Table 1 Comparison of BSCB Pathology in Traumatic SCI, neurodegenerative disease, and DCM

Pathophysiology of BSCB breakdown and reconstitution

Etiology

• Acute blunt / penetrating trauma

• Chronic inflammation

• Chronic mechanical compression

Onset / Progression of BSCB Damage

• Rapid onset and progression

• Insidious onset and progression

Ongoing compression:

• Gradual and dependent on clinical severity

Reperfusion injury after decompression:

• Rapid onset, subacute injury

BSCB reconstitution

• Early; complete recovery by 3–4 weeks

• Unresolved, unless treatment of underlying disease

Ongoing compression:

• Unresolved due to persistent, progressive compression

After decompression:

• Reconstitution in DCM of mild to moderate clinical severity, prolonged reconstitution / persistent deficits with severe clinical severity

Histological and molecular features

Presence of edema

• Present at acute stage, resolves by 1–2 weeks

• Not present

•Infrequent, observed only in severe DCM

Cystic cavitation

• Present in 1–5 % of SCI patients [62]

• Not present

• Infrequent, observed only in severe DCM [63]

MMP9 expression

• Present

• Present

• Present

Erythrocyte or tracer dye extravasation

• Extensive extravasation upon spinal cord hemorrhage

• Continuous low-level extravasation, leading to parenchymal accumulation of cytotoxic iron and lipofuscin [64, 65]

• Erythrocyte extravasation unknown

• Evans Blue extravasation observed during ongoing compression in experimental animal models

Others

• Extravasation of hemolysates and proteases

• Prolonged BSCB permeability at sites with microglial clusters

• Enlarged perivascular space with infiltrating leukocytes

• Decreased TJs

• BSCB impairment marks early-stage ALS and precedes clinical presentation

• Swollen endothelial cells filled with caveolae-like vesicles

• Abnormal TJs with large gaps, thickened basement membrane

• Thickened basement membrane