DOCSLIB.ORG

Basal Ganglia Physiology Neuroanatomy > Basal Ganglia > Basal Ganglia

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Basal Ganglia Physiology Neuroanatomy > Basal Ganglia > Basal Ganglia Basal Ganglia Physiology Neuroanatomy > Basal Ganglia > Basal Ganglia BASAL GANGLIA PHYSIOLOGY THE DIRECT & INDIRECT PATHWAYS OVERALL CIRCUITRY Key Structures • Cerebral cortex • Thalamus • Spinal motor neurons • Striatum, which is the: - Caudate & - Putamen CONNECTIVITY • The thalamus excites the cerebral cortex, which stimulates the spinal motor neurons. • The cortex excites the striatum. THE DIRECT PATHWAY Key Structures • The combined globus pallidus internal segment and the substantia nigra reticulata - GPi/STNr Connectivity • The striatum (primarily the putamen) inhibits GPi/STNr. 1 / 5 • GPi/STNr inhibits the thalamus. The direct pathway is overall excitatory THE INDIRECT PATHWAY Key Structures • The globus pallidus external segment - GPe Connectivity • GPe is inhibited by the Striatum. • GPe inhibits GPi/STNr The indirect pathway is overall inhibitory Subthalamic nucleus • The Indirect Pathway via the subthalamic nucleus Connectivity • The subthalamic nucleus excites GPi/STNr. • GPe inhibits the subthalamic nucleus Indirect Pathway: Summary • Whether it is because of GPe inhibition of the GPi/STNr • OR because of GPe inhibition of the subthalamic nucleus, • The indirect pathway is always overall inhibitory. HEMIBALLISMUS & PARKINSON'S DISEASE Hemiballismus Clinical Correlation: Hemiballismus • When the subthalamic nucleus is selectively injured, patients develop a loss of motor inhibition on the side contralateral to the subthalamic nucleus lesion, they develop wild ballistic, flinging movements, called hemiballismus. 2 / 5 Parkinson's Disease Clinical Correlation: Parkinson's disease • Substantia nigra compacta degeneration causes Parkinson's disease. • It is a disorder of slowness and asymmetric muscle rigidity, often associated with tremor. Dopamine Receptors • The substantia nigra compacta releases dopamine. • The two most prominent dopamine (D) receptors in the striatum are: - The D1 receptor, which is part of the direct pathway and is excited by dopamine. - The D2 receptor, which is part of the indirect pathway and is inhibited by dopamine. Dopamine • Dopamine from the substantia nigra compacta: - Excites the direct pathway - Inhibits the indirect pathway Both effects promote movement Corticostriatal Fibers • Many frontal-subcortical pathways project through the basal ganglia in addition to the motor pathways we have drawn. • Through the corticostriatal fibers — the Muratoff bundle and the external capsule — the cerebral cortex targets the striatum in a topographic manner. • These pathways help drive a multitude of processes, including emotional, behavioral, somatosensory, and cognitive functional modalities. ANATOMY OF THE DIRECT AND INDIRECT PATHWAYS THE FIELDS OF FOREL Direct pathway comprises: • Ansa lenticularis • Lenticular fasciculus 3 / 5 • Thalamic fasciculus The indirect pathway comprises: • Subthalamic fasciculus Fields of Forel • Field H lies medial to the subthalamic nucleus and inferior to the zona incerta. • Field H1 lies in between the thalamus and zona incerta - Medial to the zona incerta and inferolateral to the thalamus. • Field H2 lies lateral to the zona incerta and medial to the internal capsule. Direct Pathway • The direct pathway fibers comprise the pallidothalamic pathways and emanate from the internal segment of the globus pallidus. - The ansa lenticularis projects inferomedially from the globus pallidus internal segment, courses beneath the subthalamic nucleus, then turns superiorly to pass through Field H and Field H1 to enter the thalamus. - The lenticular fasciculus projects from the internal segment of the globus pallidus across the internal capsule, through Field H2 and then Field H, and then superiorly through Field H1 to enter the thalamus. - Where the ansa lenticularis and the lenticular fasciculus run together in Field H1, they are collectively called the thalamic fasciculus (for further discussion of this, see the end of the chapter). Indirect Pathway • The indirect pathway is subserved by the globus pallidus external segment projections, which involve the subthalamic nucleus and substantia nigra. - Via the subthalamic fasciculus, the external segment of the globus pallidus projects to the subthalamic nucleus, which projects back to the external segment of the globus pallidus and also to the internal segment of the globus pallidus. - The subthalamic nucleus also communicates with the substantia nigra. - The globus pallidus external segment projects to the substantia nigra, which projects fibers through Fields H and H1 to enter the thalamus. KEY DOPAMINERGIC PATHWAYS Mesocortical Pathway 4 / 5 • Projections from ventral tegmental area to prefrontal cortex. • Decreased activity from psychotropic agents reduces the positive (psychotic) symptoms of schizophrenia. Mesolimbic Pathway • Projections from ventral tegmental area to forebrain (esp. nucleus accumbens in the basal forebrain). • Responsible for cognitive and emotional function. • Decreased activity from psychotropic agents reduce: - Cognitive/Executive function (dorsolateral) - Emotion/Affect (ventromedial) Nigrostriatal Pathway • Projections from the substantia nigra to striatum (caudate and putamen). • Responsible for movement. • Decreased activity from psychotropic agents reduce movement: pseudoparkinsonism. Tuberoinfundibular pathway • Projections from the hypothalamus to the pituitary gland. - The origins of the pathway are classically assigned to the periventricular and arcuate (infundibular) nuclei. - The termination within the pituitary gland is in the median eminence. • Responsible for prolactin release: prolactin is under tonic inhibition by dopamine. • Decreased activity from psychotropic agents reduces prolactin inhibition and results in prolactin release: gynecomastia, galactorrhea, amenorrhea, infertility, etc... Powered by TCPDF (www.tcpdf.org) 5 / 5.
Load more

Recommended publications
  • Differential Deep Brain Stimulation Sites and Networks for Cervical Vs
    medRxiv preprint doi: https://doi.org/10.1101/2021.07.28.21261289; this version posted July 31, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission. Title Differential Deep Brain Stimulation Sites and Networks for Cervical vs. Generalized Dystonia Authors Andreas Horn*1, Martin Reich*2, Siobhan Ewert*1, Ningfei Li1, Bassam Al-Fatly1, Florian Lange2, Jonas Roothans2, Simon Oxenford1, Isabel Horn1, Steffen Paschen3, Joachim Runge4, Fritz Wodarg5, Karsten Witt6, Robert C. Nickl7, Matthias Wittstock8, Gerd-Helge Schneider9, Philipp Mahlknecht10, Werner Poewe10, Wilhelm Eisner11, Ann-Kristin Helmers12, Cordula Matthies7, Joachim K. Krauss4, Günther Deuschl3, Jens Volkmann2, Andrea Kühn1 Author Affiliations 1. Charité – Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Movement Disorders and Neuromodulation Unit, Department of Neurology, Berlin, Germany. 2. Julius-Maximilians-University Würzburg, Department of Neurology, Germany 3. University Kiel, Department of Neurology, Germany 4. Department of Neurosurgery, Medical School Hannover, MHH, Hannover, Germany. 5. University Kiel, Department of Radiology, Germany 6. University Oldenburg, Department of Neurology, Germany 7. Julius-Maximilians-University Würzburg, Department of Neurosurgery, Germany 8. University Rostock, Department
    [Show full text]
  • Neuromodulators and Long-Term Synaptic Plasticity in Learning and Memory: a Steered-Glutamatergic Perspective
    brain sciences Review Neuromodulators and Long-Term Synaptic Plasticity in Learning and Memory: A Steered-Glutamatergic Perspective Amjad H. Bazzari * and H. Rheinallt Parri School of Life and Health Sciences, Aston University, Birmingham B4 7ET, UK; [email protected] * Correspondence: [email protected]; Tel.: +44-(0)1212044186 Received: 7 October 2019; Accepted: 29 October 2019; Published: 31 October 2019 Abstract: The molecular pathways underlying the induction and maintenance of long-term synaptic plasticity have been extensively investigated revealing various mechanisms by which neurons control their synaptic strength. The dynamic nature of neuronal connections combined with plasticity-mediated long-lasting structural and functional alterations provide valuable insights into neuronal encoding processes as molecular substrates of not only learning and memory but potentially other sensory, motor and behavioural functions that reflect previous experience. However, one key element receiving little attention in the study of synaptic plasticity is the role of neuromodulators, which are known to orchestrate neuronal activity on brain-wide, network and synaptic scales. We aim to review current evidence on the mechanisms by which certain modulators, namely dopamine, acetylcholine, noradrenaline and serotonin, control synaptic plasticity induction through corresponding metabotropic receptors in a pathway-specific manner. Lastly, we propose that neuromodulators control plasticity outcomes through steering glutamatergic transmission, thereby gating its induction and maintenance. Keywords: neuromodulators; synaptic plasticity; learning; memory; LTP; LTD; GPCR; astrocytes 1. Introduction A huge emphasis has been put into discovering the molecular pathways that govern synaptic plasticity induction since it was first discovered [1], which markedly improved our understanding of the functional aspects of plasticity while introducing a surprisingly tremendous complexity due to numerous mechanisms involved despite sharing common “glutamatergic” mediators [2].
    [Show full text]
  • Basal Ganglia & Cerebellum
    1/2/2019 This power point is made available as an educational resource or study aid for your use only. This presentation may not be duplicated for others and should not be redistributed or posted anywhere on the internet or on any personal websites. Your use of this resource is with the acknowledgment and acceptance of those restrictions. Basal Ganglia & Cerebellum – a quick overview MHD-Neuroanatomy – Neuroscience Block Gregory Gruener, MD, MBA, MHPE Vice Dean for Education, SSOM Professor, Department of Neurology LUHS a member of Trinity Health Outcomes you want to accomplish Basal ganglia review Define and identify the major divisions of the basal ganglia List the major basal ganglia functional loops and roles List the components of the basal ganglia functional “circuitry” and associated neurotransmitters Describe the direct and indirect motor pathways and relevance/role of the substantia nigra compacta 1 1/2/2019 Basal Ganglia Terminology Striatum Caudate nucleus Nucleus accumbens Putamen Globus pallidus (pallidum) internal segment (GPi) external segment (GPe) Subthalamic nucleus Substantia nigra compact part (SNc) reticular part (SNr) Basal ganglia “circuitry” • BG have no major outputs to LMNs – Influence LMNs via the cerebral cortex • Input to striatum from cortex is excitatory – Glutamate is the neurotransmitter • Principal output from BG is via GPi + SNr – Output to thalamus, GABA is the neurotransmitter • Thalamocortical projections are excitatory – Concerned with motor “intention” • Balance of excitatory & inhibitory inputs to striatum, determine whether thalamus is suppressed BG circuits are parallel loops • Motor loop – Concerned with learned movements • Cognitive loop – Concerned with motor “intention” • Limbic loop – Emotional aspects of movements • Oculomotor loop – Concerned with voluntary saccades (fast eye-movements) 2 1/2/2019 Basal ganglia “circuitry” Cortex Striatum Thalamus GPi + SNr Nolte.
    [Show full text]
  • Basal Ganglia Anatomy, Physiology, and Function Ns201c
    Basal Ganglia Anatomy, Physiology, and Function NS201c Human Basal Ganglia Anatomy Basal Ganglia Circuits: The ‘Classical’ Model of Direct and Indirect Pathway Function Motor Cortex Premotor Cortex + Glutamate Striatum GPe GPi/SNr Dopamine + - GABA - Motor Thalamus SNc STN Analagous rodent basal ganglia nuclei Gross anatomy of the striatum: gateway to the basal ganglia rodent Dorsomedial striatum: -Inputs predominantly from mPFC, thalamus, VTA Dorsolateral striatum: -Inputs from sensorimotor cortex, thalamus, SNc Ventral striatum: Striatal subregions: Dorsomedial (caudate) -Inputs from vPFC, hippocampus, amygdala, Dorsolateral (putamen) thalamus, VTA Ventral (nucleus accumbens) Gross anatomy of the striatum: patch and matrix compartments Patch/Striosome: -substance P -mu-opioid receptor Matrix: -ChAT and AChE -somatostatin Microanatomy of the striatum: cell types Projection neurons: MSN: medium spiny neuron (GABA) •striatonigral projecting – ‘direct pathway’ •striatopallidal projecting – ‘indirect pathway’ Interneurons: FS: fast-spiking interneuron (GABA) LTS: low-threshold spiking interneuron (GABA) LA: large aspiny neuron (ACh) 30 um Cellular properties of striatal neurons Microanatomy of the striatum: striatal microcircuits • Feedforward inhibition (mediated by fast-spiking interneurons) • Lateral feedback inhibition (mediated by MSN collaterals) Basal Ganglia Circuits: The ‘Classical’ Model of Direct and Indirect Pathway Function Motor Cortex Premotor Cortex + Glutamate Striatum GPe GPi/SNr Dopamine + - GABA - Motor Thalamus SNc STN The simplified ‘classical’ model of basal ganglia circuit function • Information encoded as firing rate • Basal ganglia circuit is linear and unidirectional • Dopamine exerts opposing effects on direct and indirect pathway MSNs Basal ganglia motor circuit: direct pathway Motor Cortex Premotor Cortex Glutamate Striatum GPe GPi/SNr Dopamine + GABA Motor Thalamus SNc STN Direct pathway MSNs express: D1, M4 receptors, Sub.
    [Show full text]
  • A Bilateral Cortico-Striate Projection
    J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.28.1.71 on 1 February 1965. Downloaded from J. Neurol. Neurosurg. Psychiat., 1965, 28, 71 A bilateral cortico-striate projection J. B. CARMAN, W. M. COWAN, T. P. S. POWELL, AND K. E. WEBSTER From the Departments of Anatomy, University of Oxford, and University College, London During the course of studies on the projection of the ined, and evidence for a bilateral projection has been cerebral cortex upon the striatum in the rabbit found in 20 animals. The evidence for this projec- (Carman, Cowan, and Powell, 1963) and the cat tion depends upon the collective findings in several (Webster, 1964) degeneration was seen bilaterally in brains, but only a few typical examples will be Nauta preparations of the striatum in some, but not described in full. The findings in the remaining all, animals. For two main reasons this observation experiments will be summarized in composite was not included in the earlier study. First, because figures. of the difficulty of interpreting any findings of Experiment R30 is representative of the rabbit bilateral degeneration in silver preparations, and, brains in which a projection to the contralateral particularly as it is well known that the striatum striatum was found after a lesion involving the sen- commonly shows pseudo-degeneration, it was im- sori-motor cortex. The cortical damage in this brain perative to exclude this possibility by the prepara- is in the form of a broad strip along the dorsal guest. Protected by copyright. tion of further material using both the frozen and surface of the hemisphere from just behind the paraffin Nauta methods.
    [Show full text]
  • Gene Expression of Prohormone and Proprotein Convertases in the Rat CNS: a Comparative in Situ Hybridization Analysis
    The Journal of Neuroscience, March 1993. 73(3): 1258-1279 Gene Expression of Prohormone and Proprotein Convertases in the Rat CNS: A Comparative in situ Hybridization Analysis Martin K.-H. Schafer,i-a Robert Day,* William E. Cullinan,’ Michel Chri?tien,3 Nabil G. Seidah,* and Stanley J. Watson’ ‘Mental Health Research Institute, University of Michigan, Ann Arbor, Michigan 48109-0720 and J. A. DeSeve Laboratory of *Biochemical and 3Molecular Neuroendocrinology, Clinical Research Institute of Montreal, Montreal, Quebec, Canada H2W lR7 Posttranslational processing of proproteins and prohor- The participation of neuropeptides in the modulation of a va- mones is an essential step in the formation of bioactive riety of CNS functions is well established. Many neuropeptides peptides, which is of particular importance in the nervous are synthesized as inactive precursor proteins, which undergo system. Following a long search for the enzymes responsible an enzymatic cascade of posttranslational processing and mod- for protein precursor cleavage, a family of Kexin/subtilisin- ification events during their intracellular transport before the like convertases known as PCl, PC2, and furin have recently final bioactive products are secreted and act at either pre- or been characterized in mammalian species. Their presence postsynaptic receptors. Initial endoproteolytic cleavage occurs in endocrine and neuroendocrine tissues has been dem- C-terminal to pairs of basic amino acids such as lysine-arginine onstrated. This study examines the mRNA distribution of (Docherty and Steiner, 1982) and is followed by the removal these convertases in the rat CNS and compares their ex- of the basic residues by exopeptidases. Further modifications pression with the previously characterized processing en- can occur in the form of N-terminal acetylation or C-terminal zymes carboxypeptidase E (CPE) and peptidylglycine a-am- amidation, which is essential for the bioactivity of many neu- idating monooxygenase (PAM) using in situ hybridization ropeptides.
    [Show full text]
  • Semmelweis University, Department of Anatomy, Histology and Embryology the Position of the Diencephalon in the Brain Parts of the Diencephalon
    Microscopy of the diencephalon Árpád Dobolyi Semmelweis University, Department of Anatomy, Histology and Embryology The position of the diencephalon in the brain Parts of the diencephalon • Thalamus • Epithalamus – Pineal body – Habenulae – Trigonum habenulae – Habenular nuclei – Stria medullaris – Habenular commissure • Metathalamus – Medial geniculate body – Lateral geniculate body • Subthalamus – Subthalamic nucleus – Zona incerta – H fields of Forel • Hypothalamus Nuclear groups and nuclei of the thalamus Frontal sections of the thalamus Anterior section Middle section Functional classification of thalamic nuclei • Specific nuclei: specific input, project to specific part of the cortex - sensory relay nuclei: VPL, VPM, MGB, LGB - motor relay nuclei: VA, VL - limbic relay nuclei: AV, AD, AM • Association nuclei: cortical input, project to associative areas of the cortex - MD, LD, LP, pulvinar • Non-specific nuclei: ascending input, diffuse projection to the cortex - midline and intralaminar nuclei • Nuclei not projecting to the cerebral cortex - n. reticularis thalami, n. parafascicularis, n. subparafascicularis Cortical projections of (specific and association) thalamic nuclei mediosagittal view lateral view Specific sensory relay nuclei The VPL relays sensory inputs from the body to the cerebral cortex (Input: spinothalamic tract and the medial lemniscus) The VPM relays sensory inputs from the head to the cerebral cortex (Input: trigeminal and dorsal trigeminal lemniscus pathways) Relay of gustatory inputs to the cortex takes place
    [Show full text]
  • Imaging of the Confused Patient: Toxic Metabolic Disorders Dara G
    Imaging of the Confused Patient: Toxic Metabolic Disorders Dara G. Jamieson, M.D. Weill Cornell Medicine, New York, NY The patient who presents with either acute or subacute confusion, in the absence of a clearly defined speech disorder and focality on neurological examination that would indicate an underlying mass lesion, needs to be evaluated for a multitude of neurological conditions. Many of the conditions that produce the recent onset of alteration in mental status, that ranges from mild confusion to florid delirium, may be due to infectious or inflammatory conditions that warrant acute intervention such as antimicrobial drugs, steroids or plasma exchange. However, some patients with recent onset of confusion have an underlying toxic-metabolic disorders indicating a specific diagnosis with need for appropriate treatment. The clinical presentations of some patients may indicate the diagnosis (e.g. hypoglycemia, chronic alcoholism) while the imaging patterns must be recognized to make the diagnosis in other patients. Toxic-metabolic disorders constitute a group of diseases and syndromes with diverse causes and clinical presentations. Many toxic-metabolic disorders have no specific neuroimaging correlates, either at early clinical stages or when florid symptoms develop. However, some toxic-metabolic disorders have characteristic abnormalities on neuroimaging, as certain areas of the central nervous system appear particularly vulnerable to specific toxins and metabolic perturbations. Areas of particular vulnerability in the brain include: 1) areas of high-oxygen demand (e.g. basal ganglia, cerebellum, hippocampus), 2) the cerebral white matter and 3) the mid-brain. Brain areas of high-oxygen demand are particularly vulnerable to toxins that interfere with cellular respiratory metabolism.
    [Show full text]
  • Electrophysiological and Morphological Evidence for a Gabaergic Nigrostriatal Pathway
    The Journal of Neuroscience, June 1, 1999, 19(11):4682–4694 Electrophysiological and Morphological Evidence for a GABAergic Nigrostriatal Pathway Manuel Rodrı´guez1 and Toma´ s Gonza´ lez-Herna´ ndez2 Departments of 1Physiology and 2Anatomy, Faculty of Medicine, University of La Laguna, La Laguna, Tenerife, Canary Islands, Spain The electrophysiological and neurochemical characteristics of gic neurons, a percentage that reached 81–84% after 6-OHDA the nondopaminergic nigrostriatal (NO-DA) cells and their func- injection. Electrophysiologically, NO-DA cells showed a behavior tional response to the degeneration of dopaminergic nigrostri- similar to that found in other nigral GABAergic (nigrothalamic) atal (DA) cells were studied. Three different criteria were used to cells. In addition, the 6-OHDA degeneration of DA cells induced a identify NO-DA cells: (1) antidromic response to striatal stimu- modification of their electrophysiological pattern similar to that lation with an electrophysiological behavior (firing rate, inter- found in GABAergic nigrothalamic neurons. Taken together, the spike interval variability, and conduction velocity) different from present data indicate the existence of a small GABAergic nigro- that of DA cells; (2) retrograde labeling after striatal injection of striatal pathway and suggest their involvement in the pathophys- HRP but showing immunonegativity for DA cell markers (ty- iology of Parkinson’s disease. rosine hydroxylase, calretinin, calbindin-D28k, and cholecysto- kinin); and (3) resistance to neurotoxic effect of 6-hydroxydomine Key words: nigrostriatal pathway; dopaminergic cells; (6-OHDA). Our results showed that under normal conditions, GABAergic cells; GABA; glutamic acid decarboxylase; parval- 5–8% of nigrostriatal neurons are immunoreactive for GABA, glu- bumin; calretinin; calbindin-D28k; cholecystokinin; Parkinson’s tamic acid decarboxylase, and parvalbumin, markers of GABAer- disease The substantia nigra (SN) is a major output center of the basal paminergic (Grace and Bunney, 1980, 1983a).
    [Show full text]
  • Optogenetic Activation of Dopamine Neurons in the Ventral Tegmental Area Induces Reanimation from General Anesthesia
    CORE Metadata, citation and similar papers at core.ac.uk Provided by DSpace@MIT Optogenetic activation of dopamine neurons in the ventral tegmental area induces reanimation from general anesthesia Norman E. Taylora,b,c, Christa J. Van Dorta,b,c, Jonathan D. Kennya,c, JunZhu Peia,c, Jennifer A. Guideraa,c, Ksenia Y. Vlasova,c, Justin T. Leea,c, Edward S. Boydenc,d,e,f, Emery N. Browna,b,c,g,h,1,2, and Ken Solta,b,c,1 aDepartment of Anesthesia, Critical Care and Pain Medicine, Massachusetts General Hospital, Boston, MA 02114; bDepartment of Anaesthesia, Harvard Medical School, Boston, MA 02114; cDepartment of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139; dMedia Lab, Massachusetts Institute of Technology, Cambridge, MA 02139; eMcGovern Institute, Massachusetts Institute of Technology, Cambridge, MA 02139; fDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139; gThe Picower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA 02139; and hInstitute for Medical Engineering and Science, Massachusetts Institute of Technology, Cambridge, MA 02139 Contributed by Emery N. Brown, September 14, 2016 (sent for review February 29, 2016; reviewed by Loren M. Frank, Robert W. Gereau, and Andrew Jenkins) Dopamine (DA) promotes wakefulness, and DA transporter inhibi- There are currently no clinically approved pharmacologic or cir- tors such as dextroamphetamine and methylphenidate are effective cuit-level interventions that can induce active emergence or for increasing arousal and inducing reanimation, or active emer- reanimation from general anesthesia (10). Dopamine (DA) is a gence from general anesthesia. DA neurons in the ventral tegmental neurotransmitter that is well-known to elicit wakefulness (11).
    [Show full text]
  • Rhesus Monkey Brain Atlas Subcortical Gray Structures
    Rhesus Monkey Brain Atlas: Subcortical Gray Structures Manual Tracing for Hippocampus, Amygdala, Caudate, and Putamen Overview of Tracing Guidelines A) Tracing is done in a combination of the three orthogonal planes, as specified in the detailed methods that follow. B) Each region of interest was originally defined in the right hemisphere. The labels were then reflected onto the left hemisphere and all borders checked and adjusted manually when necessary. C) For the initial parcellation, the user used the “paint over function” of IRIS/SNAP on the T1 template of the atlas. I. Hippocampus Major Boundaries Superior boundary is the lateral ventricle/temporal horn in the majority of slices. At its most lateral extent (subiculum) the superior boundary is white matter. The inferior boundary is white matter. The anterior boundary is the lateral ventricle/temporal horn and the amygdala; the posterior boundary is lateral ventricle or white matter. The medial boundary is CSF at the center of the brain in all but the most posterior slices (where the medial boundary is white matter). The lateral boundary is white matter. The hippocampal trace includes dentate gyrus, the CA3 through CA1 regions of the hippocamopus, subiculum, parasubiculum, and presubiculum. Tracing A) Tracing is done primarily in the sagittal plane, working lateral to medial a. Locate the most lateral extent of the subiculum, which is bounded on all sides by white matter, and trace. b. As you page medially, tracing the hippocampus in each slice, the superior, anterior, and posterior boundaries of the hippocampus become the lateral ventricle/temporal horn. c. Even further medially, the anterior boundary becomes amygdala and the posterior boundary white matter.
    [Show full text]
  • MRI Atlas of the Human Deep Brain Jean-Jacques Lemaire
    MRI Atlas of the Human Deep Brain Jean-Jacques Lemaire To cite this version: Jean-Jacques Lemaire. MRI Atlas of the Human Deep Brain. 2019. hal-02116633 HAL Id: hal-02116633 https://hal.uca.fr/hal-02116633 Preprint submitted on 1 May 2019 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. Distributed under a Creative Commons Attribution - NonCommercial - NoDerivatives| 4.0 International License MRI ATLAS of the HUMAN DEEP BRAIN Jean-Jacques Lemaire, MD, PhD, neurosurgeon, University Hospital of Clermont-Ferrand, Université Clermont Auvergne, CNRS, SIGMA, France This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/4.0/ or send a letter to Creative Commons, PO Box 1866, Mountain View, CA 94042, USA. Terminologia Foundational Model Terminologia MRI Deep Brain Atlas NeuroNames (ID) neuroanatomica usages, classical and french terminologies of Anatomy (ID) Anatomica 1998 (ID) 2017 http://fipat.library.dal.ca In
    [Show full text]