American Journal of Physical Medicine & Rehabilitation:
Department of Physical Medicine and Rehabilitation, Baylor College of Medicine, Houston, Texas (KHN, CGK); and Department of Radiology, Baylor College of Medicine and St. Luke’s Episcopal Hospital, Houston, Texas (JJN).
*All correspondence and requests for reprints should be addressed to C. George Kevorkian, MD, 6624 Fannin Suite 2330, Houston, TX 77030.
One month before admission to an acute tertiary general hospital, a 66-yr-old African American female began to notice numbness and paresthesia in her bilateral lower extremities with radiating low-back pain. A local physician diagnosed her with sciatica and arthritis and prescribed an opiod analgesic and a muscle relaxant. However, she ultimately developed difficulty with ambulation and became incontinent of bowel and bladder.
On admission, her physical exam revealed uniform 3/5 muscle strength of the left lower limb and 2/5 on the right. Sensory level was at L5 on the left and L3 on the right, with absent lower-limb reflexes. Thoracolumbar magnetic resonance imaging showed leptomeningeal enhancement along the distal thoracic and lumbar cord extending to the clonus, and a fusiform enlargement was noted on sagittal views (Fig. 1). Also noted was an enhancing 3.9 × 4.0-cm mass in the right paratracheal region just lateral to the aortic arch and posterior to the superior vena cava. Chest computed tomography performed for further evaluation found right paratracheal and prevascular lymphadenopathy.
A mediastinoscopy was performed with right paratracheal mass biopsy, and the pathologic analysis demonstrated widespread noncaseating granulomata (Fig. 2). Fungal and acid-fast bacilli cultures of the mass were negative, and the diagnosis of sarcoidosis was endorsed. Although there was not a specific pathologic diagnosis of neurosarcoidosis based on the radiologic and chest biopsy pathologic evidence, the opinion of the treating physicians was that neurosarcoidosis was the most likely cause of the patient’s symptom complex. Because the mainstay of treatment for neurosarcoidosis is corticosteroid therapy, the patient was started on high-dose oral prednisone.
The patient was transferred to the hospital rehabilitation unit, where she made excellent progress. Bilateral lower-extremity strength improved to 4/5, and she regained the ability to ambulate independently with a rolling walker. Initially, she was unable to empty her bladder, but dramatic improvement was noted with the corticosteroid treatment and commencement of bethanechol and tamsulosin. At discharge, she was continent of bowel and bladder and was free of lower-back and leg pain. Repeat thoracolumbar magnetic resonance imaging performed after 3 wks of prednisone therapy showed resolution of the enhancement attributed to neurosarcoidosis.
In approximately 5% of patients with sarcoidosis, neurologic complications are present. Because both the central and peripheral nervous systems may be affected, clinical features can run the gamut from meningeal involvement masquerading as meningitis or parenchymal association disguised as primary or metastatic tumors to a perivascular or spinal cord inflammation producing a radiculopathy or myelopathy. The neuroimaging modality of preference is contrast-enhanced magnetic resonance imaging, which allows the physician to detect inflammation by enhancement of the parenchyma, meninges, and cauda equina, or to view white-matter lesions throughout the nervous system.
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