Systemic non-Hodgkin's Lymphoma Manifesting as Neurogenic Respiratory Failure

Abstract

enth day after admission. At the time of discharge, she continued to complain of extremity pain. Neurologic examination at 3week follow-up was normal although she continued to complain of extremity pain. EMG did not show any significant abnormality except for slightly prolonged distal sensory latencies in the left median nerve. Repeat brain MRI at 6 weeks showed nearly complete resolution of the supratentorial white matter and cerebellar abnormalities (figure, C). At a recent follow-up, the patient's symptoms of painful hands and feet persisted with some response to nocturnal amitriptyline, and examination remained normal. Repeat EMG was normal.Discussion. Animal studies in dogs have shown Purkinje cell damage after prolonged administration of high doses of metron i d a~o l e .~ Labeled metronidazole has been localized in the rat brain, spinal cord, and dorsal root ganglia, and there is radioisotope activity in RNA of the nervous t i~s u e .~ Metronidazole or its metabolites may bind to neuronal RNA and inhibits protein synthesis, resulting in axonal degeneration. Histologic section of rat brain after treatment with 800 m g k g of metronidazole has shown symmetric lesions in the ventricular and cochlear nuclei as well as in the cerebellar roof nuclei, colliculus, and superior olive.6 These lesions were histologically similar to those in Wernicke's encephalopathy in humans. Metronidazole crosses the blood-brain barrier in humans. ' Our patient had symptoms attributable to metronidazole toxicity, including dizziness, ataxia, confusion, nausea, vomiting, joint pain resembling serum sickness, and peripheral neuropathy. All of the symptoms cleared on discontinuation of the medication except for dysesthesia in the extremities. Since these dysesthesias may be due to degeneration of sensory fibers, they may persist for several months until regeneration of these fibers can occur.The MRI lesions involving supratentorial white matter and the deep cerebellar nuclei account for the patient's encephalopathy and cerebellar dysfunction, including vertigo. As the MRI findings were reversible, they were not due to a demyelinating process. A more likely explanation is that the acute toxic insult produces axonal swelling with increased water content, resulting in T, prolongation. Wilson et a17 reported a case of reversible MRI changes due to cyclosporin A toxicity where pathologic examination showed swollen myelin sheaths with only a few minute demyelinating lesions. An alternative explanation for the MRI signal changes is vascular spasm that might produce mild reversible localized ischemia.The differential diagnosis of multifocal, fairly symmetric lesions involving both white and gray matter without significant mass effect in MRI must include demyelinating diseases as well as metabolic infectious and inflammatory processes in addition to drug toxicity. Multiple sclerosis and acute disseminated encephalomyelitis could account for the MRI findings, but involvement of gray matter, normal CSF, and temporal profile make these possibil...

Nucleus of the Tractus Solitarius Metastasis: Relationship to Respiratory Arrest?

“…2,6,[17][18][19][21][22][23] Dorsolateral, dorsomedial and ventrolateral medullary regions are often destroyed in cases that provide detailed findings. 2,5,6,18,19,21,22 Respiratory failure has only been reported in tumors metastatic to the medulla on a few occasions. 1,2,6 A question arises concerning the role of a small, unilateral medullary lesion in causing respiratory arrest.…”

“…This includes a thin zone of immediately surrounding pallor that indicates edema which would be expected to be disruptive to passing axons of the reticular formation. Since the NTS is a major integration centre with known involvement in cases of respiratory difficulty, [3][4][5][6][7][8][9][10][11][12][13][14][15][16] and since effects of the rim of apparent edema around the metastatic deposit would have only enhanced the dysfunction of adjacent central autonomic centres, the unilateral NTS-centred lesion is probably ultimately responsible for respiratory dysregulation leading to respiratory arrest.…”