Cerebral Hyperperfusion Syndrome (CHS)

KEY FACTS

TERMINOLOGY

• Rare (1-3%) disorder most commonly occurring as

complication of cerebral revascularization

○ Other etiologies less common

– Status epilepticus

– MELAS

• Major increase in ipsilateral cerebral blood flow (CBF) well

above normal metabolic demands

IMAGING

• Ipsilateral gyral swelling, sulcal effacement in post-carotid

endarterectomy (CEA) patient

• ↑ CBF, CBV on perfusion MR, perfusion CT

TOP DIFFERENTIAL DIAGNOSES

• Acute cerebral ischemia-infarction

• Status epilepticus

• MELAS

• Acute hypertensive encephalopathy, PRES

• Hypercapnia

PATHOLOGY

• Cerebral hyperperfusion syndrome (CHS) probably caused

by maladaptive autoregulatory mechanisms, altered

cerebral hemodynamics

○ Normal perfusion pressure breakthrough

○ Rapid restoration of normal perfusion following

revascularization → hyperperfusion in previously

underperfused brain

CLINICAL ISSUES

• ~ 3% of post-CEA patients develop CHS

• Classic: Triad of unilateral headache, neurologic deficit, &

seizures

○ Variable cognitive impairment; ipsilateral face, eye pain

DIAGNOSTIC CHECKLIST

• Need to distinguish stroke/TIA from CHS

(Left) A 56-year-old man with

> 70% stenosis of proximal left

cervical ICA underwent carotid

endarterectomy. A few hours

after surgery, he became

acutely confused and

developed right-sided

weakness; perfusion source

image shows markedly

increased vasculature in the

left hemisphere ﬊. (Right) CT

perfusion obtained in the

same patient appears

relatively normal, but cerebral

blood flow on the left (as

measured by circled regions of

interest 2a, 2b) increased

compared to the right side (1a,

1b).

(Left) Time to peak (TTP) in

the same patient is even more

striking. The abnormal side is

not the right middle carotid

artery distribution (green) but

is the left side ſt (blue),

where the TTP is markedly

shortened. (Right) Axial T2WI

in the same patient shows

gyral swelling, sulcal

effacement, and

hyperintensity in the left

temporal and parietooccipital

cortex/subcortical white

matter ſt, basal ganglia st.

DWI (not shown) was normal.

This is a classic example of

postcarotid endarterectomy

hyperperfusion syndrome.

Trauma, and Stroke

Brain: Pathology-Based Diagnoses: Malformations,

103