Seeing the Hidden Danger: How MRI Scans of Carotid Plaques Help Predict Stroke Risk

Table of Contents

• Key Points
• Why This Research Matters: Carotid Plaques and Stroke
• What Makes a Plaque Dangerous? Insights from Pathology
• How MRI Visualizes Carotid Plaques: The Technical Toolbox
• Measuring Plaque Burden: Beyond Simple Artery Narrowing
• Intraplaque Hemorrhage (IPH): The Hidden Bleeding Inside Plaques
• The Lipid-Rich Necrotic Core: The Soft Center of Danger
• The Fibrous Cap: The Plaque's Protective Shield
• Ulceration: When Plaques Break Open
• Inflammation and Neovascularization: The Plaque's Hidden Activity
• What MRI Findings Mean for Stroke Risk
• Clinical Implications: What This Means for Patients
• Limitations: What MRI Cannot Yet Tell Us
• Recommendations: What Patients Should Know
• Frequently Asked Questions
• Source Information

Key Points

• Carotid plaque MRI can identify dangerous features like intraplaque hemorrhage, lipid-rich necrotic core, and thin/ruptured fibrous cap.
• Intraplaque hemorrhage on MRI is an independent stroke risk predictor stronger than any known clinical risk factor, per a large individual-patient meta-analysis.
• MRI measures plaque burden, which accounts for Glagov remodeling and is a better risk predictor than artery narrowing alone.
• For moderate carotid stenosis, MRI-detected hemorrhage or thin/ruptured fibrous cap may lead to more aggressive treatment such as surgery or stenting.
• Carotid MRI is painless and radiation-free; it may use gadolinium contrast to better visualize plaque features.

Why This Research Matters: Carotid Plaques and Stroke

For decades, doctors focused on how narrowed the carotid arteries were when assessing stroke risk. But numerous histopathological studies (studies examining diseased tissue under a microscope) have revealed a more complex story: it is often the rupture of a vulnerable plaque, not just blood flow problems from narrowing, that triggers a stroke.

Atherosclerosis—the underlying disease—is a chronic inflammatory condition of the large arteries. It begins with the accumulation of lipids (fats) in the vessel wall and the formation of fibrous (scar-like) tissue. Plaques tend to form at artery bifurcations, where arteries branch, because of locally reduced wall shear stress (the friction force of blood flow on the vessel wall), which impairs the function of the endothelium (the artery's inner lining).

As plaques become more advanced, they develop a lipid-rich necrotic core (LRNC)—a soft, dead-fat center—separated from the bloodstream by a fibrous cap (FC). Plaques can become increasingly complex, developing calcifications, ulcerations (open sores), and intraplaque hemorrhage (IPH; bleeding inside the plaque), each change increasing the risk of rupture.

The research community has established that specific plaque features—IPH, a large LRNC, and a thin or ruptured fibrous cap (TRFC)—are strongly associated with cerebrovascular symptoms (stroke or transient ischemic attack, sometimes called a mini-stroke).

What Makes a Plaque Dangerous? Insights from Pathology

Histopathological studies have played a crucial role in building the concept that rupture of the fibrous cap, followed by blood clot formation (thrombosis) and embolization (a clot traveling to the brain), is the most important cause of stroke and myocardial infarction (heart attack).

Patients with symptomatic carotid artery disease (those who have already had a stroke or mini-stroke) consistently show:

• An enlarged lipid-rich necrotic core
• A higher prevalence of thin or ruptured fibrous caps

Inflammation is another hallmark of vulnerable plaques, mainly represented by activated macrophages (immune cells that engulf debris). Leaky angiogenic micro-vessels (new, fragile blood vessels that grow into the plaque) can serve as entry points for inflammatory cells and red blood cells, causing further plaque destabilization.

IPH is considered a key factor associated with neurological symptoms and is thought to actively stimulate plaque progression. Importantly, the histological (microscopic) plaque composition in patients who underwent carotid endarterectomy (CEA; surgery to remove plaque from the carotid artery) is an independent predictor of future cardiovascular events.

In short, pathology research identified the key imaging targets: macrophage-mediated inflammation, new blood vessel growth (neo-angiogenesis), IPH, large LRNC, and fibrous cap status.

How MRI Visualizes Carotid Plaques: The Technical Toolbox

In the last two decades, MRI has become the preferred non-invasive imaging method for studying carotid plaque features. High-resolution, multi-contrast MRI can identify and quantify atherosclerotic plaque components, and its validity has been extensively proven using histopathology as the reference standard (Table 1 provides the sensitivity, specificity, and correlation values from validation studies). Large multicenter MRI studies have confirmed its feasibility in real-world settings.

Toussaint and colleagues were the first to show that MRI allows in-vivo (living body) discrimination of the LRNC, calcifications, and IPH. A year later, von Ingersleben and colleagues confirmed that hemorrhagic regions, calcium, lipid deposits, and fibrous tissue within carotid plaques could all be identified using MRI.

Different plaque components can be distinguished by combining various MRI pulse sequences:

• Pre- and post-contrast T1-weighted (T1w) turbo-spin echo — for identifying the LRNC and fibrous cap
• Magnetization-prepared rapid acquisition gradient echo (MPRAGE) — especially sensitive for detecting IPH
• Time of flight (TOF) — a bright-blood sequence used to visualize the artery lumen and juxtaluminal calcifications

Fat suppression is required to reduce signals from perivascular and subcutaneous adipose (fat) tissue. Black blood pre-pulses are crucial to optimize the contrast between the vessel wall and the lumen. While T2-weighted (T2w) MRI was initially used to identify the LRNC, later studies revealed that contrast-enhanced MRI (CE-MRI) enables improved discrimination of the fibrous cap and LRNC compared with conventional T2w MRI.

Ultrasmall superparamagnetic iron oxide particles (USPIO, also known as ferumoxtran-10) can be used to quantify plaque inflammation, but this contrast medium is not widely available. Dynamic contrast-enhanced (DCE)-MRI allows researchers to study plaque microvasculature (the tiny blood vessels feeding the plaque).

Initially, most studies used 1.5 Tesla (T) MRI scanners. Later, 3.0T scanners enabled improved spatial resolution and a better signal-to-noise ratio (SNR)—that is, clearer images with less background interference. Dedicated multi-element carotid radiofrequency coils can be used to achieve high SNR and/or high spatial resolution, which is especially important when visualizing small structures like the fibrous cap. It has been shown that IPH can also be detected using a standard neurovascular coil, making the technique more accessible.

Recent advancements in three-dimensional (3D) sequences overcome earlier limitations of 2D black blood sequences, which were constrained by slice thickness and hampered reproducible quantification due to partial volume effects. Newer 3D sequences provide isotropic 3D images of the entire cervical carotid arteries and enable multi-planar reformatting (viewing the artery from any angle).

Novel sequences such as multi-contrast atherosclerosis characterization (MATCH) and simultaneous non-contrast angiography and IPH (SNAP) can generate multi-contrast images with a single sequence, leading to a tremendous reduction in scan time and inherent image co-registration. Expert recommendations on vessel wall MRI protocol have recently been described in a white paper.

Table 1 highlights the key validation results of carotid MRI against histology:

• IPH detection with MPRAGE: 84% sensitivity/84% specificity (Moody) and 93%/96% (validated study); SNAP vs. MPRAGE agreement κ=0.82; meta-analysis: 87% sensitivity/92% specificity
• LRNC with pre/post-contrast T1w: 98% sensitivity/100% specificity; strong correlation with histology (Pearson's r=0.84, P<0.001); inter-observer agreement ICC 0.89 (95% CI: 0.81–0.93)
• LRNC with T2w (when contrast is contraindicated): 85%/92%, 90%/84%, and 95%/76% in different studies; correlation with histology r=0.75 (P<0.001); inter-reader reproducibility ICC 0.92 (95% CI: 0.82–0.97)
• Thin/ruptured fibrous cap with pre/post-contrast T1w: correlation with histology r=0.80 (P<0.001); inter-observer agreement ICC 0.78 (95% CI: 0.68–0.86); with T2w or TOF: 90% sensitivity/84% specificity; agreement with histology κ=0.87
• Calcifications with bright blood plus one other weighting: correlation with histology r=0.74 (P<0.001); inter-observer agreement ICC 0.9 (95% CI: 0.77–0.96); agreement with histology κ=0.75 (95% CI: 0.66–0.84)
• Ulceration with contrast-enhanced MR angiography (CE-MRA): inter-observer agreement κ=0.86 (95% CI: 0.77–0.95); with TOF: 81% sensitivity/90% specificity; κ=0.72 (95% CI: 0.58–0.86); SNAP vs. conventional multi-contrast κ=0.82 (95% CI: 0.65–0.99)

Measuring Plaque Burden: Beyond Simple Artery Narrowing

Luminal stenosis (the percentage of artery narrowing) does not adequately represent the true plaque burden. This is because of Glagov remodeling—the artery's compensatory enlargement in response to plaque growth. The vessel wall expands outward, so a severely diseased artery may still appear open on traditional angiography.

Therefore, imaging modalities that assess vessel wall dimensions—the actual amount of plaque—provide a more accurate measure of plaque size and severity than stenosis measurement alone. MRI is the most suited imaging technique for this because it obtains high-resolution 3D images with high contrast between the vessel wall, the lumen, and the surrounding tissue.

Plaque burden measurements are commonly obtained by subtracting the luminal (inner) area from the area encompassing the outer vessel wall, summing these areas across all MRI slices, and multiplying by slice thickness (accounting for slice gap). The normalized wall index (NWI)—defined as the wall area divided by the total vessel area—was proposed to account for the varying sizes of carotid arteries among individuals. It is a highly accurate and reproducible measure.

Early black blood MRI using double inversion recovery prepulses revealed that MRI measurements of vessel wall dimensions (wall volume, maximum wall area, and minimum luminal area) are highly correlated with volumetric measurements of removed carotid plaque specimens (Pearson's R≥0.90). The quadruple inversion recovery technique was later developed to acquire black blood images before and after contrast injection using the same sequence.

MRI can also measure the common carotid artery wall dimensions. These correlate well (r=0.89, P<0.001) with intima-media thickness (IMT) measured by B-mode ultrasound, but with much smaller measurement variability for MRI. This means that when using common carotid artery wall thickness as a surrogate measure in cardiovascular prevention trials, smaller sample sizes and potentially shorter study durations may be possible with MRI compared to ultrasound.

The authors also note a point of confusion in the literature: some ultrasound studies have measured the thickness of the far wall of the distal common carotid artery at a site where there is no plaque, while others included plaque thickness in their IMT measurement. The latter approach results in invalid comparisons, since vessel wall thickness in patients with and without plaque represents distinct features.

Intraplaque Hemorrhage (IPH): The Hidden Bleeding Inside Plaques

To date, IPH is the most widely described predictor of stroke from carotid plaque MRI. This bleeding inside the plaque appears as a hyper-intense (bright) signal compared to surrounding muscle tissue on MPRAGE images—a finding first presented by Moody and colleagues.

The brightness occurs because of the relatively short T1 relaxation time of methemoglobin (a form of hemoglobin found in older blood). IPH is therefore hyper-intense on all T1-weighted images. Cappendijk and colleagues demonstrated a high detection rate of IPH on MPRAGE images (also known as T1-weighted inversion recovery turbo-field echo, or IR-TFE) using histology as the reference standard, with detection rates greater than 80%.

The IR-TFE sequence performed superior to a black blood T1w turbo-spin echo (TSE) sequence for IPH detection. Inter-observer agreement was high for IR-TFE (κ=0.73) but low for the T1w TSE sequence (κ=0.35). Ota and colleagues confirmed that MPRAGE has higher specificity (97%) and sensitivity (80%) for IPH detection compared to fast-spin echo and TOF sequences.

Semi-automatic quantification of IPH volume on MRI correlates well with histology. IPH can also be identified on contrast-enhanced MR angiography (CE-MRA) mask images. The newer 3D-SNAP sequence detects lumen stenosis and IPH in a single sequence with inherent image co-registration, and its performance for identifying IPH is comparable to MPRAGE (κ=0.82).

The MATCH sequence simultaneously obtains three different contrast weightings (hyper-T1w, T1w, and gray blood) in a 5-minute scan to image IPH, LRNC, and calcifications. However, larger validation studies for MATCH are still required.

A meta-analysis on the diagnostic performance of MRI for detecting IPH across multiple studies revealed excellent specificity (92%) and good sensitivity (87%). Additionally, carotid plaque T1 mapping has been developed to obtain more quantitative, reproducible measurements of IPH.

The Lipid-Rich Necrotic Core: The Soft Center of Danger

The lipid-rich necrotic core (LRNC) has a short transverse relaxation time (T2) compared to surrounding fibrous tissue, which means it appears hypo-intense (dark) on T2-weighted images. Later research showed that the contrast between the LRNC and fibrous tissue actually increases after contrast injection.

On contrast-enhanced T1-weighted images, the LRNC appears as a focal non-enhancing region—a dark spot that does not light up because the necrotic (dead) core has no blood supply to carry the contrast agent into it. This is a key identifying feature.

One practical advantage of contrast-enhanced images: the LRNC area can be measured more reproducibly on contrast-enhanced than on pre-contrast-enhanced images. The coefficient of variation (a measure of measurement variability) decreased from 33.5% to 17.6% for inter-reader measurements, meaning contrast enhancement roughly halved the variability between different readers.

The Fibrous Cap: The Plaque's Protective Shield

Fibrous cap rupture exposes the thrombogenic (clot-promoting) interior of the plaque to platelets and coagulation factors in the blood. This can lead to thrombus formation (a blood clot) and distal embolization (the clot traveling downstream to block a brain vessel), with clinical consequences like stroke.

Hatsukami and colleagues were the first to show that fibrous cap status can be determined with MRI using a 3D TOF sequence. High sensitivity (0.81) and specificity (0.90) for identifying fibrous cap status were achieved by combining multiple sequences (TOF, T1w, proton density, and T2w).

Contrast-enhanced MRI, using a gadolinium-based contrast agent, enables direct measurement of fibrous cap dimensions. After gadolinium administration, the fibrous cap strongly enhances (lights up), whereas the LRNC enhances only slightly—a difference that allows clear distinction between these two structures. Inter-observer agreement for assessing fibrous cap status using pre- and post-contrast T1w TSE MRI is good (κ=0.64–0.74).

Ulceration: When Plaques Break Open

Computed tomography angiography (CTA) is considered the best noninvasive imaging method for evaluating carotid plaque ulceration, with a sensitivity of 94% and specificity of 99%. However, MR angiography (MRA) can also identify carotid ulcerations with sensitivity similar to CTA.

CE-MRA was found to be superior (sensitivity: 82%) to TOF-MRA (sensitivity: 55%) for detecting carotid ulcerations. CE-MRA carries an additional advantage: it can identify ulcerations in heavily calcified plaques—a situation that is considered a limitation of CTA because calcium causes streaking artifacts that obscure detail.

Adding a longitudinal black blood MRA to a cross-sectional multi-sequence vessel wall MRI protocol increases the accuracy of detecting carotid atherosclerotic plaque ulcerations.

Inflammation and Neovascularization: The Plaque's Hidden Activity

Inflammation is a key driver of plaque vulnerability, and MRI can assess it indirectly. DCE-MRI (dynamic contrast-enhanced MRI) allows researchers to quantify plaque microvasculature. The Ktrans value (volume transfer coefficient), derived from pharmacokinetic modeling of DCE-MRI data, showed a significant correlation with excised plaque neo-vascularity (new blood vessel growth), with correlation coefficients (R) ranging from 0.41 to 0.70 across studies.

This technique is highly reproducible and reliable, with a coefficient of variation of 16% for Ktrans measurements. In simpler terms, repeated measurements produce consistent results within about a 16% margin of variability.

Alternatively, gadofosveset-enhanced MRI can visualize plaque microvasculature without the need for pharmacokinetic modeling. USPIO (ferumoxtran-10) particles are taken up by macrophages, and their presence on MRI has been shown to correlate strongly with carotid plaque macrophage infiltration on histology. However, ferumoxtran-10 is not broadly available. As an alternative, PET/MRI (positron emission tomography combined with MRI) can be used to study plaque inflammation and composition in a single examination.

What MRI Findings Mean for Stroke Risk

Multiple proof-of-concept studies have demonstrated the ability of MRI to distinguish high-risk from low-risk plaques. Enlarged plaque burden, IPH, LRNC, thin or ruptured fibrous cap, inflammation, and neovascularization are all more common in symptomatic lesions (those that have already caused symptoms).

Cross-sectional evidence linking plaque features to stroke:

Studies have shown that carotid plaque burden is greater in patients with recurrent stroke than in those with first-time stroke. Carotid plaque burden is significantly associated with ipsilateral acute cerebral infarction volume (the amount of brain tissue damaged by a stroke on the same side), independent of the degree of carotid stenosis.

Liu and colleagues showed that carotid plaque burden in patients with ≥1.5 mm carotid plaques was associated with the presence of acute stroke. Based on numerous ultrasound studies, plaque burden is a better parameter for risk prediction than measurement of the common carotid artery intima-media thickness.

IPH and stroke risk: Carotid IPH is strongly associated with ipsilateral stroke (stroke on the same side as the plaque) in patients with ≥50% carotid stenosis. Notably, IPH is more prevalent on the symptomatic side. It was found in 60% of ipsilateral carotid arteries versus 36% of contralateral, asymptomatic arteries.

Perhaps most striking is the finding in patients diagnosed with cryptogenic stroke (a stroke with no identifiable cause after standard workup) who have non-stenotic (<50%) carotid plaques. Several studies have reported a higher prevalence of IPH on the ipsilateral side in these patients, suggesting that IPH may well have been the underlying cause of the stroke in a meaningful subgroup of these patients. This challenges the traditional view that only severely narrowed arteries require attention.

Clinical Implications: What This Means for Patients

The findings from this review have significant implications for stroke prevention:

1. IPH as a powerful stroke predictor: In a large meta-analysis based on individual patient data from both asymptomatic and symptomatic individuals with carotid artery stenosis, IPH detected on MRI was shown to be an independent risk predictor for stroke—stronger than any known clinical risk parameter (such as blood pressure, cholesterol levels, or degree of stenosis).
2. Risk reclassification: For patients with moderate carotid stenosis (where treatment decisions are often uncertain), the presence of IPH or a thin/ruptured fibrous cap on MRI could tip the balance toward more aggressive intervention, such as carotid endarterectomy (surgical removal of plaque) or stenting.
3. Guidance for cryptogenic stroke: In patients with cryptogenic stroke and non-stenotic plaques, carotid MRI can help identify IPH as a probable cause, which may change management strategies.
4. Monitoring treatment effects: Carotid MRI can be used to evaluate whether treatments (such as statins or other medications) are reducing plaque burden, shrinking the lipid-rich necrotic core, or thickening the fibrous cap over time.
5. Standardized protocols: Expert recommendations on carotid plaque MRI protocols were published in a white paper, which will help standardize imaging across centers and facilitate wider clinical adoption.

Limitations: What MRI Cannot Yet Tell Us

While carotid plaque MRI is a powerful and well-validated technique, several limitations remain:

• Contrast agent availability: Some specialized contrast agents, particularly ferumoxtran-10 (USPIO) for inflammation imaging, are not widely available in clinical practice.
• Technical complexity: The most accurate assessments require multiple pulse sequences, which increases scan time and requires specialized expertise in both acquisition and interpretation.
• Validation gaps: While MPRAGE and conventional multi-sequence protocols are extensively validated, newer multi-contrast sequences like MATCH still require larger validation studies before they can be widely adopted.
• 2D sequence limitations: Older 2D black blood sequences are limited by slice thickness, which hampers reproducible quantification due to partial volume effects—though newer 3D sequences largely overcome this.
• Statistical correlation vs. causation: While the associations between MRI-identified plaque features and stroke are strong, some cross-sectional studies cannot prove causality. Longitudinal studies, however, are increasingly addressing this gap.

Recommendations: What Patients Should Know

Based on the evidence presented in this review, here is what patients should understand:

• Carotid MRI is not yet a routine test for everyone. It is currently most valuable for patients with moderate carotid stenosis where treatment decisions are uncertain, and for selected patients with cryptogenic stroke where a non-stenotic plaque may be the hidden cause.
• If your doctor recommends a carotid MRI, it is a painless, non-invasive procedure with no ionizing radiation. You will lie still in the scanner while images are acquired, and you may receive an intravenous contrast agent (gadolinium) to help visualize plaque features more clearly.
• Ask about plaque features, not just stenosis. If you undergo carotid imaging, ask your doctor whether the report mentions plaque composition—particularly the presence of intraplaque hemorrhage (IPH), a lipid-rich necrotic core, or a thin/ruptured fibrous cap. These features carry important risk information beyond the degree of narrowing.
• IPH matters even without significant narrowing. The evidence suggests that even plaques causing less than 50% stenosis can be dangerous if they contain hemorrhage. If you have had a stroke of unclear cause (cryptogenic stroke), carotid plaque MRI may help identify the underlying mechanism.
• MRI can track treatment response. Ask whether repeat MRI might be useful to see if your plaque is responding to medications such as statins over time.
• Continue proven prevention strategies. While MRI provides powerful new information, it complements—not replaces—standard stroke prevention measures: controlling blood pressure, managing cholesterol, not smoking, and following your doctor's recommendations regarding medications (such as antiplatelet agents and statins).

Frequently Asked Questions

What is a vulnerable plaque and why does it increase stroke risk?

A vulnerable plaque is a soft, unstable fatty buildup in the carotid artery. Rather than the degree of narrowing, its rupture is a major cause of stroke. Dangerous features include intraplaque hemorrhage, a large lipid-rich necrotic core, and a thin or ruptured fibrous cap. MRI can identify these features inside the plaque.

How does MRI help predict stroke risk from carotid plaques?

MRI is a radiation-free imaging method that can see inside carotid plaques. It identifies features linked to higher stroke risk, such as intraplaque hemorrhage, large lipid-rich necrotic core, thin or ruptured fibrous cap, ulceration, and inflammation. MRI also measures plaque burden, which is more accurate than simple artery narrowing for assessing severity.

What is intraplaque hemorrhage (IPH) and how does MRI detect it?

Intraplaque hemorrhage is bleeding inside the plaque. On MRI, it appears as a bright signal on MPRAGE or T1-weighted images. IPH is strongly associated with stroke on the same side and is more common in symptomatic carotid arteries. A meta-analysis showed MRI detects IPH with 87% sensitivity and 92% specificity.

I have moderate carotid stenosis. Could MRI change my treatment?

Yes, possibly. In patients with moderate carotid stenosis, treatment decisions are sometimes uncertain. If MRI shows intraplaque hemorrhage or a thin/ruptured fibrous cap, this could lead to more aggressive treatments, such as carotid endarterectomy or stenting. However, carotid MRI is not yet a routine test for everyone.

Is a carotid MRI safe and does it involve radiation?

Carotid MRI is a painless, non-invasive procedure that uses no ionizing radiation. You lie still in the scanner while images are taken. You may receive an intravenous contrast agent called gadolinium to help visualize plaque features more clearly. It is generally considered safe, but discuss any concerns with your doctor.

What does a lipid-rich necrotic core mean for my stroke risk?

A lipid-rich necrotic core is a soft, dead-fat center inside the plaque. It appears as a dark, non-enhancing region on contrast-enhanced MRI. Larger cores are found in patients with symptoms, and this feature is associated with plaque rupture. MRI can measure it, helping assess your risk beyond just the degree of narrowing.

Can MRI show if my stroke-prevention treatment is working?

Yes. Repeat carotid MRI can evaluate whether treatments such as statins are reducing plaque burden, shrinking the lipid-rich necrotic core, or thickening the fibrous cap over time. This can help your doctor monitor how well your medication is working and adjust your treatment plan as needed.

Should I get a second opinion before deciding on carotid surgery if my MRI shows intraplaque hemorrhage but my stenosis is only moderate?

A second opinion is particularly useful when your carotid MRI shows intraplaque hemorrhage (IPH) or a thin or ruptured fibrous cap, but your carotid narrowing is only moderate. These high-risk plaque features can be more important than the degree of stenosis, and may change the decision about surgery or stenting. A second opinion can review your images and confirm whether the MRI findings truly warrant more aggressive treatment, or whether conservative medical management is appropriate. Diagnostic Detectives Network provides independent expert second opinions.

Source Information

Original article: "Magnetic resonance imaging of carotid plaques: current status and clinical perspectives"

Authors: Mohamed Kassem, Alexandru Florea, Felix M. Mottaghy, Robert van Oostenbrugge, M. Eline Kooi

Journal: Annals of Translational Medicine, Vol 8, No 19, October 2020, page 1266. Published in the special series "Carotid Artery Stenosis and Stroke: Prevention and Treatment Part I"

DOI: 10.21037/atm-2020-cass-16

Affiliations: CARIM School for Cardiovascular Diseases, Maastricht University, The Netherlands; Department of Radiology and Nuclear Medicine, Maastricht University Medical Center (MUMC+), The Netherlands; Department of Nuclear Medicine, University Hospital RWTH Aachen, Germany; Department of Neurology, MUMC+, The Netherlands.

This patient-friendly article is based on peer-reviewed research. It is intended for educational purposes and should not replace professional medical advice. Always consult your healthcare provider about your specific condition and treatment options.