Files

T

Ross f8775d1f7e .

2025-10-21 21:56:33 +01:00

31 KiB

Raw Permalink Blame History

title, docid, authors, breadcrumbs, category, cmeTopicId, documentVersionId, imageCount, lastUpdated, pageDescription, pageKeywords, pageTitle, enhancedTitle, type, references, breadcrumbs

title

docid

authors

breadcrumbs

KEY FACTS

Terminology
- Reversible stenosis of intracranial arteries
- Caused by exposure to blood breakdown products
Imaging
- General features (CTA/MRA/DSA) - Typically occurs 4-14 days after subarachnoid hemorrhage (SAH) - Smooth, relatively long segmental stenoses - Seen as arterial luminal irregularity/undulations - Multiple arteries, usually > 1 vascular territory
- Transcranial Doppler (TCD) - > 80% accuracy for vasospasm detection if mean velocity in MCA > 120 cm/s, basilar artery > 70 cm/s - Lindegaard ratio 3-6 mild to moderate vasospasm; ratio > 6 severe vasospasm - ↑ flow velocities with Lindegaard ratio < 3 suggest hyperemia or other physiologic/induced state
- CT perfusion - ↑ TTD, ↑ TTP, ↑ MTT, ↓ cerebral blood flow (CBF) - ↓ cerebral blood volume (CBV) in areas of infarct - TTD best parameter for delayed cerebral ischemia
- Vessel wall MR (VW-MR) - Vessel wall enhancement → vasospasm later
Top Differential Diagnoses
- Reversible cerebral vasoconstriction syndrome (RCVS), vasculitis, atherosclerosis - VW-MR helps in differentiation
- Flow diverter-induced subacute segmental vasospasm - 3-5 weeks after flow diversion, obscure pathophysiology
- Meningitis, acute hypertensive encephalopathy (PRES), migraine headache
Pathology
- Blood breakdown products (e.g., oxyHgb) coat vessel walls → release of free radicals from vessel wall
- Multifactorial-like release of factors like serotonin, ↓ nitric oxide activity from endothelium, ↑ endothelin-1 activity
- Prolonged exposure of vessel wall to blood components
Clinical Issues
- Delayed ischemic neurological deficit (DIND) - ~ 1 week after SAH is typical
- "Triple H" therapy
- Endovascular (chemical or balloon angioplasty)
Diagnostic Checklist
- TCD for proximal arteries, DSA for more distal vasospasm

TERMINOLOGY

Synonyms
- Subarachnoid hemorrhage (SAH) vasospasm
Definitions
- Exposure to blood breakdown products → reversible stenosis of intracranial arteries - Mild vasospasm: < 25% reduction in vessel patency - Severe vasospasm: > 50% reduction in vessel patency

IMAGING

General Features

Best diagnostic clue

- Segmental stenoses (CTA/MRA/DSA)
        - DSA is gold standard; typically 4-14 days after SAH

Location

- Affects any intradural (subarachnoid) artery
- Worst vasospasm typically adjacent to site of ruptured aneurysm (highest concentration of SAH)

Imaging Recommendations

Best imaging tool

- Gold standard is DSA (100% sensitive but nonspecific)
        - May follow with intraarterial (IA) therapy
- Transcranial Doppler (TCD) useful as bedside monitoring/screening tool

Protocol advice

- Multiterritorial vascular involvement is typical
- Visualize both carotids, dominant vertebral artery

CT Findings
- NECT
```
- May see residual SAH
- Otherwise normal (unless ischemia/stroke)
- Hypodensity in involved vascular territory may herald ischemia/infarction
- Differentiate from retraction edema
        - Adjacent to surgical clip, not confined to vascular territory
```
- CTA
```
- Screening tool for involvement of large vessels
        - Circle of Willis, M1 segment, basilar artery
- Attenuation/stenosis of arteries
        - Typically multiterritorial but asymmetric
- Insensitive for smaller vessels (e.g., M2, distal segments)
```
- CT perfusion (pCT) - Hypoperfusion - Ischemic penumbra: ↑ TTD, ↑ TTP, ↑ MTT, ↓ cerebral blood flow (CBF) - Preserved or ↑ cerebral blood volume (CBV) indicates adequacy of collateral flow - Irreversible ischemia with infarct: Further worse above parameters, & CBV is critically low - TTD best parameter for delayed cerebral ischemia - TTD defined as time to start + MTT; measures time for contrast agent to pass away from analyzed voxel - Diagnostic accuracy for TTD & MTT significantly higher than other perfusion parameters - TTD higher sensitivity than MTT; severity of vasospasm on TTD maps significantly higher correlation with DSA than other perfusion maps - pCT maps generated using deconvolution algorithm (CBV, CBF, MTT, TTD) better than maps using maximum slope method (CBV, CBF, TTP) - Deconvolution method provides significantly higher diagnostic accuracy for detecting arterial vasospasm, & higher correlation with angiographic findings - May miss distal vasospasm if pCT limited to 2 slices - Whole brain volume pCT recommended
MR Findings
- DWI
```
- Most sensitive for vasospasm sequelae
        - If ischemia → infarction
```
- MRA
```
- Not usually utilized for screening
- CT more easily performed in patients in ICU S/P SAH
- Vessel stenosis → signal void on TOF imaging
        - Depends on vasospasm severity
```
- Vessel wall MR (VW-MR) - Vessel wall enhancement (concentric in majority, eccentric in few) after endovascular treatment of ruptured aneurysms → angiographic vasospasm later - Consider early preventive treatment to reduce potential severe morbidity & mortality - Arterial wall enhancement in aneurysmal SAH likely due to inflammation & ultrastructural vessel wall changes - Like tight junction disruption & endothelial & smooth muscle cell injury - Endovascular procedure-related arterial vessel wall enhancement in segments which underwent balloon or stent-assisted coiling or flow diverter stenting - May not → subsequent vasospasm - Be aware of flow diverter-induced subacute segmental vasospasm at ~ 1 month - Number of enhancing vessel wall segments much lower with treated unruptured aneurysms - Could be even preexisting nonstenotic atherosclerotic plaques not detected on luminal imaging
Ultrasonographic Findings
- TCD - Bernoulli principle: ↑ mean flow velocity occurs due to ↓ arterial cross-sectional area from vasospasm/stenosis - Low-frequency transducer used to evaluate larger arteries at base of brain - Transtemporal window absent in 10% of patients - > 80% accuracy for vasospasm detection if mean velocity in middle cerebral artery (MCA) > 120 cm/s, basilar artery > 70 cm/s - Mean MCA velocity: Normal 55 cm/s; vasospasm: Mild > 120, moderate > 160, & severe > 200 cm/s - Lindegaard ratio: Mean MCA velocity:ipsilateral extracranial internal carotid artery (ICA) velocity ratio - Ratio 3-6 mild to moderate vasospasm; ratio > 6 severe vasospasm - ↑ flow velocities with Lindegaard ratio < 3 suggest hyperemia or other physiologic/induced state - Sensitivity ~ 60% (operator dependent) - Specificity > 95% (in patients with known SAH) - Upward trends in mean velocities may be more indicative of vasospasm than absolute values
Angiographic Findings
- Arterial luminal irregularity/undulations
- Smooth, relatively long-segment stenoses - Multiple arteries, > 1 vascular territory typical

DIFFERENTIAL DIAGNOSIS

Atherosclerosis
- Usually older patients
- Short- > long-segment stenoses
- Cavernous/extracranial ICA, vertebral artery often affected
- VW-MR shows eccentric arterial wall thickening - With contrast-enhancing inner layer of plaque near lumen, outer nonenhancing layer, & occasionally another enhancing thin layer at periphery
Reversible Cerebral Vasoconstriction Syndrome, Migraine Headaches
- Transient, may look identical
- VW-MR shows no enhancement or only minimal concentric arterial wall enhancement
- Sometimes more than minimal wall enhancement, cannot be differentiated from vasculitis then
- Arterial smooth muscle cells shorten & overlap → 5x ↑ in wall thickness for 60% luminal narrowing
Vasculitis
- Can look identical to vasospasm, reversible cerebral vasoconstriction syndrome; typically shorter segmental stenoses/"beading" in vasculitis
- Absence of SAH on NECT is typical (SAH secondary to vasculitis is rare) - Subacute SAH may be iso-/hypodense on NECT; CSF analysis may help to detect blood breakdown products
- Inflammatory markers in serum, CSF often elevated
- VW-MR typically shows smooth, homogeneous, concentric arterial wall thickening & enhancement
- Vasculitis sometimes shows eccentric wall findings like atherosclerosis (but lacks layered plaque appearance)
Flow Diverter-Induced Subacute Segmental Vasospasm
- Frequent pathophysiologically obscure vascular reaction after aneurysm treatment with flow diverters in small cerebral arteries
- Potentially cause symptomatic ischemia or stroke, 3-5 weeks post procedure
Acute Hypertensive Encephalopathy
- Posterior > anterior circulation
Meningitis
- Sulcal/cisternal enhancement

PATHOLOGY

General Features

Etiology

- SAH vasospasm most commonly seen after aneurysm rupture
        - Other causes of SAH (e.g., trauma, arteriovenous malformation rupture) may also cause vasospasm
        - Diffuse nonaneurysmal SAH has potential for vasospasm similar to aneurysmal SAH (aSAH)
- Exact pathophysiology unknown, likely multifactorial
        - Blood breakdown products (e.g., oxyHgb) coat vessel walls → release of free radicals from vessel wall
        - Release of factors, including serotonin, angiotensin, prostaglandins, thromboxane, protein kinase C, phospholipase C & A2
        - Possible role of ↓ nitric oxide activity from endothelium, ↑ endothelin-1 activity

Staging, Grading, & Classification
- Fisher CT score corresponds to risk of vasospasm development - 1: No SAH - 2: Small SAH, < 1-mm vertical layers - 3: Extensive SAH, > 1-mm vertical layers - 4: Intraventricular hemorrhage
Microscopic Features
- Prolonged exposure of vessel wall to blood components → thickening of tunica media, intimal edema, subintimal cellular proliferation with muscle cells & fibroblasts

CLINICAL ISSUES

Presentation

Most common signs/symptoms

- 70% of patients after aSAH develop vasospasm seen on DSA; only 30% symptomatic
- Vasospasm is significant source of morbidity & mortality in patients with SAH
- Delayed ischemic neurologic deficit ~ 1 week after SAH is typical
- Focal neurologic deficit(s): Motor, language, vision

Other signs/symptoms

- Altered mental status, ↓ level of consciousness

Demographics

Age

- Any age; more common in younger patients

Epidemiology

- 30,000 people per year have SAH in USA

Natural History & Prognosis
- ~ time course of vasospasm following SAH: Day 3-4: Vasospasm begins; day 7-10: Vasospasm peaks; day 14-21: Vasospasm subsides
- Hyperacute vasospasm occurs in 10% of patients (onset < 48 hours from SAH)
- Flow diverter-induced subacute segmental vasospasm occurs at 3-5 weeks
- Aggressive treatment/prophylaxis in SAH patients can prevent stroke, death from ischemic sequela
Treatment
- Medical management - "Triple H" therapy: Hypertension, hemodilution, hypervolemia - Oral or IV Ca⁺⁺ antagonists (e.g., nimodipine) - Magnesium
- Endovascular - Chemical angioplasty: IA infusion of Ca⁺⁺ antagonist has superseded papaverine - Less technically demanding than balloon angioplasty, can treat smaller distal vessels - Duration of effect may be up to 24 hours, additional IA treatments may be needed - Relatively low risk: Side effect = hypotension, which could exacerbate hypoperfusion - Balloon angioplasty - Progressive dilatation of larger basal arteries: Intradural ICA & vertebral arteries, basilar artery, MCA (M1 ± M2 segments), anterior cerebral artery (ACA) (A1 segment), posterior cerebral artery (PCA) (P1 segment) - 1% risk of fatal vessel rupture, thromboembolic stroke, vessel dissection - Intracisternal thrombolytic therapy - Several clinical trials have shown moderate success; not widely accepted Rx - Recombinant tPA infused via ventriculostomy to lyse blood in subarachnoid spaces → ↓ breakdown to oxyHgb → prevent vasospasm

DIAGNOSTIC CHECKLIST

Consider
- Vasospasm as etiology of clinical deterioration, ischemic changes on NECT 4-14 days after aSAH
Image Interpretation Pearls
- TCD is insensitive to changes in vessels beyond intradural ICA, M1, A1, & basilar arteries - Do DSA if more distal vessel involvement suspected (e.g., pericallosal aneurysm rupture, nonaneurysmal SAH)

45be7813-c057-4ff8-b70a-520e014e7ab9

References

Selected References

Images

Selected Images

Autopsied case of ruptured MCA aneurysm with subarachnoid hemorrhage (SAH) in a patient who survived several days shows severe vasospasm of the parent MCA .

T1 SPACE C+ vessel wall MR (VW-MR) in a patient with SAH shows concentric enhancement in multiple MCA branches . DSA after a few days shows mutifocal MCA branch stenoses . Consider early preventive measures initiation to reduce vasospasm later, if VW-MR done during presentation with SAH shows arterial wall enhancement.

AP right ICA DSA in a patient with SAH in right sylvian & anterior interhemispheric fissures shows severe vasospasm in the right MCA M1 & M2 segments & in the right ACA A2 segment & carotid terminus .

DSA after 25-mg verapamil infusion into right ICA shows increase in caliber of all vasospastic segments. The patient received additional IA verapamil in the following days. Recurrent vasospasm after chemical angioplasty is to be expected, but balloon angioplasty is more durable.

Coronal reformatted NECT in a patient with severe headache shows extensive hyperdense acute SAH in the bilateral MCA cisterns, sylvian fissures, suprasellar cistern, & anterior interhemispheric fissure. Note a slight hyperdense space occupying lesion (SOL) in the left inferior frontal parasagittal region .

Coronal reformatted MIP image of a CT angiogram in the same setting shows that the SOL is actually a ruptured left terminal ICA aneurysm . Patient underwent emergent aneurysm coiling.

CT perfusion done after 4 days, axial time to drain (TTD) CT perfusion map generated using deconvolution algorithm (DC) shows abnormal increased TTD in bilateral parasagittal frontoparietal ACA territories .

Axial mean transit time (MTT) CT perfusion map generated using DC shows abnormal increased MTT in the same regions . Cerebral blood flow (CBF) was also reduced in these regions (not shown). As seen here, TTD has higher sensitivity to demonstrate ischemia than other color parametric maps.

AP DSA of the right ICA in the same patient 3 hours after the CT perfusion study shows severe right A1 ACA and mild right M1 MCA vasospasm.

AP DSA of the left ICA shows severe left M1 MCA vasospasm. The left A1 ACA also had vasospasm seen in oblique projections (not shown). Vasospasm responded well to IA verapamil (images not shown). Note the aneurysm coil mass , which completely obliterates the flow in the left ICA aneurysm. SAH-associated vasospasm usually begins after 3-4 days.

Additional Images

Axial NECT in a 43-year-old male in the ER with "worst headache of life" shows diffuse SAH in the basal cisterns, especially in the left sylvian fissure.

CT angiogram in the same patient shows a lobulated aneurysm at the left distal ICA bifurcation.

Four days after emergency clipping of the aneurysm, the patient became drowsy and developed right-sided weakness. AP DSA of the left ICA shows mass effect, vasospasm , seen here as narrowing of the proximal ACA and MCA. The patient responded well to IA infusion of verapamil.

Axial NECT in a patient S/P resection of a sphenoidal ridge meningioma complicated by significant intraoperative hemorrhage shows SAH in the right sylvian fissure and anterior interhemispheric fissure .

Axial NECT obtained 10 days later when the patient developed hemiparesis shows a focal area of low attenuation in the right frontal lobe , consistent with infarction. There is blurring of both the superficial and deep gray-white interface adjacent to the infarct.

Anteroposterior 3D TOF MRA MIP image in the same patient shows no signal from flow-related enhancement along the right M1 segment . The M2 vessels are attenuated compared with the left side, suggestive of reduced flow.

Axial DTI MR shows a large area of ischemia/infarction in the right frontal lobe . The constellation of imaging findings along with the delayed clinical deterioration 10 days after documented SAH made vasospasm the most likely etiology.

31 KiB Raw Permalink Blame History

KEY FACTS

Terminology

Imaging

Top Differential Diagnoses

Pathology

Clinical Issues

Diagnostic Checklist

TERMINOLOGY

Synonyms

Definitions

IMAGING

General Features

Best diagnostic clue

Location

Imaging Recommendations

Best imaging tool

Protocol advice

CT Findings

NECT

CTA

MR Findings

DWI

MRA

Ultrasonographic Findings

Angiographic Findings

DIFFERENTIAL DIAGNOSIS

Flow Diverter-Induced Subacute Segmental Vasospasm

PATHOLOGY

General Features

Etiology

Staging, Grading, & Classification

Microscopic Features

CLINICAL ISSUES

Presentation

Most common signs/symptoms

Other signs/symptoms

Demographics

Age

Epidemiology

Natural History & Prognosis

Treatment

DIAGNOSTIC CHECKLIST

Consider

Image Interpretation Pearls

References

Selected References

Images

Selected Images

Additional Images

31 KiB

Raw Permalink Blame History