Mild traumatic brain injury impairs the coordination of intrinsic and motor-related neural dynamics.

Mild traumatic brain injury (mTBI) poses a considerable burden on healthcare systems. Whilst most patients recover quickly, a significant number suffer from sequelae that are not accompanied by measurable structural damage. Understanding the neural underpinnings of these debilitating effects and developing a means to detect injury, would address an important unmet clinical need. It could inform interventions and help predict prognosis. Magnetoencephalography (MEG) affords excellent sensitivity in probing neural function and presents significant promise for assessing mTBI, with abnormal neural oscillations being a potential specific biomarker. However, growing evidence suggests that neural dynamics are (at least in part) driven by transient, pan-spectral bursting and in this paper, we employ this model to investigate mTBI. We applied a Hidden Markov Model to MEG data recorded during resting state and a motor task and show that previous findings of diminished intrinsic beta amplitude in individuals with mTBI are largely due to the reduced beta band spectral content of bursts, and that diminished beta connectivity results from a loss in the temporal coincidence of burst states. In a motor task, mTBI results in diminished burst amplitude, altered modulation of burst probability during movement, and a loss in connectivity in motor networks. These results suggest that, mechanistically, mTBI disrupts the structural framework underlying neural synchrony, which impairs network function. Whilst the damage may be too subtle for structural imaging to see, the functional consequences are detectable and persist after injury. Our work shows that mTBI impairs the dynamic coordination of neural network activity and proposes a potent new method for understanding mTBI.

Magnetoencephalography abnormalities in adult mild traumatic brain injury: A systematic review.

BACKGROUND: The global incidence of traumatic brain injuries is rising, with at least 80% being classified as mild. These mild injuries are not visible on routine clinical imaging. The potential clinical role of a specific imaging biomarker be it diagnostic, prognostic or directing and monitoring progress of personalised treatment and rehabilitation has driven the exploration of several new neuroimaging modalities. This systematic review examined the evidence for magnetoencephalography (MEG) to provide an imaging biomarker in mild traumatic brain injury (mTBI). METHODS: Our review was prospectively registered on PROSPERO: CRD42019151387. We searched EMBASE, MEDLINE, trial registers, PsycINFO, Cochrane Library and conference abstracts and identified 37 papers describing MEG changes in mTBI eligible for inclusion. Since meta-analysis was not possible, based on the heterogeneity of reported outcomes, we provide a narrative synthesis of results. RESULTS: The two most promising MEG biomarkers are excess resting state low frequency power, and widespread connectivity changes in all frequency bands. These may represent biomarkers with potential for diagnostic application, which reflect time sensitive changes, or may be capable of offering clinically relevant prognostic information. In addition, the rich data that MEG produces are well-suited to new methods of machine learning analysis, which is now being actively explored. INTERPRETATION: MEG reveals several promising biomarkers, in the absence of structural abnormalities demonstrable with either computerised tomography or magnetic resonance imaging. This review has not identified sufficient evidence to support routine clinical use of MEG in mTBI currently. However, verifying MEG's potential would help meet an urgent clinical need within civilian, sports and military medicine.

Winston Churchill (1874-1965), Dr Robson Roose, MD Brux, FRCPE (1848-1905) and Dr Joseph Rutter, MD Lond, MRCP (1834-1913): Treatment for pneumonia in March 1886.

This paper will review Winston Churchill's severe respiratory illness in March 1886 when he developed pneumonia of the right lung as an 11-year-old boy. Winston was treated supportively with 'nourishment, stimulants [probably alcohol] and close watching' at his school by the 'celebrated' family physician, Dr Robson Roose, with the assistance of Dr Joseph Rutter. Roose was exemplary in his commitment to his young patient and assiduous in informing Lord Randolph Churchill of his son's clinical progress by letter.

Did Winston Churchill suffer a myocardial infarction in the White House at Christmas 1941?

While staying in the White House over Christmas 1941, Churchill developed chest pain on trying to open a window in his bedroom. Sir Charles Wilson, his personal physician, diagnosed a 'heart attack' (myocardial infarction). Wilson, for political and personal reasons, decided not to inform his patient of the diagnosis or obtain assistance from US medical colleagues. On Churchill's return to London, Wilson sought a second opinion from Dr John Parkinson who did not support the diagnosis of coronary thrombosis (myocardial infarction) and reassured Churchill accordingly.