Perilesional Reorganization in a Patient With Brain Tumor

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Excerpt

A 54-yr-old female patient underwent surgery to remove a meningioma at the neurosurgery department of a university hospital. Three weeks after surgery, she was admitted to the rehabilitation department of another university hospital. T2-weighted brain magnetic resonance images (MRIs) showed a leukomalactic lesion in the leg somatopic area of the right primary sensorimotor cortex and right supplementary motor area (Fig. 1A). The patient had motor weakness of the left leg (Manual Muscle Test: hip flexo, 3/5; knee extensor, 3/5; ankle dorsiflexor, 3−/5). She underwent comprehensive rehabilitative management for 4 wks, and her left leg weakness recovered to a subnormal state (hip flexor, 4+/5; knee extensor, 4+/5; ankle dorsiflexor, 4/5). We performed functional MRI and diffusion tensor imaging to investigate the mechanism of motor recovery in this patient.
Functional MRI measurements were performed using the echo planar imaging technique. Using a block paradigm (20-sec control, 20-sec stimulation: 3 cycles), toe flexion-extension movements(1 Hz) were performed for stimulation. The right primary sensorimotor cortex was activated during movements of the right (unaffected) toes (Fig. 1B). However, the perilesional areas were activated during movements of the left(affected) toes.
Diffusion tensor imaging data were acquired twice (3 and 7 wks after onset). For analysis of the corticospinal tracts (CSTs), the first and second regions of interest were placed on the lower and upper pons, respectively.1 Diffusion tensor tractography (DTT) 3 wks later showed that the right CST was discontinued at the corona radiata level. In contrast, the discontinued right CST was extended to the cerebral cortex through the perilesional white matter on DTT at 7 wks (Fig. 1C).
In this study, using functional MRI and DTT, we attempted to find change of the affected (right) CST responsible for motor recovery of the affected (left) leg and it seems that motor function of the left leg recovered as a result of healing of the CST, which passed through the perilesional area, for the following reasons: motor function of the affected leg recovered to a subnormal state after 4 wks of rehabilitation, and this indicated that other than the injured right leg somatotopic area was responsible for the motor function of the affected motor function. The perilesional area was activated by movements of the left leg on the 7-wk functional MRI and the left CST descended through the perilesional white matter on the 7-wk DTT. It seems that the motor function of the affected leg in this patient probably reorganized into the intact peri-infarct areas.

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