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Hand function deficits in hemiplegic children are a major cause of disability, but there is a lack of appropriate instruments for evaluating the evolution of this deficit over time and for verifying the efficacy of its treatment. We evaluated changes in upper limb function in relation to age and the course of individual rehabilitation treatment in 20 children (13 males and 7 females) who were first seen within the first four years of life and subsequently followed until a mean age of 13 years and four months (range, 11-17 years) in accordance with a diagnostic/rehabilitation program initiated in our division in 1989. All of the children were treated by us; those whose paretic upper limb functioned well were not treated in any specific or directed manner. The protocol involved a qualitative evaluation of the spontaneous use of the paretic hand and a quantitative evaluation of grip. Analysis of the results revealed an age-related global improvement over time, occurring within the first five years of life and more pronounced in terms of grip than spontaneous use. This finding makes our protocol more specific than those currently used because it more reliably establishes the real capacity to use the paretic hand in different situations of everyday life. The most important changes concerned the children with more impaired functional capacity, whereas the children who presented with good functional skill retained this capacity over time, thus confirming the initial decision not to treat them.
The purpose of this study was to see 1) if there is a relationship between side of hemiparesis and subsequent lower extremity amputation and 2) if time from onset of cerebrovascular accident (CVA) to onset of amputation is less in patients with diabetes mellitus than in those without that disease. Twenty-two subjects with a mean age of 63.9 +/- 11.4 years met the criterion of having a CVA followed by a lower extremity amputation. Date and side of hemiparesis and amputation were noted and a relationship was determined using the two-tailed chi-square test. Twenty-one of 22 subjects had the amputation on the same side as their hemiparesis which represents a significant relationship (chi 2 = 18.16, p less than 0.001). Mean time from CVA to amputation was 32.5 +/- 26.12 mo for diabetics and 55.0 +/- 33.1 mo for nondiabetics which also represents a significant difference (t = 1.74, p less than 0.05). It is concluded there is a strong relationship between side of hemiparesis and subsequent lower extremity amputation with the amputation occurring most often on the hemiparetic side and earlier in patients with diabetes mellitus. The causal relationship between side of CVA and subsequent same sided amputation may be due to altered autonomic nervous system control, altered sensation with increased incidence of local unobserved trauma or decreased/altered muscle fiber use on the affected side. Implications for clinical rehabilitation include education for skin protection and attempting to increase muscle fiber activity.
Twenty-two patients with cerebral vascular accident (CVA), clinically confirmed by head computed tomography, were observed for symptoms of the reflex sympathetic dystrophy syndrome (RSDS). All patients received triple phase bone scans; 16 scans were positive for RSDS. Patients with negative scans had no symptoms of RSDS. Five patients with positive scans had RSDS symptoms at the time of bone scanning. Seven of 11 patients with positive scans but no symptoms of RSDS at the time of bone scan developed symptoms of RSDS within six months. We found a significant relationship between positive bone scans and the subsequent development of RSDS (p < 0.01). Considering only those patients who were asymptomatic for RSDS at the time of bone scanning, we found bone scanning to be a good predictor for the future development of clinical RSDS. We found the correlation between positive bone scans and the subsequent development of clinical RSDS in previously asymptomatic individuals to be statistically significant (p < 0.05). We conclude that bone scans may be a good predictor of patients at risk for developing clinical RSDS after CVA.
The effects of systemic phenytoin administration on the motor deficit resulting from a cortical lesion were studied in rats trained to walk coordinately on a narrow beam. The somatomotor cortex lesion was produced by an indwelling cannula through which saline or GABA were infused chronically via an osmotic minipump. Phenytoin (50 mg/kg i.p.) administered between days 3 and 5 after the intracortical catheter implantation produced a significant increase in the severity of the resulting hemiplegic syndrome. This DPH effect was more noticeable in those animals also receiving intracortical GABA infusions. The anticonvulsant at the dose used had no effect on motor performance when administered preoperatively or when given to the animals 14 days after surgical intervention when their hemiplegic syndrome had cleared. These findings suggest that phenytoin administration to brain-damaged individuals in the initial postlesion stage may be deleterious.
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An electrophysiological study of the blink reflex was undertaken in 20 normal subjects and in 28 patients complaining of central facial palsy caused by unilateral hemispheral damage. In normal subjects, the latency, amplitude and organization of R1 and R2 responses are well known. Habituation of R2 responses occurred between 1 and 2 c/sec stimulation rate. R1 responses habituated at a higher stimulation rate (5 c/sec). In patients with unilateral hemispheral lesion, our results showed that changes in the blink reflex responses were bilateral. On the hemiplegic side the responses showed a decreased amplitude, while they were facilitated on the "normal" side. However, there was no change in latency of the two components of the reflex, on both sides. On the other hand, habituation of the late component occurred on the hemiplegic side for low stimulation rates: (0.5--1 c/sec), while on the "normal" side there was less habituation (3--4 c/sec), as compared with normal subjects. These results agree with those of experimental studies on cortical modulatory influences on brain-stem nuclei. They suggest a tactile origin of the two components of the blink reflex.
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