Effects of emotional valence and intensity on cognitive and affective empathy after insula lesions.

The insula plays a central role in empathy. However, the complex structure of cognitive (CE) and affective empathy (AE) deficits following insular damage is not fully understood. In the present study, patients with insular lesions (n = 20) and demographically matched healthy controls (n = 24) viewed ecologically valid videos that varied in terms of valence and emotional intensity. The videos showed a person (target) narrating a personal life event. In CE conditions, subjects continuously rated the affective state of the target, while in AE conditions, they continuously rated their own affect. Mean squared error (MSE) assessed deviations between subject and target ratings. Patients differed from controls only in negative, low-intensity AE, rating their own affective state less negative than the target. This deficit was not related to trait empathy, neuropsychological or clinical parameters, or laterality of lesion. Empathic functions may be widely spared after insular damage in a naturalistic, dynamic setting, potentially due to the intact interpretation of social context by residual networks outside the lesion. The particular role of the insula in AE for negative states may evolve specifically in situations that bear higher uncertainty pointing to a threshold role of the insula in online ratings of AE.

Lateralized deficits in arousal processing after insula lesions: Behavioral and autonomic evidence.

A large body of evidence ascribes a pivotal role in emotion processing to the insular cortex. However, the complex structure and lateralization of emotional deficits following insular damage are not understood. Here, we investigated emotional ratings of valence and arousal and skin conductance responses (SCR) to a graded series of emotionally arousing scenes in patients with left (n = 10) or right (n = 9) insular damage and in healthy controls (n = 18). We found a significant reduction in overall SCRs, arousal ratings and valence extremity scores in right-lesioned patients, as compared to left-lesioned patients and healthy controls. The degree of right insular damage was significantly correlated with the degree of arousal, SCR and extremity attenuation. Additional analyses of correlations between subjective arousal ratings resp. SCR and normative arousal ratings revealed that both lesion groups had evaluative and physiological difficulties to discover changes in stimulus arousal. Although no group differences emerged on overall ratings of valence, analysis of correlations between subjective and normative valence ratings displayed markedly reduced accuracy in right-lesioned patients, as compared to left-lesioned patients and healthy controls. Our findings support the hypothesis that the left and right insulae subserve different functions in emotion processing, potentially due to asymmetrical representations of autonomic information in the left and right human forebrain. The right insula may serve as integral node for sympathetic arousal and cognitive-affective processing.

Phasic alerting increases visual processing speed in amnestic mild cognitive impairment.

External warning cues temporarily increase the brain's sensitivity for upcoming events, helping individuals to flexibly adapt their reactions to the requirements of complex visual environments. Previous studies reported that younger and cognitively normal older adults profit from phasic alerting cues. Such an intact phasic alerting mechanism could be even more relevant in individuals with Alzheimer's disease who are characterized by reduced processing capacities. The present study employed a theory of visual attention based verbal whole report paradigm with auditory cues in order to investigate phasic alerting effects in amnestic mild cognitive impairment (aMCI). Patients with aMCI were also compared to a previously reported sample of cognitively normal older adults. In patients with aMCI, visual processing speed was higher in the cue compared to the no-cue condition. Further, visual processing speed was reduced in patients with aMCI compared to cognitively normal older adults. Taken together, the results suggest that the processing system of patients with aMCI exhibits general declines but can still integrate auditory warning signals on a perceptual level.

Effects of Temporary Functional Deafferentation in Chronic Stroke Patients: Who Profits More?

Temporary functional deafferentation (TFD) by an anesthetic cream on the stroke-affected forearm was shown to improve sensorimotor abilities of stroke patients. The present study investigated different predictors for sensorimotor improvements during TFD and indicated outcome differences between patients grouped in subcortical lesions only and lesions with any cortical involvement. Thirty-four chronic stroke patients were temporarily deafferented on the more affected forearm by an anesthetic cream. Somatosensory performance was assessed using von Frey Hair and grating orientation task; motor performance was assessed by a shape-sorter-drum task. Seven potential predictors were entered into three linear multiple regression models. Furthermore, effects of TFD on outcome variables for the two groups (cortical versus subcortical lesion) were compared. Sex and sensory deficit were significant predictors for changes in motor function while age accounted for changes in grating orienting task. Males, patients with a stronger sensory deficit, and older patients profited more. None of the potential predictors made significant contributions to changes in threshold for touch. Furthermore, there were no differences in sensorimotor improvement between lesion site groups. The effects of TFD together with the low predictability of the investigated parameters suggest that characteristics of patients alone are not suitable to exclude some patients from TFD.

Neuro-cognitive mechanisms of simultanagnosia in patients with posterior cortical atrophy.

Posterior cortical atrophy is dominated by progressive degradation of parieto-occipital grey and white matter, and represents in most cases a variant of Alzheimer's disease. Patients with posterior cortical atrophy are characterized by increasing higher visual and visuo-spatial impairments. In particular, a key symptom of posterior cortical atrophy is simultanagnosia i.e. the inability to perceive multiple visual objects at the same time. Two neuro-cognitive mechanisms have been suggested to underlie simultanagnosia, either reduced visual short-term memory capacity or decreased visual processing speed possibly resulting from white matter impairments over and above damage to cortical brain areas. To test these distinct hypotheses, we investigated a group of 12 patients suffering from posterior cortical atrophy with homogenous lesion sides in parieto-occipital cortices and varying severity of grey and white matter loss. More specifically, we (i) tested whether impaired short-term memory capacity or processing speed underlie symptoms of simultanagnosia; (ii) assessed the link to grey and white matter damage; and (iii) integrated those findings into a neuro-cognitive model of simultanagnosia in patients with posterior cortical atrophy. To this end, simultaneous perception of multiple visual objects was tested in patients with posterior cortical atrophy mostly with positive Alzheimer's disease biomarkers and healthy age-matched controls. Critical outcome measures were identification of overlapping relative to non-overlapping figures and visuo-spatial performance in tests sensitive to simultanagnosia. Using whole report of briefly presented letter arrays based on the mathematically formulated 'Theory of Visual Attention', we furthermore quantified parameters of visual short-term memory capacity and visual processing speed. Grey and white matter atrophy was assessed by voxel-based morphometry analyses of structural magnetic resonance data. All patients showed severe deficits of simultaneous perception. Compared to controls, we observed a specific slowing of visual processing speed, while visual short-term memory capacity was preserved. In a regression analysis, processing speed was identified as the only significant predictor of simultaneous perception deficits that explained a high degree of variance (70-82%) across simultanagnosia tasks. More severe slowing was also indicative for more severe impairments in reading and scene comprehension. Voxel-based morphometry yielded extensive reductions of grey and white matter in parieto-occipital and thalamic brain areas. Importantly, the degree of individual atrophy of white matter in left superior parietal lobe, but not of any grey matter region, was associated with processing speed. Based on these findings, we propose that atrophy of white matter commonly observed in posterior cortical atrophy leads to slowing of visual processing speed, which underlies the overt clinical symptoms of simultanagnosia.

Serum S100B Protein is Specifically Related to White Matter Changes in Schizophrenia.

BACKGROUND: Schizophrenia can be conceptualized as a form of dysconnectivity between brain regions.To investigate the neurobiological foundation of dysconnectivity, one approach is to analyze white matter structures, such as the pathology of fiber tracks. S100B is considered a marker protein for glial cells, in particular oligodendrocytes and astroglia, that passes the blood brain barrier and is detectable in peripheral blood. Earlier Studies have consistently reported increased S100B levels in schizophrenia. In this study, we aim to investigate associations between S100B and structural white matter abnormalities. METHODS: We analyzed data of 17 unmedicated schizophrenic patients (first and recurrent episode) and 22 controls. We used voxel based morphometry (VBM) to detect group differences of white matter structures as obtained from T1-weighted MR-images and considered S100B serum levels as a regressor in an age-corrected interaction analysis. RESULTS: S100B was increased in both patient subgroups. Using VBM, we found clusters indicating significant differences of the association between S100B concentration and white matter. Involved anatomical structures are the posterior cingulate bundle and temporal white matter structures assigned to the superior longitudinal fasciculus. CONCLUSIONS: S100B-associated alterations of white matter are shown to be existent already at time of first manifestation of psychosis and are distinct from findings in recurrent episode patients. This suggests involvement of S100B in an ongoing and dynamic process associated with structural brain changes in schizophrenia. However, it remains elusive whether increased S100B serum concentrations in psychotic patients represent a protective response to a continuous pathogenic process or if elevated S100B levels are actively involved in promoting structural brain damage.

Differences in somatosensory and motor improvement during temporary functional deafferentation in stroke patients and healthy subjects.

Temporary functional deafferentation is of interest to become an additional tool in neurorehabilitative treatments. Temporary functional deafferentation is known to improve sensory and motor outcomes in chronic stroke patients and healthy subjects. The present study soughts to indicate differences in the efficiency of pharmacologically induced temporary functional deafferentation between chronic stroke patients and matched healthy subjects. 46 chronic stroke patients and 20 age- and gender-matched healthy subjects were deafferented on one forearm by an anesthetic cream. Somatosensory performance was assessed using von-Frey Hair testing and Grating orientation task; motor performance was assessed by means of a shape-sorter-drum task. Grating orientation task and shape-sorter-drum task were significantly improved during temporary functional deafferentation in stroke patients but not in healthy subjects. Von-Frey Hair testing revealed no improvement of absolute tactile thresholds during temporary functional deafferentation in both groups. Furthermore, the stroke patients showed deficits at baseline measurement in all assessments except the von-Frey Hair test. Temporary functional deafferentation of a forearm by an anesthetic cream results in improvements of motor performance and somatosensory discrimination in stroke patients but not in healthy subjects. Therefore, it is reasonable to test in a next step whether temporary functional deafferentation might become an additional tool in motor rehabilitation of post stroke patients.

Effects of temporary functional deafferentation on the brain, sensation, and behavior of stroke patients.

Following stroke, many patients suffer from chronic motor impairment and reduced somatosensation in the stroke-affected body parts. Recent experimental studies suggest that temporary functional deafferentation (TFD) of parts of the stroke-affected upper limb or of the less-affected contralateral limb might improve the sensorimotor capacity of the stroke-affected hand. The present study sought evidence of cortical reorganization and related sensory and motor improvements following pharmacologically induced TFD of the stroke-affected forearm. Examination was performed during 2 d of Constraint-Induced Movement Therapy. Thirty-six human patients were deafferented on the stroke-affected forearm by an anesthetic cream (containing lidocaine and prilocaine) on one of the 2 d, and a placebo cream was applied on the other. The order of TFD and placebo treatment was counterbalanced across patients. Somatosensory and motor performance were assessed using a Grating orienting task and a Shape-sorter-drum task, and with somatosensory-evoked magnetic fields. Evoked magnetic fields showed significant pre- to postevaluation magnitude increases in response to tactile stimulation of the thumb of the stroke-affected hand during TFD but not following placebo treatment. We also observed a rapid extension of the distance between cortical representations of the stroke-affected thumb and little finger following TFD but not following placebo treatment. Moreover, somatosensory and motor performance of the stroke-affected hand was significantly enhanced during TFD but not during placebo treatment. Thus, pharmacologically induced TFD of a stroke-affected forearm might improve the somatosensory and motor functions of the stroke-affected upper limb, accompanied by cortical plasticity.

Deafferentation of the affected arm: a method to improve rehabilitation?

BACKGROUND AND PURPOSE: Reduced somatosensation is a common impairment after stroke. This somatosensory deficit is known to be a reliable predictor of poor rehabilitation outcome. Several methods of physical therapy have addressed this problem, but with only moderate success. Here, we used a new neural plasticity-based approach, ie, a simple, inexpensive, pharmacologically induced temporary functional deafferentation (TFD) of the forearm to investigate whether TFD might result in beneficial effects on the somatosensory sensibility and motor capacity of the stroke-affected hand. METHODS: Examination was performed over 2 consecutive days of an efficient rehabilitation program for stroke patients referred to as constraint-induced movement therapy. Patients were deafferented on one of these days but not on the other (placebo session). The order of deafferentation and nondeafferentation was counterbalanced across patients. TFD of the stroke-affected forearm was realized using an anesthetic cream. Somatosensory abilities were assessed by a Grating orienting task, and a shape-sorter drum task was used to test motor performance. Both tests were performed each day before and after the constraint-induced movement therapy training session. RESULTS: We found significantly better outcomes for Grating orienting task and shape-sorter drum task after TFD on the forearm as compared to placebo, indicating increased somatosensory abilities and motor performance in stroke patients using the simple TFD procedure. CONCLUSIONS: The improvement was achieved during the course of one of the best established poststroke rehabilitation programs, suggesting that TFD on the more affected forearm might become an efficient additional tool in stroke rehabilitation.

Functional deactivations: multiple ipsilateral brain areas engaged in the processing of somatosensory information.

Somatosensory signals modulate activity throughout a widespread network in both of the brain hemispheres: the contralateral as well as the ipsilateral side of the brain relative to the stimulated limb. To analyze the ipsilateral somatosensory brain areas that are engaged during limb stimulation, we performed functional magnetic resonance imaging (fMRI) in 12 healthy subjects during electrical median nerve stimulation using both a block- and an event-related fMRI design. Data were analyzed through the use of model-dependent (SPM) and model-independent (ICA) approaches. Beyond the well-known positive blood oxygenation level-dependent (BOLD) responses, negative deflections of the BOLD response were found consistently in several ipsilateral brain areas, including the primary somatosensory cortex, the supplementary motor area, the insula, the dorsal part of the posterior cingulate cortex, and the contralateral cerebellum. Compared to their positive counterparts, the negative hemodynamic responses showed a different time course, with an onset time delay of 2.4 s and a peak delay of 0.7 s. This characteristic delay was observed in all investigated areas and verified by a second (purely tactile) event-related paradigm, suggesting a systematic difference for brain areas involved in the processing of somatosensory information. These findings may indicate that the physiological basis of these deactivations differs from that of the positive BOLD responses. Therefore, an altered model for the negative BOLD response may be beneficial to further model-dependent fMRI analyses.

Phospholipase A2 activity is associated with structural brain changes in schizophrenia.

Regional structural brain changes are among the most robust biological findings in schizophrenia, yet the underlying pathophysiological changes remain poorly understood. Recent evidence suggests that abnormal neuronal/dendritic plasticity is related to alterations in membrane lipids. We examined whether serum activity of membrane lipid remodelling/repairing cytosolic phospholipase A(2) (PLA(2)) were related to regional brain structure in magnetic resonance images (MRI). The study involved 24 schizophrenia patients, who were either drug-naïve or off antipsychotic medication, and 25 healthy controls. Using voxel-based morphometry (VBM) analysis of T1-high-resolution MRI-images, we correlated both gray matter and white matter changes with serum PLA(2)-activity. PLA(2) activity was increased in patients, consistent with previous findings. VBM group comparison of patients vs. controls showed abnormalities of frontal and medial temporal cortices/hippocampus, and left middle/superior temporal gyrus in first-episode patients. Group comparison of VBM/PLA(2)-correlations revealed a distinct pattern of disease-related interactions between gray/white matter changes in patients and PLA(2)-activity: in first-episode patients (n=13), PLA(2)-activity was associated with structural alterations in the left prefrontal cortex and the bilateral thalamus. Recurrent-episode patients (n=11) showed a wide-spread pattern of associations between PLA(2)-activity and structural changes in the left (less right) prefrontal and inferior parietal cortex, the left (less right) thalamus and caudate nucleus, the left medial temporal and orbitofrontal cortex and anterior cingulum, and the cerebellum. Our findings demonstrate a potential association between membrane lipid biochemistry and focal brain structural abnormalities in schizophrenia. Differential patterns in first-episode vs. chronic patients might be related to PLA(2)-increase at disease-onset reflecting localized regenerative activity, whereas correlations in recurrent-episode patients might point to less specific neurodegenerative aspects of disease progression.

No impairment of recognition and experience of disgust in a patient with a right-hemispheric lesion of the insula and basal ganglia.

An influential single case study (Calder, Keane, Manes, Antoun, & Young, 2000, Nature Neuroscience, 3, 1077-1078) recently showed a marked multimodal impairment in the recognition and experience of disgust in a patient with a left-hemispheric lesion of the basal ganglia and the insular cortex. Here, we investigated whether a similar deficit will be observed in a patient with a comparable lesion of the insula and basal ganglia in the right hemisphere. Remarkably, the patient showed no impairments in the recognition or experience of disgust and also no notable impairments in the recognition and experience of other emotions, across a range of stimuli, as compared to healthy comparison subjects. Thus, either deficits in disgust processing are not reliably observed in patients with lesion of the insula and basal ganglia regardless of the laterality of the lesion; or right-hemispheric lesions, in contrast to left-hemispheric lesions, do not seem to induce impairments in the processing of disgust.

Unilateral optic neuropathy following subdural hematoma: a case report.

INTRODUCTION: Unilateral optic neuropathy is commonly due to a prechiasmatic affliction of the anterior visual pathway, while losses in visual hemifields result from the damage to brain hemispheres. Here we report the unusual case of a patient who suffered from acute optic neuropathy following hemispherical subdural hematoma. Although confirmed up to now only through necropsy studies, our case strongly suggests a local, microcirculatory deficit identified through magnetic resonance imaging in vivo. CASE PRESENTATION: A 70-year-old Caucasian German who developed a massive left hemispheric subdural hematoma under oral anticoagulation presented with acute, severe visual impairment on his left eye, which was noticed after surgical decompression. Neurologic and ophthalmologic examinations indicated sinistral optic neuropathy with visual acuity reduced nearly to amaurosis. Ocular pathology such as vitreous body hemorrhage, papilledema, and central retinal artery occlusion were excluded. An orbital lesion was ruled out by means of orbital magnetic resonance imaging. However, cerebral diffusion-weighted imaging and T2 maps of magnetic resonance imaging revealed a circumscribed ischemic lesion within the edematous, slightly herniated temporomesial lobe within the immediate vicinity of the affected optic nerve. Thus, the clinical course and morphologic magnetic resonance imaging findings suggest the occurrence of pressure-induced posterior ischemic optic neuropathy due to microcirculatory compromise. CONCLUSION: Although lesions of the second cranial nerve following subdural hematoma have been reported individually, their pathogenesis was preferentially proposed from autopsy studies. Here we discuss a dual, pressure-induced and secondarily ischemic pathomechanism on the base of in vivo magnetic resonance imaging diagnostics which may remain unconsidered by computed tomography.

Positional brain deformation visualized with magnetic resonance morphometry.

OBJECTIVE: To assess and visualize gravitational effects on brain morphology and the position of the brain within the skull by magnetic resonance (MR) morphometry in order to identify confounding effects and possible sources of error for accurate planning of neurosurgical interventions. METHODS: Three-dimensional MR imaging data sets of 13 healthy adults were acquired in different positions in the scanner. With a morphometric approach, data sets were evaluated by deformation field analysis and the brain boundary shift integral. Distortions of the brain were assessed comparing right versus left and prone versus supine positioning, respectively. RESULTS: Two effects could be differentiated: 1) greatest brain deformation of up to 1.7 mm predominantly located around central brain structures in the lateral direction and a less pronounced change after position changes in posterior-anterior direction, and 2) the brain boundary shift integral depicted position-dependent brain shift relative to the inner skull. CONCLUSION: Position-dependent effects on brain structure may undermine the accuracy of neuronavigational and other neurosurgical procedures. Furthermore, in longitudinal MR volumetric studies, gravitational effects should be kept in mind and the scanning position should be rigidly controlled for.

Cerebral involvement in a patient with Goodpasture's disease due to shortened induction therapy: a case report.

INTRODUCTION: Goodpasture's disease is a rare immunological disease with formation of pathognomonic antibodies against renal and pulmonary basement membranes. Cerebral involvement has been reported in several cases in the literature, yet the pathogenetic mechanism is not entirely clear. CASE PRESENTATION: A 21-year-old Caucasian man with Goodpasture's disease and end-stage renal disease presented with two generalized seizures after a period of mild cognitive disturbance. Blood pressure and routine laboratory tests did not exceed the patient's usual values, and examination of cerebrospinal fluid was unremarkable. Cerebral magnetic resonance imaging (MRI) revealed multiple cortical and subcortical lesions on fluid-attenuated inversion recovery sequences. Since antiglomerular basement membrane antibodies were found to be positive with high titers, plasmapheresis was started. In addition, cyclophosphamide pulse therapy was given on day 13. Encephalopathy and MRI lesions disappeared during this therapy, and antiglomerular basement membrane antibodies were significantly reduced. Previous immunosuppressive therapy was performed without corticosteroids and terminated early after 3 months. The differential diagnostic considerations were cerebral vasculitis and posterior reversible encephalopathy syndrome. Vasculitis could be seen as an extrarenal manifestation of the underlying disease. Posterior reversible encephalopathy syndrome, on the other hand, can be triggered by immunosuppressive therapy and may appear without a hypertensive crisis. CONCLUSION: A combination of central nervous system symptoms with a positive antiglomerular basement membrane test in a patient with Goodpasture's disease should immediately be treated as an acute exacerbation of the disease with likely cross-reactivity of antibodies with the choroid plexus. In our patient, a discontinuous strategy of immunosuppressive therapy may have favored recurrence of Goodpasture's disease.

Characterization of cortical thickness and ventricular width in normal aging: a morphometric study at 3 Tesla.

PURPOSE: To describe loss of cortical thickness and ventricular enlargement during normal aging in a sample of 525 neurologically and psychiatrically inconspicuous subjects (17-68 years old). MATERIALS AND METHODS: An automated segmentation algorithm was applied to assess cortical thickness and compared with conventional measurements of ventricular indices (ventricular body index (VBI), anterior horn index (AHI), and third ventricular width) as performed in clinical practice. Regression analysis was performed to elucidate the relationship between a decrease of the cortical mantle and increase in ventricular width with aging. RESULTS: Cortical thickness decreases with age (r = -0.49, P < 0.01; r = -0.502 in male and r = -0.461 in female subjects). Regarding the ventricular indices, we found a significant correlation with age for both the whole sample and the subdivision by gender. Cortical thickness and ventricular width are closely correlated (r = -0.43 in women, r = -0.468 in men, P < 0.001 each). The bandwidth of variance scales up with aging in all parameters. The results are discussed in terms of the underlying mechanisms of normal aging. CONCLUSION: Our findings suggest that a decrease in cortical thickness and increase in ventricular width occur with normal aging. The enlargement of the third ventricle correlates the most strongly with age.

Cognitive sequelae of diffuse axonal injury.

BACKGROUND: The results of recent studies on cognitive disability after traumatic brain injury-associated diffuse axonal injury (DAI) are inconsistent. In these studies, the diagnosis of DAI relied on cranial computed tomography. OBJECTIVE: To further clarify the extent and severity of a possibly DAI-associated cognitive impairment by the use of magnetic resonance imaging (MRI) and detailed neuropsychological testing. DESIGN AND PARTICIPANTS: From a databank of 299 patients with traumatic brain injury, 18 patients (age range, 17-50 years; median initial Glasgow Coma Scale score, 5) who showed an MRI lesion pattern compatible with pure DAI were identified. All of the patients had undergone MRI on a 3-T system. Pure DAI was defined by the findings of traumatic microbleeds on T2*-weighted gradient-echo images in the absence of otherwise traumatic or nontraumatic MRI abnormalities. MAIN OUTCOME MEASURES: Neuropsychological performance in the categories of attention and psychomotor speed, executive functions, spans, learning and memory, and intelligence 4 to 55 months (median, 9 months) after traumatic brain injury. RESULTS: All of the patients showed impairments of 1 or more cognitive subfunctions, and no cognitive domain was fundamentally spared. Memory and executive dysfunctions were most frequent, the former reaching a moderate to severe degree in half of the patients. In comparison, deficits of attention, executive functions, and short-term memory were mostly mild. Correlations between the amount of traumatic microbleeds and specific or global cognitive performance were absent. CONCLUSIONS: An MRI lesion pattern compatible with isolated DAI is associated with persistent cognitive impairment. The traumatic microbleed load is no sufficient parameter for the assessment of DAI severity or functional outcome.

Spontaneous slow hemodynamic oscillations are impaired in cerebral microangiopathy.

Small-vessel disease or cerebral microangiopathy (CMA) is a common finding in elderly people. It is related to a variety of vascular risk factors and may finally lead to subcortical ischemic vascular dementia. Because vessel stiffness is increased, we hypothesized that slow spontaneous oscillations are reduced in cerebral hemodynamics. Accordingly, we examined spontaneous oscillations in the visual cortex of 13 patients suffering from CMA, and compared them with 14 age-matched controls. As an imaging method we applied functional near-infrared spectroscopy, because it is particularly sensitive to the microvasculature. Spontaneous low-frequency oscillations (LFOs) (0.07 to 0.12 Hz) were specifically impaired in CMA in contrast to spontaneous very-low-frequency oscillations (0.01 to 0.05 Hz), which remained unaltered. Vascular reagibility was reduced during visual stimulation. Interestingly, changes were tightly related to neuropsychological deficits, namely executive dysfunction. Vascular alterations had to be attributed mainly to the vascular risk factor arterial hypertension. Further, results suggest that the impairments might be, at least partly, reversed by medical treatment such as angiotensin-converting enzyme inhibitors/angiotensin II receptor blockers. Results indicate that functional near-infrared spectroscopy may detect changes in the microvasculature due to CMA, namely an impairment of spontaneous LFOs, and of vascular reagibility. Hence, CMA accelerates microvascular changes due to aging, leading to impairments of autoregulation.

Morphometry demonstrates loss of cortical thickness in cerebral microangiopathy.

OBJECTIVE: To evaluate the role of MR morphometry in the characterization of cerebral microangiopathy (CMA) in relation to clinical and neuropsychological impairment. SUBJECTS AND METHODS: 3D MR images of 27 patients and 27 age-matched controls were morphometrically analysed for regional thickness. The normalized values were related to the patients' clinical and neuropsychological scores. The patients were categorised according to the amount of structural MR signal changes. A ventricle index reflecting internal atrophy was related to MR morphology and cortical thickness as an indicator for external atrophy. RESULTS: Cortical thickness was significantly reduced in the patients group (3.03 mm +/- 0.26 vs. 3.22 mm +/-0.13 in controls, p=0.001). The severest loss of cortical thickness occurred in severe CMA. Internal and external atrophy evolved in parallel and both showed a significant relationship with structural MR-abnormalities (p<0.05; r=-0.7; r=0.67; r=-0.74, respectively). Neuropsychological performance correlated strongly with the loss of cortical thickness. CONCLUSIONS: Cortical thickness was identified as the most sensitive parameter to characterize CMA. A strong correlation was found of morphometric parameters to the severity of CMA based on a score derived from T2-weighted MRI. The degree of cortical atrophy was directly related to the degree of neuropsychological impairment. Our findings suggest that the cortical thickness is a valid marker in the structural and clinical characterization of CMA.