Rehabilitation medicine focuses on the diagnosis, treatment and management of people with disabling medical conditions and dysmobility. Physiatrists work with people with disabilities to reduce the impact of their disease or disability on their daily life activities. On the other hand, clinical neurophysiology is a medical specialty that studies the central and peripheral nervous systems through the recording of bioelectrical activity, whether spontaneous or stimulated. Tests conducted are concerned with measuring the electrical functions of the brain, spinal cord, and nerves in the limbs and muscles. It can give the precise definition of site, the type and degree of the lesion, along with revealing the abnormalities that are in question. Due to these abilities, clinical neurophysiology is used to mainly help diagnose diseases. However, because it records bioelectrical activity, clinical neurophysiology is also useful as a treatment method i.e. electroencephalogram (EEG) biofeedback and electromyography (EMG). Recently, EEG-based brainmachine interfaces (BMI) have been used for people with disabilities. As a BMI signal source, event-related desynchronization of alpha-band EEG during motor imagery (mu ERD), which is interpreted as desynchronized activity of the activated neurons, is commonly used. The ERD represents motor cortex excitability in normal people. ERD is also recorded over the affected side in M 1 and represents motor cortex excitability in stroke patients. BCI EEG feedback is thought to induce some improvement in motor function and brain plasticity. BCI technology therefore will be useful for restoring brain function in patients with stroke. So, owing to these treatment capabilities, clinical neurophysiology is also a medical subspecialty in Rehabilitation Medicine.

A multicenter review of the medical records of Japanese post-stroke patients with spastic hemiplegia was conducted to investigate the clinical use of botulinum toxin type A (BoNT/A) by physicians with expertise in the treatment of upper and lower limb spasticity. An analysis of the data from 307 patients treated with BoNT/A during the period January 1, 2012 to November 30, 2013 provided a variety of information on factors relating to BoNT/A injection outcomes, including the total dose of BoNT/A per treatment session, the dose of BoNT/A per muscle, the number of injection sites per muscle, the method used to locate the muscles to be injected, and the dilution of reconstituted BoNT/A. Our analysis indicated that the dose of BoNT/A administered per muscle was usually selected by taking into consideration the severity of spasticity, rather than the patient's body size. Since the technical expertise of experienced clinicians is summarized in this data, it may serve as a useful reference for the use of BoNT/A in routine clinical practice.

Patients with focal hand dystonia demonstrate abnormally increased corticospinal excitability, which has been reported to be ameliorated, at least for a short term, with low frequency repetitive transcranial magnetic stimulation (rTMS). Transcranial direct current stimulation (tDCS), which is less costly and easier to apply than rTMS, is also known to modulate cortical excitability. Especially with cathodal tDCS, cortical excitability can be reduced. On the other hand, upper extremity splinting is also known to reduce dystonic symptoms by inhibiting abnormal movement. We therefore combined cathodal tDCS with finger splinting to treat focal hand dystonia in a 34-year-old man with traumatic brain injury who showed involuntary movement of his right fingers during writing and chopsticks use. After 5 days of cathodal tDCS sessions (1mA, 10min), he was encouraged to use interphalangeal joint splints for his thumb and index finger during these activities. We assessed computer-rated handwriting, reciprocal inhibition and intracortical inhibition before, 24 hours and 3 months after the 5-day tDCS sessions. Before the treatment, his flexor pollicis longus (FPL) and first dorsal interosseous (FDI) muscles showed 4Hz rhythmic hyperactivity during writing, and reciprocal inhibition at interstimulus intervals (ISI) of 20 and 100 ms were lost. Paired pulse TMS also revealed disinhibited short interval intracortical inhibition (SICI) at an ISI of 2 and 3 ms. The 5-day tDCS sessions reduced FPL and FDI EMG activities, and SICI and RI at 20 and 100 ms were also restored. Wearing the finger splints, these improvements were maintained at the 3-month follow-up. This case report is the first to demonstrate the possible long-term effects of tDCS combined with splinting for focal hand dystonia. It is supposed that splinting after tDCS plays an important role in making the tDCS aftereffects last longer.

This report illustrates a case of chronic inflammatory demyelinating polyneuropathy (CIDP) masquerading as neurofibromatosis caused by multifocal enlargements of spinal nerve roots. At age 73, the patient reported a 6-year history of numbness, weakness and pain in the hands and legs, but he could but he could walk independently with a cane. And although tremor was present, he could still draw. T2-weighted magnetic resonance imaging (MRI) through the cervical spine demonstrated spinal cord compression bilaterally at C 6-7, caused by neurofibroma-like cervical root tumors and enlargement of the spinal nerve roots and the brachial and lumbosacral nerve plexuses. Nerve conduction studies showed very little evoked response, with the exception of the median nerve which demonstrated prolonged distal latency and reduced compound muscle action potential with temporal dispersion, suggesting a diagnosis of demyelinating neuropathy. Somatosensory evoked potentials of the median nerve revealed prolonged latency, and motor evoked potentials obtained from the abductor pollicis brevis and abductor digiti minimi by transcranial magnetic stimulation demonstrated prolonged latency and temporal dispersion. Sural nerve biopsies showed segmental demyelination, remyelination (onion-bulb formation), axonal loss, and lymphocyte infiltration suggesting CIDP. The patient did not have a positive family history and declined further genetic studies. We could therefore not rule out the possibility of a hereditary hypertrophic neuropathy such as Charcot-Marie-Tooth disease.