Stretch reflex

Spasticity A motor disorder characterized by an increase in muscle tone with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex. 

A reflex is initiated by stimulation of a sensory receptor located at the peripheral ending of an afferent or first-order sensory neuron. This afferent neuron transmits impulses to the spinal cord. Within the gray matter of the spinal cord, the afferent neuron synapses with other neurons. As such, the spinal cord serves as an integrating center for the sensory input. The afferent neuron must ultimately synapse with an efferent or motor neuron. When the afferent neuron synapses directly with the motor neuron, it forms a monosynaptic reflex. An example of this type of reflex is the stretch reflex. When the afferent neuron synapses with an intemeuron that then synapses with the motor neuron, it forms a polysynaptic reflex, e.g., the withdrawal reflex. Most reflexes are polysynaptic. The motor neuron then exits the spinal cord to innervate an effector tissue, which carries out the reflex response. 

If all species-wide behaviors are adaptive, however, this criterion is not specific for emotions. A stretch reflex is surely adaptive but is not an emotion. We can rule out reflexes as emotions because they do not involve the behavior of the whole organism they are local. So another criterion of an emotion might be involving the whole organism. In fact, many reflexes can be regarded as part of an emotion complex. The release of saliva in response to... 

There is only one monosynaptic reflex known to exist in humans - the stretch reflex. For this reason, it is commonly examined and an overview of its components and their functions is given below. 

Muscarinic antagonists can cause urinary retention by blocking the excitatory effect of ACh on the detrusor muscle of the bladder. During urination, cholinergic input to this smooth muscle is activated by a stretch reflex. 

Diagram of the structures involved in the stretch reflex arc. I is an inhibitory interneuron E indicates an excitatory presynaptic terminal la is a primary intrafusal afferent fiber Ca2+ denotes activator calcium stored in the sarcoplasmic reticulum of skeletal muscle RyR channels indicates the Ca2+ release channels. 

Drugs that modify this reflex arc may modulate excitatory or inhibitory synapses (see Chapter 21). Thus, to reduce the hyperactive stretch reflex, it is desirable to reduce the activity of the la fibers that excite the primary motoneuron or to enhance the activity of the inhibitory internuncial neurons. These structures are shown in greater detail in Figure 27-11. 

Cyclobenzaprine Poorly understood inhibition of muscle stretch reflex in spinal cord Reduction in hyperactive muscle reflexes antimuscarinic effects Acute spasm due to muscle injury inflammation Hepatic metabolism duration, 4-6 h Toxicities Strong antimuscarinic effects... 

FIGURE 13-1 Schematic illustration of the basic components of the stretch reflex. Normally, higher CNS centers control the sensitivity of this reflex by inhibiting synaptic connections within the spinal cord. Spasticity is thought to occur when this higher center influence is lost because of cerebral trauma or damage to descending pathways in the spinal cord. 

Skeletal muscle spasms are used to describe the increased tension often seen in skeletal muscle after certain musculoskeletal injuries and inflammation (muscle strains, nerve root impingements, etc.) occur.20,96 This tension is involuntary, so the patient is unable to relax the muscle. Spasms differ from spasticity because spasms typically arise from an orthopedic injury to a musculoskeletal structure or peripheral nerve root rather than an injury to the CNS. Likewise, muscle spasms are often a continuous, tonic contraction of specific muscles rather than the velocity-dependent increase in stretch reflex activity commonly associated with spasticity. The exact reasons for muscle spasms are poorly understood. According to some authorities, muscle spasms occur because a vicious cycle is created when the initial injury causes muscular pain and spasm, which increases afferent nociceptive input to the spinal cord, further exciting the alpha motor neuron to cause more spasms, and so on.61,96 Other experts believe that muscle spasms occur because of a complex protective mechanism, whereby muscular contractions are intended to support an injured vertebral structure or peripheral joint.96 Regardless of the exact reason, tonic contraction of the affected muscle is often quite painful because of the buildup of pain-mediating metabolites (e.g., lactate). 

It has been suggested that botulinum toxin might have other effects on neuronal excitability. This toxin, for example, might also inhibit contraction of intrafusal muscle fibers that are located within skeletal muscle, and help control sensitivity of the stretch reflex.33 Inhibiting these intrafusal fibers would diminish activity in the afferent limb of the stretch reflex, thereby contributing to the antispasticity effects of this intervention.33... 

Khalili AA, Benton JG. A physiologic approach to the evaluation and the management of spasticity with procaine and phenol nerve block including a review of the physiology of the stretch reflex. Clin Orthop Relat Res 1966 47 97-104. 

Spasticity is a central feature of multiple sclerosis (MS) and spinal cord injury (SCI). It consists of a velocity-dependent increase in tonic stretch reflexes with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex as one component of the upper motor syndrome (Young 1994). Existing drug therapy is far from satisfactory in terms of efficacy and unwanted effects (Panegyres 1992). Tremor, ataxia and lower urinary tract symptoms are frequently troublesome in MS. Both neuropathic and nociceptive pain (dealt with in Sect. 2.3) are also common in MS and SCI, and dozens of very painful muscle spasms can occur each day. Small wonder that there is also a high incidence of anxiety and depression in these conditions. 

Blocking stretch reflex response in mice induced by intraperitoneal injection of phenyl quinone. 

As discussed previously (Sec. II.B), bronchial smooth muscle tone is under autonomic control. Cold air and stimulation of receptors by irritants such as cigarette smoke, dust particles, and sulfur dioxide can also cause increased tone and hence bronchoconstriction (229). Bronchomotor tone is also modulated by vagal stretch reflexes and varies inversely with lung volume. Paradoxically, the rise in bronchomotor tone and/or increase in FRC during an attack of asthma may partially reverse the reduction in airway caliber that occurs in this condition, making assessment of response to therapy complex. Similarly, bronchodilators have been shown to cause paradoxical reductions in airflow and desaturation in some infants with history of wheeze, a phenomenon that has been attributed at least partially to changes in airway wall compliance (230-232). 

Kearney, R.E. and Hunter, l.W. 1983. System identification of human triceps surae stretch reflex dynamics. Exp. Brain Res. 51 117-127. 

The designation of the thalamus as the epicentre for tremorogenesis is not unequivocal [214], however, and, for example, it is clear that the integrity of the brain-stem reticular formation is essential for the production of tremor [234,235]. Indeed, electrical stimulation of this structure produces tremor [236], and its influence on the gamma-efferents involved in the stretch-reflex mechanism suggest that it may produce tremor via oscillations in an unstable servo-loop [8, 237]. Furthermore, the variety of sites in the brain which can influence tremor upon stimulation or lesion lends support to the idea of a multicentric origin of tremorogenesis [8, 238]. 

Slow stretch of the length of the receptor portion of the muscle spindle produces the static stretch reflex. The rtumber of impulses transmitted fi-om the primary arrd secondary endings increase in proportion to the amount of stretch. 

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