NEUROMUSCULAR ELECTRICAL STIMULATION IN NEUROREHABILITATION

You get to ask your doctor what protocols were created as part of this and how they have been updated in the 13 years since then.  Since nothing will have occurred, you get to ask your doctor; 'DO YOU PREFER YOUR INCOMPETENCE NOT KNOWING? OR NOT DOING?'

NEUROMUSCULAR ELECTRICAL STIMULATION IN NEUROREHABILITATION

  LYNNE R. SHEFFLER, MD, and JOHN CHAE, MD
Cleveland Functional Electrical Stimulation Center, Case Western Reserve University,2500 MetroHealth Drive, Cleveland, Ohio 44109, USA
Accepted 4 January 2007
This article provides a comprehensive review of the clinical uses of neuromuscular electrical stimulation(NMES) in neurological rehabilitation. NMES refers to the electrical stimulation of an intact lower motor neuron (LMN) to activate paralyzed or paretic muscles. Clinical applications of NMES provide either a functional or therapeutic benefit. Moe and Post
207
introduced the term functional electrical stimulation (FES) to describe the use of NMES to activate paralyzed muscles in precise sequence and magnitude so as to directly accomplish functional tasks. In present day applications, functional tasks may include standing or ambulatory activities, upper limb performance of activities of daily living, and control of respiration and bladder function. A neuropros-thesis is a device or system that provides FES. Accordingly, a neuroprosthetic effect is the enhancement of functional activity that results when a neuroprosthesis is utilized. NMES is also used for therapeutic purposes. NMES may lead to a specific effect that enhances function but does not directly provide function. One therapeutic effect is motor relearning, which is defined as “the recovery of previously learned motor skills that have been lost following localized damage to the central nervous system.”¹⁸⁰ Evolving basic science and clinical studies on central motor neuroplasticity now support the role of active repetitive movement training of a paralyzed limb. If active repetitive-movement training facilitates motor relearning, then NMES mediated repetitive movement training may also facilitate motor relearning.Other examples of therapeutic applications include treatment of hemiplegic shoulder pain, cardiovascular conditioning, treatment of spasticity, and prevention of muscle atrophy, disuse osteoporosis, and deep venous thrombosis (DVT). This review focuses on the clinical uses of NMES for functional and therapeutic applications in patients with spinal cord injury or stroke. In order to provide a foundation for the various clinical applications, the neurophysiology of NMES and components of NMES systems are briefly reviewed. The specific neuroprosthetic or “functional” applications include upper- and lower-limb motor movement for self-care tasks and mobility, respectively, bladder function, and respiratory control. Specific therapeutic applications include poststroke motor relearning as well as the examples mentioned earlier. Lastly,perspectives on future developments and clinical applications of NMES are presented.
NEUROPHYSIOLOGY OF NMES
NMES is initiated with the excitation of peripheral nervous tissue. The mathematical characterization of neuronal action potential generation is largely predicated on the seminal work of scientists and neurophysiologists including Galvani¹⁰⁶
Lapicque¹⁷⁵

andHodgkin and Huxley¹³⁰.
More recently, McNeal²⁰⁰
mathematically defined the time course of events following stimulus application to the propagation of the action potential in a normal healthy myelinated nerve.The term “stimulus threshold” defines the lowest level of electrical charge that generates an action potential.The “all or none” phenomenon of the action potential produced by natural physiologic means is identical to the action potential induced by NMES.Conduction of impulses in a nerve is influencedconsiderably by the nerve’s cable properties.Hodgkin and Rushton in 1946¹³¹
used extracellular electrodes to measure applied current along lobster axons to describe the spread of current along nervefibers of uniform diameter composed of a central conductor and insulating sheath. Nerve fiber recruitment and resultant force characteristics of muscle contraction are modulated by both stimulus pulse width
and stimulus frequency.³
Other variables include distance from the stimulating electrode and membrane capacitance. The threshold for eliciting a nerve fiber action potential is 100 to 1,000 times less than the threshold for muscle fiber stimulation.²⁰⁹
Thus, clinical NMES systems stimulate either the nerve directly or the motor point of the nerve proximal to the neuromuscular junction.The nerve fiber recruitment properties elicited by NMES differ from those elicited by normal physiologic means. An action potential produced by normal physiologic mechanisms initially recruits the smallest diameter neurons prior to recruitment of larger-diameter fibers, such as alpha motor neurons.¹²⁷
Rushton²⁴⁸
 was one of the first researchers toexamine the theoretical relationship between fiberdiameter and conduction velocity. Hodgkin¹³²
proposed that the velocity of action potential propagation should vary directly with the square root of thefiber diameter. The Henneman size principle of voluntary motor unit recruitment described this pro-gressive size-dependent recruitment of motor units.¹²⁸
 Arbuthnott et al.⁹
examined in detail this relationship between fiber diameter and conduction velocity in peripheral nerve. The nerve fiber recruitment pattern mediated by NMES follows the principle of “reverse recruitment order” wherein the nerve stimulus threshold is inversely proportional to the diameter of the neuron. Thus, large-diameter nervefibers, which innervate larger motor units, are recruited preferentially. Recent work by Lertmanorat and Durand¹⁸³
proposes the clinical applicability of are shaping of the extracellular voltage that may allow the reversal of the “reverse recruitment order” elicited by NMES. NMES is dependent on an intact (alpha) LMN.Several studies document the therapeutic benefit of electrical stimulation on muscle-fiber regeneration in LMN denervation^50,149,280
; however, the clinical application of NMES is presently limited to neurologic injuries involving the upper motor neuron (UMN) such as spinal cord injury (SCI), stroke,brain injury, multiple sclerosis, and cerebral palsy. NMES is delivered as a waveform of electrical cur-rent characterized by stimulus frequency, amplitude,and pulse width. The amplitude and pulse width determine the number of muscle fibers that are activated.²⁰⁹
Temporal summation is determined by the rate at which stimulus pulses are applied to muscle. The strength of the resultant muscle con-traction is modulated by adjustment of the stimulus parameters. The minimum stimulus frequency that generates a fused muscle response is 12.5 Hz. Higher stimulus frequencies generate higher forcesbut result in muscle fiber fatigue and rapid decrement in contractile force. An optimal NMES system utilizes the minimal stimulus frequency that produces a fused response.
^26,173,200 Ideal stimulation frequencies range from 12–16 Hz for upper-limb applications and 18–25 Hz for lower-limb applications(frequency range for NMES systems is 10–50 Hz
). Greater muscle force generation is accomplished by either increasing the pulse duration (typically 200

s) or stimulus amplitude to activate neurons at a greater distance from the activating electrode. Parameters for safe stimulation for implanted NMES systems have been established experimentally.²⁰⁹ 209
The clinical application of NMES systems is complicated by the fact that the contractile force of muscle is highly nonlinear and variable over time. Muscle force generation is also impacted by multiple factors distinct from the stimulation parameters of the NMES system. These factors include the inherent length tension characteristics of the muscle, impact of the joint angle on changes in the tendon arm momentarm,and volume conduction of the current that may recruit muscles beyond the targeted muscle.^115,153 Skeletal muscle contains “fast” and “slow” musclefibers that are distinguished on the basis of contrac-tion kinetics. These fiber types are generally catego-rized according to the specific myosin heavy chain(MHC) isoforms that they express.^104,144 Histochem-ical analysis led to the original designations of types I and II muscle fibers. Slow-twitch, oxidative type Ifibers generate lower forces, but are fatigue resistant;fast-twitch glycolytic type II fibers generate higherforces but fatigue more rapidly. Muscle fibers are typed using histochemical staining for myosin ATPase, MHC isoform identification, and biochemical identification of metabolic enzymes. Myosin ATPase histochemistry energy metabolism distinguishes the muscle fibers that comprise a motor unit,all of which exhibit similar contractile and fatigue characteristics. Motor units are thus classified based on fiber type contractile characteristics as either slow-twitch (S) or fast-twitch (F). The F motor units are classified as either fast-twitch fatigue-resistant (FR), fast-twitch fatigue-intermediate (Fint), or fast-twitch fatigable (FF).²⁵⁶  An alteration in functional demands result in conversion of muscle fiber types via altered gene expression, changes in the expression of contractile proteins and metabolic enzymes³⁵, and adaptationsin the cellular electrophysiologic properties (expression or function of ion channels).^171,312 Disuse muscle atrophy common in an UMN injury is characterized by conversion of type I muscle fibers to type IIfibers.²⁴²  An ideal application of NMES allows pref-erential stimulation of fatigue-resistant type I fibers.However, NMES systems preferentially recruit type IIfibers due to lower stimulation thresholds. Chronicelectrical stimulation facilitates reversal of fiber typeconversion secondary to motor unit plasticity. ²²⁴ This reversal of fiber type conversion may be related to the motor neuron firing patterns that control expression of contractile proteins and metabolic enzymes in muscle fibers during electrostimulation.¹⁷²