A patient with a midbrain lesion at the level of the intercollicular transection develops extension of all four limbs, opisthotonus, and marked resistance to passive flexion. Section of the dorsal roots abolishes the rigidity. The mechanism of the extensor hypertonia is:

• A Unopposed lateral vestibulospinal and reticulospinal facilitation of gamma motor neurons, sensitizing muscle spindles ✓
• B Loss of cortical facilitation of gamma motor neurons with intact rubrospinal drive
• C Direct overactivation of alpha motor neurons by intact vestibulospinal tracts alone
• D Loss of cerebellar Purkinje cell output to the ventrolateral thalamus

Explanation

Decerebrate rigidity follows transection between the superior and inferior colliculi, removing descending input from the red nucleus and cortex while leaving the pontine reticular formation and lateral vestibular nucleus intact. Their unopposed facilitation drives gamma motor neurons, increasing spindle sensitivity; the resulting Ia afferent barrage reflexly activates alpha motor neurons of extensors. This gamma rigidity is abolished by dorsal root section, which is the discriminating experimental fact. Rubrospinal loss removes flexor bias, explaining the extensor posture.

Reference: Guyton and Hall Textbook of Medical Physiology, 14th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.