Intracranial Aneurysm Diagnosis
Early and accurate diagnosis is critical for management and prevention of complications.
1. Clinical Presentation
Patients with an intracranial aneurysm may present with:
- Asymptomatic (incidental finding in imaging)
- Warning signs (sentinel headaches, cranial nerve palsies)
- Acute rupture → Subarachnoid Hemorrhage (SAH)
- Sudden, severe “thunderclap” headache
- Nausea, vomiting
- Photophobia, neck stiffness (meningeal irritation)
- Altered consciousness, seizures
- Focal neurological deficits (depending on aneurysm location)
2. Imaging Modalities
Different imaging techniques are used for aneurysm detection and characterization.
| Imaging Technique | Sensitivity | Specificity | Advantages | Limitations |
|---|---|---|---|---|
| Computed Tomography Angiography (CTA) | 85-95% | 90-98% | Rapid, non-invasive, good for screening | Lower resolution for small aneurysms (<3mm), bone artifacts |
| Multiphase CTA (MP-CTA) | High | High | Improves detection in slow-flow aneurysms | Lacks dynamic flow assessment |
| Magnetic Resonance Angiography (MRA) | 85-95% | High | No radiation, good for follow-up | Longer acquisition time, motion artifacts |
| Digital Subtraction Angiography (DSA) | Nearly 100% | Nearly 100% | Gold standard, dynamic blood flow assessment | Invasive, risk of stroke/vascular injury |
| Non-Contrast CT (NCCT) | Low | High for SAH | Best for acute SAH detection | Cannot visualize unruptured aneurysms |
3. When to Use Each Modality
- First-line screening → CTA or MRA
- Acute SAH suspicion → NCCT, followed by CTA
- Definitive diagnosis (unclear cases, pre-surgical planning) → DSA
- Long-term follow-up → MRA (preferred for radiation avoidance), CTA if needed
4. Risk Factors for Aneurysm Development
- Genetic predisposition (family history, connective tissue disorders)
- Hypertension
- Smoking
- Excessive alcohol consumption
- Female sex, postmenopausal status
- Previous SAH or multiple aneurysms
- Polycystic kidney disease (PKD)
5. Management Considerations
- Small, unruptured aneurysms (<5mm): Conservative management, risk factor control, follow-up imaging
- Aneurysms ≥5mm or symptomatic: Endovascular (coiling) or surgical (clipping) intervention
- Ruptured aneurysm: Urgent aneurysm occlusion and SAH management (ICU care, BP control, vasospasm prevention)
6. Conclusion
Intracranial aneurysm diagnosis requires a multi-modal imaging approach based on clinical presentation. CTA and MRA are useful for screening, while DSA remains the gold standard for definitive evaluation and treatment planning.
Screening
The low 1.14% per-person year risk of DNIA detection and small DNIA size at detection cannot justify routine screening for DNIAs in all patients with a personal history of IAs. If imaging follow-up is considered for selected patients, early screening will likely yield the most benefit in patients who continue to smoke cigarettes 1).
Since its introduction, digital subtraction angiography has been considered the gold standard in diagnostic imaging for neurovascular disease. Modern post-processing techniques have made angiography even more informative to the cerebrovascular neurosurgeon or neurointerventionalist.
In patients with a head computed tomography scan performed less than 6 h after headache onset and reported negative by a staff radiologist, lumbar puncture can be withheld. 2). Intracranial vascular lesions, such as a vascular loop, infundibulum, and stump of an occluded vessel, are sometimes misdiagnosed as aneurysms during imaging examinations 3).
It is difficult to differentiate such lesions from aneurysms on the basis of imaging findings 4) 5).
For Aneurysmal subarachnoid hemorrhage diagnosis in the early phase, during the first 24 hours, cerebral CT, combined with intracranial CT angiography is recommended to make a positive diagnosis of SAH, to identify the cause and to investigate for an intracranial aneurysm.
Cranial magnetic resonance imaging may be proposed if the patient's clinical condition allows it. FLAIR imaging is more sensitive than CT to demonstrate a subarachnoid hemorrhage and offers greater degrees of sensitivity for the diagnosis of restricted subarachnoid hemorrhage in cortical sulcus. A lumbar puncture should be performed if these investigations are normal while clinical suspicion is high 6).
CT angiography is an appropriate initial investigation to detect macrovascular causes of non-traumatic Intracerebral hemorrhage, but accuracy is modest. Additional MRI/MRA may find cavernomas or alternative diagnoses, but DSA is needed to diagnose macrovascular causes undetected by CT angiography or MRI/MRA 7).
Spinal magnetic resonance imaging
The yield and clinical relevance of MRI of the spinal axis in patients who present with nonperimesencephalic subarachnoid hemorrhage (NPSAH) is low. Germans et al. do not recommend routine MRI of the spinal axis in this patient population, but it might be justified in a subgroup of patients 8).
The yield and clinical relevance of MRI of the spinal axis in patients who present with NPSAH is low. Germans et al. do not recommend routine MRI of the spinal axis in this patient population, but it might be justified in a subgroup of patients 9) 10).
Computed tomography angiography
Cerebral angiography
Cerebral angiography for subarachnoid hemorrhage
| Feature | Multiphase CT Angiography (MP-CTA) | Digital Subtraction Angiography (DSA) |
|---|---|---|
| Sensitivity | 85-95% (lower for small aneurysms) | Nearly 100% (gold standard) |
| Specificity | 90-98% | Nearly 100% |
| Invasiveness | Non-invasive | Invasive (catheter-based) |
| Risk of complications | Minimal (radiation & contrast risks) | Higher (stroke, vessel injury, hematoma) |
| Imaging speed | Fast (minutes) | Longer procedure |
| Visualization of small aneurysms (<3mm) | Limited accuracy | Superior resolution |
| Dynamic flow assessment | No (static images) | Yes (real-time blood flow visualization) |
| Artifact issues | Bone & vessel overlap may affect clarity | Minimal artifacts |
| Best for… | Screening, emergency cases, preoperative planning in some cases | Definitive diagnosis, pre-surgical/endovascular planning |
| Limitations | May miss small/complex aneurysms, no dynamic blood flow info | Requires arterial access, risk of complications |
see Subarachnoid hemorrhage diagnosis.
Although intracranial arterial aneurysms (IAAs) of childhood are usually idiopathic, it is possible that underlying arteriopathy escapes detection when using conventional diagnostic tools. Quantitative arterial tortuosity (QAT) has been studied as a biomarker of arteriopathy. The authors analyzed cervicocerebral QAT in children with idiopathic IAAs to assess the possibility of arteriopathy.
METHODS: Cases were identified by text-string searches of imaging reports spanning the period January 1993 through June 2017. QAT of cervicocerebral arterial segments was measured from cross-sectional studies using image-processing software. Other imaging and clinical data were confirmed by retrospective electronic record review. Children with idiopathic IAAs and positive case controls, with congenital arteriopathy differentiated according to aneurysm status (with and without an aneurysm), were compared to each other and to healthy controls without vascular risk factors.
RESULTS: Cervicocerebral QAT was measured in 314 children: 24 with idiopathic IAAs, 163 with congenital arteriopathy (including 14 arteriopathic IAAs), and 127 healthy controls. QAT of all vertebrobasilar segments was larger in children with IAAs (idiopathic and arteriopathic forms) (p < 0.05). In children with congenital arteriopathy without an aneurysm, QAT was decreased for the distal cervical vertebral arteries and increased for the supraspinal vertebral artery relative to healthy children. QAT of specific cervicocerebral segments correlated with IAA size and rupture status.
CONCLUSIONS: Cervicocerebral QAT is a biomarker of arteriopathy in children with IAA, even in the absence of other disease markers. Additional findings suggest a correlation of cervicocerebral QAT with IAA size and rupture status and with the presence of IAA in children with congenital arteriopathy 11).