Splinting for carpal tunnel syndrome: prognostic indicators of success.

OBJECTIVES: To identify (combinations of) prognostic indicators for the long term success of splinting in patients with electrophysiologically confirmed idiopathic carpal tunnel syndrome (CTS). METHODS: This study was conducted within the framework of a randomised controlled trial on the efficacy of splinting and surgery for CTS. Patients randomised to splinting received a wrist splint, which they had to wear during the night for at least six weeks. To assess the long term success, patients were asked to indicate whether there was any improvement 12 months after randomisation. Potential prognostic indicators included variables from the history taking and physical examination, self administered questionnaires on severity of symptoms, and electrodiagnostic studies. Multiple logistic regression was used to identify (combinations of) prognostic indicators. RESULTS: Of the 89 patients randomised to splinting, 83 attended the follow up measurement at 12 months, of whom 60 reported improvement. However, 34 patients had received one or more additional types of treatment during the follow up period and were therefore considered as treatment failures for splinting, resulting in a final success rate of 31% for splinting (26 of 83 patients). Only two prognostic indicators could be identified, namely a short duration of CTS complaints (one year or less) and a score of 6 or less for severity of paraesthesia at night at baseline. CONCLUSIONS: For patients to whom both factors applied, the predicted probability of treatment success, according to the model, was 62%. The overall percentage of patients who were correctly classified by the model was 78% (95% CI 69% to 87%).

Autoradiographic study of striatal dopamine re-uptake sites and dopamine D1 and D2 receptors in a 6-hydroxydopamine and quinolinic acid double-lesion rat model of striatonigral degeneration (multiple system atrophy) and effects of embryonic ventral mesencephalic, striatal or co-grafts.

The influence of embryonic mesencephalic, striatal and mesencephalic/striatal co-grafts on amphetamine- and apomorphine-induced rotation behaviour was assessed in a rat model of multiple system atrophy/striatonigral degeneration type using dopamine D1 ([3H]SCH23390) and D2 ([3H]spiperone) receptor and dopamine re-uptake ([3H]mazindol) autoradiography. Male Wistar rats subjected to a sequential unilateral 6-hydroxydopamine lesion of the medial forebrain bundle followed by a quinolinic acid lesion of the ipsilateral striatum were divided into four treatment groups, receiving either mesencephalic, striatal, mesencephalic/striatal co-grafts or sham grafts. Amphetamine- and apomorphine-induced rotation behaviour was recorded prior to and up to 10 weeks following transplantation. 6-Hydroxydopamine-lesioned animals showed ipsiversive amphetamine-induced and contraversive apomorphine-induced rotation behaviour. Amphetamine-induced rotation rates persisted after the subsequent quinolinic acid lesion, whereas rotation induced by apomorphine was decreased. In 11 of 14 animals receiving mesencephalic or mesencephalic/striatal co-grafts, amphetamine-induced rotation scores were decreased by >50% at the 10-week post-grafting time-point. In contrast, only one of 12 animals receiving non-mesencephalic (striatal or sham) grafts exhibited diminished rotation rates at this time-point. Apomorphine-induced rotation rates were significantly increased following transplantation of mesencephalic, striatal or sham grafts. The largest increase of apomorphine-induced rotation rates approaching post-6-hydroxydopamine levels were observed in animals with striatal grafts. In contrast, in the co-graft group, there was no significant increase of apomorphine-induced rotation compared to the post-quinolinic acid time-point. Morphometric analysis revealed a 63-74% reduction of striatal surface areas across the treatment groups. Striatal [3H]mazindol binding on the lesioned side (excluding the demarcated graft area) revealed a marked loss of dopamine re-uptake sites across all treatment groups, indicating missing graft-induced dopaminergic re-innervation of the host. In eight (73%) of the 11 animals with mesencephalic grafts and reduced amphetamine-induced circling, discrete areas of [3H]mazindol binding ("hot spots") were observed, indicating graft survival. Dopamine D1 and D2 receptor binding was preserved in the remaining lesioned striatum irrespective of treatment assignment, except for a significant reduction of D2 receptor binding in animals receiving mesencephalic grafts. "Hot spots" of dopamine D1 and D2 receptor binding were observed in 10 (83%) and nine (75%) of 12 animals receiving striatal grafts or co-grafts, consistent with survival of embryonic primordial striatum grafted into a severely denervated and lesioned striatum. Our study confirms that functional improvement may be obtained from embryonic neuronal grafts in a double-lesion rat model of multiple system atrophy/striatonigral degeneration type. Co-grafts appear to be required for reversal of both amphetamine- and apomorphine-induced rotation behaviour in this model. We propose that the partial reversal of amphetamine-induced rotation asymmetry in double-lesioned rats receiving mesencephalic or mesencephalic/striatal co-grafts reflects non-synaptic graft-derived dopamine release. The changes of apomorphine-induced rotation following transplantation are likely to reflect a complex interaction of graft- and host-derived striatal projection pathways and basal ganglia output nuclei. Further studies in a larger number of animals are required to determine whether morphological parameters and behavioural improvement in the neurotransplantation multiple system atrophy rat model correlate.

Reversal of behavioural abnormalities by fetal allografts in a novel rat model of striatonigral degeneration.

We have developed a rodent model of striatonigral degeneration, one of the core pathologies underlying the disease multiple system atrophy (MSA). 6-Hydroxydopamine (6-OHDA) was administered into the left medial forebrain bundle of male Wistar rats, followed 3-4 weeks later by intrastriatal injection of quinolinic acid into the ipsilateral striatum. The 6-OHDA lesion resulted in ipsilateral rotation to (+)-amphetamine and contralateral rotation to apomorphine. Following the subsequent striatal lesion, amphetamine-induced ipsilateral rotation persisted, but apomorphine-induced contralateral rotation was reduced or abolished. Subsequently, the lesioned striatum was implanted with fetal CNS allografts consisting of cell suspensions derived from striatal primordium alone or combined with cografts of ventral mesencephalon. Cografted rats showed a reduction or reversal of amphetamine-induced rotation. This was not observed in animals receiving striatal grafts alone. Apomorphine-induced contralateral rotation was restored after striatal grafts alone, but only partially in animals receiving sham or cografts. Tyrosine hydroxylase (TH) and dopamine- and cyclic adenosine 3':5'-monophosphate-regulated phosphoprotein (DARPP 32) immunocytochemistry showed mesencephalic and striatal graft survival in most animals. However, dopaminergic outgrowth was restricted to the graft deposit. The latter was surrounded by a markedly gliotic glial fibrillary acidic protein-positive capsule continuous with corpus callosum. Dopaminergic reinnervation of denervated and lesioned adult striatum itself was absent, suggesting that rotational recovery was due to diffuse dopamine release. The study shows that combined unilateral lesioning of rodent medial forebrain bundle and striatum results in a characteristic drug-induced rotational response that can be partly restored by mesencephalic/striatal cografts.

Copper-zinc superoxide dismutase in cerebrospinal fluid: implications for oxygen-radical stress in the central nervous system.

We determined the concentration of copper zinc superoxide dismutase (CuZnSOD) in cerebrospinal fluid (CSF) and plasma of 36 persons without neurological illness or with various central and peripheral nervous system disorders not supposed to generate abnormal radical formation. The CuZnSOD concentration in CSF was significantly higher compared with plasma, suggesting the presence of a high oxygen-radical load on the central nervous system. Our data may be considered to reflect normal values.

Follow-up magnetic resonance imaging in Hallervorden-Spatz disease.

Bilateral high signal emitting areas in the globus pallidus surrounded by low signal emitting areas have been described as a typical MRI finding in Hallervorden-Spatz disease (HSD). We made a diagnosis of HSD in an 11-year-old girl with progressive dystonia of 4 years duration who showed these typical MRI abnormalities. An initial MRI at the age of 9 was normal. Pathological confirmation of these typical MRI findings has not yet been described, but earlier reports as well as our case suggest that MRI may be helpful in making a clinical diagnosis of HSD. This case further shows that MRI may be normal in an early stage of the disease.

Postinfectious encephalitis in two siblings.

A 33-year-old man and his 32-year-old sister developed, with an interval of 2 years, an acute fatal encephalitis following an upper respiratory tract infection of unknown etiology. Autopsy documented postinfectious encephalitis in both. This is the first report of postinfectious encephalitis occurring in first degree relatives, suggesting that specific genetic factors play a role in the pathogenesis of this disease.

Cognition in patients with multiple sclerosis After four years.

This study reports on a 4-year follow-up of cognitive functioning in 33 MS patients and 18 healthy control subjects. As a group, and in agreement with the results in the previous assessment. MS patients have significantly weaker performances than controls in motor speed, reaction time, learning tasks, reading aloud and figure copying. Tasks addressing visuospatial problem solving, behavioural flexibility, and linguistic aspects of oral and written communication do not distinguish between the two groups. Influence of impaired movement is acknowledged in performances utilising speech and reading under instructions of speed, and in figure copying. Cognition per sé remained undisturbed in 25 patients (76%). A uniform MS-related development of cognitive deficits could not be identified, improvement, stability and further deterioration being found at reassessment.

The incidence of EEG abnormalities and outcome of infants paralyzed with neuromuscular blocking agents.

The EEGs of 40 infants paralyzed with D-tubocurarine or pancuronium during the neonatal period were reviewed retrospectively. The 23 infants who survived were re-examined at 1-3 yr of age. Sixteen infants had normal or mildly abnormal EEGs in the neonatal period; 3 died of nonneurologic causes; the remainder were normal at follow-up. Three of 8 infants with moderately abnormal EEGs in the neonatal period died, 2 had neurologic sequelae at follow-up, and 3 were normal at follow-up. Eleven of 16 infants with markedly abnormal EEGs died, and 5 had neurologic deficits at follow-up. Seizures occurred in 16 infants. Ten (63%) of the 16 died, whereas only 7 (29%) of 24 infants without seizures died (p less than .1). Eight infants had seizures only during paralysis. The EEG was statistically the best predictor of neurologic outcome when compared with the following variables recorded before paralysis: estimated gestational age (EGA), birth weight, Apgar score at 1 and 5 min, lowest PO2 and pH and highest PCO2. This study establishes the value of the EEG in the neurologic assessment of iatrogenically paralyzed newborns in the detection of seizures, and confirms previous studies which showed the value of EEG in predicting outcome.