The Stretch Reflex (07/10/13 prac)

Seite 1

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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