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At least 19 recordsLinked to original sources
PubMed1992

The significance of diagnostic imaging in acute and chronic brain damage in boxing. A prospective study in amateur boxing using magnetic resonance imaging (MRI).

The significance and possible extent of structural damage to the central nervous system (CNS) due to boxing are investigated. Bleeding, especially microhematomas, is considered to be one probable cause of the chronic encephalopathy in boxers. In a prospective study, 13 amateur boxers were investigated with the help of MRI several times before and after their fights. The MRI investigations were accompanied by neurologic examinations before and after the fights. Among the 13 boxes, 5 demonstrated focal neurological signs following the fights, without evidence of small hematoma or other structural alterations. The number of head punches did not correlate with the occurrence of neurologic signs. These results indicate that up to now imaging methods cannot clarify the development of chronic encephalopathy.

Acute Disease↗
PubMed1982

Is chronic brain damage in boxing a hazard of the past?

Of fourteen boxers with a mean age of 31 years who had been Finnish, Scandinavian, or European champions, only one showed deficits in neurological status and he and one other had had episodes of inappropriate behaviour which were attributed to boxing. However, computed tomography revealed pathological findings attributable to brain injury in four of six professional and one of eight amateur boxers. Two of the professionals and four of the amateurs had electroencephalographic abnormalities which may have been caused by brain injury. Twelve of the boxers had psychological test results which suggested brain injury, although only two professionals had definite deviation from normal. The results indicate that modern medical control of boxing cannot prevent chronic brain injuries but may create a dangerous illusion of safety. The only way to prevent brain injuries is to disqualify blows to the head.

Adolescent↗
PubMed1985

Boxing and chronic brain damage.

A chronic, and at times, progressive neurologic syndrome associated with boxing has been recognized for some time by boxing fans and people involved with the sport. Since Martland's first description of the syndrome in 1929, there has been only one randomly selected study of ex-boxers, that of Roberts, which showed a 17 per cent prevalence of this syndrome among boxers who fought between 1929 and 1955. This syndrome can be progressive but often is not. Furthermore, the extent of occupational exposure is probably a significant risk factor. Because of this, it would be expected that the prevalance of the syndrome in the modern boxer, as well as the amateur, would be significantly less than during the first half of the century, and, indeed, several studies appear to support this. Recent studies provide evidence that brain damage does exist in modern boxers and suggests that "subclinical" brain damage is likely to be more prevalent than obvious clinical dysfunction. There is clearly a discrepancy between subclinical evidence of neurologic involvement (for example, an abnormal CT scan) and signs of clinical neurologic dysfunction (for example, clinical exam and neuropsychological testing). The latter tend to show less frequent and consistent evidence of brain damage in boxers than does the CT scan. Although it is tempting to assume that an abnormal CT scan presages the development of neurologic dysfunction, it is not clear that this is the case. The prevalence of the syndrome, risk for progression to functional deficit, warning signs, and the natural history cannot be defined at this time. The only way to better define these parameters would be a controlled prospective study, which has yet to be undertaken.

Athletic Injuries↗
PubMed1990

Does Swedish amateur boxing lead to chronic brain damage? 3. A retrospective clinical neurophysiological study.

The aim of the present study was to investigate possible chronic brain damage due to Swedish amateur boxing. Forty seven former amateur boxers, 22 with many (HM = high-matched) and 25 with few matches (LM = low-matched) during their career were examined and compared with two control groups of 25 soccer players and 25 track and field athletes in the same age-range. No severe EEG abnormality was found. There was a somewhat higher incidence of slight or moderate EEG deviations among HM-(32%, 7/22) and LM-(36%, 9/25) boxers than among soccer players (20%, 5/25) and track and field athletes (12%, 3/25). Brain electric activity mapping (BEAM), brainstem auditory evoked potential (BAEP) and auditory evoked P 300 potential (P 300) did not differ significantly between the groups. No neurophysiological variable was correlated to the number of bouts, number of lost fights or length of boxing career. Thus, no signs of serious chronic brain damage was found among the amateur boxers or the soccer players and the track and field athletes. However, it cannot be excluded that the EEG differences between the groups may be a sign of slight brain dysfunction in some of the amateur boxers.

Adult↗
PubMed1990

Does Swedish amateur boxing lead to chronic brain damage? 1. A retrospective medical, neurological and personality trait study.

Sweden banned professional boxing in 1969 and has also considered banning amateur boxing. We therefore analysed possible chronic brain damage in 47 former amateur boxers who started their careers after the introduction of stricter Swedish amateur boxing rules. The boxers were compared with three control groups--25 soccer players, 25 track and field athletes and 19 conscripts. All athletes were interviewed about their sports career, medical history and social variables. They then underwent a physical and a neurological examination, including a mini-mental state examination. Personality traits were investigated and related to their platelet MAO activity in the athletes as well as in the conscripts. No significant differences were found between the groups in any of the physical or neurological examinations. All had a normal mini-mental state examination. Thus, results from these test methods did not reveal any signs of chronic brain damage from Swedish amateur boxing. Neither were any significant differences found with regard to platelet MAO activity, while significant differences were found in some of the social and personality traits variables.

Adult↗
PubMed1991

Does Swedish amateur boxing lead to chronic brain damage? 4. A retrospective neuropsychological study.

Does Swedish amateur boxing lead to any permanent neuropsychological deficit, caused by chronic brain damage? Fifty Swedish former amateur boxers, 25 soccer players, and 25 track and field athletes were investigated by standardized neuropsychological tests. In only one test did the groups differ significantly. Boxers who had taken part in a large number of bouts had a slightly inferior finger-tapping performance. None of the boxers were considered to have definite signs of intellectual impairment. In conclusion modern Swedish amateur boxing does not seem to lead to significant signs of neuropsychological impairment or "punch drunkenness", nor does it seem to differ in this respect from soccer playing or track and field sports.

Adult↗
PubMedDate not supplied

Does amateur boxing lead to chronic brain damage? A review of some recent investigations.

Fifty former amateur boxers were examined and compared with two control groups of soccer players and track and field athletes. All subjects were interviewed regarding their sports career, medical history, and social variables. They underwent a physical and a neurologic examination. Personality traits were investigated and related to the platelet monoamine oxidase activity. Cerebral morphologic changes were evaluated using computed tomography and magnetic resonance imaging. Further, clinical neurophysiologic tests were made as well as neuropsychologic tests. No significant differences were found between the groups in any of the physical or neurologic examinations or in platelet monoamine oxidase activity. Socially, the boxers had a lower degree of education and had chosen less intellectual professions, but they were less impulsive and more socialized. The computed tomography images and magnetic resonance imaging studies showed no significant differences between the groups. There was a significantly higher incidence of slight or moderate electroencephalography deviations among the boxers. Neuropsychologically, the boxers had an inferior finger-tapping performance. Thus, no signs of serious chronic brain damage were found among any of the groups studied. However, the electroencephalography and finger-tapping differences between the groups might indicate slight brain dysfunction in some of the amateur boxers.

Adult↗
PubMed1993

Assessing chronic brain damage by quantification of regional volumes in postischemic rat brains.

The present study provides data on fresh volumes of 39 anatomically defined brain regions after a 10 min transient forebrain ischemia in the rat. Ischemia was induced by occlusion of the carotid arteries and simultaneous hypotension. After a survival period of 3 months the rats were transcardially perfusion-fixed with Bodian's solution, and the brains processed for paraffin embedding and serially sectioned. The sections were Nissl-stained for delineation of the brain regions. The volume of a brain region was calculated from 8-10 equidistant sections, using the Cavalieri method and corrected for shrinkage of the brain. Fresh volumes were reduced by 27-50% in the layers of the hippocampal CA1 sector, by 40-46% in the substantia nigra, by 19% in the caudate nucleus, by 13% in the subiculum and the cingulate areas 1-3, by 12-14% in the retrosplenial and temporal areas. The results show that determination of fresh volumes is a sensitive method for quantification and localization of ischemic brain damage in the whole brain.

Animals↗
PubMed1980

Peer-facilitated sign language training for a geriatric stroke victim with chronic brain damage.

The possibility of sign language training for a psycho-geriatric, aphasic, brain damaged patient was investigated over a 66-week period. Training progressed from finger dexterity tasks, physical manipulation of the patient's hand, and visual prompting to requests for a particular sign without supplementary cues. Midway through the program a peer was included in an effort to generalize the use of sign to others on the ward. The patient learned 14 signs. Data on sign language usage and social behaviors taken during three measurement periods indicate that, when the peer was present during training, performance was highest and there was an increase in the patient's level of socialization as measured by eye contact, gestures, and attempted speech. Retention of the signs and increased social responsivity were still observed two and four months after the termination of the program.

Aged↗
PubMed1990

Does Swedish amateur boxing lead to chronic brain damage? 2. A retrospective study with CT and MRI.

It is well known that professional boxers can develop chronic traumatic encephalopathy (dementia pugilistica) due to repeated head trauma. Beside CT findings indicating cerebral atrophy, the presence of a cavum septum pellucidum has been reported to indicate encephalopathy. CT findings in amateur boxers are not as well documented. The aim of this study was to find out if morphological changes could be demonstrated among former amateur boxers using CT and MRI. Two control groups of soccer players and track and field athletes in the same age-range were used for comparison. No significant differences in the width of the ventricular system, anterior horn index, width of cortical sulci, signs of vermian atrophy, or the occurrence of a cavum septum pellucidum were found between boxers and controls. A cavum septum pellucidum was found more often in the controls than in the boxers and is probably not a sign of earlier head trauma. MRI confirm no more findings than CT in this retrospective study.

Adult↗
PubMed1980

Relative mortality of chronically ill geriatric patients with organic brain damage, before and after relocation.

Elderly patients in whom mental impairment is associated with organic brain damage (chronic brain syndrome) usually bear a higher mortality risk than do other sick geriatric patients, especially under the stress of relocation. When Ste. Anne's Hospital moved, the patients with chronic brain syndrome had the highest mortality rate during the following year. Apparently these brain-damaged subjects failed to cope with the situation until it became real (after relocation). Thus, in a stress prevention program adopted when a geriatric institution plans to move, special attention should be paid to the subpopulation with chronic brain syndrome in the period immediately following the relocation.

Aged↗
PubMed2000

The neuroimaging evidence for chronic brain damage due to boxing.

A number of imaging techniques have been used to investigate changes produced in the brain by boxing. Most morphological studies have failed to show significant correlations between putative abnormalities on imaging and clinical evidence of brain damage. Fenestration of the septum pellucidum, with formation of a cavum, one of the most frequent observations, does not appear to correlate with neurological or physiological evidence of brain damage. Serial studies on large groups may be more informative. Magnetic resonance spectroscopy and cerebral blood flow studies have been reported in only small numbers of boxers; serial studies are not available to date.

Athletic Injuries↗
PubMed1997

Chronic cerebral hypoperfusion by permanent internal carotid ligation produces learning impairment without brain damage in rats.

To investigate the influence of cerebral hypoperfusion on learning behaviours, we developed a novel rat cerebral hypoperfusion model, in which the bilateral internal carotid arteries were permanently ligated to reduce the cerebral blood flow, and examined its behavioural and histopathological consequences in comparison to those occurring after bilateral common carotid ligation. In the Morris water maze task, rats with common carotid ligation exhibited a learning deficit, whereas rats with internal carotid ligation exhibited normal learning. Both models exhibited significant learning impairments in the eight-arm radial maze task, although the impairment was less severe in internal carotid-ligated rats than in common carotid-ligated rats. The cerebral blood flow of rats with common carotid ligation was reduced significantly both two and 10 days after ligation, and was still below normal three months after ligation. A milder, but significant reduction in the cerebral blood flow was observed in internal carotid-ligated rats. Shrinkage of the optic nerves and a circadian activity rhythm desynchronized to the light/dark cycle were exhibited by the rats with common carotid ligation, whereas these parameters remained unaffected in the rats with internal carotid ligation, suggesting that permanent ligation of common carotid arteries but not internal carotid arteries impairs visual functions. The main pathological changes observed in the brain following common carotid ligation were rarefaction and gliosis of the white matter and neuronal loss in the hippocampal CA1 region. On the other hand, the rats with internal carotid ligation had no significant brain damage. Chronic treatment with idebenone (1.5 and 15 mg/kg/day), a cerebral energy metabolism enhancer, over a three-month period, commencing five days after ligation, ameliorated the impairment of water maze learning in rats with common carotid ligation. The treatment also significantly improved the learning impairment in the radial maze task of internal carotid-ligated rats. Idebenone had no effect on the histopathological changes that followed cerebral hypoperfusion. It is concluded that cerebral hypoperfusion induced by permanent internal carotid ligation impairs the working memory without causing pathological damage to the brain tissues and the visual system, and the learning impairment can be ameliorated by a cerebral energy metabolism enhancer. These findings have the clinical implication that a reduction in blood flow may be an important factor that causes or exacerbates cognitive decline in dementias.

Animals↗
PubMed1985

Chronic alcoholic brain damage: trends in the use of services in North Canterbury.

National published data, Sunnyside Hospital records and a survey of private institutions were used to ascertain trends over time in the use of services for alcohol-related brain damage in the Canterbury region. One hundred and forty-three individuals in long-term care in 1982 were identified, a rate of 42 per 100 000 population. The proportion of psychiatric hospital beds occupied by these patients rose from 3% in 1971 to 12% in 1981. The rate of first admissions remained stable during this period while readmissions rose sharply, then levelled off. Average length of stay and number of readmissions increased and average age of admissions dropped; however these differences were not statistically significant. The data, together with changes in hospital programmes and diagnostic practice over the same period, suggest that the rise in bed occupancy may reflect an extension of the hospital's services to a group not previously offered long-term care, particularly less disabled persons.

Adult↗
PubMed1993

Neuropsychological differentiation of chronic schizophrenia.

Four groups of 20 each (chronic brain-damaged schizophrenics, chronic non-brain-damaged schizophrenics, chronic non-brain-damaged with "acute" exacerbation, and control subjects) were individually administered Form I of the Luria Nebraska Neuropsychological Battery (LNNB). Control subjects scored significantly lower than all clinical groups on all scales except for the chronic non-brain-damaged schizophrenics on the Reading Scale. "Acute" schizophrenics scored higher on Motor, Visual, Receptive Speech, Intellectual Processes, Pathognomonic, Right Hemisphere and Profile Elevations scales than the other clinical groups. Chronic brain-damaged schizophrenics scored significantly higher than chronic non-brain-damaged schizophrenics on the Profile Elevation scale. To examine the possibility that LNNB performance of the schizophrenic groups may have been related to neuroleptic medication, analyses were completed on the relationship between medication levels and LNNB scores. These results suggested that while the three clinical groups differed in their chlorpromazine equivalents (CPZE), LNNB scores were not related to CPZE dosage.

Acute Disease↗