Typical imaging findings
The main pathological changes are detected by magnetic resonance imaging. The classic MRI pattern includes bilateral hyperintense lesions affecting the cortex and subcortical white matter in the parieto-occipital lobes. These changes are best visualized on T2 and T2-FLAIR (fluid-attenuated inversion recovery) sequences.
A crucial characteristic of the typical course is an increase in apparent diffusion coefficient (ADC) values on ADC maps (ADC maps). This indicates that there is no true diffusion restriction in the affected tissues, which typically points to acute cytotoxic edema.
When performing 3D time-of-flight MR angiography (TOF MRA), irregularity of the intracranial arterial walls is frequently revealed. This phenomenon is caused by vasoconstriction. It is believed that the imaging presentation of PRES partially overlaps with reversible cerebral vasoconstriction syndrome (RCVS), and both of these conditions may belong to the same spectrum of disorders.
Severe forms and poor prognosis
In the classic variant, the pathological changes are reversible, but severe forms of the syndrome exist. They are associated with a poor prognosis, and when they develop, tissue recovery is only partial.
Reliable MRI signs of a severe course include:
- Hemorrhagic complications. Intracerebral microhemorrhages may occur, hematomas can form, or, most commonly, a subarachnoid hemorrhage may develop.
- Specific contrast enhancement. Following intravenous gadolinium administration, leptomeningeal or gyriform (following the course of the gyri) contrast enhancement is observed.
- True diffusion restriction (restricted diffusivity). Unlike the classic increase in ADC, this sign indicates deeper damage to cellular structures.
Differential diagnosis: MERS
PRES must be differentiated from mild encephalopathy with a reversible lesion of the splenium of the corpus callosum (using the abbreviations MERS, RESLES, or CLOCC).
The pathophysiology of this condition remains currently unknown. Etiologically, it develops secondary to systemic infections, infectious encephalitis, seizures, discontinuation of antiepileptic drugs, or pronounced metabolic disorders (e.g., in hypoglycemia or hypernatremia). Clinically, it manifests as encephalopathy—headache, psychiatric disorders, and altered consciousness, but strictly without disconnection syndrome.
The MRI picture of MERS has distinct differences:
- The reversible lesion is localized in the splenium of the corpus callosum (splenium of the corpus callosum).
- Hyperintensity is observed on T2-weighted images.
- True diffusion restriction is present.
- The lesions typically do not show contrast enhancement after gadolinium administration.
Note: sometimes the syndrome may be accompanied by bilateral hyperintense lesions in the frontoparietal white matter on T2, which exhibit the same reversibility as the splenium lesion.
Other similar MRI patterns
When performing differential diagnosis, the following conditions should be kept in mind:
Delayed methotrexate-induced leukoencephalopathy. Occurs after specific therapy (e.g., in the treatment of osteosarcoma). T2-FLAIR visualizes diffuse and symmetric areas of hyperintense signal in the white matter. A key differential diagnostic sign is that subcortical U-fibers remain intact. ADC maps show increased diffusion values (as in mild PRES), indicating demyelination or spongiform changes rather than acute cytotoxic edema.
Gadolinium deposition in the brain. It is important not to confuse true tissue damage with contrast retention. Risk factors include repeated injections of linear gadolinium-based chelates (e.g., during long-term monitoring of meningiomas) and chronic renal failure. Non-contrast T1-weighted images reveal symmetric zones of hyperintensity in the dentate nuclei of the cerebellum, globus pallidus, and subthalamic nuclei. To date, no neurological symptoms associated with this MRI finding have been identified.
Briefly: answers to topical questions
What diseases must be differentiated from PRES syndrome based on MRI data?
Based on MRI data, posterior reversible encephalopathy syndrome must be differentiated from reversible cerebral vasoconstriction syndrome.
- Reversible cerebral vasoconstriction syndrome (RCVS) — the imaging presentation partially overlaps with PRES; it is hypothesized that both conditions may belong to the same spectrum of disorders. Vasogenic edema in this syndrome sometimes visually resembles changes characteristic of PRES.
What clinical symptoms are characteristic of the classic course of PRES syndrome?
The classic course of posterior reversible encephalopathy syndrome is characterized by the development of a complex of neurological disorders.
The clinical presentation includes the following symptoms:
- Headache — a typical manifestation of the disease.
- Seizures — convulsive syndrome of varying severity.
- Visual impairment — visual disturbances.
- Encephalopathy — impaired brain function.
- Focal neurological deficit — focal neurological symptoms.
What pathophysiological mechanisms underlie the development of posterior reversible encephalopathy syndrome?
The development of posterior reversible encephalopathy syndrome is based on the formation of local subcortical reversible vasogenic brain edema.
Key pathophysiological mechanisms include:
- Blood-brain barrier (BBB) permeability impairment.
- Arterial hypertension — a blood pressure elevation exceeding the limits of cerebral blood flow autoregulation.
- Reversible cerebral vasoconstriction syndrome — vascular spasm.
As a result of these processes, vasogenic edema develops, predominantly affecting the white matter of the parietal, occipital, and temporal lobes.
Class and exam questions
Are pathological changes in PRES always completely reversible?
No. In severe forms of the syndrome accompanied by diffusion restriction, hemorrhages, or leptomeningeal contrast enhancement, brain changes are often only partially reversible.
How to distinguish PRES from delayed methotrexate-induced leukoencephalopathy on MRI?
The key sign of methotrexate-induced encephalopathy is the sparing of subcortical U-fibers against the background of diffuse symmetric white matter damage.
Do lesion sites show contrast enhancement in MERS?
In the vast majority of cases of mild encephalopathy with a reversible splenial lesion (MERS), the lesions do not accumulate gadolinium despite the presence of restricted diffusion.
What else to study on this topic
- Pathophysiological relationship between PRES and reversible cerebral vasoconstriction syndrome (RCVS)
- MRI semiotics of delayed methotrexate-induced leukoencephalopathy
- Etiological factors and triggers for the development of MERS (RESLES/CLOCC)
- Mechanisms of gadolinium retention in brain structures and risk factors
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