There have been many improvements regarding transport conditions, pre-slaughter handling, and captive-bolt stunning of cattle at commercial abattoirs, but many challenges still exist. Animals unaccustomed to human-animal contact, such as free-range beef cattle, may be especially difficult to handle on the day of slaughter. Shifting of the slaughter process from the abattoir to the animals’ familiar environment could improve animal welfare at slaughter. In 2011, the German government passed an amendment allowing farmers to slaughter free-range cattle, on-farm, using a rifle. A proper stun is vital when employing this method but neither sufficient practical experience nor scientific knowledge are in place to allow this. Thus, this study aimed to examine shot placement and the effect of diverse ammunition by means of shooting at cattle heads, post mortem, with a rifle. Impact was assessed using brain tissue damage observed from skull dissections. Placing the shot frontally at the forehead resulted in severe brain damage significantly more frequently than targeting laterally. A precise frontal shot, utilising both large and small bore calibres, caused severe brain damage that would almost certainly have led to immediate unconsciousness and death. One of the small bore calibres caused minimal brain damage apart from the trajectory. However, this was the only calibre not passing straight through. Due to the fact that the bullet remains within the skull, thus transferring all of its energy to the skull and brain, the impact of this calibre on the brain would also be expected to be rapidly fatal. A projectile that does not exit the skull would also be advantageous as regards safety.

A minimal brain damage examination was carried out in 73 schizophrenic patients divided into three groups according to their season of birth. Results showed no statistically significant difference among groups in the prevalence of neurological soft signs.

Objectives: Anosognosia for motor impairment is a complex syndrome that can manifest itself under different forms, guiding patients’ behavior and task decisions. However, current diagnostic tools tend to evaluate only more explicit aspects of anosognosia (asking the patients about their motor abilities) and fail to address more subtle features of awareness. We have developed a new assessment measure, the ECT (Errand Choice Test), where patients are asked to judge task difficulty rather than estimate their own impairment. Methods: We assessed awareness in a group of 73 unilateral left- and right-brain damaged (30 LBD and 43 RBD, respectively) patients by means of the VATAm, which explicitly requires them to evaluate their own motor abilities, and the ECT. A control group of 65 healthy volunteers was asked to perform the ECT under two conditions: Current condition (i.e., using both hands) and Simulated conditions (i.e., simulating hemiplegia). Results: A total of 27% of the patients showed different performance on the VATAm and ECT, 21% of the patients showing lack of awareness only on VATAm and 6% only on ECT. Moreover, despite the ECT identified a higher frequency of anosognosia after RBD (33.3%) than LBD (27.6%), this hemispheric asymmetry was not significant. Remarkably, anosognosic patients performed very similarly to controls in the “current condition”, suggesting that anosognosic patients’ ability to perceive the complexity of each task per se is not altered. Conclusion: Different methods may be able to tackle different aspects of awareness and the ECT proved to be able to detect less evident forms of awareness. (JINS, 2018, 24, 45–56)

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.

Grafts of embryonic neural tissue into the brains of adult patients are currently being used to treat Parkinson's disease and are under serious consideration as therapy for a variety of other degenerative and traumatic disorders. This target article evaluates the use of transplants to promote recovery from brain injury and highlights the kinds of questions and problems that must be addressed before this form of therapy is routinely applied. It has been argued that neural transplantation can promote functional recovery through the replacement of damaged nerve cells, the reestablishment of specific nerve pathways lost as a result of injury, the release of specific neurotransmitters, or the production of factors that promote neuronal growth. The latter two mechanisms, which need not rely on anatomical connections to the host brain, are open to examination for nonsurgical, less intrusive therapeutic use. Certain subjective judgments used to select patients who will receive grafts and in assessment of the outcome of graft therapy make it difficult to evaluate the procedure. In addition, little long-term assessment of transplant efficacy and effect has been done in nonhuman primates. Carefully controlled human studies, with multiple testing paradigms, are also needed to establish the efficacy of transplant therapy.

Although the use of ECT has declined dramatically from its inception, this decrease has recently shown signs of leveling out because of ECT's powerful therapeutic effect in severely ill depressed individuals who either do not respond to pharmacologic alternatives or are too ill to tolerate a relatively lengthy drug trial. Notwithstanding its therapeutic benefits, ECT has also remained a controversial treatment modality, particularly in the eye of the public. Given the unsavory qualities associated with the word “electroconvulsive,” claims of possible, probable, or even certain brain damage with ECT have easily found listeners. A careful, nonselective assessment of data covering the areas of pathology, radiology, electrophysiology, biochemistry, and neuropsychology leads both to certain conclusions and to certain unanswered questions. ECT is not the devastating purveyor of wholesale brain damage that some of its detractors claim. For the typical individual receiving ECT, no detectable correlates of irreversible brain damage appear to occur. Still, there remains the possibility that either subtle, objectively undetectable persistent deficits, particularly in the area of autobiographic memory function, occur, or that a rarely occurring syndrome of more pervasive persistent deficits related to ECT use may be present. Clearly, more research directed toward answering these questions needs to be carried out so that the role of ECT can be more rigorously defined. While such research is pending, however, we cannot expect that the conditions that predispose to clinical referrals for ECT will disappear. Given the misery, anguish, and risk of death by suicide, starvation, or debilitation associated with severe depressive illness, for example, it still appears that ECT, at least for the present, must continue to be available.

A multicenter randomized control trial (RCT) was conducted to evaluate the effects of a treatment for dysexecutive problems after acquired brain injury (ABI) on daily life functioning. Seventy-five ABI patients were randomly allocated to either the experimental treatment, multifaceted strategy training for executive dysfunction, or a control treatment, computerized cognitive function training. Assessment took place before, directly after, and 6 months post-treatment. The primary outcome measure, the Role Resumption List (RRL), and two other follow-up measures, the Treatment Goal Attainment (TGA) and the Executive Secretarial Task (EST), were indications of daily life executive functioning. The experimental group improved significantly more over time than the controls on the RRL and attained significantly higher scores on the TGA and EST. We conclude that our treatment has resulted in significant improvements of executive functioning in daily life, lasting at least 6 months post-treatment. Although control patients’ satisfaction and subjective well-being were at the same level, the experimental group had better abilities to set and accomplish realistic goals, to plan, initiate, and regulate a series of real-life tasks, and to resume previous roles with respect to work, social relations, leisure activities, and mobility. (JINS, 2010, 16, 118–129.)

The purpose of the present study was to assess changes in the levels of cytochrome oxidase (CO) activity in the dorsal lateral geniculate nucleus (dLGN) of the adult cat following removal of primary visual cortical areas 17 and 18 on the day of birth (P1), P28, or in adulthood (≫6 months). Cytochrome oxidase activity was measured in histological sections 9 or more months after the cortical ablation. Control measures obtained from intact cats show that CO activity is normally highest in the A-laminae of dLGN, and slightly lower in the C-complex. Following visual cortex ablations incurred at any age, CO activity levels are reduced in the A-laminae. This reduction is most profound following ablations incurred on P28 or in adulthood. In contrast, CO activity in the C-complex of dLGN is at nearly normal levels following ablations on P1 or P28, but not in adulthood. These findings contribute to our understanding of the role played by the dLGN in the transfer of visual signals along retino-geniculo-extrastriate pathways that expand following early removal of areas 17 and 18. Moreover, they have implications for our understanding of spared behavioral functions attributed to the extrastriate cortex in cats which incurred early damage of areas 17 and 18.

Previous studies indicate that cortical areas 17 and 18 play a prominent role in generating the direction selectivities of neurons in the superior colliculus of the cat. This hypothesis was tested by quantifying the activities of neurons in the superficial collicular layers in intact cats and cats which incurred ablation of areas 17 and 18 and part of area 19. In addition, since behavioral and anatomical studies suggest a functional adjustment in the superior colliculus following removal of inputs from areas 17, 18, and 19 in the neonatal cat, we included a group of neonatally lesioned cats. Computation of an index of directionality indicated that the majority of neurons in intact cats preferred movement in one direction, thus confirming reports of others. Following ablation of areas 17 and 18 and part of area 19 in both groups of lesioned cats, only modest changes in the population indices were detected when poorly responsive neurons were eliminated from the analyses. Based upon levels of visually evoked neuronal activity, our data suggest a physiological compensation by neurons in stratum griseum superficiale following removal of areas 17, 18, and 19 inputs. In the intact and neonatally operated groups, activity in stratum griseum superficiale is high, whereas in the adult lesioned group activity is low. In stratum opticum, neuronal activity was similar in all three groups of cats. These results show that neurons in stratum griseum superficiale undergo a physiological compensation following removal of immature areas 17 and 18.

Tritiated proline and leucine were injected into areas 17 and 18 of intact cats and into the medial bank of the lateral suprasylvian (LS) cortex of intact cats and cats from which areas 17 and 18 had been removed on postnatal day 1 (P1), P28, or in adulthood (A). The density of label transported to the superior colliculus was quantified using image-analysis equipment. The results from the intact cats confirmed previous reports that areas 17 and 18 project most heavily to stratum zonale (SZ) and stratum griseum superficiale (SGS) and LS cortex projects most heavily to stratum opticum (SO) of the superior colliculus. However, in cats with lesions of areas 17 and 18, the projections from LS cortex showed an age-dependent reorganization. LS projections to SGS and SZ were enhanced following ablation of areas 17 and 18 on P1, and projections to SGS were enhanced following an ablation on P28. The pattern of LS-collicular projection following ablations incurred in adulthood was indistinguishable from the pattern presented by intact cats. This study demonstrates that the LS corticocollicular projection expands in SGS and possibly substitutes for inputs eliminated by the removal of areas 17 and 18 from the immature brain. This enhanced pathway may contribute to compensatory neuronal changes and to spared behaviors that accompany damage of immature cortex.