Mechanism of Decorticate & Decerebrate Posturing? Also why is only Decorticate Rigidity a misnomer?
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!