Neurochemical aftermath of amateur boxing

Zetterberg, Henrik; Hietala, Max Albert; Jonsson, Michael; Andreasen, Neils; Styrud, Ewa; Karlsson, Ingvar; Edman, Åke; Popa, Cornel; Rasulzada, Abdullah; Wahlund, L.-O.; Mehta, Preeti; Rosengren, Lars; Blennow, K.; Wallin, Anders

doi:10.1111/j.1600-0838.2006.00610_2.x

Cited by 69 publications

(110 citation statements)

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“…Zetterberg et al (2006) examined cerebrospinal fluid (CSF) taken by from lumbar puncture in 14 amateur boxers 7 to 10 days and 3 months after a bout compared to matched controls without any contact. They used several markers of neuronal and astroglial injury that can be readily detected in the CSF, finding significant indicators of neuronal injury byproducts in CSF that were positively related to the actual number of hits during a bout, most apparent in the initial samples taken after the amateur boxing contest.…”

Section: Pathophysiology Of Concussionmentioning

confidence: 99%

Neuropsychology and clinical neuroscience of persistent post-concussive syndrome

Bigler

2007

J Int Neuropsychol Soc

359

248

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On the mild end of the acquired brain injury spectrum, the terms concussion and mild traumatic brain injury (mTBI) have been used interchangeably, where persistent post-concussive syndrome (PPCS) has been a label given when symptoms persist for more than three months post-concussion. Whereas a brief history of concussion research is overviewed, the focus of this review is on the current status of PPCS as a clinical entity from the perspective of recent advances in the biomechanical modeling of concussion in human and animal studies, particularly directed at a better understanding of the neuropathology associated with concussion. These studies implicate common regions of injury, including the upper brainstem, base of the frontal lobe, hypothalamic-pituitary axis, medial temporal lobe, fornix, and corpus callosum. Limitations of current neuropsychological techniques for the clinical assessment of memory and executive function are explored and recommendations for improved research designs offered, that may enhance the study of long-term neuropsychological sequelae of concussion. (JINS, 2008, 14, 1-22.)

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Section: Pathophysiology Of Concussionmentioning

confidence: 99%

Neuropsychology and clinical neuroscience of persistent post-concussive syndrome

Bigler

2007

J Int Neuropsychol Soc

359

248

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“…Patients with stroke initially have increased T-tau levels, which normalize after a few months (Hesse et al 2001). In amateur boxers, head trauma leads to increased T-tau levels, which normalize after a few months of rest (Zetterberg et al 2006). In patients treated with electroconvulsive therapy, T-tau levels are stable after up to six treatment sessions, indicating that such treatment does not induce neuronal damage (Zachrisson et al 2000).…”

Section: Amyloid Markersmentioning

confidence: 99%

Miglustat Treatment May Reduce Cerebrospinal Fluid Levels of the Axonal Degeneration Marker Tau in Niemann–Pick Type C

et al. 2011

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Introduction: Niemann-Pick disease type C (NPC) is a lysosomal storage disorder that leads to progressive neurodegeneration. The glucosylceramide synthase blocker miglustat is being used to treat NPC, but monitoring of disease progression and treatment response is difficult. NPC patients have elevated cerebrospinal fluid (CSF) levels of total-tau (T-tau) indicating axonal degeneration, and increased CSF amyloid b (Ab) indicating abnormal brain amyloid metabolism, but it is unknown if start of miglustat treatment affects these biomarker levels.Methods: Biomarkers were measured in serial CSF samples from NPC patients who started miglustat between samplings (N ¼ 5), were untreated at both samplings (N ¼ 5) or received treatment during the whole study (N ¼ 6) (median time between samplings 309 days [range 175-644]). CSF was analyzed for Ab 38 , Ab 40 , Ab 42 , a-cleaved soluble APP, b-cleaved soluble APP, T-tau and phospho-tau.Results: T-tau levels decreased in patients who started miglustat treatment (median 955 [range 338-1,271] ng/L at baseline vs. 382 ng/L at follow-up, p ¼ 0.043). Untreated patients and continuously treated patients had stable levels (p > 0.05). No changes were seen in the other biomarkers.Conclusion: Reduced CSF T-tau suggests that miglustat treatment might affect axonal degeneration in NPC. However, the results must be interpreted with caution and verified in future studies, since this pilot study was small, treatment was not randomized, and patients starting treatment had higher baseline CSF T-tau than untreated patients.

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“…148 Studies have demonstrated that the ratio of CSF to serum albumin can be used as a means to detect disruption of the BBB in severe brain injury; however, these results were not replicated in cases of mTBI. 15,29,67,147 Tau protein and neurofilaments have emerged as biomarker candidates for axonal injury in CSF because these molecules represent the pathognomonic features found in neurodegenerative diseases, including CTE. Two prospective studies, consisting of 30 and 14 amateur boxers, compared levels of neurofilament light protein and total tau in the CSF to nonboxing healthy controls.…”

mentioning

confidence: 99%

Sports-related brain injuries: connecting pathology to diagnosis

Pan¹,

Connolly²,

Dangelmajer³

et al. 2016

FOC

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Neurosurg Focus 40 (4):E14, 2016M any sports-related brain injuries involve mild traumatic brain injuries (mTBIs), which result from physical blows to the head sustained over a period of time. Sports associated with an increased risk of head injury include American football, ice hockey, soccer, rugby, the martial arts, boxing, and bicycling. 21,90 These injuries are often unrecognized, undiagnosed, or underreported, which reflects the fact that this is a growing medical concern, often labeled a "silent epidemic." 8,66 Chronic exposure to mild brain injuries can result in long-term neurological consequences and represents a spectrum of disorders. The most remarkable outcome of mTBI is termed chronic traumatic encephalopathy (CTE), a clinical syndrome that is associated with neurodegeneration and behavioral, cognitive, and/or motor deficits. Although this disease has distinct pathological features, CTE is considered a diagnosis of exclusion because only postmortem biopsies can confirm the diagnosis. Therefore, new diagnostic methods need to be developed to: 1) inform patients of a definitive diagnosis, 2) better understand the epidemiology and risk factors of the disease, and 3) implement intervention programs to prevent any potential long-term complications. This review examines how understanding the pathology and molecular changes associated with repeated head trauma can lead to the discovery of novel imaging techniques and biomarkers. Mild Traumatic Brain Injury and CTEChronic traumatic encephalopathy has evolved from the so-called punch-drunk syndrome, which was used to describe a distinct neuropsychiatric condition that seemed to affect boxers, eventually becoming known as dementia pugilistica during the 1920s and 1930s. Symptoms such ABBrEvIATIoNs AD = Alzheimer's disease; APOE = apolipoprotein E; ASL = arterial spin labeling; BBB = blood-brain barrier; BOLD = blood oxygen level-dependent; CA = cornu ammonis; CTE = chronic traumatic encephalopathy; DTI = diffusion tensor imaging; FA = fractional anisotropy; fMRI = functional MRI; GFAP = glial fibrillary acidic protein; GRE = gradient recall echo; miRNA = microRNA; MRS = MR spectroscopy; mTBI = mild traumatic brain injury; NFL = National Football League; NFT = neurofibrillary tangle; NINDS = National Institute of Neurological Disorders and Stroke; NSE = neuron-specific enolase; p-tau = phosphorylated tau; SWI = susceptibility-weighted imaging; TDP-43 = TAR DNA-binding protein 43;18 F-FDDNP = 2-(1-{6- [(2-[fluorine-18] Brain injuries are becoming increasingly common in athletes and represent an important diagnostic challenge. Early detection and management of brain injuries in sports are of utmost importance in preventing chronic neurological and psychiatric decline. These types of injuries incurred during sports are referred to as mild traumatic brain injuries, which represent a heterogeneous spectrum of disease. The most dramatic manifestation of chronic mild traumatic brain injuries is termed chronic traumatic encephalopathy, which is associated with profo...

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Neurochemical aftermath of amateur boxing

Cited by 69 publications

References 0 publications

Neuropsychology and clinical neuroscience of persistent post-concussive syndrome

Neuropsychology and clinical neuroscience of persistent post-concussive syndrome

Miglustat Treatment May Reduce Cerebrospinal Fluid Levels of the Axonal Degeneration Marker Tau in Niemann–Pick Type C

Sports-related brain injuries: connecting pathology to diagnosis

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