We investigated the problems of re-entrance to ordinary schools after inpatient rehabilitation for traumatic brain injury in 18 children. Only 2 cases could not move by themselves and 4 cases showed mental deterioration at discharge. Some help was given by the rehabilitation center for re-entrance, such as meetings among the staff, teachers and families, and by the schools, such as reconstruction of school rooms. Actually, there were many problems as to study, safety, and behavior. It is important for each child with traumatic brain injury that the rehabilitation staff, teachers and families consider individual programs for re-entrance to ordinary schools all together.

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We reported a case of a ten-year-old boy who experienced multiple spontaneous fractures subsequent to hypoxic brain damage. In August 1996, he developed spastic tetraplegia due to asphyxia caused by near-drowning at the age of eight. In October 1997, with no obvious cause, he suffered a left femoral neck fracture. In November 1999, 6 days after he was brought to our clinic for consultation for the first time, he suffered a left femoral subtrochanteric fracture, followed by a suprachondylar fracture of the left femur, and 5 months later, a suprachondylar fracture of the right femur, all spontaneously. No traumatic episodes that might provoke these fractures were found. Although the causes of spontaneous fractures are usually multifactorial, such as osteoporosis, nutritional deficiency, adverse effects of anticonvulsants, and accelerated calcium excretion, it is suspected that the major causes for these fractures were severe spasticity and contractures on the lower extremities. To prevent spontaneous fractures and plan for early diagnosis and treatment, physiatrists should be aware of uncommon muscloskeletal complications in children with severe disability.

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Neuropathic pain is defined as pain initiated or caused by a primary lesion or dysfunction in the nervous system. It is found in many disorders including reflex sympathetic dystrophy (RSD) and causalgia. The motor abnormalities of dystonia, tremor and spasm associated with RSD or causalgia have been described in some reports. We reported two patients who had dystonia with neuropathic pain. One patient had fixed dystonic posture with persistent pain of the thigh and calf after hip surgery. This patient exhibited obvious changes of RSD in the foot. Another patient had suffered from Machado-Joseph disease and frequently fell down. This patient had fixed dystonic posture with neuropathic pain of the shoulder and upper arm after trivial trauma. Several therapies involving medication and sympathetic blocks were not effective. We tried to treat them with local blocks of the musculotendinous parts that were painful and dystonic followed by standard physical therapy. With our treatments, satisfactory control of pain and dystonia was achieved.

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Neurophysiological investigations of corticospinal integration, corticocortical interaction, and motor pathway facilitation using transcranial magnetic stimulation (TMS), and safety issues involved with TMS are reviewed. TMS activates fast-conducting corticospinal neurons directly or transsynaptically, resulting in a D wave followed by I waves recorded over the cervical cord. An increase in the firing probability of a single motor unit induced by the corticospinal descending volleys emerges as peaks in the peristimulus-time histogram (PSTH). Based on studies using PSTH and epidural electrode recording, it is believed that the D wave originates at an initial segment of the corticospinal axon, and I waves are generated by transsynaptic activation of the corticospinal neurons. Induced current with a lateromedial direction preferentially generates D waves, while a posteroanterior current preferentially generates I waves, when hand representation areas are stimulated. Because voluntary movements involve motor pathways other than the fast-conducting corticospinal tract, the appearance of motor evoked potentials (MEP) in response to TMS and voluntary motor-unit firing may be dissociated. Thus, the prognostic value of MEP in stroke hemiplegia is limited. Intracortical inhibition can be observed by paired TMS. Submotor-threshold TMS inhibits MEP of hand muscles in response to supramotor-threshold TMS with short interstimulus intervals (1-6msec). Later I waves are preferentially inhibited by submotor-threshold conditioning stimuli. It has been reported that such intracortical inhibition is diminished in patients with Parkinson's disease, task-related focal dystonia, and amyotrophic lateral sclerosis, although no disease-specific abnormalities were found. Interhemispheric inhibition and intracortical facilitation have also been reported. Cortical mechanisms for MEP facilitation induced by either voluntary contraction or motor imagery of the tested muscle have been investigated. Voluntary contraction of the tested muscle increases I waves, but has little effect on the threshold for descending volleys. Motor imagery decreases intracortical inhibition. On the other hand, voluntary contraction of ipsilateral heteronymous muscles has been shown to have different effects on MEP, background EMG, and H reflexes of the tested muscles. Additional studies of this type would help to clarify muscle interactions between joints and between agonist and antagonist muscles. Repetitive TMS induces convulsions even in healthy subjects when magnetic stimuli with high intensity and frequency, long duration, and short inter-train intervals are delivered. Safety ranges of each parameter for repetitive TMS to prevent excitation spread and convulsions have been suggested. However, such safety ranges can be used only for TMS to the primary motor cortex. We determined short-lasting (200-600msec) electroencephalographic (EEG) changes induced by TMS using an artifact-reducing circuit. Heating of EEG electrodes is negligible unless rapid-rate TMS is delivered. When stimulating the cerebral cortex in areas other than the primary motor area, EEG monitoring may be recommended.

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