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Abbas F. Sadikot - One of the best experts on this subject based on the ideXlab platform.
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The impact of ventrolateral thalamotomy on tremor and voluntary motor behavior in patients with Parkinson’s disease
Experimental Brain Research, 2006Co-Authors: Christian Duval, Michel Panisset, Antonio P. Strafella, Abbas F. SadikotAbstract:A preferred target for parkinsonian tremor alleviation is the ventrolateral (VL) thalamus. The goal of the present study is to determine how lesions involving the presumed cerebellar and pallidal recipient areas of the “motor” thalamus would alter the tremor and motor behavior of ten patients with Parkinson’s disease (PD). Tremor amplitude, power dispersion (a measure of sharpness of the power spectrum of tremor), and power distribution were quantified using a laser displacement sensor prior to, and a week after, VL thalamotomy. As well, the impact of surgery on tremor seen during movement was quantified in a manual-tracking (MT) task. Tremor-induced noise (a measure of the amount of tremor present during movement) and ERROR (difference between subject’s performance and target) were quantified. Finally, bradykinesia was assessed with a rapid alternating movement (RAM) task. Duration, range, and amplitude irregularity of wrist pronation–supination cycles were computed. Both motor tasks were quantified using a highly sensitive forearm rotational sensor. Healthy age-matched control subjects were also tested. Magnetic resonance images with an integrated atlas of thalamic nuclei were used to confirm lesion location. Results show that the lesions were centered upon the Posterior portion of the Ventral lateral (VLp) Nucleus of the thalamus, included the Posterior part of the Ventral lateral anterior Nucleus (VLa), and extended Posteriorly to encroach upon the most rostral sector of the sensory Ventral Posterior Nucleus (VPLa). VL thalamotomy significantly decreased tremor amplitude in all cases. Power dispersion was increased significantly so that it became similar to that of control subjects. Changes in power distribution indicate that thalamotomy selectively targeted PD tremor oscillations. Tremor detected during the MT task was also markedly decreased, becoming similar to that of controls. Patients also showed significant decrease in ERROR during MT. RAM duration and range were not significantly modified by the surgery, and patients’ performance remained impaired compared to healthy control subjects. Collectively, these results suggest that lesions involving the presumed “cerebellar” and “pallidal” recipient sectors of the motor thalamus do not worsen bradykinesia, suggesting that neural circuits other than the pallido-thalamo-cortical loop may be involved in slowness of movement in PD. A review of alternate pathways is presented.
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The impact of ventrolateral thalamotomy on tremor and voluntary motor behavior in patients with Parkinson's disease.
Experimental Brain Research, 2005Co-Authors: Christian Duval, Michel Panisset, Antonio P. Strafella, Abbas F. SadikotAbstract:A preferred target for parkinsonian tremor alleviation is the ventrolateral (VL) thalamus. The goal of the present study is to determine how lesions involving the presumed cerebellar and pallidal recipient areas of the “motor” thalamus would alter the tremor and motor behavior of ten patients with Parkinson’s disease (PD). Tremor amplitude, power dispersion (a measure of sharpness of the power spectrum of tremor), and power distribution were quantified using a laser displacement sensor prior to, and a week after, VL thalamotomy. As well, the impact of surgery on tremor seen during movement was quantified in a manual-tracking (MT) task. Tremor-induced noise (a measure of the amount of tremor present during movement) and ERROR (difference between subject’s performance and target) were quantified. Finally, bradykinesia was assessed with a rapid alternating movement (RAM) task. Duration, range, and amplitude irregularity of wrist pronation–supination cycles were computed. Both motor tasks were quantified using a highly sensitive forearm rotational sensor. Healthy age-matched control subjects were also tested. Magnetic resonance images with an integrated atlas of thalamic nuclei were used to confirm lesion location. Results show that the lesions were centered upon the Posterior portion of the Ventral lateral (VLp) Nucleus of the thalamus, included the Posterior part of the Ventral lateral anterior Nucleus (VLa), and extended Posteriorly to encroach upon the most rostral sector of the sensory Ventral Posterior Nucleus (VPLa). VL thalamotomy significantly decreased tremor amplitude in all cases. Power dispersion was increased significantly so that it became similar to that of control subjects. Changes in power distribution indicate that thalamotomy selectively targeted PD tremor oscillations. Tremor detected during the MT task was also markedly decreased, becoming similar to that of controls. Patients also showed significant decrease in ERROR during MT. RAM duration and range were not significantly modified by the surgery, and patients’ performance remained impaired compared to healthy control subjects. Collectively, these results suggest that lesions involving the presumed “cerebellar” and “pallidal” recipient sectors of the motor thalamus do not worsen bradykinesia, suggesting that neural circuits other than the pallido-thalamo-cortical loop may be involved in slowness of movement in PD. A review of alternate pathways is presented.
Edward G. Jones - One of the best experts on this subject based on the ideXlab platform.
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Vesicular glutamate transporters define two sets of glutamatergic afferents to the somatosensory thalamus and two thalamocortical projections in the mouse.
The Journal of Comparative Neurology, 2008Co-Authors: Alessandro Graziano, Karl D Murray, Edward G. JonesAbstract:The Ventral Posterior Nucleus of the thalamus (VP) receives two major sets of excitatory inputs, one from the ascending somatosensory pathways originating in the dorsal horn, dorsal column nuclei, and trigeminal nuclei, and the other originating from the cerebral cortex. Both systems use glutamate as neurotransmitter, as do the thalamocortical axons relaying somatosensory information from the VP to the primary somatosensory cortex (SI). The synapses formed by these projection systems differ anatomically, physiologically, and in their capacity for short-term synaptic plasticity. Glutamate uptake into synaptic vesicles and its release at central synapses depend on two isoforms of vesicular glutamate transporters, VGluT1 and VGluT2. Despite ample evidence of their complementary distribution, some instances exist of co-localization in the same brain areas or at the same synapses. In the thalamus, the two transcripts coexist in cells of the VP and other nuclei but not in the Posterior or intralaminar nuclei. We show that the two isoforms are completely segregated at VP synapses, despite their widespread expression throughout the dorsal and Ventral thalamus. We present immunocytochemical, ultrastructural, gene expression, and connectional evidence that VGluT1 in the VP is only found at corticothalamic synapses, whereas VGluT2 is only found at terminals made by axons originating in the spinal cord and brainstem. By contrast, the two VGluT isoforms are co-localized in thalamocortical axon terminals targeting layer IV, but not in those targeting layer I, suggesting the presence of two distinct projection systems related to the core/matrix pattern of organization of thalamocortical connectivity described in other mammals. J. Comp. Neurol. 507:1258–1276, 2008. © 2008 Wiley-Liss, Inc.
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Reticular Nucleus-specific changes in α3 subunit protein at GABA synapses in genetically epilepsy-prone rats
Proceedings of the National Academy of Sciences of the United States of America, 2007Co-Authors: Jeffrey Coble, Gilles Van Luijtelaar, Edward G. JonesAbstract:Differential composition of GABAA receptor (GABAAR) subunits underlies the variability of fast inhibitory synaptic transmission; alteration of specific GABAAR subunits in localized brain regions may contribute to abnormal brain states such as absence epilepsy. We combined immunocytochemistry and high-resolution ImmunoGold electron microscopy to study cellular and subcellular localization of GABAAR α1, α3, and β2/β3 subunits in Ventral Posterior Nucleus (VP) and reticular Nucleus (RTN) of control rats and WAG/Rij rats, a genetic model of absence epilepsy. In control rats, α1 subunits were prominent at inhibitory synapses in VP and much less prominent in RTN; in contrast, the α3 subunit was highly evident at inhibitory synapses in RTN. β2/β3 subunits were evenly distributed at inhibitory synapses in both VP and RTN. ImmunoGold particles representing all subunits were concentrated at postsynaptic densities with no extrasynaptic localization. Calculated mean number of particles for α1 subunit per postsynaptic density in nonepileptic VP was 6.1 ± 3.7, for α3 subunit in RTN it was 6.6 ± 3.4, and for β2/β3 subunits in VP and RTN the mean numbers were 3.7 ± 1.3 and 3.5 ± 1.2, respectively. In WAG/Rij rats, there was a specific loss of α3 subunit immunoreactivity at inhibitory synapses in RTN, without reduction in α3 subunit mRNA or significant change in immunostaining for other markers of RTN cell identity such as GABA or parvalbumin. α3 immunostaining in cortex was unchanged. Subtle, localized changes in GABAAR expression acting at highly specific points in the interconnected thalamocortical network lie at the heart of idiopathic generalized epilepsy.
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The thalamus of the monotremes: cyto- and myeloarchitecture and chemical neuroanatomy.
Philosophical Transactions of the Royal Society B, 2007Co-Authors: Shawn Mikula, Paul R. Manger, Edward G. JonesAbstract:Echidna and platypus brains were sectioned and stained by Nissl or myelin stains or immunocytochemically for calcium-binding proteins, gamma aminobutyric acid (GABA) or other antigens. Cyto- and myeloarchitecture revealed thalami that are fundamentally mammalian in organization, with the three principal divisions of the thalamus (epithalamus, dorsal thalamus and Ventral thalamus) identifiable as in marsupials and eutherian mammals. The dorsal thalamus exhibits more nuclear parcellation than hitherto described, but lack of an internal medullary lamina, caused by splaying out of afferent fibre tracts that contribute to it in other mammals, makes identification of anterior, medial and intralaminar nuclear groups difficult. Differentiation of the Ventral nuclei is evident with the Ventral Posterior Nucleus of the platypus enormously expanded into the interior of the cerebral hemisphere, where it adopts a relationship to the striatum not seen in other mammals. Other nuclei such as the lateral dorsal become identifiable by expression of patterns of calcium-binding proteins identical to those found in other mammals. GABA cells are present in the Ventral and dorsal thalamic nuclei, and in the Ventral thalamus form a remarkable continuum with GABA cells of the two segments of the globus pallidus and pars reticulata of the substantia nigra.
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Switching of NMDA Receptor 2A and 2B Subunits at Thalamic and Cortical Synapses during Early Postnatal Development
The Journal of Neuroscience, 2004Co-Authors: Karl D Murray, Edward G. JonesAbstract:Switching of the NMDA receptor 2A (NR2A) and NR2B subunits at NMDA receptors is thought to underlie the functional changes that occur in NMDA receptor properties during the developmental epoch when neural plasticity is most pronounced. The cellular expression of NR2A and NR2B and the NR2 synaptic binding protein postsynaptic density-95 (PSD-95) was examined in the mouse somatosensory cortex and thalamus from postnatal day 2 (P2) to P15 using reverse transcription-PCR, in situ hybridization histochemistry, and immunocytochemistry. The localization of NR2A and NR2B subunits and PSD-95 was then studied at synapses in layer IV of somatosensory cortex and in the Ventral Posterior Nucleus of the thalamus using high-resolution immunoelectron microscopy. At both cortical and thalamic synapses, a quantitative switch in the dominant synaptic subunit from NR2B to NR2A was accompanied by a similar change in the cellular expression of NR2A but not of NR2B. Synaptic PSD-95 developed independently, although both NR2A and NR2B colocalized with PSD-95. Displacement of NR2B subunits from synapses was not accompanied by an increase in an extrasynaptic pool of this subunit. Thus, the switch in synaptic NR2 subunit predominance does not occur by changes in expression or displacement from synapses and may reflect the formation of new synapses from which NR2B is lacking.
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A pain in the thalamus.
The Journal of Pain, 2002Co-Authors: Edward G. JonesAbstract:The review of Willis et al is one that clearly needed to be written. It raises two important issues, one of them perennial, the other current if probably ephemeral. The first stems from the idea that the pathway running from lamina I of the dorsal horn of the spinal cord can be regarded as “the” painand thermospecific pathway and that it relays in regions of the thalamus outside the classic somatosensory relay nuclei, en route to areas of cerebral cortex in the insular and cingulate regions. The second deals with the exact localization of the part of the thalamus identified by Craig and coworkers as the relevant relay center. The idea that all aspects of the phenomenon we know as pain can be explained on the basis of a single hardwired line of connections running from the small nerve fibers of peripheral nerves, through lamina I of the dorsal horn, and terminating outside the primary somatosensory areas of the cortex is by no means novel, but it has received considerable currency and, as PD Wall pointed out some years ago in the pages of this journal, if correct it would be a God-send to patients seeking relief from intractable chronic pain. In reading the article by Willis et al, one cannot fail to be struck by the large body of evidence that exists for the involvement of the primary somatosensory relay Nucleus (Ventral Posterior medial [VPM] and Ventral Posterior lateral [VPL]) of the thalamus and its cortical projection in the postcentral gyrus in the discrimination of pain intensity and localization. It would be surprising if the detailed fine grain topographic maps of the body surface that exist in the primary somatosensory areas were excluded from the discriminative apparatus underlying pain localization in favor of the insula in which topographic maps and modality segregation are not the norm. I think the view that any part of the thalamus that excludes the Ventral Posterior Nucleus and the primary somatosensory areas of the cortex in the pathways leading to pain perception cannot be sustained in the face of the broad range of data presented here by Willis et al. Even if one accepts, which as pointed out by Wall earlier many do not, the belief that lamina I cells can provide all the information necessary for the appreciation of pain and temperature, the evidence that they project exclusively to targets outside the VPM and VPL nuclei and/or that these targets are only innervated by layer I cells is weak at best. Craig et al in their initial article described labeled axons in a region they called VMpo and located outside the confines of VPL and VPM after injections of anatomic tracers putatively restricted to layer I of the dorsal horn. The restriction of an injection to lamina I is a remarkable technical feat, given the small dimensions of lamina I, and even if true, any injection restricted to lamina I inevitably has to be very tiny and cannot possibly label a sufficient number of cells to permit projections to other sites to be ruled out. The studies involving retrograde labeling of layer I cells after injections of tracers in the thalamus itself clearly show labeling of lamina I cells after injections well outside the supposed pain relay center, proving the existence of a lamina I projection there, as the results of a large number of physiologic studies bear out. Injections of retrograde tracers targeted at the new thalamic pain center did not selectively involve it. Also there are no data that rule out the projection of deeper spinothalamic cells to it. Trying to identify the region referred to as VMpo presents difficulties, as Willis et al point out. These difficulties to some extent arise from the relative paucity of studies now being conducted on thalamic anatomy. With much of the emphasis in modern studies of the thalamus having gone off anatomy and connection tracing in favor of investigating the physiologic properties of thalamic neurons and the network of which they form a part, the demand for reproducibility of anatomic results often takes longer to be met than in a previous era. Anyone can now more or less draw a line around any part of the thalamus and call it something that reflects a particular point of view without much concern for antecedent work or the expectation that new studies may soon prove it to be an oversimplification. The problem with “VMpo” is that it has never been adequately described and, where illustrated, it has usually been either as a small blob of immunoreactivity against a blank background or in an isolated section or two matched to others in which the Nissl staining is washed out and of little localizing value. If the preexisting literature was considered at all, it was only dismissively. The preexisting literature presents a rather different picture of the nuclear delineations of the Posterior part of the primate thalamus on the basis of a far more comprehensive study of immunostaining for the calcium binding proteins. The basic difference between his analysis and that of the earlier studies, according to Craig (and restated in the Willis et al article), is that the antibodies against 28-kd calbindin used in the two sets of studies label different things—the commercial Sigma monoclonal antibody used by Craig only fibers, and the polyclonal antiserum used by us only cells. Given that they are directed against identical epitopes, this would be a remarkable differential specificity, if only it were true. Our studies had in fact emphasized staining of fiFrom the Center for Neuroscience, University of California, Davis, CA. Address reprint requests to Dr. Edward Jones, University of California, Davis, Center for Neuroscience, 1544 Newton Court, Davis, CA 95615. © 2002 by the American Pain Society 1526-5900/2002 $35.00/0 doi:10.1054/jpai.2002.122952
Herbert P Killackey - One of the best experts on this subject based on the ideXlab platform.
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Corticothalamic projections from the rat primary somatosensory cortex.
The Journal of Neuroscience, 2003Co-Authors: Herbert P Killackey, S. Murray ShermanAbstract:To study the cells of origin of corticothalamic inputs to the Ventral Posterior and Posterior medial nuclei of the somatosensory thalamus in rats, we injected small aliquots of tracer into each Nucleus and analyzed the pattern of retrograde labeling in the posteromedial barrel subfield of primary somatosensory cortex, which can be divided into barrel and nonbarrel zones. The Ventral Posterior Nucleus is innervated by neurons in layer VIa of both zones, whereas the Posterior medial Nucleus is innervated by neurons in layers Vb and VIb of both zones with additional innervation from layer VIa of nonbarrel cortex. Thus, only the Posterior medial Nucleus receives a layer Vb input. Because the layer Vb input is interpreted as the initiation of a feedforward cortico-thalamocortical pathway, this implies that the target of the Posterior medial Nucleus, which includes the nonbarrel cortex, is a higher-order cortical area. We thus suggest that this cortical zone, which is classically considered part of the primary somatosensory cortex, should be reclassified as higher-order cortex.
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Distinguishing topography and somatotopy in the thalamocortical projections of the developing rat.
Developmental Brain Research, 2003Co-Authors: Douglas R. Dawson, Herbert P KillackeyAbstract:We placed discrete injections of HRP into the somatosensory cortex of the rat on the day of birth and found discrete, ordered patterns of retrogradely labelled cells in the Ventral Posterior Nucleus. We interpret these results as suggesting that topographic relations between thalamus and cortex develop independently of the periphery.
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thalamic processing of vibrissal information in the rat ii morphological and functional properties of medial Ventral Posterior Nucleus and Posterior Nucleus neurons
The Journal of Comparative Neurology, 1991Co-Authors: Nicolas L Chiaia, Robert W Rhoades, Stephen E Fish, Herbert P KillackeyAbstract:: Extracellular recording, intracellular recording, intracellular horseradish peroxidase injection, and receptive field mapping techniques were employed to evaluate the physiological and morphological properties of medial Ventral Posterior Nucleus (VPM) and Posterior Nucleus (POm) neurons in normal adult rats. Overall, we physiologically characterized 148 VPM and 121 POm neurons. Over 82% of the VPM cells were excited only by deflection of one or more mystacial vibrissae, 10% were activated by displacement of guard hairs, and the remainder were either excited by indentation of the skin or were unresponsive. Less than 40% of the POm cells were activated by vibrissa deflection, 18% were excited by displacement of guard hairs, and another 17% were unresponsive. Most of the rest of the POm cells were excited by stimulation of skin, mucosa, or activation of muscle-related afferents. Small percentages of POm cells responded only to noxious stimulation, were classified as having a wide dynamic range, or were inhibited by peripheral stimulation. Electrical stimulation of either PrV or SpI activated most neurons in both VPM and POm. This excitation was almost invariably followed by a long-lasting hyperpolarization which was generally strong enough to prevent responses to either electrical stimuli delivered in the brainstem or mechanical stimulation of the periphery. The receptive fields of vibrissa-sensitive cells in POm were generally much larger than those of cells in VPM. Data obtained with extracellular recording indicated that VPM and POm cells responded to an average of 1.4 and 4.0 vibrissae, respectively. Intracellular recording from smaller samples of VPM and POm cells demonstrated the existence of inputs that were insufficient to produce spikes from the cell, but did yield epsp's. When both sub- and suprathreshold excitation were considered, the average number of vibrissa in the receptive field of a VPM cell was 2.7 and the value for POm cells became 7.8. HRP-filled neurons recovered in POm (N = 20) generally had much larger dendritic arbors than neurons in VPM (N = 31). For the former cells, the size of the dendritic tree was significantly correlated with the number of vibrissa to which the cell responded; for the latter neurons, it was not.
Christian Duval - One of the best experts on this subject based on the ideXlab platform.
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The impact of ventrolateral thalamotomy on tremor and voluntary motor behavior in patients with Parkinson’s disease
Experimental Brain Research, 2006Co-Authors: Christian Duval, Michel Panisset, Antonio P. Strafella, Abbas F. SadikotAbstract:A preferred target for parkinsonian tremor alleviation is the ventrolateral (VL) thalamus. The goal of the present study is to determine how lesions involving the presumed cerebellar and pallidal recipient areas of the “motor” thalamus would alter the tremor and motor behavior of ten patients with Parkinson’s disease (PD). Tremor amplitude, power dispersion (a measure of sharpness of the power spectrum of tremor), and power distribution were quantified using a laser displacement sensor prior to, and a week after, VL thalamotomy. As well, the impact of surgery on tremor seen during movement was quantified in a manual-tracking (MT) task. Tremor-induced noise (a measure of the amount of tremor present during movement) and ERROR (difference between subject’s performance and target) were quantified. Finally, bradykinesia was assessed with a rapid alternating movement (RAM) task. Duration, range, and amplitude irregularity of wrist pronation–supination cycles were computed. Both motor tasks were quantified using a highly sensitive forearm rotational sensor. Healthy age-matched control subjects were also tested. Magnetic resonance images with an integrated atlas of thalamic nuclei were used to confirm lesion location. Results show that the lesions were centered upon the Posterior portion of the Ventral lateral (VLp) Nucleus of the thalamus, included the Posterior part of the Ventral lateral anterior Nucleus (VLa), and extended Posteriorly to encroach upon the most rostral sector of the sensory Ventral Posterior Nucleus (VPLa). VL thalamotomy significantly decreased tremor amplitude in all cases. Power dispersion was increased significantly so that it became similar to that of control subjects. Changes in power distribution indicate that thalamotomy selectively targeted PD tremor oscillations. Tremor detected during the MT task was also markedly decreased, becoming similar to that of controls. Patients also showed significant decrease in ERROR during MT. RAM duration and range were not significantly modified by the surgery, and patients’ performance remained impaired compared to healthy control subjects. Collectively, these results suggest that lesions involving the presumed “cerebellar” and “pallidal” recipient sectors of the motor thalamus do not worsen bradykinesia, suggesting that neural circuits other than the pallido-thalamo-cortical loop may be involved in slowness of movement in PD. A review of alternate pathways is presented.
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The impact of ventrolateral thalamotomy on tremor and voluntary motor behavior in patients with Parkinson's disease.
Experimental Brain Research, 2005Co-Authors: Christian Duval, Michel Panisset, Antonio P. Strafella, Abbas F. SadikotAbstract:A preferred target for parkinsonian tremor alleviation is the ventrolateral (VL) thalamus. The goal of the present study is to determine how lesions involving the presumed cerebellar and pallidal recipient areas of the “motor” thalamus would alter the tremor and motor behavior of ten patients with Parkinson’s disease (PD). Tremor amplitude, power dispersion (a measure of sharpness of the power spectrum of tremor), and power distribution were quantified using a laser displacement sensor prior to, and a week after, VL thalamotomy. As well, the impact of surgery on tremor seen during movement was quantified in a manual-tracking (MT) task. Tremor-induced noise (a measure of the amount of tremor present during movement) and ERROR (difference between subject’s performance and target) were quantified. Finally, bradykinesia was assessed with a rapid alternating movement (RAM) task. Duration, range, and amplitude irregularity of wrist pronation–supination cycles were computed. Both motor tasks were quantified using a highly sensitive forearm rotational sensor. Healthy age-matched control subjects were also tested. Magnetic resonance images with an integrated atlas of thalamic nuclei were used to confirm lesion location. Results show that the lesions were centered upon the Posterior portion of the Ventral lateral (VLp) Nucleus of the thalamus, included the Posterior part of the Ventral lateral anterior Nucleus (VLa), and extended Posteriorly to encroach upon the most rostral sector of the sensory Ventral Posterior Nucleus (VPLa). VL thalamotomy significantly decreased tremor amplitude in all cases. Power dispersion was increased significantly so that it became similar to that of control subjects. Changes in power distribution indicate that thalamotomy selectively targeted PD tremor oscillations. Tremor detected during the MT task was also markedly decreased, becoming similar to that of controls. Patients also showed significant decrease in ERROR during MT. RAM duration and range were not significantly modified by the surgery, and patients’ performance remained impaired compared to healthy control subjects. Collectively, these results suggest that lesions involving the presumed “cerebellar” and “pallidal” recipient sectors of the motor thalamus do not worsen bradykinesia, suggesting that neural circuits other than the pallido-thalamo-cortical loop may be involved in slowness of movement in PD. A review of alternate pathways is presented.
Iain D. Wilkinson - One of the best experts on this subject based on the ideXlab platform.
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The Anatomy of the Medial Lemniscus within the Brainstem Demonstrated at 3 Tesla with High Resolution Fat Suppressed T1-Weighted Images and Diffusion Tensor Imaging.
Rivista Di Neuroradiologia, 2011Co-Authors: Charles A. J. Romanowski, Jeremy Rowe, Daniel J Warren, Joel Bigley, John Yianni, M. Hutton, Iain D. WilkinsonAbstract:: The medial lemniscus is part of the main somatosensory pathways ascending within the brainstem. It is formed by the heavily myelinated axons of the second order neurones of the dorsal column nuclei. This pathway ascends through the rostral medulla, pons and mesencephalon to finally terminate by synapsing with third order neurones in the Ventral Posterior Nucleus of the thalamus. The medial lemniscus conveys proprioception and fine tactile discrimination as part of the somatosensory system. Conventional MRI studies of the brainstem have been relatively poor in demonstrating these fibre pathways. Diffusion tensor imaging and tractography may demostrated fibre pathways in the brainstem. These techniques do however suffer from relatively poor spatial resolution and some degree of image distortion - especially if based on echo planar imaging techniques. Knowledge of the anatomical relationships of the medial lemniscus is important for the understanding of clinical manifestations of disease processes affecting the somatosensory pathways and also to demonstrate important adjacent structures. Specifically, the pedunculopontine Nucleus (PPN) lies in close anatomical relationship to the medial lemniscus and the decussation of the superior cerebellar peduncle. This Nucleus is a promising target for deep brain stimulator placement for alleviation of non-dopamine responsive dystonias. Six healthy male volunteers (mean age 33 years) were imaged at 3 Tesla. Imaging protocols consisted of thin section, high resolution, fat suppressed T1-weighted sequences as well as thin section, high isotropic resolution diffusion tensor imaging (DTI), which was analysed to generate colour fractional anisotropy (FA) maps. These were correlated with the fat suppressed T1 weighted images. In all volunteers the medial lemniscus was seen as a pair of bands of low signal on axial, high resolution, fat suppressed T1-weighted images. They were indentified through the upper medulla, pons and mesencephalon. They correlated well with the head to foot orientated fibres on the colour FA maps generated from the DTI data. This study of normal volunteers has illustrated the value of high resolution, fat suppressed T1-weighted images in demonstrating the anatomy of the heavily myelinated medial lemniscus within the brainstem. These high resolution images with good spatial accuracy can potentially be used to aid the localisation of other nuclei, such as the PPN.
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the anatomy of the medial lemniscus within the brainstem demonstrated at 3 tesla with high resolution fat suppressed t1 weighted images and diffusion tensor imaging
Rivista Di Neuroradiologia, 2011Co-Authors: Charles A. J. Romanowski, Jeremy Rowe, Daniel J Warren, Joel Bigley, John Yianni, M. Hutton, Iain D. WilkinsonAbstract:The medial lemniscus is part of the main somatosensory pathways ascending within the brainstem. It is formed by the heavily myelinated axons of the second order neurones of the dorsal column nuclei. This pathway ascends through the rostral medulla, pons and mesencephalon to finally terminate by synapsing with third order neurones in the Ventral Posterior Nucleus of the thalamus. The medial lemniscus conveys proprioception and fine tactile discrimination as part of the somatosensory system. Conventional MRI studies of the brainstem have been relatively poor in demonstrating these fibre pathways. Diffusion tensor imaging and tractography may demostrated fibre pathways in the brainstem. These techniques do however suffer from relatively poor spatial resolution and some degree of image distortion – especially if based on echo planar imaging techniques. Knowledge of the anatomical relationships of the medial lemniscus is important for the understanding of clinical manifestations of disease processes affecting ...
