|
 
 |
| CASE REPORT |
|
| Year : 2022 | Volume
: 23
| Issue : 2 | Page : 141-144 |
|
A chronic alcoholic with central pontine myelinolysis: Victim of double hit
Sreekarthik Pratapa1, Mamidipalli Sai Spoorthy2, Parul Gupta3
1 Resident, Department of Medicine, Jawaharlal Nehru Medical College, DMIMS, Wardha, Maharashtra, India
2 Assistant Professor, Department of Psychiatry, Jawaharlal Nehru Medical College, DMIMS, Wardha, Maharashtra, India
3 Resident, Department of Psychiatry, Jawaharlal Nehru Medical College, DMIMS, Wardha, Maharashtra, India
| Date of Submission | 12-Jul-2021 |
| Date of Acceptance | 08-Oct-2021 |
| Date of Web Publication | 23-Nov-2021 |
Correspondence Address:
Dr. Parul Gupta
Department of Psychiatry, Jawaharlal Nehru Medical College, Datta Meghe Institute of Medical Sciences, Sawangi (Meghe), Wardha, Maharashtra
India
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/amh.amh_100_21
Central pontine myelinolysis (CPM), is a potentially fatal neurological disorder identified by demyelination at the bottom of the pons. Osmotic stress, endothelial dysfunction, blood–brain barrier damage, and rapid correction of hyponatremia believed to be the main causes. Chronic alcoholism may influence the CPM. We report a case of chronic alcoholism and normonatremia, who presented with sudden onset of drowsiness and quadriparesis, after sudden abstinence from alcohol who was eventually diagnosed with CPM. Evidence of elevated serum ammonia level indicated encephalopathy. Our case emphasizes that CPM can manifest in patients with chronic alcoholism. CPM must be distinguished from the natural course of alcohol withdrawal delirium and Wernicke's encephalopathy, which necessitates clinical astuteness and a high level of suspicion on the part of the physician.
Keywords: Central pontine myelinolysis, chronic alcoholism, Wernicke's encephalopathy
How to cite this article:
Pratapa S, Spoorthy MS, Gupta P. A chronic alcoholic with central pontine myelinolysis: Victim of double hit. Arch Ment Health 2022;23:141-4 |
| Introduction | |  |
Central pontine myelinolysis (CPM) belongs to the spectrum of Osmotic Demyelination Syndrome (ODS), a potentially fatal debilitating neurological condition, which was first described in 1959 in a study on malnourished and alcoholic patients.[1]
Osmotic stress, endothelial dysfunction, and damage of the blood-brain barrier are the main pathogenic features in the development of demyelination in CPM and may be influenced at multiple levels by alcohol-related pathogenic mechanisms. The pathology consists of demyelination without inflammation in the base of the pons, with relative sparing of axons and nerve cells. This condition often presents in a devastated fashion usually with quadriparesis and pseudobulbar palsy, although less severe presentations may occur. Progressive lethargy, quadriparesis, dysarthria, ophthalmoplegia, and ataxia are frequent manifestations of this condition.[2]
Comorbidities associated with CPM include dialysis, liver failure, and transplantation, severe bacterial infections, acute hemorrhagic pancreatitis, chronic alcoholism, and pellagra.[3],[4]
| Case Report | | |
A 52-year-old male, who has a history of chronic alcohol intake for 20 years, presented to us with sudden onset of drowsiness and quadriparesis, 15 days after sudden abstinence from alcohol.
There were no similar episodes in the past as narrated by his son. There was no history of seizures, vertigo, fall, or head trauma. There was no history of diabetes mellitus or hypertension. He was not on any medication previously.
On examination
His built was ectomorphic. He was drowsy with eye-opening on verbal stimuli and again falling asleep (GCS: E3V1M1). His Pulse rate was 128/min, regular and synchronous. Blood pressure measured in the right arm in the supine position was found to be 130/80 mmHg, Jugular venous pulse was normal, Respiratory rate was 12 breaths/min and SpO2 of 96% while breathing the ambient air.
Central nervous system examination revealed
Pupils-bilateral 1 mm reacting to light, there was no gaze deviation, eye movements and blinking was preserved. Motor system examination revealed quadriparesis; reflexes were normal, planters were mute bilaterally. Because of increased oral secretions and altered consciousness, an airway was secured with endotracheal intubation and the patient was ventilated through t-piece, Arterial blood gas revealed mild respiratory acidosis, and other blood investigations were in a normal range indicating no sepsis, no electrolyte abnormalities, and normal renal function test. Liver function test revealed: serum bilirubin - total bilirubin: 2.8 mg/dl, direct bilirubin: 1.9 mg/dl, indirect bilirubin: 0.9 mg/dl. Aspartate transaminase: 398 IU, alanine transaminase: 86 IU, and serum ammonia was about 210 μmol/L.
Magnetic resonance imaging brain revealed
Increased T2 and flair signals in the central basis pontis consistent with CPM [Figure 1] and [Figure 2].
The patient was treated with intravenous (IV) thiamine 100 mg/day, IV dextrose and tablet rifaximin 550 mg OD through Ryles tube for 6 days and syrup lactulose 30 ml TDS and other supportive treatment. Clinical Institute Withdrawal Assessment for Alcohol-Revised version was applied and a score of 8 (mild) was noted. Detoxification with benzodiazepines was not required. The patient's condition improved over the next week and was discharged.
| Discussion | | |
CPM (ODS) in most cases are associated with rapid correction of hyponatremia and hyperosmolar states and clinical symptoms are observed in few days after rapid sodium correction. Yet, it is also seen in normonatremic individuals with a history of chronic alcohol abuse, like in our patient whose reports showed normal sodium levels with no history of correction. A study by Ayus et al., identified rapid correction of sodium into the hypernatremic range, especially in the setting of hepatic encephalopathy to be contributing factor in the demyelinating process.[5]
In our patient, there was evidence of elevated serum ammonia levels indicating the patient was in encephalopathy concomitant with CPM leading to the symptoms with which the patient had presented. The neuropsychiatric symptoms of CPM can be similar to those seen in alcohol withdrawal, further recognizing the subtle neurological changes of development of CPM in a patient experiencing alcohol withdrawal can be more difficult due to the confounding effects of sedative use.
Acute withdrawal causes delirium tremens which usually lasts for 1–5 days, a duration beyond the expected duration should raise a concern about further workup in view of CPM, as seen in this patient. CPM also had to be distinguished from Wernicke's encephalopathy, a similar condition that usually occurs in patients with a similar history. Patients of Wernicke's encephalopathy present with nystagmus and/or ophthalmoplegia, altered mental status and ataxic gait, magnetic resonance imaging (MRI) brain shows hypersignal intensity at bilateral medial thalamus on diffusion-weighted imaging and enlargement of mammillary bodies on T1 imaging of MRI.[6],[7]
Our patient had no such symptoms on presentations and MRI brain suggested signs of CPM against those of Wernicke's encephalopathy. Hence, Wernicke's encephalopathy was ruled out of diagnosis, thus narrowing down to the diagnosis of hepatic encephalopathy-induced myelinolysis leading to CPM.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given his consent for his images and other clinical information to be reported in the journal. The patient understands that name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | Adams RD, Victor M, Mancall EL. Central pontine myelinolysis: A hitherto undescribed disease occurring in alcoholic and malnourished patients. AMA Arch Neurol Psychiatry 1959;81:154-72.  |
| 2. | Karp BI, Laureno R. Pontine and extrapontine myelinolysis: A neurologic disorder following rapid correction of hyponatremia. Medicine (Baltimore) 1993;72:359-73. |
| 3. | Laureno R, Karp BI. Myelinolysis after correction of hyponatremia. Ann Intern Med 1997;126:57-62. |
| 4. | Ashrafian H, Davey P. A review of the causes of central pontine myelinosis: Yet another apoptotic illness? Eur J Neurol 2001;8:103-9. |
| 5. | Ayus JC, Krothapalli RK, Arieff AI. Treatment of symptomatic hyponatremia and its relation to brain damage. A prospective study. N Engl J Med 1987;317:1190-5. |
| 6. | Lukose A, Tyer NM. A Woman with Alcohol Use Disorder, Wernicke-Korsakoff Syndrome, and Central Pontine Myelinolysis: A Case Report and Review of the Literature. J Addict Behav Ther Rehabil 8:1. of. 2019;3:2. |
| 7. | Sutamnartpong P, Muengtaweepongsa S, Kulkantrakorn K. Wernicke's encephalopathy and central pontine myelinolysis in hyperemesis gravidarum. J Neurosci Rural Pract 2013;4:39-41. [ PUBMED] [Full text] |
[Figure 1], [Figure 2]
|
Search Pubmed for