The Human Central Pattern Generator for Locomotion: Does It Exist and Contribute to Walking?

Descibing a possible solution but not enough to do any good. More followup needed which will never occur. My takeaway from this is that if they figure how to make this work, people like me that have dead pre-motor cortexes should be able to walk normally again.


http://journals.sagepub.com/doi/abs/10.1177/1073858417699790

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Karen Minassian, Ursula S. Hofstoetter, Florin Dzeladini, ...

First Published March 28, 2017 Review Article

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Abstract

The ability of dedicated spinal circuits, referred to as central pattern generators (CPGs), to produce the basic rhythm and neural activation patterns underlying locomotion can be demonstrated under specific experimental conditions in reduced animal preparations. The existence of CPGs in humans is a matter of debate. Equally elusive is the contribution of CPGs to normal bipedal locomotion. To address these points, we focus on human studies that utilized spinal cord stimulation or pharmacological neuromodulation to generate rhythmic activity in individuals with spinal cord injury, and on neuromechanical modeling of human locomotion. In the absence of volitional motor control and step-specific sensory feedback, the human lumbar spinal cord can produce rhythmic muscle activation patterns that closely resemble CPG-induced neural activity of the isolated animal spinal cord. In this sense, CPGs in humans can be defined by the activity they produce. During normal locomotion, CPGs could contribute to the activation patterns during specific phases of the step cycle and simplify supraspinal control of step cycle frequency as a feedforward component to achieve a targeted speed. Determining how the human CPGs operate will be essential to advance the theory of neural control of locomotion and develop new locomotor neurorehabilitation paradigms.

Rethinking Stimulation of the Brain in Stroke Rehabilitation Why Higher Motor Areas Might Be Better Alternatives for Patients with Greater Impairments

Going after the pre-motor cortex wouldn't help me at all, most of mine is dead. I wish someone would tackle the extremely difficult problem of moving functions that were in dead areas to new locations. Now that would be worthy of a Nobel prize. You will need to send your doctor after exactly how they are stimulating the PMAs.
http://nro.sagepub.com/content/21/3/225?etoc

1. Ela B. Plow1,2
2. David A. Cunningham1,3
3. Nicole Varnerin1
4. Andre Machado4

1. ¹Department of Biomedical Engineering, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA
2. ²Department of Physical Medicine & Rehabilitation, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA
3. ³School of Biomedical Sciences, Kent State University, Kent, OH, USA
4. ⁴Center for Neurological Restoration, Neurological Institute, Cleveland Clinic, Cleveland, OH, USA

1. Ela B. Plow, Department of Biomedical Engineering, Lerner Research Institute, Cleveland Clinic, 9500 Euclid Avenue, ND20, Cleveland, OH 44195, USA. Email: plowe2@ccf.org

Abstract

Stimulating the brain to drive its adaptive plastic potential is promising to accelerate rehabilitative outcomes in stroke. The ipsilesional primary motor cortex (M1) is invariably facilitated. However, evidence supporting its efficacy is divided, indicating that we may have overgeneralized its potential. Since the M1 and its corticospinal output are frequently damaged in patients with serious lesions and impairments, ipsilesional premotor areas (PMAs) could be useful alternates instead. We base our premise on their higher probability of survival, greater descending projections, and adaptive potential, which is causal for recovery across the seriously impaired. Using a conceptual model, we describe how chronically stimulating PMAs would strongly affect key mechanisms of stroke motor recovery, such as facilitating the plasticity of alternate descending output, restoring interhemispheric balance, and establishing widespread connectivity. Although at this time it is difficult to predict whether PMAs would be “better,” it is important to at least investigate whether they are reasonable substitutes for the M1. Even if the stimulation of the M1 may benefit those with maximum recovery potential, while that of PMAs may only help the more disadvantaged, it may still be reasonable to achieve some recovery across the majority rather than stimulate a single locus fated to be inconsistently effective across all.

Reflecting on mirror neurons

This is a blog posting from Mo Costandi.
http://www.theguardian.com/science/neurophilosophy/2013/aug/23/mirror-neurons
This line is what I am most concerned about.
The cells in question are located in the premotor cortex, a part of the brain involved in planning and executing movements, so the finding was not in itself particularly surprising.

If true, I'm screwed because I was planning on using action observation to relocate motor function areas that are dead. That's going to be damn hard since most of my pre-motor cortex looks like a black hole. Unless I can get the ipsilateral working.
Damnably depressing.