Abstract:Osmotic demyelination syndrome is a rare entity characterized by noninflammatory demyelination afflicting the central pons, basal ganglia, thalami, peripheral cortex, and hippocampi. Histopathologically, there is a destruction of myelin sheaths sparing the underlying neuronal axons due to the susceptibility of oligodendrocytes to rapid osmotic shifts often encountered in chronically debilitated patients. We present the temporal progression of signal abnormalities on sequential magnetic resonance imaging (MRI) … Show more
The basal ganglia and thalami are paired deep grey matter structures with extensive metabolic activity that renders them susceptible to injury by various diseases. Most pathological processes lead to bilateral lesions, which may be symmetric or asymmetric, frequently showing characteristic patterns on imaging studies. In this comprehensive pictorial review, the most common and/or typical genetic, acquired metabolic/toxic, infectious, inflammatory, vascular and neoplastic pathologies affecting the central grey matter are subdivided according to the preferential location of the lesions: in the basal ganglia, in the thalami or both. The characteristic imaging findings are described with emphasis on the differential diagnosis and clinical context.
The basal ganglia and thalami are paired deep grey matter structures with extensive metabolic activity that renders them susceptible to injury by various diseases. Most pathological processes lead to bilateral lesions, which may be symmetric or asymmetric, frequently showing characteristic patterns on imaging studies. In this comprehensive pictorial review, the most common and/or typical genetic, acquired metabolic/toxic, infectious, inflammatory, vascular and neoplastic pathologies affecting the central grey matter are subdivided according to the preferential location of the lesions: in the basal ganglia, in the thalami or both. The characteristic imaging findings are described with emphasis on the differential diagnosis and clinical context.
“…12 Furthermore, the percentage of patients involved with ODS has increased recently due to a more frequent magnetic resonance imaging (MRI) utilization in clinical settings. 10,[13][14][15][16][17][18][19][20][21][22][23] Chronic hyponatremia with subsequent ODS can occur in diverse conditions as soon as homeostatic level of [Na+] is perturbed [24][25][26][27][28] and can be more frequent in aging population. 29 In the old and current literature, number of reports of regional CPM and EPM ODS defects showed as consequences of abrupt adjustment of a temporary or chronic deficiency of the homeostatic sodium gradient.…”
“…CPM involves the basis pontis symmetrically, the pontocerebellar fibers, and usually spares the ventrolateral pons. EPM commonly involves the basal ganglia, thalami, and cerebral white matter [5]. We are presenting the case of an alcoholic patient who developed ODS despite the normal rate of the correction of hyponatremia.…”
Acute demyelination of the pons or extrapontine areas results in an osmotic demyelination syndrome (ODS), previously referred to as central pontine myelinolysis (CPM) or extra pontine myelinolysis (EPM). It is caused by osmotic dysregulation in the brain. Multiple risk factors have been known to contribute to these osmotic disturbances. Among them, osmotic stress caused by rapid correction of hyponatremia is the most common cause. Other risk factors include liver failure, alcohol dependence, malnutrition, and malignancy. Symptoms can vary depending on the location of the demyelination. It has a high rate of morbidity and mortality. We present a case of ODS in a malnourished patient who was found to have alcoholic hepatitis and invasive colon cancer. The initial presentation was sepsis secondary to pneumonia. The patient was found to be severely hyponatremic at the time of admission, and the hyponatremia was corrected as per the recommendations. The initial non-contrast head computed tomography (CT) scan was unremarkable. However, the hospital course was complicated by a deteriorating neurological exam with encephalopathy despite not overcorrecting the sodium. A short-term follow-up brain magnetic resonance imaging (MRI) eventually revealed ODS. Initially, the findings of ODS were masked due to symptoms of alcohol withdrawal. However, the patient had a quick recovery with the improvement of all the neurological findings.
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