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Heart rate variability (HRV) refers to variation in the interval between successive heart beats. Low HRV is an indicator of potential autonomic nervous system dysfunction. People with chronic pain often display autonomic dysregulation, especially in the parasympathetic nervous system. The hormone oxytocin has been shown to increase HRV in non-clinical samples, but its potential impact on HRV in persons with chronic pain is unknown. This study investigated the impact of intranasal oxytocin on HRV in persons with chronic neck and shoulder pain. Participants included 24 individuals with chronic neck and shoulder pain lasting > 12 months and 24 age- and sex-matched pain-free controls. In a randomised double-blind, placebo-controlled, cross-over study, participants self-administered intranasal oxytocin (24 IU) in one session, and placebo in another, before HRV was recorded at rest and during a mental arithmetic task. Intranasal oxytocin did not influence HRV at rest. However, compared to placebo, intranasal oxytocin elicited small decreases in low-frequency and high-frequency HRV in both groups during the mental arithmetic task. These results suggest that intranasal oxytocin may enhance the salience of the mental arithmetic task, leading to reduced engagement of the parasympathetic nervous system when completing the task. Further investigation and replication of these findings are required to improve our understanding of the effects of intranasal oxytocin on autonomic functioning both at rest and under cognitive stress. [ABSTRACT FROM AUTHOR]

Lower limb spasticity compromises the independence of people with Friedreich’s ataxia (FRDA). This study sought to examine lower limb spasticity in FRDA in order to offer new insight as to the best approach and timing of spasticity management. Gastrocnemius and soleus spasticity and muscle length were measured by the Modified Tardieu Scale (MTS) in 31 participants with typical and late-onset FRDA. Relationships between the MTS and the Friedreich Ataxia Rating Scale (FARS), Functional Independence Measure (FIM), and disease duration were analysed. Differences between ambulant (n = 18) and non-ambulant (n = 13) participants were also examined. All participants had spasticity in at least one muscle, and 38.9% of ambulant and 69.2% of non-ambulant participants had contracture in one or both of their gastrocnemius muscles. Significant negative correlations were found between both gastrocnemius and soleus angle of catch and the FARS score. The FIM score also demonstrated significant correlations with gastrocnemius muscle length and angle of catch. Gastrocnemius and soleus spasticity and contracture is apparent in people with FRDA. Spasticity is evident early in the disease and in ambulant participants. Management of spasticity and reduced muscle length should be considered in people with FRDA at disease onset to optimise function. [ABSTRACT FROM AUTHOR]

In an acute environment pain has potential protective benefits. However when pain becomes chronic this protective effect is lost and the pain becomes an encumbrance. Previously unheralded substances are being investigated in an attempt to alleviate the burden of living with chronic pain. Oxytocin, a neuropeptide hormone, is one prospective pharmacotherapeutic agent gaining popularity. Oxytocin has the potential to modulate the pain experience due to its ubiquitous involvement in central and peripheral psychological and physiological processes, and thus offers promise as a therapeutic agent. In this review, we discuss previous effective applications of oxytocin in pain-free clinical populations and its potential use in the modulation of pain experience. We also address the slowly growing body of literature investigating the administration of oxytocin in clinical and experimentally induced pain in order to investigate the potential mechanisms of its reported analgesic actions. We conclude that oxytocin offers a potential novel avenue for modulating the experience of pain, and that further research into this area is required to map its therapeutic benefit. [ABSTRACT FROM AUTHOR]

Abstract: Huntington''s disease (HD) results in progressive impairment of motor and cognitive function and neuropsychiatric disturbance. There are no disease-modifying treatments available, but HD research is entering a critical phase where promising disease-specific therapies are on the horizon. Thus, a pressing need exists for biomarkers capable of monitoring progression and ultimately determining drug efficacy. Neuroimaging provides a powerful tool for assessing disease progression. However, in order to be accepted as biomarkers for clinical trials, imaging measures must be reproducible, robust to scanner differences, sensitive to disease-related change and demonstrate a relationship to clinically meaningful measures. We provide a review of the current structural imaging literature in HD and highlight inconsistencies between studies. We make recommendations for the standardisation of reporting for future studies, such as appropriate cohort characterisation and documentation of methodologies to facilitate comparisons and inform trial design. We also argue for an intensified effort to consider issues highlighted here so that we have the best chance of assessing the efficacy of the therapeutic benefit in forestalling this devastating disease. [Copyright &y& Elsevier]

Abstract: Deficits in cortical inhibition (CI) have been implicated in the pathophysiology of schizophrenia, including decreased transcallosal inhibition (TCI). A closely related phenomenon, which has not yet been studied in schizophrenia, is transcallosal facilitation (TCF). TCI and TCF are thought to maintain a complimentary existence, allowing for the performance of tasks such as unilateral voluntary movement. Therefore, deficient TCI may lead to abnormal expression of TCF. This study aims to confirm the presence of TCI deficits in schizophrenia, and to examine TCF. Thirty consenting participants took part in the study (15 with schizophrenia and 15 healthy controls), although not all were able to complete all aspects of the study. TCI and TCF were measured using dual-pulse transcranial magnetic stimulation methodologies. Patients with schizophrenia exhibited significantly less TCI than controls; there was no difference in TCF, however. The lack of significant TCF findings is discussed in light of the methodological limitations, while the theoretical significance of deficient TCI to the pathophysiology of schizophrenia is considered. [Copyright &y& Elsevier]

Abstract: Cognitive deficits in Huntington''s disease (HD) have been attributed to neuronal degeneration within the striatum; however, postmortem and structural imaging studies have revealed more widespread morphological changes. To examine the impact of HD-related changes in regions outside the striatum, we used functional magnetic resonance imaging (fMRI) in HD to examine brain activation patterns using a Simon task that required a button press response to either congruent or incongruent arrow stimuli. Twenty mild to moderate stage HD patients and 17 healthy controls were scanned using a 3T GE scanner. Data analysis involved the use of statistical parametric mapping software with a random effects analysis model to investigate group differences brain activation patterns compared to baseline. HD patients recruited frontal and parietal cortical regions to perform the task, and also showed significantly greater activation, compared to controls, in the caudal anterior cingulate, insula, inferior parietal lobules, superior temporal gyrus bilaterally, right inferior frontal gyrus, right precuneus/superior parietal lobule, left precentral gyrus, and left dorsal premotor cortex. The significantly increased activation in anterior cingulate–frontal–motor–parietal cortex in HD may represent a primary dysfunction due to direct cell loss or damage in cortical regions, and/or a secondary compensatory mechanism of increased cortical recruitment due to primary striatal deficits. [Copyright &y& Elsevier]

Abstract: Motor disturbances in major depressive disorder (MDD) are increasingly recognized and may differentiate melancholic, from non-melancholic depression. Motor impairments in melancholic depression have been likened to Parkinson''s disease and proposed to have a frontostriatal basis. This study investigated self-pacing and reprogramming skills, thought to rely on frontostriatal functioning, in groups of healthy individuals (n =15), non-melancholic depression patients (n =10) and melancholic depression patients (n =9) using ocular motor tasks. Self-paced saccades were requested to be performed at a rhythm of 1Hz between two continuously illuminated targets, before and after external cueing. Saccade reprogramming, for direction and amplitude, was explored using a saccadic “oddball” task. Results indicated no group differences for accuracy, intersaccadic intervals (during the self-paced task), latency or peak velocity. However, the melancholic group showed greater intrasubject variability of latencies than the control group, lower peak saccade velocities compared to the non-melancholic group, and reduced accuracy of the primary saccade when compared to the control and the non-melancholic groups. These findings provide further support for distinct motor impairments associated with melancholia that may reflect frontostriatal abnormalities. [Copyright &y& Elsevier]

Abstract: There is limited documentation regarding cognitive function in individuals with Friedreich ataxia (FRDA), possibly because FRDA is widely held to predominantly affect the spinal cord, peripheral sensory nerves and cerebellum and not to affect cognition. Traditionally, the cerebellum has been thought to coordinate voluntary movement and motor tone, posture and gait. However, recent studies have implicated the cerebellum in a range of cognitive functions including executive function, visuospatial organisation and memory. We review the available data on cognitive function and neuroimaging in FRDA and the role of the cerebellum in cognitive function. We conclude with recommendations for future research including correlating cognitive function in individuals with FRDA with possible determinants of disease severity, such as age of onset and the causative genetic mutation. [Copyright &y& Elsevier]

Abstract: A predictive central-cueing paradigm was used to compare visuospatial deficits in patients with Parkinson''s (PD) and Huntington''s diseases (HD), employing directionally valid and invalid visual cues over a range of stimulus onset asynchronies (SOA) to elicit a saccadic response. Compared to age-matched control groups, both PD and HD patients responded erroneously to cue stimuli more frequently, increasing significantly over longer SOAs. Both valid and invalid cues resulted in elevated latencies compared to un-cued visually guided saccades, the associated ‘cost’ of invalid cueing significantly greater than that for valid cueing, over all SOAs. Unlike control subjects, PD and HD patients demonstrated temporal variation with cue presentation. For PD patients, latencies following directionally invalid cues were significantly longer for intermediate SOAs, suggesting difficulty overcoming a build-up of inhibitory activity over time. No validity effect was found at 1000ms. For HD patients, latencies for validly cued saccades with 150ms SOAs were shorter than latencies for no-cue trials, representing a ‘benefit’ of valid cueing. For 500ms SOAs latencies were comparably elevated following directionally valid and invalid cues, and for 1000ms SOAs neither cue condition resulted in increased latencies. These findings reflect the consequence of disruption to the balance of activity over the basal ganglia facilitatory and inhibitory pathways. Imbalance in PD resulted in difficulty sustaining goal-directed behaviour, and in HD, difficulty gating inappropriate behaviour. [Copyright &y& Elsevier]

Presymptomatic individuals carrying the gene for Huntington’s disease (HD) provide researchers with a unique opportunity of learning more about the neuropathophysiology, symptom onset, behavioural functioning, and mediating factors of this fatal disease. In this review, we attempt to demonstrate that research over the last 8 years, since the isolation of the gene, has remained at large controversial. Although we are aware of some of the factors that can influence age at onset and disease progression, we are still unable to determine exactly when an individual will develop HD symptoms, and how fast these symptoms will progress. In an era rapidly advancing with respect to therapeutic intervention that could forestall the onset and progression of HD, systematic research with improved inclusion criteria is paramount. A greater understanding of the time course of the disease would be beneficial not only in monitoring the effectiveness of future treatments, but also in determining the most appropriate time to administer them. Finally, we present various ethical considerations, as well as put forward various recommendations that could assist in better diagnosing preclinical deficits in presymptomatic individuals. [Copyright &y& Elsevier]

Friedreich ataxia (FRDA) is an inherited degenerative disorder affecting multiple systems of the body and resulting in symptoms which include progressive ataxia, dysarthria, and cardiomyopathy. Central nervous system pathology has been traditionally ascribed to the spinal cord and dentate nucleus of the cerebellum. However, cerebral abnormalities in FRDA are being increasingly documented via multiple neuroimaging techniques. Understanding the nature and implications of cerebral abnormalities in FRDA provides more comprehensive knowledge of nervous system involvement in this disorder and increases the prospects of identifying effective treatment targets. We review the cerebellar and the cerebral involvement with a focus on the emerging in vivo human neuroimaging findings suggesting wide-spread cerebral involvement, including aberrant cerebellar-cerebral connectivity. We synthesise the findings by proposing potential mechanisms that may drive these effects. Finally, we identify future research directions which, we argue, will lead to a better understanding of the extent and potential mechanisms of cerebral aberrations in FRDA. [ABSTRACT FROM AUTHOR]

Chronic neck and shoulder pain (CNSP) is a common musculoskeletal disorder in adults, which is linked to hypersensitivity to noxious stimuli. The hormone oxytocin has been implicated as a potential therapeutic for the management of chronic pain disorders, and has been suggested to have sex-specific effects on the salience of threatening stimuli. This study investigated the influence of intranasal oxytocin on the perception of noxious thermal stimuli. Participants were 24 individuals with CNSP lasting >12 months (eight women), and 24 age- and sex-matched healthy, pain-free controls. In a randomised double-blind, placebo-controlled, cross-over study, participants attended two sessions, self-administering intranasal oxytocin (24 IU) in one session, and placebo in another. Participants rated intensity and unpleasantness of thermal heat stimuli at three body sites: the cervical spine, deltoid, and tibialis anterior, on 11-point numerical rating scales. Compared with placebo, intranasal oxytocin increased the perceived intensity of noxious heat stimuli in women with CNSP (Cohen’s d = 0.71), but not in men with CNSP, or healthy, pain-free controls. Men and women displayed divergent sensitivity across target sites for ratings of pain intensity (partial eta squared = 0.12) and pain unpleasantness (partial eta squared = 0.24), irrespective of drug condition. Men were more sensitive at the cervical spine and deltoid, whereas women were more sensitive at the tibialis. These findings suggest that oxytocin and endogenous sex hormones may interact to influence the salience of noxious stimuli. The hyperalgesic effects of oxytocin in women suggest that caution should be taken when considering oxytocin in the management of chronic pain. Trial Registration: CT-2016-CTN-01313-1; ACTRN12616000532404 [ABSTRACT FROM AUTHOR]

Abstract: This paper reviews the current literature on “empathy for pain”, the ability to understand pain observed in another person, in the context of a newly documented form of pain empathy “synaesthesia for pain”. In synaesthesia for pain a person not only empathises with another''s pain but experiences the observed or imagined pain as if it was their own. Neural mechanisms potentially involved in synaesthesia for pain include “mirror systems”: neural systems active both when observing an action, or experiencing an emotion or sensation and when executing the same action, or personally experiencing the same emotion or sensation. For example, we may know that someone is in pain in part because observation activates similar neural networks as if we were experiencing that pain ourselves. We propose that synaesthesia for pain may be the result of painful and/or traumatic experiences causing disinhibition in the mirror system underlying empathy for pain. We will discuss this theory in the context of a documented group of amputees who experience synaesthesia for pain in phantom limbs. [Copyright &y& Elsevier]

Abstract: Bodily experience is a complex, mostly unconscious, process that requires the integration of multiple sensory inputs. This paper reviews the sensory systems involved in internal representations of the body—primarily the proprioceptive, motor, vestibular, and visual systems. Various neurological disorders are defined by aberrations in bodily experience—including the perceptual ablation or disembodiment of body parts, “filling in” of amputated body parts, or reduplication of body parts. These perceptual aberrations are discussed and their implications for the central and peripheral systems involved in updating and retrieving internal representations of the body are highlighted. Bodily perception and egocentric frames of reference can be experimentally manipulated through visual capture (e.g., using rubber limbs), functional adaptation and embodiment of tools and prostheses, and changes in afferent sensory feedback (e.g., through stimulation of muscle spindles). These perceptual illusions are described, and discussed for their implications for the mechanisms underlying bodily perception. [Copyright &y& Elsevier]

Abstract: The negative symptoms of schizophrenia are perhaps the most unremitting and burdensome features of the disorder. Negative symptoms have been associated with distinct motor, cognitive and neuropathological impairments, possibly stemming from prefrontal dysfunction. Eye movement paradigms can be used to investigate basic sensorimotor functions, as well as higher order cognitive aspects of motor control such as inhibition and spatial working memory — functions subserved by the prefrontal cortex. This study investigated inhibitory control and spatial working memory in the saccadic system of 21 patients with schizophrenia (10 with high negative symptoms scores and 11 with low negative symptom scores) and 14 healthy controls. Tasks explored suppression of reflexive saccades during qualitatively different tasks, the generation of express and anticipatory saccades, and the ability to respond to occasional, unpredictable (“oddball”) targets that occurred during a sequence of well-learned, reciprocating saccades between horizontal targets. Spatial working memory was assessed using a single and a two-step memory-guided task (involving a visually-guided saccade during the delay period). Results indicated significant increases in response suppression errors, as well as increased response selection impairments, during the oddball task, in schizophrenia patients with prominent negative symptoms. The variability of memory-guided saccade accuracy was also increased in patients with prominent negative symptom scores. Collectively, these findings provide further support for the proposed association between prefrontal dysfunction and negative symptoms. [Copyright &y& Elsevier]

The ‘reserve’ hypothesis posits that the brain undergoes structural and functional reorganisation to actively cope with brain damage or disease. Consistent with passive and active components of ‘reserve’, the brain moderates its biological substrates ( brain reserve ) and differentially changes the level of neural activity in tasks-specific networks and/or by recruiting additional non-task related brain regions ( cognitive reserve ) to optimise behavioural performance. How the ‘reserve’ hypothesis applies in neurodegenerative disorders such as Huntington’s disease (HD) remains unknown. We postulate that unless the ‘reserve’ hypothesis is tested empirically, it is impossible to draw firm conclusions about how task-related neural activity is providing a neuroplastic change in HD and possibly other neurodegenerative disorders. We conclude that there is a pressing need to operationalise cognitive reserve, as well as incorporate different biological substrates into a model of ‘reserve’. We suggest that it is important to identify and embed potential neuroprotective modulating factors of ‘reserve’ in randomised controlled multi-domain non-pharmaceutical interventions to potentially enhance ‘reserve’ and thus preserve cognitive and psychosocial functioning in HD patients. [ABSTRACT FROM AUTHOR]

People with Huntington's disease (HD) exhibit altered processing of emotional information, especially disgust and other negative emotions. These impairments are likely due to the effects of the disease on underlying brain networks. We examined whether oxytocin, when given intranasally, would normalise aberrant brain reactivity to emotional faces in participants with the gene-expansion for HD. In a double-blind placebo-controlled cross-over design, we measured brain activity, using functional magnetic resonance imaging, whilst nine medication-free HD carriers, and ten control participants viewed emotional (disgust, fear, angry, sad, surprise, happy) and neutral faces, following acute intranasal oxytocin (24 IU) and placebo. Subjective mood changes were assessed before and after the neuroimaging on each visit. Permutation-based non-parametric statistical testing for the whole brain, showed significant group × drug interactions ( p 's < 0.05, TFCE corrected) in areas of the left frontal pole, superior frontal, and middle frontal gyri cortically, and left putamen and thalamus sub-cortically. Parameter estimates extracted from the middle frontal gyrus and putamen showed that, under placebo, the HD group had lower brain activity to disgust stimuli, compared with controls. After intranasal oxytocin, the pattern of activation to disgust stimuli was normalised in the HD group to similar levels as controls; eight of the nine HD carriers showed increased response in the middle frontal gyrus, and seven of the nine HD carriers showed increased response in the putamen. The observed effects of oxytocin occurred in the absence of changes in subjective mood or state anxiety. These findings provide early evidence for a physiological role of oxytocin in the neuropathology of HD. Our findings are the first reported oxytocin effects in a neurodegenerative disease. Further research should examine the therapeutic benefits of oxytocin in alleviating emotional and social cognition deficits in HD and related disorders. [ABSTRACT FROM AUTHOR]

Recent evidence indicates that adults with a premutation (PM: 55–199 CGG repeats) expansion in the fragile X mental retardation 1 ( FMR1 ) gene show postural control deficits that may reflect disruption to cerebellar motor regions. Less is known about the influence of reduced cerebellar volume and structural changes, and increase in CGG repeat and FMR1 mRNA levels on the attentional demands of step initiation in PM males. We investigated the effects of a concurrent cognitive task on choice stepping reaction time (CSRT) and explored the associations between CSRT performance, cerebellar volume, CGG size, and FMR1 mRNA levels in blood in PM males. We examined 19 PM males (ages 28–75) and 23 matched controls (CGG <44; ages 26–77), who performed a verbal fluency task during CSRT performance and single-task stepping without a secondary cognitive task. Our results provide preliminary evidence that smaller cerebellar volume (β = −2.73, p = 0.002) and increasing CGG repeat length (β = 1.69, p = 0.003) were associated with greater dual-task step initiation times in PM males, but not in controls. There was evidence of a mediating effect of cerebellar volume on the relationship between FMR1 mRNA levels and single-task CSRT performance in PM males (estimate coefficient = 8.69, standard error = 4.42, p = 0.049). These findings suggest increasing CGG repeat and FMR1 mRNA levels have neurotoxic effects on cerebellar regions underlying anticipatory postural responses during stepping. Cerebellar postural changes may be predictive of the increased risk of falls in older PM males. [ABSTRACT FROM AUTHOR]

Huntington's disease (HD) affects GABA-mediated inhibitory circuitry in the cortex. As there is evidence that sex hormones affect GABAergic function, we investigated whether gender modulates GABA-related pathophysiological changes in HD. Fifteen premanifest HD, 11 symptomatic HD and 16 healthy control participants were assessed with paired-pulse transcranial magnetic stimulation applied to the primary motor cortex. Cortical inhibition was significantly reduced in symptomatic HD, compared with premanifest HD and controls. There was reduced inhibition in females overall, but no Group-by-Sex interaction. These findings suggest that sex hormones do not exert a direct influence on the mechanisms underpinning cortical inhibitory deficits in HD. [ABSTRACT FROM AUTHOR]

Abstract: Recent studies report a higher risk of dementia and motor symptoms in females with the fragile X mental retardation 1 premutation (PM-carriers) than has hitherto been appreciated. Here, we use dual-task gait paradigms to identify potential markers of cognitive and motor decline in female PM-carriers. Spatiotemporal gait characteristics and variability of gait were assessed during single- and dual-task conditions in 28 female PM-carriers (mean age 41.32 ± 8.03 years) and 31 female controls with normal fragile X mental retardation 1 alleles (mean age 41.61 ± 8.30 years). Despite comparable gait characteristics at baseline, gait performance was significantly poorer for PM-carriers when performing concurrent working memory tasks (counting backwards by 3′s or 7′s) when compared with controls. Correlational analyses showed that low working memory capacity was significantly associated with dual-task interference for the gait domains of pace (speed, step length) and variability (step time, swing time) in PM-carriers. Multiple regression analyses further showed that the interaction between age and CGG repeat length was strongly predictive of gait variability during dual-task performance. These findings indicate for the first time that vulnerability in specific domains of gait control may act as sensitive surrogate markers of future decline in female PM-carriers. [Copyright &y& Elsevier]

Highlights: [•] Neuroimaging tools have been critical for understanding pre- and symptomatic HD. [•] The relationship between pathophysiology and phenotype in HD is poorly understood. [•] TMS can inform causal relationships between neural circuitry and behaviour. [•] TMS–EEG can assess the integrity of neural networks in non-motor brain areas. [•] Neurophysiological measures may prove sensitive markers of progression in HD. [ABSTRACT FROM AUTHOR]

Abstract: For years, premutation-carriers of fragile X-syndrome (FXS) were assumed free from any deleterious phenotype. In this review, we discuss the current literature on neurocognitive, emotional and neuromotor profiles emerging in females with the fragile-X premutation, and discuss phenotypic profiles in male premutation-carriers to gain insights into possible underlying mechanisms associated with FMR1 gene expression. We contend that this emerging phenotypic profile in females with the fragile-X premutation needs further investigation using experimentally-driven tasks sensitive to neural networks especially vulnerable to FMR1 gene expression. Further investigation of developmental aspects of the female carrier profile is needed to determine the extent to which emotional, cognitive and neurobehavioural challenges indicate at-risk profiles for later degenerative decline, or rather a stable developmental phenotype. These future research avenues will provide critical new information which will enable identification of women at greatest risk for subtle age-dependent neurobehavioural changes well before the onset of more serious clinical consequences alongside the identification of biomarkers which may be useful in establishing the efficacy of future therapeutic interventions. [Copyright &y& Elsevier]

Abstract: ‘Mirror pain’ describes when the observation of another''s pain experience induces a personal experience of pain. It has been suggested that mirror pain could result from changes in neural excitability or inhibition. In this study we used transcranial magnetic stimulation (TMS) to investigate motor cortical excitability in lower-limb amputees who experience mirror pain. Using paired-pulse TMS to assess motor cortical inhibition (CI) and cortical facilitation (CF), recordings were taken from the right first dorsal interosseus in lower-limb amputees who experience mirror pain (MP+), lower-limb amputees who do not experience mirror pain (MP−), and non-amputee controls. No differences in CI or CF were observed between the MP+ and both control groups. Thus, when not paired with a pain-related stimulus, changes in motor cortical excitability do not appear to contribute to the experience of mirror pain in lower-limb amputees. [Copyright &y& Elsevier]

Abstract: Recent research suggests the observation or imagination of somatosensory stimulation in another (e.g., touch or pain) can induce a similar somatosensory experience in oneself. Some researchers have presented this experience as a type of synaesthesia, whereas others consider it an extreme experience of an otherwise normal perception. Here, we present an argument that these descriptions are not mutually exclusive. They may describe the extreme version of the normal process of understanding somatosensation in others. It becomes synaesthesia, however, when this process results in a conscious experience comparable to the observed person''s state. We describe these experiences as ‘mirror-sensory synaesthesia’; a type of synaesthesia identified by its distinct social component where the induced synaesthetic experience is a similar sensory experience to that perceived in another person. Through the operationalisation of this intriguing experience as synaesthesia, existing neurobiological models of synaesthesia can be used as a framework to explore how mechanisms may act upon social cognitive processes to produce conscious experiences similar to another person''s observed state. [Copyright &y& Elsevier]

Abstract: Synaesthesia for pain is a phenomenon where a person experiences pain when observing or imagining another in pain. Anecdotal reports of this type of experience have most commonly occurred in individuals who have lost a limb. Distinct from phantom pain, synaesthesia for pain is triggered specifically in response to pain in another. Here, we provide the first preliminary investigation into synaesthesia for pain in amputees to determine the incidence and characteristics of this intriguing phenomenon. Self-referring amputees (n =74) answered questions on synaesthesia for pain within a broader survey of phantom pain. Of the participants, 16.2% reported that observing or imagining pain in another person triggers their phantom pain. Further understanding of synaesthesia for pain may provide a greater insight to abnormal empathic function in clinical populations as well as therapeutic intervention for at risk groups. [ABSTRACT FROM AUTHOR]

Abstract: Guidelines for assessing fitness to drive in individuals with neurodegenerative disorders, such as Parkinson''s disease (PD), are subjective. It is therefore timely to review the current status of the literature not only for health professionals who are required to assess fitness to drive, but also for the development of future research directions. This review, in the context of PD, outlines the complex changes in driving behaviours, motor vehicle crash rates, driving simulator and on-road driving ability assessments, the relationship between disease severity, duration, medication dose and driving performance, the relationship between driving and neuropsychological test performance, and the effect of dopaminergic medications on driving. While it provides a current overview of the ongoing research, more comprehensive research is required for the full and proper development of policies and guidelines for assessing fitness to drive in PD. [Copyright &y& Elsevier]

The occurrence of motor dysfunction as a sign of schizophrenia, in addition to being a side effect of medication, has received considerable support in recent years. The current study aimed to systematically investigate both the presence and pattern of one such motor dysfunction, motor overflow. It was hypothesised that patients with schizophrenia would show significantly greater motor overflow than controls, and that the pattern of motor overflow occurrence would also vary significantly between the groups. A finger flexion task was used to examine the presence and pattern of motor overflow. Subjects were asked to maintain target forces, using either their index or small finger, representing 25, 50 or 75% of the maximum strength capacity for whichever finger was performing the task. Patients were found to exhibit significantly greater motor overflow than controls. There were also significant findings with respect to the patterns of motor overflow produced, specifically in regards to fine motor control and performance variability. In summary, patients differed significantly from controls in both the degree and pattern of overflow exhibited. [Copyright &y& Elsevier]