The indirect effect of positive aspects of caregiving on the relationship between cognitive decline and dementia caregiver burden.

BACKGROUND: Research has linked increased cognitive decline in a dementia care recipient to worsening caregiver burden, but the presence of positive aspects of caregiving is associated with better outcomes. As cognitive decline worsens, a lack of positive caregiving experiences could lead to burden for the caregiver. This study investigated relationships among dementia caregiver burden, cognitive decline, and positive aspects of caregiving in dementia, predicting an indirect effect of positive aspects of caregiving. METHODS: Data from 724 patients of an outpatient memory clinic in Ohio were examined and dyads included based on clinically supported patient diagnoses on the dementia spectrum. Caregivers completed the Zarit Burden Interview (ZBI) and Positive Aspects of Caregiving (PAC) measures. The Montreal Cognitive Assessment and Mini-Mental State Examination were used to estimate cognitive decline, standardized to create a single variable. Multiple potential covariates were considered for inclusion in the model. A cross-sectional mediation analysis using the Hayes PROCESS macro explored the presence of an indirect effect of PAC on the relationship between cognitive decline and ZBI using 5000 bootstrap samples. RESULTS: Only the potential covariate caregiver age was correlated with any of the primary variables; this variable was controlled in analyses. Significant relationships emerged between cognitive decline and ZBI (r = -0.12, P < 0.001), between PAC and ZBI (r = -0.23, P < 0.001), and between cognitive decline and PAC (r = -0.07, P < 0.05). An indirect effect of positive aspects of caregiving on the relationship between cognitive decline and ZBI was statistically significant (B = 0.0092, 95% bias-corrected confidence interval: 0.0008, 0.0185), accounting for 14.4% of the variance in the model. CONCLUSIONS: A lack of positive aspects of caregiving could be partially responsible for development of dementia caregiver burden as cognitive decline worsens. Longitudinal examination of these relationships is needed to understand causality fully. Findings may help healthcare providers tailor treatment to alleviate caregiver burden.

Does low-dose botulinum toxin help the recovery of arm function when given early after stroke? A phase II randomized controlled pilot study to estimate effect size.

OBJECTIVE: Spasticity after stroke may be associated with worse functional outcome. Our study aim is to establish whether a low dose of botulinum toxin, given early post stroke before clinically evident spasticity warrants treatment, will improve recovery of arm function. DESIGN: A double-blind randomized placebo-controlled trial. SETTING: An acute stroke unit. SUBJECTS: Individuals recruited within three weeks of stroke onset with severe arm function deficits. INTERVENTIONS: Injections of quarter and half standard dose botulinum toxin A to the upper limb, with a control of normal saline injections. MAIN MEASURES: Arm function, active and passive movement, and spasticity at elbow and wrist were recorded at baseline, and at 4, 8, 12 and 20 weeks post intervention. A pre-planned subgroup analysis included only subjects with no arm function at baseline (Action Research Arm Test score = 0). RESULTS: Thirty subjects were recruited, and 21 completed all assessments. Arm function scores improved in all three groups between baseline and week 20. There was no benefit for active treatment over control in the whole group analysis. In the subgroup analysis the active groups improved when compared with the control group and effect sizes for improvement in this subgroup were 0.6 and 0.5 for the quarter dose and half dose groups respectively. CONCLUSIONS: Individuals with no arm function within three weeks of stroke may benefit functionally from botulinum toxin. Using the effect size of 0.5, further studies would need a minimum of 101 participants in each group to confirm this finding.

Quantitative measurement of poststroke spasticity and response to treatment with botulinum toxin: a 2-patient case report.

BACKGROUND AND PURPOSE: Spasticity (hypertonicity) is a frequent problem that can develop after stroke and can lead to a number of secondary complications, such as contractures and pain. Consequently, many rehabilitation resources are used in treating the condition and its secondary complications. At present, the clinical assessment of spasticity incorporates descriptive scales of resistance to passive movement, but the use of a neurophysiological measure of muscle activity levels has been advocated. This case report focuses on the diagnosis of spasticity through the use of a neurophysiological measure. CASE DESCRIPTION: . Two individuals who required botulinum toxin treatment for poststroke spasticity were assessed over a course of 20 weeks with both clinical (Modified Ashworth Scale) and neurophysiological (surface electromyography recording of levels of muscle activity) measures of spasticity. Additionally, arm function, arm movement, and pain were measured. The individuals' responses to treatment with botulinum toxin and overall recovery after stroke are described. OUTCOMES: There were discrepancies between the clinical and the neurophysiological measures of spasticity. The clinical measure of spasticity was not effective in consistently identifying the presence of spasticity and, therefore, also was ineffective in documenting the individuals' responses to treatment. The neurophysiological measure was able to identify when muscle activity levels had been reduced, but a reduction in muscle activity levels did not always correspond with a reduction in Modified Ashworth Scale scores. DISCUSSION: The accurate identification of spasticity is important not only for assessment but also for the selection of appropriate treatments after stroke.

An investigation into the agreement between clinical, biomechanical and neurophysiological measures of spasticity.

OBJECTIVE: To quantify agreement between three clinically usable methods of measuring spasticity. METHODS: Patients with a first stroke who had no useful functional movement in the upper limb within six weeks from stroke onset were eligible to participate. Spasticity at the wrist joint was simultaneously measured using three methods, during an externally imposed passive stretch at two (uncontrolled) displacement velocities. The measures used were a common clinical measure (modified Ashworth Scale), a biomechanical measure (resistance to passive movement) and a neurophysiological measure (muscle activity). RESULTS: One hundred patients (54 men and 46 women) with a median age of 74 years (range 43-91) participated. Median time since stroke was three weeks (range 1-6), the right side was affected in 52 patients and the left in 48 patients. Based on muscle activity measurement, 87 patients had spasticity. According to the modified Ashworth score 44 patients had spasticity. Sensitivity of modified Ashworth score, when compared with muscle activity recordings, was 0.5 and specificity was 0.92. Based on muscle activity patterns, patients could be classified into five subgroups. The biomechanical measures showed no consistent relationship with the other measures. CONCLUSION: The presentations of spasticity are variable and are not always consistent with existing definitions. Existing clinical scales that depend on the quantification of muscle tone may lack the sensitivity to quantify the abnormal muscle activation and stiffness associated with common definitions of spasticity. Neurophysiological measures may provide more clinically useful information for the management and assessment of spasticity.