International Journal of Health Sciences and Research ISSN:

Similar documents
Multiple system atrophy (MSA) is a sporadic adult-onset

MULTI SYSTEM ATROPHY: REPORT OF TWO CASES Dipu Bhuyan 1, Rohit Kr. Chandak 2, Pankaj Kr. Patel 3, Sushant Agarwal 4, Debjanee Phukan 5

ORIGINAL CONTRIBUTION. Brain Magnetic Resonance Imaging in Multiple-System Atrophy and Parkinson Disease

FDG-PET e parkinsonismi

1.1. Parkinson disease

DISTRIBUTION OF NEURONAL CYTOPLASMIC INCLUSIONS IN MULTIPLE SYSTEM ATROPHY

Drunk When You re Not A 67 year old male presents with feeling off balance

Usefulness of Diffusion-Weighted MRI for Differentiation between Parkinson s Disease and Parkinson Variant of Multiple System Atrophy

VIII. 3. In vivo Visualization of α-synuclein Deposition by [ 11 C]BF-227 PET in Multiple System Atrophy

Pietro Cortelli. IRCCS Istituto delle Scienze Neurologiche di Bologna DIBINEM, Alma Mater Studiorum - Università di Bologna

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative

Clinical Characteristics of Patients with Multiple System Atrophy in Singapore

Functional Distinctions

Role of Magnetic Resonance Imaging in the Diagnosis of Adult Onset Movement Disorders

CN V! touch! pain! Touch! P/T!

Reduction of Neuromelanin-Positive Nigral Volume in Patients with MSA, PSP and CBD

III./3.1. Movement disorders with akinetic rigid symptoms

Brainstem. Steven McLoon Department of Neuroscience University of Minnesota

Unit VIII Problem 5 Physiology: Cerebellum

DISORDERS OF THE MOTOR SYSTEM. Jeanette J. Norden, Ph.D. Professor Emerita Vanderbilt University School of Medicine

Parts of the motor circuits

SWI including phase and magnitude images

Biomedical Technology Research Center 2011 Workshop San Francisco, CA

The neurvous system senses, interprets, and responds to changes in the environment. Two types of cells makes this possible:

An update on advances in magnetic resonance imaging of multiple system atrophy

Patterns of Cerebral Glucose Metabolism Detected with Positron Emission Tomography Dfier in Multiple System Atrophy and Olivopontocerebellar Atrophy

Dizziness, postural hypotension and postural blackouts: Two cases suggesting multiple system atrophy

I: To describe the pyramidal and extrapyramidal tracts. II: To discuss the functions of the descending tracts.

Multiple System Atrophy

Characteristic diffusion tensor tractography. in multiple system atrophy with predominant cerebellar ataxia. and cortical cerebellar atrophy

Role of Diffusion weighted Imaging in the Evaluation of Intracranial Tumors

Brain Advance Access published June 30, doi: /brain/awl166 Brain (2006) Page 1 of 9

MACHADO-Joseph disease

Essentials of Clinical MR, 2 nd edition. 14. Ischemia and Infarction II

Diffusion-Weighted and Conventional MR Imaging Findings of Neuroaxonal Dystrophy

Biological Bases of Behavior. 8: Control of Movement

By Dr. Saeed Vohra & Dr. Sanaa Alshaarawy

10/3/2016. T1 Anatomical structures are clearly identified, white matter (which has a high fat content) appears bright.

Niall Quinn. Professor of Clinical Neurology UCL IoN & NHNN Queen Square London UK

Neurodegenerative Disease. April 12, Cunningham. Department of Neurosciences

Orthostatic hypotension and nicotine sensitivity in a case of multiple system atrophy

SHORT ANSWER. Write the word or phrase that best completes each statement or answers the question.

BRAIN STEM AND CEREBELLUM..

VL VA BASAL GANGLIA. FUNCTIONAl COMPONENTS. Function Component Deficits Start/initiation Basal Ganglia Spontan movements

Deep Brain Stimulation in Multiple System Atrophy Mimicking Idiopathic Parkinson s Disease

Nsci 2100: Human Neuroanatomy 2017 Examination 3

Cheyenne 11/28 Neurological Disorders II. Transmissible Spongiform Encephalopathy

brain MRI for neuropsychiatrists: what do you need to know

Lecture XIII. Brain Diseases I - Parkinsonism! Brain Diseases I!

Review Article Brain MR Contribution to the Differential Diagnosis of Parkinsonian Syndromes: An Update

Pathogenesis of Degenerative Diseases and Dementias. D r. Ali Eltayb ( U. of Omdurman. I ). M. Path (U. of Alexandria)

Brainstem. Amadi O. Ihunwo, PhD School of Anatomical Sciences

Overview. Overview. Parkinson s disease. Secondary Parkinsonism. Parkinsonism: Motor symptoms associated with impairment in basal ganglia circuits

Role of MRI in acute disseminated encephalomyelitis

Course Calendar - Neuroscience

General Sensory Pathways of the Trunk and Limbs

The Central Nervous System I. Chapter 12

Internal Organisation of the Brainstem

Pearls and Pitfalls in Neuroradiology of Cerebrovascular Disease The Essentials with MR and CT

Course Calendar

ORIGINAL CONTRIBUTION. FMR1 Premutations Associated With Fragile X Associated Tremor/Ataxia Syndrome in Multiple System Atrophy

Voluntary Movement. Ch. 14: Supplemental Images

Atypical parkinsonism

Case 9511 Hypertensive microangiopathy

Sleep-Disordered Breathing and Risk of Sudden Death in Multiple System Atrophy

ORIGINAL CONTRIBUTION. Transcranial Brain Sonography Findings in Discriminating Between Parkinsonism and Idiopathic Parkinson Disease

Introduction to the Central Nervous System: Internal Structure

Movement Disorders. Psychology 372 Physiological Psychology. Background. Myasthenia Gravis. Many Types

Magnetic resonance imaging in degenerative

Multiple system atrophy: an update

NACC Vascular Consortium. NACC Vascular Consortium. NACC Vascular Consortium

Treatment of Neurological Disorders. David Stamler, MD Chief Medical Officer and SVP, Clinical Development January, 2018

Hyperintense putaminal rim at 1.5 T: prevalence in normal subjects and distinguishing features from multiple system atrophy

Cerebellum. Steven McLoon Department of Neuroscience University of Minnesota

Making Things Happen 2: Motor Disorders

Movement Disorders: A Brief Overview

Cerebellum John T. Povlishock, Ph.D.

Chapter 8. Control of movement

MRI for the differential diagnosis of neurodegenerative parkinsonism in clinical practice

Investigating molecular mechanisms of progression of Parkinson s Disease in human brain

Multiple System Atrophy

Basal nuclei, cerebellum and movement

MRI OF THE THALAMUS. Mohammed J. Zafar, MD, FAAN Kalamazoo, MI

Progression of dysautonomia in multiple system atrophy: a prospective study of self-perceived impairment

DEVELOPMENT OF BRAIN

Biological Bases of Behavior. 3: Structure of the Nervous System

New Approach to Parkinson s Disease: Synuclein Immunotherapy

Patologie infiammatorie encefaliche e midollari

Cerebral Peduncle Angle: An Objective Criterion for Assessing Progressive Supranuclear Palsy Richardson Syndrome

Systems Neuroscience Dan Kiper. Today: Wolfger von der Behrens

Multiple System Atrophy Manifested by Bilateral Vocal Cord Palsy as an Initial Sign

MOVEMENT OUTLINE. The Control of Movement: Muscles! Motor Reflexes Brain Mechanisms of Movement Mirror Neurons Disorders of Movement

Pontine pathology: narrowing the radiological differential

Chapter 3. Structure and Function of the Nervous System. Copyright (c) Allyn and Bacon 2004

Dr. Farah Nabil Abbas. MBChB, MSc, PhD

Exam 2 PSYC Fall (2 points) Match a brain structure that is located closest to the following portions of the ventricular system

CNS consists of brain and spinal cord PNS consists of nerves

1 MS Lesions in T2-Weighted Images

DIFFERENTIAL DIAGNOSIS SARAH MARRINAN

who have been unresponsive to L-dopa therapy

Transcription:

International Journal of Health Sciences and Research www.ijhsr.org ISSN: 2249-9571 Case Report Multiple System Atrophy-Cerebellar Type (MSA-C): A Case Report Mohd Abbas Ilyas, Pramod Shaha, Kulamani Sahoo, Rahul Khetawat, Gaurav Khairnar Department of Radiodiagnosis: Krishna Institute of Medical Sciences, Karad, Maharashtra, India 415110. Corresponding Author: Mohd Abbas Ilyas Received: 08/12/2016 Revised: 19/12/2016 Accepted: 21/12/2016 ABSTRACT Introduction: Multiple system atrophy (MSA) is a sporadic, progressive neurodegenerative disorder has clinical symptoms characterized by variable combination of Parkinsonism disease like symptoms, cerebellar ataxia & / or autonomic failure. Presentation of Case: We describe one patient having cerebellar signs with MRI features predominant of MSA-C or olivopontocerebellar atrophy showing pontine Hot cross Bun sign with having unusual focal hemorrhages in bilateral globus pallidus. Discussion: Striatonigral degeneration (MSA-P), characterized clinically by parkinsonian symptoms with degenerative changes predominantly affect basal ganglia, particularly the putamen. Shy-Drager syndrome (MSA-SDS) characterized by autonomic nervous system failure with somewhat variable pathologic changes, characterize by neuronal loss in the substantia nigra and the intermediolateral cell column of the spinal cord. Olivopontocerebellar atrophy (OPCA or MSA-C) characterized by predominantly by cerebellar signs, with predominant olivopontocerebellar atrophy. Conclusion: We mainly draw attention to an uncommon case with predominant MSA-C signs& findings showing pontine Hot cross Bun sign having having unusual focal hemorrhages in bilateral globus pallidus. Key words: Multiple system atrophy; olivopontocerebellar atrophy; Striatonigral degeneration; Shy-Dager Syndrome. INTRODUCTION Multiple system atrophy (MSA) is a sporadic, adult onset, progressive neurodegenerative disorder that involves, to varying degrees, the basal ganglia, the olivopontocerebellar complex and the autonomic system. [1,2] The term MSA was first proposed in 1969 by Graham and Oppenheimer based on their observations that Striatonigral degeneration, olivopontocerebellar complex, and Shy- Drager syndrome commonly coexist clinically and pathologically. [3] MSA-P is synonymous with Striatonigral degeneration when parkinsonism features predominates, with MSA-C when olivopontocerebellar atrophy (OPCA) or cerebellar signs predominates, and MSA SDS(Shy-Drager syndrome) when autonomic failure is dominant. [1,4-7] The incidence is 0.6 cases/ 100000/ year and the prevalence ranges from 1.86 to 4.9 cases/100000. [8] Pathologically, presence of Glial cytoplasmic inclusions containing alpha synuclein clump aggregates is a criterion for definite diagnosis of MSA. [9-11] Alpha synuclein, which is also a major component of the Lewy body, which is the pathologic hallmark lesion in Parkinson disease and dementia with Lewy bodies Recently the term synucleinopathy has been proposed to encompass a presumed common International Journal of Health Sciences & Research (www.ijhsr.org) 321

pathogenic process shared by these neurodegenerative disorders. [12,13] Axial FLAIR Axial T2 WI Figure 1: Cruciform hyperintensity in inferior pons Hot Cross Bun Sign Cerebellar atrophy Cruciform hyperintensity on T2WI/FLAIR involving inferior pons referred to as Hot Cross Bun Sign. Small concave appearing bilateral middle cerebellar peduncles. Loss of Bulge / Flattening of inferior surface of pons. Loss of inferior olivary nucleus bulge. Diffuse Cortical Atrophy. Axial T2WI Figure 2: T2WI- upper medulla- loss of normal olivary bulge on anterolateral aspect of medulla PRESENTATION OF CASE 58 year old normotensive, nondiabetic male came with case of progressive ataxia and right sided weakness since 1 year with single episode of history of fall and unconsciousness having signs of bilateral finger nose ataxia, ataxic gate, brisk exaggerated tendon reflexes & plantar extensors. MRI Brain was performed on 1.5 T Siemens Avanto using short TR /TE (450 / 10 ms), Long TR/TE (3600 / 80ms), FLAIR, DWI, ADC, SWI, PHASE. On MRI Brain : Sag T1WI Figure 3: Loss of bulge in inferior pons & Cerebellar atrophy International Journal of Health Sciences & Research (www.ijhsr.org) 322

Axial T2WI Axial FLAIR Figure 4: Slight Hyperintensity along lateral margin of putamen bilaterally. GRE SWI PHASE Figure 5: Focal hemorrhage in bilateral globus pallidus DISCUSSION MSA parkinsonism (MSA-P), formerly called striatonigral degeneration, is characterized clinically by parkinsonian symptoms with prominence of rigidity, with neuroimaging and gross pathology showing atrophy of the striatum as a result of neuronal loss, involving putamen more than caudate. [14,15] On long TR/TE MR images, a hyperintense rim at the putaminal edge, putaminal atrophy without any intrinsic signal intensity change in putamen, hypointense signal of the putamen, particularly along its posterolateral margin, on T2-weighted images which may be accompanied by a thin rim of hyperintense signal. The hypointense signal is due to abnormal deposition of iron the accompanying hyperintense signal likely reflects increased water associated with cell loss and/or gliosis. [15,16] In contrast to PD, where well more than 90% of patients show a therapeutic response to levodopa, only 13% to 20% of patients with MSA-P show a therapeutic response. [17] MSA-SDS is characterized by autonomic nervous system failure (orthostatic hypotension, urinary incontinence, and inability to sweat). Although the pathologic changes are somewhat variable, neuronal loss in the substantia nigra and the intermediolateral cell column of the spinal cord, accompanied by gliosis, commonly occurs. [18] MSA-SDS may occur alone, although typically it occurs in association International Journal of Health Sciences & Research (www.ijhsr.org) 323

with the clinical, pathologic, and radiologic features of MSA-P and/or MSA-C. [7] On MR, patients with MSA-SDS associated with MSA show typical findings of MSA-P and/or MSA-C. MR exams in pure autonomic failure patients are normal. [7] MSA-Cerebellum (MSA-C) formerly called as olivopontocerebellar degeneration [1] onset varying between early childhood to old age. The primary degeneration centers in Pons, with a subsequent progressive anterograde degeneration of pontocerebellar fibers and of the cerebellum (hemispheres greater than vermis). [18,19] Pontocerebellar fibers originate in the pontine nuclei, have a transverse course in the pons (thus they are called transverse pontine fibers), run to the cerebellum through the middle cerebellar peduncles, and terminate in all lobules of the cerebellar hemisphere and cerebellar vermis. The degeneration in MSA-C is characterized by myelin sheath loss and gliosis of this pontocerebellar pathway and neuronal loss of the cerebellar cortex. This in turn leading to retrograde degeneration of the inferior olives, whose fibers originate in the contralateral inferior olive and reach the cerebellum via the inferior cerebellar peduncle. [8,19] On MR Signal changes & atrophy of Pons, middle cerebellar peduncles, the cerebellum, inferior cerebellar peduncle & olives. On Axial T2WI and FLAIR sequences-typically hyperintensity in cruciform pattern described as Hot Cross Bun Sign is seen consisting of the transverse pontine fibers coursing mediolaterally and the pontine raphe [20] coursing anteroposteriorly. Atrophy &hyperintensity involving middle cerebellar peduncles along with atrophy of Cerebellum & loss of bulge of inferior olives. The midline sagittal section shows selective pontine atrophy with flattening / loss of normal inferior pontine bulge. The characteristic T2 hyper intense sign in pons and middle cerebellar peduncle ( cross sign ) reflects pontocerebellar fibers degeneration and despite very suggestive of MSA it can be found in other forms of parkinsonism. [21] CONCLUSION This is an uncommon case of an MSA C in a 58 year old male with predominant cerebellar signs. MRI revealed Atrophy with abnormal signal intensity of pons, middle cerebellar peduncles, cerebellum & inferior olivary nucleus features indicating atrophy of olivopontocerebellar pathway. Hyperintensity on T2WI involving the lateral margin of putamen on right side probably due to increase water content without intrinsic putamen signal change, likely representing striatonigral degeneration component. Focal hemorrhages in bilateral globus pallidus remain unexplained. We did not come across this in any literature. MRI features likely indicate Predominant MSA C type involvement correlating with cerebellar signs. Our case is classified as probable MSA, since the diagnosis of MSA is defined just with pathological analysis. There is no specific treatment to MSA until the present, only symptomatic interventions. [22] ACKNOWLEDGEMENT We are thankful to Nazirpeerjade, Department of Radiodiagnosis for his secretarial help. REFERENCES 1. Joseph KA, Ashlog JE, Klos KJ et al. Neurologic manifestations in welders with pallidial MRI T1 Hyperintensity. Neurology 2005; 64:2033-2039. 2. Ozawa T et al. The spectrum of pathological involvement of the striatonigral and olivopontocerebellar systems in multiple system atrophy: clinicopathological correlations. Brain 2004; 127:2657-2671. 3. Graham JG, Oppenheimer DR. Orthostatic hypotension: a clinicpathological study J Neurol Neurosurg Psychiatry 1969; 2:522-527. International Journal of Health Sciences & Research (www.ijhsr.org) 324

4. DejerineJ, Thomas AA. L atrophieolivo - ponto - cerebelleuse. NouvIconogr Salpetr 1900; 13:330-370. 5. Adams RD, Van Bogaert L, Vandereecken H. Degenerescencenigrostrieeetcerebello - nigro - striee. PsychiatrNeurol 1961; 142:219-259. 6. Shy GM, Drager GA. A neurological syndrome associated with orthostatic hypotension: a clinico-pathological study. Arch Neurol 1960;2:522-527 7. Brown R, PolinskyRJ, DiChiro G etal. MRI in autonomic Failure.J neurol Nuurosurgery Psychiatry 1987; 50:913-914. 8. Vanacore N. Epidemiological evidence on multiple system atrophy. J Neural Transm 2005; 112:1605-1612. 9. Papp MI, Kahn JE, Lantos PL, et al. Glialcytoplasmic inclusions in the CNS of patients with multiple system atrophy (striatonigral degeneration, olivopontocerebellar atrophy and Shy-Drager syndrome). J NeurolSci1989; 94:79-100. 10. Dickson DW, Lin W, Liu WK, et al. multiple system atrophy: a sporadic synucleinopathy. Brain Pathol1999; 9:721-32. 11. TrojanowskiJQ, Revesz T. Proposed Neuropathological criteria for the postmortem diagnosis of multiple system atrophy. Neuropatholappl Neurobiol 2007; 33(6):615-620. 12. Spillantini MG, Crowther RA, Jakes R, et al. Filamentous alpha-synuclein inclusions link multiple system atrophy with Parkinson s disease and dementia with Lewy bodies. NeurosciLett 1998; 251:205-08. 13. Galvin JE, Lee VMY, Trojanowski JQ. Synucleinopathies: clinical and pathological implications. Arch Neurol 2001; 58:186-90. 14. Pastakia B, Polinsky RJ, DiChiro G, et al. Multiple system atrophy (Shy-Drager syndrome): MR imaging. Radiology 1986;159:499-505 15. Kraft E, Schwarz J, Trenkwalder C, et al. The combination of hypointense and hyperintense signal changes on T2- weighted magnetic resonance imaging sequences: a specific marker of multiple system atrophy? Arch Neurol 1999; 56: 225-228. 16. Block SA, Bakshi R. FLAIR MRI of striatonigral degeneration. Neurology 2001; 56:1200. 17. Lang AE, Lozano AM. Parkinson's diseaseâ! First of two parts. N Engl J Med.1998; 339:1044-1053. 18. Schoene WC. Degenerative diseases of Central nervous system. In: Davis RL, Robertson DM, eds. Textbook of Neuropathology. Baltimore: Williams &Wilkins, 1985:788-823. 19. Savoiardo M, Strada L, Girotti F, et al. Olivopontocerebellar atrophy: MR diagnosis and relationship to multisystem atrophy. Radiology 1990; 174:693-96. 20. Schrag A, Kingsley D, Phatouros C, et al. Clinical usefulness of magnetic resonance imaging in multiple system atrophy. J Neurol Neurosurg Psychiatry 1998; 65:65-71. 21. Seppi K, Schocke MF, Wenning GK, Poewe W. How to diagnose MSA early: the role of magnetic resonance imaging. J Neural Transm 2005; 112:1625-1634. 22. Colosimo C, Tiple D, Wenning GK. Management of MSA: state of the art. J Neurol Transm 2005;112:1695-1704 How to cite this article: Ilyas MA, Shaha P, Sahoo K et al. Multiple system atrophy-cerebellar type (MSA-C): a case report. Int J Health Sci Res. 2017; 7(1):321-325. *********** International Journal of Health Sciences & Research (www.ijhsr.org) 325