Bernhard Baier

Awareness of the Functioning of One's Own Limbs Mediated by the Insular Cortex?

Normally, we are aware of the current functions of our arms and legs. However, this self-evident status may change dramatically after brain damage. Some patients with “anosognosia” typically are convinced that their limbs function normally, although they have obvious motor defects after stroke. Such patients may experience their own paretic limbs as strange or as not belonging to them and may even attribute ownership to another person and try to push their paralyzed limb out of bed. These odd beliefs have been attributed to disturbances somewhere in the right hemisphere. Here, we use lesion mapping in 27 stroke patients to show that the right posterior insula is commonly damaged in patients with anosognosia for hemiplegia/hemiparesis but is significantly less involved in hemiplegic/hemiparetic patients without anosognosia. The function of the posterior insular cortex has been controversially discussed. Recent neuroimaging results in healthy subjects revealed specific involvement of this area in the subjects feeling of being versus not being involved in a movement. Our finding corresponds with this observation and suggests that the insular cortex is integral to self-awareness and to ones beliefs about the functioning of body parts.

Tight Link Between Our Sense of Limb Ownership and Self-Awareness of Actions

Background and Purpose— Hemiparetic stroke patients with disturbed awareness for their motor weakness (anosognosia for hemiparesis/-plegia [AHP]) may exhibit further abnormal attitudes toward or perceptions of the affected limb(s). The present study investigated the clinical relationship and the anatomy of such abnormal attitudes and AHP. Methods— In a new series of 79 consecutively admitted acute stroke patients with right brain damage and hemiparesis/ -plegia, different types of abnormal attitudes toward the hemiparetic/plegic limb (asomatognosia, somatoparaphrenia, anosodiaphoria, misoplegia, personification, kinaesthetic hallucinations, supernumerary phantom limb) were investigated. Results— Ninty-two percent of the patients with AHP showed additional “disturbed sensation of limb ownership” (DSO) for the paretic/plegic limb. The patients had the feeling that their contralesional limb(s) do not belong to their body or even belong to another person. Analysis of lesion location revealed that the right posterior insula is a crucial structure involved in these phenomena. Conclusions— DSO for hemiparetic/-plegic limbs and AHP are tightly linked both clinically and anatomically. The right posterior insula seems to be a crucial structure involved in the genesis of our sense of limb ownership and self-awareness of actions.

Right insula for our sense of limb ownership and self-awareness of actions

Normally, we are aware that our arms and legs belong to us and not to someone else. However, some stroke patients with hemiparesis/-plegia after right-sided stroke show a disturbed sensation of limb ownership and a disturbed self-awareness of actions and such patients with anosognosia for hemiparesis/plegia typically deny their paresis/-plegia and are convinced that their limbs function normally. They may experience their limb(s) as not belonging to them and may even attribute them to other persons. Modern lesion analyses techniques in such patients and recent neuroimaging results in healthy subjects suggest a prominent role of the right insula for our sense of limb ownership as well as for our feeling of being involved in a movement—our sense of agency. We thus hypothesize that the right insular cortex constitutes a central node of a network involved in human body scheme representation.

Keeping Memory Clear and Stable—The Contribution of Human Basal Ganglia and Prefrontal Cortex to Working Memory

Successful remembering involves both hindering irrelevant information from entering working memory (WM) and actively maintaining relevant information online. Using a voxelwise lesion–behavior brain mapping approach in stroke patients, we observed that lesions of the left basal ganglia render WM susceptible to irrelevant information. Lesions of the right prefrontal cortex on the other hand make it difficult to keep more than a few items in WM. These findings support basal ganglia–prefrontal cortex models of WM whereby the basal ganglia play a gatekeeper role and allow only relevant information to enter prefrontal cortex where this information then is actively maintained in WM.

Cross-modal processing in early visual and auditory cortices depends on expected statistical relationship of multisensory information.

Previous studies have shown that processing information in one sensory modality can either be enhanced or attenuated by concurrent stimulation of another modality. Here, we reconcile these apparently contradictory results by showing that the sign of cross-modal interactions depends on whether the content of two modalities is associated or not. When concurrently presented auditory and visual stimuli are paired by chance, cue-induced preparatory neural activity is strongly enhanced in the task-relevant sensory system and suppressed in the irrelevant system. Conversely, when information in the two modalities is reliably associated, activity is enhanced in both systems regardless of which modality is task relevant. Our findings illustrate an ecologically optimal flexibility of the neural mechanisms that govern multisensory processing: facilitation occurs when integration is expected, and suppression occurs when distraction is expected. Because thalamic structures were more active when the senses needed to operate separately, we propose them to serve gatekeeper functions in early cross-modal interactions.

Neural correlates of disturbed perception of verticality

Objective: Perception of verticality can be perturbed after cortical stroke. However, a relationship between lesion location and pathologic perception of verticality is still a matter of debate since previous studies revealed contradictory results. Thus, the aim of the current study was to test whether specific cortical lesions were associated with tilts of subjective visual vertical (SVV) and to determine the critical brain areas that cause such tilts in the case of a lesion. Methods: SVV was systematically studied in 54 patients (22 patients with left-sided and 32 patients with right-sided lesions) with acute unilateral strokes, analyzed by modern voxel-wise lesion-behavior mapping techniques. Results: The data give evidence for an association between tilt of SVV and the insular cortex (IC) and inferior frontal gyrus (IFG) in both hemispheres. Whereas the IC seems to be the prominent structure in the left hemisphere, the IFG is most affected in the right hemisphere. Furthermore, other cortical regions such as the superior temporal gyrus (STG) and the rolandic operculum as well as—subcortically—the inferior occipitofrontal fascicle and the superior longitudinal fascicle seem to be involved in the vestibulo-cortical network for the perception of verticality in the roll plane. Conclusion: Damage to these regions might lead to an imbalance within the vestibular network of one hemisphere due to a deficit in multimodal signal processing.

Anatomical correlates of ocular motor deficits in cerebellar lesions

Humans are able to stabilize the images of moving targets on the retina by means of smooth pursuit eye movements. After the pontine level, all smooth pursuit pathways pass through the cerebellum. Previous animal studies gave evidence that two specific lesion sites within the cerebellum cause smooth pursuit disorders: those of the flocculus/paraflocculus and the vermis including lobule VI, VII, the uvula and the deep cerebellar nuclei. To date, there have been only a few lesion studies in patients with smooth pursuit disorders that do not allow direct comparison with a control group. In the present study, new lesion mapping techniques determined which cerebellar structures were involved in patients with deficits of smooth pursuit eye movements, slow phase of optokinetic nystagmus (OKN) and fixation suppression of vestibulo-ocular reflex, i.e. in eye movements that are considered to belong to the smooth pursuit system. The aim was to elucidate whether there is an anatomical and clinical link between these different eye movement disorders. Seventeen patients with acute, mainly unilateral cerebellar infarctions and an intact gain of the smooth pursuit system were compared with 11 patients with cerebellar lesions and deficient gain of sinusoidal smooth pursuit eye movements by means of lesion-mapping imaging. In addition, lesion analyses were conducted in subgroups with impaired fixation suppression of vestibulo-ocular reflex and deficient gain of the slow phase of the OKN. The uvula and partly the vermal pyramid were found to be the structures commonly damaged in patients with deficient gain of the horizontal sinusoidal smooth pursuit eye movement, of the slow phase of the OKN and impaired fixation suppression of vestibulo-ocular reflex; and were less involved in patients with intact smooth pursuit system. The present data give evidence for an anatomical link between sinusoidal smooth pursuit eye movements, fixation suppression of vestibulo-ocular reflex and the slow phases of OKN implying that the uvula and the vermal pyramid are important structures for generating slow phases within the smooth pursuit network in humans.

Vestibular migraine : effects of prophylactic therapy with various drugs : A retrospective study

Vertigo is frequently associated with migraine, and sometimes it is the cardinal symptom. This type of migraine is called “vestibular migraine”, “migrainous vertigo”, or “migraine-associated vertigo”. Earlier findings on effective prophylactic medication for such migraine attacks and their clinical features are few and insufficient. Our aim was to study the influence of prophylactic therapy on this type of migraine and to specify its clinical features. In a retrospective approach 100 patients (median age 47 years, range 21–72 years) with definite or probable vestibular migraine [1] were divided into two groups: those with (74 patients) and those without drug prophylaxis (26 patients). They were then interviewed by telephone at least 6 months after beginning therapy. All patients receiving medical prophylaxis showed a decrease of duration, intensity, and frequency of episodic vertigo as well as nearly all its associated features (p < 0.01). The group without medical prophylactic therapy showed only a reduction of vertigo intensity. Only 39 % of the 100 patients met the current IHS criteria for a basilartype migraine [2]. Thus, we propose that a new category – “vestibular migraine” – should be added to the HIS criteria. Furthermore, our data show that prophylactic medication may be effective for treating vestibular migraine and its associated symptoms; therefore, patient’s response to medical therapy may provide guidance in the diagnostic process of vestibular migraine.

Vestibular-evoked myogenic potentials in "vestibular migraine" and Menière's disease: a sign of an electrophysiological link?

Characterizations of the signs and symptoms of “vestibular migraine” and of Menières disease seem to overlap, suggesting that both diseases might be due to a common peripheral vestibular dysfunction. Thus, the aim of the present study was to assess vestibular‐evoked myogenic potentials (VEMPs) in both disorders to determine whether there might be an electrophysiological link between the two disorders. The amplitude and latency of VEMPs were measured from the sternocleidomastoid muscle in 63 patients with vestibular migraine (median age 47 years, range 24–70 years) and in 16 patients with Menières disease (median age 52 years, range 36–72 years), and compared with those of 63 sex‐ and age‐matched healthy controls (median age 46 years, range 17–73 years). In comparison to the controls, 43 of the 63 patients with vestibular migraine (68%) and 11 patients with Menières disease (69%) had reduced electromyography ‐corrected VEMP amplitudes, whereas no difference was seen in the latencies. Thus, these data provide evidence that the saccule may be affected in both disorders, indicating a possibly related labyrinthine cause for the pathogenesis of vestibular migraine and Menières disease.

Repetition Suppression versus Enhancement—It's Quantity That Matters

Upon repetition, certain stimuli induce reduced neural responses (i.e., repetition suppression), whereas others evoke stronger signals (i.e., repetition enhancement). It has been hypothesized that stimulus properties (e.g., visibility) determine the direction of the repetition effect. Here, we show that the very same stimuli can induce both repetition suppression and enhancement, whereby the only determining factor is the number of repetitions. Repeating the same, initially novel low-visible pictures of scenes for up to 5 times enhanced the blood oxygen level-dependent (BOLD) response in scene-selective areas, that is, the parahippocampal place area (PPA) and the transverse occipital sulcus (TOS), presumably reflecting the strengthening of the internal representation. Additional repetitions (6-9) resulted in progressively attenuated neural responses indicating a more efficient representation of the now familiar stimulus. Behaviorally, repetition led to increasingly faster responses and higher visibility ratings. Novel scenes induced the largest BOLD response in the PPA and also higher activity in yet another scene-selective region, the retrospenial cortex (RSC). We propose that 2 separable processes modulate activity in the PPA: one process optimizes the internal stimulus representation and involves TOS and the other differentiates between familiar and novel scenes and involves RSC.