Traumatic Brain Injury
Traumatic Brain Injury (TBI)
Traumatic Brain Injury (TBI) is a leading cause of death and disability in the United States. The most common causes of TBI include Falls, Motor Vehicle Accidents, Assaults, and Object-to-head impacts. Alcohol (ethanol) is a contributing factor in 40-56% of cases.
Individuals 75 years of age and older have the highest rates of hospitalization and death following traumatic brain injury. Importantly, a history of traumatic brain injury increases the risk for future TBI events.
About 40% of patients who suffer TBI develop neuropsychiatric symptoms that do not correlate with the severity of the injury. That is, mild TBI without loss of consciousness or hospitalization can lead to significant neuropsychiatric problems in vulnerable individuals.
TBI can be divided into 3 categories (mild, moderate, severe) according to severity and duration of altered mental status. The severity is often based on the Glasgow Coma Scale* (Eye Opening, Verbal Response, Motor Response) with lower Glasgow Coma Scores associated with more severe injury and poorer recovery outcomes.
Primary and Secondary Injuries
TBI can be divided into Primary and Secondary brain injuries. Primary injury refers to the “initial blow” or the immediate injuries following the event whereas the secondary injury refers to the physiological responses to the primary injury.
Primary Injuries can be further divided into Focal and Diffuse injuries
Most focal injuries occur in the polar temporal lobes and on the inferior surface of the frontal lobes (coup-contrecoup mechanism, see image below). Examples of focal injuries include hematomas and contusions.
Epidural hematomas: Lateral Skull Fractures with tearing of middle meningeal artery and vein often leading to involvement of the temporal and temporoparietal regions. Usually a period of initial loss of consciousness followed by a lucid period and finally a period of neurological decline. SURGICAL EVACUATION is often needed.
Subdural hematomas: More common than epidural hematomas. Caused by tearing of bridging vein between cortex and venous sinus and accumulation of blood in the subdural space. The underlying brain injury usually determines outcome in 80% of cases. SURGICAL EVACUATION is often needed.
Cerebral Contusions: Initial period of loss of consciousness followed by slow recovery period with intermittent fluctuations in consciousness, seizures, and focal neurological deficits from the edema that develops. Usually NO SURGERY in these cases.
Diffuse injuries are more dispersed and disseminated. Diffuse Axonal Injury is a common type of diffuse injury. Diffuse injuries usually occur due to rapid acceleration, deceleration, and/or rotational events. Commonly involved regions include the Reticular formation (brainstem), basal ganglia, superior cerebellar peduncles, limbic fornices, hypothalamus, and corpus callosum. Computerized Tomography is usually not helpful in identifying diffuse injuries. Diffusion-weighted MRI is preferred because it is sensitive to axonal edema.
Problems with arousal, attention, and processing speed often result from diffuse axonal injury
Secondary injuries result from the brain’s response to the initial injury.
Pathogenesis: Edema and/or intracranial bleeding leads to increased intracranial pressure and subsequent compression and deformation of brain tissue. Inflammatory mediators (e.g. cytokines), neurotoxic neuropeptides, and glutamate toxicity likely contribute to the damage of surrounding brain tissue. Some experts believe the secondary response is more damaging than the primary response as inflammation and edema are damaging to brain tissue.
Clinical Signs and Symptoms of Traumatic Brain Injury
Also called “Post Concussive Syndrome”
- Cognitive disturbances
- Disordered Sleep
- Anxiety Disorders
- Depression (common)
- Affective Lability
- Personality Changes
- Apathy/lack of spontaneity
- Psychosis (rare)
- Mania (rare)
Management of Traumatic Brain Injury (TBI)
Patients with TBI are more sensitive to medication side effects (e.g., extrapyramidal side effects, sedation, orthostasis, etc.). Therefore, patients are started on medications at much lower doses with slower titrations.
Medications to avoid, if possible:
- Typical antipsychotics (EPS risk)
- Clozapine (seizure risk, sedation, cognitive impairment)
- Benzodiazepines (delirium risk, falls, cognitive impairment, paradoxical disinhibition)
- Barbiturates (delirium risk, falls, cognitive impairment, paradoxical disinhibition)
- Anticholinergics (delirium risk)
- Antihistamines (delirium risk)
- Alpha-1 blockers (falls, orthostasis)
- Selective Serotonin Reuptake Inhibitors (e.g., Citalopram, Fluoxetine, Sertraline)
- Psychostimulants (Methylphenidate, Amphetamines)
- Electroconvulsive Therapy (ECT)*
- Valproic acid, Carbamazepine
- Atypical Antipsychotics**
*Except in patients with mass occupying lesions
**Animal research suggests some antipsychotics may interfere with neural plasticity and are associated with longer post-traumatic amnesia and worse outcomes
NOTE: While not covered here, it is worth mentioning that psychosocial/behavioral/cognitive interventions are essential for long term recovery. Below is a great review article.
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