Active elite rugby participation is associated with altered precentral cortical thickness.

There is growing concern that elite rugby participation may negatively influence brain health, but the underlying mechanisms are unclear. Cortical thickness is a widely applied biomarker of grey matter structure, but there is limited research into how it may be altered in active professional rugby players. Cross-sectional MRI data from 44 active elite rugby players, including 21 assessed within 1 week of head injury, and 47 healthy controls were analysed. We investigated how active elite rugby participation with and without sub-acute traumatic brain injury influenced grey matter structure using whole cortex and region of interest cortical thickness analyses. Relationships between cortical thickness and biomarkers of traumatic brain injury, including fractional anisotropy, plasma neurofilament light and glial fibrillary acidic protein, were also examined. In whole-cortex analyses, precentral cortical thickness in the right hemisphere was lower in rugby players compared with controls, which was due to reductions in non-injured players. Post hoc region of interest analyses showed non-injured rugby players had reduced cortical thickness in the inferior precentral sulcal thickness bilaterally (P = 0.005) and the left central sulcus (P = 0.037) relative to controls. In contrast, players in the sub-acute phase of mild traumatic brain injury had higher inferior precentral sulcal cortical thickness in the right hemisphere (P = 0.015). Plasma glial fibrillary acidic protein, a marker of astrocyte activation, was positively associated with right inferior precentral sulcal cortical thickness in injured rugby players (P = 0.0012). Elite rugby participation is associated with localized alterations in cortical thickness, specifically in sulcal motor regions. Sub-acute changes after mild traumatic brain injury are associated with evidence of astrocytic activation. The combination of cortical thickness and glial fibrillary acidic protein may be useful in understanding the pathophysiological relationship between sporting head injury and brain health.

White matter abnormalities in active elite adult rugby players.

The recognition, diagnosis and management of mild traumatic brain injuries are difficult and confusing. It is unclear how the severity and number of injuries sustained relate to brain injuries, such as diffuse axonal injury, diffuse vascular injury and progressive neurodegeneration. Advances in neuroimaging techniques enable the investigation of neuropathologies associated with acute and long-term effects of injury. Head injuries are the most commonly reported injury seen during professional rugby. There is increased vigilance for the immediate effects of these injuries in matches, but there has been surprisingly little research investigating the longer-term effects of rugby participation. Here, we present a longitudinal observational study investigating the relationship of exposure to rugby participation and sub-acute head injuries in professional adult male and female rugby union and league players using advanced MRI. Diffusion tensor imaging and susceptibility weighted imaging was used to assess white matter structure and evidence of axonal and diffuse vascular injury. We also studied changes in brain structure over time using Jacobian Determinant statistics extracted from serial volumetric imaging. We tested 41 male and 3 female adult elite rugby players, of whom 21 attended study visits after a head injury, alongside 32 non-sporting controls, 15 non-collision-sport athletic controls and 16 longitudinally assessed controls. Eighteen rugby players participated in the longitudinal arm of the study, with a second visit at least 6 months after their first scan. Neuroimaging evidence of either axonal injury or diffuse vascular injury was present in 23% (10/44) of players. In the non-acutely injured group of rugby players, abnormalities of fractional anisotropy and other diffusion measures were seen. In contrast, non-collision-sport athletic controls were not classified as showing abnormalities. A group level contrast also showed evidence of sub-acute injury using diffusion tensor imaging in rugby players. Examination of longitudinal imaging revealed unexpected reductions in white matter volume in the elite rugby players studied. These changes were not related to self-reported head injury history or neuropsychological test scores and might indicate excess neurodegeneration in white matter tracts affected by injury. Taken together, our findings suggest an association of participation in elite adult rugby with changes in brain structure. Further well-designed large-scale studies are needed to understand the impact of both repeated sports-related head impacts and head injuries on brain structure, and to clarify whether the abnormalities we have observed are related to an increased risk of neurodegenerative disease and impaired neurocognitive function following elite rugby participation.

Plasma glial fibrillary acidic protein and neurofilament light chain, but not tau, are biomarkers of sports-related mild traumatic brain injury.

Mild traumatic brain injury is a relatively common event in contact sports and there is increasing interest in the long-term neurocognitive effects. The diagnosis largely relies on symptom reporting and there is a need for objective tools to aid diagnosis and prognosis. There are recent reports that blood biomarkers could potentially help triage patients with suspected injury and normal CT findings. We have measured plasma concentrations of glial and neuronal proteins and explored their potential in the assessment of mild traumatic brain injury in contact sport. We recruited a prospective cohort of active male rugby players, who had pre-season baseline plasma sampling. From this prospective cohort, we recruited 25 players diagnosed with mild traumatic brain injury. We sampled post-match rugby players without head injuries as post-match controls. We measured plasma neurofilament light chain, tau and glial fibrillary acidic protein levels using ultrasensitive single molecule array technology. The data were analysed at the group and individual player level. Plasma glial fibrillary acidic protein concentration was significantly increased 1-h post-injury in mild traumatic brain injury cases compared to the non-injured group (P = 0.017). Pairwise comparison also showed that glial fibrillary acidic protein levels were higher in players after a head injury in comparison to their pre-season levels at both 1-h and 3- to 10-day post-injury time points (P = 0.039 and 0.040, respectively). There was also an increase in neurofilament light chain concentration in brain injury cases compared to the pre-season levels within the same individual at both time points (P = 0.023 and 0.002, respectively). Tau was elevated in both the non-injured control group and the 1-h post-injury group compared to pre-season levels (P = 0.007 and 0.015, respectively). Furthermore, receiver operating characteristic analysis showed that glial fibrillary acidic protein and neurofilament light chain can separate head injury cases from control players. The highest diagnostic power was detected when biomarkers were combined in differentiating 1-h post-match control players from 1-h post-head injury players (area under curve 0.90, 95% confidence interval 0.79-1.00, P < 0.0002). The brain astrocytic marker glial fibrillary acidic protein is elevated in blood 1 h after mild traumatic brain injury and in combination with neurofilament light chain displayed the potential as a reliable biomarker for brain injury evaluation. Plasma total tau is elevated following competitive rugby with and without a head injury, perhaps related to peripheral nerve trauma and therefore total tau does not appear to be suitable as a blood biomarker.

Peripartum isolated cortical vein thrombosis in a mother with postdural puncture headache treated with an epidural blood patch.

A 32-year-old woman presented with low pressure headache 3 days after delivery of her baby. An assessment of postdural puncture headache was made. This was initially treated with analgesia, caffeine, and fluids for the presumed cerebrospinal fluid (CSF) leak. The woman was readmitted two days after her hospital discharge with generalised seizures. A brain scan showed features of intracranial hypotension, and she was treated for CSF leak using an epidural blood patch. Her symptoms worsened and three days later, she developed a left homonymous quadrantanopia. An MRI scan confirmed a right parietal haematoma with evidence of isolated cortical vein thrombosis (ICVT).

Acute ischaemic ventricular inferoseptal defect in a pyretic patient: a diagnostic challenge.

A 78-year-old Caucasian male presented with a 5-day progressive history of fever, vomiting and dyspnoea. Initial clinical examination revealed fever, sinus tachycardia, hypotension, peripheral cyanosis and a systolic murmur. Investigations revealed a multiple organ dysfunction syndrome. A repeat trans-thoracic echocardiogram showed a basal inferoseptum aneurysm associated with an acquired ventricular septal defect not demonstrated on initial scan. An intra-aortic balloon pump was urgently inserted and he underwent surgical repair of the defect, 7 days after his initial presentation. He unfortunately died from postoperative complications.

Sexual history: its importance in averting detrimental misdiagnosis and delayed diagnosis.

Two cases where the sexual history proved important in reaching the diagnosis are presented. Case 1 concerns a 37-year-old HIV positive homosexual man, who presented with symptoms of rectal pain associated with bleeding. He was unsuccessfully treated for Crohn disease. A subsequent review of his sexual history led to investigations for venereal infections. A final diagnosis of proctitis secondary to lymphogranuloma venereum was made. The patient was successfully treated with doxycycline and spared an unnecessary colectomy. Case 2 concerns a 22-year-old Caucasian woman under investigation for possible lymphoma. However, the doctor carrying out the biopsy experienced a needle stick injury and the ensuing investigations revealed the patient's HIV positive status and thus the explanation for her hitherto undiagnosed lymphadenopathy. A prior review of her sexual history could have hastened the diagnosis and prevented the need for invasive tests.

Pre-emptive treatment for Clostridium tetani: importance of early recognition and treatment in the community.

The case of a 79-year-old woman with neurotoxin producing Clostridium tetani identified in a lower limb laceration that was promptly treated is presented; the patient developed no symptoms of tetanus. Her antibody levels were measured as 0.01 U/ml (protective levels >0.01 U/ml) and were therefore not protective. The isolate of C tetani was identified by 16S sequencing. The potential to produce tetanus toxin was determined by detection of a fragment of the C tetani neurotoxin gene. She was given a week long course of oral flucloxacillin, 500 mg four times a day and metronidazole, 400 mg three times a day, for 5 days. The patient was subsequently given prophylactic immunoglobulin (500 IU) as per guidelines. The fact that the patient did not manifest any symptoms of localised or generalised tetanus could be attributed to prompt management when she presented to her primary care site.

Sporadic Creutzfeldt-Jakob disease: early signs and pre-mortem diagnosis.

A 71-year-old Caucasian woman presented with a 3 week history of progressive ataxia followed by rapid cognitive decline. Examination on admission showed cerebellar ataxia. This was followed by multifocal dementia with cortical, subcortical and brainstem involvements during her hospital stay. Protein 14-3-3 was identified in the cerebrospinal fluid (CSF) as well as a markedly increased S100b. The patient was reviewed by the National CJD Surveillance Unit and the National Prion Unit who supported the pre-mortem diagnosis of probable Sporadic Creutzfeldt-Jakob disease. The patient deteriorated rapidly, became cortically blind, bed bound and died in May 2009, 4 months after the onset of symptoms.