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Posture and PositioningGift of Positioning
Reflexes: Sensorimotor Integrative Behavior at a Basic Level
Mechanics of Postural Stability
Postural Analysis: Neuromechanical Principles and Considerations
Postural Disability: Positioning Challenges, Accommodations
Gift of PositioningThe gift of positioning enables a person to orient oneself, and to interact in various ways with the environment. This requires voluntary movement, often involving coordination of many parts of the body, all while maintaining mechanical stability. This is the topic of other courses, including courses taught in the past by this instructor, and some offered here at Marquette by Drs. Harris, Schmit and Scheidt. Thus this section will be brief. There is a considerable literature in this area, including two 47-chapter books that I have had the pleasure of editing. Reflexes (in the Context of Usability and Disability)Sensing within Musculoskeletal TissueMusculoskeletal tissue is loaded with sensors. Some regions have a greater density of sensors (e.g., hands-forearms, neck) that others (e.g., abdomen). A key type of sensor within muscle is the muscle spindle, which resides within muscle. One of many good web sites on the anatomy of the spindle is given at King's College / University of London. Basically, intrafusal fibers (nuclear bag, nuclear chain) are structurally in parallel with the main (extrafusal) muscle fibers. Within the intrafusal fibers, contractile machinery (excited by the gamma motoneurons) is in series with regions that contain stretch-sensitive nerve endings, yielding the primary (1a) and secondary (II) afferents. The primary afferents are especially sensitive to the rate of change of stretch of muscle, and thus we often think of these as velocity sensors, though in fact their sensitivity is nonlinear. For instance, for ramp (velocity) stretches, they are more sensitive to an initial "short range" stretch. The secondary afferents are viewed primarily as muscle length sensors, though because they are in series with intrafusal contractile tissue they are often hypothesized to sense more of a relative length, and are somewhat sensitive to rate of change. The gamma motoneurons that excite intrafusal fibers are the size of small alpha motoneurons.
The alpha motoneurons that excite the main (extrafusal) muscle fibers come in a range of sizes. As seen above, the larger motoneurons (MNs) tend to innervate fast-fatiguable (FF) muscle fibers, and the smaller slow-fatigue-resistant muscle fibers (SR). The collection of muscle fibers innervated by a particular MN is called its motor unit. As seen below, MNs receive and must integrate converging signals from many sources, some from the higher brain, some from spinal interneuron circuits, and some from sensory neurons. Normally, within a motor pool (a collection of motor neurons that innervate muscles to a given muscle or functional part of a muscle), there is orderly recruitment in which the smallest MN cells (both in terms of cell body size and axon diameter) are recruited first. Small alpha MNs tend to innervate slow-twitch muscle fibers that are more fatigue-resistant, having better access to oxygen (e.g., more mitochondria, better blood vessel access). Larger alpha motoneurons aren't even recruited until a muscle generates about 50% of maximum force, and thus might not even become active over the course of a day. See a separate page for more information on muscle fiber composition and orderly recruitment. Typically larger motoneurons have a larger motor unit, i.e. they innervate a larger number of muscle fibers (as high as several hundred).
Often there is alpha-gamma coactivation within the motor pool, and to a first (crude) approximation the gamma motoneurons can be thought of as small alpha motoneurons. These are the first to be recruited, and continue to increase their firing rate as the drive to the motor pool increases and larger motoneurons become recruited. Another key type of sensor is the Golgi Tendon organ, which resides near where muscle fibers and tendon meet. We typically assume that it is sensitive to muscle force, and its rate of change. There are also other sensors within musculoskeletal tissue, including nerve ends sensitive to pressure, temperature, pain, and joint orientation. All appear part of a cohesive plan that aims at informing the CNS about the state of the musculoskeletal system. For instance, it has been shown that both foot and knee mechanoreceptors, located within tissues associated with joints, send signals that affect leg reflex-induced muscle activity. There are also interneurons that are near the motoneurons that have stereotyped roles, the most notable being the small Renshaw cells that surround motoneurons. These receive collateral input from a motoneuron and inhibit nearby motoneurons. Another important class of interneurons are those that provide reciprocal inhibition between classic "antagonistic" muscles. Sensorimotor "Reflexes"Sensory afferents connect via synapses to other neurons in the spinal cord, traveling at velocities up to 120 m/s (or 12 cm per ms) for those with the largest axons. Most provide synaptic excitation to interneurons, but some make direct contact to motoneurons. There are a number of interneuronal circuits that are beyond the scope of this course, and well as collateral branch signals that head up spinal tracts to the brain. To understand the normal and pathological role of reflexes, one starts by understanding the converging synaptic drive to motoneurons. Each MN receives hundreds if not thousands of converging synaptic inputs to its dendridic tree, some coming from local sensory neurons or spinal interneurons, others from distant parts of the CNS such as the sensorimotor cortex. Some connections are inhibitory, some excitatory, and all contribute via electrotonic spread to a summing region where an action potential can be initiated. There are also more complex connections that enable pre-synaptic inhibition/excitation. Thus in a very real way, no one pathway or source of excitation would normally dominate unless it was really strong, and (in some cases) other pathways allow it to dominate. Importantly, "higher brain" inputs appear to carefully regulate reflex strengths, in particular by keeping their loop gains low most of the time. With neurological impairment (e.g., cerebral palsy, stroke, spinal cord injury), often reflexes are more prominent because the higher brain drive is not functioning in a normal way. This can lead to spasticity, excessive muscle tone, tremors, and other types of functional impairment.
With the above as a context, the classic "stretch reflex" has several components: a more "dynamic stretch reflex" that is more sensitive to sudden changes in length (and more associated with primary afferent drive) and the "static stretch reflex" that is more prolonged and more associated with secondary afferents and gamma drive. But remember that these reflexes normally have low gains, and might provide a response that is well under 10% of maximum, hits only after about a 40 ms loop delay, and is over within a few hundred milliseconds! There are many posture-related "reflexes" and "synergies" and "responses" that are relevant to neurorehab, including:
Structural Neuro-Mechanical Intimacy and Multi-Segmental ReflexesThere is also structural order within the musculoskeletal apparatus, the spinal circuitry, and higher brain structure. This holistic design becomes apparent in many ways, often more so after a traumatic event of the sort that requires rehabilitative therapy. For example:
One cannot help but notice that neuromotor structure and properties are profoundly influenced by mechanics, especially issues related to postural stability. Mechanics of Postural StabilityBy the age of two, most children have "learned" an incredible amount of postural mechanics, as seen by their ability to move and then maintain a remarkable variety of postures, without falling, within a gravitational field. The mechanics behind postural stability is remarkably complex:
Lets assume that the body consists of a collection of masses within a gravitational field, with an example being the simplified head-neck system shown below. Thus it functions as a compound inverted pendulum. Such systems normally have a tendency to collapse. Pragmatically, to be stable, the potential energy lost by falling masses must be more than offset by the potential energy gained by spring-like structures within the system. Wood is stiff but spring-like, and for a tree, for any cross-section the trunk must be large enough in diameter to have the appropriate level of stiffness. But trees don't move (except in Lord of the Rings), and people do, via joints. Thus the body's solution is to have spring-like structures across joints.
Most joint articulations move freely, and thus joint stiffness is due to tissues crossing the joint, such as ligaments and muscles. Typically ligaments provide significant force and stiffness only for joint angles near the range of motion extremes, and thus for the primary range stiffness due to muscles tends to dominate. Thus for stable equilibrium (one that doesn't drift off with perturbation), the joint "stiffness" that is mostly due to of muscles (whether through in intrinsic muscle stiffness and/or reflexes) must be above a certain threshold stiffness:
It is well established that muscle dynamic stiffness increases with muscle force - this is primarily a reflection of a series elastic (SE) property of the muscle and tendon unit, which can be tough of as conceptually in series with the contractile tissue. This contractile tissue exhibits another type of stiffness that relates to the degree of overlap between the myosin and actin filaments of muscle: the so-called "tension-length" properties of muscle. This is not nearly as stiff as the SE component, and tends to dominate intrinsic "quasi-static" length-dependent changes in muscle force. It tends to be a lower magnitude of stiffness, and muscles such as the quadriceps can even become negative over a part of the functional range of motion. These are sources of intrinsic muscle stiffness, and are best understood by using muscle models. There is also reflex-based stiffness. For instance, when a muscle is stretched, sensors (e.g., 1a primary afferents within muscle spindles) feed back signals to the spinal cord that in turn cause an increase in motoneuron drive the the stretched muscle, which can cause an increase in muscle force (e.g., via increased motoneuronal drive). This is a spring-like behavior, though unlike for intrinsic stiffness, there is a transmission time delay. Also, the gains for such reflexes is typically low. Thus this is more of a "backup" source of spring-like behavior. Each muscle that generates force will produce a moment about the joints that it crosses. For most joints there are antagonistic muscles crossing the joint, i.e. their joint torques oppose each other. Thus the overall joint torque is a sum of individual torques that often differ in sign. These resultant joint torques are what matters for static equilibrium. If the brain chooses to coactive antagonists, such as the biceps and triceps of the arm, the added muscle toques subtract from each other. In contrast, individual joint stiffnesses due to muscles add to the joint stiffness. Thus coactivation becomes a mechanism for leads to smaller overall joint torques but larger joint stiffnesses, or more generally, impedance. Thus the brain has access to a great built-in mechanism for helping deal with stability challenges: cocontraction of antagonists. Using cocontraction, we can change the dynamic joint stiffness by about an order of magnitude within the time it takes to contract the opposing muscles, about a quarter of a second. It is a great design, and an excellent example of how the brain can take advantage of nonlinearity (variable joint stiffness) to improve control. It turns out that for large-scale postural systems such as a standing biped, stable posture is a "balancing act" between joint moments (related to statics, but also dynamics of movement), joint muscle/reflex spring-like behavior (related to stability of posture), and joint mobility (related to movement transition). It also turns out that neural structures such as the cerebellum "understand" mechanical stability to a remarkable level. Indeed, it is considerations of postural stability rather than movement generation that have proved to be the greatest challenge in implementing walking systems such as for robots or functional neuromuscular stimulation. We tend to take these intrinsic postural mechanisms for granted. But with neuromotor impairment it is often intrinsic postural mechanisms that pose the greatest challenges. Postural Analysis: Neuromechanical Principles and ConsiderationsMovement as a Transition in Posture (sometimes)One way of solving the complex problem of voluntary movement is to assume, as seen in the previous section, that muscles/reflexes are spring-like. Transitioning from one posture to another then can be done by changing the equilibrium point of the musculoskeletal system, with movement occurring until a minimum potential energy is reached. There have been a number of opposing theories on how this could be done, but at a basic level they come down to changing the stiffness K and/or rest length Xo of spring-like muscle-reflex actuators. In these theories a given posture is "released" (e.g., by lowering muscle activations of agonists) and a new posture within the large-scale system occurs when the musculoskeletal system comes to a new resting configuration. Integrative Neuromechanical Perspective of Posture and BalanceNot yet mentioned is two other critical aspects of posture and balance: the role of the vestibular system (and also vision and neck sensors), and the role of multisegmental "righting" reflexes. Embedded within the head, as part of the apparatus of the inner ear, are two pairs of three semicircular canals that are oriented orthogonally to each other. These measure angular acceleration (and essentially angular velocity via a "neural integrator" in the brain stem). There are also structures called the otoliths that measure translational kinematics. Both send signals to the vestibular nuclei, which sends signals to many other brain structures. Collectively, this vestibular system provides a constant stream of sensor information on head kinematics. It is augmented by a rich collection of kinematic sensors within neck muscles and connective soft tissues, plus information via vision. These signals are an important component of our postural control system. There are also many intrinsic multisegmental reflexes, in particular related to limb extensor and flexor synergies. These tend to be more obvious during during certain early stages in motor development of a child. However, they are intrinsic, and often are exhibited strongly in persons with neurological impairment such as spinal cord injury. Indeed, the recovery process after trauma such as stroke often reflects developmental stages. Dr. Schmit is one of the leading researchers studying such reflexes, focusing on reflex synergies in individuals with spinal cord injury. Coordinated Responses to Perturbations to Balance, and Anticipated Postural AdjustmentsWhole-body postural stability during standing or everyday activities requires not only that stability within internal body segments, but also of the whole body. We lack claws on or feet or glue on our shoes, and thus cannot easily pass a moment between ourselves and the ground. Thus, for static equilibrium while on earth, our "center of gravity" must be within our base of support. For periods of time this criteria can be violated and we can remain in "dynamic equilibrium," such as during single-support phases of walking where we plant a foot in front of us to prevent a fall. Many mechanisms are available to maintain this form of postural stability, with sensors ranging from the vestibular apparatus within the head to pressure sensors within the footpad, and integrative neuromotor systems including roles for the cerebellum and basal ganglia. To indicate just how intertwined and subconscious these intrinsic neuromechanical mechanisms are, consider the following:
Positioning Challenges and Accommodations in Rehabilitation and DisabilityIt is difficult to underestimate the relationship between neuromotor impairment and postural neurocontrol mechanisms: virtually any neuromotor impairment has postural consequences. Indeed, there is little reason to make a list of diseases or types of impairment, since all neuromotor activities with the possible exception of hand function have a significant postural component. Most activities of daily living (ADL's) are performed slowly enough that they can be viewed as transitions in posture. This is especially true for individuals with disabilities, who often successfully complete activities such as eating at slower (but acceptable) rates. Even walking, when performed slowly as is often the case after stroke, is essentially a postural task. Rehabilitation professionals probably spend more time addressing postural challenges than any other. Classic examples of dysfunction causing postural challenges include:
In most cases, the challenges and accommodations relate to finding alternative solutions rather than addressing the root of the problem. For instance, other than medications there is often a limited amount that can be done about spacticity, muscle weakness, dysfunctional synergies, or tremor. In addition to interventional therapies (e.g., medication to reduce spasticity, physical therapy to increase strength or improve motor patterns), accommodations include assistive technologies and orthotics. Thus the HAAT conceptual model applies, but with every case being different. Here are a few of the classic categories of functional activities that may need to be addressed, and where there is often a role for rehabilitation engineers:
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