Prevalence of Spasticity and Below-Level Neuropathic Pain Related to Spinal Cord Injury Level and Damage to the Lower Spinal Segments.

OBJECTIVE: To evaluate spasticity and below-level spinal cord injury neuropathic pain after spinal cord injury in patients with, or without, damage to the lumbar spinal cord and roots. DESIGN/PATIENTS: Chart review of 269 patients with spinal cord injury from segments C1 to T11. METHODS: Patients were interviewed concerning leg spasticity and below-level spinal cord injury neuropathic pain in the lower trunk and legs. Damage to the lumbar spinal cord and roots was inferred where there was radiological evidence of a vertebral fracture, spinal stenosis or the narrowing of spinal foramina of a vertebra from thoracic 11 to lumbar 5, or; magnetic resonance imaging showing evidence of damage to the lumbar spinal cord and roots. RESULTS: Among 161 patients without damage to the lumbar spinal cord and roots, 87% of those with cervical spinal cord injury experienced spasticity, compared with 85% with thoracic spinal cord injury. The corresponding figures for patients in whom damage to the lumbar spinal cord and roots was present were 57% and 52%, respectively. Below-level spinal cord injury neuropathic pain was not associated with damage to the lumbar spinal cord and roots. In those patients with no damage to the lumbar spinal cord and roots, regression showed that neither outcome was significantly associated with the level of spinal cord injury. CONCLUSION: The lack of segmental dependency for spinal cord injury and spasticity suggests mechanisms restricted mainly to the lumbar spinal cord. For below-level spinal cord injury neuropathic pain, additional mechanisms, other than lesions of the spino-thalamic tract, must be considered.

Intrathecal Baclofen Dosage for Long-Term Treatment of Patients With Spasticity Due to Traumatic Spinal Cord Injuries or Multiple Sclerosis.

OBJECTIVE: To investigate dosage changes in intrathecal baclofen during long-term treatment of patients with severe leg spasticity. METHODS: We performed a retrospective chart review of 49 patients treated with an intrathecal baclofen pump (ITB) because of severe leg spasticity, for a minimum of 7 years. Eight patients were excluded due to catheter/pump failure or factors aggravating spasticity. Of the remaining 41 patients, 19 had spinal cord injury (SCI) and 22 were diagnosed with multiple sclerosis (MS). Among the SCI patients, 15 had cervical and 4 thoracic SCI, with 7 patients showing the American Spinal Injury Association impairment scale (AIS) A and 12 patients with AIS B-D. The dose was regulated by discussion among the patients and their physicians, usually 4-10 times annually, to reduce leg spasticity and also avoid leg/trunk weakness. RESULTS: After 1 year patients on ITB needed a median dose of 168 mg/24 hr (range, 30-725 mg) for an optimal effect. After 7 to 10 years the dosage needed to reduce leg spasticity in the MS patients was significantly increased compared with the initial dose (mean 157%, n=22 and mean 194%, n=18). In contrast, the SCI patients needed only a modest increase (mean 113% and 121%). The difference between MS and SCI patients was significant (t-test p=0.006 and p=0.004). CONCLUSION: The increased dosage in MS patients compared with patients diagnosed with SCI probably reflects the progressive disease course. The need for a large dosage increase in patients with SCI suggests possible pump failure, triggering factors for spasticity or progressive spinal disease.

Clinical Assessment of Spasticity in People With Spinal Cord Damage: Recommendations From the Ability Network, an International Initiative.

A thorough assessment of the extent and severity of spasticity, and its effect on functioning, is central to the effective management of spasticity in persons with spinal cord damage (SCD). These individuals however do not always receive adequate assessment of their spasticity. Inadequate assessment compromises management when the effect of spasticity and/or need for intervention are not fully recognized. Assessment is also central to determining treatment efficacy. A barrier to spasticity assessment has been the lack of consensus on clinical and functional measures suitable for routine clinical practice. To extend on existing work, a working group of the Ability Network identified and consolidated information on possible measures, and then synthesized and formulated findings into practical recommendations for assessing spasticity and its effect on function in persons with SCD. Sixteen clinical and functional measures that have been used for this purpose were identified using a targeted literature review. These were mapped to the relevant domains of the International Classification of Functioning, Disability and Health to assess the breadth of their coverage; coverage of many domains was found to be lacking, suggesting a focus for future work. The advantages, disadvantages, and usefulness of the measures were assessed using a range of criteria, with a focus on usefulness and feasibility in routine clinical practice. Based on this evaluation, a selection of measures suitable for initial and follow-up assessments are recommended. The recommendations are intended to have broad applicability to a variety of health care settings where people with SCD are managed.

The outcome spectrum of multiple sclerosis: disability, mortality, and a cluster of predictors from onset.

Interest in the long-term natural history of multiple sclerosis (MS) is being revived, as disability endpoints become increasingly important with the advent of highly efficacious long range but potentially harmful drugs. MS had an increasingly benign course, probably due to better assessment and changing diagnostic criteria. Incidence cohorts reduce inclusion bias, capturing both extreme benign and severe cases. We conducted a 50-year follow-up of an incidence cohort of Gothenburg residents with MS onset in 1950-1964 (n = 254; 212 with an initial relapsing-remitting course and 42 with a monophasic course, diagnostic criteria according to Poser). Patients were followed longitudinally until censoring, death, or study termination in 2012 and evaluated using Kaplan-Meier estimates and Cox regression analysis. Median time to secondary progression was 15 years. Median time to EDSS6 and EDSS7 was 26 and 48 years (n = 254), respectively. The cumulative risk of reaching EDSS6 was 50% at 55 years of age and 80% at 80 years of age (n = 212). A score based on a cluster of clinical features at onset predicted secondary progression, EDSS6, EDSS7, and EDSS10 (hazard ratio 1.6-2.3 per score unit for women, 0.99-1.49 for men). This score predicted the disease course during five decades indirectly, by predicting time to secondary progression. Age at onset predicted the course in men, with 3-6% yearly increase in the risk of reaching disability milestones. The present incidence cohort provided hard outcome data in untreated patients over several decades.

Continuous prediction of secondary progression in the individual course of multiple sclerosis.

BACKGROUND: Prediction of the course of multiple sclerosis (MS) was traditionally based on features close to onset. OBJECTIVE: To evaluate predictors of the individual risk of secondary progression (SP) identified at any time during relapsing-remitting MS. METHODS: We analysed a database comprising an untreated MS incidence cohort (n=306) with five decades of follow-up. Data regarding predictors of all attacks (n=749) and demographics from patients (n=157) with at least one distinct second attack were included as covariates in a Poisson regression analysis with SP as outcome. RESULTS: The average hazard function of transition to SPMS was 0.046 events per patient year, showing a maximum at age 33. Three covariates were significant predictors: age, a descriptor of the most recent relapse, and the interaction between the descriptor and time since the relapse. A hazard function termed "prediction score" estimated the risk of SP as number of transition events per patient year (range <0.01 to >0.15). CONCLUSIONS: The insights gained from this study are that the risk of transition to SP varies over time in individual patients, that the risk of SP is linked to previous relapses, that predictors in the later stages of the course are more effective than the traditional onset predictors, and that the number of potential predictors can be reduced to a few (three in this study) essential items. This advanced simplification facilitates adaption of the "prediction score" to other (more recent, benign or treated) materials, and allows for compact web-based applications (http://msprediction.com).

A representative cohort of patients with non-progressive multiple sclerosis at the age of normal life expectancy.

Multiple sclerosis may have a non-progressive symptomatology for decades; however, it is not clear whether the disease activity may abate completely. We identified a cohort of patients, resident in Gothenburg at the time of disease onset, between the years 1950-64 (n = 307). These geographical and temporal restrictions, along with favourable conditions for a 'spider' epidemiological study, were optimal for an unbiased selection; this 15-year incidence cohort was essentially followed prospectively for 37-59 years after onset. The shortest follow-up time for patients without primary or secondary progression was 45 years. For patients with an initial relapsing-remitting course and multiple sclerosis diagnosis according to the Poser criteria (n = 202), the probability of non-progressive disease after 40 years was 22% (standard error 3.0%), and after 50 years it was 14% (standard error 3.2%). For attack onset including patients with possible multiple sclerosis, the corresponding probabilities after 40 and 50 years were 35% (standard error 3.3%) and 28% (standard error 3.5%), respectively. At the last follow-up in 2009-10, when patients reached the average age of the Swedish population life expectancy, only 13 patients from the multiple sclerosis diagnosis cohort, according to the Poser criteria, remained alive and non-progressive. Their annualized attack frequency diminished with time from 0.29 to 0.015. These patients had been functioning well socially. Nine patients had an Expanded Disability Status Scale score of 0-2.5, and four patients had a score of 3 or 3.5, with deficits dating back to attacks decades ago. Eight patients participated in a complete neuropsychological examination, which showed a slight difference (P < 0.01) concerning verbal memory and executive function compared to an age and socially matched reference group, whereas results for five other cognitive domains were within the normal range. Magnetic resonance images fulfilled the Barkhof-Tintoré criteria for multiple sclerosis in 10 of 11 patients, with conspicuously few subcortical lesions relative to extensive periventricular lesions and lesions extending from the inferior midline aspect of the corpus callosum. Prediction of the non-progressive stage was possible with moderate hazard ratios and low sensitivity. Early features that predicted a non-progressive course were complete remission of the onset attack, low or moderate initial relapse frequency and-when the patients with possible multiple sclerosis were included-dominating afferent symptoms. The clinical disease activity had abated in these 13 patients, with the caveat that transition to secondary progression continued to occur after four decades, albeit with decreasing risk.