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Somatosensory
Terms modified by Somatosensory Selected AbstractsTaste deficits after middle ear surgery for otosclerosis: taste somatosensory interactionsEUROPEAN JOURNAL OF ORAL SCIENCES, Issue 5 2008Marie-Violaine Berteretche The aim of this study was to evaluate the postoperative consequences of chorda tympani reclining during middle ear surgery for otosclerosis. Electrogustometric taste thresholds were measured at 11 loci on the tongue and the soft palate in 14 patients before surgery, and 8 d, 1 month and (in some cases) 6 months after surgery. A significant increase in thresholds was observed on the ipsilateral side of the tongue after surgery. The extent of the deficit and the recovery time course depended on tongue locus. The tip of the tongue displayed a limited deficit, suggesting bilateral chorda tympani innervation. The edge of the tongue was less impaired than the dorsal or the lateral tip loci; it may be dually innervated by both chorda tympani and glossopharyngeal nerves in humans, as already shown in rats. Likewise for the fungiform papillae located just anterior to the circumvallate papillae. Somatosensory early complaints suggest a derepression of chorda tympani on lingual nerve signals. In a second stage, relief of complaints before electrogustometric threshold recovery suggested trigeminal compensation of the chorda tympani deficit. Relief of complaints seems to involve central integrative processes, whereas the evolution of electrogustometric threshold represents the actual recovery time course of chorda tympani peripheral sensitivity. [source] Somatosensory working memory performance in humans depends on both engagement and disengagement of regions in a distributed networkHUMAN BRAIN MAPPING, Issue 1 2010Saskia Haegens Abstract Successful working memory (WM) requires the engagement of relevant brain areas but possibly also the disengagement of irrelevant areas. We used magnetoencephalography (MEG) to elucidate the temporal dynamics of areas involved in a somatosensory WM task. We found an increase in gamma band activity in the primary and secondary somatosensory areas during encoding and retention, respectively. This was accompanied by an increase of alpha band activity over task-irrelevant regions including posterior and ipsilateral somatosensory cortex. Importantly, the alpha band increase was strongest during successful WM performance. Furthermore, we found frontal gamma band activity that correlated both with behavioral performance and the alpha band increase. We suggest that somatosensory gamma band activity reflects maintenance and attention-related components of WM operations, whereas alpha band activity reflects frontally controlled disengagement of task-irrelevant regions. Our results demonstrate that resource allocation involving the engagement of task-relevant and disengagement of task-irrelevant regions is needed for optimal task execution. Hum Brain Mapp, 2010. © 2009 Wiley-Liss, Inc. [source] HTLV-II infection associated with a chronic neurodegenerative disease: Clinical and molecular analysisJOURNAL OF MEDICAL VIROLOGY, Issue 2 2002Edimilson A. Silva Abstract HTLV II is a retrovirus endemic in some Amerindian tribes and spread worldwide with a high prevalence among intravenous drug abusers. It has three different genetic subtypes a, b, and d, defined mainly by the long terminal repeat (LTR) region. HTLV II has been associated with a neurodegenerative disease in few cases. We describe the first well-documented case in Brazil where the virus is endemic in isolated ethnic groups. The patient is a 55-year-old woman with a chronic and painful syndrome characterized by spastic paraparesis, hyperactive reflexes and spastic bladder. Somatosensory evoked potential indicates a thoracic spinal cord lesion. Computer tomography showed periventricular demyelination. Enzyme-linked immunosorbent assay was positive for HTLV I/II whereas the discriminatory Western blot was indeterminate. Molecular analysis of the Tax region revealed a HTLV II pattern that was also confirmed through sequencing the LTR region. Phylogenetic analysis of the LTR sequence shows an HTLV IIa subtype that clustered with the virus isolated from Kayapo Indians and Brazilian urban intravenous drug users. Indeterminate Western blots are frequently found using commercial kits, therefore we recommend that all cases in which a myelopathy is associated with an indeterminate serological result should be evaluated by PCR to determine the actual number of HTLV II associated myelopathy cases. J. Med. Virol. 66:253,257, 2002. © 2002 Wiley-Liss, Inc. [source] Abstracts of the 8th Meeting of the Italian Peripheral Nerve Study Group: 83JOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 1 2003G Lauria We describe a 64-year-old patient complaining of progressive gait disturbance, referred to the compressive effect of multiple discal protrusions, for about 3 years. At the age of 62 he presented epileptic seizures during a febrile episode. Cerebral MRI showed bilateral frontobasal T2-weighted hyperintensity involving cortex and white matter. Partial seizures reappeared one year later and a MRI revealed a mild frontobasal atrophy. At the moment of our observation, neurological examination showed waddling gait with bilateral foot drop, muscular atrophy and weakness limited to the gluteal muscles and widespread deep tendon areflexia. Nerve conduction studies showed absent F-waves at both upper and lower limb examination, with normal distal sensorimotor nerve conduction. Needle EMG examination detected mild chronic partial denervation, predominant in proximal muscles of lower limbs. Somatosensory evoked potentials recorded from upper extremities showed bilateral increase in early latencies (N9). Overall, neurophysiological findings indicated a widespread radiculopathy. Serum exams revealed positive anti-nucleus (1:640, granular). CSF examination detected increased IgG level and several oligoclonal bands. Chest radiogram was normal. Soon after our first observation, the patient showed symptoms of respiratory insufficiency. A CT scans revealed a thoracic mass compatible with microcytoma, whereas anti-Hu (3 +) antibodies and increased NSE (neuronal specific enolase) titer were found. In the following two weeks, the patient showed a progressive worsening of the general clinical conditions and died. We interpreted this complex neurological picture, which included an atypical limbic encephalitis and a slowly progressive polyradiculopathy, as a paraneoplastic syndrome. The almost complete resolution of the encephalitic process and the subtle chronic involvement of the peripheral nervous system, characterized by a limited, though widespread, radicular impairment, are rather peculiar features. [source] RE: Somatosensory evoked potentials predict neurolysis outcome in meralgia paraestheticaANZ JOURNAL OF SURGERY, Issue 9 2004Gavin Davis FRACS No abstract is available for this article. [source] GABAergic modulation of primary gustatory afferent synaptic efficacyDEVELOPMENTAL NEUROBIOLOGY, Issue 2 2002Andrew A. Sharp Abstract Modulation of synaptic transmission at the primary sensory afferent synapse is well documented for the somatosensory and olfactory systems. The present study was undertaken to test whether GABA impacts on transmission of gustatory information at the primary afferent synapse. In goldfish, the vagal gustatory input terminates in a laminated structure, the vagal lobes, whose sensory layers are homologous to the mammalian nucleus of the solitary tract. We relied on immunoreactivity for the GABA-transporter, GAT-1, to determine the distribution of GABAergic synapses in the vagal lobe. Immunocytochemistry showed dense, punctate GAT-1 immunoreactivity coincident with the layers of termination of primary afferent fibers. The laminar nature and polarized dendritic structure of the vagal lobe make it amenable to an in vitro slice preparation to study early synaptic events in the transmission of gustatory input. Electrical stimulation of the gustatory nerves in vitro produces synaptic field potentials (fEPSPs) predominantly mediated by ionotropic glutamate receptors. Bath application of either the GABAA receptor agonist muscimol or the GABAB receptor agonist baclofen caused a nearly complete suppression of the primary fEPSP. Coapplication of the appropriate GABAA or GABAB receptor antagonist bicuculline or CGP-55845 significantly reversed the effects of the agonists. These data indicate that GABAergic terminals situated in proximity to primary gustatory afferent terminals can modulate primary afferent input via both GABAA and GABAB receptors. The mechanism of action of GABAB receptors suggests a presynaptic locus of action for that receptor. © 2002 Wiley Periodicals, Inc. J Neurobiol 52: 133,143, 2002 [source] Revisiting the role of the insula in refractory partial epilepsyEPILEPSIA, Issue 3 2009Dang Khoa Nguyen Summary Purpose:, Recent evidence suggesting that some epilepsy surgery failures could be related to unrecognized insular epilepsy have led us to lower our threshold to sample the insula with intracerebral electrodes. In this study, we report our experience resulting from this change in strategy. Methods:, During the period extending from October 2004 to June 2007, 18 patients had an intracranial study including 10 with insular coverage. The decision to sample the insula with intracerebral electrodes was made in the context of (1) nonlesional parietal lobe-like epilepsy; (2) nonlesional frontal lobe-like epilepsy; (3) nonlesional temporal lobe-like epilepsy; and (4) atypical temporal lobe-like epilepsy. Results:, Intracerebral recordings confirmed the presence of insular lobe seizures in four patients. Cortical stimulation performed in 9 of 10 patients with insular electrodes elicited, in decreasing order of frequency, somatosensory, viscerosensory, motor, auditory, vestibular, and speech symptoms. Discussion:, Our results suggest that insular cortex epilepsy may mimic temporal, frontal, and parietal lobe epilepsies and that a nonnegligeable proportion of surgical candidates with drug-resistant epilepsy have an epileptogenic zone that involves the insula. [source] Parietal Lobe Epilepsy: The Semiology, Yield of Diagnostic Workup, and Surgical OutcomeEPILEPSIA, Issue 6 2004Dong Wook Kim Summary: Purpose: To characterize the clinical features, the prognostic value, and diagnostic sensitivities of various presurgical evaluations and the surgical outcomes in parietal lobe epilepsy (PLE), we describe 40 patients who were diagnosed as having PLE, including 27 surgically treated patients. Methods: The diagnosis was established by means of a standard presurgical evaluation, including magnetic resonance imaging (MRI), fluorodeoxyglucose,positron emission tomography (FDG-PET), ictal single-photon emission tomography (SPECT), and scalp video-electroencephalography (EEG) monitoring, with additional intracranial EEG monitoring in selected cases. Results: Among the 40 patients, 27 experienced at least one type of aura. The most common auras were somatosensory (13 patients), followed by affective, vertiginous, and visual auras. The patients had diverse manifestations. Eighteen patients showed simple motor seizure, followed by automotor seizure, and dialeptic seizure. Two patients manifested generalized tonic,clonic seizures only, and 19 patients experienced more than one type of seizure. The surgical outcome was favorable in 22 of 26 patients including 14 who were seizure free. Patients with localized MRI abnormality had a higher probability to be seizure free, with marginal significance (p = 0.062), whereas other diagnostic modalities failed to predict the surgical outcome. In the seizure-free group, localization sensitivity was 64.3% by MRI, 50% by PET, 45.5% by ictal SPECT, and 35.7% by ictal EEG. The concordance rate of the various diagnostic modalities was higher in the seizure-free group than in the non,seizure-free group, although it did not reach statistical significance. Conclusions: Seizures, in the case of PLE, can manifest themselves in a wider variety of ways than was previously thought. Surgical outcome was favorable in most of the patients. MRI abnormality and concordance of different diagnostic modalities were associated with high seizure-free rate. [source] Lumbosacral spinal cord somatosensory evoked potentials for quantification of nociception in horsesEQUINE VETERINARY JOURNAL, Issue 3 2010J. P. A. M. Van LOON Summary Reasons for performing study: There is a need for objective evaluation and quantification of the efficacy of analgesic drugs and analgesic techniques in horses. Objectives: To determine whether lumbosacral spinal cord somatosensory evoked potentials (SSEP) can be a useful and reliable tool to assess nociception in equines. Methods: SSEPs and electromyograms (EMG) from the epaxial muscles were recorded simultaneously, following electrical stimulation applied to the distal hindlimb in lightly anaesthetised Shetland ponies (n = 7). In order to validate the model, the effect of increasing stimulus intensity was documented and the conduction velocities (CV) of the stimulated nerves were calculated. The effect of epidurally applied methadone (0.4 mg/kg bwt) in a randomised, crossover design was investigated. Results: Two distinct complexes (N1P1 and N2P2) were identified in the SSEP waveform. Based on their latency and conduction velocity and the depressant effect of epidurally applied methadone, the SSEP N2P2 was ascribed to nociceptive A,-afferent stimulation. The SSEP N1P1 originated from non-nociceptive A,-afferent stimulation and was not influenced by epidurally applied methadone. Conclusions and potential relevance: The nociceptive A, component of the SSEP, the N2P2 complex, is presented as a valid and quantitative parameter of spinal nociceptive processing in the horse. Validation of the equine SSEP model enables the analgesic effects of new analgesics/analgesic techniques to be quantified and analgesia protocols for caudal epidural analgesia in equidae improved. [source] Constitutive opioid receptor activation: a prerequisite mechanism involved in acute opioid withdrawalADDICTION BIOLOGY, Issue 2 2005E Freye The opioid receptor antagonist naltrexone, which is used in detoxification and rehabilitation programmes in opioid addicts, can precipitate opioid withdrawal symptoms even in patients who have no opioid present. We tested the hypothesis that in order to precipitate withdrawal, opioids need to convert the inactive opioid receptor site via protein kinase C into a constitutively active form on which the antagonist precipitates withdrawal. Acute abstinence symptoms were induced by the potent opioid receptor agonist sufentanil (21?,g/kg), given for 6 days, which was followed by the antagonist naltrexone (20?,g/kg i.v.) in the awake trained canine (n,=,10). Abrupt displacement of opioid binding resulted in acute withdrawal symptoms: increase in blood pressure, heart rate, increase in amplitude height of somatosensory evoked potential, reduced tolerance to colon distention and a significant increase in grading of vegetative variables (restlessness, panting, thrashing of the head, whining, yawning, gnawing, salivation and/or rhinorrhoea, mydriasis, stepping of extremities and vomiting). Following a washout period of 14 days, the same animals were given the highly specific protein kinase C inhibitor H7 (250?,g/kg) prior to the same dosages of sufentanil and naltrexone. Such pretreatment was able to either attenuate or completely abolish the acute withdrawal symptoms. The data suggest that for precipitation of withdrawal, intracellular phosphorylation is a prerequisite in order to activate the opioid ,-receptor. In such a setting, naltrexone acts like an ,inverse agonist? relative to the action of the antagonist on a non-preoccupied receptor site not being exposed previously to a potent opioid agonist. [source] Effect of vitamin E supplementation in patients with ataxia with vitamin E deficiencyEUROPEAN JOURNAL OF NEUROLOGY, Issue 5 2001S. Gabsi Ataxia with vitamin E (Vit E) defciency (AVED) is an autosomal recessive disorder caused by mutations of the , tocopherol transfer protein gene. The Friedreich ataxia phenotype is the most frequent clinical presentation. In AVED patients, serum Vit E levels are very low in the absence of intestinal malabsorption. As Vit E is a major antioxidant agent, Vit E deficiency is supposed to be responsible for the pathological process. Twenty-four AVED patients were fully investigated (electromyography, nerve conduction velocity (NVC) studies, somatosensory evoked potentials, cerebral computed tomography scan, sural nerve biopsy, genetic studies) and supplemented with Vit E (800 mg daily) during a 1-year period. Clinical evaluation was mainly based on the Ataxia Rating Scale (ARS) for cerebellar ataxia assessment and serum Vit E levels were monitored. Serum Vit E levels normalized and ARS scores decreased moderately but significantly suggesting clinical improvement. Better results were noted with mean disease duration , 15 years. Reflexes remained abolished and posterior column disturbances unchanged. Vitamin E supplementation in AVED patients stabilizes the neurological signs and can lead to mild improvement of cerebellar ataxia, especially in early stages of the disease. [source] Heteromodal connections supporting multisensory integration at low levels of cortical processing in the monkeyEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 11 2005Céline Cappe Abstract While multisensory integration is thought to occur in higher hierarchical cortical areas, recent studies in man and monkey have revealed plurisensory modulations of activity in areas previously thought to be unimodal. To determine the cortical network involved in multisensory interactions, we performed multiple injections of different retrograde tracers in unimodal auditory (core), somatosensory (1/3b) and visual (V2 and MT) cortical areas of the marmoset. We found three types of heteromodal connections linking unimodal sensory areas. Visuo-somatosensory projections were observed originating from visual areas [probably the ventral and dorsal fundus of the superior temporal area (FSTv and FSTd), and middle temporal crescent (MTc)] toward areas 1/3b. Somatosensory projections to the auditory cortex were present from S2 and the anterior bank of the lateral sulcus. Finally, a visuo-auditory projection arises from an area anterior to the superior temporal sulcus (STS) toward the auditory core. Injections in different sensory regions allow us to define the frontal convexity and the temporal opercular caudal cortex as putative polysensory areas. A quantitative analysis of the laminar distribution of projecting neurons showed that heteromodal connections could be either feedback or feedforward. Taken together, our results provide the anatomical pathway for multisensory integration at low levels of information processing in the primate and argue against a strict hierarchical model. [source] Demonstration of long-range GABAergic connections distributed throughout the mouse neocortexEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 6 2005Ryohei Tomioka Abstract ,-Aminobutyric acid (GABA)ergic neurons in the neocortex have been mainly regarded as interneurons and thought to provide local interactions. Recently, however, glutamate decarboxylase (GAD) immunocytochemistry combined with retrograde labeling experiments revealed the existence of GABAergic projection neurons in the neocortex. We further studied the network of GABAergic projection neurons in the neocortex by using GAD67-green fluorescent protein (GFP) knock-in mice for retrograde labeling and a novel neocortical GABAergic neuron labeling method for axon tracing. Many GFP-positive neurons were retrogradely labeled after Fast Blue injection into the primary somatosensory, motor and visual cortices. These neurons were labeled not only around the injection site, but also at a long distance from the injection site. Of the retrogradely labeled GABAergic neurons remote from the injection sites, the vast majority (91%) exhibited somatostatin immunoreactivity, and were preferentially distributed in layer II, layer VI and in the white matter. In addition, most of GABAergic projection neurons were positive for neuropeptide Y (82%) and neuronal nitric oxide synthase (71%). We confirmed the long-range projections by tracing GFP-labeled GABAergic neurons with axon branches traveled rostro-caudally and medio-laterally. Axon branches could be traced up to 2 mm. Some (n = 2 of 4) were shown to cross the areal boundaries. The GABAergic projection neurons preferentially received neocortical inputs. From these results, we conclude that GABAergic projection neurons are distributed throughout the neocortex and are part of a corticocortical network. [source] Taste deficits related to dental deafferentation: an electrogustometric study in humansEUROPEAN JOURNAL OF ORAL SCIENCES, Issue 6 2006Yves Boucher Dental treatments, the prevalence of which increases with age, can cause orofacial somatosensory deficits. In order to examine whether they may also affect taste sensitivity, electrogustometric thresholds were measured at 9 loci on the tongue surface in 391 healthy non-smoking, non-medicated subjects. Results showed that the greater the number of deafferented teeth, the higher the thresholds. Irrespective of age, subjects with more than 7 deafferented teeth exhibited significantly higher thresholds than subjects with fewer than 7 deafferented teeth. Conversely, across age groups, no statistical difference was observed among subjects with no, or few, deafferented teeth. Hence, a taste deficit, which was not correlated to aging, was observed. An association was noticed between the location of taste deficits and the location of deafferented teeth. Higher thresholds at anterior sites, with no possible traumatic injury relationship, suggested that neurophysiological convergence between dental somatosensory and taste pathways , possibly in the nucleus tractus solitarius , could be responsible for these relative decreases of taste sensitivity when dental afferences were lacking. Among trigeminal contributions, lingual nerve and inferior alveolar nerve may synergize taste. [source] From learning to forgetting: Behavioral, circuitry, and molecular properties define the different functional states of the recognition memory traceHIPPOCAMPUS, Issue 5 2010Rocío Romero-Granados Abstract Neuropsychological analyses of amnesic patients, as well as lesion experiments, indicate that the temporal lobe is essential for the encoding, storage, and expression of object recognition memory (ORM). However, temporal lobe structures directly involved in the consolidation and reconsolidation of these memories are not yet well-defined. We report here that systemic administration of a protein synthesis inhibitor before or up to 4 h after training or reactivation sessions impairs consolidation and reconsolidation of ORM, without affecting short-term memory. We have also observed that ORM reconsolidation is sensitive to protein synthesis inhibition, independently of the ORM trace age. Using bdnf and egr-1 gene expression analysis, we defined temporal lobe areas related to consolidation and reconsolidation of ORM. Training and reactivation 21 days after ORM acquisition sessions provoked changes in bdnf mRNA in somatosensory, perirhinal, and hippocampal cortices. Reactivation 2 days after the training session elicited changes in bdnf and egr-1 mRNA in entorhinal and prefrontal cortices, while reactivation 9 days post-training provoked an increase in egr-1 transcription in somatosensory and entorhinal cortices. The differences in activated circuits and in the capacity to recall the memory trace after 9 or 21 days post-training suggest that memory trace suffers functional changes in this period of time. All these results indicate that the functional state of the recognition memory trace, from acquisition to forgetting, can be specifically defined by behavioral, circuitry, and molecular properties. © 2009 Wiley-Liss, Inc. [source] Somatosensory working memory performance in humans depends on both engagement and disengagement of regions in a distributed networkHUMAN BRAIN MAPPING, Issue 1 2010Saskia Haegens Abstract Successful working memory (WM) requires the engagement of relevant brain areas but possibly also the disengagement of irrelevant areas. We used magnetoencephalography (MEG) to elucidate the temporal dynamics of areas involved in a somatosensory WM task. We found an increase in gamma band activity in the primary and secondary somatosensory areas during encoding and retention, respectively. This was accompanied by an increase of alpha band activity over task-irrelevant regions including posterior and ipsilateral somatosensory cortex. Importantly, the alpha band increase was strongest during successful WM performance. Furthermore, we found frontal gamma band activity that correlated both with behavioral performance and the alpha band increase. We suggest that somatosensory gamma band activity reflects maintenance and attention-related components of WM operations, whereas alpha band activity reflects frontally controlled disengagement of task-irrelevant regions. Our results demonstrate that resource allocation involving the engagement of task-relevant and disengagement of task-irrelevant regions is needed for optimal task execution. Hum Brain Mapp, 2010. © 2009 Wiley-Liss, Inc. [source] Movement gating of beta/gamma oscillations involved in the N30 somatosensory evoked potentialHUMAN BRAIN MAPPING, Issue 5 2009Ana Maria Cebolla Abstract Evoked potential modulation allows the study of dynamic brain processing. The mechanism of movement gating of the frontal N30 component of somatosensory evoked potentials (SEP) produced by the stimulation of the median nerve at wrist remains to be elucidated. At rest, a power enhancement and a significant phase-locking of the electroencephalographic (EEG) oscillation in the beta/gamma range (25,35 Hz) are related to the emergence of the N30. The latter was also perfectly identified in presence of pure phase-locking situation. Here, we investigated the contribution of these rhythmic activities to the specific gating of the N30 component during movement. We demonstrated that concomitant execution of finger movement of the stimulated hand impinges such temporal concentration of the ongoing beta/gamma EEG oscillations and abolishes the N30 component throughout their large topographical extent on the scalp. This also proves that the phase-locking phenomenon is one of the main actors for the N30 generation. These findings could be explained by the involvement of neuronal populations of the sensorimotor cortex and other related areas, which are unable to respond to the phasic sensory activation and to phase-lock their firing discharges to the external sensory input during the movement. This new insight into the contribution of phase-locked oscillation in the emergence of the N30 and in its gating behavior calls for a reappraisal of fundamental and clinical interpretation of the frontal N30 component. Hum Brain Mapp 2009. © 2008 Wiley-Liss, Inc. [source] Rolandic alpha and beta EEG rhythms' strengths are inversely related to fMRI-BOLD signal in primary somatosensory and motor cortexHUMAN BRAIN MAPPING, Issue 4 2009Petra Ritter Abstract Similar to the posterior alpha rhythm, pericentral (Rolandic) EEG rhythms in the alpha and beta frequency range are referred to as "idle rhythms" indicating a "resting state" of the respective system. The precise function of these rhythms is not clear. We used simultaneous EEG-fMRI during a bimanual motor task to localize brain areas involved in Rolandic alpha and beta EEG rhythms. The identification of these rhythms in the MR environment was achieved by a blind source separation algorithm. Rhythm "strength", i.e. spectral power determined by wavelet analysis, inversely correlated most strongly with the fMRI-BOLD signal in the postcentral cortex for the Rolandic alpha (mu) rhythm and in the precentral cortex for the Rolandic beta rhythm. FMRI correlates of Rolandic alpha and beta rhythms were distinct from those associated with the posterior "classical" alpha rhythm, which correlated inversely with the BOLD signal in the occipital cortex. An inverse correlation with the BOLD signal in the respective sensory area seems to be a general feature of "idle rhythms". Hum Brain Mapp 2009. © 2008 Wiley-Liss, Inc. [source] Coherent corticomuscular oscillations originate from primary motor cortex: Evidence from patients with early brain lesionsHUMAN BRAIN MAPPING, Issue 10 2006Christian Gerloff Abstract Coherent oscillations of neurons in the primary motor cortex (M1) have been shown to be involved in the corticospinal control of muscle activity. This interaction between M1 and muscle can be measured by the analysis of corticomuscular coherence in the ,-frequency range (,-CMCoh; 14,30 Hz). Largely based on magnetoencephalographic (MEG) source-modeling data, it is widely assumed that ,-CMCoh reflects direct coupling between M1 and muscle. Deafferentation is capable of modulating ,-CMCoh, however, and therefore the influence of reafferent somatosensory signaling and corresponding neuronal activity in the somatosensory cortex (S1) has been unclear. We present transcranial magnetic stimulation (TMS) and MEG data from three adult patients suffering from congenital hemiparesis due to pre- and perinatally acquired lesions of the pyramidal tract. In these patients, interhemispheric reorganization had resulted in relocation of M1 to the contralesional hemisphere, ipsilateral to the paretic hand, whereas S1 had remained in the lesioned hemisphere. This topographic dichotomy allowed for an unequivocal topographic differentiation of M1 and S1 with MEG (which is not possible if M1 and S1 are directly adjacent within one hemisphere). In all patients, ,-CMCoh originated from the contralesional M1, in accordance with the TMS-evoked motor responses, and in contrast to the somatosensory evoked fields (SEFs) for which the sources (N20m) were localized in S1 of the lesioned hemisphere. These data provide direct evidence for the concept that ,-CMCoh reflects the motorcortical efferent drive from M1 to the spinal motoneuron pool and muscle. No evidence was found for a relevant contribution of neuronal activity in S1 to ,-CMCoh. Hum Brain Mapp, 2006. © 2006 Wiley-Liss, Inc. [source] Difference in somatosensory evoked fields elicited by mechanical and electrical stimulations: Elucidation of the human homunculus by a noninvasive methodHUMAN BRAIN MAPPING, Issue 4 2005Ken Inoue Abstract We recently recorded somatosensory evoked fields (SEFs) elicited by compressing the glabrous skin of the finger and decompressing it by using a photosensor trigger. In that study, the equivalent current dipoles (ECDs) for these evoked fields appeared to be physiologically similar to the ECDs of P30m in median nerve stimulation. We sought to determine the relations of evoked fields elicited by mechanically stimulating the glabrous skin of the great toe and those of electrically produced P40m. We studied SEFs elicited by mechanical and electrical stimulations from the median and tibial nerves. The orientations of dipoles from the mechanical stimulations were from anterior-to-posterior, similar to the orientations of dipoles for P30m. The direction of the dipole around the peak of N20m from median nerve electrical stimulation was opposite to these directions. The orientations of dipoles around the peak of P40m by tibial nerve stimulation were transverse, whereas those by the compression and decompression stimulation of the toe were directed from anterior-to-posterior. The concordance of the orientations in ECDs for evoked fields elicited by mechanical and electrical stimulations suggests that the ECDs of P40m are physiologically similar to those of P30m but not to those of N20m. The discrepancy in orientations in ECDs for evoked field elicited by these stimulations in the lower extremity suggests that electrical and compression stimulations elicit evoked fields responding to fast surface rubbing stimuli and/or stimuli to the muscle and joint. Hum. Brain Mapping 24:274,283, 2005. © 2005 Wiley-Liss, Inc. [source] Neural connectivity in hand sensorimotor brain areas: An evaluation by evoked field morphologyHUMAN BRAIN MAPPING, Issue 2 2005Franca Tecchio Abstract The connectivity pattern of the neural network devoted to sensory processing depends on the timing of relay recruitment from receptors to cortical areas. The aim of the present work was to uncover and quantify the way the cortical relay recruitment is reflected in the shape of the brain-evoked responses. We recorded the magnetic somatosensory evoked fields (SEF) generated in 36 volunteers by separate bilateral electrical stimulation of median nerve, thumb, and little fingers. After defining an index that quantifies the shape similarity of two SEF traces, we studied the morphologic characteristics of the recorded SEFs within the 20-ms time window that followed the impulse arrival at the primary sensory cortex. Based on our similarity criterion, the shape of the SEFs obtained stimulating the median nerve was observed to be more similar to the one obtained from the thumb (same median nerve innervation) than to the one obtained from the little finger (ulnar nerve innervation). In addition, SEF shapes associated with different brain regions were more similar within an individual than between subjects. Because the SEF morphologic characteristics turned out to be quite diverse among subjects, we defined similarity levels that allowed us to identify three main classes of SEF shapes in normalcy. We show evidence that the morphology of the evoked response describes the anatomo-functional connectivity pattern in the primary sensory areas. Our findings suggest the possible existence of a thalamo-cortico-thalamic responsiveness loop related to the different classes. Hum Brain Mapp 24:99,108, 2005. © 2004 Wiley-Liss, Inc. [source] Afferent pathway dysfunction in children with primary nocturnal enuresisINTERNATIONAL JOURNAL OF UROLOGY, Issue 2 2010Linya Lv Objectives: To investigate afferent pathway dysfunction in children with primary nocturnal enuresis by measuring pudendal somatosensory evoked potential and tibial somatosensory evoked potential. Methods: Subjects with primary nocturnal enuresis, 36 boys and 18 girls, aged from 5 to 16 years, were enrolled in this study: 24 subjects had complicated primary enuresis (CPE) and 30 subjects had monosymptomatic primary enuresis (MPE). There were no differences in bodyweight or gender between the MPE and CPE groups (P > 0.05). All of the children underwent physical examination, urine analysis, urinary ultrasound and spinal magnetic resonance imaging. Only subjects without urological and neurological abnormalities (with the exception of spina bifida occulta, which was found in some of the patients) were included in this neurophysiological study. Results: There were 20 children who were positively recorded with pudendal somatosensory evoked potential in the CPE group, and all of the children in the MPE group were positively recorded (P < 0.05). Positive records of tibial somatosensory evoked potential were successfully achieved in both groups. Furthermore, the pudendal and tibial conductive velocity were slower as compared to the normal range, especially in children in the CPE group (P < 0.001). Conclusions: Afferent pathway function may be impaired by some factors, which should be considered by both clinicians and parents. [source] Whole-brain functional magnetic resonance imaging mapping of acute nociceptive responses induced by formalin in rats using atlas registration-based event-related analysisJOURNAL OF NEUROSCIENCE RESEARCH, Issue 8 2008Yen-Yu I. Shih Abstract Nociceptive neuronal activation in subcortical regions has not been well investigated in functional magnetic resonance imaging (fMRI) studies. The present report aimed to use the blood oxygenation level-dependent (BOLD) fMRI technique to map nociceptive responses in both subcortical and cortical regions by employing a refined data processing method, the atlas registration-based event-related (ARBER) analysis technique. During fMRI acquisition, 5% formalin (50 ,l) was injected into the left hindpaw to induce nociception. ARBER was then used to normalize the data among rats, and images were analyzed using automatic selection of the atlas-based region of interest. It was found that formalin-induced nociceptive processing increased BOLD signals in both cortical and subcortical regions. The cortical activation was distributed over the cingulate, motor, somatosensory, insular, and visual cortices, and the subcortical activation involved the caudate putamen, hippocampus, periaqueductal gray, superior colliculus, thalamus, and hypothalamus. With the aid of ARBER, the present study revealed a detailed activation pattern that possibly indicated the recruitment of various parts of the nociceptive system. The results also demonstrated the utilization of ARBER in establishing an fMRI-based whole-brain nociceptive map. The formalin induced nociceptive images may serve as a template of central nociceptive responses, which can facilitate the future use of fMRI in evaluation of new drugs and preclinical therapies for pain. © 2008 Wiley-Liss, Inc. [source] Chronic nicotine administration increases NGF-like immunoreactivity in frontoparietal cerebral cortexJOURNAL OF NEUROSCIENCE RESEARCH, Issue 5 2003R. Martínez-Rodríguez Abstract Nicotine/nicotine agonists, which have been proposed as therapeutic agents for the treatment of Alzheimer's disease and other neurodegenerative disorders, produce a wide variety of effects on the nervous system. Some mechanisms involved remain poorly understood. In this work, immunohistochemical techniques were used to determine the effect of nicotine on nerve growth factor (NGF) in the frontoparietal (motor, somatosensory) brain cortex of the albino rat. Nicotine was chronically administered intraperitoneally using osmotic pumps (0.35 mg nicotine base/kg body weight/day for 14 days). An increase in the number and the immunoreaction intensity of NGF-like positive pyramidal and nonpyramidal neurons of these cortical areas was observed after treatment. Immunopositive astroglial cells were always seen in sections of treated animals but not in controls. The neuropil of control animals was, in general, devoid of reaction, but in treated animals, immunopositive prolongations were located randomly, some in close association with capillaries. At the electron microscopic level, these prolongations were demonstrated as belonging to neurons (dendrites and axons) and astroglial cells. Nicotinic activation of selected neurons and glial cells seems to trigger NGF/neurotrophic mechanisms, suggesting their use may be of benefit in prevention and treatment of neurodegenerative diseases. © 2003 Wiley-Liss, Inc. [source] Mechanisms of oral somatosensory and motor functions and their clinical correlates,JOURNAL OF ORAL REHABILITATION, Issue 4 2006B. J. SESSLE summary, This article provides a review of somatosensory and motor pathways and processes involved in oral sensorimotor function and dysfunction. It reviews somatosensory processes in peripheral tissues, brainstem and higher brain centres such as thalamus and cerebral cortex, with a particular emphasis on nociceptive mechanisms. It also outlines some of the circuits and processes involved in reflexes and motor control. In addition, it emphasizes the concept of neuroplasticity and its applicability to oro-facial pain, to motor control and motor learning, and to adaptation to changes in the oral sensory environment such as may occur with the placement of dental implants. [source] Spinal somatosensory evoked potential evaluation of acute nerve-root injury associated with pedicle-screw placement procedures: An experimental studyJOURNAL OF ORTHOPAEDIC RESEARCH, Issue 2 2003I-Ming Jou Pedicle screws for spinal fixation risk neural damage because of the proximity between screw and nerve root. We assessed whether spinal somatosensory evoked potential (SSEP) could selectively detect pedicle-screw-related acute isolated nerve injury. Because pedicle screws are too large for a rat's spine, we inserted a K-wire close to the pedicle in 32 rats, intending not to injure the nerve root in eight (controls), and to injure the L4 or L5 root in 24. We used sciatic-nerve-elicited SSEP pre- and postinsertion. Radiologic, histologic, and postmortem observations confirmed the level and degree of root injury. Sciatic (SFI), tibial (TFI), and peroneal function indices (PFI) were calculated and correlated with changes in potential. Although not specific for injuries to different roots, amplitude reduction immediately postinsertion was significant in the experimental groups. Animals with the offending wire left in place for one hour showed a further non-significant deterioration of amplitude. Electrophysiologic changes correlated with SFI and histologic findings in all groups. SSEP monitoring provided reliable, useful diagnostic and intraoperative information about the functional integrity of single nerve-root injury. These findings are clinically relevant to acute nerve-root injury and pedicle-screw insertion. If a nerve-root irritant remains in place, a considerable neurologic deficit will occur. © 2002 Orthopaedic Research Society. Published by Elsevier Science Ltd. All rights reserved. [source] Genotype,phenotype correlation in some autosomal recessive hereditary spastic paraplegiasJOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 2 2004F Manganelli Hereditary spastic paraplegias (HSPs) are a group of clinically and genetically inherited disorders. Spastic paraparesis (SP), the main clinical feature of all HSPs can occur in relative isolation in the "pure" form or in combination with other neurological deficits in "complicated" forms. Autosomal dominant, autosomal recessive (AR) and X-linked recessive inheritance pattern of HSPs have been reported. At present, among AR-HSPs, three genes, paraplegin (SPG7), spartin (SPG20 , Troyer syndrome) and maspardin (SPG21) have been identified and six genetic loci have been mapped (SPG5, SPG11, SPG14, SPG15, SPG24, SPG25). We have evaluated 11 patients belonging to six AR-HSP families genetically identified as SPG5, SPG7, SPG11 and SPG15. In all patients electromyography, nerve conduction velocity studies, visual (VEPs), somatosensory (SSEPs), brainstem auditory (BAEPs) and magnetic motor (MMEPs) evoked potentials were performed. All 4 SPG5 patients, affected by a pure form of SP, showed abnormalities of both MMEPs and SSEPs, and two of them also VEP alterations. In the two SPG7 patients with complicated SP, MMEP abnormalities only were discovered. Among the three SPG11 patients affected by SP, complicated by mental retardation and thin corpus callosum, electrophysiological studies revealed MMEP abnormalities and signs of motor neuropathy in one of them. Finally, in the SPG15 family, presenting with SP associated with mental retardation and neurosensorial deafness, MMEP and BAEP alterations were found. [source] Bicuculline-induced brain activation in mice detected by functional magnetic resonance imagingMAGNETIC RESONANCE IN MEDICINE, Issue 2 2001Thomas Mueggler Abstract Dynamic measurements of local changes in relative cerebral blood volume (CBVrel) during a pharmacological stimulation paradigm were performed in mice. Using magnetite nanoparticles as an intravascular contrast agent, high-resolution CBVrel maps were obtained. Intravenous administration of the GABAA antagonist bicuculline prompted increases in local CBVrel as assessed by MRI with a high spatial resolution of 0.2 × 0.2 mm2 and a temporal resolution of 21 s. Signal changes occurred 20,30 s after the onset of drug infusion in the somatosensory and motor cortex, followed by other cortical and subcortical structures. The magnitudes of the CBVrel increases were 18% ± 4%, 46% ± 14%, and 67% ± 7%, as compared to prestimulation values for the cortex, and 9% ± 3%, 25% ± 4%, and 36% ± 7% for the caudate putamen for bicuculline doses of 0.6, 1.25, and 1.5 mg/kg, respectively. On-line monitoring of transcutaneous carbon dioxide tension PtcCO2 reflecting arterial PaCO2 did not show any alteration during the stimulation paradigm. One of five of the mice receiving the highest bicuculline dose, and three of seven receiving the intermediate dose displayed a different cortical response pattern. After a CBVrel increase of 40% lasting for approximately 1 min, significant CBVrelreductions by 80% have been observed. Subcortical structures did not display this behavior. The present study suggests that this noninvasive approach of functional MRI (fMRI) can be applied to study drug-induced brain activation by central nervous system (CNS) drugs in mice under normal and pathological situations. Magn Reson Med 46:292,298, 2001. © 2001 Wiley-Liss, Inc. [source] Temperature modulated histamine-itch in lesional and nonlesional skin in atopic eczema , a combined psychophysical and neuroimaging studyALLERGY, Issue 1 2010F. Pfab Abstract Background: Itch is the major symptom of many allergic diseases; yet it is still difficult to measure objectively. The aim of this study was to use an evaluated itch stimulus model in lesional (LS) and nonlesional (NLS) atopic eczema (AE) skin and to characterize cerebral responses using functional magnetic resonance imaging (fMRI). Methods: Thermal modulation was performed on a histamine stimulus in randomized order on LS or NLS in rapid alternating order from 32°C (warm) to 25°C (cold). Subjective itch ratings were recorded. Additionally, fMRI measurements were used to analyze the cerebral processing (n = 13). Healthy skin (HS) of age-matched volunteers served as control (n = 9). Results: Mean VAS itch intensity was significantly (P < 0.0001) higher during the relative cold [55.2 ± 8.3% (LS); 48.6 ± 8.2% (NLS)] compared to the relative warm blocks [36.0 ± 7.3% (LS); 33.7 ± 7.6% (NLS)]. Compared to HS, the itch response was delayed in LS and NLS. Itch intensity was perceived highest in LS, followed by NLS and HS. For NLS, fMRI revealed at the beginning of the itch provocation a cerebral deactivation pattern in itch processing structures (thalamus, prefrontal, cingulate, insular, somatosensory and motor cortex). During the course of stimulation, the cerebral deactivation was reduced with time and instead an activation of the basal ganglia occurred. In contrast LS showed an activation instead of deactivation pattern already at the beginning of the stimulation in the above mentioned structures. Conclusions: Moderate short-term temperature modulation led to a reproducible, significant enhancement of histamine-induced itch with the strongest effect in LS. The differences in itch perception and itch kinetics between healthy volunteers and NLS in patients point towards an ongoing central inhibitory activity patients with AE, especially at the beginning of the itch provocation. [source] Improvement in a quantitative measure of bradykinesia after microelectrode recording in patients with Parkinson's disease during deep brain stimulation surgeryMOVEMENT DISORDERS, Issue 5 2006Mandy Miller Koop MS Abstract It is widely accepted that patients with Parkinson's disease experience immediate but temporary improvement in motor signs after surgical implantation of subthalamic nucleus (STN) deep brain stimulating electrodes before the electrodes are activated, although this has never been formally studied. Based on anecdotal observations that limb mobility improved just after microelectrode recording (MER) during deep brain stimulation (DBS) procedures, we designed a prospective study to measure upper extremity bradykinesia using a quantitative measure of angular velocity. Measurements were made pre- and post-MER and during intraoperative DBS. Analysis of 98 STN DBS procedures performed on 61 patients showed that MER did not create adverse clinical symptoms despite concerns that MER increases morbidity. Quantitative upper extremity bradykinesia improved after MER alone, and further improvement was seen during intraoperative DBS. Electrophysiological data from each case were then compared to the improvement in bradykinesia post-MER alone and a significant correlation was found between the improvement in arm bradykinesia, the number of passes through the STN with somatosensory driving, and also with the number of arm cells with somatosensory driving in the STN, but not with total number of passes, total number of passes through the STN, or total number of cells with somatosensory driving in the STN. This study demonstrates that there is a significant improvement in upper extremity bradykinesia just after MER, before inserting or activating the DBS electrode in patients with Parkinson's disease who undergo STN DBS. © 2006 Movement Disorder Society [source] | ||||||||||||||||||||||||||||