SUMMARY Permanent brain damage may result from closed head injury if coma lasts more than 30 minutes. In whiplash without head injury, substantial loss of consciousness may signal permanent brain-cell injury. In most late whiplash, the mechanism of cognitive difficulties remains speculative. PET and SPECT abnormalities are not fulfilling their early promise as specific biological markers of MTBI. Under-diagnosed injuries better explain chronic disability after whiplash.
Permanent brain damage may result from closed head injury if coma lasts more than 30 minutes.
In head-injured patients, Mild Traumatic Brain Injury (MTBI) with loss of consciousness and amnesia of 30-35 minutes has been shown to cause modest Diffuse Axonal Injury (DAI) 1. DAI is the histopathological (tissue damage) marker for disruption of brain cells.
Unless MTBI patients happen to die shortly after injury from other injuries or unrelated causes and there is autopsy study of the brain, we are unlikely to know in the near future whether there is such visible disruption of brain cells 2.
In whiplash without head injury, substantial loss of consciousness may signal permanent brain-cell injury.
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PRACTICE POINT Injury to brain cells (DAI) is present after Moderate and Severe Traumatic Brain Injury |
In lightly anesthetised non-human primates, severe whiplash without head injury causes organic brain damage 3. The amount of physical damage to brain cells parallels the length of coma and the severity of subsequent neurological abnormalities and changes in behaviour.
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PRACTICE POINT The threshold indicator for permanent brain-cell injury is probably around 30 minutes of unconsciousness |
However, even disregarding the greater anatomical resilience of the human neck, there is no support in these animal experiments for causation of brain cell injury by common human whiplash with only a few minutes of altered consciousness or amnesia.
In most late whiplash, the mechanism of cognitive difficulties remains speculative.
Prospective studies of MTBI without loss of consciousness and amnesia of up to 15 minutes have shown mild cognitive impairment lasting a few days 4, 5.
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PRACTICE POINT Neuropsychological testing does not clarify the genesis of cognitive difficulty following MTBI or whiplash |
Cognitive symptoms - forgetfulness, slowness, distractability and poor concentration - are common following MTBI, but they are also prevalent in otherwise similar patients who have not suffered TBI 6 and in personal injury litigants without a history or claim of head injury 7. Studies of normal populations show how common these symptoms are without any recognised illness or injury 8.
Thus, the presence of cognitive symptoms following MTBI does not prove a causal relationship. Even when de novo development of neuropsychological abnormality is demonstrated following consecutive injuries, organic brain damage is not proven.
PET and SPECT abnormalities are not fulfilling their early promise as specific biological markers of MTBI.
We previously commented ( MLN* V1,I3 and V2,I9) on the hope that blood-flow abnormalities shown by Positron Emission Tomography (PET) and Single Photon Emission Computed Tomography (SPECT) would prove to be biological markers for long-term or permanent brain damage following MTBI.
It has subsequently become clearer that similar abnormalities in blood-flow to the frontal lobes and anterior temporal region of the brain occur in depression 9, 10 and that the frontal lobe abnormalities are common to anxiety states also 11.
Not only are we left again with no objective evidence of permanent physical injury following MTBI or common whiplash, but the diagnosis and severity assessment of depression, anxiety states and chronic headache are themselves based on purely subjective data.
These disorders are, of course, very common in the aftermath of MTBI and whiplash. There is presently no sound medical evidence on which to attribute these diagnostic imaging abnormalities to physical rather than psychological injury.
Under-diagnosed injuries better explain chronic disability after whiplash.
What causes long-term suffering and disability to occur in only one-in-five (15-25%) whiplash or MTBI victims - the bulk of personal injury litigants?
Pre-existing psychological and psychosocial factors are poor predictors of adverse response to such mild injury.
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PRACTICE POINT Disability is not determined by severity of whiplash or TBI |
There is some evidence that it is those who experience a greater severity of chronic pain that are most troubled by cognitive problems 12. Indeed, Mild TBI patients with chronic pain report greater ongoing cognitive difficulty than Severe TBI victims without associated pain.
Expectation and attitude appear to play a large role 13. Some patients react to injury with greater anxiety ("Will I ever get better?") or depression ("I'll never be the same.")
Over-solicitous attention by family, friends and caregivers may encourage this response 14, that has been dubbed not psycho-somatic (the mind making the body sick) but rather somato-psychic (a psychological over-reaction to bodily injury)13.
We have elsewhere alluded to the well-established permanent adverse effect that pursuing litigation has on recovery following personal injury. "Compensation neurosis" carries quite the wrong connotation, for disability is not alleviated by legal settlement.
In summary, the jury is still out on whether permanent and hitherto unrecognised mechanical injury to brain cells occurs following TBI and whiplash without substantial unconsciousness or amnesia.
Medicine and the law persist in a dichotomous view of body and mind. Physicians and lawyers are not far apart in our prejudices that what we experience with our senses is somehow more real than that which depends on inductive reasoning.
Specifically, lawyers feel more comfortable putting a dollar figure on organic brain damage caused by head-injury or whiplash than on psychological disability appearing de novo after such injury.
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PRACTICE POINT Routinely request psychiatric assessment of MTBI and late whiplash claimants |
Many physicians and lawyers seem to believe, despite considerable evidence to the contrary, that psychological health cannot adversely or beneficially influence physical healing. They remain uncertain whether, by taking thought, the claimant could not cure his/her psychological injury.
A practical medical response to this uncertainty is exhaustive diagnosis and treatment of the secondary psychological complications of head-injury or whiplash.
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PRACTICE POINT Known causes of disability in late whiplash 1. Chronic headache |
An alternative medicolegal approach is routinely to refer MTBI and late whiplash claimants for assessment of both malingering and somatoform disorder, and for the common psychological consequences - chronic pain, depression and anxiety states, including Post Traumatic Stress Disorder.
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