Arizona Advanced Medicine Clinic

Post Concussion Syndrome, Chronic "Mild" Traumatic Brain Injury

Post Concussion Syndrome, Chronic “Mild” Traumatic Brain Injury

Incidence

According to the Centers for Disease Control statistics1, 1.4 million people in the United States sustain a traumatic brain injury each year. Of these, 50,000 die, 235,000 are hospitalized, and 1.1 million are treated and released from Emergency Departments. Physical recovery is often rapid, but emotional instability and slowing of the intellect seem to be more long-lasting and very debilitating effects. The brain scans are normal, but function is clearly not normal.

Symptoms

Sufferers experience significant physical, cognitive and emotional problems, even from mild traumatic brain injury.

Physical symptoms may range from headaches and dizziness to fatigue, sleep disturbance, light and sound sensitivity, sexual dysfunction, nausea, vomiting, ringing in the ears (tinnitus) and seizures.

Cognitive symptoms include poor attention and concentration, forgetfulness, poor short-term memory, slowing of neural processing, disturbed complex thinking and organization, word substitutions, word reversals.

Emotional symptoms may include easy irritability, low frustration threshold, anxiety, depression, explosive temper, and sensation of easy overloading by too much stimulation.

Recovery from traumatic brain injury

Rehabilitation, according to standard Western medicine, consists pretty much of cognitive-behavioral therapy and psychotherapy and drugs to control behavior, and “watchful waiting” until the condition heals itself. In other words, “get over it” seems to be the message from allopathic medicine.

Is there no hope for those who are still having symptoms months to years later? Does the brain really require pharmaceutical medications in order to have a chance of healing? Do pharmaceuticals really help? Is there no other way?

Indeed, there is tremendous hope… as long as we are careful about first eliminating hindrances to healing (toxicities like certain foods, heavy metals, organic pollutants, solvents), and second, providing the brain with specific treatment to help restore its normal pathways. Beyond conventional medicine and pharmaceuticals, there are many options available for both diagnosis and treatment.

Blockages to healing

Food allergy or sensitivity is the first place to look. Chronic inflammatory reactions to the gluten contained in wheat, barley, rye, and other gluten-containing grains can cause tremendous brain dysfunction, with clear evidence of white matter abnormalities even in the absence of abdominal or digestive symptoms.5

Genetics seem to play a role in healing as well. Apolipoprotein E4 genotype recover from head injury less quickly than those with the ApoE3 or ApoE2 genotype.6,7

Nutritional status is important. Zinc deficiency can cause decreased survival from head injury, and presumably by extension, impaired recovery.8 Significantly more inflammation after brain injury was seen in zinc deficient rat brains than in those whose zinc levels were adequate.9 Magnesium deficiency also has an impact on brain recovery.10 The dietary supplement creatine may be protective in the presence of brain injury. This protective effect seems to be related to maintenance of mitochondrial function which is essential to produce the energy needed for healing.11 Deficiency of iodine during intrauterine growth is associated with marked brain dysfunction (called cretinism).12

Total body burden of toxicity is also significantly related to our ability to heal. Heavy metals like mercury, arsenic, cadmium and lead have a tremendous impact on our neurologic function, starting with intra-uterine growth and continuing on into adulthood and old age. The ApoE4 genotype has been used as a marker for mercury toxicity, since people with that genotype are unable to excrete mercury as well as the rest of the population. It is more than probable that mercury and other heavy metals are also instrumental in delayed healing from head injury.

Brain training

Even though the blockages to healing have been removed, and good nutritional status has been restored, often the system has been sufficiently disrupted for long enough that the symptoms are not yet completely relieved. Disorganization of thoughts, problems with planning and short-term memory disturbances continue to be an issue.


1 http://www.cdc.gov/ncipc/tbi/TBI.htm

2 Fleminger S. Managing agitation and aggression after head injury. BMJ 2003;327:4-5 (5 July).

3 Feeney DM, Gonzalez A, Law WA. Amphetamine, haloperidol, and experience interact to affect rate of recovery after motor cortex surgery. Science 1982;217: 855-7.

4 Tateno A, Jorge RE et al. Clinical Correlates of Aggressive Behavior After Traumatic Brain Injury. J Neuropsychiatry Clin Neurosci 15:155-160, May 2003.

5 Kieslich M, Errazuriz G et al. Brain White-matter lesions in celiac disease: a Prospective Study of 75 Diet-Treated Patients. Pediatrics 108;2:e21

6 Friedman G , Froom P. Apolipoprotein E-epsilon4 genotype predicts a poor outcome in survivors of traumatic brain injury.Neurology. 1999 Jan 15;52(2):244-8.

7 Crawford FC, Vanderploeg RD et al. APOE genotype influences acquisition and recall following traumatic brain injury. Neurology 2002;58:1115-1118.

8 Young B, Ott L. Zinc supplementation is associated with improved neurologic recovery rate and visceral protein levels of patients with severe closed head injury. J Neurotrauma. 1996 Jan;13(1):25-34.

9 Penkowa M, Giralt M et al. Zinc or Copper Deficiency-Induced Impaired Inflammatory Response to Brain Trauma May Be Caused by the Concomitant Metallothionein Changes. J Neurotrauma Apr 2001, 18;4:447-463.

10 Hoane MR. Magnesium therapy and recovery of function in experimental models of brain injury and neurodegenerative disease. Clin Calcium. 2004 Aug;14(8):65-70.

11 Sullivan PG, Geiger JD. Dietary supplement creatine protects against traumatic brain injury. Ann Neurol. 2000 Nov;48(5):723-9.

12 Sandstead HH. A Brief History of the Influence of Trace Elements on Brain Function. AJCN 43: 293-98 (Feb 1986).

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