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In order to evaluate brain stem dysfunction related to ischemic process, the authors monitored the Brainstem Auditory Evoked Responses (BAERs) with time in a brain stem ischemic model. 19 adult mongrel cats were divided into two groups: embolization (n=14) and sham operated control (n=5). Embolization was done by injecting cylindrical silicone embolus to the right vertebral artery. Each successful embolization of the basilar artery was then confirmed by vertebral angiography. BAERs were monitored before embolization and then 5-10 min, 15 min, 30 min, 60 min, 3 hr and 6 hr after embolization. The presence of ischemic lesion caused by embolization was confirmed by injecting 2% Evans blue solution 30 min before sacrificing the animals. Leakage of the dye was observed. In embolized animals, significant (Student t test, p<0.05) delay of interpeak latencies of waves 1-3, 3-5, and 1-5 was observed 15 min after embolization. This delay became more significant (p<0.01) 30 min after embolization. These results provide evidence for the usefulness of BAERs monitoring which can be used to complement other diagnostic methods for patients with vertebrobasilar insufficiency and/or infarction.

type:text, The vascular anatomy and microvascular architecture of the vertebrobasilar system, especially within the brainstem, was investigated in cats. The main branches of the basilar artery were observed and the inner diameters of these vessels were measured on vertebral angiograms. The three-dimensional microvascular architecture was constructed using molded vascular models. The arterial anastomoses between the arteries inside the brainstem were studied using contact microangiograms. The paramedian branch penetrated into the brainstem in a retrograde fashion from the cranial basilar artery, and in an anterograde fashion from the caudal basilar artery. Arterial anastomoses were noted between the circumferential arteries. The frequency of arterial anastomoses was higher and diameters of the anastomotic vessels were larger in the ventrolateral region of the brainstem than in the ventromedial region. Regarding the perforating arteries, the arterial anastomoses were present outside the brainstem. No arterial anastomoses were found inside the brainstem.

The vascular anatomy and microvascular architecture of the vertebrobasilar system, especially within the brainstem, was investigated in cats. The main branches of the basilar artery were observed and the inner diameters of these vessels were measured on vertebral angiograms. The three-dimensional microvascular architecture was constructed using molded vascular models. The arterial anastomoses between the arteries inside the brainstem were studied using contact microangiograms. The paramedian branch penetrated into the brainstem in a retrograde fashion from the cranial basilar artery, and in an anterograde fashion from the caudal basilar artery. Arterial anastomoses were noted between the circumferential arteries. The frequency of arterial anastomoses was higher and diameters of the anastomotic vessels were larger in the ventrolateral region of the brainstem than in the ventromedial region. Regarding the perforating arteries, the arterial anastomoses were present outside the brainstem. No arterial anastomoses were found inside the brainstem.

The vascular anatomy and microvascular architecture of the vertebrobasilar system, especially within the brainstem, was investigated in cats. The main branches of the basilar artery were observed and the inner diameters of these vessels were measured on vertebral angiograms. The three-dimensional microvascular architecture was constructed using molded vascular models. The arterial anastomoses between the arteries inside the brainstem were studied using contact microangiograms. The paramedian branch penetrated into the brainstem in a retrograde fashion from the cranial basilar artery, and in an anterograde fashion from the caudal basilar artery. Arterial anastomoses were noted between the circumferential arteries. The frequency of arterial anastomoses was higher and diameters of the anastomotic vessels were larger in the ventrolateral region of the brainstem than in the ventromedial region. Regarding the perforating arteries, the arterial anastomoses were present outside the brainstem. No arterial anastomoses were found inside the brainstem.

type:text, A report is presented on two cases of chronic subdural hematoma which occurred after craniotomy, removal of the hematoma and external decompression for traumatic intracranial hematoma. As for the pathogenesis of chronic subdural hematoma of these two cases, these chronic subdural hematomas were considered to have originated from the subdural collection of mixed fluid of cerebrospinal fluid and blood caused by tearing of the arachnoid on head injury or craniotomy in the space between the brain and dural plasty. Opening and irrigating the hematoma cavity proved adequate as treatment at cranioplasty.

type:text, In six subarachnoid hemorrhage (SAH) cases due to aneurysmal rupture, effects of cisternal administration of Nicardipine hydrochloride (nicardipine) on vasospasm wer studied. Nicardipine is one of calcium antagonists. All aneurysms were clipped within 48 hr after the onset of SAH with ventricular and cisternal drainages. Subarachnoid clot was removed as much as possible. Nicardipine or mixture of nicardipine and urokinase was administered through cisternal drainage once a day for 10 days postoperatively. The dose of nicardipine was 2 mg or 4 mg, and that of urokinase was 6,000 units or 24,000 units. On the 7th day after the onset of SAH, angiograms were performed before and 30 min after the cisternal administration of nicardipine. Then the diameters of each arteries were compared in order to estimate the vasodilative effects of nicardipine angiographically. In this study nicardipine was considered to have some prophylactic effect on vasospasm because vasospasm was not observed either angiographically or clinically in 2 out of 3 severe SAH cases on CT.

In six subarachnoid hemorrhage (SAH) cases due to aneurysmal rupture, effects of cisternal administration of Nicardipine hydrochloride (nicardipine) on vasospasm wer studied. Nicardipine is one of calcium antagonists. All aneurysms were clipped within 48 hr after the onset of SAH with ventricular and cisternal drainages. Subarachnoid clot was removed as much as possible. Nicardipine or mixture of nicardipine and urokinase was administered through cisternal drainage once a day for 10 days postoperatively. The dose of nicardipine was 2 mg or 4 mg, and that of urokinase was 6,000 units or 24,000 units. On the 7th day after the onset of SAH, angiograms were performed before and 30 min after the cisternal administration of nicardipine. Then the diameters of each arteries were compared in order to estimate the vasodilative effects of nicardipine angiographically. In this study nicardipine was considered to have some prophylactic effect on vasospasm because vasospasm was not observed either angiographically or clinically in 2 out of 3 severe SAH cases on CT.

A report is presented on two cases of chronic subdural hematoma which occurred after craniotomy, removal of the hematoma and external decompression for traumatic intracranial hematoma. As for the pathogenesis of chronic subdural hematoma of these two cases, these chronic subdural hematomas were considered to have originated from the subdural collection of mixed fluid of cerebrospinal fluid and blood caused by tearing of the arachnoid on head injury or craniotomy in the space between the brain and dural plasty. Opening and irrigating the hematoma cavity proved adequate as treatment at cranioplasty.

In six subarachnoid hemorrhage (SAH) cases due to aneurysmal rupture, effects of cisternal administration of Nicardipine hydrochloride (nicardipine) on vasospasm wer studied. Nicardipine is one of calcium antagonists. All aneurysms were clipped within 48 hr after the onset of SAH with ventricular and cisternal drainages. Subarachnoid clot was removed as much as possible. Nicardipine or mixture of nicardipine and urokinase was administered through cisternal drainage once a day for 10 days postoperatively. The dose of nicardipine was 2 mg or 4 mg, and that of urokinase was 6,000 units or 24,000 units. On the 7th day after the onset of SAH, angiograms were performed before and 30 min after the cisternal administration of nicardipine. Then the diameters of each arteries were compared in order to estimate the vasodilative effects of nicardipine angiographically. In this study nicardipine was considered to have some prophylactic effect on vasospasm because vasospasm was not observed either angiographically or clinically in 2 out of 3 severe SAH cases on CT.

A report is presented on two cases of chronic subdural hematoma which occurred after craniotomy, removal of the hematoma and external decompression for traumatic intracranial hematoma. As for the pathogenesis of chronic subdural hematoma of these two cases, these chronic subdural hematomas were considered to have originated from the subdural collection of mixed fluid of cerebrospinal fluid and blood caused by tearing of the arachnoid on head injury or craniotomy in the space between the brain and dural plasty. Opening and irrigating the hematoma cavity proved adequate as treatment at cranioplasty.

The vascular anatomy and microvascular architecture of the vertebrobasilar system, especially within the brainstem, was investigated in cats. The main branches of the basilar artery were observed and the inner diameters of these vessels were measured on vertebral angiograms. The three-dimensional microvascular architecture was constructed using molded vascular models. The arterial anastomoses between the arteries inside the brainstem were studied using contact microangiograms. The paramedian branch penetrated into the brainstem in a retrograde fashion from the cranial basilar artery, and in an anterograde fashion from the caudal basilar artery. Arterial anastomoses were noted between the circumferential arteries. The frequency of arterial anastomoses was higher and diameters of the anastomotic vessels were larger in the ventrolateral region of the brainstem than in the ventromedial region. Regarding the perforating arteries, the arterial anastomoses were present outside the brainstem. No arterial anastomoses were found inside the brainstem.

We present a case of ruptured distal posterior inferior cerebellar artery (PICA) aneurysm, and review the literature and discuss the treatment strategy. A 77-year-old woman presented with the sudden onset of severe headache, nausea and vomiting. Computed tomography revealed an intraventricular hemorrhage, predominantly in the fourth ventricle and hydrocephalus with a thin subarachinoid hemorrhage (SAH). Angiography revealed an aneurysm arising at the turning point of the vessel, from the telovelotonsillar segment of the right PICA. On the 17 day after the onset, repeated angiography revealed a smaller aneurysm than the one detected on the first day at the same place and with no spasm. On the 22 day, the aneurysm was proved to be partially thrombosed and was safely clipped via a right lateral suboccipital approach. SAH with a fourth ventricular hemorrhage or an isolated fourth ventricle hemorrhage should raise the suspicion of a distal PICA aneurysm. Aneurysms of the distal PICA have often been reported to arise at a turning point of the artery rather than at a junction of the vessel. It is suggested that the pathogenesis could be hemodynamic stress that has developed due to embryological factors. Distal PICA aneurysms have often gone detected in many previous cases because of thrombosis inside the aneurysms. Thus, particularly in the case of intentionally delayed surgery, we recommend repeated angiography under various conditions to identify how the aneurysm develops just before surgery.

In six subarachnoid hemorrhage (SAH) cases due to aneurysmal rupture, effects of cisternal administration of Nicardipine hydrochloride (nicardipine) on vasospasm wer studied. Nicardipine is one of calcium antagonists. All aneurysms were clipped within 48 hr after the onset of SAH with ventricular and cisternal drainages. Subarachnoid clot was removed as much as possible. Nicardipine or mixture of nicardipine and urokinase was administered through cisternal drainage once a day for 10 days postoperatively. The dose of nicardipine was 2 mg or 4 mg, and that of urokinase was 6,000 units or 24,000 units. On the 7th day after the onset of SAH, angiograms were performed before and 30 min after the cisternal administration of nicardipine. Then the diameters of each arteries were compared in order to estimate the vasodilative effects of nicardipine angiographically. In this study nicardipine was considered to have some prophylactic effect on vasospasm because vasospasm was not observed either angiographically or clinically in 2 out of 3 severe SAH cases on CT.

A report is presented on two cases of chronic subdural hematoma which occurred after craniotomy, removal of the hematoma and external decompression for traumatic intracranial hematoma. As for the pathogenesis of chronic subdural hematoma of these two cases, these chronic subdural hematomas were considered to have originated from the subdural collection of mixed fluid of cerebrospinal fluid and blood caused by tearing of the arachnoid on head injury or craniotomy in the space between the brain and dural plasty. Opening and irrigating the hematoma cavity proved adequate as treatment at cranioplasty.