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Intracranial vertebral artery dissection (IVAD) is rare and potentially fatal due to the risk of secondary subarachnoid hemorrhage once ruptured. Unruptured traumatic IVAD is even rarer and can result in ischemic stroke, yet mostly benign when timely diagnosed. Herein, we present an uncommon case of a patient who underwent a fatal ischemic stroke induced by unruptured traumatic IVAD. The patient was symptomatic soon after being physically assaulted but left untreated until acute deterioration for multiple brain infarctions occurred, secondary to IVAD-induced cerebellar stroke. Fifteen days later, he died, regardless of an urgently performed thrombectomy. Multiple serial histologic examinations revealed an unruptured dissection of the intracranial vertebral artery with a slit-like tear of the intimal and medial layers, considered to be the culprit lesion. The 15-day prolonged onset of stroke was rare in traumatic IVADs. Furthermore, the slit-like tear of the intimal layer in our case may support the initial intimal laceration hypothesis for VAD pathogenesis. Since limited pathohistological information is available regarding ischemic IVAD, we believe this rare case will be beneficial in understanding the pathophysiology of ischemic IVAD.

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Hemorrhagic intracranial artery dissections are unstable lesions, with a high propensity for rebleeding (up to 40%) in the acute period. Imaging plays an important role in the diagnosis and management of intracranial artery dissections. In this paper, we describe 2 cases in which the dissected intracranial artery underwent rapid morphological change within 3 days or less, highlighting the importance of short-term follow-up imaging in patients with these hemorrhagic lesions.

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OBJECTIVE: Unruptured intracranial vertebral artery dissection (VAD) generally heals spontaneously. A chronological evaluation of intramural hematoma (IMH) using T1-weighted vessel wall imaging (VWI) may provide a more detailed understanding of the pathophysiology of VAD. We herein investigated the relationship between chronological signal changes in IMH on VWI and the spontaneous healing of VAD. MATERIALS AND METHODS: We retrospectively investigated 26 patients with 27 unruptured VADs who underwent magnetic resonance (MR) imaging more than three times during the follow-up period. Morphological changes were evaluated using MR angiography (MRA). The relative signal intensity (RSI) of IMH against the posterior cervical muscle on T1-weighted VWI was calculated. The ratio of chronological RSI changes was defined as follows: maximum RSI/minimum RSI (RSI max/min). Based on the median value of RSI max/min, 27 VADs were divided into VADs with and without chronological RSI changes. Statistical analyses were performed to compare clinical and radiological findings between the two groups. RESULTS: Spontaneous healing occurred in 17 out of 27 VADs (63%). The median value of RSI max/min was 1.48. The RSI of VADs with chronological RSI changes (RSI max/min ≥ 1.48) increased until three weeks after their onset and decreased over time, while that of VADs without chronological RSI changes (RSI max/min < 1.48) showed no change. The frequency of healing was significantly higher in VADs with than without chronological RSI changes (100% vs 23%, p < 0.0001). CONCLUSIONS: Chronological signal changes in IMH on T1-weighted VWI have potential as a diagnostic imaging marker of the spontaneous healing of VAD.

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BACKGROUND: Man in the barrel syndrome (MBS) is a condition of brachial diplegia initially described after a bilateral watershed cerebral infarct between the anterior and the middle cerebral artery territories. OBJECTIVE: To report a case of MBS as a consequence of anterior spinal artery infarct due to vertebral artery dissection. DISCUSSION: More recently, nonischemic lesions in brain and brain stem have also been described as etiologies of MBS. There are few reports describing spinal cord infarction leading to MBS. The anterior spinal artery syndrome with only brachial diplegia also represents a rare and atypical pattern. CONCLUSION: The conventional neurological consideration that MBS provides a precise anatomical localization is now challenged. The finding of a brachial diplegia leads to the need to investigate the brain, the spinal cord, and the peripheral nervous system.

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BACKGROUND AND PURPOSE: Headache may be a warning sign of subsequent stroke in patients with vertebral artery dissection (VAD). Even though the headache characteristics of VAD have been described predominantly in patients with extracranial VAD and neurological complications, headache semiology is not well known in patients with uncomplicated intracranial vertebral artery dissection (ICVAD). In the present study, we attempt to identify the headache semiology that characterizes ICVAD and validate the revised version of the International Classification of Headache Disorders (ICHD-3 beta) criteria for headache attributed to intracranial artery dissection. METHODS: Six patients with neurologically uncomplicated ICVAD presented at a participating medical center, and eight similar patients were reviewed in the literature. Combining these data, we analyzed headache characteristics of patients with uncomplicated ICVAD according to their pain onset and duration, nature, intensity, location, aggravating and relieving factors, associated symptoms, response to medication, and prognosis. RESULTS: Headache in uncomplicated ICVAD usually has an acute mode of onset (11/14) and persistent (10/14) temporal feature. Pain that has a throbbing quality (nine of 14) and severe intensity (13/14) on the ipsilesional (10/14) and occipitonuchal area (12/14) is a headache prototype in ICVAD. Additionally, headache was intensified by head flexion and rotation (three of six), and relieved by head extension and supine positioning (five of six). Headache of all patients in the present study fulfilled the ICHD-3 beta criteria. CONCLUSION: Headache semiology of uncomplicated ICVAD is mostly homogenous in the present study. These characteristics may be helpful in the diagnosis of uncomplicated ICVAD.

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