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Prior studies have shown that patients suffering from chronic Low Back Pain (cLBP) have impaired somatosensory processing including reduced tactile acuity, i.e. reduced ability to resolve fine spatial details with the perception of touch. The central mechanism(s) underlying reduced tactile acuity are unknown but may include changes in specific brain circuitries (e.g. neuroplasticity in the primary somatosensory cortex, S1). Furthermore, little is known about the linkage between changes in tactile acuity and the amelioration of cLBP by somatically-directed therapeutic interventions, such as acupuncture. In this longitudinal neuroimaging study, we evaluated healthy control adults (HC, N ​= ​50) and a large sample of cLBP patients (N ​= ​102) with structural brain imaging (T1-weighted MRI for Voxel-Based Morphometry, VBM; Diffusion Tensor Imaging, DTI) and tactile acuity testing using two-point discrimination threshold (2PDT) over the lower back (site of pain) and finger (control) locations. Patients were evaluated at baseline and following a 4-week course of acupuncture, with patients randomized to either verum acupuncture, two different forms of sham acupuncture (designed with or without somatosensory afference), or no-intervention usual care control. At baseline, cLBP patients demonstrated reduced acuity (greater 2PDT, P ​= ​0.01) over the low back, but not finger (P ​= ​0.29) locations compared to HC, suggesting that chronic pain affects tactile acuity specifically at body regions encoding the experience of clinical pain. At baseline, Gray Matter Volume (GMV) was elevated and Fractional Anisotropy (FA) was reduced, respectively, in the S1-back region of cLBP patients compared to controls (P ​< ​0.05). GMV in cLBP correlated with greater 2PDT-back scores (ρ ​= ​0.27, P ​= ​0.02). Following verum acupuncture, tactile acuity over the back was improved (reduced 2PDT) and greater improvements were associated with reduced S1-back GMV (ρ ​= ​0.52, P ​= ​0.03) and increased S1-back adjacent white matter FA (ρ ​= ​−0.56, P ​= ​0.01). These associations were not seen for non-verum control interventions. Thus, S1 neuroplasticity in cLBP is linked with deficits in tactile acuity and, following acupuncture therapy, may represent early mechanistic changes in somatosensory processing that track with improved tactile acuity.

Objective: To evaluate the effects of individual or group mirror therapy on sensorimotor function, activities of daily living, quality of life and visuospatial neglect in patients with a severe arm paresis after stroke. Design: Randomized controlled trial. Setting: Inpatient rehabilitation centre. Subject: Sixty patients with a severe paresis of the arm within three months after stroke. Interventions: Three groups: (1) individual mirror therapy, (2) group mirror therapy and (3) control intervention with restricted view on the affected arm. Main measures: Motor function on impairment (Fugl-Meyer Test) and activity level (Action Research Arm Test), independence in activities of daily living (Barthel Index), quality of life (Stroke Impact Scale) and visuospatial neglect (Star Cancellation Test). Results: After five weeks, no significant group differences for motor function were found (P > 0.05). Pre–post differences for the Action Research Arm Test and Fugl-Meyer Test: individual mirror therapy: 3.4 (7.1) and 3.2 (3.8), group mirror therapy: 1.1 (3.1) and 5.1 (10.0) and control therapy: 2.8 (6.7) and 5.2 (8.7). However, a significant effect on visuospatial neglect for patients in the individual mirror therapy compared to control group could be shown (P < 0.01). Furthermore, it was possible to integrate a mirror therapy group intervention for severely affected patients after stroke. Conclusion: This study showed no effect on sensorimotor function of the arm, activities of daily living and quality of life of mirror therapy compared to a control intervention after stroke. However, a positive effect on visuospatial neglect was indicated.

A review of published brain-damaged patients showing delusional beliefs concerning the contralesional side of the body (somatoparaphrenia) is presented. Somatoparaphrenia has been reported, with a few exceptions, in right-brain-damaged patients, with motor and somatosensory deficits, and the syndrome of unilateral spatial neglect. Somatoparaphrenia, most often characterized by a delusion of disownership of left-sided body parts, may however occur without associated anosognosia for motor deficits, and personal neglect. Also somatosensory deficits may not be a core pathological mechanism of somatoparaphrenia, and visual field disorders may be absent. Deficits of proprioception, however, may play a relevant role. Somatoparaphrenia is often brought about by extensive right-sided lesions, but patients with posterior (parietal-temporal), and insular damage are on record, as well as a few patients with subcortical lesions. Possible pathological factors include a deranged representation of the body concerned with ownership, mainly right-hemisphere-based, and deficits of multisensory integration. Finally, the rubber hand illusion, that brings about a bodily misattribution in neurologically unimpaired participants, as somatoparaphrenia does in brain-damaged patients, is briefly discussed.

Lack of awareness of deficits, known as anosognosia, is a very impressive neuropsychiatric symptom of Alzheimer's disease (AD). It often appears in the early stages of the disease and worsens over time. According to our dual-path hypothesis, the occurrence of anosognosia in AD would depend on a critical failure of the error-monitoring system, reflecting either (i) local alterations in the cingulate cortex (direct pathway), with particular emphasis on its anterior and posterior parts (ACC and PCC, key brain regions at the origin of error-related potentials, ErrP); and/or (ii) an inability to link error-monitoring and emotional processing for adaptive behavior due to impairments in the latter system (indirect pathway), mainly affecting the orbitofrontal cortex (OFC) and the amygdala. This study focused on a subgroup of the longitudinal ADNI cohort characterized by 125 subjects who progressed from mild cognitive impairment, MCI, to AD. Our main goal was to investigate which brain structures and specific areas, without any a priori out of a total of 360, contributed the most to unawareness of deficits over time. The results show that self-awareness deterioration correlated with cortical thickness changes in specific areas of two brain structures: the OFC (area p32, right hemisphere, p <0.01, corrected; a25, left hemisphere, p = 0.051, corrected) and the ACC (area a24, left hemisphere, p = 0.051, corrected). These findings strongly support our dual-path model for the emergence of anosognosia in AD, bringing to the front the relevance of the indirect pathway, linking emotional processing to error-monitoring, in the self-awareness loop.

Anosognosia for hemiplegia (AHP) is known to be associated with lesions to the motor system combined with varying lesions to the right insula, premotor cortex, parietal lobe or hippocampus. Due to this widespread cortical lesion distribution, AHP can be understood best as a network disorder. We used lesion maps and behavioral data (n ​= ​49) from two previous studies on AHP and performed a lesion network-symptom-mapping (LNSM) analysis. This new approach permits the identification of relationships between behavior and regions connected to the lesion site based on normative functional connectome data. In a first step, using ordinary voxel-based lesion-symptom mapping, we found an association of AHP with lesions in the right posterior insula. This is in accordance with previous studies. Applying LNSM, we were able to additionally identify a region in the right posterior hippocampus where AHP was associated with significantly higher normative lesion connectivity. Notably, this region was spared by infarction in all patients. We therefore argue that remote neuronal dysfunction caused by disrupted functional connections between the lesion site and the hippocampus (i.e. diaschisis) contributed to the phenotype of AHP. An indirect affection of the hippocampus may lead to memory deficits which, in turn, impair the stable encoding of updated beliefs on the bodily state thus contributing to the multifactorial phenomenon of AHP. •In VLSM, right insular lesions are associated with anosognosia for hemiplegia (AHP).•Lesion-network symptom-mapping can locate remote dysfunction after brain lesions.•In LNSM, higher lesion connectivity of the right hippocampus is associated with AHP.•Thus direct and indirect (e.g. diaschisis) lesion effects contribute to AHP.

Optic Aphasia (OA) and Associative Visual Agnosia (AVA) are neuropsychological disorders characterized by impaired naming on visual presentation. From a cognitive point of view, while stimulus identification is largely unimpaired in OA (where access to semantic knowledge is still possible), in AVA it is not. OA has been linked with right hemianopia and disconnection of the occipital right-hemisphere (RH) visual processing from the left hemisphere (LH) language areas. In this paper, we describe the case of AA, an 81-year-old housewife suffering from a deficit in naming visually presented stimuli after left occipital lesion and damage to the interhemispheric splenial pathway. AA has been tested through a set of tasks assessing different levels of visual object processing. We discuss behavioral performance as well as the pattern of lesion and disconnection in relation to a neurocognitive model adapted from Luzzatti and colleagues ( 1998 ). Despite the complexity of the neuropsychological picture, behavioral data suggest that semantic access from visual input is possible, while a lesion-based structural disconnectome investigation demonstrated the splenial involvement. Altogether, neuropsychological and neuroanatomical findings support the assumption of visuo-verbal callosal disconnection compatible with a diagnosis of OA.

Anosognosia, defined as a lack of knowledge of the disease, was originally identified in neurological disorders and is common in schizophrenia. These deficits are commonly referred to as “lack of insight” or “unawareness of illness.” They include challenges in accurate judgments of the reality of experience, as well as global and specific personal abilities. Related to inaccuracies in self-assessment are response biases when an incorrect self-assessment is made. We adopted a perspective focused on Introspective Accuracy (IA) and Introspective Bias (IB). IA is the ability to accurately judge several domains of experience and functioning. These include the reality of clinical symptoms, the experience of mood states, momentary competence in the performance of cognitive assessments and everyday functional skills, and the ability to accurately anticipate the success of future performance. IB is the direction of response bias in the context of impairments in IA. Deficits in insight, judgment inaccuracies, and response bias are highly relevant as these difficulties come with downstream impacts including difficulties with treatment adherence, an increase in severity of symptoms, greater everyday disability, reduced response to cognitive training interventions, and a need for increased intensity of interventions to maintain community residence. In this article, we review the research in IA and IB in schizophrenia, including differences in momentary versus global self-assessments, and the clinical correlates and functional impacts of inaccurate self-assessments and response biases in the context of self-assessment errors. We also examine the existing data regarding the neurobiological basis of impairments in IA.

Stereoscopic depth perception requires considerable neural computation, including the initial correspondence of the two retinal images, comparison across the local regions of the visual field and integration with other cues to depth. The most common cause for loss of stereoscopic vision is amblyopia, in which one eye has failed to form an adequate input to the visual cortex, usually due to strabismus (deviating eye) or anisometropia. However, the significant cortical processing required to produce the percept of depth means that, even when the retinal input is intact from both eyes, brain damage or dysfunction can interfere with stereoscopic vision. In this review, I examine the evidence for impairment of binocular vision and depth perception that can result from insults to the brain, including both discrete damage, temporal lobectomy and more systemic diseases such as posterior cortical atrophy. This article is part of the themed issue ‘Vision in our three-dimensional world’.

While Cognitive impairment (CI) has been identified as an independent risk factors for mortality in patients undergoing peritoneal dialysis (PD), it is inadequately assessed. We evaluated the applicability of the Modified Mini-Mental State Examination (3MS) in assessing specific cognitive function and compared it to a detailed neuropsychological test battery as the reference standard. In this multicentric cross-sectional study, we enrolled 445 clinically stable patients from five PD units, who were undergoing PD for at least 3 months. The 3MS was evaluated for general cognitive function. A detailed neuropsychological battery including domains of immediate memory, delayed memory, executive function, language, and visuospatial ability were evaluated as reference standards. Sensitivity and specificity of the 3MS was determined by using receiver operating characteristic (ROC) analysis. The CI prevalence evaluated by 3MS was 23.6%. PD patients with CI performed worse in all cognitive domains. The 3MS correlated well with specific cognitive domains. However, 18.5%, 57.4%, 12.6%, 8.8%, and 41.2% of patients whom were idendified as normal by 3MS still showed executive dysfunction, immediate memory impairment, delayed memory impairment, and language-ability and visuospatial-ability impairment, respectively. The 3MS identified patients having specific cognitive dysfunction with varied extent of diagnostic value, with 0.50, 0.42, 0.35, 0.34, and 0.26 of Youden index in executive function, delayed memory, language ability, immediate memory, and visuospatial ability, respectively. The 3MS is not a comprehensive instrument for major cognitive domains in PD patients. It could, however, be used for executive dysfunction and delayed memory impairment screening.

This review explores the relationships between depression, apathy, and anosognosia in Alzheimer's disease. Depressed mood is found to be associated with less anosognosia, while greater apathy is associated with more anosognosia, and the contrasting reasons for these associations are discussed. The review also describes recent research findings indicating a dissociation between impaired awareness of condition/deficit and preserved emotional reactivity in response to illness-related material or the experience of failure in tests. We conclude by pointing to future directions for this area of research and clinical implications. (JINS, 2014, 20, 2–7)