CASE REPORT

ACUTE TRANSVERSE MYELITIS

Click to edit Master subtitle style

PRESENTATOR: - PRYMA SUGEARTO - ITHA PAULINA SIAHAAN

9/18/11

BACKGROUND

Acute Transverse Myelitis (ATM) is a rare disease in childhood and adolescence and the incidence has been estimated at 1.34 in 1,000,000 people in Israel but there has been no specific evaluation of pediatric incidence. It is characterized by bilateral spinal cord dysfunction presenting as 9/18/11lower extremity weakness with or

OBJECTIVE
-

To explore more about the theoritical aspects on acute transverse myelitis To integrate the theory and application of acute transverse myelitis case in daily life.

9/18/11

LITERATURE REVIEW
Click to edit Master subtitle style

9/18/11

DEFINITION

Acute transverse myelitis (ATM) refers to the inflammatory subtype of transverse myelopathy, which is an acute or subacute clinical syndrome in which injury to the spinal cord results in neurologic deficits, manifesting as weakness, sensory loss and autonomic dysfunction. This inflammation generally results in motor, sensory and autonomic dysfunction that progressively worsens 9/18/11

EPIDEMIOLOGY

The incidence of ATM is between 1.34 and 4.6 per million per year with bimodal peaks between ages 1019 and 3039 years. Estimates of the annual incidence of idiopathic or postinfectious transverse myelitis range from 1.3 to 8 cases per million. The incidence increases to 24.6 cases per million annually if acquired demyelinating causes, especially multiple sclerosis, are included.
9/18/11 There is no clear pattern among cases of

ETIOLOGY

Viral infection(2040% of these cases) although a specific virus is rarely isolated. Enterovirus is the leading causative virus, especially Coxsackie virus A7, A9, and A23 and Coxsackie virus B serotypes, which are frequently implicated in cases of meningoencephalitis. ATM occurs in systemic autoimmune
9/18/11

CRITERIA FOR IDIOPATHIC ATM Development of sensory,

motor, or autonomic dysfunction attributable to the spinal cord. Bilateral signs and/or symptoms (though not necesarily symetric. Clearly defined sensory level. Exclusion of extra axial compressive etiology by neuroimaging (MRI or myelography, CT of spine not adequate). 9/18/11

9/18/11

CSF pleocytosis or elevated IgG index or gadolinium enhancement. If none of the inflammation criteria is met at symptom onset, repeat MRI and lumbal puncture evaluation between 2 and seven days following symptom onset meet criteria.

TREATMENT

High-dose intravenous corticosteroid therapy Plasma exchange ( severe demyelination) Cyclophosphamid IVIG can be other choice Rehabilitative care
9/18/11

PROGNOSIS

One third recover with little to no sequelae One third have moderate degree of residual disability One third may have severe disabilities Rapid progression of symptoms and spinal shock predicts poor recovery. Recovery begins within 2 to 12 weeks of the onset of symptoms and may continue for up to 2 years
9/18/11

If there is no improvement within the first