August 03, 2008

Controlling The Spindle Servo Arm

The muscle spindle is regulated at many hierarchical levels. At the level of the cord segment (segmental level), we see that if the sensory nerve is damaged, by afflictions like Tabes dorsalis (damages the dorsal horn) the reflex arc will be interrupted. Similarly, in acute anterior poliomyelitis, the ventral or anterior root, the pathway of motor outflow, is damaged. In both the cases, hypotonia or loss of muscle tone will ensue, as expected.

regulation of muscle spindleThere is also additional supra-segmental inputs on the said reflex circuit. They come from the basal ganglia, the cerebellum, and cerebral cortex. Refer to the picture on the left. There are two balloon like stuff in the medulla (and pons). The one in red is the bulbo-reticular facilitatory area, which is tonically firing and naturally facilitating the reflex arc. The one in green represent reticular inhibitory area and is normally silent. The descending pathways from both of them travel via lateral funiculus to gamma neurons and constitute the reticulospinal tract. The inhibitory property of the inhibitory area arises from the inhibitory inputs it gets from the cortex (suppressor strip or 4s of M1 or motor cortex; Brodmann area 4) and from the basal ganglia. Cerebellum also inhibits this area (inhibitory fibers shown in green, stimulatory in red). Please note that the cerebellum also inhibits the vestibular nucleus, a structure that stimulates the arc via anterior funiculus. Fibers from vestibular nucleus form the vestibulospinal tract and end supplying the alpha motor neurons.

Now if you cut along the line as shown, as Sherrington did, you would then stop the inhibitory inputs from both the cortex and the basal ganglia. Decerebrate rigidity of Sherringtonian type will occur. All the four limbs and the tail of the animal will be extended, the tail will stand up and the animal will take up a backwardly arched posture (opisthotonus). This is gamma rigidity, since outflow to the A-gamma is responsible for it. To produce decerebrate rigidity of ischaemic type, both the carotid arteries are tied and the basilar artery is tied at the junction of pons and medulla. The anterior lobe of cerebellum is damaged, causing inhibitory output to the vestibular nucleus to stop. Vestibulospinal outflow continues unabated and alpha motor discharge is enhanced causing alpha rigidity. Decerebrate rigidity of Sherringtonian type can be stopped by deafferentation (sectioning of afferent 1a fibers) but the ischemic type rigidity is not diminished by the procedure.

In most kinds of stroke, there is ischaemia or hemorrhage in the internal capsule. It is through this portion of the brain, the corticospinal tract descends. Thus, if you look at the figure, you can see that the fibers to the inhibitory reticular area get damaged, resulting in decorticate rigidity. This type of rigidity can also be produced by surgically destroying the cortex.

But all these mentioned are not rigidities, strictly speaking, since either the flexor or the extensor group is involved. True rigidity is found in Parkinson's disease where both muscle groups are involved. Lead-pipe type of rigidity is more common, but cog-wheel rigidity is also seen in Parkinsonism, a disease caused by lesion in the basal ganglia.

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Reference: Principles of physiology, Debasis Pramanik, 2e, p447-448
Review of Medical Physiology, William F. Ganong,22e, p210-212
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