Symptoms - of the Disease

Fact Explanation
Introduction Central pontine myelinolysis is a non-inflammatory, usually symmetrical demyelination of the central basis pontis. The exact mechanism is yet to be found. Any way it occurs when the prolonged and severe hyponatraemia is corrected rapidly. In around 10% of patients with central pontine demyelination there would be other regions of the brain as well, especially mid brain, thalamus, basal nuclei, and cerebellum. Several theories are proposed. Most theories suggest the pathology due to the effect of osmosis. The cellular edema may occur due to the fluctuating osmotic forces which leads compression on fibres tracts and resulting demyelination. The oedema occurs when the prolonged or severer hyponatraemia is corrected rapidly with sodium.During the time of hyponatraemia in patient the intracellular charged protein moieties are altered, but the rapid correction with sodium will not correct in a parallel manner. Therefore those intracellular electrolyte imbalance also contributes to the myelinolysis. The localization of the pathology to the pons and other extra-pontine areas will be due to the nature of compact gray and white matter.There are several risk factors and conditions making it is more susceptible which are discussed latter. Patients following liver transplant is vulnerable. The condition is usually irreversible and can be fatal. Improvement may take weeks and months. Patients who recovered also will have persistent disability. The disease doesn't have a gender preference. [1][2]
History of hyponatraemia The patient or family members may know about the history of hyponatraemia or will give a history of vomiting, loose stool, consumption of drugs or infection causing hyponatraemia. Patient has usually recovered from the delirium and confusion with IV fluids and sodium replacement. So for around 48 hours following the recovery the patient may assymptomatic functioning well. Patient may start to deteriorate following that period of well being. Those symptoms are as follows. [1][2][3]
Confusion Due to the evolving pathology as mentioned above patient may be confused. It could be due to the cerebral edema. Delirium and coma also can be present due to lesions in potine tegmentum or thalamus. [2][4]
Diplopia on lateral vision or inability to look lateral. Due to the involvement of pons there would be a lateral gaze palsy. Lesions in mid brain may cause verticle gaze palsy. [5]
Inability to move limbs The patient will have features of spastic quadriplegia which are further discussed later. [6]
Head and neck weakness Due to the pseudobulbar palsy the head and neck weakness is present. [6]
Dysphagia or dysarthria Again due to the pseudobulbar palsy the dysphagia or dysarthria can be present. [6]
References
  1. GRAFF-RADFORD J, FUGATE JE, KAUFMANN TJ, MANDREKAR JN, RABINSTEIN AA. Clinical and Radiologic Correlations of Central Pontine Myelinolysis Syndrome Mayo Clin Proc [online] 2011 Nov, 86(11):1063-1067 [viewed 02 January 2015] Available from: doi:10.4065/mcp.2011.0239
  2. MARTIN R. CENTRAL PONTINE AND EXTRAPONTINE MYELINOLYSIS: THE OSMOTIC DEMYELINATION SYNDROMES J Neurol Neurosurg Psychiatry [online] 2004 Sep, 75(Suppl 3):iii22-iii28 [viewed 02 January 2015] Available from: doi:10.1136/jnnp.2004.045906
  3. AL-SALMAN J, KEMP D, RANDALL D. Hyponatremia West J Med [online] 2002 May, 176(3):173-176 [viewed 02 January 2015] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1071707
  4. LOVE S. Demyelinating diseases J Clin Pathol [online] 2006 Nov, 59(11):1151-1159 [viewed 02 January 2015] Available from: doi:10.1136/jcp.2005.031195
  5. LAI CC, TAN CK, LIN SH, CHEN HW. Central pontine myelinolysis CMAJ [online] 2011 Jun 14, 183(9):E605 [viewed 02 January 2015] Available from: doi:10.1503/cmaj.090186
  6. MARTIN PJ, YOUNG CA. Central pontine myelinolysis: clinical and MRI correlates. Postgrad Med J [online] 1995 Jul, 71(837):430-432 [viewed 02 January 2015] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2397973

Symptoms - of Complications

Fact Explanation
Locked-in-syndrome The spastic quadriplegia, pseudobulbar palsy causing head and neck muscle weakness with dysphagia and dysarthria or even mutism may cause locked-in-syndrome in where the patient is unresponsive and immobile. But in locked in syndrome usually the blinking, vertical eye movements, breathing and alertness is intact. [1][2]
Comatose states Due to the involvement of pontine tegmentum, reticular activating system or thalumus the patient may be in coma, the patient is unconsciousness and unable to be awakened. [3][4]
Features of aspiration pneumonia Due to the immobility, swallowing difficulty, impaired reflexes there is a high chance of having orthostatic and aspiration pneumonia. Those could be fever, breathing difficulty, phlegm production. [5]
Features of deep vein thrombosis and pulmonary embolism Due to the immobility patients are in risk to have deep vein thrombosis and pulmonary embolism. Features are calf pain, fever, leg swelling, shortness of breath and chest pain. [6]
Bed sores Patients are bed bound and more prone to get pressure ulcers. [7]
Contractures Due to the long term disuse of muscles there may be contactures. [8]
Disability following recovery Even though some patients may recover over weeks and months they might develop disability in later. These could be behavioral or intellectual impairment or movement disorders like parkinsonism especially if extra pontine.[9][10]
References
  1. HECKMANN JG, DINKEL HP. Recovery of locked-in syndrome in central pontine myelinolysis Am J Case Rep [online] :219-220 [viewed 02 January 2015] Available from: doi:10.12659/AJCR.889378
  2. SOHN MK, NAM JH. Locked-in Syndrome due to Central Pontine Myelinolysis: Case Report Ann Rehabil Med [online] 2014 Oct, 38(5):702-706 [viewed 02 January 2015] Available from: doi:10.5535/arm.2014.38.5.702
  3. CAMPBELL MC. Hyponatremia and Central Pontine Myelinolysis as a Result of Beer Potomania: A Case Report Prim Care Companion J Clin Psychiatry [online] 2010, 12(4):PCC.09100936 [viewed 02 January 2015] Available from: doi:10.4088/PCC.09l00936ecr
  4. GRAFF-RADFORD J, FUGATE JE, KAUFMANN TJ, MANDREKAR JN, RABINSTEIN AA. Clinical and Radiologic Correlations of Central Pontine Myelinolysis Syndrome Mayo Clin Proc [online] 2011 Nov, 86(11):1063-1067 [viewed 02 January 2015] Available from: doi:10.4065/mcp.2011.0239
  5. RAGHAVENDRAN K, NEMZEK J, NAPOLITANO LM, KNIGHT PR. Aspiration-Induced lung injury Crit Care Med [online] 2011 Apr, 39(4):818-826 [viewed 02 January 2015] Available from: doi:10.1097/CCM.0b013e31820a856b
  6. GALSON SK. PREVENTION OF DEEP VEIN THROMBOSIS AND PULMONARY EMBOLISM Public Health Rep [online] 2008, 123(4):420-421 [viewed 02 January 2015] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2430635
  7. WAKE WT. Pressure Ulcers: What Clinicians Need to Know Perm J [online] 2010, 14(2):56-60 [viewed 02 January 2015] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2912087
  8. CLAVET H, HéBERT PC, FERGUSSON D, DOUCETTE S, TRUDEL G. Joint contracture following prolonged stay in the intensive care unit CMAJ [online] 2008 Mar 11, 178(6):691-697 [viewed 02 January 2015] Available from: doi:10.1503/cmaj.071056
  9. POST B, VAN GOOL WA, TIJSSEN MA. Transient parkinsonism in isolated extrapontine myelinolysis Neurol Sci [online] 2009 Aug, 30(4):325-328 [viewed 02 January 2015] Available from: doi:10.1007/s10072-009-0088-9
  10. IMAM YZ, SAQQUR M, ALHAIL H, DELEU D. Extrapontine Myelinolysis-Induced Parkinsonism in a Patient with Adrenal Crisis Case Rep Neurol Med [online] 2012:327058 [viewed 02 January 2015] Available from: doi:10.1155/2012/327058

Risk Factors

Fact Explanation
Hyponatraemia As mentioned previously hyponatraemia is the sole predisposing factor for the disease. So such history can be elicited as above. [1][2]
Liver transplantation Liver transplantation surgeries can be complicated with central pontine myelinolysis and it is well known. It has to be suspected when confusion and weakness is present during post operative recovery. But the typical funding of myelinolysis may be masked due to concurrent neuropathy and myopathy in these patients. [3]
Other predisposing factors Alcoholism, malnutrition, immunodeficiency (HIV/AIDS), severe burns and liver disease also known to predispose central pontine myelinolysis. [3][4]
References
  1. MARTIN R. CENTRAL PONTINE AND EXTRAPONTINE MYELINOLYSIS: THE OSMOTIC DEMYELINATION SYNDROMES J Neurol Neurosurg Psychiatry [online] 2004 Sep, 75(Suppl 3):iii22-iii28 [viewed 02 January 2015] Available from: doi:10.1136/jnnp.2004.045906
  2. CAMPBELL MC. Hyponatremia and Central Pontine Myelinolysis as a Result of Beer Potomania: A Case Report Prim Care Companion J Clin Psychiatry [online] 2010, 12(4):PCC.09100936 [viewed 02 January 2015] Available from: doi:10.4088/PCC.09l00936ecr
  3. BOON AP, CAREY MP, ADAMS DH, BUCKELS J, MCMASTER P. Central pontine myelinolysis in liver transplantation. J Clin Pathol [online] 1991 Nov, 44(11):909-914 [viewed 02 January 2015] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC496628
  4. HOLMES AH, ESIRI M, MORRIS CS, EDWARDS A. Central pontine myelinolysis in a patient with AIDS. J Neurol Neurosurg Psychiatry [online] 1992 Jul, 55(7):631-632 [viewed 02 January 2015] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC489187

Signs - of the Disease

Fact Explanation
Level of consciousness The patient may be confused with disorientation in time, place and person. There may be memory impairment and disability in recalling. Delirium may be present and some patients may be comatose with out being aroused or unresponsive to deep stimuli. [1][2]
Gaze paralysis with the involvement of pons there may be a horizontal gaze paralysis and rarely there would be a vertical gaze paralysis with involvement of mid brain. Therefore the vertical eye movement is usually spared. [3]
Motor examination of limbs Typically there would be a spastic quadriplegia. The deep tendon reflexes are exaggerated and Babinski's sign is positive due to the involvement of upper tracts. [4][5]
Cranial nerves and head and neck examination with the pseudobulbar palsy 9th, 10th, 11th, 12th cranial nerves are paralysed and patient will have dysarthria and dysphagia. It also causes weakness of head and neck muscles. when these symptoms are combined with the severe quadriplegia the patient is aware about the exterior but unable respond to the exterior. This status is called as "locked in syndrome". [6]
References
  1. LOVE S. Demyelinating diseases J Clin Pathol [online] 2006 Nov, 59(11):1151-1159 [viewed 02 January 2015] Available from: doi:10.1136/jcp.2005.031195
  2. CAMPBELL MC. Hyponatremia and Central Pontine Myelinolysis as a Result of Beer Potomania: A Case Report Prim Care Companion J Clin Psychiatry [online] 2010, 12(4):PCC.09100936 [viewed 02 January 2015] Available from: doi:10.4088/PCC.09l00936ecr
  3. LAI CC, TAN CK, LIN SH, CHEN HW. Central pontine myelinolysis CMAJ [online] 2011 Jun 14, 183(9):E605 [viewed 02 January 2015] Available from: doi:10.1503/cmaj.090186
  4. EL MOGHAZY W, GALA-LOPEZ B, WONG W, KNETEMAN N. Recovery of locked-in syndrome following liver transplantation with calcineurin inhibitor cessation and supportive treatment Am J Case Rep [online] :16-19 [viewed 02 January 2015] Available from: doi:10.12659/AJCR.883748
  5. KOUL PA, KHAN UH, JAN RA, SHAH S, QADRI AB, WANI B, ASHRAF M, AHMAD F, BAZAZ SR. Osmotic demyelination syndrome following slow correction of hyponatremia: Possible role of hypokalemia Indian J Crit Care Med [online] 2013, 17(4):231-233 [viewed 02 January 2015] Available from: doi:10.4103/0972-5229.118433
  6. MARTIN PJ, YOUNG CA. Central pontine myelinolysis: clinical and MRI correlates. Postgrad Med J [online] 1995 Jul, 71(837):430-432 [viewed 02 January 2015] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2397973

Signs - of Complications

Fact Explanation
Severely disturbed conscious level or state of unresponsiveness As mentioned previously the patient may be comatose or may be in "locked in syndrome". Glasgow coma scale has to be assessed. There by the patient would be immobile and bed bound leading multiple complications including follows and pressure ulcers. [1][2][3][4]
Features of aspiration pneumonia Patient may be in respiratory distress and will be febrile. Auscultation and respiratory tract examination may reveal the evidence of consolidation. [5]
Evidence of deep vein thrombosis and pulmonary embolism The patient due to the prolonged bed bound status may develop DVT with tender swollen calves which may be associated with low grade fever. Patient may be restless, dyspnoeic, tachycardic and hypotensive when complicated with pulmonary embolism. [6]
Evidence of joint contractures Due to the prolonged disuse of the skeletal muscles there would be fixed or dynamic contractures involving large and small joints. [7]
Long term complications As a long term complication patient may develop intellectual disability and parkinsonism features. Tremor, stooped gait, rigidity, hypokinesia has to be checked in these patients. [8][9]
References
  1. MARTIN PJ, YOUNG CA. Central pontine myelinolysis: clinical and MRI correlates. Postgrad Med J [online] 1995 Jul, 71(837):430-432 [viewed 02 January 2015] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2397973
  2. GRAFF-RADFORD J, FUGATE JE, KAUFMANN TJ, MANDREKAR JN, RABINSTEIN AA. Clinical and Radiologic Correlations of Central Pontine Myelinolysis Syndrome Mayo Clin Proc [online] 2011 Nov, 86(11):1063-1067 [viewed 02 January 2015] Available from: doi:10.4065/mcp.2011.0239
  3. CAMPBELL MC. Hyponatremia and Central Pontine Myelinolysis as a Result of Beer Potomania: A Case Report Prim Care Companion J Clin Psychiatry [online] 2010, 12(4):PCC.09100936 [viewed 02 January 2015] Available from: doi:10.4088/PCC.09l00936ecr
  4. HECKMANN JG, DINKEL HP. Recovery of locked-in syndrome in central pontine myelinolysis Am J Case Rep [online] :219-220 [viewed 02 January 2015] Available from: doi:10.12659/AJCR.889378
  5. RAGHAVENDRAN K, NEMZEK J, NAPOLITANO LM, KNIGHT PR. Aspiration-Induced lung injury Crit Care Med [online] 2011 Apr, 39(4):818-826 [viewed 02 January 2015] Available from: doi:10.1097/CCM.0b013e31820a856b
  6. RABUKA CE, AZOULAY LY, KAHN SR. Predictors of a positive duplex scan in patients with a clinical presentation compatible with deep vein thrombosis or cellulitis Can J Infect Dis [online] 2003, 14(4):210-214 [viewed 02 January 2015] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2094940
  7. CLAVET H, HéBERT PC, FERGUSSON D, DOUCETTE S, TRUDEL G. Joint contracture following prolonged stay in the intensive care unit CMAJ [online] 2008 Mar 11, 178(6):691-697 [viewed 02 January 2015] Available from: doi:10.1503/cmaj.071056
  8. POST B, VAN GOOL WA, TIJSSEN MA. Transient parkinsonism in isolated extrapontine myelinolysis Neurol Sci [online] 2009 Aug, 30(4):325-328 [viewed 02 January 2015] Available from: doi:10.1007/s10072-009-0088-9
  9. SEISER A, SCHWARZ S, AICHINGER-STEINER M, FUNK G, SCHNIDER P, BRAININ M. Parkinsonism and dystonia in central pontine and extrapontine myelinolysis J Neurol Neurosurg Psychiatry [online] 1998 Jul, 65(1):119-121 [viewed 02 January 2015] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2170170

Differential Diagnoses

Fact Explanation
Strokes Strokes are sudden onset and typically presents with unilateral symptoms. There may be underlying cerebro vascular risk factors rather than a history of rapidly corrected hyponatraemia. Altered level of consciousness is less likely in strokes but may occur in cases of intra cranial haemorrhages, brain stem infarctions or infarctions with significant cerebral oedema. Imaging with CT may find the area with ischaemic or haemorrhagic stroke. If any suspicion MRI brain can be carried out. [1]
Meningitis including basal meningitis and encephalitis The typical history of hyponatraemia is absent and patient may have fever, headache, photophobia. On examination there will be neck stiffness and positive Kernig's sign. Quadriplegia is less likely and multiple cranial nerve palsies with opthalmoplegia may be present in basal meningitis (specially tuberculous) . Imaging, inflammatory markers and CSF analysis usually conclude the diagnosis. Imaging with MRI, EEG and seroligical investigations may find the diagnosis of encephalitis. Acute demyelinating encephalomyelitis may also have similar diffuse neurological manifestations. [2][3]
Multiple sclerosis This is a episodic demyelinating condition of central nervous system which may present with visual impairment, limb weakness and cranial nerve palsies. The level of consciousness is largely spared in early cases. Episodic and progressive nature of the disease with imaging with MRI may differentiate the illness. [4]
Guillen barre syndrome This is an acute inflammatory demyelination causing ascending paralysis with respiratory distress as an complication. Level of consciousness is largely spared and typical history with nerve conduction study finding may give the diagnosis. [5]
Hydrocephalus Hydrocephalus is the enlargement of cerebral ventrical with or with out and obstruction to CSF flow. Patient may have headache, urinary incontinence, limb and cranial nerve palsies. Imaging will conclude the diagnosis. [6]
Space occupying lesions including tumors of the brain (Primary or seccondary) Space occupying lesion may occur as a progressive illness associated with headache, seizures, limb weakness. Symptoms and signs are variable according to the site of the lesion. Imaging is essential in suspected cases. [7][8]
References
  1. USTRELL X, PELLISé A. Cardiac Workup of Ischemic Stroke Curr Cardiol Rev [online] 2010 Aug, 6(3):175-183 [viewed 02 January 2015] Available from: doi:10.2174/157340310791658721
  2. ELHASSANIEN AF, AZIZ HA. Acute demyelinating encephalomyelitis: Clinical characteristics and outcome J Pediatr Neurosci [online] 2013, 8(1):26-30 [viewed 02 January 2015] Available from: doi:10.4103/1817-1745.111418
  3. SOLOMON T, DUNG NM, KNEEN R, GAINSBOROUGH M, VAUGHN D, KHANH VT. Japanese encephalitis J Neurol Neurosurg Psychiatry [online] 2000 Apr, 68(4):405-415 [viewed 02 January 2015] Available from: doi:10.1136/jnnp.68.4.405
  4. GOLDENBERG MM. Multiple Sclerosis Review P T [online] 2012 Mar, 37(3):175-184 [viewed 02 January 2015] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3351877
  5. SENEVIRATNE U. Guillain-Barré syndrome Postgrad Med J [online] 2000 Dec, 76(902):774-782 [viewed 02 January 2015] Available from: doi:10.1136/pmj.76.902.774
  6. DE OLIVEIRA MF, PINTO FC, NISHIKUNI K, BOTELHO RV, LIMA AM, ROTTA JM. Revisiting Hydrocephalus as a Model to Study Brain Resilience Front Hum Neurosci [online] :181 [viewed 02 January 2015] Available from: doi:10.3389/fnhum.2011.00181
  7. SYMON L, PASZTOR E, BRANSTON NM, DORSCH NW. Effect of supratentorial space-occupying lesions on regional intracranial pressure and local cerebral blood flow: an experimental study in baboons J Neurol Neurosurg Psychiatry [online] 1974 Jun, 37(6):617-626 [viewed 02 January 2015] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC494722
  8. HOLLAND EC. Glioblastoma multiforme: The terminator Proc Natl Acad Sci U S A [online] 2000 Jun 6, 97(12):6242-6244 [viewed 02 January 2015] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3399

Investigations - for Diagnosis

Fact Explanation
Imaging with MRI scan of the brain and brain stem MRI is the method of imaging to detect central pontine myelinolysis. Initial imaging may not show a change and a series of MRI may be needed. It should be T2 weighted imaging and will show areas of demyelination. [1][2]
Electroencephalography (EEG) EEG will show typical diffuse bihemispheric slowing. [3]
Brainstem-evoked potentials This is used when the imaging is unsuccessful in concluding a the diagnosis. [4]
Series of serum sodium If these sodium values are available it will give the most important clue regarding the previous hyponatraemia which has been corrected rapidly. [2]
CSF analysis CSF analysis is not essential and can be carried out in doubtful situations. But it is usually normal. That will demonstrate elevated protein, increased opening pressure or mononuclear pleocytosis. [4]
References
  1. THOMPSON PD, MILLER D, GLEDHILL RF, ROSSOR MN. Magnetic resonance imaging in central pontine myelinolysis. J Neurol Neurosurg Psychiatry [online] 1989 May, 52(5):675-677 [viewed 02 January 2015] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1032189
  2. GRAFF-RADFORD J, FUGATE JE, KAUFMANN TJ, MANDREKAR JN, RABINSTEIN AA. Clinical and Radiologic Correlations of Central Pontine Myelinolysis Syndrome Mayo Clin Proc [online] 2011 Nov, 86(11):1063-1067 [viewed 02 January 2015] Available from: doi:10.4065/mcp.2011.0239
  3. IMAM YZ, SAQQUR M, ALHAIL H, DELEU D. Extrapontine Myelinolysis-Induced Parkinsonism in a Patient with Adrenal Crisis Case Rep Neurol Med [online] 2012:327058 [viewed 02 January 2015] Available from: doi:10.1155/2012/327058
  4. LOVE S. Demyelinating diseases J Clin Pathol [online] 2006 Nov, 59(11):1151-1159 [viewed 02 January 2015] Available from: doi:10.1136/jcp.2005.031195

Investigations - for Management

Fact Explanation
Serum electrolytes As mentioned above for the diagnosis as well as for the management available series of serum sodium is far important. It will show the previous degree of hyponatraemia and rate of its correction. This will guide the further electrolyte management. [1][2]
Basic investigations with full blood count and other renal function tests including creatine This will give the patients base line status and will be needed to repeat during the disease course. Increased wBC may denote the infection and renal funtion has to be assessed regularly. [3]
Liver function tests including serum protein levels Malnutrition, alcoholism and liver diseases may predispose the central pontine myelinolysis and have to be identified. If present vitamin supplementation is needed. [3]
Inflammatory markers such as CRP, ESR These will denote the occurrence of complicating infections such as aspiration pneumonia, infected bed sore and urinary tract infection. [4]
Chest X ray Is needed when the respiratory signs are present to diagnose and assess the aspiration pneumonoa. [4]
D-dimer and lower limb venous duplex when the DVT or pulmonary embolism is suspected these investigations has to be carried out. [5]
ECG, CT pulmonary angiogram (CTPA) These are needed when the pulmonary embolism is suspected. [6]
References
  1. LIEN YH, SHAPIRO JI, CHAN L. Study of brain electrolytes and organic osmolytes during correction of chronic hyponatremia. Implications for the pathogenesis of central pontine myelinolysis. J Clin Invest [online] 1991 Jul, 88(1):303-309 [viewed 02 January 2015] Available from: doi:10.1172/JCI115292
  2. GRAFF-RADFORD J, FUGATE JE, KAUFMANN TJ, MANDREKAR JN, RABINSTEIN AA. Clinical and Radiologic Correlations of Central Pontine Myelinolysis Syndrome Mayo Clin Proc [online] 2011 Nov, 86(11):1063-1067 [viewed 02 January 2015] Available from: doi:10.4065/mcp.2011.0239
  3. JACOB S, GUPTA H, NIKOLIC D, GUNDOGDU B, ONG S. Central Pontine and Extrapontine Myelinolysis: The Great Masquerader—An Autopsy Case Report Case Rep Neurol Med [online] 2014:745347 [viewed 02 January 2015] Available from: doi:10.1155/2014/745347
  4. HOLM A, NEXOE J, BISTRUP LA, PEDERSEN SS, OBEL N, NIELSEN LP, PEDERSEN C. Aetiology and prediction of pneumonia in lower respiratory tract infection in primary care Br J Gen Pract [online] 2007 Jul 1, 57(540):547-554 [viewed 02 January 2015] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2099637
  5. RABUKA CE, AZOULAY LY, KAHN SR. Predictors of a positive duplex scan in patients with a clinical presentation compatible with deep vein thrombosis or cellulitis Can J Infect Dis [online] 2003, 14(4):210-214 [viewed 02 January 2015] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2094940
  6. SCHELLHAAß A, WALTHER A, KONSTANTINIDES S, BöTTIGER BW. The Diagnosis and Treatment of Acute Pulmonary Embolism Dtsch Arztebl Int [online] 2010 Aug, 107(34-35):589-595 [viewed 02 January 2015] Available from: doi:10.3238/arztebl.2010.0589

Management - General Measures

Fact Explanation
Prevention The prevention of the central pontine myelinolysis is far important as the established condition is having poor prognosis with risk of death. Meticulous correction of hyponatraemia is the sole method to prevent it via preventing rapid correction of hyponatraemia. [1][2]
Health education Patient and specially the family members should be informed regarding the natural course of the illness and the poor prognosis. Family members should be educated about the lack of active interventions and available supportive care. [3][4]
Prevention of bed sores when the patients are bed bound they are more prone to have pressure ulcers. Timely turning, using an air mattress, timely wound dressing may prevent the extensive bed sores. [5]
Nutrition when the patients are having dysphagia naso gastric feeding is indicated. Malnutrition also aggravates the condition and nutritional supplementation may be necessary. [6]
Bladder and bowel care when the patient is having incontinence patient has to be catheterized. Bowel care should be continued to maintain a good hygiene in bed bound patient. [7]
Chest physiotherapy and feeding in propped up position These measures will minimize the risk of having aspiration pneumonia. [8]
Prevention of deep vein thrombosis Better hydration, physiotherapy, class I stocking and prophylactic anti coagulation may prevent the occurrence of DVT and pulmonary embolism. Physiotherapy also prevents the occurrence of joint contractures. [9]
Neurorehabilitation Patient may have permanent cognitive and intellectual even following recovery. Some may have parkinsonism. These patients has to be properly rehabilitated. Drug management for the parkinsonism may be needed. [10][11]
References
  1. MARTIN R. CENTRAL PONTINE AND EXTRAPONTINE MYELINOLYSIS: THE OSMOTIC DEMYELINATION SYNDROMES J Neurol Neurosurg Psychiatry [online] 2004 Sep, 75(Suppl 3):iii22-iii28 [viewed 02 January 2015] Available from: doi:10.1136/jnnp.2004.045906
  2. GRAFF-RADFORD J, FUGATE JE, KAUFMANN TJ, MANDREKAR JN, RABINSTEIN AA. Clinical and Radiologic Correlations of Central Pontine Myelinolysis Syndrome Mayo Clin Proc [online] 2011 Nov, 86(11):1063-1067 [viewed 02 January 2015] Available from: doi:10.4065/mcp.2011.0239
  3. JOAD AS, MAYAMOL T, CHATURVEDI M. What Does the Informal Caregiver of a Terminally Ill Cancer Patient Need? A Study from a Cancer Centre Indian J Palliat Care [online] 2011, 17(3):191-196 [viewed 02 January 2015] Available from: doi:10.4103/0973-1075.92335
  4. ELLERSHAW J, WARD C. Care of the dying patient: the last hours or days of life BMJ [online] 2003 Jan 4, 326(7379):30-34 [viewed 02 January 2015] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1124925
  5. ANDERS J, HEINEMANN A, LEFFMANN C, LEUTENEGGER M, PRöFENER F, VON RENTELN-KRUSE W. Decubitus Ulcers: Pathophysiology and Primary Prevention Dtsch Arztebl Int [online] 2010 May, 107(21):371-382 [viewed 02 January 2015] Available from: doi:10.3238/arztebl.2010.0371
  6. HEGAZI RA, WISCHMEYER PE. Clinical review: optimizing enteral nutrition for critically ill patients - a simple data-driven formula Crit Care [online] 2011, 15(6):234 [viewed 02 January 2015] Available from: doi:10.1186/cc10430
  7. Bladder Management for Adults with Spinal Cord Injury: A Clinical Practice Guideline for Health-Care Providers J Spinal Cord Med [online] 2006, 29(5):527-573 [viewed 02 January 2015] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1949036
  8. ARMSTRONG JR, MOSHER BD. Aspiration Pneumonia After Stroke: Intervention and Prevention Neurohospitalist [online] 2011 Apr, 1(2):85-93 [viewed 02 January 2015] Available from: doi:10.1177/1941875210395775
  9. GALSON SK. PREVENTION OF DEEP VEIN THROMBOSIS AND PULMONARY EMBOLISM Public Health Rep [online] 2008, 123(4):420-421 [viewed 02 January 2015] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2430635
  10. SOHN MK, NAM JH. Locked-in Syndrome due to Central Pontine Myelinolysis: Case Report Ann Rehabil Med [online] 2014 Oct, 38(5):702-706 [viewed 02 January 2015] Available from: doi:10.5535/arm.2014.38.5.702
  11. ABBOTT R, SILBER E, FELBER J, EKPO E. Osmotic demyelination syndrome BMJ [online] 2005 Oct 8, 331(7520):829-830 [viewed 02 January 2015] Available from: doi:10.1136/bmj.331.7520.829

Management - Specific Treatments

Fact Explanation
Supportive management only, no specific management. As mentioned previously there is no specific management for central pontine myelinolysis other than the prevention and the supportive care. Any specific reason for the electrolyte imbalance has to be found and treated promptly if present. [1][2][3]
References
  1. KHOSYA S, MEENA H. Central pontine myelinolysis Indian J Med Res [online] 2013 May, 137(5):993-994 [viewed 02 January 2015] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3734697
  2. MARTIN R. CENTRAL PONTINE AND EXTRAPONTINE MYELINOLYSIS: THE OSMOTIC DEMYELINATION SYNDROMES J Neurol Neurosurg Psychiatry [online] 2004 Sep, 75(Suppl 3):iii22-iii28 [viewed 02 January 2015] Available from: doi:10.1136/jnnp.2004.045906
  3. GRAFF-RADFORD J, FUGATE JE, KAUFMANN TJ, MANDREKAR JN, RABINSTEIN AA. Clinical and Radiologic Correlations of Central Pontine Myelinolysis Syndrome Mayo Clin Proc [online] 2011 Nov, 86(11):1063-1067 [viewed 02 January 2015] Available from: doi:10.4065/mcp.2011.0239