Muscle reflexes stretch reflex

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

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. 

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... 

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... 

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. 

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). 

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. 

Servo-assist function of the muscle spindle reflex. If the extrafusal fibers contract less than the intrafusal fibers, then the muscle spindles will maintain a stretch reflex to further excite the extrafusal fibers. This technique is used in active resistive myofascial therapy. 

Reciprocal innervation. When a stretch reflex excites one muscle, it simultaneously inhibits the antagonist muscle. Reciprocal... 

A stimulatory effect on the stretch reflex in hypotonic muscles. 

Stretch reflex. The stretch of a muscle excites the muscle spindle mechanism, resulting in reflex contraction of that muscle. This is to be avoided when applying passive myofascial techniques to contracted or con-tractured muscles. It can be avoided by applying slow, even force and releasing that force slowly and evenly. However, the stretch reflex is to be used during active myofascial... 

Reciprocal inhibition. This is used in active myofascial techniques with or without resistance. When a stretch reflex stimulates one muscle, it simultaneously inhibits the antagonist muscle e.g., if the stretch reflex excites the biceps, reciprocal inhibition inhibits the triceps. 

The pharmacological effects of this complex mixture of alkaloids in opium may, in some respects, be more beneficial than the effects of an individual alkaloid. The effect of opium in the treatment of diarrhoea is better than that of either morphine or codeine given individually. It is possible to calm the gastrointestinal tract with a dose which contains only half of the dose which would be necessary for morphine alone. The combination of the increase in stretch reflex caused by morphine and the inhibition of increased peristaltic action by papaverine leads to a better therapeutic effect. The increase in muscle tone due to morphine is reduced by papaverine, and other benzylisoquinolines also participate in this tranquillisation of the g.i. tract. In the normal 50 mg dosage of opium used for the treatment of diarrhoea there is about 5 mg of morphine, 0.5 mg of papaverine and 3 mg of nos-capine which contrasts markedly with a dose of 100—200 mg of papaverine if this were given alone. The analgaesic activity of opium is due mainly to the morphine present, as the levels of codeine, neopine and papaverine are relatively small. The respiratory depression effect of opium is also due to the morphine content and the antagonistic effects of noscapine and narcotoline are not so pronounced. Thus the main use of opium in medicine is for the treatment of diarrhoea. 

The large diameter A/l-afferent fibre enters the dorsal horn of the spinal cord through the medial division of the dorsal root. It then descends through the medial region of lamina I or II, or alternatively, curves around the medial (central) edge of the dorsal horn down to the ventral horn. On reaching deeper laminae, laminae IV and V, the AjS-fibres ascend back up into laminae III and IV where they repeatedly subdivide and form a characteristic termination pattern. The densest arborisation appears to occur in lamina III. Axons originating from specialised muscle stretch receptors have collaterals that pass ventrally to make monosynaptic connections with neurons of laminae V, VI and VII. Some also extend to laminae VIII and IX of the ventral horn where they synapse directly onto motor neurons and form the basis of monosynaptic reflexes. 

Because baroreceptors respond to stretch or distension of the blood vessel walls, they are also referred to as stretch receptors. A change in blood pressure will elicit the baroreceptor reflex, which involves negative feedback responses that return blood pressure to normal (see Figure 15.6). For example, an increase in blood pressure causes distension of the aorta and carotid arteries, thus stimulating the baroreceptors. As a result, the number of afferent nerve impulses transmitted to the vasomotor center increases. The vasomotor center processes this information and adjusts the activity of the autonomic nervous system accordingly. Sympathetic stimulation of vascular smooth muscle and the heart is decreased and parasympathetic stimulation of the heart is increased. As a result, venous return, CO, and TPR decrease so that MAP is decreased back toward its normal value. 

Pulmonary stretch receptors are responsible for initiating the Hering-Breuer reflex. These stretch receptors are located within the smooth muscle of large and small airways. They are stimulated when the tidal volume exceeds 1 1. Nerve impulses are transmitted by the vagus nerve to the medullary respiratory center and inhibit the inspiratory neurons. The primary function of these receptors and the Hering-Breuer reflex is to prevent overinflation of the lungs. 

Tension is the force that is being opposed by the muscle and is a different concept to stretch. The reflex can be summarized as below. 

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