ed:
• Transient confusion, disorientation, or impaired consciousness;
• Dysfunction of memory around the time of injury [antegrade or retro- grade amnesia];
• Loss of consciousness lasting less than thirty minutes. Observed signs of neurological or
neuropsychological dysfunction, such as: • Seizures acutely following injury to the head;
• Among infants and very young chil- dren: irritability, lethargy, or vomit- ing following head injury;
• Symptoms among older children and adults such as headache, diz- ziness, irritability, fatigue or poor concentration, when identified soon after injury, can be used to support the diagnosis of mild TBI, but cannot be used to make the di- agnosis in the absence of loss of consciousness or altered conscious- ness.16
One of the differences between this definition and the ACRM definition is that ACRM includes “dazed” as well as “con- fused or disoriented” in explaining what constitutes “altered consciousness.” There is professional dispute on this issue, as dis- cussed in a 2009 National Academy of Neu-
ropsychological Education Paper published in the Archives of Clinical Neuropsycholo- gy17
Focal Neurologic Signs of MTBI
(the “Position Paper”). The Position Pa- per identifies other challenges in diagnos- ing MTBI that are more practically signifi- cant than this subtle difference in wording. For example, “even when patients are re- viewed by emergency medical personnel at the scene of the injury, various acute symp- toms, including a brief LOC, might have been present prior to their arrival at the scene.”18
Furthermore, “[b]ecause post-traumatic confusion or amnesia usually persists for a period beyond LOC, patients are typically unable to accurately self-report if—and for how long—they were unconscious. Some patients assume they were unconscious during the period for which they have no recall.” This can lead to a situation where the plaintiff reports being unconscious un- til “waking up” in the ambulance, yet is re- ported to have been talking at the scene. This discrepancy can create a credibility is- sue, if not clearly understood. Even assess- ing loss of memory for events before or af- ter the accident can be challenging since many patients report what they were told about the accident instead of what they ac- tually remember, without drawing this fine, but important distinction.
The definitions do not spell out various focal neurologic signs that occasionally ap- pear and, as the Position Paper indicates, should be used to diagnose MTBI. These signs may be
associated with injury to one or more of the systems affecting vision, hear- ing, language, sensory-perceptual, or motor functions. The most common focal signs of brain injury,19
including
those in the WHO definition, are: post- traumatic seizures, intracranial lesions (e.g. contusion, hematoma, hemor- rhage, or edema) anosmia/hyposmia; other cranial nerve deficits; visual field cuts, diplopia, or other visual symp- toms caused by CNS injury; acute non- fluent (expressive) aphasia; and gait/ balance problems.20
Needless to say, when any of these condi- tions are confirmed, the challenge of prov- ing a brain injury is much less.
One of the conditions on this list that is often overlooked is anosmia, or loss of sense of smell. There is a substantial body of work (and several peer-reviewed articles) from Nils Varney that provides powerful ev- idence indicating that post-traumatic an- osmia is a clinical sign of significant orbito-
14
THE VERMONT BAR JOURNAL • SPRING 2012
www.vtbar.org
Proving a “Mild” Traumatic Brain Injury
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