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I read these two from various books, and got confused. The confusion is -

Reticulospinal tracts control gamma motor neurons. Gamma motor neurons control tone of muscle. In decerebrate rigidity, the reticulospinal tracts are cut, so the gamma motor neurons start firing excessively, and SPASTICITY develops. I understood this part and why Decerebrate Rigidity is a misnomer as it is actually spasticity.

Question is, in decorticate rigidity, the cerebral cortex is damaged. The basal ganglia are intact. One explanation I found is that the basal ganglia keep the reticulospinal tract activated so gamma motor neuron is under control. But if basal ganglia have no direct communication with brainstem or spinal cord, and their efferents pass through cerebral cortex, then even in decorticate rigidity, the reticulospinal tract should not be working, and thus the gamma motor neurons should fire excessively, in which case the decorticate rigidity also becomes a spasticity.

Am I missing anything? I am keeping red nucleus and vesticular nuclei out of this just to make matter simple. My question is about activity of gamma motor neurons in these two conditions. I hope you got the question. Thank you.

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    $\begingroup$ Interesting question, and presented with nice explanation of your difficulty. +1 $\endgroup$ – anongoodnurse Jan 25 '15 at 23:54
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1)

a. Decorticate posturing means rubrospinal tract is the dominant output to the motor neurons of the body... maybe dominant is the wrong word, I am not all that knowledgable on this subject, but it is certainly altering the standard reticulospinal tract based extensor posturing.

http://en.wikipedia.org/wiki/Rubrospinal_tract

It is responsible for the strange flexion of upper limbs (aka arms). I say strange because when you think coma you think extension, not flexion. The lower limbs (aka legs), as always is extensor. Why the upper limb but not the lower limb? The red nucleus may play an additional role in controlling muscles of the shoulder and upper arm via projections of its magnocellular part.

b. In decerebrate posturing the rubrospinal tract is also cut, since the lesion is below the red nucleus. In this scenario the reticular activating system (aka reticulospinal tract) is the dominant output to the motor neurons of the body. Here you get the classic extensor pose, for both upper and lower limbs...

The point is: Rubrospinal tract was what you were missing. The red nucleus is the specific part of the basal ganglia that is involved...


2) the difference between spasticity vs rigidity:

  • spasticity is an increased resistance to the passive movement of a joint due to abnormally high muscle tone (hypertonus) which varies with the amplitude and speed of displacement of a joint.
  • rigidity is an increased resistance to the passive movement of a joint which is constant throughout the range of joint displacement and not related to the speed of joint movement.

your supposed to test this out on patients to get a feel for what's the difference.

spaciticity is the case for upper motor neurons lesions (ex. stroke), since the spinal reflexes are not being inhibited from above...

an example of rigidity in neurology is Parkinson's disease, which is the loss of the substantial nigra, which like the red nucleus is also in the midbrain... while the the substantial nigra and basal ganglia loop do influence the motor control of the body... they are not upper motor neurons. Upper motor neuron is specific to the corticospianl tract, it is the neuron going from cortex to anterior horn of spinal cord. Basal ganglia does influence the motor cortex but it isn't part of the corticospinal tract, hence not an upper motor neuron lesion.


3) Role of muscle spindles in spasticity from upper motor neuron lesions:

I am using this website for this part of my answer:

http://www.d.umn.edu it's from university of minnisota, which is funny because their acronym is UMN

high resistance to stretch occurs when the spindles are overactive (usually due to high rate of gamma motor neuron discharge) --> HYPERTONIC (SPASTIC)

removing inhibitory inputs to the gamma motor neurons increases their discharge rate, and increases spindle output

this can happen when there is an UPPER MOTOR NEURON lesion

It seems that with an upper motor neuron lesion, the gamma motor neuron is uninhibited, thus the gamma fibers have a constitutively increased discharge rate and muscle spindles are overactive. The machanoreceptors in the spindles then decrease their afferent sign, which should lead to relaxation of a/g-motor neurons, and well, I dunno, I am thoroughly confused on the precise mechanism of UMN lesion causing spasticity. Reflexes are intact so the a/g-motor neurons should relax, since only UMN damaged and not any part of the reflex arc. I seem to be missing something here.

I'm calling for back up, someone please help!

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  • $\begingroup$ I'm sorry but this doesn't answer my question. My question is why only in Decerebrate rigidity, we see gamma motor neuron overactivity. Red nucleus plays a part in pathogenesis I agree, but the rubrospinal tract ends on alpha motor neurons and not on gamma motor neurons. Another thing which I would like to correct, Red Nucleus is not a part of basal ganglia, but a part of extrapyramidal system. Also basal ganglia have no direct connection to brain stem, they have indirect connection through cortex. $\endgroup$ – gautampw Jan 26 '15 at 8:52
  • $\begingroup$ this website has something at the very bottom of the page: d.umn.edu/~jfitzake/Lectures/DMED/MuscleReceptors/… It seems that with an upper motor neuron lesion, the gamma motor neuron is uninhibited, thus the gamma fibers have a constitutively increased discharge rate and muscle spindles are overactive. The machanoreceptors in the spindles then decrease their afferent sign, which should lead to relaxation of a/g-motor neurons, and well, I dunno, I am thoroughly confused on the precise mechanism of UMN lesion causing spasticity. Reflexes intact, only UMN damaged. $\endgroup$ – Jasand Pruski Jan 26 '15 at 16:51
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Not sure if this helps but its what i know after reading my class notes on reticular formation.This may not help but as I trying to learn also I will share.

Decorticate - The motor part way/Rubrospinal no longer has the influence of the higher centers such as the corticospinal - Flexor Response

Decerebrate - The lesion happens below the red nucleus therefore the rubrospinal spinal tract is not functioning - Extensor Response

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Since in decorticate posture the lesion is at the level of neurons which originate from cortexand relay in the basal ganglia...but since basal ganglia are still intact they do influence in controlling increased discharge rates of gamma motor neuron. Moreover red nucleus is dominant here since no input from motor cortex flexor posture is present that too in upperlimbs since rubrospinal tract ends in cervical spinal cord.

Decerebrate means no rubro no cortex no basal ganglia...so gamma motor neuron are like "yay, i'm free now" so they keep increasingly discharging causing spastic extensor response...

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  • $\begingroup$ Overall well-written answer... Please add some reliable references though $\endgroup$ – L.B. Jul 26 '17 at 13:59

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