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← Theoretical 2

Q74 — Pathophysiology of Traumatic Brain Injury

Theoretical 2 Real exam question — full text reproduced under IBO's CC BY-NC-SA 4.0 license
Nervous System Physiology

The biochemical and physiological processes accompanying cerebral injuries frequently turn into sources of secondary tissue damage themselves. These processes can be caused by many factors, e.g., dysfunction of mitochondria, anaerobic stress, peroxide-mediated oxidation of lipids, axon degeneration and cell death. Due to demyelination and disruption of the axonal cytoskeleton, the accumulation of transport proteins at the axon terminus takes place, which leads to accumulation of neurotransmitters in the synaptic cleft. Then, NMDA and AMPA receptors in postsynaptic membranes are activated, thus enhancing Ca2+ influx from intracellular stores.

Schematic of traumatic brain injury pathophysiology showing endothelia, basement membrane, and astrocytes releasing inflammatory cytokines, chemokines, and ROS; accumulation of transport proteins at the axon terminus leading to glutamate buildup in the synaptic cleft; activation of calpains; mitochondrial involvement with cytochrome release; nuclear DNA damage; and activation of caspases leading to cell death. Figure. Schematic representation of the pathophysiology of traumatic brain injury (TBI). ROS = reactive oxygen species; AMPAR = α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor; NMDAR = N-methyl-D-aspartate receptor; ER = endoplasmic reticulum; AIF = apoptosis-inducing factor protein.

Using this information, determine whether the following statements are true or false.

A. Demyelination of the axons causes disruption of the axonal cytoskeleton leading to accumulation of transport proteins at the axon terminus, and thus, making it hyperactive.
B. Ca2+ channel blockers have potential therapeutic value in spinal cord injuries.
C. Accumulation of free radicals results in intensive peroxidation of membraneous lipids, which leads to mitochondrial dysfunction
D. Excess glutamate is released following head injury which activates AMPA and NMDA receptors.
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Question reproduced from IBO 2022, Theoretical Paper 2, licensed under CC BY-NC-SA 4.0 — attributed to the International Biology Olympiad. Open the full exam PDF · Community solutions (unofficial)