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Future generations of upper limb prosthesis will have dexterous hand with individual fingers and will be controlled directly by neural signals. Neurons from the primary motor (M1) cortex code for finger movements and provide the source for neural control of dexterous prosthesis. Each neuron’s activation can be quantified by the change in firing rate before and after finger movement, and the quantified value is then represented by the neural activity over each trial for the intended movement. Since this neural activity varies with the intended movement, we define the relative importance of each neuron independent of specific intended movements. The relative importance of each neuron is determined by the inter-movement variance of the neural activities for respective intended movements. Neurons are ranked by the relative importance and then a subpopulation of rank-ordered neurons is selected for the neural decoding. The use of the proposed neuron selection method in individual finger movements improved decoding accuracy by 21.5% in the case of decoding with only 5 neurons and by 9.2% in the case of decoding with only 10 neurons. With only 15 highly-ranked neurons, a decoding accuracy of 99.5% was achieved. The performance improvement is still maintained when combined movements of two fingers were included though the decoding accuracy fell to 95.7%. Since the proposed neuron selection method can achieve the targeting accuracy of decoding algorithms with less number of input neurons, it can be significant for developing brain-machine interfaces for direct neural control of hand prostheses.

A 66-year-old male with a history of hypertension and type 2 diabetes mellitus was admitted to the hospital with complaints of vomiting for 2 weeks and bilateral loss of vision for 2 days. Ophthalmology examination for visual acuity revealed no perception of light in both eyes. Pupils were symmetrically dilated and completely nonreactive to light, as shown in Figure 1. Bilateral mild papilledema with moderate pale-appearing discs was seen on fundoscopy. It is interesting to note that we did not see any changes of hypertensive or diabetic retinopathy. Intraocular pressures were normal. The patient was hemodynamically stable. The remaining neurological system history and examination were unremarkable. The patient was oliguric. Laboratory tests revealed blood urea nitrogen of 174 mg/dl, serum creatinine of 11.91 mg/dl, and significant anion gap metabolic acidosis without an osmolal gap. Toxicology screens for serum and urine were negative. Urine microscopy showed heme granular casts. Serum calcium was 6.0 mg/dl, phosphorus was 9.6 mg/dl, and intact parathyroid hormone was 843 pg/ml. Anti-neutrophil cytoplasmic antibody panel, anti-nuclear antibody, anti-glomerular basement membrane antibody, erythrocyte sedimentation rate, and ultrasound of kidneys were normal. Magnetic resonance imaging of the brain, carotid doppler, and 2D-echocardiography were normal. The patient refused lumbar puncture. Hemodialysis was performed daily for 4 days. The vomiting resolved, urine output improved, predialysis serum creatinine improved, and therefore hemodialysis was discontinued. Serum creatinine on the 7th day of hospitalization was 1.57 mg/dl. Acute kidney injury (AKI) was attributed to acute tubular necrosis. Unfortunately, despite recovery of the renal functions, there was no improvement in his vision, and the pupils remained dilated and nonreactive to light on the seventh day of hospitalization.