NEURORADIOLOGY


Case 45 :

A 24 year old male presented with fever, neck rigidity, altered sensorium, paraplegia and bowel-bladder incontinence.
CSF study revealed leukocytosis, high protein and low sugar. Gram staining of CSF revealed gram positive cocci.
MRI of brain and spine was performed

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Diagnosis

Pyogenic Meningitis with corpus callosal  infarct and spinal cord infarct.

Findings

Two irregular lesions in the posterior body of corpus callosum and splenium which are hypointense on T1sag and hyperintense on FLAIR sagittal and axial images.On diffusion weighted images the lesion is bright and appears black on ADC map which suggests that its is an acute infarct.
Axial Gradient Echo image through lower thoracic spine shows patchy cord hyperintensities . DWI through the thoracic cord reveals restricted diffusion, probably representing spinal cord ischemia.

Discussion:

Sudden onset of focal neurological deficits, including monoplegia, hemiplegia, aphasia, and tetraparesis, has been reported in meningitis. Although these could be postictal phenomena, they mostly are due to vasculitic changes resulting in ischemia. While some of these could be the result of proliferative arachnoiditis or hydrocephalus, vasculitis still appears to be the leading cause.
Vasculitis with resultant thrombosis and hemorrhagic infarction may develop in vessels that traverse the basilar or spinal exudate or lie within the brain substance. Microorganisms or Mycobacteriaalso may invade the adventitia directly and initiate the process of vasculitis. An early neutrophilic reaction is followed by infiltration of lymphocytes, plasma cells, and macrophages, leading to progressive destruction of the adventitia, disruption of elastic fibers, and, finally, intimal destruction. Eventually, fibrinoid degeneration within small arteries and veins produces aneurysms, multiple thrombi, and focal hemorrhages, alone or in combination. It is this phenomenon which can give rise to infarct.
Isolated corpus callosal infarcts are rare. In the setting of meningitis any small vessel territory may be involved with ischemia.
Tuberculous spinal meningitis may manifest as an acute, subacute, or chronic form.

    • The clinical picture in primary spinal meningitis is often characterized by myelopathy, with progressive ascending paralysis, eventually resulting in basal meningitis and associated sequelae.
    • In some cases with acute onset, in addition to variable constitutional symptoms, patients develop acute paraplegia with sensory deficits and urinary retention. The clinical picture often mimics transverse myelitis or Guillain-Barré syndrome.
    • The subacute form is often dominated by myeloradiculopathy, with radicular pain and progressive paraplegia or tetraplegia.
    • A less virulent chronic form might mimic a very slowly progressive spinal cord compression or a nonspecific arachnoiditis.
    • The dorsal cord seems to be affected most commonly, followed by the lumbar and the cervical regions.

Dr Paresh Desai, Goa