerve conduction studies, thermal and vibratory threshold determination. Twenty-eight (77.8%) patients had abnormal pupillography results, but only 20 patients (56%) had signs of PN or CAN. In nine patients with PN, only pupillography identified autonomic neuropathy. Four patients had pupillary dysfunction but no CAN or PN. In comparison to controls, patients had reduced PD, late DV, RA and CV indicating sympathetic and parasympathetic dysfunction. The incidence and severity of pupillary abnormalities did not differ between patients with and without CAN or PN. LRP demonstrates sympathetic and parasympathetic pupillary dysfunction independently from PN or CAN and thus refines the diagnosis of autonomic neuropathy in type-II diabetics.

Adult↗