Overview of Traumatic Brain Injury (TBI)

Table of Contents

Overview

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 may not always correlate with the severity of the injury (i.e., mild TBI without LOC or Hospitalization can lead to significant neuropsychiatric problems in vulnerable individuals). TBI is categorized into 3 categories 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. There appears to be increased morbidity associated with lower IQ, history of substance abuse, older age, and previous traumatic brain injury.

Pathophysiology

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 that ensue from the Primary injury. 

Primary Injuries

Primary Injuries can be further divided into Focal and Diffuse injuries

Focal 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

These 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

Secondary Injuries result from physiological responses 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

“Post Concussive Syndrome”

  • Cognitive disturbances (may mimic symptoms of schizophrenia)
  • Fatigue
  • Disordered Sleep
  • Headache
  • Vertigo
  • Irritability/Aggression
  • Anxiety/Anxiety Disorders (GAD, PTSD, OCD, Panic Disorder)
  • Depression (most common)
  • Affective Lability
  • Personality Changes
  • Apathy/lack of spontaneity
  • Psychosis (rare, usually seen with frontal and temporal lobe injuries and seizures)
  • Mania (rare)

Management of Traumatic Brain Injury (TBI)

Medication-Based Management

General Principles

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 and titrated much more slowly. 

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)

Medication Options

  • Selective Serotonin Reuptake Inhibitors (Citalopram, Fluoxetine, Sertraline): For depression, anxiety, irritability, and agitation
  • Propranolol: For aggression
  • Amantadine: For cognitive impairment/Executive dysfunction
  • Modafinil/Armodafinil: For cognitive impairment/Executive dysfunction
  • Psychostimulants (Methylphenidate, Amphetamines): for depression, apathy, fatigue, cognitive deficits
  • Buspirone: for depression, anxiety, irritability, and aggression
  • Electroconvulsive Therapy (ECT): Except in patients with mass occupying lesions
  • Valproic acid: For Mania, Aggression, Irritability, Anxiety, Agitation
  • Carbamazepine: For Mania, Aggression, Irritability, Anxiety, Agitation
  • Atypical (2nd generation) Antipsychotics: Try to avoid agents that lower the seizure threshold (e.g., clozapine, Olanzapine)
  • Lithium: Controversial. Some data suggests neurotoxicity, others demonstrate neuro-protection. If seizure history, try to avoid. 

*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

References

  1. Levenson, J. L. (2019). The American Psychiatric Association Publishing textbook of psychosomatic medicine and consultation-liaison psychiatry. Washington, D.C.: American Psychiatric Association Publishing.
  2. Stern, T. A., Freudenreich, O., Fricchione, G., Rosenbaum, J. F., & Smith, F. A. (2018). Massachusetts General Hospital handbook of general hospital psychiatry. Edinburgh: Elsevier.
  3. J. Ferrando, J. L. Levenson, & J. A. Owen (Eds.), Clinical manual of psychopharmacology in the medically ill(pp. 3-38). Arlington, VA, US: American Psychiatric Publishing, Inc.
  4. Schatzberg, A. F., & DeBattista, C. (2015). Manual of clinical psychopharmacology. Washington, DC: American Psychiatric Publishing.
  5. Arciniegas, Yudofsky, Hales (editors). The American Psychiatric Association Publishing Textbook Of Neuropsychiatry And Clinical Neurosciences. Sixth Edition.
  6. Schatzberg, A. F., & Nemeroff, C. B. (2017). The American Psychiatric Association Publishing textbook of psychopharmacology. Arlington, VA: American Psychiatric Association Publishing.
  7. Mendez, M. F., Clark, D. L., Boutros, N. N. (2018). The Brain and Behavior: An Introduction to Behavioral Neuroanatomy. United States: Cambridge University Press.
  8. Hales et al. The American Psychiatric Association Publishing Textbook of Psychiatry. Sixth Edition

Leave a Reply