Central pontine myelinolysis

Last updated
Central pontine myelinolysis
Other namesOsmotic demyelination syndrome, central pontine demyelination
MRI Central Pontine Myelinolysis fat sat T2.jpg
Axial fat-saturated T2-weighted image showing hyperintensity in the pons with sparing of the peripheral fibers, the patient was an alcoholic admitted with a serum Na of 101 treated with hypertonic saline, he was left with quadriparesis, dysarthria, and altered mental status
Specialty Neurology
Causes Alcoholism, malnutrition

Central pontine myelinolysis is a neurological condition involving severe damage to the myelin sheath of nerve cells in the pons (an area of the brainstem). It is predominately iatrogenic (treatment-induced), and is characterized by acute paralysis, dysphagia (difficulty swallowing), dysarthria (difficulty speaking), and other neurological symptoms.

Contents

Central pontine myelinolysis was first described as a disorder in 1959. The original paper described four cases with fatal outcomes, and the findings on autopsy. The disease was described as a disease of alcoholics and malnutrition. [1] 'Central pontine' indicated the site of the lesion and 'myelinolysis' was used to emphasise that myelin was affected. The authors intentionally avoided the term 'demyelination' to describe the condition, in order to differentiate this condition from multiple sclerosis and other neuroinflammatory disorders. [2]

Since this original description, demyelination in other areas of the central nervous system associated with osmotic stress has been described outside the pons (extrapontine). [3] Osmotic demyelination syndrome is the term used for both central pontine myelinolysis and extrapontine myelinolysis. [4]

Central pontine myelinolysis, and osmotic demyelination syndrome, present most commonly as a complication of treatment of patients with profound hyponatremia (low sodium), which can result from a varied spectrum of conditions, based on different mechanisms. It occurs as a consequence of a rapid rise in serum tonicity following treatment in individuals with chronic, severe hyponatremia who have made intracellular adaptations to the prevailing hypotonicity. [5] [6]

Signs and symptoms

T2 weighted magnetic resonance scan image showing bilaterally symmetrical hyperintensities in caudate nucleus (small, thin arrow), putamen (long arrow), with sparing of globus pallidus (broad arrow), suggestive of extrapontine myelinolysis (osmotic demyelination syndrome) Extrapontine myelinolysis T2 01.jpg
T2 weighted magnetic resonance scan image showing bilaterally symmetrical hyperintensities in caudate nucleus (small, thin arrow), putamen (long arrow), with sparing of globus pallidus (broad arrow), suggestive of extrapontine myelinolysis (osmotic demyelination syndrome)

Symptoms depend on the regions of the brain involved. Prior to its onset, patients may present with the neurological signs and symptoms of hyponatraemic encephalopathy such as nausea and vomiting, confusion, headache and seizures. These symptoms may resolve with normalisation of the serum sodium concentration. Three to five days later, a second phase of neurological manifestations occurs correlating with the onset of myelinolysis. Observable immediate precursors may include seizures, disturbed consciousness, gait changes, and decrease or cessation of respiratory function. [7] [8]

The classical clinical presentation is the progressive development of spastic quadriparesis, pseudobulbar palsy, and emotional lability (pseudobulbar affect), with other more variable neurological features associated with brainstem damage. These result from a rapid myelinolysis of the corticobulbar and corticospinal tracts in the brainstem. [9]

In about ten per cent of people with central pontine myelinolysis, extrapontine myelinolysis is also found. In these cases symptoms of Parkinson's disease may be generated. [1]

Causes

Loss of myelinated fibers at the basilar part of the pons in the brainstem (Luxol-Fast blue stain) Pontine myelinolysis.jpg
Loss of myelinated fibers at the basilar part of the pons in the brainstem (Luxol-Fast blue stain)

The most common cause is overly-rapid correction of low blood sodium levels (hyponatremia). [10] Apart from rapid correction of hyponatraemia, there are case reports of central pontine myelinolysis in association with hypokalaemia, anorexia nervosa when feeding is started, patients undergoing dialysis and burn victims. There is a case report of central pontine myelinolysis occurring in the context of refeeding syndrome, in the absence of hyponatremia. [2]

It has also been known to occur in patients suffering withdrawal symptoms of chronic alcoholism. [1] In these instances, occurrence may be entirely unrelated to hyponatremia or rapid correction of hyponatremia. It could affect patients who take some prescription medicines that are able to cross the blood-brain barrier and cause abnormal thirst reception - in this scenario the central pontine myelinolysis is caused by polydipsia leading to low blood sodium levels (hyponatremia).[ citation needed ]

In schizophrenic patients with psychogenic polydipsia, inadequate thirst reception leads to excessive water intake, severely diluting serum sodium. [11] With this excessive thirst combined with psychotic symptoms, brain damage such as central pontine myelinolysis [12] may result from hyperosmolarity caused by excess intake of fluids, (primary polydipsia) although this is difficult to determine because such patients are often institutionalised and have a long history of mental health conditions. [13]

It has been observed following hematopoietic stem cell transplantation. [14]

Central pontine myelinolysis may also occur in patients prone to hyponatremia affected by:

Pathophysiology

The currently accepted theory states that the brain cells adjust their osmolarities by changing levels of certain osmolytes like inositol, betaine, and glutamine in response to varying serum osmolality. In the context of chronic low plasma sodium (hyponatremia), the brain compensates by decreasing the levels of these osmolytes within the cells, so that they can remain relatively isotonic with their surroundings and not absorb too much fluid. The reverse is true in hypernatremia, in which the cells increase their intracellular osmolytes so as not to lose too much fluid to the extracellular space. [26]

With correction of the hyponatremia with intravenous fluids, the extracellular tonicity increases, followed by an increase in intracellular tonicity. When the correction is too rapid, not enough time is allowed for the brain's cells to adjust to the new tonicity, namely by increasing the intracellular osmoles mentioned earlier. If the serum sodium levels rise too rapidly, the increased extracellular tonicity will continue to drive water out of the brain's cells. This can lead to cellular dysfunction and central pontine myelinolysis. [27] [28]

Diagnosis

It can be diagnosed clinically in the appropriate context, but may be difficult to confirm radiologically using conventional imaging techniques. Changes are more prominent on MRI than on CT, but often take days or weeks after acute symptom onset to develop. Imaging by MRI typically demonstrates areas of hyperintensity on T2-weighted images. [29]

Treatment

To minimise the risk of this condition developing from its most common cause, overly rapid reversal of hyponatremia, the hyponatremia should be corrected at a rate not exceeding 10 mmol/L/24 h or 0.5 mEq/L/h; or 18 mEq/L/48hrs; thus avoiding demyelination. [28] No large clinical trials have been performed to examine the efficacy of therapeutic re-lowering of serum sodium, or other interventions sometimes advocated such as steroids or plasma exchange. [28] Alcoholic patients should receive vitamin supplementation and a formal evaluation of their nutritional status. [30] [31]

Once osmotic demyelination has begun, there is no cure or specific treatment. Care is mainly supportive. Alcoholics are usually given vitamins to correct for other deficiencies. The favourable factors contributing to the good outcome in central pontine myelinolysis without hyponatremia were: concurrent treatment of all electrolyte disturbances, early intensive care unit involvement at the advent of respiratory complications, early introduction of feeding including thiamine supplements with close monitoring of the electrolyte changes and input. [2]

Research has led to improved outcomes. [32] Animal studies suggest that inositol reduces the severity of osmotic demyelination syndrome if given before attempting to correct chronic hyponatraemia. [33] Further study is required before using inositol in humans for this purpose. [34]

Prognosis

Though traditionally the prognosis is considered poor, a good functional recovery is possible. All patients at risk of developing refeeding syndrome should have their electrolytes closely monitored, including sodium, potassium, magnesium, glucose and phosphate. [2] Recent data indicate that the prognosis of critically ill patients may even be better than what is generally considered, [35] despite severe initial clinical manifestations and a tendency by the intensivists to underestimate a possible favorable evolution. [36] While some patients die, most survive and of the survivors, approximately one-third recover; one-third are disabled but are able to live independently; one-third are severely disabled. [37] Permanent disabilities range from minor tremors and ataxia to signs of severe brain damage, such as spastic quadriparesis and locked-in syndrome. [38] Some improvements may be seen over the course of the first several months after the condition stabilizes.[ citation needed ]

The degree of recovery depends on the extent of the original axonal damage. [27]

Related Research Articles

<span class="mw-page-title-main">Locked-in syndrome</span> Condition in which a patient is aware but completely paralysed

Locked-in syndrome (LIS), also known as pseudocoma, is a condition in which a patient is aware but cannot move or communicate verbally due to complete paralysis of nearly all voluntary muscles in the body except for vertical eye movements and blinking. The individual is conscious and sufficiently intact cognitively to be able to communicate with eye movements. Electroencephalography results are normal in locked-in syndrome. Total locked-in syndrome, or completely locked-in state (CLIS), is a version of locked-in syndrome wherein the eyes are paralyzed as well. Fred Plum and Jerome B. Posner coined the term for this disorder in 1966.

Hyponatremia or hyponatraemia is a low concentration of sodium in the blood. It is generally defined as a sodium concentration of less than 135 mmol/L (135 mEq/L), with severe hyponatremia being below 120 mEq/L. Symptoms can be absent, mild or severe. Mild symptoms include a decreased ability to think, headaches, nausea, and poor balance. Severe symptoms include confusion, seizures, and coma; death can ensue.

<span class="mw-page-title-main">Cerebral edema</span> Excess accumulation of fluid (edema) in the intracellular or extracellular spaces of the brain

Cerebral edema is excess accumulation of fluid (edema) in the intracellular or extracellular spaces of the brain. This typically causes impaired nerve function, increased pressure within the skull, and can eventually lead to direct compression of brain tissue and blood vessels. Symptoms vary based on the location and extent of edema and generally include headaches, nausea, vomiting, seizures, drowsiness, visual disturbances, dizziness, and in severe cases, death.

Polydipsia is excessive thirst or excess drinking. The word derives from the Greek πολυδίψιος (poludípsios) "very thirsty", which is derived from πολύς + δίψα. Polydipsia is a nonspecific symptom in various medical disorders. It also occurs as an abnormal behaviour in some non-human animals, such as in birds.

<span class="mw-page-title-main">Demyelinating disease</span> Any neurological disease in which the myelin sheath of neurons is damaged

A demyelinating disease refers to any disease affecting the nervous system where the myelin sheath surrounding neurons is damaged. This damage disrupts the transmission of signals through the affected nerves, resulting in a decrease in their conduction ability. Consequently, this reduction in conduction can lead to deficiencies in sensation, movement, cognition, or other functions depending on the nerves affected.

<span class="mw-page-title-main">Electrolyte imbalance</span> Medical condition

Electrolyte imbalance, or water-electrolyte imbalance, is an abnormality in the concentration of electrolytes in the body. Electrolytes play a vital role in maintaining homeostasis in the body. They help to regulate heart and neurological function, fluid balance, oxygen delivery, acid–base balance and much more. Electrolyte imbalances can develop by consuming too little or too much electrolyte as well as excreting too little or too much electrolyte. Examples of electrolytes include calcium, chloride, magnesium, phosphate, potassium, and sodium.

Hypernatremia, also spelled hypernatraemia, is a high concentration of sodium in the blood. Early symptoms may include a strong feeling of thirst, weakness, nausea, and loss of appetite. Severe symptoms include confusion, muscle twitching, and bleeding in or around the brain. Normal serum sodium levels are 135–145 mmol/L. Hypernatremia is generally defined as a serum sodium level of more than 145 mmol/L. Severe symptoms typically only occur when levels are above 160 mmol/L.

The syndrome of inappropriate antidiuretic hormone secretion (SIADH), also known as the syndrome of inappropriate antidiuresis (SIAD), is characterized by a physiologically inappropriate release of antidiuretic hormone (ADH) either from the posterior pituitary gland, or an abnormal non-pituitary source. Unsuppressed ADH causes a physiologically inappropriate increase in solute-free water being reabsorbed by the tubules of the kidney to the venous circulation leading to hypotonic hyponatremia.

<span class="mw-page-title-main">Water intoxication</span> Potentially fatal overhydration

Water intoxication, also known as water poisoning, hyperhydration, overhydration, water toxemia or hyponatremia is a potentially fatal disturbance in brain functions that can result when the normal balance of electrolytes in the body is pushed outside safe limits by excessive water intake.

Cerebral salt-wasting syndrome (CSWS), also written cerebral salt wasting syndrome, is a rare endocrine condition featuring a low blood sodium concentration and dehydration in response to injury (trauma) or the presence of tumors in or surrounding the brain. In this condition, the kidney is functioning normally but excreting excessive sodium. The condition was initially described in 1950. Its cause and management remain controversial. In the current literature across several fields, including neurology, neurosurgery, nephrology, and critical care medicine, there is controversy over whether CSWS is a distinct condition, or a special form of syndrome of inappropriate antidiuretic hormone secretion (SIADH).

<span class="mw-page-title-main">Saline (medicine)</span> Saline water for medical purposes

Saline is a mixture of sodium chloride (salt) and water. It has a number of uses in medicine including cleaning wounds, removal and storage of contact lenses, and help with dry eyes. By injection into a vein, it is used to treat dehydration such as that from gastroenteritis and diabetic ketoacidosis. Large amounts may result in fluid overload, swelling, acidosis, and high blood sodium. In those with long-standing low blood sodium, excessive use may result in osmotic demyelination syndrome.

Toxic encephalopathy is a neurologic disorder caused by exposure to neurotoxic organic solvents such as toluene, following exposure to heavy metals such as manganese, as a side effect of melarsoprol treatment for African trypanosomiasis, adverse effects to prescription drugs, or exposure to extreme concentrations of any natural toxin such as cyanotoxins found in shellfish or freshwater cyanobacteria crusts. Toxic encephalopathy can occur following acute or chronic exposure to neurotoxicants, which includes all natural toxins. Exposure to toxic substances can lead to a variety of symptoms, characterized by an altered mental status, memory loss, and visual problems. Toxic encephalopathy can be caused by various chemicals, some of which are commonly used in everyday life, or cyanotoxins which are bio-accumulated from harmful algal blooms (HABs) which have settled on the benthic layer of a waterbody. Toxic encephalopathy can permanently damage the brain and currently treatment is mainly just for the symptoms.

<span class="mw-page-title-main">Primary polydipsia</span> Medical condition

Primary polydipsia and psychogenic polydipsia are forms of polydipsia characterised by excessive fluid intake in the absence of physiological stimuli to drink. Psychogenic polydipsia which is caused by psychiatric disorders, often schizophrenia, is often accompanied by the sensation of dry mouth. Some forms of polydipsia are explicitly non-psychogenic. Primary polydipsia is a diagnosis of exclusion.

<span class="mw-page-title-main">Marchiafava–Bignami disease</span> Medical condition

Marchiafava–Bignami disease is a progressive neurological disease of alcohol use disorder, characterized by corpus callosum demyelination and necrosis and subsequent atrophy. The disease was first described in 1903 by the Italian pathologists Amico Bignami and Ettore Marchiafava in an Italian Chianti drinker. In this autopsy, Marchiafava and Bignami noticed that the middle two-thirds of the corpus callosum were necrotic. It is very difficult to diagnose and there is no specific treatment. Until 2008 only around 300 cases had been reported. If caught early enough, most patients survive.

Hypoosmolar hyponatremia is a condition where hyponatremia is associated with a low plasma osmolality. The term "hypotonic hyponatremia" is also sometimes used.

Raymond Delacy Adams was an American neurologist, neuropathologist, Bullard Professor of Neuropathology at Harvard Medical School and chief of neurology at Massachusetts General Hospital. Along with Maurice Victor, Adams was the author of Adams and Victor's Principles of Neurology, the 12th edition of which appeared, 50 years after the original.

<span class="mw-page-title-main">Potomania</span> Medical condition

Potomania is a specific hypo-osmolality syndrome related to massive consumption of beer, which is poor in solutes and electrolytes. With little food or other sources of electrolytes, consumption of large amounts of beer or other dilute alcoholic drinks leads to electrolyte disturbances, where the body does not have enough nutrients known as electrolytes, namely sodium, potassium, and magnesium. The symptoms of potomania are similar to other causes of hyponatremia and include dizziness, muscular weakness, neurological impairment and seizures, all related to hyponatremia and hypokalaemia. While the symptoms of potomania are similar to other causes of hyponatremia and acute water intoxication, it should be considered an independent clinical entity because of its often chronic nature of onset, pathophysiology, and presentation of symptoms.

<span class="mw-page-title-main">Adipsia</span> Medical condition

Adipsia, also known as hypodipsia, is a symptom of inappropriately decreased or absent feelings of thirst. It involves an increased osmolality or concentration of solute in the urine, which stimulates secretion of antidiuretic hormone (ADH) from the hypothalamus to the kidneys. This causes the person to retain water and ultimately become unable to feel thirst. Due to its rarity, the disorder has not been the subject of many research studies.

Transurethral resection of the prostate (TURP) syndrome is a rare but potentially life-threatening complication of a transurethral resection of the prostate procedure. It occurs as a consequence of the absorption of the fluids used to irrigate the bladder during the operation into the prostatic venous sinuses. Symptoms and signs are varied and unpredictable, and result from fluid overload and disturbed electrolyte balance and hyponatremia. Treatment is largely supportive and relies on removal of the underlying cause, and organ and physiological support. Pre-operative prevention strategies are extremely important.

Exercise-associated hyponatremia (EAH) is a fluid-electrolyte disorder caused by a decrease in sodium levels (hyponatremia) during or up to 24 hours after prolonged physical activity. This disorder can develop when marathon runners or endurance event athletes drink more fluid, usually water or sports drinks, than their kidneys can excrete. This excess water can severely dilute the level of sodium in the blood needed for organs, especially the brain, to function properly.

References

  1. 1 2 3 Yoon B, Shim YS, Chung SW (2008). "Central pontine and extrapontine myelinolysis after alcohol withdrawal". Alcohol and Alcoholism. 43 (6): 647–649. doi: 10.1093/alcalc/agn050 . PMID   18678596.
  2. 1 2 3 4 Bose P, Kunnacherry A, Maliakal P (September 2011). "Central pontine myelinolysis without hyponatraemia". The Journal of the Royal College of Physicians of Edinburgh. 41 (3): 211–214. doi: 10.4997/JRCPE.2011.305 . PMID   21949915.
  3. ↑ Gocht A, Colmant HJ (1987). "Central pontine and extrapontine myelinolysis: a report of 58 cases". Clinical Neuropathology. 6 (6): 262–270. PMID   3322623.
  4. ↑ Lampl C, Yazdi K (2002). "Central pontine myelinolysis". European Neurology. 47 (1): 3–10. doi:10.1159/000047939. PMID   11803185. S2CID   46885398. Archived from the original on 2012-03-06.
  5. ↑ Babar SM (October 2013). "SIADH associated with ciprofloxacin". The Annals of Pharmacotherapy. 47 (10): 1359–1363. doi:10.1177/1060028013502457. PMID   24259701. S2CID   36759747.
  6. ↑ Yoon B, Shim YS, Chung SW (2008). "Central pontine and extrapontine myelinolysis after alcohol withdrawal". Alcohol and Alcoholism. 43 (6): 647–649. doi: 10.1093/alcalc/agn050 . PMID   18678596.
  7. ↑ Musana AK, Yale SH (August 2005). "Central pontine myelinolysis: case series and review". WMJ. 104 (6): 56–60. PMID   16218318.
  8. ↑ Odier C, Nguyen DK, Panisset M (July 2010). "Central pontine and extrapontine myelinolysis: from epileptic and other manifestations to cognitive prognosis". Journal of Neurology. 257 (7): 1176–1180. doi:10.1007/s00415-010-5486-7. PMID   20148334. S2CID   25301314.
  9. ↑ Karp BI, Laureno R (November 1993). "Pontine and extrapontine myelinolysis: a neurologic disorder following rapid correction of hyponatremia". Medicine. 72 (6): 359–373. doi: 10.1097/00005792-199311000-00001 . PMID   8231786. S2CID   24829955.
  10. ↑ Bernsen HJ, Prick MJ (September 1999). "Improvement of central pontine myelinolysis as demonstrated by repeated magnetic resonance imaging in a patient without evidence of hyponatremia". Acta Neurologica Belgica. 99 (3): 189–193. PMID   10544728.
  11. ↑ Donald H. "Psychogenic Polydipsia (Excessive Fluid seeking Behaviour)" (PDF). American Psychological Society Divisions. Archived (PDF) from the original on 2015-04-07.
  12. ↑ Lim L, Krystal A (June 2007). "Psychotic disorder in a patient with central and extrapontine myelinolysis". Psychiatry and Clinical Neurosciences. 61 (3): 320–322. doi: 10.1111/j.1440-1819.2007.01648.x . PMID   17472602.
  13. ↑ Gill M, McCauley M (2015-01-21). "Psychogenic polydipsia: the result, or cause of, deteriorating psychotic symptoms? A case report of the consequences of water intoxication". Case Reports in Psychiatry. 2015: 846459. doi: 10.1155/2015/846459 . PMC   4320790 . PMID   25688318.
  14. ↑ Lim KH, Kim S, Lee YS, Kim KH, Kim J, Rhee J, et al. (April 2008). "Central pontine myelinolysis in a patient with acute lymphoblastic leukemia after hematopoietic stem cell transplantation: a case report". Journal of Korean Medical Science. 23 (2): 324–327. doi:10.3346/jkms.2008.23.2.324. PMC   2526450 . PMID   18437020. Archived from the original on 2009-02-27.
  15. ↑ Singh N, Yu VL, Gayowski T (March 1994). "Central nervous system lesions in adult liver transplant recipients: clinical review with implications for management". Medicine. 73 (2): 110–118. doi: 10.1097/00005792-199403000-00004 . PMID   8152365. S2CID   37808180.
  16. ↑ Kato T, Hattori H, Nagato M, Kiuchi T, Uemoto S, Nakahata T, Tanaka K (April 2002). "Subclinical central pontine myelinolysis following liver transplantation". Brain & Development. 24 (3): 179–182. doi:10.1016/S0387-7604(02)00013-X. PMID   11934516. S2CID   22140717.
  17. ↑ Martinez AJ, Estol C, Faris AA (May 1988). "Neurologic complications of liver transplantation". Neurologic Clinics. 6 (2): 327–348. doi:10.1016/S0733-8619(18)30873-9. PMID   3047544.
  18. ↑ McKee AC, Winkelman MD, Banker BQ (August 1988). "Central pontine myelinolysis in severely burned patients: relationship to serum hyperosmolality". Neurology. 38 (8): 1211–1217. doi:10.1212/wnl.38.8.1211. PMID   3399069. S2CID   42068902.
  19. ↑ Winkelman MD, Galloway PG (September 1992). "Central nervous system complications of thermal burns. A postmortem study of 139 patients". Medicine. 71 (5): 271–283. doi: 10.1097/00005792-199209000-00002 . PMID   1522803. S2CID   12872586.
  20. ↑ Sugimoto T, Murata T, Omori M, Wada Y (March 2003). "Central pontine myelinolysis associated with hypokalaemia in anorexia nervosa". Journal of Neurology, Neurosurgery, and Psychiatry. 74 (3): 353–355. doi:10.1136/jnnp.74.3.353. PMC   1738317 . PMID   12588925.
  21. ↑ Keswani SC (April 2004). "Central pontine myelinolysis associated with hypokalaemia in anorexia nervosa". Journal of Neurology, Neurosurgery, and Psychiatry. 75 (4): 663, author reply 663. PMC   1739009 . PMID   15026526.
  22. ↑ Leroy S, Gout A, Husson B, de Tournemire R, Tardieu M (June 2012). "Centropontine myelinolysis related to refeeding syndrome in an adolescent suffering from anorexia nervosa". Neuropediatrics. 43 (3): 152–154. doi:10.1055/s-0032-1307458. PMID   22473289. S2CID   22751051.
  23. ↑ Bergin PS, Harvey P (August 1992). "Wernicke's encephalopathy and central pontine myelinolysis associated with hyperemesis gravidarum". BMJ. 305 (6852): 517–518. doi:10.1136/bmj.305.6852.517. PMC   1882865 . PMID   1393001.
  24. ↑ Sutamnartpong P, Muengtaweepongsa S, Kulkantrakorn K (January 2013). "Wernicke's encephalopathy and central pontine myelinolysis in hyperemesis gravidarum". Journal of Neurosciences in Rural Practice. 4 (1): 39–41. doi: 10.4103/0976-3147.105608 . PMC   3579041 . PMID   23546346.
  25. ↑ Kishimoto Y, Ikeda K, Murata K, Kawabe K, Hirayama T, Iwasaki Y (2012). "Rapid development of central pontine myelinolysis after recovery from Wernicke encephalopathy: a non-alcoholic case without hyponatremia". Internal Medicine. 51 (12): 1599–1603. doi: 10.2169/internalmedicine.51.7498 . PMID   22728498.
  26. ↑ Gankam Kengne, Fabrice; Decaux, Guy (2017-09-01). "Hyponatremia and the Brain". Kidney International Reports. 3 (1): 24–35. doi:10.1016/j.ekir.2017.08.015. ISSN   2468-0249. PMC   5762960 . PMID   29340311.
  27. 1 2 Medana IM, Esiri MM (March 2003). "Axonal damage: a key predictor of outcome in human CNS diseases". Brain. 126 (Pt 3): 515–530. doi: 10.1093/brain/awg061 . PMID   12566274.
  28. 1 2 3 Spasovski G, Vanholder R, Allolio B, Annane D, Ball S, Bichet D, et al. (March 2014). "Clinical practice guideline on diagnosis and treatment of hyponatraemia". European Journal of Endocrinology. 170 (3): G1-47. doi: 10.1530/eje-13-1020 . PMID   24569125.
  29. ↑ Zimny A, Neska-Matuszewska M, Bladowska J, Sąsiadek MJ (2015). "Intracranial Lesions with Low Signal Intensity on T2-weighted MR Images - Review of Pathologies". Polish Journal of Radiology. 80: 40–50. doi:10.12659/PJR.892146. PMC   4307690 . PMID   25628772.
  30. ↑ Kleinschmidt-DeMasters BK, Norenberg MD (March 1981). "Rapid correction of hyponatremia causes demyelination: relation to central pontine myelinolysis". Science. 211 (4486): 1068–1070. Bibcode:1981Sci...211.1068K. doi:10.1126/science.7466381. PMID   7466381.
  31. ↑ Laureno R (1980). "Experimental pontine and extrapontine myelinolysis". Transactions of the American Neurological Association. 105: 354–358. PMID   7348981.
  32. ↑ Brown WD (December 2000). "Osmotic demyelination disorders: central pontine and extrapontine myelinolysis". Current Opinion in Neurology. 13 (6): 691–697. doi:10.1097/00019052-200012000-00014. PMID   11148672. S2CID   36063964.
  33. ↑ Silver SM, Schroeder BM, Sterns RH, Rojiani AM (January 2006). "Myoinositol administration improves survival and reduces myelinolysis after rapid correction of chronic hyponatremia in rats". Journal of Neuropathology and Experimental Neurology. 65 (1): 37–44. doi: 10.1097/01.jnen.0000195938.02292.39 . PMID   16410747.
  34. ↑ "INOSITOL: Overview, Uses, Side Effects, Precautions, Interactions, Dosing and Reviews". www.webmd.com. Retrieved 2021-10-14.
  35. ↑ Louis G, Megarbane B, Lavoué S, Lassalle V, Argaud L, Poussel JF, et al. (March 2012). "Long-term outcome of patients hospitalized in intensive care units with central or extrapontine myelinolysis*". Critical Care Medicine. 40 (3): 970–972. doi:10.1097/CCM.0b013e318236f152. PMID   22036854. S2CID   205542487.
  36. ↑ Young GB (March 2012). "Central pontine myelinolysis: a lesson in humility*". Critical Care Medicine. 40 (3): 1026–1027. doi:10.1097/CCM.0b013e31823b8e0b. PMID   22343870.
  37. ↑ Abbott R, Silber E, Felber J, Ekpo E (October 2005). "Osmotic demyelination syndrome". BMJ. 331 (7520): 829–830. doi:10.1136/bmj.331.7520.829. PMC   1246086 . PMID   16210283.
  38. ↑ Luzzio C (17 November 2015). "Central Pontine Myelinolysis". Medscape. Retrieved 14 March 2017.
This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.