Neuromodulation : journal of the International Neuromodulation Society
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Intractable neuropathic facial pain resulting from injury to the peripheral branches of the trigeminal nerve presents a significant challenge for neurologists, pain specialists, and neurosurgeons. In this paper, we describe our technique of peripheral nerve stimulation of the infraorbital and supraorbital nerves to treat patients with medically intractable facial pain. Stimulation of the infraorbital and supraorbital nerves is performed using percutaneously inserted electrodes that are positioned in the epifascial plane, traversing the course of the infraorbital or supraorbital nerves. ⋯ In patients who underwent permanent electrode implantation, stimulation resulted in long lasting pain relief; complications were rare and minor. We conclude that trigeminal branch stimulation is a simple technique that can be used in selected patients with neuropathic pain in the distribution of the infraorbital or supraorbital nerves. This procedure may provide relief of medically intractable pain, without the need for destructive procedures or more central modulation approaches.
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During the course of rehabilitation hemiplegic patients who have Chedoke McMaster Stages of Motor Recovery scores 4 and 5 measured three weeks after onset of stroke often improve their arm and hand function to the point that they can later use it in the activities of daily living (ADL) (1). These patients can be considered to have mild arm and hand paralysis since they can grasp objects and manipulate them with minor restrictions in the range of movement and force. On the other hand, hemiplegic patients who have Chedoke McMaster Stages of Motor Recovery scores 1 and 2 measured three weeks after onset of stroke, during the course of rehabilitation seldom improve their arm and hand function, and when they do, the improvements are not sufficient to allow these patients to use the arm and hand in ADL (1). ⋯ The treated and control patients had approximately the same time allocated for arm and hand therapy. After the treatment program was completed, the patients treated with the neuroprosthesis significantly improved their reaching and grasping functions and were able to use them in ADL. However, the majority of the control patients did not improve their arm and hand functions significantly and were not able to use them in ADL.
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In recent years, part of the muscle resistance in spastic patients has been explained by changes in the elastic properties of muscles. However, the adaptive spinal mechanisms responsible for the exaggeration of stretch reflex activity also contribute to muscle stiffness. The available data suggest that no single spinal mechanism is responsible for the development of spasticity but that failure of different spinal inhibitory mechanisms (reciprocal IA inhibition, presynaptic inhibition, IB inhibition, recurrent inhibition) are involved in different patients depending on the site of lesion and the etiology of the spastic symptoms. ⋯ This is ensured by increasing transmission in several spinal inhibitory pathways. In spastic patients, this control is inadequate, and therefore stretch reflexes in antagonist muscles are easily evoked at the beginning of voluntary movements or in the transition from flexor to extensor muscle activity. This problem is contradicted by the fact that antispastic therapy to improve voluntary movements should be directed.