Transverse myelopathy mimicking conus medullaris syndrome
Is a clinical syndrome attributable to a spinal cord disorder that interrupts ascending and descending neuroanatomic pathways within (or passing through) the transverse plane of the spinal cord.■ The first priority in the evaluation of a patient with an acute transverse myelopathy is to obtain an MRI of the entire spinal cord, with and without contrast, to search for a cord-compressive etiology that may be amenable to prompt neurosurgical decompression to prevent cord infarction.
■ Once cord-compressive etiologies are excluded, the next priority is to evaluate findings from MRIs and CSF analysis that will further categorize the myelopathy as inflammatory or noninflammatory.
■ Once criteria for spinal cord inflammation are met, the next priority is to test for etiologies known to induce CNS inflammation.
■ When initial laboratory testing does not reveal a specific diagnosis, further evaluation is based on the extent of demyelination seen on MRI and whether the pattern of myelitis is consistent with a partial versus a longitudinally extensive myelitis.
A previously healthy 53-year-old man presented to his primary care physician's office after awaking that morning with numbness below the waist. The numbness involved the perineal area, genitals, buttocks, posterior aspect of the right leg, and plantar aspect of both feet. The patient reported erectile dysfunction (ED), along with difficulties eliminating urine and stool as a result of pelvic floor and sphincter paralysis; he denied incontinence. The patient also noted a mild gait imbalance resulting from foot numbness and mild weakness of his right hip but denied any back or leg pain. He recalled several episodes of transient genital numbness a few months earlier. Prior to the current problem, he had been in his usual state of good health, except for an upper respiratory tract infection 3 weeks before this encounter.
History Past neurologic history was significant for migraine headaches with aura beginning at age 30 years. Three years ago, while on vacation in New Zealand, he developed diplopia that was attributed to a left cranial nerve palsy that gradually resolved over an 8-week period. MRI of the brain (with and without contrast) was read by a neurologist as normal, and the palsy was presumed to be microvascular in etiology. The patient also reported a history of chronic gastroesophageal reflux disease (GERD), hereditary hemochromatosis, and childhood asthma. Current therapies included esomeprazole and famotidine for the GERD and periodic maintenance phlebotomies for hemochromatosis. Family history was negative for neurologic disorders, diabetes mellitus, multisystemic autoimmune or vasculitic diseases, and coagulopathies.
Migraine Headache White Matter Ischemia - News

An MRI of the brain showed no evidence of acute or chronic ischemia; significant, active, white matter processes; or vascular abnormalities. A repeat MRI of the lumbar spine 1 week later revealed no changes from the previous scan.
Migraine Headache White Matter Ischemia - Bookshelf
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