Sport-Related Structural Brain Injury and Return to Play: Systematic Review and Expert Insight.

BACKGROUND: Sport-related structural brain injury (SRSBI) is intracranial pathology incurred during sport. Management mirrors that of non-sport-related brain injury. An empirical vacuum exists regarding return to play (RTP) following SRSBI. OBJECTIVE: To provide key insight for operative management and RTP following SRSBI using a (1) focused systematic review and (2) survey of expert opinions. METHODS: A systematic literature review of SRSBI from 2012 to present in accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines and a cross-sectional survey of RTP in SRSBI by 31 international neurosurgeons was conducted. RESULTS: Of 27 included articles out of 241 systematically reviewed, 9 (33.0%) case reports provided RTP information for 12 athletes. To assess expert opinion, 31 of 32 neurosurgeons (96.9%) provided survey responses. For acute, asymptomatic SRSBI, 12 (38.7%) would not operate. Of the 19 (61.3%) who would operate, midline shift (63.2%) and hemorrhage size > 10 mm (52.6%) were the most common indications. Following SRSBI with resolved hemorrhage, with or without burr holes, the majority of experts (>75%) allowed RTP to high-contact/collision sports at 6 to 12 mo. Approximately 80% of experts did not endorse RTP to high-contact/collision sports for athletes with persistent hemorrhage. Following craniotomy for SRSBI, 40% to 50% of experts considered RTP at 6 to 12 mo. Linear regression revealed that experts allowed earlier RTP at higher levels of play (ß = -0.58, 95% CI -0.111, -0.005, P = .033). CONCLUSION: RTP decisions following structural brain injury in athletes are markedly heterogeneous. While individualized RTP decisions are critical, aggregated expert opinions from 31 international sports neurosurgeons provide key insight. Level of play was found to be an important consideration in RTP determinations.

Bilateral trigeminal neuralgia associated with limited systemic sclerosis.

A young patient with limited systemic sclerosis and medically resistant bilateral trigeminal neuralgia was successfully treated with microvascular decompression. To our knowledge, this is the first published report of this type of case.

Intracranial pressure: more than a number.

Many doctors involved in the critical care of head-injured patients understand intracranial pressure (ICP) as a number, characterizing the state of the brain pressure-volume relationships. However, the dynamics of ICP, its waveform, and secondarily derived indices portray useful information about brain homeostasis. There is circumstantial evidence that this information can be used to modify and optimize patients' treatment. Secondary variables, such as pulse amplitude and the magnitude of slow waves, index of compensatory reserve, and pressure-reactivity index (PRx), look promising in clinical practice. The optimal cerebral perfusion pressure (CPP) derived using the PRx is a new concept that may help to avoid excessive use of vasopressors in CPP-oriented therapy. However, the use of secondary ICP indices remains to be confirmed in clinical trials.

A small animal model for early cerebral aneurysm pathology.

Prior studies, using systemic hypertension and elastase infusion, have induced cerebral aneurysm (CA) formation in mice. However, the CAs induced were rapidly formed, relatively large, and often ruptured. These features are not completely representative of human CAs. We set out to develop a mouse model representative of the early pathological features of human CA. Twenty male C57/BL6 mice were placed in a stereotactic frame. Low dose elastase solution (2µl/min) was manually injected into the right basal cistern. Human angiotensin II (0.11µl/h) was infused subcutaneously. Mice were observed for 2-3weeks prior to euthanasia. Early CA histopathological features including endothelial change (EC) and internal elastic lamina degeneration (IELD) were systematically sought at major cerebral arterial bifurcations. Brains were harvested from 11 of 15 mice, yielding 27 bifurcations. Sub-arachnoid haemorrhage (SAH) without CA formation was observed in one brain. Macroscopic CA without SAH was observed in another brain. Early CA features were observed in 8/11 (73%) brains. All bifurcations with IELD demonstrated EC: where EC was absent, IELD was also absent. EC severity appeared to correlate with IELD severity. EC and IELD were both severe within the CA. Using lower dose elastase solution than previously employed, we developed a model of early CA pathology. Our model demonstrated that the spectrum of known early CA pathology can be created at multiple bifurcations in mice, with EC severity appearing to correlate with IELD severity. This model permits the study of factors which potentially advance or retard the progression of CA formation.

A technique for producing demyelination of the rat optic nerves.

Demyelination is a major cause of neurological disability within the human population, and the end product of a number of pathological processes, though the most common is the disease multiple sclerosis. This disease commonly affects the optic pathway, particularly the optic nerve and chiasm. This paper reports a novel technique of producing chemical glial toxin induced demyelination in the rat optic nerves and chiasm by the direct instillation of the glial toxin ethidium bromide into the rat cranial subarachnoid space causing demyelination of the optic nerves and chiasm. This model, because of its involvement of the optic pathways, will allow both histological and functional assessments of the processes of demyelination and remyelination in the rat animal model.

Post-traumatic amnesia.

Of patients hospitalised for traumatic brain injury (TBI), most pass through a state of altered consciousness known as "post-traumatic amnesia" (PTA). Despite the lack of a consistent definition, PTA is widely used as a construct in neurosurgical practice to guide decision-making and prognosis. Accurate PTA assessment is important, because over-evaluation leads to excess social, financial and opportunity costs, whilst under-evaluation risks patient welfare. Whilst anterograde memory is certainly disrupted in PTA, PTA in fact involves a far more extensive memory disturbance. More instructively, the complete "post-TBI syndrome" also comprises an extensive cognitive deficit which includes a confusional state, as well as a behavioural disturbance characterised by acute agitation. Recently, impairments in attention and executive functioning have also been emphasised; indeed, some consider these the primary disturbance with PTA. Although all of these features were fully described (or implied) by the earliest pioneers, most current PTA scores do not assess the complete "post-TBI syndrome". Currently, the Westmead PTA scale (WPTAS) directs most in-hospital TBI management throughout Australasia: however, in addition to general defects, specific limitations have been identified in the levels of evidence for WPTAS validity. We review the literature regarding PTA and, in particular, the continued role of the WPTAS in directing neurosurgical practice.