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Description : Check out this medical presentation on Neurology, which is titled "TRANSVERSE MYELITIS", to know about transverse myelitis.

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Published on : Aug 18, 2021 | Views : 4612 | Downloads : 45

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RESIDENT LECTURE 03/29/2018 KARTHIKA VEERAPANENI,MD ASSISTANT PROFESSOR NEUROLOGY UAMS
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TRANSVERSE MYELITIS
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Transverse Myelitis Definition: A pathogenically heterogeneous focal inflammatory disorder of the spinal cord characterized by acute or sub acute development of motor weakness, sensory impairment, and autonomic dysfunction. A rare acquired neuro-immune spinal cord disorder that can present with the rapid onset of weakness, sensory alterations, and bowel or bladder dysfunction The term myelitis refers to inflammation of the spinal cord; transverse simply describes the position of the inflammation, that is, across the width of the spinal cord. Epidemiology: Incidence between 1-8 new cases per million per year. Affects people of all ages, with a range of six months to 88 years. Bimodal peaks between the ages of 10 to 19 years and 30 to 39 years. Approximately 25% of cases are in children. There is no gender or familial association with TM. It is estimated that about 1,400 new cases of transverse myelitis are diagnosed each year in the United States.
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Transverse Myelitis Results of inflammation: Demyelination and Axonal Injury/Necrosis Etiology: Infectious Non Infectious inflammatory type Idiopathic
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Transverse myelitis Infectious: I. Viral: A. Enter viruses (groups A and B Coxsackievirus, poliomyelitis, others) B. Herpes zoster C. Myelitis of AIDS D. Epstein-Barr virus (EBV), cytomegalovirus (CMV), herpes simplex E. Rabies F. Arboviruses-Flaviviruses (Japanese, West Nile, etc.) G. HTLV-I (human T-cell lymphotropic virus type I; tropical spastic paraparesis)
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Transverse myelitis II. Bacterial/fungal/parasitic: A. Mycoplasma pneumonia B. Burrelia burdorferi ( Lyme disease) C. Pyogenic myelitis 1.Acute epidural abscess and granuloma 2. Abscess of spinal cord D. Tuberculous myelitis E. Syphilitic myelitis F. Parasitic and fungal infections producing epidural granuloma, localized meningitis, or meningomyelitis and abscess, especially certain forms of schistosomiasis
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Transverse myelitis Noninfectious inflammatory type: Postvaccinal myelitis Acute and chronic relapsing or progressive multiple sclerosis (MS) Subacute necrotizing myelitis and Devic’s disease(NMO) Myelopathy with lupus or other forms of connective tissue diseases Para neoplastic myelopathy Traumatic Idiopathic : Clinical events that are consistent with TM but that are not associated with CSF abnormalities or abnormalities detected on MRI and that have no identifiable underlying cause are characterized as possible idiopathic TM.
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Transverse Myelitis IMMUNOPATHOGENESIS: -pathologic heterogeneity with involvement of both gray and white matter -TM is not a pure demyelinating disorder but rather a mixed inflammatory disorder that affects neurons, axons, and oligodendrocytes and myelin. -autopsy reports have described lymphocytic infiltration with demyelination and axonal loss -30 to 60 percent of the idiopathic TM cases, there is an antecedent respiratory, gastrointestinal, or systemic illness.
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Transverse Myelitis IMMUNOPATHOGENESIS: -In parainfectious TM, the injury may be associated with direct microbial infection of the central nervous system, or with the systemic response to infection by a variety of agents such as varicella zoster virus, herpes virus, and Listeria monocytogenes. -Molecular mimicry with Enterobius vermicularis (pinworm) in a patient with elevated titers of cross-reacting antibodies. -Microbial super antigens such as staphylococcal enterotoxins A through I, toxic shock syndrome toxin-1, and streptococcus pyogenes exotoxin, have also been purported to stimulate the immune system and are known to be capable of activating T-lymphocytes without costimulatory molecules, thereby triggering autoimmune disease by activating auto-reactive T cell clones. -Lupus-associated TM could be associated with central nervous system vasculitis or thrombotic infarction of the spinal cord. -Role of autoantibodies in patients with Neuromyelitis optica and recurrent TM. Autoantibodies-Activate other components of the immune system by crossing the blood-brain barrier. Polyclonal derangement of the immune system. Some autoantibodies initiate a direct and selective injury of neurons that express antigens that cross-react with antibodies directed against infectious pathogens. -TM can occur as part of the spectrum of multiple sclerosis
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Transverse myelitis Symptoms of TM typically develop rapidly over several hours Approximately 37 percent of patients worsen maximally within 24 hours Some cases worsen more slowly, over several weeks. Clinical Presentation: 4 Symptom groups Motor Sensory Autonomic Pain
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Transverse Myelitis Motor: Depends on level, lesion extent: Examples: C3-C5 Quadriplegia, Respiratory Paralysis( diaphragm) T1-T2:Spastic paraplegia L1-S5:UMN/LMN in lower extremities, Bowel/bladder dysfunction (urinary retention) Spinal shock: Sometimes in hyper acute stage( legs flaccid/areflexia); then spasticity develops Sensory: Paraesthesias, numbness, altered temp sensations., etc. L'hermitte sign (Paresthesias in the limbs, elicited by neck flexion)
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Autonomic: Urinary urgency, incontinence, nocturia, urine retention Bowel: Urgency, incontinence, retention Sexual Dysfunction Pain: “Burning” radicular pain “Tight squeezing” “banding” sensation Note: Severe cases of ascending myelitis involving the cervical spinal cord may cause neurogenic respiratory failure. Longitudinally extensive TM can produce hiccups due to involvement of the medulla, and persistent nausea and vomiting due to involvement of the area postrema
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Diagnostic Criteria for Transverse Myelitis* Bilateral (not necessarily symmetric) sensorimotor and autonomic spinal cord dysfunction Clearly defined sensory level Progression to nadir of clinical deficits between 4 hours and 21 days after symptom onset Demonstration of spinal cord inflammation: cerebrospinal fluid pleocytosis or elevated IgG index,† or MRI revealing a gadolinium-enhancing cord lesion Exclusion of compressive, post radiation, neoplastic, and vascular causes * Clinical events that are consistent with transverse myelitis but that are not associated with cerebrospinal fluid abnormalities or abnormalities detected on MRI and that have no identifiable underlying cause are categorized as possible idiopathic transverse myelitis. † The IgG index is a measure of intrathecal synthesis of immunoglobulin and is calculated with the use of the following formula: (CSF IgG ÷ serum IgG) ÷ (CSF albumin ÷ serum albumin).
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Types: Complete: Usually longer (>3 vertebral segments) and Central-->Symmetric decrease in motor/sensory functions associated with decreased sphincter functions. Incomplete: Shorter( <3 vertebral segments), peripheral lesions involving limited tracts, usually incomplete loss of function.
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Classification based on spinal cord lesion characteristics: Acute partial TM: Para infectious Asymmetric lesions typically of 1 or 2 vertebral segments in length Usually mild to moderate in severity High risk for MS when MRI brain reveals WM lesions compatible with demyelination. Longitudinally extensive TM: Asymmetric or symmetric spinal cord lesions that span ≥3 contiguous vertebral segments. Usually moderate to very severe Most commonly associated with high risk for NMO spectrum disorders in the setting of seropositivity for NMO- IgG
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Interpretation of clinical spinal cord syndromes Complete cord syndrome: Loss of all motor and sensory modalities below the level of the lesion Associated with acute, severe, "necrotizing" myelitis. Brown-Sequard syndrome (partial or complete): Dysfunction of the corticospinal tracts and dorsal columns( symptoms ipsilateral to the lesion) and spinothalamic tract dysfunction( symptoms contralateral to the lesion) Conus-Medullaris syndrome: Can be associated with Viral or post-viral myelitis syndromes.
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Key points: At the first occurrence of a partial myelitis, the presence of two or more brain lesions indicates an 88% chance of conversion to MS in the next 20 years. With a normal MRI, the risk is only 19%. In one study, 38% of patients with a first episode of TM were seropositive for NMO-IgG The risk of developing recurrent myelitis or new onset optic neuritis in patients with an isolated longitudinally extensive transverse myelitis was more than 50% among those who were NMO-IgG seropositive, compared with 0% in those who were NMO-IgG seronegative. About 25%–40% of cases of transverse myelitis are caused by viral infections. The frequency of transverse myelitis during or after varicella infection is reported to be 0.3%.
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Diagnosis Diagnosis of TM is based on clinical and Radiological findings CSF studies: Usually depends on etiology Most commonly, Cerebrospinal fluid (CSF) is abnormal in half of patients, with elevated protein level (usually 100 to 120 mg/100 mL) and moderate lymphocytosis (usually <100/mm3). Glucose levels are normal. Oligoclonal bands are usually not present in isolated TM, and when present suggest a higher risk of subsequent MS. Lab work up depends on suspected etiology. Imaging: Lesions may occur anywhere within the cord, however the thoracic cord is the most frequently involved site. CT Spine variable enlargement of the spinal cord variable contrast enhancement patterns (including no enhancement)
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MRI Spine Up to 40% of cases have no findings on MRI. In the remainder, the appearance is variable and non-specific. large variation in lesion size, however they most commonly extend for 3-4 spinal segments. lesions typically occupy greater than two thirds of the cross-sectional area of the cord. variable enlargement of the spinal cord. an intrinsic spinal cord lesion that usually enhances with gadolinium administration. It is critically important to exclude compressive lesions of the spinal cord, such as spinal epidural abscess, that require specific treatment. Typical signal characteristics on MRI brain include: T1 : isointense or hypointense T2 : poorly delineated hyperintense signal T1 C+ (Gd) : variable enhancement patterns (none, diffuse, patchy, peripheral)
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TM-Treatment Corticosteroids, typically methylprednisolone (1 g intravenously daily for 3-5 days). Plasma exchange or cyclophosphamide may be useful in steroid-unresponsive patients. Patients tend to improve over several months, but may have residual deficits, and mortality rates in excess of 30% have been reported. Also, treatment includes disease specific treatment.
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TM-PROGNOSIS Most patients with idiopathic TM have at least a partial recovery, which usually begins within one to three months. Some degree of persistent disability is common, occurring in about 40 percent Significant recovery is unlikely if there is no improvement by three months. A very rapid onset with complete paraplegia and spinal shock have been associated with poorer outcomes. TM is generally a monophasic illness. However, a small percentage of patients may suffer a recurrence. Cont………….
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TM-PROGNOSIS(cont…) While patients are often treated with parenteral corticosteroid therapy, there is limited evidence that this approach alters outcomes. MS is more likely to develop in those with partial and asymmetric cord involvement versus a complete cord syndrome. A finding of demyelinating lesions on brain MRI also identifies those at higher risk for MS.
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CASE 48 y/o RHF with PMH DM2, Asthma, Depression presented with c/o progressive, ascending lower extremity numbness and weakness for 3 days. Symptoms first began in toes and ascended to waist. History also positive for Bowel/bladder incontinence. No h/o HA/vision changes/dysphagia/dysarthria or other neurological symptoms except as described above. ROS: Diarrhea for one day, rash in back of head PMH: DM2, asthma, shingles and depression PSH: Pancreatectomy 2/2 cyst, cholecystectomy FH: adopted
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Allergies: Demerol (rash) MEDS: Fluoxetine 20 mg daily Gabapentin 300 mg TID Lantus 10 units BID Albuterol 2 puffs QID Social History: Lives with boyfriend in San Antonio unemployed Smoking:4 cigarettes per day EtOH:5 beers on the weekend Illicit drugs: denied
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Physical Exam: Significant for Gen: diaphoresis HEENT: Swelling in posterior aspect of neck , Scratch marks on back of head CVS: Tachycardia Lungs: CTAB Neuro exam: MS: within normal limits CNs: 2-12 grossly intact Motor: Increased tone in LUE Strength: 4/5 b/l deltoids, 5/5 in rest of the muscle groups in b/l UEs, 1/5 Strength in b/l LEs all throughout Sensory: Absent sensation from xiphoid process to toes Reflexes: BR Bic Tri Pat Ach Plantar Clonus Right 2+ 2+ 2+ 2+ 0 mute absent Left 2+ 2+ 2+ 2+ 0 mute absent Cerebellar: intact finger-to-nose and rapid alternating movements Gait: Unable to walk
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Labs: CBC: 6.6/13.9/40.6/270 BMP: 141/3.9/109/23/18/0.67/240 LFTs: wnl CRP elevated 15, ESR elevated 27 RPR, HIV, and Acute Hepatitis Panel are negative. CSF Studies: clear, colorless, TNC 240, RBC 34, seg granulocytes 0, lymphocytes 86%, monocytes 6%, Eosinophils 8% Protein high143, glucose normal 56, Lymphocyte count high 86% Aquaporin Ab Neg, ANA neg, SSA, SSB Ab neg, West nile IgG/IgM serum neg, LDH serum normal
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MRI C-Spine w/ Contrast Sagittal-T1 POST-GAD MRI C-Spine w/o Contrast Sagittal-T1 Sagittal-T2 MRI C-spine w/o contrast Axial – T2
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Based on history and imaging, D/D included: 1. Acute Inflammatory transverse myelitis 2. Acute demyelinating encephalomyelitis 3. Multiple sclerosis
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Although the occurrence of Post Herpetic TM is rare, with history of recent shingles and based on imaging, we thought our patient had Post Herpetic Transverse Myelitis . Patient was started on IV steroids and acyclovir while pending CSF studies. CSF viral studies negative for CMV, EBV, Enterovirus, HSV and VZV As CSF studies were negative for VZV, we discontinued Acyclovir but per ID recommendations, we restarted Acyclovir the next day and finished 14 days of antiviral therapy Patient’s strength in LEs improved from 1/5 to 4/5 in b/l LEs and sensation minimally improved in b/l LEs and abdomen but not returned to normal Patient was eventually sent to Rehab. 6 months later, she was back to baseline.
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Thank You