[Image Note] Reversible posterior encephalopathy syndrome (PRES)

Overview — PRES

Definition: is a clinical-imaging syndrome
with reversible neurological lesions and specific radiographic findings.

Age of onset: can occur at any age, more common in
young women.

Clinical manifestations: Acute or subacute onset depending on the location and extent of injury, mainly including: sudden increase in blood pressure, headache, nausea, vomiting, blurred vision, seizures, impaired consciousness and mental abnormalities
.
Timely and effective treatment of the cause is found, and clinical symptoms and imaging manifestations can be completely restored or restored to the pre-onset level
.

Laboratory tests: elevated LDH levels can precede clinical and imaging findings and can be used to detect the degree of
cerebral edema in patients with PRES.

pathogen

Common causes

Malignant hypertension (most common)

Pregnancy and perinatal eclampsia, preeclampsia, etc

Various serious kidney diseases (such as acute glomerulonephritis, chronic renal insufficiency, etc.
)

Application of immunosuppressive drugs and cytotoxic drugs (immunoglobulin, interferon, cyclosporine, etc.
) after organ and tissue transplantation

Oncology chemotherapy drugs (ifosfamide, cisplatin, etc.
)

Rare causes

Connective tissue diseases (e.
g.
, SLE, nodular arteritis, Behcet's disease)

Hemolytic uremic syndrome

Multi-organ failure

Thrombotic thrombocytopenic purpura

Massive blood transfusions

AIDS and alcoholism

Pathological mechanism

Cerebral perfusion pressure breakthrough theory: (most accepted)

Blood pressure rises sharply, exceeding the upper limit of cerebral vascular self-regulation, cerebral vascular passive dilation, cerebral perfusion pressure increases, capillary endothelial cells are tightly connected and open, capillary permeability increases, the blood-brain barrier is damaged, plasma components penetrate into the brain parenchyma, resulting in vasogenic edema or petechial hemorrhage without cerebral infarction
.
White matter is looser than gray matter, and liquid is easy to retain; The sympathetic nerve fibers of the posterior circulation vessels are less distributed and easy to expand, so vasogenic cerebral edema is more likely to appear in the back of the
brain.

The theory of vasospasm

Vascular endothelial injury theory

Radiographic findings

Place:

Typical site: parieto-occipital lobe, may be associated with cortical involvement
.

Atypical sites: involvement beyond the parietal occipital area (eg, only frontal and temporal lobes; posterior frontal lobe and corpus callosum pressure; It can also involve only the brainstem, cerebellum, basal ganglia, thalamus, etc.
)

Distribution: symmetrical on both sides, white matter is heavier than gray matter, and the posterior cycle is heavier than the anterior circulation
.

CT findings: lack of specificity, mostly manifested as bilateral parietal occipital lobes symmetrical patchy low-density opacities, no mass effect
.

MR performance:

T1 and other low intensity, T2 and FLAIR high intensity, FLAIR is more sensitive, can find cortical lesions
.
DWI is low or high signal, and ADC is high signal
.
There is generally no reinforcement after enhancement, but due to the destruction of the blood-brain barrier, strengthening
is occasionally seen.
May be combined with bleeding, mostly oozing, multiple or single primary swelling or microbleeding
.
MRV shows patency of cerebral veins and sinuses without stenosis, abnormal dilation, and signs of thrombosis
.