Undead research has provided some insights into the underlying pathophysiology of the zombie disposition. However we are still a long way from understanding precisely the pattern of neurological activity responsible for the behaviour we see in zombie subjects. In this essay we outline the likely neural correlates of zombie behaviour and propose possible mechanisms by which the virus may animate the human body. The discussion is based mainly on observed zombie behaviour and aims to further our understanding of this pathology so that we may better defend ourselves when the need arises.
The nature of the virus
Zombies clearly have no need for a functioning circulatory system as can be inferred by their ability to operate with congealed blood[i] or severe blood loss. Similarly, they are not affected by even severe traumas unless there is significant damage to the central nervous system (CNS). The virus must therefore work by sustaining the metabolic activity of neurons independent of blood flow. One can envisage several possible mechanisms; perhaps injection of RNA that codes for enzymes capable of maintaining mitochondrial activity. However, it is highly implausible that such a mechanism could continue indefinitely, unless there is a way for these translated enzymes to sustain neurons anaerobically. Since no zombie outbreak has lasted long enough, we can only speculate as to the longevity of the virus.
The virus must also be able to invade other body tissues including muscle and—by a similar process—maintain metabolic activity of these tissues independent of blood flow. The likelihood is that the virus reaches the CNS first and then spreads out to muscle tissue, or it reaches the nervous system via retrograde transmission from other body tissue. Note that continued function of nervous system and muscle tissue is sufficient to make zombies ‘viable’. Maintenance of other tissue is superfluous even if possible.
Every study from Night Of The Living Dead to Resident Evil confirms that transmission is most common via zombie bites or scratches. Sufficiently high viraemia can only be achieved by direct transmission of the virus into the blood which evidently can be achieved by a mere scratch. The virus is then able to enter the nervous system from the vasculature leading to characteristic patterns of neural activity.
Judging by the low overall level of brain activity in zombies, the virus is either selective in its spread or varies functionally in different types of neurons or CNS regions. Higher cortical activity is almost completely absent in zombies. The virus has a specific pattern of spread that includes almost the entirety of the peripheral nervous system (PNS), brainstem and parts of the diencephalon with little or no activation in the prosencephalon (forebrain), which could either be down to an inability of the virus to effectively spread to these regions or an inability to function in this region in a similar way to other CNS regions. Since the prosencephalon is embryologically distinct (at the five vesicle stage) we would expect that some embryologically defined anatomical or physiological boundary exists that prevents viral spread or activity in this region.
It is not known exactly how the virus is able to kill humans, but presumably there is an initial period during which viral spread to the nervous system leads to complete shutdown (death) followed by reanimation. Alternatively, it may be the case that there is a direct transition between ‘living’ neural activity and Undead neural activity. Attempts to track neural activity of subjects undergoing transformation using fMRI have so far been unsuccessful due to the difficulty of restraining subjects once they have transformed.
General brain activation
As was alluded to in the previous section, zombies lack behaviour associated with higher cortical processes, such as cognition, memory, emotions…etc. The Undead subject exhibits a lack of awareness of him/her/itself and has little or no problem-solving ability. Tasks typically performed by zombies include walking (though ataxic), eating, lunging, oculomotor function, and basic response to stimuli. All these tasks require only brainstem and spinal cord activation but can be modulated by higher cortical input. There is inconclusive evidence that some internally generated, planned movements can be exhibited by zombies. These include functions like twisting door knobs[ii] and attempts to smash windows. Such functions demonstrate activity in the basal ganglia and some motor areas as well as (controversially) some activation even of frontal cortical areas involved in internally motivated movements. It should be noted that without external stimuli zombies usually go dormant and even shut their eyes so the majority of their movement constitutes responses to sensory information. Lack of fine motor coordination of the fingers however suggests that there is insufficient primary motor cortex activation.
Zombie sensory system
The capacity to respond to visual, auditory, somatosensory and olfactory stimuli suggests that the virus leads to robust midbrain activation. Zombies can localize and respond to visual cues, indicating an intact functioning circuit between the retina and superior colliculus and hypothalamus, via the lateral geniculate nucleus. Similarly, auditory localisation suggests intact circuits between the spiral ganglion and both the inferior colliculus and medial geniculate nucleus. In both these cases, The Undead lack the ability to recognise the significance of different visual and auditory stimuli and there is no reason to suggest that zombies have any conscious perception of these stimuli, which leads us to conclude that they lack primary and association cortices for these sensory pathways.
In terms of olfaction, we see a remarkable ability in zombies to distinguish the smell of fresh and decomposing tissue. The surprising implication is that zombies may exhibit some activation of the orbitofrontal cortex and may even be able to consciously perceive different smells. There may also be an affective component involved. The Undead demonstrate a change in affective state when in the presence of fresh meat, which suggests some co-activation of the amygdala and entorhinal cortex (parts of the limbic system), in response to olfactory cues.
Several examples of zombies being hit and shot reveal that zombies do not appear to have even basic nociceptive input. Zombies do not flinch in response to gunshots or blunt trauma. This would suggest that the virus is unable to activate (or prevents firing of) nociceptive pathways even as low as the spinal cord (e.g. nociceptive reflex arcs). Since nociceptors are anatomically and physiologically distinct to other types of neurons, they may be less susceptible to viral animation than other larger neurons (i.e. Aβ involved in mechanoreception). Some conflicting evidence exists in this area; some zombies, for example, howl when subjected to extreme thermal stimuli[iii]. There may be selective activation of some nociceptors but not others (e.g. C-fibres responsible for sensing thermal stimuli may be more susceptible to animation than Aδ fibres) however this distinction is not straightforward, and more data is needed on zombie responses to noxious stimuli.
Insatiable appetite
Zombie subjects display a bottomless appetite and apparent craving for flesh. This is likely down to strong activation of the lateral hypothalamic area (feeding centre) by the virus which receives olfactory input via the medial forebrain bundle. This view is consistent with the hypothesis that the zombie olfactory circuits are most robustly activated by the virus. The virus also fails to activate the ventromedial nucleus (satiety centre) and the result is a never-ending urge to eat.
Do zombies feel emotion?
Zombies display a singular lack of emotions except for an occasional expression of anger (see fig. 1). These signs of anger may suggest some limbic activation and, therefore, a small affective component to zombie behaviour. However it is also plausible that robust activation of the lateral hypothalamus leads to expressions of anger when certain circuits are activated but that the feeling of anger is not present. Since zombies express no other emotions (such as fear, happiness and sadness) it would seem prima facie more plausible that there is little limbic activity. Even with limbic activity it is highly unlikely that prefrontal cortex (PFC) activation necessary for processing of emotion is present in zombies.
Fig.1 Night Of The Living Dead, angry facial expression suggests lateral hypothalamic activation.
Zombie gait
Walking does not require cortical input; pattern generators in the spinal cord are sufficient. However cortical input is needed to refine the ungainly movements generated by the spinal cord alone. Studying zombie locomotion can help elucidate the extent of cortical activation and descending modulation.
The characteristic shuffling gait of The Undead suggests elements of Parkinsonism with complicated cerebellar deficits. The wide staggering gait is reminiscent of damage to the cerebellum while the slowness of movement, shuffling, and delay in onset of movement resembles Parkinsonism. Nigrostriatal dopaminergic neurons are sensitive to oxidative stress and have high metabolic demand so the virus achieves a partial but incomplete activation. Deficits in balance and posture suggest a suboptimal activation of the cerebellum by the virus, most notably, deficits in balance and posture associated with the vermis.
Conclusion
We therefore propose that the only way one can ‘kill’ a zombie is destruction of the brainstem. Although this may not kill the virus which will go on to support isolated neurons, it will effectively destroy the circuits required for almost all of the zombie’s functions. Future research into zombie neurophysiology will require a greater integration of psychometric and neurometric data so that we can pin down exactly how neural activity is influencing behaviour. Moreover histological preparations are lacking in this field and would provide indispensable insight into the underlying pathology. In vivo experiments remain problematic until anaesthetics can be developed with demonstrable efficacy in zombies.
mahmoodnaji 