Prolonged muscular flaccidity: frequency and association with unilateral spatial neglect after stroke

Formisano, Rita; Barbanti, Piero; Catarci, Teresa; Vuono, G. De; Calisse, P. G.; Razzano, Carmelina

doi:10.1111/j.1600-0404.1993.tb05349.x

Cited by 21 publications

(10 citation statements)

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“…The remaining half of the patients either showed improvement (nearly 20% of cases) or a decrease in functional ability (nearly 30% of cases). The amount of these percentages underscores the fact that, according to previous reports [9, 10], functional level may change after discharge: in many severe cases, cognitive disorders or prolonged flaccidity may delay recovery [8, 21]; or functional level may not be sufficiently consolidated to be sustained at home, may be impeded by logistic and architectural problems or may be worsened by comorbidities. It is interesting to note that functional changes were not closely related to functional status at discharge, but to specific medical and nonmedical factors.…”

Section: Discussionmentioning

confidence: 99%

One-Year Follow-Up in Stroke Patients Discharged from Rehabilitation Hospital

et al. 2000

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This study was designed to evaluate functional status at a 1-year follow-up in consecutive first-stroke patients after discharge from rehabilitation hospital and to identify reliable prognostic factors associated with changes in their abilities. Functional evaluation was made of consecutive patients 1 year after discharge to their own homes. Two multiple logistic regressions (forward stepwise) were performed using both improvement and worsening of the Barthel Index score between discharge and follow-up as dependent variables. Independent variables were medical, demographic and social factors. The final sample included 157 out of 172 patients. During the follow-up, 10 patients (5.81%) died because of a new cerebrovascular event, 1 patient died of myocardial infarction, 2 patients had new strokes and 2 fractured their paretic legs. Functionally, 43.3% of the patients maintained the level they achieved during inpatient rehabilitation treatment, 23.6% improved and the remaining 33.1% worsened. Patients with hemineglect and aged ≥65 years had a higher probability of functional worsening (odds ratio, OR = 3.77, 95% confidence interval, CI = 1.42– 10.0 and OR = 3.93, 95% CI = 1.72–8.95, respectively). Postdischarge rehabilitation (performed for 46.5% of the final sample) was significantly and positively associated with functional improvement (OR = 7.23, 95% CI = 2.89–18.05), and its absence with functional worsening (OR = 12.32, 95% CI = 4.47–37.01). In conclusion, in nearly half of the cases, functional status was still not stabilized at the time of discharge from the rehabilitation hospital. Postdischarge outpatient treatment was useful for preventing worsening of the functional ability achived during inpatient treatment and increased the possibility of further functional improvement. Age ≥65 years and hemineglect were predictors of functional worsening at follow-up.

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Section: Discussionmentioning

confidence: 99%

One-Year Follow-Up in Stroke Patients Discharged from Rehabilitation Hospital

et al. 2000

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“…In a minority of cases, flaccidity persists chronically after occurrence of a central lesion, e.g., with some spinal cord infarcts25, 132, 193 or cerebral lesions 177. Persistent flaccidity is often associated with a greater degree of paresis and poorer outcome,36, 79, 82, 133, 177, 197, 221 although this is not always the case 159, 201. Occasionally, a secondary reduction of spasticity is also observed months after spinal cord injury, which may suggest secondary impairment or degeneration of premotor neuronal circuits or of motor neurons 108…”

Section: Immediate Effects Of Central Lesionmentioning

confidence: 99%

Pathophysiology of spastic paresis. I: Paresis and soft tissue changes

2005

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Spastic paresis follows chronic disruption of the central execution of volitional command. Motor function in patients with spastic paresis is subjected over time to three fundamental insults, of which the last two are avoidable: (1) the neural insult itself, which causes paresis, i.e., reduced voluntary motor unit recruitment; (2) the relative immobilization of the paretic body part, commonly imposed by the current care environment, which causes adaptive shortening of the muscles left in a shortened position and joint contracture; and (3) the chronic disuse of the paretic body part, which is typically self-imposed in most patients. Chronic disuse causes plastic rearrangements in the higher centers that further reduce the ability to voluntarily recruit motor units, i.e., that aggravate baseline paresis. Part I of this review focuses on the pathophysiology of the first two factors causing motor impairment in spastic paresis: the vicious cycle of paresis-disuse-paresis and the contracture in soft tissues.

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“…Thesewere motor flaccidity 11 either died before discharge (n=4) or self-discharged prematurely (n=4), every stroke 124 patient admitted to the neuro-rehabilitation unit and whose medical record was 125 available was included in the study. The demographic and clinical characteristics of 126 the sample are presented in Table 1 …”

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confidence: 99%