The corticospinal tracts are excitatory in nature (Glutaminergic). So damage of the CST would mean less excitatory input to the LMN. By this logic, there should not be hypertonia. What is the mechanism behind this spastic (hypertonic) state of the muscle in UMN type of lesion?
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The main idea is that most Corticospinal tracts end up in inhibitory (GABA releasing) inter-neutrons, which then synapse directly into the Lower Motor neurons. This means that positive stimulation of inhibitory neurons occurs, which leads to overall negative regulation of Lower motor neurons.(1)
And the book goes on to say,
The corticospinal tracts are not the sole pathway for serving voluntary movement. Rather, they form the pathway that confers speed and agility to volun- tary movements and is thus used in performing rapid skilled movements. Many of the simple, basic voluntary movements are mediated by other descending tracts.
Note that the other descending tracts would be the extra-pyramidal tracts, which, are responsible for the most evident signs of UMN lesions, which include spasticity, hyper-reflexia, hyper-tonicity and severe paralysis.
Here is the list of symptoms of lesions localised to the pyramidal/coricospinal tracts:
- Positive Babinski sign.
- Absence of Cremasteric reflexes.
- Absence of Superficial abdominal reflexes.
1- South Asian Edition Of Snell's Clinical Neuroanatomy
