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					PSYCHO-Cussive OR PATHO-Cussive?
An Update on the Persistent Post-Concussive Syndrome.
by Rosemary LYNDALL WEMM, Clinical Neuropsychologist Perth, W.A.; February, 2000


The head injured are the bread and butter of the neuropsychologist in private practice. Those with massive injuries have a distinctive profile and are relatively easy to assess and report upon. At the other end of the scale are those people with minor blows to the head who have little or no loss of consciousness but who, nevertheless, suffer from a range of debilitating symptoms, at least in the short term. Most of these individuals have no evidence of neuro-pathology on conventional radiological tests. Insurance companies will usually pay worker’s compensation in the first few weeks post-injury without too much fuss. When the symptoms continue beyond a few months there is an escalating tendency for insurers and health professionals alike to attribute the victim’s self-reported suffering to malingering or to pre-existing intra-psychic weaknesses. New research suggests that this prevalent assumption is false.


The sequelae of minor traumatic head injuries are headache, neck pain, giddiness, dizziness, vertigo, tinnitus, paresthesias, sleep disturbances, fatigue, impairment of divided and selective attention, loss of concentration, decreased tolerance to bright light and loud sound, poor memory, adynamia, irritability, depression and/or other psychological disturbances (eg. panic attacks) and a decrease in the ability to tolerate alchohol. [Landy, 1998; Tysvaer, 1992; Tysvaer et al, 1989; Ettlin et al, 1989; Baroff, 1998; Chambers et al, 1996; Elkind, 1989; Bohnen et al, March 1992; Bohnen et al, May 1992; Bohnen et al, Dec, 1991; Abu-Judeh et al, 1999; Scheutzow & Wiercisiewski, 1999; Goldstein, 1991]. Most aspects of this syndrome have been found to relate to a cognitive/concussive vector rather than an emotional/vegetative vector; that is, they are likely to be the direct result of brain assault rather than a secondary consequence or reaction to the injury. However, organic factors are increasingly implicated as co-progenitors of even the socio-affective components of the syndrome; a post-concussed brain is not as resilient in the face of life’s normal set of adversities as a normal brain. Any pre-existing vulnerability in this [as in other areas of cognitive functioning] is magnified. Aggressive adversarial legal and compensatory systems, which treat the victim as well until proven otherwise, are likely to exacerbate the degree of injury and prevent or prolong recovery [Bohnen et al, Mar, 1992; Yeates et al, 1999]. # Contary to the beliefs of many lawyers and insurance agents, symptoms like post-trauma head-aches do not disappear following settlement of a compensation claim. [Packard & Ham, 1994]

These symptoms overlap, to some extent, with the whiplash syndrome (headache, vertigo, auditory disturbances, tinnitus, disturbances in concentration and memory, difficulties in swallowing, impaired vision and temporo-mandibular dysfunctions) [Otte et al, 1996; 1997] which is not surprising, given the similarity of the injuries which cause the syndromes.

--------------------------------------------------------------------------------------------------------------------# An example of the legally sanctioned and unregulated practices whereby the insurance and medico-legal
industries can create injury, cause grievous bodily harm and practise medicine without a license in the pursuance of their duty to make money for those who are rich enough to be their beneficaries.



While the majority of victims of mild head trauma recover within a few weeks, about 30 percent of victims continue to experience symptoms of a more or less permanent nature. This has been termed the persistent post-concussive syndrome (PPCS). In about 10 percent of cases the symptoms are sufficiently severe to prevent the victim from resuming pre-injury activities. [Landy, 1998; Tsyvaer, 1992; Chambers et al, 1996]. Seemingly mild injuries frequently result in persisting post-concussive syndromes. The Glascow Coma Scale, which is generally used to assess the severity of brain trauma, is not a good indicator of symptomatology for these persons. [Borszuk, 1997] Few of these individuals experience marked loss of consciousness at or around the time of the injury. [Abu-Judeh et al, 1999]. Positive CT scans [which demonstrate cerebral pathology] can occur in the absence of gross neurological deficits; it is not even necessary for an individual to have received a direct blow to the head. [Binder, 1986; Gieron, et al, 1998]. Nevertheless, the CT scans of PPCS victims are generally normal. It is this picture which has given rise to the prevailing belief that those with PPCS do not have brain pathology. Recent research challenges this assumption.


With the advent of functional assessments of brain function the argument for the absence of brain pathology in this population has weakened. Functional assessments are generally far more effective than assessments of structural integrity in detecting cerebral dysfunction and appear to be more strongly related to symptoms and recovery patterns [Levin, 1993; Tysvaer, 1992; Lewine et al, 1999; Abu-Judeh et al, 1999]. Neuropsychological assessment has been reported to detect abnormalities in about 80% of cases compared with 65% of cases with magnetic sour imaging (MSI), around 60-70% with SPECT,

0%-33% with CT scanning and around 20% with MRI and EEG [Lewine et al, 1999; Abu-Judeh et al, 1999; Tysvaer,1992; Abdel-Dayem et al, 1998]. In other words, absence of evidence of damage on standard imaging and EEG measures is not evidence of absence of damage. Research is currently being conducted on the use of S-100beta protein, and/or its relationship with the glial fibrillary acidic protein (GFAP), as a marker for brain pathology in mild closed head injuries. [Waterloo et al, 1997; Hinkle et al, 1997; Rothoerl et al, 1998; Beaudeux et al, 1999; Ingebrigtsen et al, 1999]. S-100beta is an isoform of a protein which is predominantly synthesized and secreted by glial cells. If these cells are structurally damaged then this isoform leaks into the surrounding tissue and then into the cerebro-spinal fluid and the bloodstream. The presence of S-100beta in blood samples taken shortly after injury is proof that glial cells have been damaged. It is circumstantial proof that the contiguous neurons [for which the glial cells provide nutrients] are also damaged. Ingebrigtsen reports that S-100beta it is a valid indicator of the presence and severity of brain damage if sampled within the first six hours of injury. The Ingebrigtsen team extended this work by studying victims of PCS, operationally defined as victims of minor head injury with Glasgow Coma Scale scores of 13-15 and normal CT scans. Detectable serum levels of S-100 protein were found in 28% of these victims within the first six hours post-injury. Since this figure approximates the known percentage of mild head injury victims who go on to develop persistent post-concussive symptoms in later months (30%) the test is likely to be an early marker of this eventuality as well as providing an explanation for it. Ergo, the victims of PPCS have sustained minimal brain damage. The presence of detectable S-100 correlates with MRI results. Ten percent of the total sample had an abnormal MRI. This represented less than one percent [0.01%] of the non-positive S-100 group and 29% of the positive S-100 group. That figure is consistent with the usually reported percentage of PPCS sufferers who have positive findings on an MRI [i.e. 20%]. A positive S-100 level also correlates with the presence of specific deficits on neuropsychological testing. In testing sessions conducted at 48 hours and 3 months post injury the Swedish team [Waterloo et al, 1997; Ingebrigtsen et al, 1999] found deficits of reaction time, attention and speed of information processing in this group. According to them, posttraumatic depression could not explain the differences between these individuals and the individuals who did not have positive S-100 levels. Some cognitively demanding neuro-psychological tests [eg STROOP test variants] appear to have value as predictors of which victims of mild head injury will develop PPCS [Bohnen et al, Feb 1992]. Other studies [for example, Stuss et al, 1985] demonstrate that subtle mental deficits can be detected even in patients who have apparently fully recovered from a closed head injury. Discriminate analysis of the test results in the study by Stuss et al was able to correctly classify 85% of individuals who had suffered a head injury. The main symptom was residual impairment on tests of divided attention. Litigation was not a factor. This lends further support to the notion that persisting post- concussive symptoms are primarily the result of brain pathology. Unfortunately tests of serum levels of S-100beta are not yet routinely done in the first few hours following mild head injuries. Furthermore, human brain tissue is not usually available for microscopic examination until after the death of the patient. It is not necessary, however, to have such definitive data in order to make a circumstantial diagnosis. In line with usual medical practice, patients with a characteristic symptomotology and a corroborating neuro-psychological test profile could reasonably be diagnosed as having PPCS and assumed to have the same degree of brain damage implied by the Ingebrigtsen studies.

DIAGNOSTIC CRITERIA FOR PERSISTANT POST-CONCUSSIVE SYNDROME [PPCS] 1 2 3 History of mild traumatic brain injury 3 or more months previously Little of no LOC [Glascow Coma Scale scores of 13 or above] The major symptoms are headache, neckache, iritability, fatigue, memory problems and attentional failures. Other symptoms include giddiness, dizziness, vertigo, tinnitus, paresthesias, sleep disturbances, decreased tolerance to bright light and loud sound, disturbances of divided and selective attention, loss of concentration, adynamia, irritability, decrease in the ability to tolerate alcohol, depression and other psychological disturbances [such as panic attacks]. CT scan probably normal [0-33% hit rate] MRI probably normal [20% hit rate] MSI possibly abnormal [65% hit rate] SPECT possibly abnormal [60-70% hit rate] Neuropsychological assessment [80% hit rate] reveals: immediate memory problems [eg impairment of WAIS digits forward]; short term memory problems [which are primarily impairments of aquisition], absent or impaired primacy effect on extended learning tasks [eg RAVL], problems of selective and divided attention [eg STROOP test variants], adynamia, slow mental processing speed. May also show some fronto-mesial features [eg. minor confabulations]. Peri-trauma S-100 beta protein levels positive [90% hit rate within 6 hours post-injury] May co-exist with whiplash syndrome, frontal lobe syndrome, depression, anxiety, post-traumatic stress disorder.

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Recent SPECT studies have reported that the most frequent sites of detected abnormalities in patients with persistent post-concussive symptoms are, in descending order of frequency, the basal ganglia and thalamus, frontal lobes, temporal lobes and parietal lobes. Studies conducted within 3 months of the accident found twice as many lesions as those conducted later. [AbdelDayhem et al, 1998; Abu-Judeh et al, 1999]. {These areas are more ventral than those which generally show abnormalities in the whiplash syndrome (viz. parieto-occipital areas) [Otte et al, 1996]. This validates the existence of both syndromes as legitimate and separate entities, although they may, of course, co-occur in some head-injured victims.}


There is now good evidence that the PPCS results from minor brain pathology. This will hopefully result in the victims of this syndrome being treated with more compassion than is currently the case in hospital, rehabilitation and forensic settings. This outcome could be assisted, on the one hand, by a push for Australian casualty departments to routinely test headinjured victims for blood serum levels of S-100beta, and on the other hand, by including updated information on this topic into the initial and continuing education of health and forensic professionals.


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