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A 55-year-old woman suffered from diplopia and occipital pain after shoveling snow. She was diagnosed with the right vertebral artery dissecting aneurysm at the level of the axial vertebra and repeatedly had cerebral infarctions in the posterior circulation. She had subluxation of the atlantoaxial vertebra as an underlying disease. Right vertebral angiogram with the head rotated to the left showed the right vertebral artery occlusion and left vertebral angiogram with the head rotated to the right showed stenosis at the C1-C2 level, leading to the diagnosis of Bow hunter's stroke. After wearing a cervical collar and taking 100 ‍mg of aspirin, she had no recurrence of cerebral infarction and later underwent C1-C2 posterior fusion to prevent the recurrence of cerebral infarction. She finished taking aspirin 6 months after the surgery, and there has been no recurrence of cerebral infarction. We report here a case of Bow hunter's stroke, a rare disease, with good clinical outcomes after C1-C2 posterior fusion.

Ruptured vertebral artery dissecting aneurysms(VADA) carry a poor prognosis owing to the high rates of rebleeding, stroke, and mortality without appropriate treatment. Various endovascular techniques are employed to treat these aneurysms. Deconstructive techniques, involving internal trapping with coils, often achieve complete angiographic occlusion at higher rates; however, they carry a risk of medullary infarction. Reconstructive techniques using neck-bridge stents preserve the parent vessel and reduce perioperative morbidity. Nevertheless, these techniques are associated with a higher rate of aneurysmal rebleeding or recurrence. Optimal treatment modalities should be chosen based on the anatomical characteristics of the aneurysm and the trade-off between risks and benefits.

Purpose: Sudden onset severe occipital/nuchal pain is believed to be a typical symptom of vertebral artery dissection(VAD). However, recent developments in diagnostic imaging have suggested that VAD is not always associated with such pain. This study aimed to analyze the clinical features of initial symptoms in patients with VAD., Methods: In total, this study included 29 consecutive patients who were referred to our hospital because of only headache and/or nuchal pain due to VAD between 2011 and 2016. In this study, their clinical features were precisely assessed, including the pain location, onset pattern, duration, intensity, disease period, diagnosis modality, and prognosis. Both MRI and MRA were performed for all subjects. Cerebral angiography and thin-slice T1-weighted MRI were additionally performed in selected cases., Results: Of the 29 patients, 23 presented with occipital headache and/or nuchal pain. The pain was persistent in 26/29 and ipsilateral in 29/29. However, only 16/29 reported a typical sudden onset. Only 12/29 complained of severe pain, while the other 17/29 presented with dull pain. The mean interval between onset and hospitalization was 7.4 days(0 to 30 days)and the mean interval between hospitalization and diagnosis was 3.9 days(0 to 21 days). Intramural hematoma was identified in 21/29 patients using thin-slice T1-weighted MRI., Conclusion: Only 55% of patients with VAD demonstrate typical occipital/nuchal pain with sudden onset. Both MRI and MRA should be indicated for patients who complain of persistent, unilateral pain in the occipital/nuchal regions to prevent VAD being missed during diagnosis.

A 45-year-old woman was admitted with headache following sudden disturbance of consciousness that occurred two hours beforehand. A neurological examination identified disorientation, left homonymous hemianopia, left hemiplegia, and sensory disturbance in the left limbs. Brain MRI DWI showed acute infarcts in the right occipital lobe and bilateral thalami, and MRA poorly depicted right vertebral artery and right posterior cerebral artery. Anticoagulation was started to treat acute ischemic stroke, but her consciousness level deteriorated at 12 hours after onset. MRI revealed a double lumen in the basilar artery, indicating a diagnosis of vertebrobasilar artery dissection. Serial MRA findings showed that images of the basilar artery and posterior cerebral artery changed over time, suggesting vertebral artery dissection extension to the posterior cerebral artery.

A 52-year-old man developed sudden occipital headache followed by vomiting and vertigo. On admission, he displayed right Horner syndrome with ipsilateral reduced facial sensation to pain and temperature that crossed in the body, affecting the left limbs. In addition, he had right hemiparesis. Diffusion weighted magnetic resonance images showed a high intensity lesion localized in the lower and right lateral medulla oblongata. Magnetic resonance angiography showed severe luminal stenosis in the right vertebral artery and T2-weighted sampling perfection with application optimized contrasts using different flip angle evolution (SPACE) showed arterial wall expansion. T1-weighted SPACE showed subacute intramural hematoma at that point, suggesting arterial dissection. First described in 1946, Opalski syndrome is considered a variant of Wallenberg syndrome with ipsilateral hemiparesis. This motor impairment is considered as a result of extension of the ischemia from the lateral medulla to the upper cervical cord involving corticospinal fibers caudal to pyramidal decussation. This case adds information regarding the anatomy of the pyramidal decussation.

A 34-year-old man developed right neck pain. Several hours later, he felt numbness of his extremities and presented at our hospital. He developed right hemiparesis and hypoesthesia of the right extremities. A few hours later, upbeat nystagmus and dysarthria appeared along with a sensory disturbance that spread to all extremities, and right hemiparesis progressed to tetraplegia. Brain MR diffusion-weighted images revealed a high-intensity lesion in the bilateral medial medulla oblongata and we diagnosed this bilateral medial medullary infarction. Three dimentional CT angiography revealed dissection of the right VA. We administered intravenous argatroban, edaravone, glycerin and oral clopidogrel. He was assessed as having modified Rankin scale 4 and was transferred to another hospital for rehabilitation on day 30. When the medial medulla oblongata is supplied by the unilateral VA, a unilateral VA dissection can cause bilateral medial medullary infarction.

A 46-year-old man developed central respiratory failure in the subacute phase of unilateral lateral medullary infarction. He complained of sudden headache and nausea at first. Neurological examination revealed Wallenberg's syndrome. Acute right lateral medullary infarction caused by the dissecting right vertebral artery was identified by magnetic resonance images. He was transferred to our hospital on the 3rd day after the onset. He was alert and conscious on admission, and became restless gradually later. He was intubated for sudden respiratory failure on the 9th day. Blood gas analysis showed hypercapnia and hypoxia. Central respiratory failure was indicated by the fact that various examinations showed no change of his infarction, no subarachnoid hemorrhage, or no worsening of pneumonia. Ventilatory support was required for a month because of repetitive CO2 narcosis. He was weaned from the ventilator on the 39th day. Only a few reports are available on central respiratory failure associated with the subacute phase of unilateral medullary infarction. Delayed central respiratory failure may be lethal. Careful observation is required on the subacute phase of Wallenberg's syndrome.

The objective of this study was to identify the clinical features associated with neurological deterioration within 30 days of ischemic stroke patients with spontaneous cevicocranial dissection (SCCD) and clarify the effect on outcomes. We retrospectively identified 18 patients with SCCD (1.6%, 3 women, 52 ± 16 years old) among 1,112 patients with acute ischemic stroke within 7 days after onset. Of the 18 patients, 13 (72%) had vertebrobasilar arterial dissection. Neurological deterioration was present in 4 patients (22%), and 2 patients (11%) died. All of them became worse within 3 days after onset. Their initial blood pressures were high. All of them had dominant side vertebral artery or basilar artery dissection. Subarachnoid hemorrahage (SAH) were not seen although the agressive anticoagulant therapy were performed except for a case who had aneurysmal change. The patients with neurological deterioration had poor outcome, but the patients without neurological deterioration had good outcome. Recurrent ischemic event or SAH did not occurred in 3 months if they had not neurological deterioration. When we see acute stroke patients with dissection at the dominant side vertebral artery or the basilar artery, we should observe carefully for neurological deterioration especially within three days of onset.

A 45-year-old man noted a tendency to fall to the left side on standing following headache and vomiting. Neurological findings were unremarkable except for truncal lateropulsion to the left side. Brain magnetic resonance imaging (MRI) showed a small infarct in the left inferolateral part of medulla. Clinical and imaging findings suggested vertebral artery dissection as the cause of stroke. On hospital day 6, the patient developed decreased pain and temperature sensation in the right side below T10 sensory level and decreased sweating on the left side of the face with miosis of the left pupil. Brain MRI revealed an expanded lesion of the left inferolateral part of medulla. In our patient, the involvement of the spinocerebellar tract and the lateral spinothalamic tract likely contributed to the development of truncal lateropulsion and sensory disturbance below thoracic levels, respectively. Our case is clinically important in understanding a correlation between clinical symptoms and lateral medullary lesions.

We have encountered a case of a patient with bilateral vertebral artery (VA) dissection who suffered from severe pharyngeal pain. A 61-year-old man, who initially visited a nearby hospital for investigation of mild headache, was pointed out to have a left VA aneurysm. The next morning, severe pharyngeal pain on the right side suddenly occurred. The cause was unknown even when consultation was made to an otolaryngology and oral and maxillofacial surgeon. Sore throat improved in two days. On the 12th day after pharyngeal pain, the patient entered our hospital with a diagnosis of VA dissection. Imaging studies indicated severe stenosis of the right VA and an aneurysm of the left VA which confirmed the diagnosis of bilateral VA dissection. After severe stenosis of the right VA improved a little, the trapping of the left VA aneurysm was performed with bypass surgery of the occipital artery to the posterior inferior cerebellar artery. Although there have been reports of glossopharyngeal neuralgia due to compression of dissective aneurysms of VA, no report exists in terms of a sore throat due to VA dissection without glossopharyngeal neuralgia. This symptom was considered to be involved in the referred pain.

Vertebral artery dissection(VAD)presenting as isolated occipital headache and/or neck pain is being increasingly diagnosed because of the development of magnetic resonance imaging(MRI). While a majority of the patients diagnosed with this condition shows a favorable prognosis, the pain may be a predictor of fatal stroke in some patients. We aimed to find out the features of headache with VAD, identify the clinical manifestations indicative of VAD, and determine the ideal diagnostic approach to this condition to avoid fatal stroke. We reviewed medical records of 41 consecutive patients who showed VAD with isolated headache and were diagnosed between 1995 and 2008. All patients experienced pain in the occipitocervical area ipsilateral to the affected VA. Pain showed a sudden onset in 21(51%)patients, was persistent over several days in 31(76%)patients, and was severe enough to disable daily life activities in 34(83%)patients. Progression of stenosis or aneurysmal dilatation of the vessel was identified on follow-up imaging(angiography, magnetic resonance angiography)in 7 patients(17%), and was found within 14 days after pain onset in 6 of these patients(86%). Patients with persistent, severe, and unilateral pain in the occipitocervical area should undergo MRI examination, including surface anatomy scanning(SAS)imaging, and the possibility of VAD should be considered in their diagnosis. Once VAD is diagnosed, the patient should undergo meticulous blood pressure control, bed rest, and repeated MRI examination for at least 2 weeks after onset.

We report a rare case of a ruptured vertebral artery dissecting aneurysm (VADA) with affected vertebral artery (VA) occlusion. A 66-year-old hypertensive man presented with subarachnoid hemorrhage. No cerebeller sign or cranial nerve palsy was found on admission. Initial CT angiography and digital subtraction angiography (DSA) revealed the right VA occlusion. On the three days after onset, the right VA was recanalized and visualized as a posterior inferior cerebellar artery (PICA)-involved VADA. Endovascular internal trapping of the right VA including PICA origin was performed. In conclusion, it is essential that patients of VA occlusion associated with subarachnoid hemorrhage should be carefully diagnosed considering the possibility of VADA.

A 35-year-old male experienced a sudden onset of severe headache. A CT scan revealed subarachnoid hemorrhage. By cerebral angiography, he was diagnosed as having a ruptured right vertebral artery dissecting aneurysm (VADA). It was successfully treated by endovascular occlusion of the affected site, including the aneurysm and parent artery, by using detachable coils. A follow-up angiography obtained seven months after the first treatment revealed the recanalization of the right vertebral artery and dissected aneurysm in an antegrade fashion. A skull X-ray image was useful for detecting the change in appearance of the coils. The second embolization was successfully performed in the same manner. Based on this rare case, the authors emphasize that a careful angiographic analysis and complete internal trapping of the dissecting site are important in the treatment of the ruptured VADA.

We report a 63-year-old case of the vertebral artery dissection with recurrent brain embolisms. She was admitted to the hospital because she suffered a visual symptom. She was examined by magnetic resonance imaging (MRI) and diagnosed a left vertebral artery (VA) dissection. Digital subtraction angiography (DSA) revealed the string sign on the left VA supporting the evidence of dissection. However, after DSA, multiple brain embolic stroke was occurred. She was treated with anti-platelet drug (sodium ozagrel), then, recanalization of the pseudo-lumen at the dissecting lesion was observed by MRI examination. Anti-platelet medicine (cilostazol) was taken for preventing reattack although the dissecting lesion was not closed. Following 4 weeks, brain embolisms were observed in the posterior circulation system. MRI revealed a dilated pseudo-lumen at the dissecting lesion with recurrent VA. This time, she was treated only with free radical scavenger (edarabone). After the occlusion of the dissected VA was observed, she started to take anti-platelet medicine again. It is generally accepted to use anti-platelet drug or anti-coagulant drug as a treatment of VA dissection causing brain ischemia. However, it should be assessed more carefully in cases showing recanalization of the pseudo-lumen as observed in this case. Surgical treatments should be taken into consideration at the early stage, especially for the cases presenting fragile dissecting lesions. Further study need to decide the effective treatment of the vertebral artery dissection.

A 43-year-old woman presented with weakness in her left arm and leg. She had noticed headache persisting for 2 weeks in her right occipital area 6 weeks prior to the onset of the weakness. Cranial diffusion-weighted MR image demonstrated acute infarction in the right medial part of medulla oblongata. Cerebral angiography revealed pearl and string sign in the right intracranial vertebral artery. Magnetic resonance T1-weighted image obtained when the patient complained of left-sided weakness showed a high intensity area in right vertebral artery corresponding to intramural hematoma. The diagnosis of spontaneous vertebral artery dissection was established based on clinical features, laboratory findings, MR images and angiographic findings. Generally, in patients with cervicocephalic artery dissection with ischemic onset, the occurrence of headache is either simultaneous with the ischemic symptoms, or several days prior to the ischemic symptoms. The present case showed that headache due to arterial dissection can occur several weeks prior the ischemic symptoms. Precise history of headache should be taken in patients with cervicocephalic artery dissection.

We report a case of vertebral artery (VA) dissection presenting with repeated distal embolism. A 48-year-old man was admitted to our institution with neck pain and vertigo of two day duration. MRI on arrival showed infarction of the left cerebellar hemisphere and the right occipital lobe. Emergency angiography revealed left VA dissection and occlusion of the left posterior inferior cerebellar artery and right calcaline artery. Six hours after admission, he manifested cortical blindness due to embolism of the contralateral left calcaline artery despite giving heparin and aspirin. Thrombolysis was performed but was not successful. We embolized the affected VA to prevent further embolism. We discuss here the indication and timing of treatment for VA dissection presenting with ischemic symptom.

We report a case of a dissecting vertebral aneurysm with subarachnoid hemorrhage (SAH) after ischemic onset on the same day. A 48-year-old man had abrupt vertigo and nausea. CT & MRI on admission showed no abnormality, but he complained of left hemiparesis after admission. Twelve hours after the ischemic onset he suddenly complained of severe headache and his consciousness deteriorated. The follow-up CT showed diffuse SAH. Cerebral angiography showed occlusion of the right vertebral artery at the origin of the posterior inferior cerebellar artery (PICA) and segmental stenosis of the left vertebral artery at the portion distal to the vertebral PICA junction. We treated the patient conservatively. Four days later, he suddenly fell into a coma, but CT showed no bleeding. Because of this we suspected brain stem ischemia due to deterioration of vertebral dissection. The patient died 8 hours after the ischemic reattack. We report difficulty of treatment of a dissecting vertebral aneurysm with simultaneous ischemia and subarachnoid hemorrhage.

We report here a case of atypical Wallenberg's syndrome due to spontaneous vertebral artery (VA) dissection. A 52-year-old woman was admitted to our department because of a sudden onset of left orbital pain. Emergency CT scan disclosed no evidence of intracranial hemorrhage. Neurological examination at the time of the current admission, showed dysphagia, left soft palate palsy, hoarseness, left Horner syndrome, hypalgesia with thermohypesthesia on the right side of her face, however, hypalgesia with thermohypesthesia on the right side of her body. The diagnosis of atypical Wallenberg's syndrome was based on the above findings. MR images disclosed the infarcted lesion at the left lateral medulla depicted as high-intensity on T2-weighted & FLAIR images. We carried out conservative treatment with antiplatelet & hemodilution therapies and the blood pressure control. Left vertebral angiograms obtained 18 days after the onset, showed the segmental severe stenosis of the VA between the ramification of the posterior inferior cerebellar artery (PICA) and the union of the VAs. In the venous phase, retention of contrast medium in the VA and the PICA was observed. The flow rate of the parent artery was decreased. We strongly suspected that her initial symptom of left orbital pain was due to dissection of the VA itself. Three-dimensional CT angiograms obtained 30 days after the onset, demonstrated the defect of the left VA between the ramification of the left PICA and the union of the VAs. Left vertebral angiograms obtained 36 days after the onset, showed the occlusion of the VA between the ramification of the PICA and the union of the VAs. The neurological findings gradually improved and the patient was discharged. Follow up left vertebral angiograms obtained 4 months & 16 months after the onset, revealed almost no changes of left VA occlusion.

The authors report the case of a rare manifestation by vertebral artery dissection. A 15-year-old boy who presented with left shoulder weakness and numbness of the left arm was admitted to our hospital. Neurological examination on admission revealed muscle weakness of the left deltoid muscle and sensory disturbance of the left C5 area. MRI/MRA and 3D-CT angiography demonstrated an aneurysm-like dilatation of the left vertebral artery mainly at the C4/5 level. Partial thrombosis was noted in the dilated artery. The left vertebral angiogram showed that the second and third portions of the left vertebral artery had a dilated pseudo-lumen due to arterial dissection. The pseudo-lumen of the dissected vertebral artery was largest in diameter at the C4/5 level. The patient successfully underwent proximal occlusion of the dissected vertebral artery using detachable balloon and Guglielmi detachable coils. Proximal vertebral artery occlusion using an intravascular technique was regarded as a non-invasive and effective option for patients with a cervical radiculopathy due to cervical vertebral artery dissection.

In this paper we report a case of vertebral artery occlusion caused by spontaneous extra-cranial vertebral artery dissection accompanied with cerebellar and thalamic infarctions due to recanalization. Furthermore, after a nine-week time lapse we performed PTA/stenting. A 62-year-old man with vertigo, dysarthria and nuchal pain without injury was admitted to our hospital. Emergent cerebral angiography revealed an occlusion of the right vertebral artery and the right PICA. The patient's symptoms gradually improved owing to local-fibrinolysis with urokinase for the right PICA via the left vertebral artery. Follow-up angiography (2 weeks later) showed re-canalization and dissection of the right vertebral artery. Treatment for spontaneous extra-cranial vertebral artery dissection is chosen, depending on whether there is co-lateral circulation or not. We obtained a good result using PTA/Stenting in this case of spontaneous extra-cranial vertebral artery dissection within nine weeks after onset.

A 66-year-old male presented with dysarthria and right hemiparesis. Cerebral angiography at onset showed obliteration of the basilar artery and dilatation in the left vertebral artery. The patient's clinical symptoms were exaggerated and he was finally diagnosed to as suffering locked-in syndrome. Magnetic resonance imaging showed a brain stem infarction from the pons to the left middle cerebellar peduncle. We determined that the patient suffered dissection of the left vertebral artery at the basilar artery and treated, using the conservative therapy him of strict blood pressure control. A second angiography 13 days after onset showed recanalization of the basilar artery. At 29 days after onset, the patient fell into a coma with subarachnoid hemorrhage and acute hydrocephalus. Cerebral angiography revealed improvement in the irregularity and dilatation of the basilar artery, but the point of rupture could not be clearly identified. After performing proximal occlusion of the left vertebral artery by intravascular surgery, both right STA-SCA anastomosis and proximal occlusion of the right vertebral artery were carried out. Unfortunately, the patient died. Based on there data, it is appointed out that patients with a dissection of the vertebrobasilar artery must be followed up by serial angiography, and even if an angiographical improvement of the dissection is observed, the risk of subarachnoid hemorrhage still exists in patients suffering ischemic stroke.

A-38-year-old man suddenly developed nausea, vomiting and vertigo during chiropractic neck manipulation. This was followed by right hemiplegia, right deep sensory disturbance and left hypoglossal nerve palsy, consistent with the medial medullary infarction (Dejerine syndrome). The MRI revealed infarction at left medial part of the medulla. The vertebral angiogram and MRA showed marked narrowing of the left vertebral artery. X-rays of the cervical spine showed no spondylosis, dislocation nor osteolysis of the odontoid process. The serological studies, including lupus anticoagulant, protein C, and protein S gave normal results. Although vascular accidents involving the brain stem after chiropractic neck manipulation have been reported since Pratt-Thomas and Berger, previous reports are still rare. In them lateral medullary infarction (Wallenberg syndrome) is probably the most common case. On the other hand, medial medullary syndrome (Dejerine syndrome) is absolutely rare. To our knowledge, the only one report has been made by Watanabe and his colleagues before our present case. The mechanism was suggested that rotation and tilting of the neck stretches and compresses the vertebral artery at the cervical joint causing injury to the vessel, with an intimal tearing, dissection, and pseudoaneurysm formation. Consequently, the present case may be caused by injury to the left vertebral artery with an intimal tearing during neck manipulation sufficient to cause disection and subsequent infarction of the brain stem.

Vertebral artery (VA) dissections are uncommon, but are increasingly recognized as a cause of posterior circulation stroke in young adults. We describe a patient with bilateral VA dissection who presented SAH. The patient was successfully treated by proximal coil occlusion of the bilateral vertebral arteries in two stages. In the treatment of SAH due to bilateral VA dissection, it is important to estimate the status of the treated vessels or contralateral vessels by follow-up angiography. Staged bilateral proximal VA occlusions should be considered in the case of recurrent VA dissection or progressive aneurysm enlargement.

Spontaneous dissection of the intracranial vertebral artery has been increasingly recognized as a cause of vertebrobasilar ischemic stroke. However, little is known about its natural history and clinical course. The authors report a young patient with repeated cerebral infarction in the posterior cerebral circulation caused by dissection of the vertebral artery, which was not detected on the first angiogram. The otherwise healthy 22-year-old male suddenly developed visual disturbance. Neuroradiological examination revealed right occipital infarction, but cerebral aniography revealed no caliber change or other pathological findings. He was treated with antiplatelet therapy. Two years later, he suffered vertigo, nausea, and dysarthria due to newly developed left cerebellar and medullary infarction. Cerebral angiography revealed left vertebral artery occlusion. T1-weighted MR image demonstrated Gadlinium-enhanced intramural hematoma in the occluded left vertebral artery, which was compatible to the arterial dissection. The present case argues serial neuroimaging studies especially in young patients with vertebrobasilar stroke in order to rule out the arterial dissection, even if initial angiography failed to demonstrate any radiographical evidence.

A case is reported of the vertebral arterial dissection presenting initially with cerebellar infarction, and which subsequently occurred with subarachnoid hemorrhage 14 days later. A 75-year old male was admitted because of vertigo and ataxia. MR T2-weighted imaging showed a hyperintensity areas on the left cerebellar hemisphere and MR angiography showed multiple stenotic lesions in the left vertebral artery. We diagnosed his illness as dissection of the left vertebral artery and antiplatelet therapy and the blood pressure control were carried out. Fourteen days after the onset, the patient complained of sudden onset of headache and subarachnoid hemorrhage was confirmed on CT scan. Proximal clip occlusion of the left vertebral artery and OA-PICA anastomosis was carried out immediately. The patient was discharged with slight truncal ataxia. We evaluated the features of this vertebral arterial dissection presenting with subarachnoid hemorrhage after ischemic stroke with reference to another reported cases.