Background: Previous research addressing cognitive recovery after traumatic brain injury (TBI) in adults has predominately used cross-sectional methods. This systematic review examines longitudinal research into cognitive recovery in the first 2 years following moderate-to-severe TBI in adults and aims to identify apparent methodological issues with the existing literature.

Design: Systematic review of the first 2 years post-trauma.

Setting: Data were extracted from three electronic databases and manual searches of published articles until October 2012.

Participants: Two hundred and forty-two participants with severe TBI and 281 comparison participants were used to calculate effect sizes.

Results: Twenty papers met the selection criteria, with effect sizes computed from four studies. Moderate-to-large effect sizes were initially observed between the TBI and comparison groups on most measures (range: d = 0.2–2.8). Recovery continued in all five cognitive domains over the 2 years post-injury.

Conclusions: Results demonstrated that cognitive recovery was continuous throughout the first 2 years following moderate-to-severe TBI. Findings also indicated different rates of recovery for the specific cognitive domains, highlighting the heterogeneous nature of cognitive recovery after TBI. The review highlighted several methodological issues within the limited existing literature; recommendations were developed to improve the evidence base.

After traumatic injury, the brain undergoes a prolonged period of degenerative change that is paradoxically accompanied by cognitive recovery. The spatiotemporal pattern of atrophy and the specific relationships of atrophy to cognitive changes are ill understood. The present study used tensor-based morphometry and neuropsychological testing to examine brain volume loss in 17 traumatic brain injury (TBI) patients and 13 controls over a 4-year period. Patients were scanned at 2 months, 1 year, and 4 years post-injury. High-dimensional warping procedures were used to create change maps of each subject's brain for each of the two intervals. TBI patients experienced volume loss in both cortical areas and white matter regions during the first interval. We also observed continuing volume loss in extensive regions of white matter during the second interval. Neuropsychological correlations indicated that cognitive tasks were associated with subsequent volume loss in task-relevant regions. The extensive volume loss in brain white matter observed well beyond the first year post-injury suggests that the injured brain remains malleable for an extended period, and the neuropsychological relationships suggest that this volume loss may be associated with subtle cognitive improvements. (JINS, 2012, 18, 1–13)

The effect of age at injury on outcome after acquired brain injury (ABI) has been the subject of much debate. Many argue that young brains are relatively tolerant of injury. A contrasting viewpoint due to Hebb argues that greater system integrity may be required for the initial establishment of a function than for preservation of an already-established function. A neuro-computational model of cortical map formation was adapted to examine effects of focal and distributed injury at various stages of development. This neural network model requires a period of training during which it self-organizes to establish cortical maps. Injuries were simulated by lesioning the model at various stages of this process and network function was monitored as “development” progressed to completion. Lesion effects are greater for larger, earlier, and distributed (multifocal) lesions. The mature system is relatively robust, particularly to focal injury. Activities in recovering systems injured at an early stage show changes that emerge after an asymptomatic interval. Early injuries cause qualitative changes in system behavior that emerge after a delay during which the effects of the injury are latent. Functions that are incompletely established at the time of injury may be vulnerable particularly to multifocal injury. (JINS, 2011, 17, 1030–1038)

Aims – To review developments in recovery-focussed mental health services internationally. Methods – Two forms of ‘recovery’ which have been used in the literature are considered, and international examples of recovery-focussed initiatives reviews. A ‘litmus test’ for a recovery-focussed service is proposed. Results – ‘Clinical recovery’ has emerged from professional literature, focuses on sustained remission and restoration of functioning, is invariant across individuals, and has been used to establish rates of recovery. ‘Personal recovery’ has emerged from consumer narratives, focuses on living a satisfying, hopeful and contributing life even with limitations caused by the illness, varies across individuals, and the empirical evidence base relates to stages of change more than overall prevalence rates. Clinical and personal recovery are different. Two innovative, generalisable and empirically investigated examples are given of implementing a focus on personal recovery: the Collaborative Recovery Model in Australia, and Trialogues in German-speaking Europe. The role of medication is an indicator: services in which all service users are prescribed medication, in which the term ‘compliance’ is used, in which the reasoning bias is present of attributing improvement to medication and deterioration to the person, and in which contact with and discussion about the service user revolves around medication issues, are not personal recovery-focussed services. Conclusions – The term ‘Recovery’ has been used in different ways, so conceptual clarity is important. Developing a focus on personal recovery is more than a cosmetic change – it will entail fundamental shifts in the values of mental health services.

Declaration of Interest: None.

The nature of residual cognitive deficits after out of hospital cardiac arrest (OHCA) is incompletely described and has never been defined against a cardiac control (CC) group. The objective of this study is to examine neuropsychological outcomes 3 months after OHCA in patients in a “middle range” of acute severity. Thirty prospective OHCA admissions with coma >1 day and responsive but confused at 1 week, and 30 non-OHCA coronary care admissions were administered standard tests in five cognitive domains. OHCA subjects fell into two deficit profiles. One group (N = 20) had mild memory deficits and borderline psychomotor deficits compared to the CC group; 40% had returned to work. The other group (N = 10) had severe impairments in all domains. Coma duration was associated with group. Neither group had a high prevalence of depression. For most patients within the “middle range” of acute severity of OHCA, cognitive and functional outcomes at 3 months were encouraging. (JINS, 2011, 17, 364–368)

Blindsight is the term commonly used to describe visually guided behaviour elicited by a stimulus falling within the scotoma (blind area) caused by a lesion of the striate cortex. Such “vision” is normally held to be unconscious and to be mediated by subcortical pathways involving the superior colliculus. Blindsight is of considerable theoretical importance since it suggests that destriate man is more like destriate monkey than had been previously believed and also because it supports the classical notion of two visual systems. It is also of potential clinical importance, since it has been claimed recently that systematic practice in blindsight can lead to the recovery of normal visual function in patients with cortical lesions. From a review of the literature it is concluded that all of the phenomena of blindsight can be attributed either to light scatter into unimpaired parts of the visual field or to residual vision resulting from spared striate cortex. The possible contribution f other factors is also considered. It is concluded that blindsight studies have generally failed to control for such nonblindsight interpretations partly because of poor methodology and partly because of difficulties in defining the term “blindsight.”

Experiments were carried out to investigate the extent to which subjects can exhibit performance similar to blindsight when they are using scattered light as a cue. This was done both with hemianopic subjects (by manipulating the amount of scattered and direct light coming from a stimulus) and with normal subjects (by presenting targets within their blind spots). Good blindsight performance was observed when only scattered light was available as a cue to the subjects. It is therefore concluded that an adequate case for blindsight has not been made. It is probably impossible to demonstrate the existence of blindsight on purely behavioural grounds. What is required is the establishment of relationships between visual function and independent anatomical evidence.

Cognitive deficits were produced in rats by different methods of damaging the brain: chronic ingestion of alcohol, causing widespread damage to diffuse cholinergic and aminergic projection systems; lesions (by local injection of the excitotoxins, ibotenate, quisqualate, and AMPA) of the nuclei of origin of the forebrain cholinergic projection system (FCPS), which innervates the neocortex and hippocampal formation; transient cerebral ischaemia, producing focal damage especially in the CA1 pyramidal cells of the dorsal hippocampus; and lesions (by local injection of the neurotoxin, colchicine) of the granule cells of the dentate gyrus. Following chronic alcohol or lesions of the FCPS, transplants of cholinergically rich fetal brain tissue into the terminal areas (neocortex and/or hippocampus) restored performance almost to control levels, with a time course consistent with growth of the transplants and integration with host tissue; transplants of cholinergically poor fetal tissue (hippocampus) were without effect, as were transplants of cholinergically rich tissue into the region containing the nuclei of origin of the FCPS. Grafts of primary cells enriched in glia and cultured neuroblastoma cells into the terminal areas of the FCPS were equally effective, suggesting that there are multiple mechanisms by which neural transplants can restore cognitive function following diffuse cholinergic damage. In contrast, after ischaemia- or neurotoxin-induced damage to CA1 or dentate granule cells respectively, cholinergically rich fetal transplants into the damaged hippocampal formation were ineffective in restoring performance. After ischaemic damage, however, performance was restored by suspension grafts of CA1 cells but not by transplants containing CA3 pyramidal cells or granule cells; and after colchicine damage it was restored by solid grafts containing granule but not CA1 pyramidal cells. Furthermore, electrophysiological evidence has demonstrated functional, graft type-specific host-graft functional neuronal connectivity. Thus, restoration of cognitive function by neural transplants is possible after damage to either diffuse (cholinergic) or point-to-point (intrahippocampal) forebrain systems, but the transplant must be appropriate to the damage to be repaired. Because the different types of brain damage studied provide analogues of human alcoholic dementia, Alzheimer's disease, and heart attack, these results are encouraging with regard to the eventual application of neural transplant surgery to the treatment of cognitive deficits in humans.

The primary aims of this study were to examine post-injury cognitive development in young children with traumatic brain injury (TBI) and to investigate the role of the proximal family environment in predicting cognitive outcomes. Age at injury was 3–6 years, and TBI was classified as severe (n = 23), moderate (n = 21), and complicated mild (n = 43). A comparison group of children who sustained orthopedic injuries (OI, n = 117) was also recruited. Child cognitive assessments were administered at a post-acute baseline evaluation and repeated at 6, 12, and 18 months post-injury. Assessment of the family environment consisted of baseline measures of learning support and stimulation in the home and of parenting characteristics observed during videotaped parent–child interactions. Relative to the OI group, children with severe TBI group had generalized cognitive deficiencies and those with less severe TBI had weaknesses in visual memory and executive function. Although deficits persisted or emerged across follow-up, more optimal family environments were associated with higher scores for all injury groups. The findings confirm other reports of poor recovery of cognitive skills following early childhood TBI and suggest environmental influences on outcomes. (JINS, 2010, 16, 157–168.)

While the cognitive disturbances that frequently follow severe traumatic brain injury (TBI) are relatively well understood, the ways in which these affect the psychosocial functioning of people with TBI are yet to be determined and have thus received little attention in treatment research. Growing evidence indicates that a significant proportion of individuals with TBI demonstrate an inability to recognize affective information from the face, voice, bodily movement, and posture. Because accurate interpretation of emotion in others is critical for the successful negotiation of social interactions, effective treatments are necessary. Until recently, however, there have been no rehabilitation efforts in this area. The present review examines the literature on emotion perception deficits in TBI and presents a theoretical rationale for targeted intervention. Several lines of research relevant to the remediation of emotion perception in people with TBI are considered. These include work on emotion perception remediation with other cognitively impaired populations, current neuropsychological models of emotion perception and underlying neural systems, and recent conceptualizations of remediation processes. The article concludes with a discussion of the importance of carrying out efforts to improve emotion perception within a contextualized framework in which the day-to-day relevance of training is clear to all recipients. (JINS, 2008, 14, 511–525.)

Lateralized spatial biases after brain damage are commonly assessed using batteries of paper-and-pencil tests. These tests hardly allow quantification of performance in different locations in space, and they tend to lose sensitivity along the course of recovery. We tested the dynamic Starry Night Test (SNT), a novel computerized test measuring reaction time and detection accuracy for visual target stimuli in a dynamic background, in 32 inpatients with right hemisphere stroke (RHS), 16 patients with left hemisphere stroke (LHS), and 9 healthy controls. As a group, only the RHS patients were significantly slower to respond to contralesional targets. Individually, 21 (66%) RHS patients and 5 (31%) LHS patients showed statistically significant contralateral deficits. In a number of RHS patients the SNT was more sensitive to the ipsilesional bias of spatial attention than the Behavioral Inattention Test (BIT), a standardized paper-and-pencil test battery of unilateral spatial neglect. Two illustrative case reports show that the dynamic SNT, but not the BIT, was sensitive to the spatial deficit in recovered patients, one of whom was involved in repeated car accidents. The SNT overcomes serious shortcomings of paper-and-pencil tests of unilateral neglect. It provides a simple quantitative tool for monitoring the natural and treatment-induced recovery of patients. (JINS, 2005, 11, 697–707.)Part of the data was presented in abstract form at the EBBS EuroConference on Cognitive and Neural Bases of Spatial Neglect, September 14–17, 2000, Como, Italy.

Hearing loss associated with high-voltage electric shock is a rare entity and minimal information is available in the current literature about this condition. To our knowledge, this article represents the first case report in the literature of improvement in sensorineural hearing loss sustained due to a high-voltage electric shock.

A case report of a patient who incurred various otologic problems, including hearing loss and tinnitus, is presented. An improvement in hearing loss and tinnitus was observed in the subsequent follow up after one month. Audiological findings and possible pathophysiology of hearing loss are discussed.

We recommend that further studies be done to investigate the incidence, severity and pathophysiology of hearing loss in such cases.