Improvement Of Nerve Function Research Articles

Surgical Decompression for Peroneal Nerve Palsy After Total Knee Arthroplasty

Five patients were treated by operative exploration and decompression of the peroneal nerve for peroneal nerve palsy complicating total knee arthroplasty (TKA). All patients had failed to demonstrate improvement in the peroneal nerve function despite extended conservative care. The procedure was performed five to 45 months after the index TKA. Patients were evaluated and graded preoperatively and postoperatively using the Modified Nerve Palsy Scale of Weber, Daube, and Coventry. All patients demonstrated improved nerve function. Four of five patients had full peroneal nerve recovery. All patients were able to discontinue their ankle-foot orthoses. This is a rare complication of TKA, and when conservative nonoperative measures do not lead to sufficient improvement in nerve function, consideration may be given to operative decompression of the peroneal nerve.

Diabetic autonomic neuropathy after pancreas and kidney transplantation

We have evaluated the effect of successful pancreatic and kidney transplantation on autonomic neuropathy in nine Type 1 (insulin-dependent) diabetic subjects. Cardiovascular reflex tests were performed before and at 6-24 months after transplantation. A control group of ten Type 1 diabetic patients after kidney grafting only was examined at the same time periods. For base-line comparisons results of the tests in ten healthy subjects were used. Advanced autonomic neuropathy was present in both groups of transplant recipients and no significant changes in test results could be found at post-transplant evaluation. Lack of autonomic nerve function improvement was confirmed in seven patients of the pancreatic and kidney transplantation group who were examined again after 2-4 years. Irreversible structural autonomic nerve damage is probably present in uraemic pancreatic transplantation candidates.

Peripheral nerve palsy associated with congenital constriction band syndrome

Of 21 patients with congenital constriction band syndrome treated in our clinic from 1967 to 1988, four had constriction bands proximal to the wrist. Three of these also had a peripheral nerve palsy. Late surgical decompression does not help but early diagnosis, using electrodiagnosis methods, and neurolysis or nerve grafting as soon as possible may improve nerve function.

Sorbinil: an aldose reductase inhibitor which improves nerve function in diabetic neuropathy

Sorbinil: an aldose reductase inhibitor which improves nerve function in diabetic neuropathy

Clinical studies with an aldose reductase inhibitor in the autonomic and somatic neuropathies of diabetes

Clinical investigations with the aldose reductase inhibitor (ARI) sorbinil in diabetic patients with neuropathy are described. Cardiac autonomic neuropathy was studied in 36 patients, in a double-blind, placebo-controlled, randomized, noncrossover trial. Patients received sorbinil (250 mg qd) or placebo over 6 weeks after a one-week baseline period. Diabetic control did not change over the study period, as indicated by unchanged glycohemoglobin. Response was assessed by expiration/inspiration ( E I ) ratios on EKG during 6 c/min respiration and resting minimum heart rate, both measures of vagal function. In the sorbinil group, E I ratios improved from 1.074 ± 0.012 to 1.096 ± 0.020 ( P < 0.03) with a slight decrease in the placebo group from 1.112 ± 0.023 to 1.105 ± 0.023 ( P = NS). The difference between the week 6 and week 0 changes in each group was significant ( P < 0.01). Resting minimum heart rate decreased in the sorbinil group from 76.4 ± 2.3 to 66.8 ± 2.4 beats/min ( P < 0.001), with a mean change of 10 ± 2. In the placebo group, heart rate was unchanged (77.9 ± 3.9 to 77.5 ± 3.3). The two sample t tests of the within-group differences were likewise significant ( P < 0.001). These changes in both E I ratio and resting minimum heart rate are consistent with a sorbinil-related improvement in cardiac parasympathetic nerve function. Several isolated cases with apparent sorbinil-related improvement in autonomic symptoms will also be described. Studies of somatic neuropathy have previously shown improvement in nerve conduction velocities with sorbinil. In a study of 11 patients with severly painful diabetic neuropathy treated with sorbinil for 3 weeks [placebo-controlled in single-blind fashion (n = 8)], pains (as assessed on a 0 to 20 rating scale) improved from a mean score of 16 down to 8, with deterioration following drug withdrawal. Objective improvements in sensation and strength were observed in some cases. In this group of patients, statistically significant improvements in nerve conduction velocity, E I ratios, and resting minimal heart rate, similar to those previously discussed, were also documented. Somatosensory-evoked potentials studies in the 36-patient study showed significant improvements in peripheral conduction and cortical responses. Sorbinil toxicity in 106 patients was 11.3%, with sex incidence of 7 73 males (9.6%) and 5 33 females (15.2%). The reaction, which is virtually confined to a macular-erythematous rash ± fever, in all cases occurred within the first 14 days of therapy and was followed by rapid and uneventful recovery. Our clinical experience with sorbinil has been promising and has suggested the possibility of a major role for ARIs in the treatment and perhaps prophylaxis of diabetic peripheral somatic and autonomic neuropathies.

Effects of sorbinil therapy in diabetic patients with painful peripheral neuropathy and autonomic neuropathy

Clinical investigations with the aldose reductase inhibitor sorbinil in patients with peripheral neuropathy due to diabetes are described. After an improvement in motor and sensory nerve conduction velocities was demonstrated in asymptomatic diabetic patients taking sorbinil (compared with velocities during a placebo period), 11 patients with painful diabetic neuropathy were treated with sorbinil for three weeks without alterations in diabetic management or control. Therapy was placebo-controlled in a single-blind fashion in eight patients. Pain (assessed by or on a zero to 20 rating scale), which had been constant for many months before entry into the study and unresponsive to numerous medications, improved from a mean score of 16 to 8 and returned when the drug was discontinued. Objective improvement in sensation and strength were observed in some cases. Improvements in nerve conduction velocity and cardiac autonomic function were also documented. Cardiac autonomic neuropathy was studied in 36 patients in a double-blind, placebo-controlled, randomized, noncrossover trial. Patients received one 250-mg sorbinil tablet or one placebo tablet daily for six weeks, after a one-week baseline period. Glycemic control did not change during the study period, as indicated by unaltered glycohemoglobin levels. Response was assessed by expiration-inspiration ratios, obtained on electrocardiography during six cycles per minute respiration, and by resting minimal heart rate, both measures of vagal function. In the sorbinil-treated group, expiration-inspiration ratios improved from 1.074 ± 0.012 to 1.096 ± 0.020 (p <0.03). There was a slight decrease in the ratios in the placebo-treated group, from 1.112 ± 0.023 to 1.105 ± 0.023 (not significant). The difference between the Week 0 to Week 6 changes in each group was significant (p <0.01). Resting minimal heart rate decreased in the sorbinil-treated group from 76.4 ± 2.3 to 66.8 ± 2.8 ± 2.4 beats per minute (p <0.001), with a mean change of 10 ± 2. In the placebo-treated group, heart rate was unchanged (77.9 ± 3.9 to 77.5 ± 3.3 beats per minute). The two-sample t test of the within-group differences was also significant (p <0.001). The changes in both expiration-inspiration ratios and resting minimal heart rate are consistent with a sorbinil-related improvement in cardiac parasympathetic nerve function. Several isolated cases of apparent sorbinil-related improvements in autonomic symptoms have been observed. Median nerve somatosensoryevoked potential studies in this group of patients showed statistically significant sorbinil-related improvements in peripheral conduction and cortical responses. The incidence of sorbinil toxicity in 106 patients was 11.3 percent. Side effects were confined to rash, which was sometimes accompanied by fever. These effects disappeared rapidly after discontinuation of the drug. The results of this study are promising, suggesting the possibility of a major role for aldose reductase inhibitors in the treatment of, and perhaps prophylaxis against, both somatic and autonomic components of diabetic peripheral neuropathy.

155 A REDUCTION IN CRANIAL SCLEROSIS DURING CALCITRIOL THERAPY IN A PATIENT WITH CRANIOMETAPEYSEAL DYSPLASIA

A 1 month old male presented with a left facial nerve palsy, hepatosplenomegaly, and sclerosis of long bones and the base of the skull. The original diagnosis of osteopetrosis was revised to craniometaphyseal dysplaisa (CMD) based on mandibular sclerosis and normal density of the vetebrae. by 2 months of age, hepatosplenomegaly had resolved, but the base of the skull had become more sclerotic and there was no improvement of facial nerve function. Parameters from an iliac crest biopsy included: trabecular bone volume, 15.1% (25±3%); osteoclast surface area, 2.6% (1.1±0.3%); and osteoclast number/mm trabecular bone surface, 0.37 (0.12±0.02). All these parameters differ significanly from childhood norms (±SD). Osteoblastic parameters were normal. The patient was begun on high dose (1.5 mcg/kg/d) calcitriol (Hoffmann-La-Roche) and a low calcium (15 mg/kg/d) diet (Ross Laboratories). After 7 months of therapy, the facial nerve palsy had improved. Raiographs of the base of the skull demonstrated decreased density. A CT demonstrated increased size of optic foramina and internal auditory canals. A reapeat iliac crest biopsy showed decreased osteoclast number and increased trabecular bone volume.

IMPROVED METABOLIC CONTROL-A CAUSE OF DIABETIC NEUROPATHY

Two adolescents, both 17 years, began intensified therapy to improve glycemic control (HbA1c 17.0%, 9.0%). Physical examinations were normal. Baseline neurophysiologic studies (Biothesiometry and NCV) demonstrated mild sensory nerve dysfunction, not due to heavy metal toxicity or vitamin deficiency. Intensified conventional diabetes therapy improved their diabetes control. Hb A1c values were <8.5% at 8 weeks after beginning therapy. Four to six weeks after beginning therapy, each patient developed distal, symmetrical polyneuropathy characterized by pain and/or numbness of extremities. Despite improved metabolic control, repeat neurophysiologic studies were unchanged. A 15-year-old female presented with right facial paresis and pedal dysesthesias. Her glycemic control was similarly improved(Table). Six weeks later she reported severe leg pain and worsening of existing symptoms without neurophysiologic change. In all three patients, symptoms completely subsided in 3 to 4 months without improvement in neurophysiologic tests. Improved metabolic control may exacerbate silent or overt neuropathy in young diabetics. Resolution of symptoms in response to treatment protocols may not indicate improved nerve function.

Improvement of peripheral nerve function after institution of insulin treatment in diabetes mellitus. A case-control study.

The influence of improved diabetic control on peripheral nerve function was studied before and 3-4 months after institution of insulin treatment in 22 diabetics unsatisfactorily controlled by oral hypoglycemic agents. After institution of insulin treatment, diabetic control was improved as demonstrated by decreasing levels of HbA1. There was an overall tendency towards improvement of motor and sensory conduction velocities, however significant only in the upper extremities. There was a tendency towards improved temperature sensitivity in the legs, while no changes occurred in the hands and face. The sensation for vibration did not change. It is concluded that improved diabetic control, even in elderly patients with long-standing diabetes, is followed by neurophysiological signs of improved peripheral nerve function.

Bell's palsy--a new concept of treatment.

A report is given on preliminary results of an infusion therapy which, in contrast to presently used conservative forms of treatment, is based on both an antiphlogistic and a Theological effect of high doses of cortisone in combination with dextrane plus pentoxifylline. In more than 50% of the patients, clinical and electromyographical improvement of nerve function is observed already during infusion. Compared to other conservative therapeutic procedures, the frequency of resulting complete recoveries is 7–10% higher according to clinical criteria and 10–18% higher as judged by neurophysiological parameters. Compared to the spontaneous outcome, complete recovery ranges 20% higher in our series. Facial nerve decompression seems therefore no longer justified, as little as therapeutic nihilism.

Preliminary report on ten patients with spinal cord injuries treated with hyperbaric oxygen.

A preliminary report is presented on 10 patients with spinal cord injuries who were treated with hyperbaric oxygen. The results suggest that by supporting injured spinal cord tissue with oxygen under pressure, improvement in nerve function may occur. No deterioration of motor power or sensation was evident during or after hyperbaric oxygen treatment in any of these patients. The possible contribution of ischaemia to the pathology of spinal cord injury should encourage further experimental research and clinical trials with hyperbaric oxygen.

Variations in motor conduction velocity produced by acute changes of the metabolic state in diabetic patients.

Repeated measurements of motor conduction velocity in 14 primarily untreated diabetics showed a clear improvement in nerve-function during insulin treatment. — Similar results could not he produced by measuring the threshold for vibration sense.

Peripheral nerve function in vitamin B 12 deficiency.

INVOLVEMENT of the spinal cord in patients with addisonian pernicious anemia is well known 1,2 and the defect has been clinically related to vitamin B 12 deficiency. 3-5 Although peripheral nerve dysfunction has also been described in this condition, 6,7 its documentation and relationship to vitamin B 12 deficiency is not completely established. 8,9 Recently, techniques have been developed for the measurement of the conduction velocity in the largest motor 10 and sensory fibers 11,12 in human peripheral nerves. These methods offer a sensitive index for assessing peripheral nerve function if the techniques are standardized and individual values compared with those of normals in the same age range. 13 These procedures are well tolerated by patients and testing can be repeated at various time intervals. Improvement or deterioration of nerve function can thus be determined. Pathological processes which affect large fibers are readily studied by these techniques since the

Polyneuropathy in Chronic Renal Insufficiency

Peripheral neuropathy is frequently associated with chronic renal insufficiency. It presents as progressive peripheral involvement first of sensory, then motor fibers. Loss of vibration sense is the most consistent early finding. Nerve conduction measurements aid in the detection of mild or subclinical neuropathy. Patients on long-term dialysis therapy also have neuropathy as evidenced by slowed nerve conduction. Allowing patients to become critically ill with uremia and its complications may predispose them to rapidly progressive motor neuropathy during the early phase of dialysis therapy. Since motor neuropathy may not be reversible, every effort should be made to avoid this complication by instituting dialysis therapy before severe uremia develops. Adequate dialysis appears to arrest the progression of neuropathy, and is followed by slow improvement over months or years. Successful renal transplantation greatly improved nerve function in two patients.