What is the cause of the "clasp knife" phenomenon in a stroke patient?

In patients with upper motor neurone damage, the clasp knife phenomenon may often be elicited.

What exactly is the clasp knife phenomenon?

This is best described as a sudden increase in tone when (1) rapidly and (2) passively contracting (3) the antigravity muscles. The antigravity muscles are those muscles that the body would usually use to maintain a standing posture. They include the extensors of the upper limb and the flexors of the lower limb.

Actually, the clasp knife phenomenon is a combination of two phenomena.

First, there's the spasticity of the antigravity muscles (muscles of the verebral column and the extensor muscles of the limbs). The antigravity muscles are excited by the pontine reticular nuclei and inhibited by the medullary reticular nuclei (both travel in the reticulospinal tract). Crucially, the medullary portion, unlike the pontine portion, depends heavily on input from the cerebral cortex, red nuclei and basal ganglia. In a stroke, these inputs are lost, and the medullary inhibitor system becomes non-functional, thus allowing full overactivity of the pointine excitatory system. Therefore, spasticity of the antigravity muscles develops. (This is why stroke patients with a hemiplegia typically have a 'bent' upper limb and a 'straightened' lower limb.)

Second, there's the 'give' (sudden decrease in tone) that occurs after a brief while of rapidly passively extending the muscles. This seems to be an exaggerated response to a normal phenomenon, called the stretch (or myotactic) reflex. Sudden stretching of a muscle is sensed by receptors, which cause an initial strong reflex contraction of the muscle concerned. However, this only lasts a brief while, and then is replaced by a much weaker muscular contraction. This system is again dampened by the medullary reticulospinal system, and therefore its loss in a stroke causes the reflex to become exaggerated. Thus, the clasp knife phenomenon is actually a (greatly exaggerated) sudden resistance to contraction, which then subsides after half a second or so, back to baseline spasticity.