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PubMed2006

Effects of U83836E on nerve functions, hyperalgesia and oxidative stress in experimental diabetic neuropathy.

Oxidative stress has been implicated to play an important role in the pathogenesis of diabetic neuropathy, which is the most common complication of diabetes mellitus affecting more than 50% of diabetic patients. In the present study, we have investigated the effect of U83836E [(-)-2-((4-(2,6-Di-1-pyrrolidinyl-4-pyrimidinyl)-1-piperazinyl)methyl)-3,4-dihydro-2,3,7,8-tetramethyl-2H-1-benzopyran-6-ol, 2HCl], a potent free radical scavenger in streptozotocin (STZ)-induced diabetic neuropathy in rats. STZ-induced diabetic rats showed significant deficit in motor nerve conduction velocity (MNCV), nerve blood flow (NBF) and thermal hyperalgesia after 8 weeks of diabetes induction, indicating development of diabetic neuropathy. Antioxidant enzyme (superoxide dismutase and catalase) levels were reduced and malondialdehyde (MDA) levels were significantly increased in diabetic rats as compared to the age-matched control rats, this indicates the involvement of oxidative stress in diabetic neuropathy. The 2-week treatment with U83836E (3 and 9 mg/kg, i.p.) started 6 weeks after diabetes induction significantly ameliorated the alterations in MNCV, NBF, hyperalgesia, MDA levels and antioxidant enzymes in diabetic rats. Results of the present study suggest the potential of U83836E in treatment of diabetic neuropathy.

Animals↗
PubMed2005

A family with a novel frameshift mutation in the PMP22 gene (c.433_434insC) causing a phenotype of hereditary neuropathy with liability to pressure palsies.

Hereditary neuropathy with liability to pressure palsies is usually due to PMP22 deletion. Point mutations of PMP22 causing an hereditary neuropathy with liability to pressure palsies phenotype are rare. We describe a clinical and electrodiagnostic phenotype of hereditary neuropathy with liability to pressure palsies in a 21-year-old woman, which led to our detecting a novel frameshift mutation of PMP22. This mutation was also found in her mother and brother and corresponded to an insertion of one cytidine between nucleotides 433 and 434 in the last coding exon (c.433_434insC). The mutated PMP22 protein lacks the last 15 amino acids and has a modified C terminus lengthened to 221 residues instead of 160 (Leu145fsX222). The mother and the proband had a clinical and electrophysiological hereditary neuropathy with liability to pressure palsies phenotype. The brother was asymptomatic, but the results of electrodiagnostic tests were suggestive of hereditary neuropathy with liability to pressure palsies. This observation of a new mutation mostly leading to a PMP22 haploinsufficiency provides further evidence of the diversity of phenotypes associated with frameshift PMP22 mutations.

Adult↗
PubMed2001

Internal carotid artery hypoplasia presenting as anterior ischemic optic neuropathy.

PURPOSE: To describe the occurrence of anterior ischemic optic neuropathy in a young woman with internal carotid artery hypoplasia. METHODS: Case report with clinical and radiologic observations. RESULTS: A 38-year-old woman suffered from a sudden, painless loss of vision in her right eye. The diagnosis of anterior ischemic optic neuropathy was based on the clinical course and appearance of the fundus. Doppler evaluation of the carotid arteries, computed tomography (CT) scan, magnetic resonance imaging (MRI), and CT angiogram all demonstrated internal carotid artery hypoplasia on the same side. CONCLUSION: Although carotid artery disease (mainly atherosclerosis) is not a common predisposing factor for anterior ischemic optic neuropathy, our patient had an ipsilateral coexisting internal carotid artery hypoplasia and anterior ischemic optic neuropathy. We believe that the carotid artery anomaly might have contributed to the development of anterior ischemic optic neuropathy in this patient.

Adult↗
PubMed1997

Incidence of nonarteritic anterior ischemic optic neuropathy.

PURPOSE: Nonarteritic anterior ischemic optic neuropathy is the most common acute optic nerve disease of adults over age 50 years. This study determined the incidence of acute nonarteritic anterior ischemic optic neuropathy in the circumscribed population of Olmsted County, Minnesota. METHODS: This was a retrospective study of the incidence of acute nonarteritic anterior ischemic optic neuropathy between 1981 and 1990. The Rochester Epidemiology Project medical records linkage system facilitates identification of the medical records of virtually all Olmsted County residents with a given diagnosis. All cases of acute nonarteritic anterior ischemic optic neuropathy that fulfilled certain inclusion and exclusion criteria were identified. RESULTS: Twenty-two cases in 21 patients (11 men and 10 women) were recorded. The crude annual incidence rate was 10.3 per 100,000 individuals (95% confidence interval [CI] = 5.1 to 18.4). When adjusted to the age and sex distribution of the 1990 United States white population, the incidence rate was 10.2 per 100,000 (95% CI = 6.5 to 15.6). At diagnosis, the median age was 72 years, mean visual acuity was 20/200 in the affected eye, and the most common visual field defect was an altitudinal deficit (10 cases). CONCLUSIONS: Although results of this small study should be interpreted cautiously, extrapolation of our findings to the United States white population indicates that nearly 5,700 new cases of acute nonarteritic anterior ischemic optic neuropathy may be expected to occur each year in this group.

Aged↗
PubMed1995

Cardiovascular autonomic neuropathy and proliferative diabetic retinopathy.

PURPOSE: To determine prospectively whether cardiovascular autonomic neuropathy is a risk factor for proliferative diabetic retinopathy. METHODS: A five-year follow-up study of 88 diabetic persons was performed at a center providing primary and specialized care for diabetes. Participants were white, insulin-dependent patients with diabetes of 15 to 21 years' duration. The primary end point was the presence of proliferative diabetic retinopathy, seen either on fundus photography or ophthalmologic examination. Cardiovascular autonomic neuropathy was measured at baseline by using a standard protocol. RESULTS: Fourteen patients developed proliferative diabetic retinopathy during follow-up. One measure of cardiovascular autonomic neuropathy, the 30:15 ratio, the heart rate variation at the 30th beat compared with that at the 15th beat, was lower among patients with proliferative diabetic retinopathy (P = .0049) The risk of proliferative diabetic retinopathy in patients with an abnormal cardiovascular autonomic neuropathy index was 2.59, although the estimate was not statistically significant because of the small number of patients who developed proliferative diabetic retinopathy. CONCLUSIONS: This study provides prospective evidence that cardiovascular autonomic neuropathy is associated with proliferative diabetic retinopathy. In addition to ocular determinants of proliferative diabetic retinopathy, systemic risk factors also should be considered when examining patients with diabetes mellitus.

Adolescent↗
PubMed1999

Anterior ischemic optic neuropathy following the use of a nasal decongestant.

PURPOSE: To report a case of sequential anterior ischemic optic neuropathy temporally related to the sequential use of a decongestant nasal spray. METHODS: A 43-year-old woman was evaluated for sequential bilateral vision loss following the use of oxymetazoline nasal spray. RESULTS: Thorough investigation of possible etiologies causing the bilateral anterior ischemic optic neuropathy was negative. Our patient had several predisposing risk factors for ischemic optic neuropathy, including diabetes mellitus, hypertension, and crowded optic nerve heads. Before each acute optic neuropathy, the patient used two to three puffs of oxymetazoline nasal spray. CONCLUSION: Decongestants have been associated with ischemic and hemorrhagic vascular events. Vasoconstriction secondary to oxymetazoline use may precipitate anterior ischemic optic neuropathy.

Acute Disease↗
PubMed1996

Diabetic sensory neuropathy effect on ankle joint movement perception.

OBJECTIVE: To determine if diabetic subjects with lower extremity cutaneous sensory neuropathy also have a loss of ankle joint movement perception. The strength of association between measurements of ankle joint movement perception and measures of cutaneous sensory function was also investigated. DESIGN: Diabetic subjects with and without sensory neuropathy and individuals without diabetes participated in this study. SETTING: All subjects were community-living individuals. PARTICIPANTS: Fifty-one subjects, ages 40 to 68. Seventeen of the 34 subjects with diabetes had significant distal sensory neuropathy as determined by cutaneous perception of mechanical vibration. All individuals without diabetes were volunteers from the community. Most subjects with diabetes were recruited through direct referral from their physicians. INTERVENTIONS: Ankle joint movement perception threshold (JMPT) was assessed using a device designed for this study. Cutaneous sensory function under both halluces was measured for vibration perception using a vibrometer and for touch-pressure perception using Semmes-Weinstein monofilaments. MAIN OUTCOME MEASURES: Ankle JMPTs (degrees) were compared to measurements of cutaneous vibration perception (volts) and touch-pressure perception (monofilaments force ratings). RESULTS: Diabetic subjects with cutaneous sensory neuropathy demonstrated a significant loss of ankle movement perception (p < .01). Correlation between JMPT and cutaneous sensory tests ranged from Spearman's rank r = .43 to .67. CONCLUSIONS: Although individuals with cutaneous sensory loss secondary to diabetic neuropathy also demonstrated loss of movement perception at the ankle, the relatively low explained variance between the two types of assessment (18% to 45%) indicates that the severity of ankle joint movement perception deficits cannot be directly implied from cutaneous sensory tests.

Adult↗
PubMed2000

Atypical features prompting neuroimaging in acute optic neuropathy in adults.

BACKGROUND: Acute optic neuropathy due to an intracranial lesion may masquerade as optic neuritis or nonarteritic anterior ischemic optic neuropathy (NAION). We reviewed the records of patients who presented with acute unilateral optic neuropathy that was initially diagnosed as optic neuritis or NAION but who ultimately proved to have an underlying structural lesion. METHODS: Retrospective observational case series. We reviewed the records of patients with the initial diagnosis of optic neuritis or NAION in whom the diagnosis was changed to an intracranial etiology at four tertiary care neuro-ophthalmology centres between 1995 and 1998. RESULTS: Eight cases were identified in which atypical features prompted further investigation, including neuroimaging, leading to the diagnosis of an intracranial etiology for the optic neuropathy. Five patients were discovered to have neoplasms (a tuberculum sellae meningioma in two cases, an optic nerve sheath meningioma in two cases and a metastatic lesion in one case), and three patients had intracranial sarcoidosis. Atypical features for optic neuritis included a progressive course, absence of pain, optic atrophy at presentation, lack of significant visual improvement and age over 40 years. For NAION, the atypical features included progressive course, optic atrophy on presentation, absence of vasculopathic risk factors and preceding transient visual loss. INTERPRETATION: Clinicians should be aware that patients with intracranial lesions may present with acute optic neuropathy mimicking optic neuritis or NAION and that certain atypical features should warrant consideration for neuroimaging.

Acute Disease↗
PubMed1997

Perineurium talin immunoreactivity decreases in diabetic neuropathy.

We studied the immunolocalization of Dp116 (a 116 kDa protein product of the dystrophin gene), vinculin, talin, vimentin, desmin, spectrin and titin in the sural nerve biopsies of 25 patients with peripheral neuropathies of different origin. 4 patients presented with HMSN type 1, 4 with HMSN type 2, 2 with HNPP, 4 with CIDP, 5 with chronic axonal neuropathy of unknown origin, 3 with vasculitic neuropathy, 3 with diabetic neuropathy. Expression and localization of Dp116, vinculin, vimentin, desmin, spectrin and titin did not differ from normal control cases. Spectrin and titin immunoreactivities were absent and desmin was occasionally found in few epineurial vessels. A thin rim of Dp116 binding surrounded the outermost layer of myelin sheaths. Perineurium and epineurial vessels stained deeply for vinculin. Vimentin immunoreactivity was seen in all endoneurial, perineurial and epineurial cells. Immunoreactivity for talin was normally found at endoneurial and epineurial vessel walls, perineurial cells and epineurial fibroblasts in all the sural nerves except diabetic nerves. In the latter, whereas talin binding was normal in the vessel walls and epineurial fibroblasts, it was markedly reduced in the perineurium. On immunoblot, two bands at 235 and 190 kDa were found in the sural nerves with the antibody anti-talin, and both were reduced only in the patients with diabetic neuropathy. We postulate that decreased perineurium talin in diabetic polyneuropathy may be related to the known alterations of the tight junctions of the perineurial cells, which have been proposed to be a contributory factor to impaired permeability barrier properties.

Case-Control Studies↗
PubMed2002

Neuropathology and pathogenesis of diabetic autonomic neuropathy.

Autonomic neuropathy is a significant complication of diabetes resulting in increased patient morbidity and mortality. A number of studies, which have shown correspondence between neuropathologic findings in experimental animals and human subjects, have demonstrated that axonal and dendritic pathology in sympathetic ganglia in the absence of significant neuron loss represents a neuropathologic hallmark of diabetic autonomic neuropathy. A recurring theme in sympathetic ganglia, as well as in the pot-ganglionic autonomic innervation of various end organs, is the involvement of distal portions of axons and nerve terminals by degenerative or dystrophic changes. In both animals and humans, there is a surprising selectivity of the diabetic process for subpopulations of autonomic ganglia, nerve terminals within sympathetic ganglia and end organs, from end organ to end organ, and between vascular and other targets within individual end organs. Although the involvement or autonomic axons in somatic nerves may reflect an ischemic pathogenesis, the selectivity of the diabetic process confounds simple global explanations of diabetic autonomic neuropathy as the result of diminished blood flow with resultant tissue hypoxia. A single unifying pathogenetic hypothesis has not yet emerged from clinical and experimental animal studies, and it is likely that diabetic autonomic neuropathy will be shown to have multiple causative mechanisms, which will interact to result in the variety of presentations of autonomic injury in diabetes. Some of these mechanisms will be shared with aging changes in the autonomic nervous system. The role of various neurotrophic substances and the polyol pathway in the pathogenesis and treatment of diabetic neuropathy likely represents a two-edged sword with both salutary and exacerbating effects. The basic neurobiologic process underlying the diabetes-induced development of neuroaxonal dystrophy, synaptic dysplasia, defective axonal regeneration, and alterations in neurotrophic substance may be mechanistically related.

Animals↗
PubMed2000

Ca(2+)-Mg(2+)-ATPase activity and ionized calcium in Type 2 diabetic patients with neuropathy.

Ca(2+)-Mg(2+)-ATPase is an important regulator of intracellular calcium concentration and therefore, of erythrocyte deformability. We have investigated the possible relationship between Ca(2+)-Mg(2+)-ATPase activity (ATPase) and ionized calcium (Ca(2+)), in diabetic patients with peripheral neuropathy. A total of 104 Type 2 diabetic patients (57 neuropathic and 47 non-neuropathic) and 25 non-diabetic subjects were studied. After an overnight fast, blood was taken for Ca(2+)-Mg(2+)-ATPase activity, Ca(2+), Mg(2+), PTH and HbA(1c). The neuropathy study group had significantly lower levels of ATPase, 6.6 (95% CI, 5.6-7.7) nmol/mg/min compared to controls 7. 1 (6.2-8.3) nmol/mg/min, P<0.001 and to diabetic patients without neuropathy 7.0 (6.0-8.1) nmol/mg/min, P<0.001. The study group had also lower levels of Ca(2+) (0.89+/-0.18 mmol/l vs. control 1.08+/-0. 24 mmol/l, P<0.01 and non-neuropathic 0.98+/-0.27 mmol/l, P<0.05) and Mg(2+) (0.73+/-0.13 mmol/l vs. control 0.81+/-0.14 mmol/l, P<0. 05), despite similar PTH levels. In diabetic subjects, no correlation was found between ATPase or Ca(2+) with glucose, HbA(1c), age or duration of diabetes. We conclude that in patients with diabetic neuropathy there are abnormalities of Ca(2+)-Mg(2+)-ATPase activity and Ca(2+). This provides further support for the role of microangiopathy in the pathogenesis of neuropathy.

Blood Glucose↗
PubMed2001

Evaluation of three screening tests and a risk assessment model for diagnosing peripheral neuropathy in the diabetes clinic.

OBJECTIVE: with the aim of evaluating predictive power, three simple screening tests as alternates to nerve conduction tests for diagnosing diabetic peripheral neuropathy (DPN) were investigated. Results of the screening tests, along with the subjects' demographic and clinical characteristics, were planned as the variables for the development of a risk assessment tool for predicting DPN. DESIGN: this is a cross-sectional multi-group comparison study. The study utilized a predictive model derived from one subset of the study population, and prospectively tested in the other subset to predict the presence of neuropathy. SETTING: Diabetic Neuropathy Research Clinic of the Toronto General Hospital and University Health Network in Toronto, Ontario, Canada from June 1998 to August 1999. SAMPLE POPULATION: data come from 478 subjects consisting of non-diabetic reference subjects, and patients with type 1 and type 2 diabetes mellitus. OUTCOMES MEASURES: nerve conduction studies (NCS) comprised the primary defined outcome. The three screening sensory tests examined in the study were the Semmes-Weinstein 10 g monofilament examination (SWME), superficial pain sensation, and vibration by the on-off method. RESULTS: the three screening tests are significantly and positively correlated with NCS. An increase in the number of insensate responses in the screening test is associated with an increase in the abnormal NCS score. The strength of the association between NCS and each sensory test was greater when the neuropathy severity stage of the subject was added to the model. Both the SWME and vibration by the on-off method tests demonstrated sufficient statistical power to differentiate non-diabetic control subjects from subjects with diabetes, as well as to differentiate subjects with diabetes with and without neuropathy. These two tests, when compared with NCS, also demonstrated acceptable diagnostic performance characteristics in terms of high sensitivity and specificity, total number of correctly predicted cases, and receiver-operating characteristic curves. CONCLUSION: this data, through the development of a model involving training and validation sets, demonstrates that the knowledge of clinical risk factors alters the interpretation of sensory tests for DPN. This finding lends further support to the validity of simple sensory testing maneuvers in the conditional diagnosis of DPN. We recommend annual screening with either the SWME or vibration by the on-off method in the primary care and diabetes clinics.

Cross-Sectional Studies↗
PubMed1998

Erythrocyte aldose reductase protein: a clue to elucidate risk factors for diabetic neuropathies independent of glycemic control.

Prolonged hyperglycemia has been thought to be the primary cause of diabetic complications, however, some diabetic patients develop severe complications early in duration of diabetes, while some patients have no or mild complications even after prolonged hyperglycemia. To investigate the risk factors for diabetic severe neuropathy independent of glycemic control and duration of diabetes, erythrocyte aldose reductase was determined in 43 non-insulin-dependent diabetic patients by a two-site ELISA using recombinant human aldose reductase. Among 20 patients with severe neuropathy which was developed within 5 years of diagnosis, the level of erythrocyte aldose reductase protein was significantly higher than that of 23 patients with no or mild neuropathy who had more than 8 years duration of diabetes and prolonged hyperglycemia (11.9+/-5.7 vs. 8.3+/-1.3 ng/mgHb, P < 0.0001). There was a significant stability of the erythrocyte aldose reductase (AR) in the 40 diabetic patients during 1-4 years. The logistic regression analysis revealed that the maximum body mass index (BMI) in the past minus present BMI and the level of erythrocyte aldose reductase protein were the independent risk factors for diabetic severe neuropathy. The measurement of erythrocyte AR level may be useful for predicting severe neuropathy in non-insulin-dependent diabetes mellitus (NIDDM) patients.

Aldehyde Reductase↗
PubMed2001

Hyper-responsivity in a subset of C-fiber nociceptors in a model of painful diabetic neuropathy in the rat.

While clinical characteristics of diabetic painful neuropathy are well described, the underlying electrophysiological basis of the exaggerated painful response to stimuli, as well as the presence of spontaneous pain, are poorly understood. In order to elucidate peripheral contributions to painful diabetic neuropathy, we quantitatively evaluated the function of C-fibers in a rat model of painful diabetic neuropathy, diabetes induced by the pancreatic beta-cell toxin streptozotocin. While there was no significant effect of diabetes on conduction velocity, mechanical threshold or spontaneous activity, the number of action potentials in response to sustained threshold and suprathreshold mechanical stimuli was significantly increased in the diabetic rats. Moreover, there was a clustering of responses of C-fibers in diabetic rats; while two-thirds of C-fibers fired at the same mean frequency as C-fibers in control rats, one-third of C-fibers in diabetic rats were markedly hyper-responsive, demonstrating a threefold increase in firing frequency. The high-firing-frequency C-fibers in rats with diabetes also had faster conduction velocity than the low-firing-frequency C-fibers in rats with diabetes or in C-fibers in control rats. The hyper-responsiveness was characterized by a selective increase of the shortest interspike intervals (<100ms) in the burst component (first 10s) of the response to a sustained suprathreshold stimulus; in the plateau phase (last 50s) of the response to a 60-s suprathreshold stimulus, we found a selective increase of interspike intervals between 100 and 300ms in hyper-responsive C-fibers in rats with diabetes. The hyper-responsiveness did not correlate with mechanical threshold, presence of spontaneous activity or location of the fiber's receptive field. In summary, in an established model of painful diabetic neuropathy in the rat, a subset of C-fibers demonstrated a marked hyper-responsiveness to mechanical stimuli. The subset was also found to have a greater mean conduction velocity than the fibers not demonstrating this hyper-responsivity. The present findings suggest that study of individual neurons in vitro may allow elucidation of the ionic basis of enhanced nociception in diabetic neuropathy.

Action Potentials↗
PubMed1997

Bimoclomol (BRLP-42) ameliorates peripheral neuropathy in streptozotocin-induced diabetic rats.

A reduction in nerve conduction velocity and an increase in resistance to ischemic conduction failure are early signs of neural dysfunction in both diabetic patients and animal models of diabetes. The effect of Bimoclomol (BRLP-42), a drug under clinical development for the treatment of diabetic complications, on experimental peripheral neuropathy was examined in rats made diabetic by injection of streptozotocin. Daily oral doses of Bimoclomol (10 or 20 mg/kg) or control dose of gamma-linolenic acid (260 mg/kg), an agent with known neuropathy-improving effects, were administered for 3 months. Treatments began 1 day after diabetes induction to assess the prophylactic efficacy of Bimoclomol. Neuropathy was evaluated electrophysiologically by measuring motor and sensory nerve conduction velocities and resistance to ischemic conduction failure of sciatic nerve in vivo. Bimoclomol significantly reduced nerve conduction slowing and retarded the typical elevated ischaemic resistance due to streptozotocin-induced neuropathy, suggesting that the drug might be a useful treatment for diabetic peripheral neuropathies.

Animals↗
PubMed1998

The role of copper on ethambutol's antimicrobial action and implications for ethambutol-induced optic neuropathy.

The principal side effect of the antimycobacterial agent ethambutol (EMB) is an optic neuropathy with clinical features very similar to a mitochondrial hereditary optic neuropathy (Leber's). The mechanism of EMB-induced optic neuropathy may be EMB's chelation of copper, thereby precluding normal cytochrome c oxidase activity and mitochondrial metabolism in the optic nerve. Before attempting to use therapeutic copper to replenish endogenous stores in an attempt to preclude EMB-induced optic neuropathy, we wished to determine whether EMB is still effective against mycobacteria in the presence of copper. EMB and copper, alone and in combination, were tested against six strains of Mycobacterium tuberculosis and five strains of Mycobacterium avium using a radiometric broth macrodilution assay. Copper did not effect EMB's antimicrobial actions against either species of mycobacteria. This in vitro study suggests that if copper were given to patients to prevent EMB-induced optic neuropathy, it would not compromise EMB's bacteriostatic properties.

Antitubercular Agents↗
PubMed2000

Optic neuropathy associated with laser in situ keratomileusis.

PURPOSE: To report 4 cases of optic neuropathy following laser in situ keratomileusis (LASIK). SETTING: Tertiary Care ophthalmic practices. METHODS: In this retrospective observational case series, 4 patients who developed acute visual loss following LASIK are reported. All had clinical evidence of optic neuropathy. Two had optic disc edema and 2 had normal appearing optic discs initially. None of the patients experienced significant visual recovery, and all developed optic atrophy in the affected eye. RESULTS: All patients had evaluations for alternative etiologies of their optic neuropathy, with negative results. All patients were therefore presumed to have experienced an ischemic optic neuropathy following LASIK. CONCLUSIONS: Patients who have LASIK may experience an acute anterior or retrobulbar optic neuropathy. The etiology is unknown but may be related to the marked increase in intraocular pressure that occurs during a portion of the procedure.

Adult↗
PubMedDate not supplied

Decompression of peripheral nerves for diabetic neuropathy in the lower extremity.

Consideration of the presence of a compressive neuropathy overlying an existing diabetic neuropathy in symptomatic patients and surgical decompression of these compressed nerves in selected patients is presented. The short-term results of 33 lower extremities treated with external neurolysis of the common peroneal, deep peroneal, and tarsal tunnel nerves are presented with a mean follow-up time of 3 months (range, 1 to 6 months). The surgery was performed in an attempt to relieve pain and to restore normal sensation in the foot. All procedures were performed under spinal or general anesthesia. Candidates for the procedure were type 1 or type 2 diabetics with symptomatic somatosensory neuropathy (pain, burning, tingling, and/or numbness) and preoperative computer-assisted neurosensory testing that confirmed the presence of elevated nerve threshold levels and axonal degeneration in the foot and leg. External neurolysis of the involved nerves provided good to excellent results in 90.0% of those patients with preoperative neuropathic pain, and restored sensation at good to excellent levels in 66.7% of those patients with preoperative neuropathic numbness. The mean visual analog score for pain assessment was 9.0 preoperatively and 3.2 postoperatively for those patients with pain as a symptomatic complaint (n = 30). There were 4 complications (12%) and all were early cases consisting of a noninfected wound dehiscence of the tarsal tunnel incision, which went on to heal without consequence. These initial short-term results suggest that external neurolysis of the common peroneal, deep peroneal, and tarsal tunnel nerves in selected patients with symptomatic diabetic neuropathy and an overlying compression neuropathy as determined by using computer-assisted neurosensory testing appears to be an effective treatment for providing pain relief and restoration of sensation in the foot.

Cohort Studies↗