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PubMed1984

Perilymphatic fistula--a definitive and curable cause of vertigo following head trauma.

Vertigo or disequilibrium occurring in patients after concussive and nonconcussive head trauma may be due to a pathologic perilymphatic fistula from the inner ear through the oval and round window areas of the middle ear. Of 33 patients who had successful grafting of the fistulous area at middle ear exploration, 32 had resolution of vertigo, and 12 of 23 who had an associated hearing loss had improved hearing. Perilymphatic fistulas associated with vertigo and hearing loss after head trauma can be diagnosed with great certainty and are surgically curable in the great majority of cases. Patients with post-concussive syndrome, whose symptoms include vertigo or disequilibrium, should have a thorough otologic evaluation for the possibility of a perilymphatic fistula.

Craniocerebral Trauma↗
PubMed1993

[Post-traumatic psychological disorders].

Mental disorders after closed-head injury are reviewed. Post-concussive syndrome and post-contusional disability are described with particular emphasis on consciousness disorders, amnesia, frontal disturbance and long-term outcome.

Brain Concussion↗
PubMed1993

Defrocking the fraud: the detection of malingering.

The purpose of this paper is to provide psychiatrists with practical advice on how to detect malingered mental illness. Various types of malingering are defined and the five major purposes of malingering are specified. The research literature on malingering is reviewed. Clinicians must be thoroughly grounded in the phenomenology of true mental disease to detect malingering. Detailed information about hallucinations is reviewed so that faked hallucinations that do not follow typical patterns can be more easily identified. Strategies for approaching persons suspected of malingering are suggested. Features of malingered mutism, mania, depression and mental retardation are described. The differential diagnosis of malingering, post-traumatic stress disorder, conversion disorder, and post-concussion syndromes after trauma is discussed. Clues to malingered psychoses and post-traumatic stress disorders are delineated. Finally, specific indicators of malingered insanity defenses are identified.

Depressive Disorder↗
PubMed1993

Differentiation of balance deficits through examination of selected components of static stabilometry.

Stabilometry, which measures the body's center of pressure (COP) movements, during relaxed standing, has been used to distinguish individuals with vestibular and neurologic dysfunctions from normal subjects. The purpose of this study was to determine whether mathematical differences in the magnitudes of the COP obtained from six somatosensory testing conditions could be used to discriminate between different types of balance deficits. Stabilometry measures, using a fixed force platform, were obtained from normal (N = 52) and dizzy (N = 149), peripheral vestibular dysfunction (PVD), post-concussion syndrome (PCS), psychogenic (PSG), and unknown/undetermined etiology (UNK). The data significantly differentiated CVD, PVD and PSG patients from normals and between some of the dizzy groups: CVD versus PVD, PCS; and PSG versus CVD, PVD, PCS and UNK. The measures of anterior-posterior COP movements provided the greatest discrimination.

Adolescent↗
PubMedDate not supplied

[Subjective syndrome after head injury].

UNLABELLED: DEFINITION AND CLASSIFICATION PROBLEMS: Post-traumatic or post-commotion syndrome is one of the most controversial entities in studying consequences of craniocerebral trauma. Part of this problem arises from impossibility of adequate translation of the term brain concussion. Post-concussion syndrome is a broader concept than post-commotion and includes, if not a whole, than part of the post-contusion syndrome. There are also some other terms in the literature: post-traumatic syndrome, post head injury syndrome, post head injury syndrome or symptoms and the old term post-traumatic encephalopathy. Terminological imprecisions have not been solved yet, but the notion itself is determined by relative standard symptoms often associated with closed craniocerebral trauma, but without precise connection with the severity of the trauma. In the classification of mental disorders and behavior disorders, this syndrome is coded as FO7.2. ETIOLOGY: In regard to the etiology of this syndrome some authors speak in favor of psychogenic and some of organic etiology, while Levin considers symptoms of post-commotion syndrome to start as organic and persist as psychic. Wechsler classified subjective disorders after head injuries into 4 categories: simulation, traumatic hysteria, traumatic encephalopathy and traumatic neurosis. The author does not deal with the origin of symptoms, whereas the classification itself suggests priority of psychic to organic factors (11). Those who speak in favor of organic etiology, think that axon damage and neuron damage are organic substrate in mild brain injuries, while fibrous degenerations of the cerebral hemisphere and brain stem are the organic base in severe traumas. On the other hand, many scientists primarily point to psychic moments, especially to importance of aggravation and simulation as well as compensation or rental neurosis in persistent post-traumatic syndrome. Most scientists agree that personality characteristics influence the development of post-traumatic syndrome and can predispose aggravation and simulation, whereas these symptoms more often occur in neurotic persons. The latest investigations reveal that classification in regard to etiologic factors--organic and psychogenic--is an anachronism. Long and Novac state that 80% of persons with cerebral trauma spontaneously speak about symptoms of the post-traumatic syndrome, while by targeted evaluation the percentage rises to 90%, so that they think that universality of symptoms points to their common origin. CONCLUSION: If the post-traumatic syndrome is though of as a line with organic dementia at one end and traumatic neuroses at the other, then this syndrome can be placed at different positions. Some authors put it close to the neurotic syndrome or regard it to be the neurotic syndrome itself, while others, mostly due to homogenity of the clinical picture, believe that this syndrome has an organic cause.

Brain Concussion↗
PubMed2002

Imaging of sequelae of head trauma.

The imaging of head trauma has been one of the fundamental cornerstones of neuroradiology. As the practice of neuroimaging has matured, great strides have been made in the diagnostic as well as prognostic armamentarium available to physicians. Given the vast diversity of trauma mechanisms and clinical pathways, new advanced imaging technologies have had a lasting impact on the detection, description, and depiction of head trauma. Furthermore, these new tools are allowing the imaging specialist to function not only as an interpreter of what is seen but as a 21st century radiographic oracle. We present a comprehensive review of the imaging findings of sequlae of traumatic brain injury and the growing correlation of new neuroimaging techniques and neurotraumatic outcomes.

Arachnoid Cysts↗
PubMed2002

2002 Refshauge Lecture. When to retire after concussion?

The management of an athlete with recurrent concussions, whether persistently symptomatic or not, remains anecdotal. There are no evidence-based guidelines upon which a team physician can advise the athlete. All doctors involved in athlete care need to be aware of the potential for medicolegal problems if athletes are inappropriately returned to sport prematurely or in the case of professional athletes held out of sport or retired on the basis of non-scientific recommendations.

Adult↗
PubMed2002

Prediction of post-traumatic complaints after mild traumatic brain injury: early symptoms and biochemical markers.

OBJECTIVES: To identify parameters at first presentation after mild traumatic brain injury (MTBI) that are predictive of the severity of post-traumatic complaints (PTC) after six months. Early recognition of patients with MTBI who are at risk of developing PTC would be useful because early follow up at the outpatient clinic may help to reduce the severity of these complaints in the long run. METHODS: The presence of symptoms in the emergency room (ER) (headache, dizziness, nausea, vomiting, and neck pain) and biochemical markers (neurone specific enolase and S-100B) in serum were assessed as possible predictive variables for the severity of PTC. Outcome variables were the severity of 16 PTC six months after the trauma. RESULT: After six months, the severity of most complaints had declined to pretrauma levels but medians for headache, dizziness, and drowsiness were still increased. In a series of 79 patients, 22 (28%) reported one or more PTC after six months. After adjustment for baseline variables, an at least twofold increased severity of all PTC subgroups was reported by those patients reporting headache, dizziness, or nausea in the ER. A twofold increased severity of "cognitive" and "vegetative" PTC was also found in those with increased concentrations of biochemical serum markers at first presentation. The prevalence of full recovery after six months increased from 50% in patients with three symptoms to 78% in those with no symptoms in the ER. Inclusion of biochemical markers showed that all 10 patients with no symptoms in the ER and normal markers recovered fully. CONCLUSIONS: The presence of headache, dizziness, or nausea in the ER after MTBI is strongly associated with the severity of most PTC after six months. Identifying MTBI patients in the ER without headache, dizziness, nausea, or increased serum marker concentrations may be a promising strategy for predicting a good outcome.

Adolescent↗
PubMed2001

Not just malingering: syndrome diagnosis in traumatic brain injury litigation.

When patients present with syndromes we mistrust or misunderstand, clinician are often quick to make a determination of malingering. However, the use of malingering as a default diagnosis neglects a variety of clinical possibilities that may be relevant for treatment and forensic disposition. In neuropsychology, the growing use of a malingering diagnosis has recently been fueled by the increasingly adversarial nature of forensic brain injury litigation in which the goal is often less to provide an objective evaluation of cognition and personality as to brand all personal injury claimants as manipulative frauds. Less maliciously, but still disturbing, neuropsychologists whose knowledge base and clinical experience involves mainly the administration and scoring of psychometric tests may ignorantly, if innocently, overlook alternative diagnoses and syndromes that their education and training have ill-prepared them to recognize. And some patients do indeed malinger, and it is important to identify them, if only to spare legitimately injured claimants from being tarred with the same brush. This paper describes some of the syndromes that may present in clinical and forensic practice with brain-injured patients. It is to be considered a first step toward a practice model of neuropsychology that encourages the role of knowledge and clinical judgement in guiding the meaningful clinical interpretation of tests and measures.

Brain Concussion↗
PubMed2002

Brain atrophy in mild or moderate traumatic brain injury: a longitudinal quantitative analysis.

BACKGROUND AND PURPOSE: Although mild or moderate traumatic brain injury (TBI) is known to cause persistent neurologic sequelae, the underlying structural changes remain elusive. Our purpose was to assess decreases in the volume of brain parenchyma (VBP) in patients with TBI and to determine if clinical parameters are predictors of the extent of atrophy. METHODS: We retrospectively assessed the total VBP in 14 patients with mild or moderate TBI at more than 3 months after injury and in seven patients at two time points more than 3 months apart. VBP was calculated from whole-brain MR images and then normalized by calculating the percent VBP (%VBP) to correct for intraindividual variations in cranial size. Clinical parameters at the time of trauma were evaluated for potential predictors of atrophy. Findings were compared with those of control subjects of similar ages. RESULTS: In the single time-point analysis, brain volumes, CSF volumes, and %VBP were not significantly different between patients and control subjects. In the longitudinal analysis, the rate of decline in %VBP (0.02 versus 0.0064 U/day, P =.05) and the change in %VBP between the first and second time points (-4.16 +/- 1.68 versus -1.49 +/- 1.7, P =.022 [mean +/-SD]) were significantly greater in patients. Change in %VBP was significantly greater in patients with loss of consciousness (LOC) than in those without LOC (P =.023). CONCLUSION: Whole-brain atrophy occurs after mild or moderate TBI and is evident at an average of 11 months after trauma. Injury that produces LOC leads to more atrophy. These findings may help elucidate an etiology for the persistent or new neurologic deficits that occur months after injury.

Adult↗
PubMed2001

Attentional deficits in patients with post-concussion symptoms: a componential perspective.

Attentional deficits are frequently reported by patients suffering from closed head injuries. The majority will develop a group of clinical symptoms known as post-concussion symptoms or syndromes (PCS), which are characterized by a range of subjectively experienced symptoms including headaches, dizziness, fatigue, irritability, slowed thinking, and memory dysfunction. It is posited that attentional deficit is the crucial factor for the apparent failures of memory and higher cognitive functioning, and may contribute largely to difficulty in re-integrating back into the community and resuming independent daily living. It also appears that there are large variations within these patients, in terms of both presented symptoms and neuropsychological performances. However, these variations in terms of attentional deficits have not been systematically differentiated and examined. This article aims to build up a theoretical framework to guide the investigation of the varieties of attentional deficits in patients with PCS. Current theories on attention from cognitive psychology, neuropsychology, cognitive neuroscience and clinical rehabilitation will be reviewed and integrated. It is hoped that a better understanding of the underlying mechanism of such defects will foster and guide the development of intervention.

Adhesives↗
PubMed1998

Return to play guidelines after a head injury.

Presently there are no universally accepted definitions of the grades of concussion or criteria for when to allow the athlete to return to competition after a head injury. What is agreed upon is that in order to avoid cumulative brain damage and the second impact syndrome, no athlete still suffering post-concussion symptoms should return to competition. This article is meant to serve only as a guideline as the final decision in every instance is a clinical judgement.

Biomechanical Phenomena↗
PubMed1989

The perilymph fistula syndrome defined in mild head trauma.

Neurological and neuro-otological studies were carried out on 102 adults with mild cranio-cervical trauma productive of positional vertigo and perilymph fistula as confirmed by laboratory tests, and by the finding of perilymph fistula at tympanotomy in the surgically managed group. In this patient group, all other neurological and neuro-otological diagnoses were excluded, e.g. epilepsy, cerebral palsy, multiple sclerosis, retardation; and for the neuro-otological group those with a history of ototoxicity, labyrinthitis, Meniere's disease, chronic ear infections, or developmental or familial disorders. Emphasis in this study was on mild trauma: fewer than half of the sample had been rendered unconscious in the injury of record, and a third of the cases were of whiplash type, with no loss of consciousness (LOC) and no remembered headstrike. These concomitant lesions comprise the perilymph fistula syndrome (PLFS) with a unique profile of neurological, perceptual, and cognitive deficits resembling a post-concussion injury. A complete description of the clinical picture is given, including psychological, cognitive and diagnostic tests, and the outcome of bedrest vs. surgical management. PLFS can arise from minor trauma, fistula are frequently bilateral (71/102), a mild sensorineural hearing loss is of variable occurrence (53%), secondary hydrops is not uncommon, and women appear more vulnerable than men for developing the syndrome. As based upon combined laboratory techniques and clinical symptomology, fistula were correctly predicted in 61 of 65 laser-operated ears. The positional vertigo component of PLFS was in all cases managed according to a special physical therapy program utilizing exercises for vestibular symptom habituation. Even when diagnosed late, a good-to-excellent outcome was achieved in 70% of treated patients.

Adult↗
PubMed1998

Second-impact syndrome.

Second impact syndrome (SIS) occurs when an athlete who has sustained an initial head injury, most often a concussion, sustains a second head injury before symptoms associated with the first have fully cleared. While most commonly reported in football, the SIS can occur during any sport that can produce head blows. Any athlete still complaining of post-concussion symptoms after a head injury must not be allowed to return to play.

Adolescent↗
PubMed1997

Does premorbid depression influence post-concussive symptoms and neuropsychological functioning?

We examined the contribution of premorbid affective disturbance to persistent post-concussive symptoms and neuropsychological functioning following a mild traumatic brain injury. No differences were observed on self-reported post-concussive symptoms, MMPI scales, or neuropsychological measures between two case-matched groups of patients with and without a history of pre-injury depression. Clinicians are urged to use caution in attributing post-concussive symptoms or neuropsychological deficits to the presence of a pre-existing affective disorder.

Adult↗
PubMed1994

Sequelae of minor head injury: the natural history of post-concussive symptoms and their relationship to loss of consciousness and follow-up.

The character and natural history of post-concussive symptoms were studied in two subject groups: patients admitted to hospital for observation following brief loss of consciousness (LOC) as a result of head injury and patients who attended the accident unit after head injury but not were not admitted. Follow-up data were obtained from the hospitalized group at standardized out-patient interview and from the non-hospitalized group by postal questionnaire. Two- and 12-week data are presented on 24 hospitalized and 58 non-hospitalized patients. The type and frequency of symptoms was similar in the two groups and rank ordering was significantly correlated. However, the reduction in symptom scores (number of symptoms) 12 weeks post-injury was significantly greater in the hospitalized than the non-hospitalized group. The possible significance of this is discussed.

Adolescent↗