Orienting Head Movements Resulting from Electrical Microstimulation of the Brainstem Tegmentum in the Barn Owl
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Magnetic Resonance Imaging of Multiple Sclerosis: a Study of Pulse-Technique Efficacy
691 Magnetic Resonance Imaging of Multiple Sclerosis: A Study of Pulse-Technique Efficacy Val M. Runge1 Forty-two patients with the clinical diagnosis of multiple sclerosis were examined by Ann C. Price1 proton magnetic resonance imaging (MRI) at 0.5 T. An extensive protocol was used to Howard S. Kirshner2 facilitate a comparison of the efficacy of different pulse techniques. Results were also Joseph H. Allen 1 compared in 39 cases with high-resolution x-ray computed tomography (CT). MRI revealed characteristic abnormalities in each case, whereas CT was positive in only 15 C. Leon Partain 1 of 33 patients. Milder grades 1 and 2 disease were usually undetected by CT, and in all A. Everette James, Jr.1 cases, the abnormalities noted on MRI were much more extensive than on CT. Cerebral abnormalities were best shown with the T2-weighted spin-echo sequence (TE/TR = 120/1000); brainstem lesions were best defined on the inversion-recovery sequence (TE/TI/TR =30/400/1250). Increasing TE to 120 msec and TR to 2000 msec heightened the contrast between normal and abnormal white matter. However, the signal intensity of cerebrospinal fluid with this pulse technique obscured some abnormalities. The diagnosis of multiple sclerosis continues to be a clinical challenge [1,2). The lack of an objective means of assessment further complicates the evaluation of treatment regimens. Evoked potentials, cerebrospinal fluid (CSF) analysis , and computed tomography (CT) are currently used for diagnosis, but all lack sensitivity and/or specificity. Furthermore, postmortem examinations demonstrate many more lesions than those suggested by clinical means [3). -
Brainstem: Structure & Its Mode of Action
Journal of Neurology & Neurophysiology 2021, Vol.12, Issue 3, 521 Opinion Brainstem: Structure & Its Mode of action Karthikeyan Rupani Research Fellow, Tata Medical Centre, India. Corresponding Author* The brainstem is exceptionally little, making up around as it were 2.6 percent of the brain's add up to weight. It has the basic parts of directing cardiac, and Rupani K, respiratory work, making a difference to control heart rate and breathing rate. Research Fellow, Tata Medical Centre, India; It moreover gives the most engine and tactile nerve supply to the confront and E-mail: [email protected] neck by means of the cranial nerves. Ten sets of cranial nerves come from the brainstem. Other parts incorporate the direction of the central apprehensive Copyright: 2021 Rupani K. This is an open-access article distributed under the framework and the body's sleep cycle. It is additionally of prime significance terms of the Creative Commons Attribution License, which permits unrestricted within the movement of engine and tangible pathways from the rest of the use, distribution, and reproduction in any medium, provided the original author brain to the body, and from the body back to the brain. These pathways and source are credited. incorporate the corticospinal tract (engine work), the dorsal column-medial lemniscus pathway and the spinothalamic tract [3]. The primary part of the brainstem we'll consider is the midbrain. The midbrain Received 01 March 2021; Accepted 15 March 2021; Published 22 March 2021 (too known as the mesencephalon) is the foremost prevalent of the three districts of the brainstem. It acts as a conduit between the forebrain over and the pons and cerebellum underneath. -
L4-Physiology of Motor Tracts.Pdf
: chapter 55 page 667 Objectives (1) Describe the upper and lower motor neurons. (2) Understand the pathway of Pyramidal tracts (Corticospinal & corticobulbar tracts). (3) Understand the lateral and ventral corticospinal tracts. (4) Explain functional role of corticospinal & corticobulbar tracts. (5) Describe the Extrapyramidal tracts as Rubrospinal, Vestibulospinal, Reticulospinal and Tectspinal Tracts. The name of the tract indicate its pathway, for example Corticobulbar : Terms: - cortico: cerebral cortex. Decustation: crossing. - Bulbar: brainstem. Ipsilateral : same side. *So it starts at cerebral cortex and Contralateral: opposite side. terminate at the brainstem. CNS influence the activity of skeletal muscle through two set of neurons : 1- Upper motor neurons (UMN) 2- lower motor neuron (LMN) They are neurons of motor cortex & their axons that pass to brain stem and They are Spinal motor neurons in the spinal spinal cord to activate: cord & cranial motor neurons in the brain • cranial motor neurons (in brainstem) stem which innervate muscles directly. • spinal motor neurons (in spinal cord) - These are the only neurons that innervate - Upper motor neurons (UMN) are the skeletal muscle fibers, they function as responsible for conveying impulses for the final common pathway, the final link voluntary motor activity through between the CNS and skeletal muscles. descending motor pathways that make up by the upper motor neurons. Lower motor neurons are classified based on the type of muscle fiber the innervate: There are two UMN Systems through which 1- alpha motor neurons (UMN) control (LMN): 2- gamma motor neurons 1- Pyramidal system (corticospinal tracts ). 2- Extrapyramidal system The activity of the lower motor neuron (LMN, spinal or cranial) is influenced by: 1. -
Microstimulation of the Midbrain Tegmentum Creates Learning Signals for Saccade Adaptation
The Journal of Neuroscience, April 4, 2007 • 27(14):3759–3767 • 3759 Behavioral/Systems/Cognitive Microstimulation of the Midbrain Tegmentum Creates Learning Signals for Saccade Adaptation Yoshiko Kojima, Kaoru Yoshida, and Yoshiki Iwamoto Department of Neurophysiology, Doctoral Program in Kansei Behavioral and Brain Sciences, University of Tsukuba, Tsukuba, Ibaraki 305-8574, Japan Error signals are vital to motor learning. However, we know little about pathways that transmit error signals for learning in voluntary movements. Here we show that microstimulation of the midbrain tegmentum can induce learning in saccadic eye movements in mon- keys. Weak electrical stimuli delivered ϳ200 ms after saccades in one horizontal direction produced gradual and marked changes in saccade gain. The spatial and temporal characteristics of the produced changes were similar to those of adaptation induced by real visual error. When stimulation was applied after saccades in two different directions, endpoints of these saccades gradually shifted in the same direction in two dimensions. We conclude that microstimulation created powerful learning signals that dictate the direction of adaptive shift in movement endpoints. Our findings suggest that the error signals for saccade adaptation are conveyed in a pathway that courses through the midbrain tegmentum. Key words: motor learning; electrical stimulation; midbrain; saccade; adaptation; macaque; monkey Introduction superior colliculus, a key midbrain structure that issues saccade Motor learning ensures the accuracy of the movements we exe- signals to the premotor reticular circuitry (Scudder et al., 2002). cute daily. Vital to learning is the information about the error that The colliculus also has indirect access to the cerebellum via both results from executed movements. -
Brain Structure and Function Related to Headache
Review Cephalalgia 0(0) 1–26 ! International Headache Society 2018 Brain structure and function related Reprints and permissions: sagepub.co.uk/journalsPermissions.nav to headache: Brainstem structure and DOI: 10.1177/0333102418784698 function in headache journals.sagepub.com/home/cep Marta Vila-Pueyo1 , Jan Hoffmann2 , Marcela Romero-Reyes3 and Simon Akerman3 Abstract Objective: To review and discuss the literature relevant to the role of brainstem structure and function in headache. Background: Primary headache disorders, such as migraine and cluster headache, are considered disorders of the brain. As well as head-related pain, these headache disorders are also associated with other neurological symptoms, such as those related to sensory, homeostatic, autonomic, cognitive and affective processing that can all occur before, during or even after headache has ceased. Many imaging studies demonstrate activation in brainstem areas that appear specifically associated with headache disorders, especially migraine, which may be related to the mechanisms of many of these symptoms. This is further supported by preclinical studies, which demonstrate that modulation of specific brainstem nuclei alters sensory processing relevant to these symptoms, including headache, cranial autonomic responses and homeostatic mechanisms. Review focus: This review will specifically focus on the role of brainstem structures relevant to primary headaches, including medullary, pontine, and midbrain, and describe their functional role and how they relate to mechanisms -
(Rmtg),&Nbsp;A Gabaergic Afferent to Midbrain Dopamine Neurons
Neuron Article The Rostromedial Tegmental Nucleus (RMTg), a GABAergic Afferent to Midbrain Dopamine Neurons, Encodes Aversive Stimuli and Inhibits Motor Responses Thomas C. Jhou,1,* Howard L. Fields,2 Mark G. Baxter,3 Clifford B. Saper,4 and Peter C. Holland5 1Behavioral Neuroscience Branch, National Institute on Drug Abuse, Baltimore, MD 21224, USA 2Ernest Gallo Clinic and Research Center, University of California at San Francisco, Emeryville, CA 94608, USA 3Department of Experimental Psychology, University of Oxford, OX1 3UD Oxford, UK 4Beth Israel Deaconess Medical Center, Harvard University, Boston, MA 02215, USA 5Department of Psychological and Brain Sciences, Johns Hopkins University, Baltimore, MD 21218, USA *Correspondence: [email protected] DOI 10.1016/j.neuron.2009.02.001 SUMMARY vation strongly inhibits dopamine (DA) neurons (Christoph et al., 1986; Ji and Shepard, 2007), are activated by aversive Separate studies have implicated the lateral habe- stimuli and reward omission and inhibited by reward-predictive nula (LHb) or amygdala-related regions in processing cues or unexpected rewards (Matsumoto and Hikosaka, 2007, aversive stimuli, but their relationships to each other 2009; Geisler and Trimble, 2008). These ‘‘negative reward and to appetitive motivational systems are poorly prediction errors’’ are inverse to firing patterns in putative dopa- understood. We show that neurons in the recently minergic midbrain neurons (Mirenowicz and Schultz, 1994, 1996; identified GABAergic rostromedial tegmental Hollerman and Schultz, 1998; -
Brainstem Dysfunction in Critically Ill Patients
Benghanem et al. Critical Care (2020) 24:5 https://doi.org/10.1186/s13054-019-2718-9 REVIEW Open Access Brainstem dysfunction in critically ill patients Sarah Benghanem1,2 , Aurélien Mazeraud3,4, Eric Azabou5, Vibol Chhor6, Cassia Righy Shinotsuka7,8, Jan Claassen9, Benjamin Rohaut1,9,10† and Tarek Sharshar3,4*† Abstract The brainstem conveys sensory and motor inputs between the spinal cord and the brain, and contains nuclei of the cranial nerves. It controls the sleep-wake cycle and vital functions via the ascending reticular activating system and the autonomic nuclei, respectively. Brainstem dysfunction may lead to sensory and motor deficits, cranial nerve palsies, impairment of consciousness, dysautonomia, and respiratory failure. The brainstem is prone to various primary and secondary insults, resulting in acute or chronic dysfunction. Of particular importance for characterizing brainstem dysfunction and identifying the underlying etiology are a detailed clinical examination, MRI, neurophysiologic tests such as brainstem auditory evoked potentials, and an analysis of the cerebrospinal fluid. Detection of brainstem dysfunction is challenging but of utmost importance in comatose and deeply sedated patients both to guide therapy and to support outcome prediction. In the present review, we summarize the neuroanatomy, clinical syndromes, and diagnostic techniques of critical illness-associated brainstem dysfunction for the critical care setting. Keywords: Brainstem dysfunction, Brain injured patients, Intensive care unit, Sedation, Brainstem -
Optogenetic Activation of Cholinergic Neurons in the PPT Or LDT Induces REM Sleep
Optogenetic activation of cholinergic neurons in the PPT or LDT induces REM sleep Christa J. Van Dorta,b,c,1, Daniel P. Zachsa,b,c, Jonathan D. Kennya,b,c, Shu Zhengb, Rebecca R. Goldblumb,c,d, Noah A. Gelwana,b,c, Daniel M. Ramosb,c, Michael A. Nolanb,c,d, Karen Wangb,c, Feng-Ju Wengb,e, Yingxi Linb,e, Matthew A. Wilsonb,c, and Emery N. Browna,b,d,f,1 aDepartment of Anesthesia, Critical Care, and Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114; and bDepartment of Brain and Cognitive Sciences, cPicower Institute for Learning and Memory, eMcGovern Institute for Brain Research, fHarvard-MIT Division of Health Sciences and Technology, and dInstitute for Medical Engineering and Science, Massachusetts Institute of Technology, Cambridge, MA 02139 Contributed by Emery N. Brown, December 3, 2014 (sent for review September 19, 2014; reviewed by Helen A. Baghdoyan and H. Craig Heller) Rapid eye movement (REM) sleep is an important component of REM sleep regulation, a method that can modulate specific cell the natural sleep/wake cycle, yet the mechanisms that regulate types in the behaving animal is needed. Optogenetics now pro- REM sleep remain incompletely understood. Cholinergic neurons vides this ability to target specific subpopulations of neurons in the mesopontine tegmentum have been implicated in REM sleep and control them with millisecond temporal resolution (30). regulation, but lesions of this area have had varying effects on REM Therefore, we aimed to determine the role of cholinergic sleep. Therefore, this study aimed to clarify the role of cholinergic neurons in the PPT and LDT in REM sleep regulation using neurons in the pedunculopontine tegmentum (PPT) and laterodor- optogenetics. -
Brainstem Dental 2012.Doc
Dental Neuroanatomy January 12 and 19, 10-12, 2012 Suzanne S. Stensaas, Ph.D. Dear Students: Please print these notes and bring them with you. My style is to use a Tablet PC and I draw on either a Word or pdf copy with colors. Be prepared to draw. Have at least 5 colors. Please try to look at the notes AHEAD OF TIME for each lecture in this course. This way you can see the direction and organization of the lecture and be more familiar with the terms. There will be a quiz (that does not count) at the beginning to cover topics in the two gross anatomy lectures by Dr. Morton in Phase 1. They are G 17B and GL 18 Waxman, S Clinical Neuroanatomy, 26th ed.2010. THE OLD EDITION IS FINE TOO. Review Ch 5 on the spinal cord organization, but not the tracts in the middle or lesions at the end of the chapter. Also review the basic concept of a reflex. Review or skim Ch 12 on the vascular supply of the brain. Just look at pictures and legends for the clinical part at the end. NEW material: Chapter 7 Waxman, Brainstem, but not the cerebellum part. NEW material: Chapter 8 Waxman, Cranial nerves, all of it including autonomic. BEWARE THE CRANIAL NERVES ARE KILLERS! There are about 50 copies of the following bright yellow paperback book, which can be checked out from the Eccles Health Sciences Library and kept for the duration of the course. They are on reserve as: Cranial nerves: anatomy and clinical comments Linda Wilson-Pauwels, 1988 Toronto; Philadelphia: B.C. -
Isolated Necrosis of Central Tegmental Tracts Due to Neonatal Hypoxic-Ischemic Encephalopathy: MRI Findings
Journal of Neurology & Stroke Case Report Open Access Isolated necrosis of central tegmental tracts due to neonatal hypoxic-ischemic encephalopathy: MRI findings Abstract Volume 11 Issue 1 - 2021 Perinatal hypoxia is an old entity that still prevails today and may lead to neurological Tomás de Andrade Lourenção Freddi, Luiz sequelae that can go unnoticed until a certain age, generating many costs for public health. In this case report, we demonstrate on magnetic resonance imaging an unusual pattern of Fellipe Curvêlo Ciraulo Santos, Nelson Paes perinatal hypoxia in a preterm 5-month-old infant, involving the central tegmental tracts Fortes Diniz Ferreira, Felipe Diego Gomes and briefly discuss its possible pathophysiology. Dantas Department of Radiology, Hospital do Coração, Brazil Keywords: magnetic resonance imaging, asphyxia, hypoxic-ischemic encephalopathy, tegmentum, neonates, brainstem Correspondence: Tomás de Andrade Lourenção Freddi, Hospital do Coração, 147 Desembargador Eliseu Guilherme Street, São Paulo, SP, 04004-030, Brazil, Tel +5511976059280, Email Received: May 25, 2020 | Published: Febrauary 15, 2021 Abbreviations: MRI, magnetic resonance imaging; HII, that connect the red nucleus and the inferior olivary nucleus, being hypoxic-ischemic injury; FLAIR, fluid-attenuated inversion recovery; part of the dentato-rubro-olivary system, called Guillain–Mollaret CTT, central tegmental tract; VGB, vigabatrin triangle.3–5 Introduction Hypoxic-ischemic injury (HII) is one of the most important causes of encephalopathy in neonates, irrespective of gestational age, and may occur in the uterus or during delivery by different intrapartum conditions. In preterm or very low birth weight infants, brain magnetic resonance imaging (MRI) can demonstrate multiple different findings, which a detailed description is beyond the scope of this article, although being periventricular leukomalacia the most frequent (seen in at least 50% of cases). -
Why a Midbrain? Evolution, Structure and Functions Notes
The changes cause "distortions" in the basic organization of the hindbrain • Variations in relative size of parts – Huge vagal lobe of the fresh-water buffalofish [Review] – Vagal and facial lobes of the catfish [Review] – Electric fish have an enormous and specialized cerebellum. [Review] • Cell migrations from the rostral hindbrain’s alar plate— from a proliferative region called the “rhombic lip”: – To cerebellum – To pre-cerebellar cell groups – especially the cells of the pons 1 Endbrain Midbrain Cerebellum Vagal Lobe Image by MIT OpenCourseWare. Buffalofish (Carpiodes tumidus) has a specialized palatal organ for filtering the water for food; it is innervated by the vagus nerve. 2 Olfactory Stalk Primitive Endbrain Midbrain Cerebellum Facial Lobe Vagal Lobe Image by MIT OpenCourseWare. The catfish has taste receptors all over its body innervated by the facial nerve (7th cranial nerve) 3 Amiurus melas (the small catfish) Image by MIT OpenCourseWare. 4 Courtesy of MIT Press. Used with permission. Schneider, G. E. Brain structure and its Origins: In the Development and in Evolution of Behavior and the Mind. MIT Press, 2014. ISBN: 9780262026734. The enlarged cerebellum of a Mormyrid fish Fig.6-1 5 Questions, chapter 10 16) What is the meaning of the term “pons”? (See the end of chapter 5.) What is a major input, and what is the major output, of the cells of the pontine gray matter? 17) What causes quantitative distortions of the basic structural layout of the hindbrain? What is the major distortion that occurs in the development of the hindbrain of humans and other primates? 18) What is the role of the “rhombic lip” – a structure seen during the development of the rostral hindbrain? 6 The "distortions" in the basic organization of the hindbrain, continued • Variations in relative size of parts √ Huge vagal lobe of the fresh-water buffalofish √ Vagal and facial lobes of the catfish √ Electric fish have an enormous and specialized cerebellum. -
Localization and Network of Coma- Causing Brainstem Lesions: Evidence for a Human Consciousness Network
Localization and Network of Coma- Causing Brainstem Lesions: Evidence for a Human Consciousness Network The Harvard community has made this article openly available. Please share how this access benefits you. Your story matters Citation Fischer, David B. 2016. Localization and Network of Coma-Causing Brainstem Lesions: Evidence for a Human Consciousness Network. Doctoral dissertation, Harvard Medical School. Citable link http://nrs.harvard.edu/urn-3:HUL.InstRepos:27007725 Terms of Use This article was downloaded from Harvard University’s DASH repository, and is made available under the terms and conditions applicable to Other Posted Material, as set forth at http:// nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of- use#LAA Abstract Focal brainstem lesions can disrupt arousal and cause coma, yet the exact location of the brainstem region critical to arousal and its associated network are unknown. First, we compare brainstem lesions between 12 patients with coma and 24 patients without coma to identify a region specific to coma-causing lesions. Second, we determine the network connectivity of this brainstem region and each individual coma- causing lesion using resting state functional connectivity MRI data acquired from 98 healthy subjects. Third, we evaluate the functional connectivity of this network in patients with disorders of consciousness (51 patients versus 21 controls). These analyses reveal a small, coma-specific region in the left pontine tegmentum, near the medial parabrachial nucleus. This brainstem region, and each individual coma-causing lesion, is functionally connected to the left agranular, anterior insula (AI), and pregenual anterior cingulate cortex (pACC). These cortical sites align poorly with previously defined functional networks but match the distribution of von Economo neurons (VENs).