Traumatic Brain Injury

San Antonio, Texas Traumatic Brain Injury Attorney

In recent years, great advances in neuroimaging and studies on patients have begun to develop a consensus on Traumatic Brain Injury (TBI). In August 2010 Drs. Brent Masel and Douglas De Witt published an article in the Journal of Neurotrauma, vol 37 in which they asserted that Traumatic Brain Injury (TBI) is not like a fractured bone which can be set and allowed to heal. You don’t “fix” a TBI. It is a chronic disease process that manifests itself over time.

When a Traumatic Brain Injury occurs, structures in the brain that function as message relay centers gets torn or sheared. Anoxal shearing or tearing breaks the circuits for message conduction in the brain and results in the blockage of information the brain requires to function properly. When axons break down from trauma, they emit toxic substances which infect adjacent and nearby axons, setting up a process of deterioration which results in a multiplier effect of axon damage, a kind of cascade of pathology, with attendant consequences developing over time.

A Traumatic Brain Injury thus involves, with its consequences manifesting themselves over weeks and months and years. Studies have shown that in comparison with the general population, within one year of injury a Traumatic Brain Injury victim is 37 times more likely to die from seizures, 12 times more likely to die from septicemia, 4 times more likely to die from pneumonia and 3 times more likely to die from respiratory conditions. The sequelae of Traumatic Brain Injury are ongoing and insidious.

Traumatic Brain Injury survivors don’t earn as much as non-injured persons in the general population. Other kinds of post-Traumatic Brain Injury morbidities include epilepsy, sleep disorders, and psychiatric disorders. Five percent of all epilepsy cases are from TBI. Brain injury is the leading cause of epilepsy in the young adult population. Sleep disorders such as obstructive sleep apnea are common following TBI.

Psychiatric disorders are far more common among Traumatic Brain Injury survivors, including suicide (18% of Traumatic Brain Injury survivors attempt suicide within five years), substance abuse, emotional instability, and mood changes. Job performance suffers as well (32% of Traumatic Brain Injury survivors are unemployed after 5 years.)

It is increasingly apparent that cognitive function gradually decreases after TBI, with greater declines with an increase in age. This would be a natural process anyone, but Traumatic Brain Injury accelerates it. All of the studies agree that the more severe the brain injury results in higher comorbidities.

Brain injury is a disease.
– It impacts organ systems.
– It is a disease causative and disease accelerative.
– It should be managed and paid for on a par with other diseases.

Individuals more than one-year post-TBI:

  • 50 times more likely to die from seizures.
  • 9.5 times more likely to die from septicemia.
  • 6.4 times more likely to die from aspiration pneumonia.
  • Four times are likely to die from other respiratory conditions.
  • Harrison-Felix, et al., Causes of Death Following 1 Year Post-Injury Among Individuals with Traumatic Brain Injury, 21 J. Head Trauma Rehab. 22(2006)

Post-traumatic epilepsy

  • Traumatic Brain Injury is the leading cause of epilepsy in the young adult population.
  • Patients with a Traumatic Brain Injury are 1.5 to 17 times more likely to develop seizures than the general population.
  • The risk of sudden death in epileptics is 20 times greater than the general population: risk increases with increasing seizure frequency.
  • Latency to first seizure can be as long as 17 years.
  • Of 67 children with moderate to severe TBI, 40 percent developed post-traumatic epilepsy.
  • Patients with epilepsy are three times more likely to have strokes.
  • Annegars et al., A Population-Based Study of Seizures After Traumatic Brain Injuries, 338 NEW. ENG. J. MED. 20 (1998); Shorvon & Tomson, Sudden Unexpected Death in Epilepsy, 378 LANCET 2028 (2011); Liesemer et al., Early Post-Traumatic Seizures in Moderate to Severe Pediatric Traumatic Brain Injury: Rates, Risk Factors, and Clinical Features, 28 J. NEUROTRAUMA 755 (2011).
  • Traumatic Brain Injury cohort had almost twice the incidence of subsequent stroke.
  • Severity of Traumatic Brain Injury correlated with stroke incidence and post-stroke mortality.
  • Liao at al., Stroke Risk and Outcomes in Patients with Traumatic Brain Injury: Two Nationwide Studies, 89 MAYO CLINIC PROCEEDINGS 163 (2014).
  • Patients with Traumatic Brain Injury were five times more likely to develop malignant brain tumors.
  • The more severe the TBI, the more likely to have a tumor development.
  • Chen et al., A Novel Animal Model of Closed-Head Concussive-Induced Mild Traumatic Brain Injury: Development, Implementation, and Characterization, 29 J. NEUROTRAUMA 268 (2012).
  • Subjective sleep complaints in 70 percent of chronic Traumatic Brain Injury outpatients.
  • Objective sleep disturbances in 30 to 45 percent of chronic TBI: obstructive sleep apnea, periodic limb movement disorder, narcolepsy, parathyroid hormone.
  • Cognitive issues associated with sleepiness.
  • 56,000 auto crashes annually in the United States attributed to drowsiness.
  • Hypopituitarism in 30 percent of moderate to severe TBIs more than 1-year post-injury.
  • Schneider et al., Hypothalamopituitary Dysfunction Following Traumatic Brain Injury and Aneurysmal Subarachnoid Hemorrhage: A Systematic Review, 298 JAMA 1429 (2007); Aimaretti et al., Residual pituitary Function After Brain Injury-Induced Hypopituitarism: A Prospective 12-Month Study, 90 j. clinical endocrinology & metabolism (2005).
  • Growth hormone deficiency in 20 percent of moderate to severe TBIs more than one-year post-injury.
  • Increased osteoporosis.
  • Increased cholesterol.
  • Increased abdominal fat.
  • Increased atherosclerosis: higher mortality from cardiovascular disease.
  • Decreased cognitive functioning.
  • Aimaretti et al., Residual Pituitary Function After Brain Injury-Induced Hypopituitarism: A Prospective 12-Month Study, 90 J. CLINICAL ENDOCRINOLOGY & METABOLISM (2005).

Hypothyroidism is approximately 5 percent moderate to severe more than 1-year post – TBI.

    • 10 to 15 percent more than 1-year post moderate to severe TBI.
    • 40 to 60 percent of individuals complain of sexual dysfunction post-TBI.
      • Males:
        • Decreased libido
        • Decreased muscle mass
        • Decreased strength
        • Correlation between low free testosterone and cognitive function
      • Zasler et al., Brain Injury Medicine (Demo Med. Publ’g 2007); Amar Agha & Christopher Thomson, Anterior Pituitary Dysfunction Following Traumatic Brain Injury (TBI), 64 CLINICAL ENDOCRINOLOGY 481 (2006); Tan et al., Thyroid Function and the Risk of Alzheimer’s Disease: The Framingham Study, 168 Archives Internal Med. 1514 (2008).
  • Chronic TBI:
    • Psychosis, 20 percent
    • Depression, 18 to 61 percent
    • Mania, 1 to 22 percent
    • PTSD, 3 to 59 percent
    • Aggression, 20 to 40 percent
  • Traumatic Brain Injury is associated with the high rates of suicidal ideation, suicide attempts, and completed suicide.
  • Kim et al., Neuropsychiatric Complications of Traumatic Brain Injury: A Critical Review of the Literature (a Report by the ANAP Committee on Research, 19 J. Neuropsychiatry & Clinical Neurosciences 106 (2007).
  • 23 percent developed a personality disorder after their TBI.
  • 50 percent developed major mental disorder after their TBI.
  • Koponen et al., Axis I and II Psychiatric Disorders After Traumatic Brain Injury: A 30-Year Follow-Up Study, 159 AM J. PSYCHIATRY 1315 (2002).
  • There is evidence of an association between moderate or severe Traumatic Brain Injury and psychosis.
  • Even if the Traumatic Brain Injury is severe, the psychosis does not appear during the first post – Traumatic Brain Injury year, but rather, becomes apparent in the second and third years post-TBI.

Young adults who experience a moderate or severe Traumatic Brain Injury have more than two times the risk of developing Alzheimer’s and other forms of dementia later in life. The worse the injury, the higher the risk.

  • Moderate TBI: 2.3 times the risk
  • Severe TB: Four times the risk

33 individuals with moderate to severe TBI:

  • 27 percent showed cognitive decline comparing 12-month baseline to two to five years of testing (mean 37 months).
  • Diffusion tensor imaging showed the progression of white matter injury when measured 4.5 months and 29 months post-injury in 13 moderate to severe TBIs.
  • Till et al., Post recovery Cognitive Decline in Adults with Traumatic Brain Injury, 89 ARCHIVES PHYSICAL MED. &REHAB. S25 (2008); Greenberg et al., Use of Diffusion Tensor Imaging to Examine Subacute White Matter Injury Progression in Moderate to Severe Traumatic Brain Injury, 89 ARCHIVES PHYSICAL MED & REHAB. 245 (2008).

All of these comorbidities will cause Traumatic Brain Injury victims severe mental anguish, physical impairment, and affect their quality of life. These life-altering comorbidities will greatly influence their future physical pain and mental anguish as well as his future impairment.

If your loved one has suffered a traumatic brain injury that you feel contact the Law Offices of Craig White at (210) 829-7183 for a free initial consultation to review your matter.

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