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CASE REPORT
Year : 2015  |  Volume : 24  |  Issue : 2  |  Page : 198-201  Table of Contents     

Central pontine myelinolysis in a case of alcohol dependence syndrome


1 Department of Psychiatry, Armed Forces Medical College, Pune, Maharashtra, India
2 Department of Psychiatry, Lokmanya Tilak Memorial Medical College (Sion Hospital), Mumbai, Maharashtra, India
3 Department of Psychiatry, Base Hospital, New Delhi, India
4 Department of Psychiatry, INHS Asvini, Mumbai, Maharashtra, India

Date of Web Publication4-May-2016

Correspondence Address:
Kaushik Chatterjee
Department of Psychiatry, Armed Forces Medical College, Sholapur Road, Pune - 411 040, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0972-6748.181732

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   Abstract 

Osmotic Demyelination Syndrome includes Central Pontine Myelinolysis and Extrapontine Myelinolysis. This condition has been described in cases of chronic Alcohol Dependence Syndrome and in rapid correction of hyponatremia. Though we frequently see patients with Alcohol Dependence Syndrome presenting with complicated withdrawal, Central Pontine Myelinolysis remains largely undetected and under-reported in literature. We present here a case of protracted Delirium Tremens where MRI brain revealed Central Pontine Myelinolysis. Subsequently cognitive assessment revealed significant dysfunction and brain SPECT showed hypo-perfusion of the frontal lobes. Osmotic Demyelination Syndrome should be suspected in protracted Delirium Tremens.

Keywords: Alcohol dependence syndrome, central pontine myelinolysis, delirium tremens


How to cite this article:
Chatterjee K, Fernandes AB, Goyal S, Shanker S. Central pontine myelinolysis in a case of alcohol dependence syndrome. Ind Psychiatry J 2015;24:198-201

How to cite this URL:
Chatterjee K, Fernandes AB, Goyal S, Shanker S. Central pontine myelinolysis in a case of alcohol dependence syndrome. Ind Psychiatry J [serial online] 2015 [cited 2020 Jul 12];24:198-201. Available from: http://www.industrialpsychiatry.org/text.asp?2015/24/2/198/181732

Central pontine myelinolysis (CPM) was described in 1959 by Adams et al. as a condition seen in alcoholics and malnourished individuals which is a result of an osmotic insult and demyelination of the basis pontis.[1] This concept was extended in 1962 with the recognition that lesions can occur outside the pons, so-called extrapontine myelinolysis (EPM).[2] Chronic alcohol abuse appears to be a particular risk factor for CPM and EPM. It has been reported that chronic alcoholics may be asymptomatic or have relatively few symptoms, with a better outcome of their CPM and EPM than in cases associated with an acute correction of hyponatremia.[3]

Patients with chronic alcohol dependence are commonly given intravenous fluids as part of the treatment of alcohol withdrawal. They are predisposed to chronic severe hyponatremia because of a variety of mechanisms including psuedohyponatremia, hypovolemia, cerebral salt wasting syndrome, and reset osmostat syndrome.[4]

Functional neuroimaging studies in recently detoxified alcoholics using positron emission tomography or single photon emission computed tomography (SPECT) revealed global reduced cerebral perfusion in frontal regions.[5] Frontal lobe dysfunctions are consistently described in chronic alcoholics.[6]


   Case Report Top


A 52-year-old male was admitted to medical ward for the management of a severe headache and raised blood pressure. Subsequently, he suffered a seizure and developed an irrelevant speech for which a psychiatric consultation was sought.

History revealed alcohol consumption from the age of 22 years. By the age of 45 years, he had features of alcohol dependence in the form of craving, tolerance, loss of control, withdrawal discomfort, the primacy of alcohol use, and sociooccupational deterioration. He consumed around 750 ml of rum daily. Before 2 days admission, he abruptly stopped drinking after repeated pleading by family members. He had been detected to have hypertension in 2007 and diabetes mellitus (Type II) along with dyslipidemia in 2008. There was no family history of mental illness or substance use. He is educated up to 9th class and has been employed for last 26 years. He chewed tobacco regularly for last 30 years.

He had tachycardia, raised blood pressure, bilateral coarse digital tremors, and diaphoresis. He was disoriented and had vivid visual and auditory hallucinations along with secondary delusions of persecution. There was no focal neurological deficit or neck rigidity. A urine drug screen was negative. Laboratory investigation findings are summarized in [Table 1]. A diagnosis of alcohol dependence syndrome (complicated withdrawal with seizures and delirium) was made, and the patient was treated with chlordiazepoxide in tapering doses, thiamine supplementation and parenteral haloperidol for behavioral control. His response to treatment was tardy and though his orientation improved he had difficulty in comprehending instructions even a week later. Mini- mental state examination (MMSE) score improved from 12 at admission to 26. However, he remained dull and was unable to participate in routine neurocognitive evaluation even a fortnight after admission. Progression of withdrawal and MMSE are described in [Table 2].
Table 1: Laboratory investigations

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Table 2: Alcohol Withdrawal Scale and mini-mental state examination scores

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Contrast enhanced magnetic resonance imaging (MRI) brain done then, revealed a nonenhancing area of altered signal intensity in central pons suggestive of CPM [Figure 1]. Brain SPECT showed hypoperfusion of frontal lobes (L > R) but yielded no further information about the pons [Figure 2]. Electroencephalogram showed no abnormality. By the 3rd week, cognitive functions started improving, and he was co-operative. Evaluation of lifetime drinking history [7] yielded total alcohol consumption of 496.61 kg over 30 years, with an average drinking day consumption of 80.35 g/day. Repeated after 6 weeks, MRI showed a reduction in size of pontine lesion. Repeated after 8 weeks brain, SPECT showed improvement in frontal lobe perfusion [Figure 3]. Detailed neuropsychological evaluation done at 2, 6, and 10 weeks of admission is depicted in [Table 3]. Even though there was relative improvement in scores on neuropsychological evaluation in the 6th and 10th week, cognitive deficits remained.
Figure 1: Contrast enhanced magnetic resonance imaging of brain ill-defined area of altered signal intensity in central pons (7.0 mm × 6.7 mm × 8.1 mm). (a) Sagittal section postcontrast brain shows no postcontrast enhancement. (b) On fluid-attenuated inversion recovery it is hypo-intense. (c) On magnetic resonance imaging diffusion there is true restriction of diffusion on diffusion weighted imaging and apparent diffusion coefficient map

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Figure 2: Initial brain single photon emission computed tomography hypoperfusion in frontal lobes (left hypoperfusion [15.96%] >right hypoperfusion [20.87%])

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Figure 3: Repeat brain single photon emission computed tomography (8 weeks later). Mild hypo-perfusion in frontal lobes. Perfusion in frontal lobes (left [17.91%], right [22.24%]) is better than in previous scan

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Table 3: Neuropsychological evaluation

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   Discussion Top


Various mechanisms have been proposed for the development of osmotic demyelination following chronic alcohol use. Rapid correction of hyponatremia remains the most documented etiologic factor. Oligodendroglia are particularly susceptible to dehydration and volume changes due to their physically tight alignment in the basis pontis. During rapid correction of hyponatremia, intracellular electrolyte corrections are swift, but the brain is unable to correct the loss of organic osmolytes quickly enough, resulting in cellular dehydration, damage to the myelin sheath, and oligodendrocyte degeneration. The process of maintaining an iso-osmolar environment with respect to the serum is energy consuming. If the patient is malnourished, as is typically the case in alcohol dependence, the cells may lack sufficient energy reserve to maintain the Na +/K + ATPase pump activity and to synthesize organic osmoles. Alcohol-associated thiamine deficiency may exacerbate the problem because it decreases brain glucose uptake. This energy supply–demand imbalance results in a pro-apoptotic drive.[8]

In this patient, no hyponatremia was detected, though he had been initially treated with intravenous Ringer's lactate in the medical ward for dehydration. After a protracted alcohol withdrawal, he manifested significant impairment in all cognitive domains which improved partially and gradually thereafter. This correlates with the findings of Mochizuki et al., that CPM due to alcohol use leaves neurological deficits.[5] Nicolás et al. found that two-thirds of patients of active chronic alcoholism exhibited frontal lobe impairment demonstrated by neuropsychological testing and SPECT, independent of brain atrophy.[9] Noël et al. reported that decreased blood flow in the inferior frontal gyrus assessed by SPECT was associated with executive function deficits which were related to relapse in detoxified alcohol-dependent individuals.[5]

Protracted delirium tremens is encountered frequently in patients of alcohol dependence syndrome. They should be investigated using neuroimaging and caution should be exercised while correcting their fluid and electrolyte imbalances.

Acknowledgments

  • Surg Capt R. Pant, HoD – Department of Radiology, INHS Asvini
  • Col. M. Jacob, HoD – Department of Nuclear Medicine, INHS Asvini.


Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
   References Top

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.  Back to cited text no. 1
    
2.
Martin RJ. Central pontine and extrapontine myelinolysis: The osmotic demyelination syndromes. J Neurol Neurosurg Psychiatry 2004;75 Suppl 3:iii22-8.  Back to cited text no. 2
    
3.
Mochizuki H, Masaki T, Miyakawa T, Nakane J, Yokoyama A, Nakamura Y, et al. Benign type of central pontine myelinolysis in alcoholism – Clinical, neuroradiological and electrophysiological findings. J Neurol 2003;250:1077-83.  Back to cited text no. 3
    
4.
Liamis GL, Milionis HJ, Rizos EC, Siamopoulos KC, Elisaf MS. Mechanisms of hyponatraemia in alcohol patients. Alcohol Alcohol 2000;35:612-6.  Back to cited text no. 4
    
5.
Noël X, Sferrazza R, Van Der Linden M, Paternot J, Verhas M, Hanak C, et al. Contribution of frontal cerebral blood flow measured by (99m) Tc-Bicisate spect and executive function deficits to predicting treatment outcome in alcohol-dependent patients. Alcohol Alcohol 2002;37:347-54.  Back to cited text no. 5
    
6.
Ihara H, Berrios GE, London M. Group and case study of the dysexecutive syndrome in alcoholism without amnesia. J Neurol Neurosurg Psychiatry 2000;68:731-7.  Back to cited text no. 6
    
7.
Skinner HA, Sheu WJ. Reliability of alcohol use indices. The lifetime drinking history and the MAST. J Stud Alcohol 1982;43:1157-70.  Back to cited text no. 7
    
8.
Bakst R, Kasper M, Greene R. Central pontine myelinolysis in a patient admitted for alcohol withdrawal. Hosp Physician 2008;44:23-8.  Back to cited text no. 8
    
9.
Nicolás JM, Catafau AM, Estruch R, Lomeña FJ, Salamero M, Herranz R, et al. Regional cerebral blood flow-SPECT in chronic alcoholism: Relation to neuropsychological testing. J Nucl Med 1993;34:1452-9.  Back to cited text no. 9
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]
 
 
    Tables

  [Table 1], [Table 2], [Table 3]



 

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