Reiner Sprengelmeyer

Facial expression recognition across the adult life span

We report three experiments investigating the recognition of emotion from facial expressions across the adult life span. Increasing age produced a progressive reduction in the recognition of fear and, to a lesser extent, anger. In contrast, older participants showed no reduction in recognition of disgust, rather there was some evidence of an improvement. The results are discussed in terms of studies from the neuropsychological and functional imaging literature that indicate that separate brain regions may underlie the emotions fear and disgust. We suggest that the dissociable effects found for fear and disgust are consistent with the differential effects of ageing on brain regions involved in these emotions.

S-100 Protein: Serum Marker of Focal Brain Damage After Ischemic Territorial MCA Infarction

BACKGROUND AND PURPOSE Elevations of protein S-100 (S-100) in cerebrospinal fluid and serum have been reported after cerebral infarctions. The aim of our study was to evaluate the time course of serum S-100 concentrations after territorial middle cerebral artery (MCA) infarctions in correlation with clinical data and prognosis. METHODS S-100 serum levels were serially determined in 26 patients with an acute infarction in the territory of the MCA at day 0 (within 12 hours after onset of symptoms), day 1 (24 hours after stroke onset), and days 2, 3, 4, 5, 7 or 8, and 10 after stroke and in 26 age- and sex-matched control subjects. S-100 assays were performed using a two-site radioimmunoassay technique. The clinical status was documented using the Scandinavian Stroke Scale. The functional deficit 4 weeks after stroke onset was scored by use of the modified Rankin scale. A cranial computed tomography (CCT) was performed initially and at day 4 or 5. RESULTS Elevated concentrations of S-100 (> 0.2 microgram/L) were observed in 21 of 26 patients with MCA infarction but in none of the control subjects. S-100 levels peaked at days 2 and 3 after stroke. The S-100 concentrations in serum were significantly higher in patients with severe neurological deficits at admission, with extensive infarctions and a space-occupying effect of ischemic edema as compared with the rest of the population. S-100 values were not significantly correlated with the functional prognosis. CONCLUSIONS Presence of S-100 in serum after ischemic stroke may be due to combined leakage out of necrotic glial cells and passage through an impaired brain-blood barrier, indicating severe ischemic cell injury. Therefore, S-100 in serum can be used as a peripheral marker of ischemic focal brain damage and may be helpful for therapeutic decisions in acute ischemic stroke.

Facial expression recognition in people with medicated and unmedicated Parkinson's disease.

Recognition of facial expressions of emotion was investigated in people with medicated and unmedicated Parkinsons disease (PD) and matched controls (unmedicated PD, n=16; medicated PD, n=20; controls, n=40). Participants in the medicated group showed some visual impairment (impaired contrast sensitivity) and performed less well on perception of unfamiliar face identity, but did not show significant deficits in the perception of sex, gaze direction, or familiar identity from the face. For both Parkinsons disease groups, there was evidence of impaired recognition of facial expressions in comparison to controls. These deficits were more consistently noted in the unmedicated group, who were also found to perform worse than the medicated group at recognising disgust from prototypical facial expressions, and at recognising anger and disgust in computer-manipulated images. Although both Parkinsons disease groups showed impairments of facial expression recognition, the consistently worse recognition of disgust in the unmedicated group is consistent with the hypothesis from previous studies that brain regions modulated by dopaminergic neurons are involved in the recognition of disgust.

Knowing no fear.

People with brain injuries involving the amygdala are often poor at recognizing facial expressions of fear, but the extent to which this impairment compromises other signals of the emotion of fear has not been clearly established. We investigated N.M., a person with bilateral amygdala damage and a left thalamic lesion, who was impaired at recognizing fear from facial expressions. N.M. showed an equivalent deficit affecting fear recognition from body postures and emotional sounds. His deficit of fear recognition was not linked to evidence of any problem in recognizing anger (a common feature in other reports), but for his everyday experience of emotion N.M. reported reduced anger and fear compared with neurologically normal controls. These findings show a specific deficit compromising the recognition of the emotion of fear from a wide range of social signals, and suggest a possible relationship of this type of impairment with alterations of emotional experience.

Disgust implicated in obsessive-compulsive disorder.

Psychiatric classificatory systems consider obsessions and compulsions as forms of anxiety disorder. However, the neurology of diseases associated with obsessive–compulsive symptoms suggests the involvement of fronto–striatal regions likely to be involved in the mediation of the emotion of disgust, suggesting that dysfunctions of disgust should be considered alongside anxiety in the pathogenesis of obsessive–compulsive behaviours. We therefore tested recognition of facial expressions of basic emotions (including disgust) by groups of participants with obsessive–compulsive disorder (OCD) and with Gilles de la Tourettes syndrome (GTS) with and without co–present obsessive–compulsive behaviours (GTS with OCB; GTS without OCB). A group of people suffering from panic disorder and generalized anxiety were also included in the study. Both groups with obsessive–compulsive symptoms (OCD; GTS with OCB) showed impaired recognition of facial expressions of disgust. Such problems were not evident in participants with panic disorder and generalized anxiety, or for participants with GTS without obsessions or compulsions, indicating that the deficit is closely related to the presence of obsessive–compulsive symptoms. Participants with OCD were able to assign words to emotion categories without difficulty, showing that their problem with disgust is linked to a failure to recognize this emotion in others and not a comprehension or response criterion effect. Impaired recognition of disgust is consistent with the neurology of OCD and with the idea that abnormal experience of disgust may be involved in the genesis of obsessions and compulsions.

Overactivation of fear systems to neutral faces in schizophrenia

BACKGROUND The amygdala plays a central role in detecting and responding to fear-related stimuli. A number of recent studies have reported decreased amygdala activation in schizophrenia to emotional stimuli (such as fearful faces) compared with matched neutral stimuli (such as neutral faces). We investigated whether the apparent decrease in amygdala activation in schizophrenia could actually derive from increased amygdala activation to the neutral comparator stimuli. METHODS Nineteen patients with schizophrenia and 24 matched control participants viewed pictures of faces with either fearful or neutral facial expressions, and a baseline condition, during functional magnetic resonance imaging scanning. RESULTS Patients with schizophrenia showed a relative decrease in amygdala activation to fearful faces compared with neutral faces. However, this difference resulted from an increase in amygdala activation to the neutral faces in patients with schizophrenia, not from a decreased response to the fearful faces. CONCLUSIONS Patients with schizophrenia show an increased response of the amygdala to neutral faces. This is sufficient to explain their apparent deficit in amygdala activation to fearful faces compared with neutral faces. The inappropriate activation of neural systems involved in fear to otherwise neutral stimuli may contribute to the development of psychotic symptoms in schizophrenia.

Event related potentials and the perception of intensity in facial expressions

It is well known from everyday experience, that facial expressions of emotions can very much vary in intensity, e.g. ranging from mild anger to rage, or from uneasiness and mild fear to angst and panic. However, the effect of different intensities of facial expressions of emotion on event related potentials has yet not been studied. We therefore investigated 16 healthy participants with a gender decision task to male and female faces displaying angry, disgusted and fearful facial expressions varying in intensity (50%, 100%, 150%). Analysis of ERP data showed a significant increase in amplitude of the N170 by intensity, but not by type of emotion. The intensity induced negative variation was most pronounced between 200 and 600ms at electrodes P9 and P10. For this time segment, there was a clear linear relationship between intensity and degree of negative deflection. A dipole source localisation of the intensity effect using the difference waveform (150% minus 50% intensity) revealed two symmetrically positioned generators within the inferior temporo-occipital lobe. An emotion specific effect for disgust was further found at temporal electrode sites (FT7 and FT8) at around 350-400ms. Results are summarised in a two-phase model of emotion recognition, suggesting the existence of an initial monitoring process which codes saliency of incoming facial information. In a second step, the specific emotional content of faces is decoded in emotion specific recognition systems.

The Cutest Little Baby Face A Hormonal Link to Sensitivity to Cuteness in Infant Faces

We used computer image manipulation to develop a test of perception of subtle gradations in cuteness between infant faces. We found that young women (19–26 years old) were more sensitive to differences in infant cuteness than were men (19–26 and 53–60 years old). Women aged 45 to 51 years performed at the level of the young women, whereas cuteness sensitivity in women aged 53 to 60 years was not different from that of men (19–26 and 53–60 years old). Because average age at menopause is 51 years in Britain, these findings suggest the possible involvement of reproductive hormones in cuteness sensitivity. Therefore, we compared cuteness discrimination in pre- and postmenopausal women matched for age and in women taking and not taking oral contraceptives (progestogen and estrogen). Premenopausal women and young women taking oral contraceptives (which raise hormone levels artificially) were more sensitive to variations of cuteness than their respective comparison groups. We suggest that cuteness sensitivity is modulated by female reproductive hormones.

The insular cortex and the neuroanatomy of major depression

BACKGROUND The neuroanatomical substrate underlying Major Depressive Disorder (MDD) is incompletely understood. Recent reports have implicated the insular cortex. METHODS Two cohorts of participants with MDD were tested. In the first MDD cohort, we used standardised facial expression recognition tasks. In the second cohort, we focused on facial disgust recognition, a function associated with the insular cortex. T1 weighted MR imaging was used in the second cohort to test the hypothesis of abnormal insular volume being associated with impaired disgust recognition. RESULTS Disgust recognition was particularly impaired in both cohorts. In the second cohort, the magnitude of the disgust recognition deficit correlated with reduced insula grey matter volume. Exploring the idea of insula involvement in MDD further, we identified the insular cortex and the anterior cingulate cortex as key neural correlates of core symptoms, in that scores of 3 clinical scales (the Beck Depression Inventory, the Hamilton Depression Rating Scale, and the Snaith-Hamilton Pleasure Scale) correlated with grey matter volume in these structures. LIMITATIONS MDD participants were clinically representative of specialist and academic psychiatric practice in the UK and presented with robust primary diagnoses; we did not exclude common co-morbidities such as anxiety and personality disorders. CONCLUSIONS We propose that cognitive and emotional functions assumed to be associated with the insula are adversely affected in patients with MDD and that this may, therefore, represent the substrate for some core clinical features of MDD. Further exploration of the involvement of the insular cortex in MDD is warranted.

Disgust in pre-clinical Huntington's disease: A longitudinal study

Emotion recognition from both face and voice and experience of emotions were investigated in a group of non-symptomatic people at risk of carrying the Huntingtons disease gene who presented for genetic testing. Based on the results of the DNA test, a group of people carrying the Huntingtons disease gene (HD+), and a group of non-carriers (HD-) were formed. Since we were especially interested in the time course of possible deficits in emotion recognition, all people at risk were reassessed 6 and 12 months after the initial assessment. Recognising facial expressions of disgust was significantly impaired on all three assessments in the HD+ group, while recognition of vocal emotions and the experience of emotions were largely unaffected, confirming that deficits in recognition of facial expressions of disgust are an early correlate of carrying the gene for Huntingtons disease. The inclusion of a healthy control group (n = 37) further allowed an estimate of the genetic and environmental contribution to deficits in facial emotion recognition.