Radiological Appearance and Imaging Techniques in the Diagnosis of Advanced Central Pontine Myelinolysis


Conventional magnetic resonance imaging (MRI) and computed tomography (CT) are used to diagnose central pontine myelinolysis (CPM), which is seen in the setting of osmotic changes, usually with the rapid correction of hyponatremia. However, they generally follow clinical symptoms and fail to detect myelinolytic damage within the first two weeks, which limits their effectiveness in early diagnosis. CPM can mimic ischemic brainstem changes on CT head and glioma on MRI. This case examines the relationship between observed radiological changes with clinical symptoms and serum sodium levels, combined with an examination of pioneering advances in radiomic analysis, including diffusion-weighted MRI, CT brain perfusion and MR spectroscopy.


Central pontine myelinolysis (CPM) is a rare clinical syndrome characterized by pontine white matter tract and extrapontine myelinolysis (EPM) with a variety of clinical manifestations [1]. CPM has been reported in association with electrolyte abnormalities as well as in the setting of liver transplantation, lithium poisoning, and carbamate poisoning [2-4]. Alcoholic or malnourished patients typically lack organic osmolytes, putting them at higher risk of developing osmotic demyelination syndrome [2]. The most common clinical context for CPM is the rapid correction of severe hyponatremia when serum sodium in patients with chronic hyponatremia is rapidly rectified, resulting in a rapid increase in plasma osmolality. [5]. Patients with adrenal insufficiency, metabolic disorders, malnutrition and cancer are also thought to be particularly susceptible to this disease. [6].

The clinical findings of CPM can range from moderate motor impairment that fully resolves over time to severe blocking syndrome [7]. Quadriparesis is caused by involvement of the corticospinal pathways, which is initially flaccid but eventually becomes spastic [8]. Pseudobulbar palsy caused by damage to the corticobulbar tract causes paralysis of the head and neck along with dysphagia and dysarthria [9]. Lesions of the pontine tegmentum or thalamus produce disorientation, as well as a locked-in state, marked by paralysis of the lower cranial nerves and limb muscles [7].

We described a patient whose treatment of severe hyponatremia was complicated by clinical and radiological signs of CPM.

Presentation of the case

An otherwise healthy 37-year-old man with a history of chronic alcoholism (30-40 units per day) presented with a fall and confusion.

Blood tests showed hypokalemia (K – 2.6 mmol/L), hyponatremia (Na – 113 mmol/L), acute renal failure (estimated glomerular filtration rate (eGFR) 56 mL/min/1.73 m*2 and creatinine 138 umol/L), low vitamin B12 and magnesium (B12 – 913 pg/mL, Mg – 0.62 mmol/L) but normal levels of folate. He was treated with 0.9% normal saline IV with KCl. The CT head was unremarkable by this admission. Eventually, sodium improved with an upward trend of 6-7 mmol/L per day and initially after five days of treatment. Potassium, magnesium and kidney functions returned to normal and the patient was discharged home.

He presented again five weeks later with bilateral lower extremity weakness and instability. The biochemical profile, including sodium, was within normal limits.

Brain CT demonstrated low attenuation crossing the midline in the lower bridge (Figure 1). There was no evidence of edema or worsening intracranial pressure. Although there was slight effacement of the fourth left lateral ventricle, there were no signs of hydrocephalus. The MRI brain showed a classic central symmetrical trident shape with high signal on T2-weighted (T2WI) imaging and low signal on liquid-attenuated inversion recovery (FLAIR) imaging sequence (Figure 2). On T1-weighted imaging (T1WI), there was a corresponding low central signal intensity. The descending corticospinal tracts were preserved. Diffusion-weighted imaging (DWI) sequence demonstrated only weak restricted diffusion outlining the lesion outlining the well-preserved descending corticospinal pathways (Figure 3). Thus, a diagnosis of central pontine myelinolysis was made. Figure 4 shows the mapping of DWI and apparent diffusion coefficient (ADC).

Single axial CT head at second admission 5 weeks later shows weak central attenuation in the lower bridge (between white arrows)
MRI-brain:-axial-DWI-(a)-and-ADC-(b)-demonstrates-T2-shines-through-with-weak-signal-on-DWI-(between-white-arrows)-and -corresponding -high-signal-on-ADC-board-(between-black-arrows)

His neurological function improved over time and he was discharged 10 days after admission. He had almost complete functional recovery and was independent in all activities of daily living.


The basic pathology identified in CPM is the compression and subsequent demyelination of the fiber bundles due to either a reduced adaptive capacity of the neuroglia to substantial changes in serum osmolarity or cellular edema produced by changes in electrolyte gradients. [10,11]. A dense grid-like arrangement of white and gray fibers in the central region of the bridge makes it particularly susceptible to osmotic demyelination [8]. Compression of fiber bundles caused by cellular edema produced by shifting osmotic pressures can lead to demyelination [12]. EPM occurs in areas of greatest gray and white mixing and involves the midbrain, thalamus, basal nuclei, and cerebellum [7,8].

Conventional MRI (T1WI, T2WI, and FLAIR) and CT scans are used to diagnose PMC, however, they usually follow clinical symptoms and fail to detect myelinolytic damage in the first two weeks, which limits their effectiveness in the early diagnosis of CPM. [13]. Additionally, CT imaging is much less sensitive than MRI imaging for detecting early CPM abnormalities, where the diagnosis of CPM cannot be ruled out in the presence of normal CT imaging, and therefore, if a clinical suspicion should be performed, additional imaging should be recommended. [14].

DWI, on the other hand, can identify abnormal diffusion restriction in demyelinating lesions within 24 hours of initiation, which can boost diagnostic confidence. [15]. In severe cases, however, pontine lesions may exhibit diffusion restriction, which is caused by cellular necrosis and can be mistaken for pontine infarction. [14].

A low T1WI signal intensity and a high T2WI FLAIR sequence with an oval or trident shape (trident sign) or the snout of a pig (piglet sign) are characteristic of CPM [16]. This is due to the relative sparing of the descending corticospinal and corticobulbar pathways [16]. In EPM, T2WI and FLAIR sequences show symmetrical high signal abnormalities in bilateral caudate nucleus and putamen with globus pallidus sparing [15]. Additionally, there is no contrast enhancement after intravenous administration of gadolinium in both CPM and EPM. [1].

CT perfusion demonstrates increased blood flow, decreased mean transit time, and decreased time to maximum in the pons, which could be attributed to higher metabolic demands at the site of cell injury [16]. This, in addition to inflammation of the microglia, shows avid uptake of fluorodeoxyglucose (FDG) in the pons on a PET scan performed at two weeks [17]. In magnetic resonance spectroscopy, the acute phase is marked by a drop in the N-acetyl aspartate (NAA)/creatine (Cr) ratio, an increase in the choline (Cho)/Cr ratio and a lactate/lipid peak. This shows a further increase in the Cho/Cr ratio and a decrease in the NAA/Cr ratio in the later phase [18].

Pontine lesions incidentally discovered during MRI examinations constitute a diverse group, many of which correspond more to rarefaction of pontine ischemia than to asymptomatic PMC [19]. With the right clinical information, this result can be used to make an early diagnosis of CPM [19]. The imaging features could also mimic a glioma due to the similarity of disease etiology resulting from damage to the blood-brain barrier, which produces abnormal inhomogeneous signal intensity on contrast-enhanced MRI. In such cases, follow-up could be beneficial for a definitive diagnosis. [18].


There is a high index of suspicion for CPM and a low threshold for MRI in symptomatic patients with current or recent hyponatremia, regardless of the appropriate correction rate. CPM imaging appearances may be delayed in some patients and if clinical suspicion is high, repeat imaging in 10-14 days is recommended. Imaging appearance of CPM can mimic ischemic brainstem changes on CT head and mimic glioma on MRI. In patients with a history of hyponatremia, CPM should be considered. In advanced CPM, MRI may show appearances of encephalomalacia with a T2 reflection rather than a characteristic diffusion restriction.


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