scholarly journals Clinical Evolution of Central Pontine Myelinolysis in a Patient with Alcohol Withdrawal: A Blurred Clinical Horizon

2016 ◽  
Vol 2016 ◽  
pp. 1-5 ◽  
Author(s):  
Abdul S. Mohammed ◽  
Prajwal Boddu ◽  
Dina F. Yazdani

Central pontine myelinolysis (CPM), a potentially fatal and debilitating neurological condition, was first described in 1959 in a study on alcoholic and malnourished patients. It is a condition most frequently related to rapid correction of hyponatremia. Chronic alcoholism associated CPM tends to be benign with a favorable prognosis compared to CPM secondary to rapid correction of hyponatremia. We describe a normonatremic, alcoholic patient who presented with CPM after a rapid rise in his sodium levels. Our case illustrates the fact that CPM can manifest even in patients who are normonatremic at baseline. Rapid rises in sodium levels should be promptly reversed before clinical symptoms manifest in patient with risk factors for CPM irrespective of their baseline sodium levels. Furthermore, clinical evolution of CPM can be difficult to discern from the natural course of alcohol withdrawal delirium, requiring astuteness and maintenance of a high degree of clinical suspicion on the part of the physician.

Author(s):  
Anoop AS ◽  
Lakshmiprasad L. Jadhav ◽  
Sruthy Nair ◽  
Rohan Mohandas

A 56 year old male patient was admitted to S.D.M Ayurveda Hospital, Hassan, Karnataka with the confirmed diagnosis of Central Pontine Myelinolysis (CPM) on 11/12/17. The chief complaints were weakness of both hands and legs, stiffness in both hands and legs, pain in both shoulder joints, slurred speech, difficulty in walking with gait changes. H/O chronic alcoholism. MRI brain showed pontine and basal ganglia diffusion restriction - Acute Pontine Myelinolysis. The serum electrolyte showed serum sodium level as 128 mmol/litre. This disease can be understood as Samana Avruta Vyana in hyponatremic encephalopathy stage and the stage of myelinolysis can be understood as Sarvanga Vata with Kapha Avruta Udana and Vyana. After clinical evaluation, Avarana Chikitsa was started followed by Kevala Vatika Chikitsa and significant improvement was seen. Significant result was observed in subjective and objective parameters after the treatment. The patient was discharged with oral medications for 1 month.


2021 ◽  
Vol 49 ◽  
Author(s):  
Álan Gomes Pöppl ◽  
Érico Haas Pires ◽  
Claudia Ruga Barbieri ◽  
Lucas Marques Colomé

Background: Primary hypoadrenocorticism is a rare condition resulting from immune-mediated destruction of the adrenal cortices. It can also occur due to necrosis, neoplasms, infarctions and granulomas. The clinical and laboratory changes are due to deficient secretion of glucocorticoids and mineralocorticoids, which leads to electrolyte disorders associated with hyponatremia and hyperkalemia. These disorders can cause hypotension, hypovolemia and shock, putting a patient's life at risk if inadequate hydroelectrolytic supplementation and hormone replacement is provided. Nevertheless, rapid sodium chloride supplementation is contraindicated due to the risk of central pontine myelinolysis induction. The present study aims to describe a thalamic osmotic demyelination syndrome after management of a primary hypoadrenocorticism crisis in a 2-year-old, female West White Highland Terrier. Case: The patient had a presumptive diagnosis of hypoadrenocorticism already receiving oral prednisolone and gastrointestinal protectants in the last 2 days. After prednisolone dose reduction the dog presented a severe primary hypoadrenocorticism crisis treated with intravenous sodium chloride 0.9% solution along with supportive therapy. Four days after being discharged from the hospital, the patient showed severe neurological impairment and went back to the clinic where a neurological examination revealed mental depression, drowsiness, ambulatory tetraparesis and proprioceptive deficit of the 4 limbs, postural deficits, and cranial nerves with decreased response. Due to these clinical signs, a magnetic resonance imaging was performed. It showed 2 intra-axial circular lesions, symmetrically distributed in both thalamus sides, with approximately 0.8 cm in diameter each without any other anatomical changes on magnetic resonance imaging. The images were compatible with metabolic lesions, suggesting demyelination. Furthermore, liquor analysis did not show relevant abnormalities, except for a slight increase in density and pH at the upper limit of the reference range. After treatment, the patient had a good neurological evolution secondary to standard primary hypoadrenocorticism treatment, without sequelae. Discussion: In the present case report, primary hypoadrenocorticism gastrointestinal signs seemed to be triggered by a food indiscretion episode, not responsive to the symptomatic therapies employed. The patient´s breed and age (young West White Highland Terrier bitch) is in accordance with the demographic profile of patients affected by the disease, where young females are frequently more affected. Regarding the probable thalamic osmotic demyelination syndrome documented in this case, is important to notice that myelinolysis or demyelination is an exceedingly rare noninflammatory neurological disorder, initially called central pontine myelinolysis, which can occur after rapid correction of hyponatremia. It has already been observed in dogs after correction of hyponatremia of different origins, including hypoadrenocorticism and parasitic gastrointestinal disorders. Currently, the terms "osmotic myelinolysis" or “osmotic demyelination syndrome" are considered more suitable when compared to the term "central pontine myelinolysis" since it has been demonstrated in dogs and humans the occurrence of demyelination secondary to the rapid correction of hyponatremia in distinct regions of the central nervous system including pons, basal nuclei, striatum, thalamus, cortex, hippocampus and cerebellum. The present case report emphasizes the difficulties for hormonal confirmation of primary hypoadrenocorticism in a patient already on corticosteroid treatment, as well as proposes that the current term osmotic demyelination syndrome replace the term “central pontine myelinolysis” in veterinary literature related to the management of hypoadrenocorticism crisis.Keywords: Addison Syndrome, hyponatremia, osmotic myelinolysis, magnetic resonance imaging.


2012 ◽  
Vol 2012 ◽  
pp. 1-2 ◽  
Author(s):  
Hideomi Yamada ◽  
Koji Takano ◽  
Nobuhiro Ayuzawa ◽  
George Seki ◽  
Toshiro Fujita

We report a case in whom slow correction of hyponatremia (5 mmol/day for 3 days) induced central pontine myelinolysis (CPM). After the diagnosis was confirmed by imaging, we started to relower serum Na that completely recovered the sign and symptoms of CPM. Rapid correction of serum sodium is known to be associated with CPM. However, it may occur even after slow correction of hyponatremia. Currently, there is no standard therapy for CPM other than supportive therapy. Other therapy includes sterioid, plasmaphresis and IVIG, but these therapies have not been shown to be particularly effective. The pathophysiology of CPM is related to a relative dehydration of the brain during the correction of hyponatremia, resulting in cell death and demyelination, therefore gentle rehydration with lowering serum sodium may not be an unreasonable therapy. The present case provides supportive evidence that reinduction of hyponatremia is effective in treating CPM if started immediately after the diagnosis is suggested. The present case tells us that severe chronic hyponatremia must be managed with extreme care especially in patients with chronic debilitating illness and that relowering serum Na is a treatment of choice when CPM is suggested.


2016 ◽  
Vol 22 (2) ◽  
pp. 218-221 ◽  
Author(s):  
Dae-seop Shin ◽  
Dushin Jeong ◽  
Kwang Ik Yang ◽  
Hyung Kook Park ◽  
Hyung Geun Oh

2017 ◽  
Vol 41 (1) ◽  
pp. 148 ◽  
Author(s):  
Jae Ho Kim ◽  
Sae Hyun Kim ◽  
Ho Joong Jeong ◽  
Young Joo Sim ◽  
Dong Kyu Kim ◽  
...  

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