This review discusses neuronal mechanisms controlling posture and locomotion. Volitional gait behaviors are composed of “automatic control of posture and rhythmic limb movements” that operate in conjunction with “intentional control of precise movements of the trunk, limbs, and feet.” The automatic control of posture and rhythmic limb movements is mediated by the ventromedial descending motor system from structures of the brainstem. Descending signals in this system activate spinal interneuronal circuits, which are termed central pattern generators (CPGs), to automatically generate a locomotor rhythm and pattern in cooperation with sensory afferents from muscles, joints, and skin. However, when moving, the subject requires intentional gait modification, which in turn critically involves an activation of the dorsolateral descending motor system, or the lateral corticospinal tract, arising from the motor cortical areas. An intentional gait control is always preceded by appropriate postural adjustments, which are themselves achieved by the motor programs in motor cortical areas including the supplementary motor area and premotor area. To generate and develop the motor programs, information of bodily function such as body schema, which is always updated at the temporoparietal cortex on the basis of proprioceptive, visual, vestibular and auditory sensations, can be critically required. The postural control program is propagated to the brainstem, via the cortico-reticular projection, so that anticipatory postural adjustment is performed by the activation of the ventromedial systems immediately before the onset of the intentional gait modification. Conversely, programs of intentional gait control are transmitted to the primary motor cortex so that precise limb trajectories can be generated and accurate foot placement is achieved by the activation of the corticospinal tract. Signals from the basal ganglia and the cerebellum regulate “automatic processes” by acting on the brainstem and “intentional processes” by acting on the cerebral cortex. Operation of the basal ganglia is largely affected by dopamine, and cerebellar function depends on feed-forward and feedback signals acting on the cerebellum. Dysfunction of either mechanism of the above processes may result in postural disturbance and/or gait failure. (328 words)

  With the advent of brain computer interface, several methods are developed in its application for rehabilitative treatment. We devised a new rehabilitation system using an electroencephalogram-based brain computer interface, which successfully improved paretic upper extremity function in stroke patients. Patients were requested to decrease amplitudes of sensory motor-rhythm during motor imagery. While imaging extension of the affected fingers, patients were asked to alter EEG with a visual feedback of their brain activities. In several months, new voluntary electromyographic activity was measurable in patient's paretic finger extensors.

  Subsequently patients are treated with specific electrical stimulation called integrated volitional electrical stimulation (IVES). IVES controls stimulation strength automatically following patient's will to extend their paretic fingers. Activation of the damaged hemisphere was confirmed by fMRI analysis.

  It is important to reduce spasticity of the paretic limb prior to application of these methods. Injection of botulinum toxin type A should be considered in order to make the paretic finger movement easy.

  Both the atlanto-axial joints can be exposed adequately by an unilateral extra-pharyngeal approach from the right side. The atlanto-axial dislocation can be reduced, joints can be decorticated and bone graft can be introduced into the joint. The odontoid process can be drilled and removed. The C1-C2 joint can be fixed either by 1. C1 lateral mass and C2 body screw plate bilaterally, or 2. Bilateral anterior C2-C1 transarticular screws.

  Objective : Posterior atlantoaxial (C1-2) fixation with individual screw placement in C1 and C2, commonly referred as Goel-Harms method, is one of the technical options to treat C1-2 subluxation or instability. In the present study, we demonstrated our surgical technique of posterior C1-2 fixation with the Goel-Harms method and analyzed the surgical outcome with special reference to surgery-related complications.

  Materials and methods : This study included a series of 17 consecutive patients who underwent posterior C1-2 instrumented fixation with the Goel-Harms method over the past 8 years at our institute. Unilateral or bilateral C2 nerve root resection at the sensory ganglion was performed to achieve a safe and wide exposure of the lateral atlantoaxial joints. The neurosurgical cervical spine scale (NCSS) and sensory pain scale of C2 nerve distribution were used to assess the pre-and postoperative neurological condition. Postoperative C1-2 arthrodesis was determined on the basis of plain radiography or sagittal computed tomography (CT) images.

  Results : Screw malposition resulting in vascular or neural injury was not encountered. Sensory pain scale analysis indicated that the mean score before surgery was 2.3, which significantly improved to 1.4 after surgery. No patients reported allodynia or C2 neuropathic pain at a recent follow-up. C2 nerve root resection resulted in early postoperative dysesthesia in all patients ; however, neurological examination during follow-up revealed that only 2 of 17 patients (11.7%) demonstrated C2 sensory disturbance. Radiological analysis after surgery revealed that none of the patients had pseudoarthrosis requiring revision surgery.

  Conclusion : Although C2 nerve root resection is still under debate and not fully justified, the present study suggests that C2 nerve root resection does not always result in significant morbidity and can be a safe surgical option. These findings emphasize the importance of safe and wide exposure of the lateral atlantoaxial joints to avoid surgery-related complications.

  A 25-year-old woman presented with progressive pain in the anterior aspect of her left thigh. Neurologically, no objective abnormality was identified. Neuroimaging studies including cine-magnetic resonance imaging (MRI), magnetic resonance (MR) myelography, and computed tomography (CT) myelography showed an extradural cystic mass, probably containing cerebral spinal fluid, at the left lateral intracanalicular space from vertebral levels T12-L2.

  Although the above methods failed to visualize any dural defect, 3D Turbo SE MRI revealed a possible dural defect adjacent to the left L1 nerve root where neural tissue was somewhat incarcerated.

  Using a minimally invasive posterior approach (L1 hemilaminectomy with partial hemilaminectomy of T12 and L2), the cyst wall was removed as much as possible. Neural tissue, presumably the cauda equina, protruded into the cyst cavity through the small dural defect. After removing the neural tissue into the dural canal, the dural defect was simply sutured. Fibrin glue was used to reinforce this suture for water tightness. Microscopically, the cyst wall consisted of fibrous tissue with an inner single-cell lining. Soon after the surgery, her pain was relieved. No recurrence has been observed so far.

  In order to carry out minimally invasive surgery for the treatment of an extradural arachnoid cyst, it was necessary to identify dural defect (s). However, even by using cine-MRI, MR myelography, or CT myelography, the definitive diagnosis was difficult. In our case, 3D Turbo SE MRI was useful for detecting a dural defect. 3D Turbo SE MRI can show multi-angle images in a shorter examination time. In view of the form of the dural canal, 3D Turbo SE MRI is feasible in the assessment of a dural defect. Therefore, this neuroimaging method seems to be an indispensable tool for the diagnosis of extradural extra-arachnoid cysts.

  Spinal subarachnoid hematomas are rare causes of spinal cord compression. They are usually associated with the use of anticoagulants, lumbar puncture, arteriovenous malformation (AVM), spinal artery aneurysm, etc. They may also occur spontaneously ; however, the incidence of this is rare. Herein, we report a rare case of spontaneous spinal subarachnoid hematoma in which emergency surgery was necessary. The patient was a 54-year-old woman who presented with sudden thoracodorsal pain and mild motor weakness of both lower limbs at a local hospital. Because the lower limb weakness progressed and bladder dysfunction was noticed, she was referred to our department on the third day after onset. CT and MR images revealed an intradural lesion compressing the spinal cord from the left ventral position at thoracic vertebrae (T) 2 through 9. Head CT revealed a small amount of SAH in the peripheral sulci. On spinal angiography, no clearly abnormal blood vessels were observed. Emergency surgery was performed on the day of admission. During surgery, we performed a left unilateral laminectomy from T4 to T8. No lesions were observed outside the dura mater or in the subdural cavity, and a hematoma was identified under the arachnoid membrane. Upon removing the hematoma, no abnormal blood vessels, tumors or other lesions were found. After surgery, the neurological symptoms improved. On postoperative days 4 and 5, mild disorientation was noted, but the patient recovered thereafter. CT and MRI performed 9 days after surgery revealed a hemorrhagic infarction in the right parietal lobe, which was presumably due to vasospasm. On day 10 after surgery, the patient was alert and able to walk with crutches, and was therefore transferred to a rehabilitation hospital. Spinal subarachnoid hematoma should be included in the diagnosis of thoracodorsal pain. If the patient's neurological status progressively deteriorates, early surgical treatment is recommended.