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Ayako Ro, Norimasa Kageyama, Nobuyuki Abe, Akihiro Takatsu and Tatsushige Fukunaga

Object

Subarachnoid hemorrhage (SAH) due to a ruptured intracranial vertebral artery (VA) dissection sometimes results in a sudden fatal outcome. The authors analyzed the relationship between clinical features and histopathological characteristics among fatal cases to establish valuable information for clinical diagnostics and prophylaxis.

Methods

This study included 58 medicolegal autopsy cases of ruptured intracranial VA dissection among 553 fatal nontraumatic cases of SAH that occurred between January 2000 and December 2007. Their clinical features were obtained from autopsy records. Histopathological investigations were performed on cross-sections obtained from all 4-mm segments of whole bilateral intracranial VAs and prepared with H & E and elastica van Gieson staining.

Results

The autopsy cases included 47 males and 11 females, showing a marked predilection for males. The mean age was 46.8 ± 7.7 years, with 78% of the patients in their 40s or 50s. Hypertension was the most frequently encountered history; it was found in 36% of cases from clinical history and in 55% of cases based on autopsy findings. Prodromal symptoms related to intracranial VA dissections were detected in 43% of patients. Headache or neck pain lasting hours to weeks was a frequent complaint. Of patients with prodromal symptoms, 44% had consulted doctors; however, in none of these was SAH or intracranial VA dissection diagnosed at a preventable stage.

Autopsy revealed fusiform aneurysms with medial dissecting hematomas. Apart from ruptured intracranial VA dissection, previous intracranial VA dissection was detected in 25 cases (43%); among them, 10 showed previous dissection of the bilateral intracranial VAs. The incidence of prodromal symptoms (60%) among the patients with previous intracranial VA dissection was significantly higher than that (30%) among cases without previous dissection (chi-square test; p = 0.023). Most previous intracranial VA dissections formed a single lumen resembling nonspecific atherosclerotic lesions, with the exception of 3 cases (12%) with a double lumen.

Conclusions

Intracranial VA dissection resulting in fatal SAH frequently affects middle-aged men with untreated hypertension. Related to the high frequency of prodromal symptoms, latent previous intracranial VA dissection was histopathologically detected. Furthermore, intracranial VA dissection tends to induce multiple lesions affecting both intracranial VAs recurrently. This suggests the importance of an awareness of sustained whole intracranial VA vulnerability for the prevention of recurrence. The incidence of prodromal symptoms was significantly higher among patients with previous intracranial VA dissections. Thus, earlier diagnosis of intracranial VA dissections at the unruptured stage is desirable for prophylaxis against fatal SAH.

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Ayako Ro and Norimasa Kageyama

Object

Subarachnoid hemorrhage (SAH) due to ruptured intracranial vertebral artery (VA) dissection is a life-threatening disease. Angiographic and symptomatic prognostic factors for rupture and rerupture have been investigated, but the pathological characteristics have not been fully investigated. The authors aimed to investigate these features by performing a pathomorphometic study of ruptured intracranial VA dissections.

Methods

This study included 50 administrative autopsy cases of fatal SAH due to ruptured intracranial VA dissection among 517 fatal nontraumatic cases of SAH occurring between March 2003 and May 2011.

Pathomorphometry was performed using serial 5-μm histological cross-sections with elastica van Gieson staining from each 0.2-mm segment around the ruptured intracranial VA. The longitudinal lengths of 4 types of vascular lesions—adventitial ruptures, dilated lesions where the internal elastic lamina (IEL) was ruptured with adventitial extension, intimal tears where the IEL was ruptured, and medial defects—were calculated based on the numbers of the slides in which these lesions were continuously detected (minimum 2 adjoining slides). The distance from the vertebrobasilar junction to the center of adventitial rupture was also calculated in 37 cases.

Results

All cases showed one adventitial rupture with a mean length of about 1.9 ± 1.1 mm. The center of the adventitial rupture was located 5.0–26.8 mm (mean 14.6 ± 5.5 mm) from the intracranial VA bifurcation. Adventitial ruptures existed in the centers of dilated lesions, where the adventitia was highly extended. Other vascular lesions were serially observed surrounding the adventitial rupture. The mean lengths of dilated lesions, intimal tears, and medial defects were 9.4 ± 4.8 mm, 13.2 ± 6.3 mm, and 15.6 ± 7.2 mm, respectively. The lengths between proximal lesions and distal lesions from the center of the adventitial rupture for both medial defects and intimal tears were significantly longer at proximal lesions than at distal ones (chi-square test, p < 0.01).

Conclusions

Every ruptured intracranial VA dissection has a single point of adventitial rupture where the adventitia was maximally extended, so dilation appears to be a valuable predictive factor for hemorrhagic intracranial VA dissections. The adventitial ruptures were as small as 2 mm in length, and clinically detectable dilated lesions were about 9 mm in length. However, vascular vulnerability caused by IEL ruptures and medial defects existed more widely across a length of VA of 1.3–1.5 cm. Comparatively broader protection of the intracranial VA than the clinically detected area of dissection might be desirable to prevent rebleeding. Broader protection of proximal lesions than distal lesions might be effective from the viewpoint of site distribution of vascular lesions and blood flow alteration to the pseudolumen caused by the dissecting hematoma. Medial defects are the most widely seen lesions among the 4 types of vascular lesions studied. Medial degenerative disease, known as segmental arterial mediolysis, is suspected in the pathogenesis of intracranial VA dissections.