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Objective. To compare the results of splinting and surgery in patients with carpal tunnel syndrome (CTS). Design. Randomised. Method. Patients with clinically and electrophysiologically confirmed idiopathic CTS were recruited by neurologists in 13 hospitals in the Netherlands. One hundred and seventy-six patients were included in the trial and were randomly allocated to either wrist splinting (n = 89) or open surgery (n = 87). The primary outcome measures were: perceived improvement, number of nights waking up due to symptoms, and severity of symptoms. Outcomes were assessed up to 18 months after randomisation. Intention-to-treat analyses were performed. Results. In the surgery group there were 21 men and 66 women, with an average age of 49 years (SD: II), and in the splint group there were 12 men and 77 women with an average age of 49 (SD: 12). After 3, 6, 12 and 18 months, surgery was more effective than splinting on all outcome measures. Success rates, based on perceived improvement, were 79% (62/78) for the surgery group and 53% (46/86) for the splint group after 3 months (difference: 26%; 95% CI: 12-40), and 90% (61/68) and 75% (59/79), respectively, after 18 months (difference: 15%; 95% CI: 3-27). However, by that time 32/79 patients (41%) in the splint group had also undergone surgery. Conclusion. Surgery resulted in greater clinical effects compared to splinting in patients with CTS.

CONTEXT Carpal tunnel syndrome (CTS) can be treated with nonsurgical or surgical options. However, there is no consensus on the most effective method of treatment. OBJECTIVE To compare the short-term and long-term efficacy of splinting and surgery for relieving the symptoms of CTS. DESIGN, SETTING, AND PATIENTS A randomized controlled trial conducted from October 1998 to April 2000 at 13 neurological outpatient clinics in the Netherlands. A total of 176 patients with clinically and electrophysiologically confirmed idiopathic CTS were assigned to wrist splinting during the night for at least 6 weeks (89 patients) or open carpal tunnel release (87 patients); 147 patients (84%) completed the final follow-up assessment 18 months after randomization. MAIN OUTCOME MEASURES General improvement, number of nights waking up due to symptoms, and severity of symptoms. RESULTS In the intention-to-treat analyses, surgery was more effective than splinting on all outcome measures. The success rates (based on general improvement) after 3 months were 80% for the surgery group (62/78 patients) vs 54% for the splinting group (46/86 patients), which is a difference of 26% (95% confidence interval [CI], 12%-40%; P<.001). After 18 months, the success rates increased to 90% for the surgery group (61/68 patients) vs 75% for the splinting group (59/79 patients), which is a difference of 15% (95% CI, 3%-27%; P =.02). However, by that time 41% of patients (32/79) in the splint group had also received the surgery treatment. CONCLUSION Treatment with open carpal tunnel release surgery resulted in better outcomes than treatment with wrist splinting for patients with CTS.

Background: The PRISMS study demonstrated significant clinical and MRI benefit at 2 years for interferon-beta -1a, 22 and 44 meg thrice weekly (tiw), compared with placebo in relapsing-remitting MS. Years 3 and 4 extension study results are reported. Methods: Patients initially receiving placebo were randomized to blinded interferon-beta -1a, 22 or 44 meg tiw (n = 172; crossover group); others continued blinded treatment with their originally assigned dose, 22 meg (Rx22 group) or 44 meg (Rx44 group) tiw (n = 167 per group). Patients had 3- to 6-month clinical and annual MRI assessments. Results: Relapse rates for 4 years were 1.02 (crossover), 0.80 (Rx22, p < 0.001), and 0.72 (Rx44, p < 0.001); the dose effect approached significance (p = 0.069; risk ratio, 0.88; 95% CI, 0.76-1.01). Crossover groups showed reductions in relapse count, MRI activity, and lesion-burden accumulation with interferon-p-la compared with their placebo period (p < 0.001 both doses). Time to sustained disability progression was prolonged by 18 months in the Rx44 group compared with the crossover group (p = 0.047). Rx22 and Rx44 reduced new T2 lesion number and lesion burden compared with crossover (p < 0.001); Rx44 was superior to Rx22 on several clinical and MRI outcomes. Persistent neutralizing antibodies developed in 14.3% (Rx44) and 23.7% (Rx22) of patients and were associated with reduced efficacy. Conclusions: Clinical and MRI benefit continued for both doses up to 4 years, with evidence of dose response. Outcomes were consistently better for patients treated for 4 years than for patients in crossover groups. Efficacy decreased with neutralizing antibody formation.

The usefulness of sensory symptoms in the assessment of diabetic polyneuropathy is unclear. In the present study, we studied the hypothesis that pain is associated with small nerve fibre function, and that sensory alteration is associated with large nerve fibre function. In addition, we assessed the reproducibility and the ability to detect changes in clinical status over time of the nerve function tests currently used in clinical trials. Patients (78) with stable diabetic polyneuropathy were examined on three separate occasions with a test-retest interval of 17 and 52 weeks. Small nerve fibre function was measured using temperature discrimination thresholds for warmth (TDTwarmth) and cold (TDTcold). Large nerve fibre function was measured by testing sensory and motor nerve conduction velocities (SNCV and MNCV) and vibration perception thresholds (VPT). Neuropathic pain was only significantly associated with TDTcold, and with the MNCV of the tibial nerve. Sensory alteration was associated with almost all nerve function tests except the SNCV and MNCV of the ulnar nerve. The measurements of symptom severity and the nerve function tests all proved to be sufficiently reproducible. The standardized smallest detectable difference on group level (SDD) of the measurement of sensory alteration and neuropathic pain were almost the same (9% and 12%, respectively). Among the nerve function tests, the SNCV and MNCV had the smallest SDD (3-4%), and were, therefore, potentially the most responsive instruments. The SDD of the TDT was greater than the VPT (9-14% vs 21-28%, respectively). In conclusion, neuropathic pain was not associated with small nerve fibre function, and sensory alteration was associated with both large and small fibre function. In addition, the standardized measurement of symptom severity, the SNCV and MNCV tests, and the VPT test appear to be useful for monitoring the course of polyneuropathy in clinical trials.

Aims/hypothesis. Currently, three categories of measures are used to assess cardiovascular autonomic dysfunction: measures of the Ewing-test, measures of heart-rate variability, and measures of baroreflex sensitivity. We studied the determinants of these measures obtained from cardiovascular autonomic function tests in the Hoorn Study. Methods. The study group (n = 631) consisted of a glucose-tolerance-stratified sample from a 50- to 75-year-old group of people. Cardiac cycle duration (RR interval) and continuous finger arterial pressure were measured under three conditions: during (a) spontaneous breathing, (b) six deep breaths over one minute, and (c) an active change in position from lying to standing. From these readings, ten measures of autonomic function were assessed (three Ewing, six heart-rate variability and one baroreflex sensitivity). As possible determinants we considered age, sex, glucose tolerance, cardiovascular disease, use of anti-hypertensive drugs, anthropometric factors, metabolic factors and lifestyle factors. Results. Multivariate analysis showed that eight of ten cardiovascular autonomic function measures were most strongly associated with glucose tolerance. Furthermore, measures were moderately associated with age, sex, waist-to-hip ratio, use of anti-hypertensive drugs, and insulin. The measures were weakly associated with coronary artery disease but not with lipids. The strongest determinants seemed to differ between subjects with and without diabetes: in the non-diabetic subjects the most strongly associated were age and use of anti-hypertensive drugs and in subjects with diabetes, insulin. No consistent differences in association between the three categories of measures were observed. Conclusion/interpretation. The strongest determinants of autonomic function were age, presence of diabetes and use of anti-hypertensive drugs. [Diabetologia (2000) 43: 561–570]

Objective. Distal somatic polyneuropathy is a major contributing factor in the pathogenesis of chronic foot infections and ulcers, and may lead to lower limb amputations. Both metabolic and vascular abnormalities may contribute to the development of impaired nerve function. We therefore assessed the association between hyperhomocysteinaemia, a risk factor for cardiovascular disease, and polyneuropathy.Design, setting and subjects. We studied an age-, sex- and glucose tolerance-stratified random sample of a 50- to 75-year-old general Caucasian population in the Hoorn Study (N = 629). Any polyneuropathy (N = 95) was defined as the absence of at least two of the three following sensory modalities or reflexes of either foot: light touch sense, ankle reflex and vibration sensation. Definite polyneuropathy (N = 25) was present if, in addition, the vibration perception threshold of the right big toe was abnormal.Results. The prevalence of any polyneuropathy was 12.4% (33 of 266) in subjects with normal glucose tolerance (NGT), 12.6% (21 of 167) in those with impaired glucose tolerance (IGT), and 25.3% (41 of 162) in those with type 2 diabetes. The prevalence of definite polyneuropathy was 2.6% (7 of 266) in subjects with NGT, 2.4% (4 of 167) in those with IGT and 8.7% (14 of 161) in type 2 diabetic subjects. Polyneuropathy was associated with known risk factors such as diabetes, hyperglycaemia and body height. After adjustment for age, sex, HbA(1c) and hypertension, the odds ratio (95% CI) for any polyneuropathy per 5 mu mol L-1 (about 1 SD) serum total homocysteine increment was 1.00 (0.72-1.39). After adjustment for age and sex, it was 0.62 (0.21-1.89) for definite polyneuropathy.Conclusion. Although a weak relation (as judged from the confidence intervals) cannot be excluded, we conclude that hyperhomocysteinaemia is probably not related to risk of distal somatic polyneuropathy.

Muscle & NerveVolume 20, Issue 1 p. 116-118 Short Report The assessment of diabetic polyneuropathy in daily clinical practice: Reproducibility and validity of Semmes Weinstein monofilaments examination and clinical neurological examination Gerlof D. Valk MD, Gerlof D. Valk MD Department of Neurology, Free University Hospital, Amsterdam, The NetherlandsSearch for more papers by this authorJeroen J.J. de Sonnaville MD, Jeroen J.J. de Sonnaville MD Department of Internal Medicine, Free University Hospital, Amsterdam, The NetherlandsSearch for more papers by this authorWilliam H. van Houtum MD, William H. van Houtum MD Institute for Research in Extramural Medicine, Free University Hospital, Amsterdam, The Netherlands Department of Internal Medicine, Free University Hospital, Amsterdam, The NetherlandsSearch for more papers by this authorRobert J. Heine MD, PhD, Robert J. Heine MD, PhD Department of Internal Medicine, Free University Hospital, Amsterdam, The NetherlandsSearch for more papers by this authorJacques T.M. van Eijk PhD, Jacques T.M. van Eijk PhD Department of General Practice, Nursing Home Medicine and Social Medicine, Free University Hospital, Amsterdam, The NetherlandsSearch for more papers by this authorLex M. Bouter PhD, Lex M. Bouter PhD Department of Epidemiology and Biostatistics, Free University Hospital, Amsterdam, The NetherlandsSearch for more papers by this authorFrederik W. Bertelsmann MD, PhD, Corresponding Author Frederik W. Bertelsmann MD, PhD Department of Neurology, Free University Hospital, Amsterdam, The NetherlandsDepartment of Neurology, Free University Hospital, P.O. Box 7057, 1007 MB Amsterdam, The NetherlandsSearch for more papers by this author Gerlof D. Valk MD, Gerlof D. Valk MD Department of Neurology, Free University Hospital, Amsterdam, The NetherlandsSearch for more papers by this authorJeroen J.J. de Sonnaville MD, Jeroen J.J. de Sonnaville MD Department of Internal Medicine, Free University Hospital, Amsterdam, The NetherlandsSearch for more papers by this authorWilliam H. van Houtum MD, William H. van Houtum MD Institute for Research in Extramural Medicine, Free University Hospital, Amsterdam, The Netherlands Department of Internal Medicine, Free University Hospital, Amsterdam, The NetherlandsSearch for more papers by this authorRobert J. Heine MD, PhD, Robert J. Heine MD, PhD Department of Internal Medicine, Free University Hospital, Amsterdam, The NetherlandsSearch for more papers by this authorJacques T.M. van Eijk PhD, Jacques T.M. van Eijk PhD Department of General Practice, Nursing Home Medicine and Social Medicine, Free University Hospital, Amsterdam, The NetherlandsSearch for more papers by this authorLex M. Bouter PhD, Lex M. Bouter PhD Department of Epidemiology and Biostatistics, Free University Hospital, Amsterdam, The NetherlandsSearch for more papers by this authorFrederik W. Bertelsmann MD, PhD, Corresponding Author Frederik W. Bertelsmann MD, PhD Department of Neurology, Free University Hospital, Amsterdam, The NetherlandsDepartment of Neurology, Free University Hospital, P.O. Box 7057, 1007 MB Amsterdam, The NetherlandsSearch for more papers by this author First published: 07 December 1998 https://doi.org/10.1002/(SICI)1097-4598(199701)20:1<116::AID-MUS19>3.0.CO;2-2Citations: 82AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume20, Issue1January 1997Pages 116-118 RelatedInformation

Muscle & NerveVolume 20, Issue 10 p. 1334-1335 Letter to the Editor Variation in the treatment of carpal tunnel syndrome Rob J.P.M. Scholten MD, PhD, Corresponding Author Rob J.P.M. Scholten MD, PhD Institute for Research in Extramural Medicine, Vrije Universiteit, Van der Boechorststraat 7, 1081 BT Amsterdam, The NetherlandsInstitute for Research in Extramural Medicine, Vrije Universiteit, Van der Boechorststraat 7, 1081 BT Amsterdam, The NetherlandsSearch for more papers by this authorMarc C.T.F.M. de Krom MD, PhD, Marc C.T.F.M. de Krom MD, PhD Department of Neurology, Maastricht University Hospital, Maastricht, The NetherlandsSearch for more papers by this authorFrits W. Bertelsmann MD, PhD, Frits W. Bertelsmann MD, PhD Department of Neurology, Academic Hospital of the Free University, Amsterdam, The NetherlandsSearch for more papers by this authorLex M. Bouter PhD, Lex M. Bouter PhD Department of Epidemiology and Biostatistics, Vrije Universiteit, Amsterdam, The NetherlandsSearch for more papers by this author Rob J.P.M. Scholten MD, PhD, Corresponding Author Rob J.P.M. Scholten MD, PhD Institute for Research in Extramural Medicine, Vrije Universiteit, Van der Boechorststraat 7, 1081 BT Amsterdam, The NetherlandsInstitute for Research in Extramural Medicine, Vrije Universiteit, Van der Boechorststraat 7, 1081 BT Amsterdam, The NetherlandsSearch for more papers by this authorMarc C.T.F.M. de Krom MD, PhD, Marc C.T.F.M. de Krom MD, PhD Department of Neurology, Maastricht University Hospital, Maastricht, The NetherlandsSearch for more papers by this authorFrits W. Bertelsmann MD, PhD, Frits W. Bertelsmann MD, PhD Department of Neurology, Academic Hospital of the Free University, Amsterdam, The NetherlandsSearch for more papers by this authorLex M. Bouter PhD, Lex M. Bouter PhD Department of Epidemiology and Biostatistics, Vrije Universiteit, Amsterdam, The NetherlandsSearch for more papers by this author First published: 07 December 1998 https://doi.org/10.1002/(SICI)1097-4598(199710)20:10<1334::AID-MUS25>3.0.CO;2-1Citations: 16AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume20, Issue10October 1997Pages 1334-1335 RelatedInformation

Only sparse and contradictory data are available on peripheral somatic nerve function in relation to the total range of glucose tolerance. A random sample (n = 708) of people, stratified by age, sex, and glucose tolerance, from a Caucasian population aged 50 to 74 years was invited to undergo an examination including measures of large-fibre nerve function (ankle and knee reflexes, vibration sense, vibratory perception threshold (VPT) at the foot) and one measure of small-fibre function (thermal discrimination threshold (TDT) at the foot). A total of 267 subjects with a normal glucose tolerance (NGT), 167 with impaired glucose tolerance (IGT), 90 with newly diagnosed diabetes mellitus (NDM), and 73 with previously known diabetes (KDM) were included. KDM was associated with the highest prevalence of large-fibre nerve dysfunction. Within the range from NGT to NDM, most large-fibre function measures showed a decline with decreasing glucose tolerance. The TDT showed a decrease with an increase in fasting and post-load insulin levels (p < 0.05). We conclude that glucose intolerance is associated with impaired peripheral large-fibre nerve function, an association which seems to apply even in the non-diabetic range. Higher insulin levels were associated with a better small-fibre nerve function.

There is evidence that treatment with an antibody to tumor necrosis factor alpha (TNF alpha) improves an animal model of multiple sclerosis (MS) and is beneficial in two systemic inflammatory diseases in humans, but there are no reports about anti-TNF treatment of MS. Therefore, we treated two rapidly progressive MS patients with intravenous infusions of a humanized mouse monoclonal anti-TNF antibody (cA2) in an open-label phase I safety trial and monitored their clinical status, gadolinium-enhanced brain magnetic resonance imaging (MRI), and peripheral blood and cerebrospinal fluid (CSF) immunologic status.We did not notice any clinically significant neurologic changes in either patient. The number of gadolinium-enhancing lesions increased transiently after each treatment in both patients. CSF leukocyte counts and IgG index increased after each treatment.The transient increase in the number of gadolinium-enhancing lesions that followed each infusion of cA2 together with the increase in cells and immunoglobulin in the CSF of each patient suggest that the treatment caused immune activation and an increase in disease activity. These results suggest that further use of cA2 in MS is not warranted and that studies of other agents that antagonize TNF alpha should be carried out with frequent monitoring of gadolinium-enhanced MRIs.

We report in this paper a case of a patient who developed extensive cranial nerve paresis on the left and right side after otitis externa. Investigation revealed an osteomyelitis of the skull base. We describe this disease and stress the importance of the gallium scan in the diagnostic process and therapeutic follow up.

OBJECTIVE To compare the efficacy and toxicity of 4-aminopyridine and 3,4-diaminopyridine in patients with multiple sclerosis. DESIGN Intervention study with a before-after design and a randomized, double-blind, crossover design. SETTING University referral center. PATIENTS Twenty-four patients with definite multiple sclerosis who had been treated in a previous clinical trial with 4-aminopyridine. INTERVENTIONS Nonresponders to treatment with 4-aminopyridine (14 patients) were treated with 3,4-diaminopyridine in a 4-week, open-label trial with doses up to 1.0 mg/kg of body weight (before-after design). Responders to treatment with 4-aminopyridine (10 patients) participated in a comparative study of 6 weeks' duration with 4-aminopyridine and 3,4-diaminopyridine according to a randomized, double-blind, double-crossover design. MAIN OUTCOME MEASURES Neurophysiologic variables for nonresponders, neurologic functions and symptoms on a visual analogue scale for responders, and side effects for both groups. RESULTS Toxicity profiles of 4-aminopyridine and 3,4-diaminopyridine were different, and systemic tolerability was reduced for 3,4-diaminopyridine. 4-Aminopyridine was more effective than 3,4-diaminopyridine, especially for ambulation, fatigue, and overall daily functioning. CONCLUSION Our data suggest that, concerning both efficacy and side effects, 4-aminopyridine is superior to 3,4-diaminopyridine in the treatment of patients with multiple sclerosis.

OBJECTIVE:To study the long-term efficacy and safety of 4-aminopyridine in patients with multiple sclerosis.DESIGN:Case series, follow-up varying from 6 to 32 months.SETTING:University referral center.PATIENTS:Thirty-one patients with definite MS, 23 of them being exposed to long-term administration (6 to 32 months) of 4-aminopyridine, since they showed a favorable initial response to the drug.INTERVENTIONS:Long-term oral treatment with 4-aminopyridine in daily doses of up to 0.5 mg/kg of body weight.MAIN OUTCOME MEASURES:Neurologic functions and symptoms as reported by the patients; side effects.RESULTS:Twenty of 23 patients who showed a favorable initial response benefited from long-term administration. Ambulation and fatigue (each in 13 patients) and visual function (in five patients) were most frequently reported to be improved. Three major side effects did occur during a follow-up of 406 patient months: a generalized epileptic seizure in two patients and hepatitis in one.CONCLUSIONS:Although a substantial proportion of patients with multiple sclerosis seem to benefit from long-term administration of 4-aminopyridine, additional studies are needed to clarify the exact value of the drug.

Cytomegalovirus (CMV) causes several neurological diseases in the late stages of AIDS, but their ante-mortem diagnosis is problematic.Clinical criteria (defining a presumptive diagnosis) and polymerase chain reaction $4 (PCR) assay from cerebrospinal fluid (CSF) were blindly used to predict the involvement of CMV in neurological disorders of 164 consecutive AIDS patients undergoing a lumbar puncture.During the follow-up, a definite diagnosis based on viral culture of CSF, clinical outcome and/or CNS histology was allowed in 88 patients, 27 (16 %) of whom had a proven CMV related neurological disease.The concordance between the presumptive and definite diagnosis was of 60 %, inducing a moderate agreement kappa index of 0.40.In contrast, the sensitivity and specificity of PCR were respectively of 89 and 94 %, with a positive and negative predictive values of 86 and 95 %.Cytomegalovirus related neurological diseases appeared thus as a frequent complication of AIDS, and detection of viral DNA in CSF by means of PCR seems a reliable tool for their diagnosis, allowing its use for therapeutic decisions 20 99mTC-HMPAO LEUCOCYTE SCINTIGRAPHY IN DIAGNOSIS