Learning Brainstem Anatomy: a Mnemonic Device
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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. -
Cranial Nerve Palsy
Cranial Nerve Palsy What is a cranial nerve? Cranial nerves are nerves that lead directly from the brain to parts of our head, face, and trunk. There are 12 pairs of cranial nerves and some are involved in special senses (sight, smell, hearing, taste, feeling) while others control muscles and glands. Which cranial nerves pertain to the eyes? The second cranial nerve is called the optic nerve. It sends visual information from the eye to the brain. The third cranial nerve is called the oculomotor nerve. It is involved with eye movement, eyelid movement, and the function of the pupil and lens inside the eye. The fourth cranial nerve is called the trochlear nerve and the sixth cranial nerve is called the abducens nerve. They each innervate an eye muscle involved in eye movement. The fifth cranial nerve is called the trigeminal nerve. It provides facial touch sensation (including sensation on the eye). What is a cranial nerve palsy? A palsy is a lack of function of a nerve. A cranial nerve palsy may cause a complete or partial weakness or paralysis of the areas served by the affected nerve. In the case of a cranial nerve that has multiple functions (such as the oculomotor nerve), it is possible for a palsy to affect all of the various functions or only some of the functions of that nerve. What are some causes of a cranial nerve palsy? A cranial nerve palsy can occur due to a variety of causes. It can be congenital (present at birth), traumatic, or due to blood vessel disease (hypertension, diabetes, strokes, aneurysms, etc). -
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. -
Brainstem Exclusive of the Pyramids Themselves, Which Were Blood-Supplied Through the Intact Basilar Artery
NOTE ON CONVERGENCE OF PYRAMIDAL AND PRIMARY AFFERENT IMPULSES IN THE SPINAL CORD OF THE CAT BY DAVID P. C. LLOYD THE ROCKEFELLER UNIVERSITY Communicated December 20, 1967 The burden of this note is to present an example of observations long since made but not previously published. The immediate stimulus for presenting them now was provided by the paper by R. Porter' in which a combination of im- pulses of cortical and of lingual nerve origin was shown by convergence to facilitate the response of interneurons in or near the spinal trigeminal nucleus to a level of activity greater than that of the sum of responses elicited by lingual nerve stimu- lation and corticospinal stimulation, respectively, in isolation. Experiments of the sort now to be described concern the convergence upon interneurons in the lumbar spinal enlargement of pyramidal tract impulses and primary afferent im- pulses engendered by stimulation of the seventh lumbar dorsal root. To an ex- tent these experiments are confirmatory, with respect to another location in the neuraxis, of the observations of Porter,' but they demonstrate, in addition, how one pathway by occlusion may pre-empt the interneuron from service to the other pathway. In a prior paper2 convergence at the internuncial level was im- plied by virtue of pyramidal tract facilitatory influence upon disynaptic (three- neuron-arc) reflexes in the absence of any influence upon monosynaptic (two- neuron-arc) reflexes (ref. 2, Figs. 9 and 10). Preparation and procedure were discussed in the previous publication2 and need not be restated here, except to note that the pyramidal tract impulses were "pure" because the bulbar pyramid was stimulated rostral to a lesion that sev- ered the entire brainstem exclusive of the pyramids themselves, which were blood-supplied through the intact basilar artery. -
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. -
Studies of Oculomotor-System Neural Connections Ronald S
Journal of the Arkansas Academy of Science Volume 34 Article 26 1980 How We Look: Studies of Oculomotor-System Neural Connections Ronald S. Remmel University of Arkansas for Medical Sciences Robert D. Skinner University of Arkansas for Medical Sciences Follow this and additional works at: http://scholarworks.uark.edu/jaas Part of the Sense Organs Commons Recommended Citation Remmel, Ronald S. and Skinner, Robert D. (1980) "How We Look: Studies of Oculomotor-System Neural Connections," Journal of the Arkansas Academy of Science: Vol. 34 , Article 26. Available at: http://scholarworks.uark.edu/jaas/vol34/iss1/26 This article is available for use under the Creative Commons license: Attribution-NoDerivatives 4.0 International (CC BY-ND 4.0). Users are able to read, download, copy, print, distribute, search, link to the full texts of these articles, or use them for any other lawful purpose, without asking prior permission from the publisher or the author. This Article is brought to you for free and open access by ScholarWorks@UARK. It has been accepted for inclusion in Journal of the Arkansas Academy of Science by an authorized editor of ScholarWorks@UARK. For more information, please contact [email protected], [email protected]. Journal of the Arkansas Academy of Science, Vol. 34 [1980], Art. 26 HOW WE LOOK: STUDIES OF OCULOMOTOR-SYSTEM NEURAL CONNECTIONS . R. S. REMMELandR. D. SKINNER i Department of Physiology and Biophysics and Department of Anatomy University of Arkansas forMedical Sciences Little Rock, Arkansas 72205 ABSTRACT The neural connections of the reticular formation (RF) withthe vestibular nuclei (8V)and the ascending medial longitudinal fasciculus (MLF) were studied, because many neurons in these structures carry eye-movement and head-movement (vestibular) signals and are only one or two synaptic connections removed from eye motorneurons. -
Efficacy And/Or Effectiveness of Portable Neuromodulation Stimulator (Pons®) As Treatment for Traumatic Brain Injury (TBI)”
Evidence-Based Practice Group Answers to Clinical Questions “Efficacy and/or Effectiveness of Portable Neuromodulation Stimulator (PoNS®) as Treatment for Traumatic Brain Injury (TBI)” A Rapid Systematic Review By WorkSafeBC Evidence-Based Practice Group Dr. Craig Martin Manager, Clinical Services Chair, Evidence-Based Practice Group October 2019 Clinical Services – Worker and Employer Services Efficacy and/or Effectiveness of Portable Neuromodulation Stimulator (PoNS®) as Treatment for Traumatic Brain Injury (TBI) i About this report Efficacy and/or Effectiveness of Portable Neuromodulation Stimulator (PoNS®) as Treatment for Traumatic Brain Injury (TBI) Published: October 2019 About the Evidence-Based Practice Group The Evidence-Based Practice Group was established to address the many medical and policy issues that WorkSafeBC officers deal with on a regular basis. Members apply established techniques of critical appraisal and evidence-based review of topics solicited from both WorkSafeBC staff and other interested parties such as surgeons, medical specialists, and rehabilitation providers. Suggested Citation WorkSafeBC Evidence-Based Practice Group, Martin CW. Efficacy and/or Effectiveness of Portable Neuromodulation Stimulator (PoNS®) as Treatment for Traumatic Brain Injury (TBI). Richmond, BC: WorksafeBC Evidence- Based Practice Group; October 2019. Contact Information Evidence-Based Practice Group WorkSafeBC PO Box 5350 Stn Terminal Vancouver BC V6B 5L5 Email [email protected] Phone 604 279-7417 Toll-free 1 888 967-5377 -
An EM Study of the Dorsal Nucleus of the Lateral Lemniscus: Inhibitory, Commissural, Synaptic Connections Between Ascending Auditory Pathways
The Journal of Neuroscience, March 1989, g(3): 987-982 An EM Study of the Dorsal Nucleus of the Lateral Lemniscus: Inhibitory, Commissural, Synaptic Connections Between Ascending Auditory Pathways Douglas L. Oliver and Amiram Shneiderman Department of Anatomy, The University of Connecticut Health Center, Farmington, Connecticut 06032 The dorsal nucleus of the lateral lemniscus (DNLL) and its tions between the nuclei. Crossed inhibitory connections in connections constitute one of the ascending auditory path- the DNLL pathway may be important in regulating the flow ways to the inferior colliculus. One notable feature of this of ascending auditory information. nucleus is the heavy commissural connections between DNLL on opposite sides of the midbrain. These commissural con- The dorsal nucleus of the lateral lemniscus (DNLL) holds a nections may have a significant impact on the ascending unique position in the auditory system. Astride the fibers of the pathway. In this study, the fine structure of DNLL in the cat lateral lemniscus,DNLL receives most of the sameprojections and its commissural connections were examined. Both an- that ascendto the inferior colliculus (Glendenning et al., 1981; terograde and retrograde transport methods were used si- Shneiderman et al., 1988); and DNLL also projects bilaterally multaneously at the EM level. Injections of 3H-leucine mixed to the inferior colliculus. Thus, the combined inputs and outputs with WGA-HRP were made in one DNLL. After axonal trans- of DNLL form a multisynaptic pathway, parallel to the other port, EM autoradiographic methods were used to identify the ascending pathways to the inferior colliculus (Goldberg and anterogradely labeled axonal endings from the opposite Moore, 1967; van Noort, 1969; Roth et al., 1978; Adams, 1979; DNLL. -
Neuron Numbers Increase in the Human Amygdala from Birth to Adulthood, but Not in Autism
Neuron numbers increase in the human amygdala from birth to adulthood, but not in autism Thomas A. Avinoa, Nicole Bargera, Martha V. Vargasa, Erin L. Carlsona, David G. Amarala,b,c, Melissa D. Baumana,b, and Cynthia M. Schumanna,1 aDepartment of Psychiatry and Behavioral Sciences, UC Davis MIND Institute, School of Medicine, University of California, Davis, Sacramento, CA 95817; bCalifornia National Primate Research Center, University of California, Davis, CA 95616; and cCenter for Neuroscience, University of California, Davis, CA 95618 Edited by Joseph E. LeDoux, New York University, New York, NY, and approved March 1, 2018 (received for review February 12, 2018) Remarkably little is known about the postnatal cellular develop- process, however, may also make the amygdala more susceptible ment of the human amygdala. It plays a central role in mediating to developmental or environmental insults. emotional behavior and has an unusually protracted development ASD is characterized by impairments in social communication well into adulthood, increasing in size by 40% from youth to combined with restricted interests and behaviors. Alterations in adulthood. Variation from this typical neurodevelopmental trajec- amygdala growth can be detected as early as 2 y of age (23–26) tory could have profound implications on normal emotional devel- and persist into late childhood (5, 27). The severity of the indi- vidual’s social and communicative symptoms positively correlates opment. We report the results of a stereological analysis of the – number of neurons in amygdala nuclei of 52 human brains ranging with amygdala enlargement, suggesting a potential structure from 2 to 48 years of age [24 neurotypical and 28 autism spectrum function relationship (23). -
Auditory and Vestibular Systems Objective • to Learn the Functional
Auditory and Vestibular Systems Objective • To learn the functional organization of the auditory and vestibular systems • To understand how one can use changes in auditory function following injury to localize the site of a lesion • To begin to learn the vestibular pathways, as a prelude to studying motor pathways controlling balance in a later lab. Ch 7 Key Figs: 7-1; 7-2; 7-4; 7-5 Clinical Case #2 Hearing loss and dizziness; CC4-1 Self evaluation • Be able to identify all structures listed in key terms and describe briefly their principal functions • Use neuroanatomy on the web to test your understanding ************************************************************************************** List of media F-5 Vestibular efferent connections The first order neurons of the vestibular system are bipolar cells whose cell bodies are located in the vestibular ganglion in the internal ear (NTA Fig. 7-3). The distal processes of these cells contact the receptor hair cells located within the ampulae of the semicircular canals and the utricle and saccule. The central processes of the bipolar cells constitute the vestibular portion of the vestibulocochlear (VIIIth cranial) nerve. Most of these primary vestibular afferents enter the ipsilateral brain stem inferior to the inferior cerebellar peduncle to terminate in the vestibular nuclear complex, which is located in the medulla and caudal pons. The vestibular nuclear complex (NTA Figs, 7-2, 7-3), which lies in the floor of the fourth ventricle, contains four nuclei: 1) the superior vestibular nucleus; 2) the inferior vestibular nucleus; 3) the lateral vestibular nucleus; and 4) the medial vestibular nucleus. Vestibular nuclei give rise to secondary fibers that project to the cerebellum, certain motor cranial nerve nuclei, the reticular formation, all spinal levels, and the thalamus. -
Overview of the Reticular Formation (RF)
TeachSheet Reticular Formation & Diffuse modulatory system Overview of the Reticular Formation (RF) The term reticular formation refers to the neuronal network within the brainstem, although it continues rostrally into the thalamus and hypothalamus and caudally into the propriospinal network of the spinal cord. A “coordinating system” (like the Limbic system) with “connections” to sensory, somatic motor and visceral motor systems Organization can be subdivided into two neuronal cell “columns” (medial to lateral) as well as on the basis of their neurotransmitter release Neuronal columns (many nuclei and names, but these are some of the major ones): o “Medial tegmental field” (large-celled nuclei) . Origin of the reticulospinal pathway . Role in coordinating posture, eye and head movements. o “Lateral tegmental field” (smaller and fewer cells, shorter local projections) . Extends from the medulla to the pons . Coordinate autonomic and limbic functions (e.g. micturition, swallowing, mastication and vocalization) The functions of the reticular formation include their ability to coordinate motor and sensory brainstem nuclei: o Pattern generator . Eye movements; horizontal (PPRF) and vertical (riMLF) . Rhythmical chewing movements (pons) . Posture and locomotion (midbrain and pons) . Swallowing, vomiting, coughing and sneezing (medulla) . Micturition (pons) o Respiratory control (medulla); expiratory, inspiratory, apneustic and pneumotaxic o Cardiovascular control (medulla); vasomotor pressor/depressor, cardioacceleratory and inhibitory. Afferents arise from baroreceptors (carotid sinus and aortic arch), chemoreceptors (carotid sinus, lateral reticular formation chemosensitive area in the medulla) and stretch receptors (lung and respiratory muscles) . Efferents arise from reticular formation neurons within the pons and medulla o Sensory modulation or “gate” control . The term “gating” refers to “modulation” of synaptic transmission from one set of neurons to the next.