According to higher-order theories of consciousness, a mental state is conscious only when represented by another mental state. Higher-order theories must predict there to be some brain areas (or networks of areas) such that, because they produce (the right kind of) higher-order states, the disabling of them brings about deficits in consciousness. It is commonly thought that the prefrontal cortex produces these kinds of higher-order states. In this paper, I first argue that this is likely correct, meaning that, if some (...) higher-order theory is true, prefrontal lesions should produce dramatic deficits in visual consciousness. I then survey prefrontal lesion data, looking for evidence of such deficits. I argue that no such deficits are to be found, and that this presents a compelling case against higher-order theories. (shrink)

The existence of shoulder abduction (SA) and finger extension (FE) movement capacity shortly after stroke onset is an important prognostic factor, indicating favorable functional outcome for the hemiparetic upper limb. Here we asked whether variation in lesion topography affects these two movements in a similar or a distinct way, and whether lesion impact is similar or distinct for left and right hemisphere damage. SA and FE movements were examined in 77 chronic post-stroke patients using relevant items of the Fugl-Meyer test. (...) Lesion effects were analyzed separately for left and right hemispheric damage (LHD, RHD) patient groups using voxel-based lesion-symptom mapping. In the LHD group, SA and FE were affected only by damage to the cortico-spinal tract in its passage through the corona radiata. In contrast, following RHD, these two movements were affected not only by cortico-spinal tract damage but also by damage to white matter association tracts, the putamen and the insular cortex. In both groups, voxel clusters have been found where damage affected SA and also FE, along with voxels where damage affected only one of the two movements. The capacity to execute SA and FE movements following stroke is affected significantly by damage to shared and distinct voxels in the cortico-spinal tract in LHD patients and by damage to shared and distinct voxels in a larger array of cortical and subcortical regions in RHD patients. (shrink)

The impact of stroke on motor functioning is analyzed at different levels. ‘Impairment’ denotes the loss of basic characteristics of voluntary movement. ‘Activity limitation’ denotes the loss of normal capacity for independent execution of daily activities. Recovery from impairment is accomplished by ‘restitution’ and recovery from activity limitation is accomplished by the combined effect of ‘restitution’ and ‘compensation.’ We aimed to unravel the long-term effects of variation in lesion topography on motor impairment of the hemiparetic lower limb (HLL), and gait (...) capacity as a measure of related activity limitation. Gait was assessed by the 3 m walk test (3MWT) in 67 first-event chronic stroke patients, at their homes. Enduring impairment of the HLL was assessed by the Fugl–Meyer Lower Extremity (FMA-LE) test. The impact of variation in lesion topography on HLL impairment and on walking was analyzed separately for left and right hemispheric damage (LHD, RHD) by voxel-based lesion-symptom mapping (VLSM). In the LHD group, HLL impairment tended to be affected by damage to the posterior limb of the internal capsule (PLIC). Walking capacity tended to be affected by a larger array of structures: PLIC and corona radiata, external capsule and caudate nucleus. In the RHD group, both HLL impairment and walking capacity were sensitive to damage in a much larger number of brain voxels. HLL impairment was affected by damage to the corona radiata, superior longitudinal fasciculus and insula. Walking was affected by damage to the same areas, plus the internal and external capsules, putamen, thalamus and parts of the perisylvian cortex. In both groups, voxel clusters have been found where damage affected FMA-LE and also 3MWT, along with voxels where damage affected only one of the measures (mainly 3MWT). In stroke, enduring ‘activity limitation’ is affected by damage to a much larger array of brain structures and voxels within specific structures, compared to enduring ‘impairment.’ Differences between the effects of left and right hemisphere damage are likely to reflect variation in motor-network organization and post-stroke re-organization related to hemispheric dominance. Further studies with larger sample size are required for the validation of these results. (shrink)

Falls are a leading cause of serious injury and restricted participation among persons with stroke (PwS). Reactive balance control is essential for fall prevention, however, only a few studies have explored the effects of lesion characteristics (location and extent) on balance control in PwS. We aimed to assess the impact of lesion characteristics on reactive and anticipatory balance capacity, gait, and hemiparetic lower limb function, in PwS. Forty-six subacute PwS were exposed to forward, backward, right and left unannounced horizontal surface (...) translations in 6 increasing intensities, while standing. Fall threshold (i.e., perturbation intensity that results in a fall into the harness system) was measured. In addition, the Berg Balance Scale (BBS), 6 Minute Walk Test (6MWT) and Lower Extremity Fugl-Meyer (LEFM) were measured. Lesion effects were analyzed separately for left- and right-hemisphere damaged (LHD, RHD) patients, using voxel-based lesion-symptom mapping (VLSM). Our results show that voxel clusters where damage exerted a significant impact on balance, gait and lower-limb function were found in the corticospinal tract, in its passage in the corona radiata and in the posterior limb of the internal capsule. Additional significant impact was found to lesions affecting the putamen and the external capsule. Balance, gait, and hemiparetic lower limb function showed much overlap of the corresponding ‘significant’ voxel clusters. Test scores of RHD and LHD patients were affected largely by damage to homologous regions, with the LHD group showing a wider distribution of ‘significant’ voxels. The study corroborates and extends previous findings by demonstrating that balance control, gait, and lower limb function are all affected mainly by damage to essentially the same brain structures, namely - the corticospinal tract and adjacent structures in the capsular-putaminal region. (shrink)

Data from published case and group studies bear on the trace deletion hypothesis. The deficit-lesion correlational literature does not support Grodzinsky's claim that lesions in and around Broca's area inevitably lead to comprehension deficits specifically related to coindexation of traces or his claim that other lesions spare this function.

A class of maize mutants, collectively known as disease lesion mimics, display discrete disease‐like symptoms in the absence of pathogens. It is intriguing that a majority of these lesion mimics behave as dominant gain‐of‐function mutations. The production of lesions is strongly influenced by light, temperature, developmental state and genetic background. Presently, the biological significance of this lesion mimicry is not clear, although suggestions have been made that they may represent defects in the plants' recognition of, or response to, pathogens. (...) One feature that is common to all lesion mimics is their association with cell death. In plants, as in animals, a number of developmental and pathological processes exist where controlled cell death, whether programmed or triggered in response to physiological or environmental stimuli, constitutes the normal aspect of life. Might disease lesion mimic mutations represent variants where regulation of desirable cell death has gone awry? In this paper we argue that this might be the case, and further conjecture that these mutants offer a unique opportunity for studying the genetic and cellular mechanisms of cell death in plants. (shrink)

A short discussion piece arguing that the neuropsychological phenomenon of double dissociations is most revealing of underlying cognitive architecture because of the capacities that are spared, more than the capacities that are lost.

Higher-order thought (HOT) theory says that a mental state is conscious when and only when represented by a conceptual, belief-like mental state. Plausibly, HOT theory predicts the impairment of HOT-producing brain areas to cause significant deficits in consciousness. This means that HOT theory can be refuted by identifying those brain areas that are candidates for producing HOTs, then showing that damage to these areas never produces the expected deficits of consciousness. Building this refutation is a work-in-progress, with several key components (...) of it already existing in the literature (e.g., Boly et al. in J Neurosci 37(40):9603–9613, 2017; Kozuch in Mind Lang, 37(5):790–813, 2022). This article pulls together and supplements these earlier components so as to provide a comprehensive lesion-based argument against HOT theory, one which offers extra data and arguments in support of it, and which also addresses common objections. (shrink)

As philosophers of mind we seem to hold in common no very clear view about the relevance that work in psychology or the neurosciences may or may not have to our own favourite questions—even if we call the subject ‘philosophical psychology’. For example, in the literature we find articles on pain some of which do, some of which don't, rely more or less heavily on, for example, the work of Melzack and Wall; the puzzle cases used so extensively in discussions (...) of personal identity are drawn sometimes from the pleasant exercise of scientific fantasy, at times from surprising reports of scientific fact; and there are those who deny, as well as those who affirm, the importance of the discovery of rapid-eye-movement sleep to the philosophical treatment of dreaming. A general account of the relation between scientific, and philosophical, psychology is long overdue and of the first importance. Here I shall limit myself to just one area where the two seem to connect, discussing one type of neuropsychological research and its relevance to questions in the philosophy of mind and the philosophy of psychology. (shrink)

PET studies using classical conditioning paradigms are reported. It is emphasized that PET studies show and not in learning paradigms. The importance of dissociating motor performance and learning deficits in human lesions studies is demonstrated in two exemplary studies. The different role of the cerebellum in adaptation of postural reflexes and learning of complex voluntary arm movements is discussed, [THACH].

Deep Brain Stimulation is currently being investigated as an experimental treatment for patients suffering from treatment-refractory AN, with an increasing number of case reports and small-scale trials published. Although still at an exploratory and experimental stage, initial results have been promising. Despite the risks associated with an invasive neurosurgical procedure and the long-term implantation of a foreign body, DBS has a number of advantageous features for patients with SE-AN. Stimulation can be fine-tuned to the specific needs of the particular patient, (...) is relatively reversible, and the technique also allows for the crucial issue of investigating and comparing the effects of different neural targets. However, at a time when DBS is emerging as a promising investigational treatment modality for AN, lesioning procedures in psychiatry are having a renaissance. Of concern it has been argued that the two kinds of interventions should instead be understood as rivaling, yet “mutually enriching paradigms” despite the fact that lesioning the brain is irreversible and there is no evidence base for an effective target in AN. We argue that lesioning procedures in AN are unethical at this stage of knowledge and seriously problematic for this patient group, for whom self-control is particularly central to wellbeing. They pose a greater risk of major harms that cannot justify ethical equipoise, despite the apparent superiority in reduced short term surgical harms and lower cost. (shrink)

The nuclear pore complex (NPC) is emerging as a center for recruitment of a class of “difficult to repair” lesions such as double‐strand breaks without a repair template and eroded telomeres in telomerase‐deficient cells. In addition to such pathological situations, a recent study by Su and colleagues shows that also physiological threats to genome integrity such as DNA secondary structure‐forming triplet repeat sequences relocalize to the NPC during DNA replication. Mutants that fail to reposition the triplet repeat locus to (...) the NPC cause repeat instability. Here, we review the types of DNA lesions that relocalize to the NPC, the putative mechanisms of relocalization, and the types of recombinational repair that are stimulated by the NPC, and present a model for NPC‐facilitated repair. (shrink)