Central pontine myelinolysis

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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 thebrainstem]). 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 [1] described four cases with fatal outcomes, and the findings on autopsy. The disease was described as a disease of alcoholics and malnutrition. [2] '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. [3]

Since this original description, demyelination in other areas of the central nervous system associated with osmotic stress has been described outside the pons (extrapontine). [4] Osmotic demyelination syndrome is the term used for both central pontine myelinolysis and extrapontine myelinolysis. [5]

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. [6] [7]

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. [8] [9]

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. [10]

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. [2]

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). [11] 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. [3]

It has also been known to occur in patients suffering withdrawal symptoms of chronic alcoholism. [2] 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. [12] With this excessive thirst combined with psychotic symptoms, brain damage such as central pontine myelinolysis [13] 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. [14]

It has been observed following hematopoietic stem cell transplantation. [15]

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. [27]

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. [28] [29]

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. [30]

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. [29] 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. [29] Alcoholic patients should receive vitamin supplementation and a formal evaluation of their nutritional status. [31] [32]

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. [3]

Research has led to improved outcomes. [33] Animal studies suggest that inositol reduces the severity of osmotic demyelination syndrome if given before attempting to correct chronic hyponatraemia. [34] Further study is required before using inositol in humans for this purpose. [35]

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. [3] Recent data indicate that the prognosis of critically ill patients may even be better than what is generally considered, [36] despite severe initial clinical manifestations and a tendency by the intensivists to underestimate a possible favorable evolution. [37] 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. [38] Permanent disabilities range from minor tremors and ataxia to signs of severe brain damage, such as spastic quadriparesis and locked-in syndrome. [39] 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. [28]

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 their 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 Greek πολυδίψιος (poludípsios) 'very thirsty', which is derived from Ancient Greek πολύς (polús) 'much, many' and δίψα (dípsa) 'thirst'. 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> Abnormality in the concentration of electrolytes in the body

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, or water toxemia, 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 hypovolemia 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 caused by psychiatric disorders—oftentimes schizophrenia—is frequently accompanied by the sensation of dry mouth. Some conditions with polydipsia as a symptom are non-psychogenic. Primary polydipsia is a diagnosis of exclusion.

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

Marchiafava–Bignami disease (MBD) 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.

<span class="mw-page-title-main">Basilar part of pons</span>

The basilar part of pons, also known as basis pontis, or basilar pons, is the ventral part of the pons in the brainstem; the dorsal part is known as the pontine tegmentum.

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

<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 beverages 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

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