Our brains allow us to interpret ourselves and the world around us. When we sustain a head injury, there’s a disruption in the brains’ ability to store, process, accumulate and retrieve information. Damage to the brain can interfere with our ability to control emotions and interact socially. Traumatic Brain Injury (TBI) is one of the assaults to the brain that can cause severe complications to a person’s normal function.
Traumatic brain injury is non-degenerative, non-congenital insult to the brain from an external mechanical force causing temporary or permanent neurological dysfunction, which may result in impairment of cognitive, physical and psychosocial functions. TBI severity is gauged according to a continuum from mild to moderate to severe. Although there is variation concerning the most appropriate means of defining TBI severity, three measures have regularly been used as “gold standard” indicators of TBI severity. These include: Loss of Consciousness (LOC), Post Traumatic Amnesia (PTA), and the Glasgow Coma Scale (GCS).
An estimated 57 million people worldwide have been hospitalized with one or more TBI. In the United States alone, an estimated 1.5 to 2 million individuals succumb to a traumatic brain injury annually, with 80 000 suffering from permanent severe neurological disabilities and leading to approximately 52 000 deaths each year due to TBI, furthermore, international research also indicates TBI is a primary cause of death and disability in young.
In South Africa, head injuries alone have been shown to account for 25.2% of non-natural deaths for children younger than 15 years of age. Head injuries are also the most frequently reported explanation for admission to hospital in children younger than 13 years of age.
The overall incidence of TBI in developed countries is about 200 per 100 000 population per year. Population- based studies show that the incidence of TBI is between 180 and 250 per 100 000 population per year in the United States. Incidence is higher in Europe ranging from 91 per 100 000 in Spain to 546 per 100 000 in Sweden, in Southern Australia incidence is 322 per 100 000 and in South Africa 316 per 100 000. These numbers probably underestimate the true incidence of TBI, because they typically refer to the TBI patients admitted to hospital. Many patients with mild TBI (not presenting to the hospital) or with severe TBI (associated with death at the scene of the accident or during transport to a hospital) may not, in fact, be accounted for in the epidemiological reports.
When observing trends in sex differences, researchers have found that males represent a higher proportion of TBI victims than do females. In South Africa, the same trend towards sex differences has been reported for TBI in adults, with an estimated male to female ratio of 4:1.
Approximately 50% of TBIs are the result of motor vehicle, bicycle or pedestrian–vehicle accidents. Falls are the second-commonest cause of TBI (20–30% of all TBI), being more frequent among the elderly and the very young population. Violence-related incidents account for approximately 20% of TBI, almost equally divided into firearm and non-firearm assaults.
Consequences of TBI
TBI may impair cognition i.e. concentration, memory, judgment and mood and it also affects movement abilities i.e. strength, coordination and balance. TBI also impairs sensation i.e. tactile sensation and special senses, such as vision and sexual function, leading to important behavioural changes and consequences on daily living activities.
The complications of TBI are not restricted to neurological consequences. Gastrointestinal complications occur in about 50% of patients; these patients develop hepatic dysfunction, bowel incontinence, and dysphagia, with consequent nutrition problems.
Presentation varies according to the injury. Some patients with head trauma stabilize and other patients deteriorate. A patient may present with or without neurologic deficit. Patients with concussion may have a history of seconds to minutes unconsciousness, then normal arousal. Disturbance of vision and equilibrium may also occur. Common symptoms of head injury include coma, confusion, drowsiness, personality change, seizures, nausea and vomiting, headache and a lucid interval, during which a patient appears conscious only to deteriorate later.
Most head injuries are of a benign nature and require no treatment beyond analgesics and close monitoring for potential complications such as intracranial bleeding. If the brain has been severely damaged by trauma, neurosurgical evaluation may be useful. Treatments may involve controlling elevated intracranial pressure. This can include sedation, paralytics, cerebrospinal fluid diversion. Second line alternatives include decompressive craniect, barbiturate coma, hypertonic saline and hypothermia.
- Lieberman SA, Oberoi AL, Gilkinson CR, Masel BE & Urban RJ. Prevalence of neuroendocrine dysfunction in patients recovering from traumatic brain injury. Journal of Clinical Endocrinology and Metabolism 2001 86 2752–2756.
- Masel BE. Rehabilitation and hypopituitarism after traumatic brain injury. Growth Hormone and IGF Research 2004 14 (Suppl A) S108–S113.
- Agha A, Rogers B, Sherlock M, O’Kelly P, Tormey W, Phillips J & Thompson CJ. Anterior pituitary dysfunction in survivors of traumatic brain injury. Journal of Clinical Endocrinology and Metabolism 2004 89 4929–4936.
- Elovic EP. Anterior pituitary dysfunction after traumatic brain injury. Part I. Journal of Head Trauma Rehabilitation 2003 18 541–543.
- Bruns J Jr & Hauser WA. The epidemiology of traumatic brain injury: a review. Epilepsia 2003 44 (Suppl 10) 2–10.
- Hofman K, Primack A, Keusch G, Hrynkow S. Addressing the growing burden of trauma and injury in low- and middle-income countries. Am J Public Health 2005;95:13-7
- Bowman B, Seedat M, Duncan N, Kobusingye O. Violence and injuries. In: Jamison DT, Feachem RG, Makgoba MW, Bos ER, Baingana FK, Hofman KJ, et al, eds. Disease and mortality in sub-Saharan Africa. Washington: World Bank; 2006