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W5D3H4: Pain and Reflexes Learning Objectives 1. Describe pain sensory pathways and relevant molecules involved in nociception. 2. Outline spinal reflex circuits, including those activated in the presence of a painful stimulus. 3. Describe the clinical use of reflexes as assays of motor neuron function and relate changes in pain and somatic detection to diabetic neuropathies. LO 1. Describe pain sensory pathways and relevant molecules involved in nociception nocioceptors Area on the skin that receptor responds to rapidly adapting slowly adapting rapidly adapting slowly adapting LO 1. Describe pain sensory pathways and relevant molecules involved in nociception Anatomy of nociceptors LO 1. Describe pain sensory pathways and relevant molecules involved in nociception Conduction latency Compound action potentials recoded in response to peripheral nerve stimulation LO 1. Describe pain sensory pathways and relevant molecules involved in nociception LO 1. Overview of pain response to mechanical injury: Release of protease -> Bradykinin production -> activation of free nerve endings-> action potential propagated to spinal cord & axonal branches-> nociceptor axons release substance P and CGRP -> histamine release -> vasodilation and increased pain sensation. LO2. Outline spinal reflex circuits, including those activated in the presence of a painful stimulus. "Striking the tendon below the patella gives rise to a sudden extension of the leg, known as the knee-jerk reflex.” Sir Michael Foster (1877) Textbook of Physiology 0 1 2 3 4 NINDS Reflex Assessment Scale Reflex absent Reflex small, less than normal; includes a trace response or a response brought out only with reinforcement Reflex in lower half of normal range Reflex in upper half of normal range Reflex enhanced, more than normal; includes clonus LO2. Outline spinal reflex circuits, including those activated in the presence of a painful stimulus. Characteristics of Spinal reflexes Involuntary Short latency (< 40 ms) Stereotyped responses Only require peripheral and spinal neurons LO2. Outline spinal reflex circuits, including those activated in the presence of a painful stimulus. Physiological Mechanisms Underlying Spinal Reflexes THE PATELLAR TENDON (KNEE JERK) REFLEX The patellar tendon (knee jerk) reflex illustrates a monosynaptic stretch reflex and reciprocal inhibition of the antagonistic muscle. Stimulus: Tap to tendon stretches muscle. Receptor: Muscle spindle stretches and fires. Afferent path: Action potential travels through sensory neuron. Integrating center: Sensory neuron synapses in spinal cord. Efferent path 1: Somatic motor neuron onto Effector 1: Quadriceps muscle Efferent path 2: Interneuron inhibiting somatic motor neuron Response: Quadriceps contracts, swinging lower leg forward. Effector 2: Hamstring muscle Response: Hamstring stays relaxed, allowing extension of leg (reciprocal inhibition). LO2. Outline spinal reflex circuits, including those activated in the presence of a painful stimulus. THE CROSSED EXTENSOR REFLEX A flexion reflex in one limb causes extension in the opposite limb. The coordination of reflexes with postural adjustments is essential for maintaining balance. Gray matter White matter Spinal cord Spinal cord Ascending pathways to brain Sensory neuron Painful stimulus activates nociceptor. Primary sensory neuron enters spinal cord and diverges. Nociceptor One collateral activates ascending pathways for sensation (pain) and postural adjustment (shift in center of gravity). Alpha motor neurons Painful stimulus Extensors inhibited Flexors contract, moving foot away from painful stimulus. Extensors contract as weight shifts to left leg. Flexors inhibited Withdrawal reflex pulls foot away from painful stimulus. Crossed extensor reflex supports body as weight shifts away from painful stimulus. LO2. Outline spinal reflex circuits, including those activated in the presence of a painful stimulus. Flexion and Crossed-Extensor Reflexes in arms Pain!!! LO 3. Describe the clinical use of reflexes as assays of motor neuron function and relate changes in pain and somatic detection to diabetic neuropathies. ------------------------------------------------------------------------------------------------------The type or intensity of reflexes are graded according to the following criteria: Grade Response 0+ No response or absent reflex 1+ Trace or decreased response 2+ Normal response 3+ Exaggerated or brisk response 4+ Sustained response -----------------------------------------------------------------------------------------------------Damage to spinal motor neurons, defects in synaptic transmission at the NMJ or muscle atrophy can result in grades of 0 or 1. Grades of 3 or 4 can be indicative of damage to the spinal cord or brain, which result in a condition known as ‘spasticity’ and may include clonus. LO 3. Describe the clinical use of reflexes as assays of motor neuron function: Spasticity Spasticity is a condition characterized by hypertonicity (increased muscle tone), clonus (a series of rapid muscle contractions), exaggerated tendon jerk reflexes, involuntary muscle spasms, scissoring (involuntary crossing of the legs), and stiff joints caused by co-contraction of antagonist muscles. The degree of spasticity varies from mild muscle stiffness to severe, painful, and uncontrollable muscle spasms. Spasticity can interfere with rehabilitation in patients with certain disorders, and often interferes with daily activities. Spasticity is usually caused by damage to brain or spinal neurons involved in the control of movement. It may occur in association with spinal cord injury, multiple sclerosis, cerebral palsy, anoxia, brain trauma, severe head injury, and diseases such as adrenoleukodystrophy, amyotrophic lateral sclerosis (ALS), and phenylketonuria. Inferences drawn from an animal model suggest that one of the principal mechanisms of spasticity is an increase in the excitability of motoneurons consequent to the lesion in the brain or spinal cord. The increased excitability results in sustained repetitive discharge of motoneurons in response to brief stimuli. LO 3. Describe the clinical use of reflexes as assays of motor neuron function: Clasp-Knife Reflex The clasp-knife reflex (also called the inverse myotatic reflex) is a pathological reflex that is only observed following lesions of the central nervous system that produce spasticity. In response to a rapid muscle stretch, a patient with spasticity first exhibits a strong stretch reflex, followed by a relaxation of the muscle. It is the sudden release of muscle tension when a contracting muscle is forcibly stretched that gives the reflex its name: The spastic limb initially resists flexion (because of the stretch reflex) and then collapses on itself like the blade of a jack- or clasp-knife. The reflex is thought to be mediated by group II and group III afferent fibers arising from free nerve ending receptors located in muscle fascia and aponeuroses. The spinal circuits responsible for the clasp-knife reflex are normally suppressed and only become operational only after lesions to the spinal cord or brain. Clonus is the result of a reverberating or exaggerated response Clonus movie: https://www.youtube.com/watch?v=4SrhgjGIZ30 The following is a good way to conceptualize clonus: If a person standing on the tip ends of the feet suddenly drops his or her body downward and stretches the gastrocnemius muscles, stretch reflex impulses are transmitted from the muscle spindles. Normally this helps you to not land on your heels too hard- as you are able, stand up and try it! In clonus, these impulses reflexively excite the stretched muscle, which lifts the body up again. After a fraction of a second, the reflex contraction of the muscle dies out and the body falls again, thus stretching the spindles a second time. Again, a dynamic stretch reflex lifts the body, but this too dies out after a fraction of a second, and the body falls once more to begin a new cycle. In this way, the stretch reflex of the gastrocnemius muscle continues to oscillate, often for long periods. Babinski sign • A reflex in which there is extension upward of the toes and the abduction of the toes when the sole of the foot is stroked firmly on the outer side from the heel to the front • Normal in infants under the age of 2 years but a sign of brain or spinal cord injury or disease in older persons. Watch http://www.youtube.com/watch?v=ZQh6zVxtYGc&feature=related