Coursera submission

1. Osmotic demyelination
syndrome
A demyelinating syndrome also called central pontine myelinosis

2. • A demyelinating disease is any disease of the nervous system in which
the myelin sheath of neurons is damaged (Wikepedia, 2014).
www.nature.com

3. Osmotic Demyelination Syndrome
• “central pontine myelinolysis”
• Demyelinating lesion in the brain that occurs with overly rapid
correction of hyponatremia
• Characterized by acute paralysis, dysphagia, and dysarthria
• Most common in those with chronic hyponatremia (usually caused by
alcoholism)

4. Case
• 68 y/o male admitted to hospital 1 days ago with electrolyte
disturbances, dehydration, seizures and chronic alcohol abuse.
• Day 1 of admission level of consciousness decreased to GSC 7 but
improved to 14/15. Only to deteriorate again 4 days later to 3/15
• Transferred to the critical care unit for airway management and
neurological review. CT scan of brain to be completed on transfer was
normal.
• Admission sodium level 108mmol/dl on day one increased to
128mmol/dl. Now 142mmol/Dl
• Presumed pontine demyelinating syndrome

5. Pathophysiology
• initially encephalopathic or presenting with seizures from
hyponatraemia, then recovering rapidly as normonatraemia is
restored.
• Patient deteriorate several days later. The initial signs of the Osmotic
demyelination syndrome, which reflect this second phase,
• include dysarthria and dysphagia (secondary to corticobulbar fibre
involvement),
• a flaccidquadriparesis (from corticospinal tract involvement) which later
becomes spastic.
• This originates from involvement of the basis pontis, The basilar part
of pons is the anterior portion of the pons (Martin R. J. 2004)

6. • if the lesion extends into the tegmentum of the pons:
• pupillary, oculomotor abnormalities may occur.
• There may be an apparent change in conscious level reflecting the ‘‘locked-in
syndrome’’ that a large lesion in this site is likely to produce (Martin 2004).

7. • This may give a similar presentation as discussed in this course as
related to Bobbi brain stem stroke.
• The question is would this patient recover

8. Prognosis
• Once considered bleak for most syndromes were diagnosed post
mortem
• The improvement in CT and MRI techniques now allows diagnosis
early
• Neither clinical features nor extent of radiological change are
predictive. The outcome may be death, disability, or recovery to
virtually normal level of function.
• However there is a 25% of patients from most studies who survive
with significant neurological deficits from paralysis to severe
Ataxia.(King 2010)

9. treatments
• The management of patients with CPM and ODS is prolonged
neurorehabilitation.
• In addition to the:
• generally applied therapeutic measures, there are four additional treatment
modalities. These are
• administration of TRH, plasmapheresis, corticosteroids alone or in combination with
plasmapheresis,
• intravenous immunoglobulin
• No specific choice
• Prevention is the best treatment

10. Osmotic Demyelination Syndrome
Prevention
• Controlled correction of severe hyponatremia
• Correction rate=0.5-1.0meq/L/hr, with not more than 12meq/l
correction in 24 hrs; should receive no more than 8-10mmol of
sodium per day
• Management: Supportive
• Prognosis is poor

11. References
• Bhattacharya, A. K., Bera, A B. and Roy, S. (2007) A Case Study Osmotic
Demyelination Syndrome. Journal of Indian Academy of Clinical Medicine 8 (2).
• King, Mitchel and Rosner (2010) Osmotic Demyelination syndrome. American
Journal of Medical Science, 339(6).
• Martin R. J. (2004) Central Pontine and Extra Pontine myelinosis: The Osmotic
Demylenation Syndrome. Journal Neurol Neurosurgical Psychiatry, 75
(Supplement ii).
• Nature.com (2014) available at: http://www.nature.com/scitable/content/the-
fate-of-demyelinated-axons-14463695 Accessed July 18th.
• Wikepedia, (2014) available at:
http://en.wikipedia.org/wiki/Demyelinating_disease accessed June 7th 2014.