The Zombification of Aaron Macabe and its

Effects on his Motor Control Abilities

EPHE 380: Human Motor Control

Final Exam
Stephanie Norman
V00482420
Instructor: Paul Zehr
April 14, 2014

Question:
Aaron, a healthy 22 year old male, has found himself in the middle of a zombie
apocalypse. He is hiding in an open, grassy field when he spots a zombie approaching him.
In response, he starts running from the zombie, but, alas, he started too late and his body
was not yet warmed-up, allowing the zombie (a former Olympic sprinter before he became
zombified) to catch up to Aaron, grab his right forearm, yank it backwards, and bite him on
the right lateral forearm.
The zombie virus (zombiform rhabdoviridae) acts much like the rabies virus but is
acute in its effects, lacking an incubation time due to its extraordinary replication
capabilities. It is neurotropic, and enters Aarons afferent C6 nerve within seconds of
infection, and begins its retrograde axonal transport to travel antidromically, arriving at the
dorsal root ganglia and the spinal cord. From here, spread to Aarons brain occurs. A
variety of cells in the brain are infected including in the cerebellum, the dopaminergic
neurons in the substantia nigra pars compacta in the basal ganglia, and the supplementary
motor area causing neural degeneration. The infected side of the body experiences more
neuronal cell death in the ipsilateral hemisphere of the brain, resulting in contralateral
hemiparesis due to alteration of the descending and segmental activation of muscles during
walking.
After being bitten, Aaron manages to sprint away from the zombie, and is capable of
continued running even after the zombie virus begins to exhibit its effects. How does
Aarons motor control system respond to the zombie bite, and how is his running affected
after the zombiform rhabdoviridae infection?

When Aaron first sees the zombie and starts sprinting away, many motor units are
quickly recruited, including the larger fast oxidative and fast glycolytic fibres since high
velocity and high force is required for the fast getaway. However, the fast glycolytic fibres
are quick to fatigue, which slows Aaron down from a sprint to a run, and although
asynchronous firing allows for some fatigue resistance, Aaron starts to slow down as the
fast oxidative fibres also start to fatigue, reducing the leg muscles maximal force and
power production abilities and increasing the variability of the motor unit discharge. The
zombie, on the other hand, due to his past Olympic sprint training, is quite fast despite the
virus effects because his intense training when healthy caused increased synchrony of
motor unit firing and increased doublet firing, allowing him the force to catch up to Aaron,
grab his arm, and pull the arm back to his jaws to feast upon.
Without having to turn around and look at the zombie, Aaron knows his arm is being
pulled backwards through kinesthesia and proprioception due to the muscle spindles in the
biceps brachii, joint mechanoreceptors in the shoulder and elbow, and the slowly adapting
mechanoreceptors in the skin of the arm where he is grabbed (Figure 1).
The muscle spindles in his biceps also detect the muscle stretching, which triggers
the stretch reflex and activates the biceps to contract to try and pull the arm away from the
zombie before Aaron even has time to think about consciously pulling his arm away (Figure
2). However, the zombie detects this inherent attempt to pull away and grabs the arm more
firmly just before he bites down, causing the Golgi Tendon Organs (GTOs) to fire as they
sense the sudden increase in muscle tension. Though generally GTOs inhibit the agonist
muscle, Aarons locomotion causes state-dependent reflex reversal and results in positive
force feedback, which strengthens Aarons elbow flexion, allowing him to free his arm from
the zombies grasp (Figure 2). But tragically, not before the zombie gets in his incurable
bite.
3

As Aaron is grabbed and bitten, the muscle spindles in the biceps as well as the
cutaneous receptors in the forearm fire the free nerve endings, Ruffini corpuscle and
Merkel receptors (Figure 1). A large number of these exteroceptors are activated, and they
fire with high frequency, alerting Aaron that he is getting grabbed quite hard, and making
the bite feel quite painful. The sensory information from the bite arises largely from the C6
dermatome, which carries this information to the spinal cord, and from there it is carried to
the thalamus, which receives and relays this information to the primary somatosensory
cortex. The primary somatosensory cortex gives the exteroception and proprioception of
the movement of the arm and the location of the bite, which is then relayed to the
secondary sensory cortex followed by the posterior parietal cortex, which generates an
overall picture of the body and alerts Aaron that his right arm is being bitten (Figure 3).
The nociceptors in the forearm also trigger the flexion withdrawl and crossed
extension reflex (Figure 2), which flexes Aarons right arm away from the zombie while
causing the left arm to simultaneously extend. Since Aaron is running, this extension of the
left arm may assist in getting some body torsion to help Aaron pull away from the zombie.
When the zombie grabs Aarons arm and pulls his arm back, Aaron is capable of
maintaining forward movement by remodeling his stance by leaning forward more to move
his centre of gravity to the front of his base of support. Since Aaron is in an excited and
tense state, the muscle and tendon elasticity immediately respond to the arm grab and
subsequent backwards yanking because his muscles are tense, thereby enhancing their
stiffness and due to the visco-elastic properties, to make Aaron a little stiffer and harder to
perturbate, and allowing a faster reaction to the unexpected tug backwards. The vestibular
system and proprioception components (as described above) of the equilibrial triad then
kick in, with the semi-circular canals detecting the rotation of the head as he is pulled to his
right, with the hair cells detecting the sudden deceleration. The cervicocollic vestibular
4

reflex and vestibule-occular reflex stabilizes Aarons head and gaze, respectively, so his
head rotates marginally compared to the rest of his body, and he can maintain his forward
focus. There are no anticipated postural adjustments or role of vision in his postural
adjustments because Aaron was looking forward when he was grabbed so the yank was
unexpected. However, postural synergies, a pre-programmed reaction, help him maintain
balance. Lastly, his voluntary actions are to pull his body forward and flex his right arm
while yanking it out of the zombies grasp. The voluntary actions are initiated in the primary
motor cortex, then are carried down corticospinal tracts to the musculocutaneous nerve,
which innervates the brachialis and biceps brachii muscle, causing them to contract. These
voluntary actions are aided by his reflexes and by the epinephrine circulating through his
blood, which causes vasodilation to allow more blood to reach his leg muscles.
Furthermore, by this time, Aarons muscles have warmed up, which causes increased
conduction velocity in the nerve and muscle, improved blood flow to muscle and enhanced
metabolic reactions to allow increased muscle force and providing the burst of speed that
saves him from the grasp of the zombies hands and therefore saves his brains from being
eaten from him while still in human-form.
Muscle wisdom allows Aaron to continue running because his muscles decrease the
rate of discharge from their motor neurons to match the decreased relaxation rate to cause
increases in summation and a more economical contraction. It also shifts the forcefrequency relationship so lower frequency input gives the same force output. However, the
zombie is unable to continue to pursue Aaron after biting him because the increased
synchrony of his muscles due to training leads to faster fatigue that cannot be
compensated for by muscle wisdom.
By this time, the zombie virus has arrived at Aarons brain and begins infecting its
target regions. However, the effects are not yet noticeable, and furthermore, the virus does
5

not affect the spinal cord or peripheral nerves, thereby leaving the spinal central pattern
generators (CPGs), the interneuronal reflex network, and the motoneurons intact. The
CPGs rhythmically fire and these three components work together to produce the
coordinated running pattern that helps Aaron to sprint away from the zombie. The CPGs
are already turned on because Aaron started running pre-infection, activating the CPGs
by descending drive from his brain. Furthermore, the mesencephalic locomotor region is
not targeted by the virus, allowing continued supraspinal control over the locomotor CPGs,
which is how the attacking zombie was able to chase after Aaron. Once Aaron has pulled
his arm away from the zombie, his arm CPGs continue firing, returning his arm swinging to
the normal, alternating swing seen in running that is neutrally coupled to the rhythmic leg
movement and provides some coordination between the arm and leg CPGs.
Within two minutes of the bite, as Aaron is continuing his escape from the zombie,
the viral infection is beginning its neural degeneration of the target regions. The
contralateral hemiparesis begins to develop, and Aaron begins to lose regulation and
coordination of the left side of his body. The hypoactive muscle activity reduces the
corticospinal input resulting in less feedback from the movement of the legs and causing
drop foot. This explains why zombies seem to either drag one foot behind them or shuffle
their feet forward. However, the afferent feedback from the muscle spindles, GTOs and
cutaneous afferents remain healthy, which is vital for zombies since the stumbling
response, which relies on a combination of muscle and cutaneous afferents causing
excitation in the biceps femoris and inhibition in the tibialis anterior, prevents zombies from
continually falling over as they trip due to their drop foot and loss of coordination.
The primary motor cortex is not targeted by the virus, therefore, as Aaron becomes
zombified, his ability to code for force and direction remains intact and the primary motor
cortex tries to maintain the same running speed and forward direction. The healthy primary
6

motor cortex also allows for on-line control of the locomotor CPGs, enabling even zombified
Aaron to account for perturbations in the field such as rocks and divots while he is running.
However, the supplementary motor area (SMA) is targeted, therefore the bilateral coordination between the left and right hemispheres starts to deteriorate and Aarons running
becomes even more uncoordinated. In addition, the activity of the SMA is further decreased
as the virus begins to infect the dopaminergic neurons in the substantia nigra pars
compacts in the basal ganglia, resulting in a hypokinetic basal ganglia disorder due to an
overactive indirect pathway within the basal ganglia that reduces the activity of the
thalamus and thereby reducing the activity of the SMA. This results in Aaron becoming
more rigid and bradykinetic with a shuffling gait, lack of balance reactions and lack of facial
expressions, all which are stereotypical components of zombification. The SMA lesions
also explain why zombies are unable to perform complex sequences of movements such
as dance or karate even if they were experts at performing them prior to zombification.
Zombiform rhabdoviridae heavily targets the cerebellum, leading to impaired
balance and coordination, resulting in an ataxic running gait. The comparator function of the
cerebellum also is affected; further disturbing Aarons movements as he loses the ability to
perform feedback-dependent error corrections. The resulting lesions in the cerebellum also
lead to global hypotonia, morphing Aaron into the classic limp-looking zombie who starts to
increasingly slur his words as dysarthria develops. This is why zombies are generally highly
uncoordinated and able only to grunt or groan rather than speak clearly.
In summary, Aarons running gait is substantially affected as hemiparesis develops,
and the cerebellum, the basal ganglia, and the supplementary motor area degenerate.
Nonetheless, the now fully zombified Aaron remains able to continue running due to the
amazing compensatory abilities of the unaffected human motor control systems including
the spinal CPGs, the peripheral nerves and the intact regions of the brain.
7