Anatomy and Pathophysiology of Traumatic Brain Injury (TBI) Quiz

Frontal lobe injuries are common due to their location in the front of the brain, often affected in head trauma.

CT scans are preferred for quick assessment of structural damage in TBI cases.

The brainstem controls essential autonomic functions like breathing and heart rate.

Mild TBIs typically don't involve loss of consciousness, distinguishing them from more severe injuries.

Mouthguards absorb shock and protect teeth, jaw, and mitigate head injuries in contact sports.

The frontal lobe plays a significant role in regulating emotions, decision-making, and social behavior.

Compression typically doesn't cause TBI; it's more commonly associated with spinal injuries.

Apoptosis, or programmed cell death, is a key process leading to secondary brain injury post-TBI.

Glutamate, when excessively released, can lead to excitotoxicity and neuronal damage in TBI.

Hyponatremia, an electrolyte imbalance, can occur due to hormonal disturbances after severe TBI.

Contusions result from the brain hitting the skull, causing localized bruising and injury.

Coup-contrecoup injuries occur when forces cause the brain to impact the skull on both sides, leading to injury.

GCS is a reliable tool for assessing TBI severity based on eye, verbal, and motor responses.

DAI results from rapid acceleration-deceleration, causing widespread shearing of axons.

Mannitol, an osmotic diuretic, is often used to decrease intracranial pressure in severe TBI cases.

Executive functions such as planning, decision-making, and problem-solving are frequently impaired in moderate to severe TBI.

Elevated cortisol levels, triggered by stress, can worsen secondary brain injury after TBI.

Aphasia involves language difficulties, including speaking, understanding, reading, and writing, post-TBI.