Traumatic brain injury (TBI), dubbed the “invisible injury”, is a physiological phenomenon that manifests itself in our heads. Largely invisible to the naked eye, the injury is left to display itself subjectively through psychological, cognitive and limited physical clues. The brain, plagued by unseen chronic inflammation, neuronal cell damage and death is left without any visible signature of the widespread damage and remodelling that occur.

 

Dr. Cathy Malchiodi, a psychologist and founder of Trauma-Informed Practices and Expressive Arts Therapy Institute, explains how art therapy can help with self-understanding and healing. Benefits from the process of exploring unconscious/conscious feelings, thoughts, and personal experiences through art-making with a trained professional include visual thinking, sensory processing, emotional release, communication, and a tangible product that can document internal complexities and progress (1). These concepts could be directly applicable to the cognitive processes that are impacted by traumatizing experiences. Cannabis sativa is known for its psychotropic properties, thanks to its most abundant phytocannabinoids, delta-9-tetrahydrocannabinol (THC) (2). Cannabis is colloquially known for its ability to enhance creativity and produce a psychedelic experience. Recently, cannabis has gained recognition for its potential therapeutic anti-inflammatory and neuroprotective properties (3).

 

 

How do cannabinoids, psychedelic experiences, and creativity influence TBI recovery? How can this be visually represented?

 

Through the construction of a symbolic narrative based on biological signals, we intend to blur the distinction between endogenous and exogenous states. In essence, we intend to represent TBI using electroencephalographic data (EEG) associated with art therapy/psychedelic experience as a vehicle leading to the creation of a physical artifact (sculpture), using data visualization as a mediator. We will work to represent a sequence starting from a passive and meditative (pre-injury) baseline, followed by an abrupt traumatic change (TBI), and moving through an active response symbolizing recovery through art therapy.

 

Different techniques of signal processing can be used on EEG signals to extract features that represent dimensions of the emotional experience (4), as well as features representing the complexity of the signal (5). Complexity metrics, such as measures of entropy, have proven to enable dissociation between complex mental states, such as the psychedelic experience and normal waking consciousness (6).

 

Visualizing EEG data through digital media is possible by transforming it to drive a generative process. The psychedelic graphic animations in 3D software will serve as a translation medium for the data collected at symbolic time points associated with the injury-recovery cycle. The psychedelic animations will also illustrate (symbolically) the depolarization and excitotoxicity that occurs at the moment of a TBI event, as well as the self-transformation experience throughout the therapeutic process. EEG data will also be used to create a soundscape for the creation.

 

Holistically, this fluid and responsive environment will serve as the baseline for solid figurative representation of the neurological states associated with the injury-recovery cycle and will illustrate the neurological plasticity of the recovering brain. Specifically, the digital visualization, with its rapid fluidity will illuminate the acute neurological changes taking place during and following TBI. The physical manifestation, produced using plasticine or clay, will represent the chronic neurological flexibility of the brain, which slows but never stops, in the months to years following TBI. The sculpture will act as an artifact representing a unique lived experience, encompassing the cycle of injury, the malleability of the brain and the flow from internal to external by capturing the projection from the brain to digital and then digital to matter.

 

 

TBI

 

The term Traumatic Brain Injury (TBI) is an umbrella term used to define a complex neurological event, induced by biomechanical forces to the head, face or neck, resulting in mild to serious downstream physiological, behavioural, and cognitive consequences. TBIs most commonly result from falls, sports-related injuries, car accidents, or physical assaults (7), and depending on the injury’s severity, cognitive and neurological deficits can persist long-term, causing a lifetime paradigm shift for the persons injured.

 

TBI is a multifaceted injury, characterized by numerous pathophysiological changes within the brain that have been triggered by an original structural injury, known as the primary injury (8). This mechanical primary injury causes immediate contusions to the injured area, diffuse shearing of axons and blood vessels, damage to glial cells, cytoskeletal disruptions, as well as localized hemorrhaging (9-13).

 

The secondary injury cascade involves widespread cellular, molecular, and biochemical changes that develop following the primary injury (13,14). These pathophysiological mechanisms are characterized by ion, neurotransmitter, mitochondrial, and cerebrovascular dysregulation leading to eventual cell death and resulting chronic impairments (15,16). The secondary injury evolves from minutes to years’ post-injury due to ongoing immune activation and neuroinflammation and ultimately results in tissue damage and atrophy, cell death, and the potential accumulation of troublesome proteins such as amyloid precursor and tau proteins, which are the hallmarks of Chronic Traumatic Encephalopathy (CTE) (17-19).

 

Scientific investigation has focused on the various known downstream effects of the secondary injury cascade as potential therapeutic targets to decrease functional deficits associated with the primary injury. One specific area of focus has been the widespread CNS excitotoxicity immediately following the onset of adverse biomechanical forces to the cerebrum. Regardless of injury severity, shearing forces cause micro-injuries to axons throughout the CNS, leading to adverse molecular “leakage” across the neuronal cell membrane (14,23-24). It is suggested that these micro-injuries, known as mechanoporations, allow ions who are integral in maintaining electrical and chemical homeostasis of the axon membrane, to leak out, resulting in mass depolarization of voltage- and ligand-gated ion channels, leading to damaging excitatory neurotransmitter release and Ca+2 influx (25-27). The widespread CNS excitation leads to mitochondrial dysfunction and lasting disruptions of energy production which is further perpetuated by the generation of damaging free radicals synthesized en-masse as part of the second injury cascade (28-29). When left unchecked, this spread of synaptic depression, cellular imbalances, energy deficits, and RONS accumulation contributes to post-injury complications such as seizures, critical dendritic edema and eventual cell death (30).

 

These cellular cascades trigger molecular signals driving downstream immune activation and subsequent cytokine and chemokine release, pushing the initial robust post-traumatic neuroinflammatory response that lasts for weeks to years following injury (31). According to the review of Simon et al. (2017), this inevitable and critical immune cascade resulting in persistent neuroinflammation is increasingly seen as a necessary, but potentially harmful, biological coping mechanism, and an important focal point for pharmaceutical interventions (15).

 

TBIs have an extensive impact on the quality of life of the individual and loved ones of the victim, making it important to focus on both the molecular and behavioural sides of TBI research. I use animal models to investigate molecular and behavioural aspects of TBI, but I also focus on the physical manifestation of symptoms by assessing motor and cognitive function in addition to investigating overt behavioural changes following injury.

 

The focus of my research is on the endocannabinoid system (eCS), a system within the human body that regulates numerous critical physiological and behavioural functions, actively participates in potentiating synaptic plasticity and neurogenesis. Specifically, I study how eCS mediated autoregulatory mechanisms can be modulated or dysregulated in dangerous excitatory environments. The spreading depolarization following a TBI, at both a micro or macro scale, is reminiscent of EEG activity associated with seizures and seizure-like activity. EEG recordings following TBI indicate an acute loss in global activity, and a chronic loss in theta oscillations (25). Thanks to my colleague and good friend Roebuck et al. (2020) (26), who examined the effects of smoked cannabis flower on a model of epilepsy, we were able to integrate seizure EEG data to represent the excitotoxicity so commonly seen in TBI.

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References

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