The Stretch Reflex (07/10/13 prac)

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The physiological basis, methodology, results, and clinical importance of the monosynaptic stretch reflex and the Jendrassik manoeuvre from the 07/10/13 Human Physiology practical.
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The Stretch Reflex (07/10/13 prac) A monosynaptic reflex exhibited by all skeletal muscles: Striking the tendon with a reflex hammer → stretches the main body of its attached muscle → stretches the muscle spindles contained within the muscle → activates the sensory endings of the 1a afferent fibres wrapped around the central part of the muscle spindles → action potentials travel up the 1a afferent axons → which enter the spinal cord by the dorsal roots → synapse onto the cell bodies of α-motoneurons in the ventral horn of the grey matter → stimulate action potentials which travel along the α-motoneurons, leaving the spinal cord by the ventral roots → stimulate the skeletal muscle cells of the same muscle → produce muscle action potentials (which can be recorded as EMG using surface electrodes) → muscle contraction. Also, reciprocal inhibition of the activity of antagonistic muscles occurs, to permit only the contracting muscle to move the limb. Although this response occurs under unnatural conditions, it occurs any time one uses a muscle to make a movement – it is fundamental to regulating the behaviour of muscles, helping to ensure that the right amount of tension is produced to match the aim of the movement. We explored this monosynaptic stretch reflex by attaching electrodes to the insertion of the Achilles tendon and to the gastrocnemius muscle. The subject stood and leaned against the edge of a bench shifted their weight to their non-instrumented leg, and lifted the heel of the instrumented leg. The Achilles tendon was then struck (a few cm up from its insertion point, on the heel) with a reflex hammer, also plugged into the ADI, and the latency (the time between being struck by the tendon and the gastrocnemius muscle contracting) was averaged. Typically, this is ~30ms. Next, we explored the Jendrassik manoeuvre: a technique which relies on the anterior horn cells being connected in order to prime motor neurons and make a motor response more likely. This is used when pathological latencies are recorded, or when people naturally have ‘quiet’ magnitudes, to boost them so that a response can be recorded. It involves the subject standing as before, but holding their elbows out and fingers hooked together. For 10 hammer taps, the person should keep their arms relaxed, for the next 10 they should pull their hands apart firmly, and for the last 10 they should relax once more. We recorded both the latencies (in ms) and the magnitudes (in mV). Class data: ·         Using a linear regression to establish a p-value for the slope (y=mx+c), there was only weak evidence to support the idea that height affects the stretch reflex latency (R2 = 10%, so only 10% of latency due to height). ·         Using a linear regression to establish a p-value for the slope (y=mx+c), there was no evidence to suggest that hip-ankle length affects the stretch reflex latency. ·         Using a paired T-test to establish a p-value, there was no evidence that the Jendrassik manoeuvre affected the latency of the stretch reflex. ·         Using a paired T-test to establish a p-value, there was no evidence that the Jendrassik manoeuvre affected the magnitude of the stretch reflex before and during the technique (it may have been weak evidence – p = 0.051). ·         Using a paired T-test to establish a p-value, there was no evidence that the Jendrassik manoeuvre affected the magnitude of the stretch reflex during and after the technique. o    The lack of evidence for the Jendrassik manoeuvre affecting magnitude is likely a result of improper performance of the technique. The stretch reflex can be used to assess neurological damage. Testing the stretch reflex of different areas can help to localise neurological damage - if the latency of a motor response is increased, discontinuous or is not recorded, there is likely to be a pathology. Given that the nerves branch off from particular sections in the spinal column, the damage can be localised by testing the neuromuscular responses of different muscles/limbs. Pathologies that may cause variations in stretch reflexes include: demyelination of the nerves which increases the latency of the reflex; calcium deficiency which would produce a 'normal' latency but a delayed contraction; or nerve cell death, which would produce no response.

The Stretch Reflex (07/10/13 prac) A monosynaptic reflex exhibited by all skeletal muscles: Striking the tendon with a reflex hammer → stretches the main body of its attached muscle → stretches the muscle spindles contained within the muscle → activates the sensory endings of the 1a afferent fibres wrapped around the central part of the muscle spindles → action potentials travel up the 1a afferent axons → which enter the spinal cord by the dorsal roots → synapse onto the cell bodies of α-motoneurons in the ventral horn of the grey matter → stimulate action potentials which travel along the α-motoneurons, leaving the spinal cord by the ventral roots → stimulate the skeletal muscle cells of the same muscle → produce muscle action potentials (which can be recorded as EMG using surface electrodes) → muscle contraction. Also, reciprocal inhibition of the activity of antagonistic muscles occurs, to permit only the contracting muscle to move the limb. Although this response occurs under unnatural conditions, it occurs any time one uses a muscle to make a movement – it is fundamental to regulating the behaviour of muscles, helping to ensure that the right amount of tension is produced to match the aim of the movement. We explored this monosynaptic stretch reflex by attaching electrodes to the insertion of the Achilles tendon and to the gastrocnemius muscle. The subject stood and leaned against the edge of a bench shifted their weight to their non-instrumented leg, and lifted the heel of the instrumented leg. The Achilles tendon was then struck (a few cm up from its insertion point, on the heel) with a reflex hammer, also plugged into the ADI, and the latency (the time between being struck by the tendon and the gastrocnemius muscle contracting) was averaged. Typically, this is ~30ms. Next, we explored the Jendrassik manoeuvre: a technique which relies on the anterior horn cells being connected in order to prime motor neurons and make a motor response more likely. This is used when pathological latencies are recorded, or when people naturally have ‘quiet’ magnitudes, to boost them so that a response can be recorded. It involves the subject standing as before, but holding their elbows out and fingers hooked together. For 10 hammer taps, the person should keep their arms relaxed, for the next 10 they should pull their hands apart firmly, and for the last 10 they should relax once more. We recorded both the latencies (in ms) and the magnitudes (in mV). Class data: ·         Using a linear regression to establish a p-value for the slope (y=mx+c), there was only weak evidence to support the idea that height affects the stretch reflex latency (R2 = 10%, so only 10% of latency due to height). ·         Using a linear regression to establish a p-value for the slope (y=mx+c), there was no evidence to suggest that hip-ankle length affects the stretch reflex latency. ·         Using a paired T-test to establish a p-value, there was no evidence that the Jendrassik manoeuvre affected the latency of the stretch reflex. ·         Using a paired T-test to establish a p-value, there was no evidence that the Jendrassik manoeuvre affected the magnitude of the stretch reflex before and during the technique (it may have been weak evidence – p = 0.051). ·         Using a paired T-test to establish a p-value, there was no evidence that the Jendrassik manoeuvre affected the magnitude of the stretch reflex during and after the technique. o    The lack of evidence for the Jendrassik manoeuvre affecting magnitude is likely a result of improper performance of the technique. The stretch reflex can be used to assess neurological damage. Testing the stretch reflex of different areas can help to localise neurological damage - if the latency of a motor response is increased, discontinuous or is not recorded, there is likely to be a pathology. Given that the nerves branch off from particular sections in the spinal column, the damage can be localised by testing the neuromuscular responses of different muscles/limbs. Pathologies that may cause variations in stretch reflexes include: demyelination of the nerves which increases the latency of the reflex; calcium deficiency which would produce a 'normal' latency but a delayed contraction; or nerve cell death, which would produce no response.

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