Opiod-Related Brain Injury (Toxic Brain Injury, Anoxic/Hypoxic Brain Injury)
Opiod-Related Brain Injury (Toxic Brain Injury, Anoxic/Hypoxic Brain Injury)
por Anthony Sarmiento
1. References
1.1. Jammoul, M., Jammoul, D., Wang, K. K., Kobeissy, F., & Depalma, R. G. (2024). Traumatic Brain Injury and Opioids: Twin Plagues of the Twenty-First Century. Biological Psychiatry, 95(1), 6–14. https://doi-org.acu.idm.oclc.org/10.1016/j.biopsych.2023.05.013
1.2. NJ Spotlight News. (2019, May 16). Overdose survivors face challenges of brain injury. YouTube. https://www.youtube.com/watch?v=KbiBUtaq7YM
1.3. Manasco, M. H. (2020). Introduction to Neurogenic Communication Disorders (3rd ed.). Jones & Bartlett Learning. https://reader2.yuzu.com/books/9781284209655
2. History
2.1. Depressants such as OxyContin used to provide pain relief to patients as a non-addictive alternative in the 1990s. This spiraled out of control causing this opiod epidemic we are currenly in (Manasco, 2020).
2.2. "Synthetic opioids such as illicitly manufactured fentanyl have contributed to the sharp rise in opioid overdose deaths since 2019. Overdose deaths caused by synthetic opioids (primarily fentanyl) increased from 57,834 to 71,238 between 2020 and 2021 (Jammoul, 2024)"
2.3. "Since 1999, there has been an increasing trend in opioid overdose deaths in the United States. The latest reported data reveal a staggering increase in 2020 with 68,630 deaths and in 2021 with 80,411 deaths. Synthetic opioids such as illicitly manufactured fentanyl have contributed to the sharp rise in opioid overdose deaths since 2019. Overdose deaths caused by synthetic opioids (primarily fentanyl) increased from 57,834 to 71,238 between 2020 and 2021 (Jammoul et al., 2024)"
3. Definition
3.1. "Opiod use disorder (OUD) is characterized by a chronic and compulsive need to obtain and use opioids, whether medically prescribed or illegally obtained. Opioid misuse refers to the use of a prescribed opioid beyond its medical limits by either exceeding the set dosage or combining different prescribed opioids. The term opioid use is employed to refer to the use of illicit opioids (Jammoul et al, 2024)."
3.2. Once someone overdoses and consciousness is lost, depressants continue to slow the body down eventually decreasing bodies autonomic function until the respiratory system in brain stem is inhibitited and the body stops breathing for itself (Manasco, 2020).
3.2.1. Heroine overdose takes hours to shut down respiratory system, making the opportunity to save a life more likely
3.2.2. Fentanyl overdose can be instantaneous, someone can die before emergency responders can make it on scene
3.3. Unconscious and not breathing = hypoxia or anoxia depending on the lenght of oxygen lacking in the brain
3.3.1. Anoxia: total depletion of oxygen level
3.3.2. Hypoxia: insufficient level of oxygen to maintain bodily function
3.4. Subsequent opioid exposure possibly leads to further exacerbated inflammation and neurodegeneration.
4. Site of Lesion
4.1. Depressants lower function of the Central Nervous System. Central Nervous System responsible for receiving, processing, and responding to sensory information (Manasco, 2020).
4.2. Hippocampus uniquely sensitive to low levels of oxygen in the brain leading to memory issues
4.3. Occipital lobe damage leads to visual impairment
4.4. Traumatic brain injury “first hit” induces a neuroinflammatory process involving microglial priming, which, on a second hit related to opioid exposure, exacerbates neuroinflammation, modifies synaptic plasticity, and spreads tau aggregates to promote neurodegeneration. As TBI also impairs myelin repair by oligodendrocytes, it may reduce or degrade white matter integrity in the reward circuit resulting in behavioral changes (Jammoul et al., 2024)."
4.5. "Primary injury occurs as a direct result of the initial injury and is characterized by axonal damage and neurodegeneration. Secondary injury refers to further damage beyond the initial injury and includes different mechanisms such as excitotoxicity, inflammation, increased oxidative stress, mitochondrial dysfunction, apoptosis, and neurodegeneration (Jammoul et al., 2024)"
4.6. "The processes of neuroinflammation following TBI include glial activation/proliferation, the release of proinflammatory cytokines, inflammation-related proteins (proteases, metalloproteinases, and inflammasomes), and leukocyte activation...neuroinflammation may progress leading to blood-brain barrier breakdown, edema, and increased intracranial pressure (Jammoul et al., 2024)
4.7. "One study reports that chronic opioid use triggers axonal degeneration by causing axonal deformations, decreasing the size of axonal fascicles, decreasing myelin basic protein, and increasing amyloid-β protein expression. Patients on long-term opioid therapy exhibit reduced axonal connectivity in the internal/external capsules along with the pathways of the amygdala including the stria terminalis, ventral amydalofugal connection, and uncinate fasciculus in addition to reduced functional connectivity in the anterior insula, NA, and amygdala. We hypothesize that TBI may impair myelin repair by oligodendrocytes acutely, setting the stage for further degeneration with chronic opioid use (Jammoul et al,. 2024)."
5. Cognitive, Communication, & Swallowing Function
5.1. People who have overdosed sometimes walk away thinking they have not suffered any brain trauma, chalking up cognitive impairment to long-term drug use. Returning back to normal life noticing an inability to focus, process information around them, or commmunicate properly
5.2. "Chronic changes in excitatory synaptic plasticity at the level of MSNs promote drug-seeking behavior... Thus, chronic opioid use promotes synaptic plasticity in the reward circuit (Jammoul et al,. 2024)."
5.3. "The hippocampus is another region experiencing opioid-induced synaptic plasticity changes. For example, fentanyl and morphine increase excitatory conduction in the hippocampus. Morphine induces long-term potentiation in the hippocampal synapses resulting in impaired memory formation and opioid dependence (Jammoul et al., 2024)."
6. Quality of Life
6.1. Damaged areas of the brain will affect motor movement, patient can be wheelchair bound, have trouble seeing, cant feed themselves, inability to speak, inability to feed themselves, etc (NJ Spotlight News, 2019).
6.2. Joe Hartman was hospitalized in 2016 from a fentanyl laced cocaine overdose. Patient fell into a coma. Doctors stated patient suffered brain trauma during this time due to the lack of oxygen (NJ Spotlight News, 2019) Link: https://www.youtube.com/watch?v=KbiBUtaq7YM
6.3. Brain Injury Association of America: "...those with a prior history of substance misuse before their brain injury are ten times more likely to resume past behavoir (NJ Spotlight News, 2019)."
6.3.1. Double whammy of rehabilitation focusing on drug recovery and brain recovery, but areas of the brain that help someone overcome addiciton can be affected. Decision making skills impaired and someone can get stuck in a vicious cycle of failed recovery attempts with subsequent brain trauma from any additional overdosing if patient relapses
6.3.2. Drug addiction and brain need to be treated side by side
6.3.3. "Pain, a neurological consequence of TBI, is a risk factor that increases the likelihood of opioid use/misuse after TBI. Other comorbidities including depression, anxiety, posttraumatic stress disorder, and sleep disturbances are also associated with deleterious outcomes (Jammoul et al., 2024)"