JFK’s reaction looks to be a reflex stiffening reaction showing many of the classic signs of Spastic Paralysis or Spasticity.

Similarities in the observed Z-film reactions beginning at z225/226 to Spastic Paralysis/Spasticity can be seen in the example photos below which depict spasticity. These photo examples were found as references from the American Association of Neurological Surgeons, the Pacific Movement Disorders Center, and the Premier Neurology & Wellness Center.

In the example clear frame at z248, taken after the lower neck shot occurred, the spastic paralysis or spasticity symptoms developed could have been caused by spinal trauma or damage (as opposed to flaccid paralysis which would more likely arise from extensive brain cortex and midbrain trauma or damage). Spasticity is a stretch reflex related reaction in the traumatized spinal cord area and affects the associated muscles innervated from that area of the cord.

Another example of spasticity is called pattern III seen above, taken from classifications of spasticity in upper limb positions by the German neurology Prof. Harald Hefter.

JFK’s position looks very similar to these patterns with perhaps slightly more pronation in the forearm and flexion at the wrist.

Net, Spastic Paralysis can cause symptoms of stiffness and rigidity which appears to be similar to what is seen in the Zapruder film after z225 and could likely be the cause of the upper body stiffness that ITEK commented on in the Z-film when they stated that JFK “appeared to remain in a frozen position”.

References indicate that Spastic Paralysis symptoms can happen over different time frames. Depending on person and type of trauma, the condition can develop differently in everyone; sometimes it takes weeks, while in others it happens instantly. In the JFK case it would appear to have manifested itself immediately.

Speculating on the specific mechanisms for these actions is described in more detail further below on this page.

In summary:

- JFK’s reactions starting around z225/226 (hands clenching followed by arm movements) appear to be a reflexive stiffening of the muscles similar to what is called spastic paralysis or spasticity. Spasticity of the shoulders, arms, and hands can be caused by trauma to the spinal cord in the area around the lower few cervical vertebras feeding the brachial plexus, and the major neck muscles getting innervation from spinal accessory nerve roots that exit the cord down to C4/C5 from the spinal accessory nucleus in the spinal cord.

-Looking at ballistic gel studies using a Carcano, a bullet strike that would transverse the upper back would be expected to cause significant reverberation/shockwave trauma in that area of the spine in the upper back. Additionally based on x-ray there may have been damage to the bone of the transverse process of C6 or C7 on JFK. A bullet grazing or nearly contacting the transverse process of a cervical vertebra would likely generate an impulse of compression and possible twisting/torquing of vertebra segments in that area (perhaps like a wingnut twisting around a screw) affecting the spinal cord contained within and causing bilateral cord effects.

-The onset of a reflex reaction becoming visible on film could start as fast or faster than typical rapid voluntary reactions so could be expected to be seen beginning as soon as ~200 ms after stimulus. If the spasticity type of arm/hand positioning in JFK is observed to start at about z225/226, this might give a clue to the approximate bullet strike time. Using this approach, the bullet might be estimated to have struck within ~3-4 frames earlier, or around ~z222. (To note, John Connally also apparently showed some reaction in this timeframe).

Net, observations of JFK’s motion on the Zapruder film after z225 are consistent with an apparent bullet transversal in the C6/C7 area of the neck resulting in spastic paralysis rapidly affecting the neck and shoulders, arms, hands and fingers.

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Speculating on the possible specific mechanism for spastic paralysis from an estimated z222 strike:

Local spinal cord trauma or damage (stretching/torqueing) occurred causing disruption and an imbalance in the net control signals from the upper motor neutron inhibitory input tracts resulting in decreased net lower motor neuron inhibitory signaling allowing any residual excitatory input and unrestricted stretch reflex feedback to predominate local control of the affected lower motor neurons and the innervated muscles. This could result in over activation/contraction of the associated innervated muscles. One nerve tract likely involved would be the lateral (medullary) reticulospinal tract. In that case if the inhibitory fibers were disrupted in the reticular formation this could result in the hypertonia (spasticity) as the lateral reticulospinal's are involved in inhibition, and disruption of this pathway can result in spasticity.

If all the local flexor & extensor muscles are affected about equally, the flexors (that tend to work against gravity or resistive forces) tend to be more powerful so net they win out, with the net result having the flexor muscles controlling the body parts positions that are taken, and this accounts for the presentation seen with those body parts as a result of the spasticity.

Flaccid paralysis from the extensive neurological damage caused by the z312/313 strike:

With the extensive trauma and destruction affecting the brain cortex and upper midbrain itself as a result of the z312/313 shot, what would be expected is even more extensive disruption of the total neural system. This would include complete spinal shock which can cause the loss of all muscle tone and even the spinal reflexes below the level of the damage. Eliminating all muscle control would result in immediate flaccid paralysis. This is what police and military snipers aim to achieve, especially in hostage situations.

Some recent research into the mechanism of rapid neuromuscular loss of control after head trauma is examined in a Neurological journal this past year describing the phenomenon of boxers losing consciousness immediately after a head strike with a complete loss of muscle tone (flaccid paralysis) and falling to the floor. Their latest hypothesis on this is a mechanism of pore formation in the axonal cell membrane caused by the mechanical stretching trauma which is called mechanoporation. Mechanoporation disrupts the cell membranes creating new quasi-stabilized pores and the modeling indicates this will shut down the action potentials. The model further helps explain the typically seen loss of consciousness without seizures seen in boxing knockouts (but seizures can still be a rare occurrence).

They describe this in “How can a punch knock you out” at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7649325/#!po=20.5882