A Case Presentation Discussion .


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Bobbye Thompson, MD University of Texas Medical Branch, Galveston Division of Neurosurgery. A Case Presentation & Discussion. History. 51yo F w/several months progressive BLE weakness; pain greater in LLE Bilateral numbness just above breasts & inferiorly
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Bobbye Thompson, MD University of Texas Medical Branch, Galveston Division of Neurosurgery A Case Presentation & Discussion

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History 51yo F w/a while dynamic BLE shortcoming; torment more prominent in LLE Bilateral deadness simply above bosoms & poorly Muscle throbs issues fits falls Urinary incontinence & saddle anesthesia Constipation 2wks (manual disimpaction) No history of spinal operation, harm, or injury No F/C/N/V

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Physical Exam Sensory shortfall mediocre compared to T1 respectively Decreased rectal tone Motor: LLE 2/5, RLE 5/5 Increased tone/spasticity Hyperreflexia Babinski: Bilateral upgoing toes Gait: Able to remain with asisstance; drags LLE, circumduction

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Sag T1 FS MRI Post Sag T2 MRI

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Labs/CSF Gram recolor & culture: uncommon monocytes, no living beings separated CSF glucose: 69 CSF protein: 31 Oligoclonal groups: negative

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Differential Diagnosis Tumor Astrocytoma Ependymoma Demyelinating sore: Multiple sclerosis Neuromyelitis optica Transverse myelitis ADEM

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Impression Progressive LE shortcoming Imaging reliable with Intramedullary tumor at T1 Oligoclonal groups negative Probable tumor, likely glioma Proceed with C6-T2 laminectomy with biopsy or potentially resection Midline myelotomy firm, tan tissue Frozen area: gliosis versus poor quality glioma Inflammatory invade

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Surgical Pathology

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CD68

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CD45

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Diagnosis Inflammatory demyelinating injury Multiple Sclerosis No further surgical mediation Neurology for administration of MS Follow up in center 2 months postop Motor LLE enhanced MRI Brain & C-spine

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MRI 2 mos Post Op

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Multiple Sclerosis (MS) Neuromyelitis Optica (NMO) Transverse Myelitis Acute Disseminated Encephalomyelitis (ADEM) Demyelinating Diseases Mimicking Tumors

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Multiple Sclerosis Relapsing-dispatching MS (RRMS) : Most regular 85% of MS at first analyzed Partial or aggregate recuperation between assaults Secondary-dynamic MS (SPMS) : RRMS course, however turns out to be step by step dynamic Attacks & halfway recuperations may keep on occurring Over 60% at first RRMS advance to SPMS in 10 yrs

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Multiple Sclerosis Primary-dynamic MS (PPMS) : Progressive from onset Symptoms by and large don\'t transmit Progressive inability w/o intense assaults 15% of MS at first analyzed Primary-backsliding MS (PRMS) : Same as PPMS, yet with intense assaults

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Multiple Sclerosis Clinical: Episodic, backsliding transmitting neurologic indications in a youthful grown-up (ordinarily) Neurological side effects dispersed in time & space Common presentations: monocular visual aggravations (optic neuritis), paresthesias/shortcoming (myelitis), incoordination (cerebellar), or potentially diplopia (brainstem) Labs: Oligoclonal groups positive, MBP lifted Not particular, new tests enhancing affectability/specificity Early MS versus Clinically unequivocal MBP raised in different illness forms MRI: T2 serious foci in white matter (UBOs), juxtacortical (G-W intersection including U-strands), periventricular sores, include corpus collosum (opposite expansions)

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MS C-spine

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Neuromyelitis Optica/Devic Clinical: Visual misfortune eye(s) w/myelopathy, for the most part more than a while; may happen at the same time. Course can be monophasic, yet ~2/3 backsliding. In kids: more often than not monophasic & went before by contamination. Recuperation is regularly total. ADEM variation. Labs: Oligoclonal groups negative. NMO-IgG serum can be sent (backhanded immunofluorescence test) MRI: Spinal line injuries augment > 3 levels, w/o cerebrum sores. SC injuries are cavitating, necrotic, w/intense axonal pathology.

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NMO MRI T2

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Transverse Myelitis Clinical : central provocative issue of spinal line; intense or subacute blend of engine, tangible, and autonomic shortfalls. Up to half pt will have LE loss of motion/paresis > 80% have deadness, paresthesias, or dysesthesias, regularly with a very much characterized tangible level lion\'s share encounter weakened bladder work. 1/3 finish recuperation, 1/3 direct incapacity, 1/3 extreme inability. Labs/MRI/Treatment : Variable

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Transverse Myelitis Findings that envoy analysis of MS: hilter kilter clinical discoveries power of tactile deficiencies MRI sores <3 spinal line fragments, MRI Brain: mysterious white matter sores ("filthy white matter") CSF: Oligoclonal groups positive

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Acute Disseminated Encephalomyelitis(ADEM) Clinical: "Postinfectious Encephalomyelitis" Presents as ACUTE neurological indications Fever, queasiness, spewing, positional vertigo, and modified cognizance (tired or dormant) Children taking after viral infxn or vaccination Labs: ESR, CRP, CSF pleocytosis MRI: broad sores, numerous upgrade w/gad (ring-improving injuries) Basal ganglia as well as thalami contribution Spares corpus collosum Molecular mimicry: viral epitope & myelin epitope

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ADEM MRI - Brain

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ADEM MRI - Spine

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Other Differentials Sjögren\'s disorder : copies MS by delivering intermittent multifocal neurological signs; white-matter sores on MRI and oligoclonal groups in CSF. Separate by: systemic indications (sicca-dry eyes, mouth & rheumatic elements), anomalous serology (antinuclear, SSA-Ro, or SSB-La antibodies), and discoveries of incendiary foci on salivary organ biopsy.

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Other Differentials Behçet\'s ailment : Most basic CNS presentation is a subacute brainstem disorder. Separate by: intermittent oral ulcerations (no less than 3 times in 12 months), MRI in Behçet\'s sickness: mind irregularities have a tendency to be huge, diffuse injuries limited to the brainstem .

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Red Flags Atypical components that may predict elective conclusion (not MS): Onset: too soon/late (before 15-20y, after 50y) Early onset may indicate a hereditary etiology Family history: more improbable MS (powerless hereditary assoc) Normal CSF, MRI, and additionally Evoked potential studies Systemic signs Anemia Angiokeratomas Cardiomyopathy Proteinuria Metabolic acidosis

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Summary

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Summary History & Physical Exam, Labs & MRI discoveries, AND prohibition of option judgments. ~90% of patients at last determined to have MS at first present with a clinically segregated disorder (CIS, for example, optic neuritis. X-ray can be profitable in separating. American Academy of Neurology : on estimation of MRI anticipating inevitable change of a clinically confined disorder to clinically clear MS: > 3 white-matter sores in T2 MRI is delicate indicator (>80%) of clinically unequivocal MS inside 7-10 years In Normal MRIs, <20% will have second assault w/in 10y

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The Future Development of all the more exceedingly particular criteria for this range of sicknesses. Advancement of more dependable biomolecular markers. Continuously consider demyelinating ailments in the differential conclusion of upgrading intramedullary injuries . On the off chance that list of suspicion is high, facilitate testing might be justified.

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