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(Stroke. 1999;30:1380-1383.)
© 1999 American Heart Association, Inc.

Original Contributions

Middle Cerebral Artery Stroke That Includes the Premotor Cortex Reduces Mobility Outcome

Presented in preliminary form at the 50th annual meeting of the American Academy of Neurology, Minneapolis, Minn, April 29, 1998.

Ichiro Miyai, MD, PhD; Tsunehiko Suzuki, MD, PhD; Jin Kang, MD, PhD; Kisou Kubota, MD, PhD Bruce T. Volpe, MD

From the Department of Neurology, Toneyama National Hospital, Osaka, Japan (I.M., J.K.); Bobath Memorial Hospital, Osaka, Japan (T.S., K.K.); and the Department of Neurology, Cornell University Medical College, Burke Medical Research Institute, White Plains, NY (B.T.V.).

Correspondence to Ichiro Miyai, MD, PhD, Department of Neurology, Toneyama National Hospital, 5-1-1, Toneyama, Toyonaka City, Osaka 560-8552, Japan. E-mail webeo{at}ga2 so-net.ne.jp

	Abstract

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Background and Purpose—The premotor cortex (PMC) (Brodmann 6) contributes uniquely to proximal upper and lower limb power and plays a role in the organization of motor behaviors. We assessed the degree to which PMC damage affected functional outcome.

Methods—We prospectively compared the functional outcome of patients with a first stroke in the middle cerebral artery distribution that either left the PMC intact (PMC-; n=19) or damaged the PMC (PMC+; n=12). The Functional Independence Measure for disability and the motor score of the Stroke Impairment Assessment Set for impairment assessed outcome.

Results—Demographic and clinical features and lesion volume were comparable for the PMC+ and PMC- groups. However, the PMC- group demonstrated significant gain in mobility and in proximal leg movement. This focal improvement contributed to the trend in the PMC- group toward greater independent ambulation.

Conclusions—Decreased motor recovery of proximal lower limbs in humans with PMC damage supports the idea that it is the origin of corticoreticulospinal pathways that subserve proximal lower extremity function. Furthermore, persistent proximal weakness after PMC damage may amplify other motor impairments, which include defects in planning, initiating, and sequencing. Neurorehabilitation outcomes may contribute to a more detailed functional anatomy after stroke and partial recovery.

Key Words: middle cerebral artery • stroke outcome • rehabilitation

	Introduction

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We and others have demonstrated that patients with stroke confined to the basal ganglia (BG), including the internal capsule but sparing the cortex, had diminished response to rehabilitation compared with those with comparable damage to the BG and overlying cortex.^{1 2} To further specify these findings, in the present study we assessed the effect on outcome of ischemic damage in the premotor cortex (PMC or lateral premotor cortex, Brodmann area 6) or supplementary motor area (SMA or medial premotor cortex, Brodmann area 6).^{3 4 5 6} This study focused on patients with an initial single cerebral infarction in the territory of the middle cerebral artery (MCA). Since the SMA is supplied by the anterior cerebral artery, the target patients had BG and internal capsule damage with or without PMC damage.

Damage to the PMC disrupts sequential motor tasks and causes unilateral weakness of shoulder and hip muscles.^{7 8} Recent functional imaging has demonstrated that the recovery of sequential movements, limited by scan protocol demands to finger movements, in patients with stroke was associated with bilateral activation of the PMC.⁹ Other functional imaging and neurophysiological studies have suggested that the PMC mediates motor behavior that is dependent on environmental cues of the sort that occur commonly in rehabilitation environments.^{3 7 10 11 12} We examined whether these characteristics of the functional anatomy of PMC stroke would have an effect on rehabilitation outcome.

	Subjects and Methods

Top Abstract Introduction Subjects and Methods Results Discussion References

 
We examined 42 consecutive patients who had an initial single cerebral infarction with an ischemic lesion in the territory of the MCA, including the subcortical regions of the corona radiata, internal capsule, and the BG (mainly the putamen and the globus pallidus), as well as the overlying cortex, including the primary sensorimotor cortex. All patients were transferred to the Rehabilitation Division of Bobath Memorial Hospital after initial medical treatment followed by short-term physical therapy at acute care hospitals. On average, 4 months after the onset of stroke, patients who were still nonambulatory were referred to the hospital for multidisciplinary rehabilitation (Table 1). Patients with severe medical complications participated in abbreviated rehabilitation programs and were not available for detailed weekly assessments; they were therefore excluded from the protocol. These 11 patients had congestive heart failure, myocardial infarctions, unremitting cardiac arrhythmias, pneumonia, hip fracture, deep vein thrombosis, and uncontrolled hypertension. Thirty-one patients were enrolled in the study.

View this table: [in this window] [in a new window]   Table 1. Demographic Features in Patients With Cerebral Infarction Designated PMC+ and PMC-

MRI information was obtained on admission (on average, 4 months; Table 1). The MRI protocol was identical for all patients in the study: lesions were identified with the use of a 1.0-T superconductive MRI system (Shimazu, MAGNEX Epios10). T2-weighted (repetition time, 3630 ms; echo time, 110 ms) axial spin-echo images as well as T1-weighted (repetition time, 500 ms; echo time, 15 ms) axial spin-echo images were obtained. Lesion density maps of each patient were plotted on the standardized horizontal brain templates,¹³ and digitalized files of the T2-weighted images were imported into the measuring program (NIH Image 1.60). Lesion volume was estimated by summing the area of the T2-identified infarct across contiguous slices. The slice dimensions were 8.5 mm thick with a slice gap of 1.5 mm; there was no slice overlap. On the basis of the distribution of cortical lesions, patients were divided into 2 groups: 12 patients were designated PMC+ and had damage in the subcortical regions as defined above and the overlying cortex including PMC; 19 patients were designated PMC- and had damage in subcortical regions and the overlying cortex other than PMC. No patient in either group had a thalamic lesion.

All patients received multidisciplinary inpatient rehabilitation by the neurodevelopmental technique of Bobath,¹⁴ including 45-minute sessions of physical therapy, 45-minute sessions of occupational therapy, and 45-minute sessions of speech therapy as needed, 5 days a week. At admission and discharge, functional outcome was evaluated with the use of reliable and valid measures: the Functional Independence Measure^{15 16} (FIM) for disability and the motor subscore of the Stroke Impairment Assessment Set¹⁷ (SIAS) for neurological impairment. We also analyzed the change of activities of daily living (ADL), mobility, and cognition subscores of FIM. The motor subscore of SIAS (score range, 0 to 25) consists of 2 tests for upper extremity (score range, 0 to 10) and 3 tests for lower extremity (score range, 0 to 15). Details of SIAS are described in Tables 2 and 3.

View this table: [in this window] [in a new window]   Table 2. Motor Subscores of SIAS

View this table: [in this window] [in a new window]   Table 3. Scoring of SIAS

FIM was rated by trained nursing staff who were blinded to sites of lesions, and SIAS was rated by physicians who were also blinded to sites of lesions. FIM evaluation was performed every 2 to 3 weeks, and when the FIM score reached a plateau, a discharge plan was finalized. Interrater reliability for individual items of SIAS and FIM was estimated with the use of weighted ¹⁸ (n=16). The statistics for each SIAS item were 0.91 (95% CI, 0.77 to 1.07) for knee-mouth test, 0.85 (95% CI, 0.65 to 1.04) for finger test, 0.69 (95% CI, 0.39 to 0.98) for hip flexion test, 0.70 (95% CI, 0.42 to 0.98) for knee extension test, and 0.71 (95% CI, 0.44 to 0.97) for ankle dorsiflexion test. Thus, each item of the SIAS demonstrated agreement (=0.69 to 0.91) across raters. The Spearman correlation coefficient across raters for total SIAS, SIAS for upper extremity, and SIAS for lower extremity was 0.980 (P=0.0001), 0.986 (P=0.0001), and 0.944 (P=0.0003), respectively. Reliability for each FIM item also ranged from good to very good: 0.66 (0.38 to 0.95) for eating, 0.62 (0.37 to 0.88) for grooming, 0.71 (0.45 to 0.96) for bathing, 0.67 (0.43 to 0.91) for dressing upper body, 0.84 (0.65 to 1.04) for dressing lower body, 0.68 (0.41 to 0.95) for toileting, 0.93 (0.79 to 1.06) for bladder management, 0.76 (0.50 to 1.01) for bowel management, 0.71 (0.47 to 0.96) for bed/chair transfer, 0.74 (0.49 to 0.99) for toilet transfer, 0.77 (0.55 to 0.99) for tub/shower transfer, 0.77 (0.55 to 1.00) for walk/wheelchair, 0.81 (0.52 to 1.10) for stairs, 0.85 (0.66 to 1.04) for comprehension, 0.79 (0.58 to 1.00) for expression, 0.68 (0.41 to 0.94) for social interaction, 0.72 (0.50 to 0.95) for problem solving, and 0.83 (0.60 to 1.05) for memory. The Spearman correlation coefficient for total FIM (0.973; P<0.005), ADL subscale (0.912; P<0.005), mobility subscale (0.987; P<0.005), and cognition subscale (0.976; P<0.005) was significant.

We used either a ² test or an unpaired t test to compare demographic data of the groups. Statistical analysis for functional outcome relied on the nonparametric Wilcoxon rank sum test.

	Results

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Table 1 demonstrates that the groups were similar in regard to sex, age, days after stroke, length of stay, side of stroke, type of deficits, Mini-Mental State Examination, and volume of lesion. Of note, all patients had motor plus sensory plus visual deficits. Visual fields were assessed by single and double confrontation with moving fingers and by reaction to visual threat in globally aphasic patients All patients were moderately or severely paralyzed, and no patients had limb-kinetic apraxia, ideomotor apraxia, or ideational apraxia.^{8 19} Although no patient met the criteria of the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition for organic mood disorder with depression, 2 patients in each group were treated with antidepressants. Lesion density maps of patients with cerebral infarction with and without PMC lesion showed comparable lesion volume estimation for PMC+ and PMC- (Figure) (PMC+=72.9±8.0 cm³ [±SEM]; PMC-=65.9±8.0 cm³; P=0.2403).

View larger version (78K): [in this window] [in a new window]   Figure 1. Lesion density maps of patients with cerebral infarction with (PMC+, top) and without (PMC-, bottom) PMC lesion. Each lesion was transposed to the left hemisphere of standardized horizontal brain templates.12 These images were then superimposed with the use of NIH Image version 1.60 to produce lesion density maps for each group of patients. From the readers' left to right, +3.1, 4.4, 5.6, and 7.0 cm from the canthomeatal line. L indicates lateral; M, medial.

On admission, PMC- and PMC+ were comparable on total FIM and on the mobility, ADL, and cognition subscores. PMC+ demonstrated a significantly retarded mobility outcome on discharge (Table 4) (P<0.05, Wilcoxon rank sum test). There was a trend toward greater independence in ambulation (without physical assistance or supervision) for the PMC- group (16 of 19 [84%] compared with 7 of 12 [58%] for the PMC+ group).

View this table: [in this window] [in a new window]   Table 4. Comparison of Admission and Discharge FIM Scores Between PMC+ and PMC-

To make comparisons in regions where the administrative rules for discharge vary, we calculated FIM efficiency for each patient (gain of FIM score/length of stay measured in days). The data (mean±SEM efficiency) demonstrate trends toward greater FIM efficacy for the PMC- group (PMC+/PMC-=0.085±0.024/0.141±0.036 for total FIM score; P=0.268). For purpose of comparison, these FIM efficacy scores are comparable to those of chronic stroke patients in Japan in other rehabilitation institutes.²⁰

On admission, PMC- and PMC+ were comparable on total SIAS scores and on the upper and lower extremity subscores (Table 5). There was a significant difference between PMC+ and PMC- on the gains of SIAS scores for proximal leg movement (P<0.05, Wilcoxon rank sum test) (Table 6), but the overall gain in SIAS score for upper and lower extremities was comparable.

View this table: [in this window] [in a new window]   Table 5. Comparison of Admission and Discharge SIAS Scores Between PMC+ and PMC-

View this table: [in this window] [in a new window]   Table 6. Comparison of Admission SIAS Score and Gain of SIAS for Lower Extremity Between PMC+ and PMC-

Finally, there was a significant correlation between disability (FIM) and impairment (SIAS) ratings on discharge for the hip (0.7; Z=4.41; P<0.0001) and proximal lower extremity mobility (0.7; Z=4.51; P<0.0001). In terms of disposition, there was a trend for the PMC- group to go home more often (17/19 [89%]) than the PMC+ group (8/12 [67%]).

	Discussion

Top Abstract Introduction Subjects and Methods Results Discussion References

 
In this prospective comparison of outcome in 2 groups of patients with ischemic cerebral infarction of MCA territory that differed only in lesion extension to the PMC (PMC+ or PMC-), there was a significant increase in the motor recovery of axial and proximal lower limb strength that contributed to a more favorable outcome in those without PMC damage (PMC-). These outcome differences are consistent with the current functional anatomy of stroke that damages PMC. It is crucial to note that all patients displayed comparable neurological deficits, which included hemiparesis, hemisensory loss, and homonymous hemianopia, and lesion volumes were comparable. There was no evidence for limb-kinetic apraxia, and despite a tendency of PMC+ patients to more often sustain left hemisphere damage, it was not significant (²=3.3). The initial impairment and disability levels were also comparable between the groups. Thus, the improved axial and proximal lower limb improvement undoubtedly led to the increase in acquisition of independent ambulation (84% of PMC-; 58% of PMC+), a result that also contributed to a higher rate of returning home in the PMC- group.

On the basis of current functional neuroanatomy, there are several possible mechanisms that may underlie these findings. Parallel motor pathways among the primary motor cortex, the PMC, the SMA, and the final effectors in the spinal cord are known to exist,⁶ and the persistent weakness of the PMC+ group may reflect interruption of the output projections from the PMC via the reticulospinal tract.^{7 8} The PMC appears to participate in control of the contralateral proximal musculature and also of the axial musculature bilaterally. Evidence from functional neuroimaging and neurophysiological studies^{7 10 11 12} has demonstrated that the PMC mediates motor behavior that is dependent on environmental cues, especially visual cues. Thus, in the group with PMC+, there are additional reasons for the persistent motor impairment. Positron emission tomography studies in patients with ischemic subcortical strokes have suggested that the PMC ipsilateral to the infarct undergoes enhanced positron emission tomography activation on movement of the contralateral limb.²¹ Recent functional imaging has also demonstrated that the recovery of finger movements in patients with MCA infarction was associated with bilateral activation of the PMC.⁹ Intact PMC in the PMC- group likely contributed to the improved motor outcome. A final speculation depends on the finding that the PMC is involved in motor function, which includes braking, selection, initiation, planning, and sequencing.^{22 23} Disruptions of motor behavior at this level combined with the loss of power may have made the PMC+ group more tentative, particularly with regard to ambulation.^{24 25} This trend toward less independent ambulation contributed to the decreased rate of discharge to home.

	Acknowledgments

 
The authors acknowledge support from funds for the comprehensive research on aging and health from the Ministry of Health and Welfare in Japan. We thank Naomi Hoshina for assistance with data collection.

Received February 18, 1999; revision received April 7, 1999; accepted April 7, 1999.

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Top Abstract Introduction Subjects and Methods Results Discussion References

 

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This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Miyai, I. Articles by Volpe, B. T. Search for Related Content PubMed PubMed Citation Articles by Miyai, I. Articles by Volpe, B. T. Related Collections Health policy and outcome research Embolic stroke Risk Factors for Stroke Spinal Cord Vascular Disease