[A Case of Traumatic Carotid Artery Dissection Treated with Mechanical Thrombectomy Followed by Carotid Artery Stenting].

Traumatic carotid artery dissection(TCAD)is often associated with severe traumatic brain injuries and has high rates of morbidity and mortality. Here, we report a case of TCAD that was treated with mechanical thrombectomy followed by carotid artery stenting(CAS). A 50-year-old man suffered from minor facial trauma due to a motorcycle accident and had disturbance of consciousness with left hemiplegia 2 hours after sustaining the injury. Magnetic resonance imaging scans revealed cerebral infarction in a part of the middle cerebral artery territory, and magnetic resonance angiography showed cervical internal carotid artery occlusion. The patient was diagnosed with TCAD and underwent acute revascularization. Complete recanalization was with a combined technique using a stent-retriever and an aspiration catheter. Carotid angiography revealed a dissection of the internal carotid artery on the right side, and CAS was performed on the right side. Postoperatively, the patient recovered from disturbance of consciousness and left hemiplegia and was discharged once he was ambulatory. In cases of worsening symptomatology or worsening imaging findings, an endovascular approach should be considered for the treatment of TCAD.

Fluctuations of Nutrition-Associated Markers After Decompressive Hemicraniectomy in Middle Cerebral Artery Occlusion Patients.

Cerebral infarction (CI) caused by middle cerebral artery occlusion exhibits a very high mortality rate. To reduce this rate, a decompressive hemicraniectomy (DHC) is performed clinically based on several randomized trials. In ischemic stroke, a state of malnutrition leads to poor outcomes. However, little evidence is available on nutrition state in the acute phase after DHC. This preliminary study focuses on serum markers, especially dynamic or static nutrition-associated markers including prealbumin, transferrin, retinol binding protein (RBP) and serum albumin under tube feeding with Peptamen®AF (Nestlé Health Science Japan). Blood samples were collected from four patients and analyzed at 6 time points over 14 days (preoperative day, post-operative day (POD) 1, POD 3, POD 7, POD 10, and POD 14). One-way analysis of variance (ANOVA), post hoc Least Significant Difference (LSD), was employed to analyze the blood levels at each time point. The prealbumin and RBP levels showed no significant difference between preoperation and POD 3, although they decreased gradually, while transferrin decreased significantly between the preoperative day and POD 3 (P < 0.05). The level increased significantly on POD 14 as compared to POD 3 (P < 0.05) for each dynamic marker, respectively. The albumin value decreased significantly on POD 3 to POD 7 as compared to the preoperational day (P < 0.05), while the total protein fell significantly on POD 3 (P < 0.05). The total cholesterol, HDL cholesterol, LDL cholesterol, triglyceride, glucose, transferrin, and C-reactive protein were also investigated. Some markers fluctuated significantly, especially on POD 3. The duration may represent a hypercatabolic phase for malignant cerebral infarction with DHC. Based on these findings, further investigations among these markers, the tube fed contents, physiological changes and disability could lead to better outcomes following malignant CI.

Changes of Doublecortin-Immunoreactive Cells from the Acute Phase to Chronic Phase After Transient Global Brain Ischemia in Rat Cingulate Cortex.

Doublecortin (DCX)-immunoreactive (-ir) cells play important roles in adult cortical remodeling. We previously reported that DCX-ir cells decrease after transient global brain ischemia (GBI) in the cingulate cortex (Cg) of rats. In the present study, we examined the changes of DCX-ir cells from the acute to the chronic phase after GBI in rats. Transient GBI was induced by a four-vessel occlusion model as described previously. Thirty-six rats were divided into six groups: day 7 after sham operation (Group Sham+A), day 7 after 3 min GBI (Group GBI3+A), day 7 after 10 min GBI (Group GBI10+A), day 90 after sham operation (Group Sham+C), day 90 after 3 min GBI (Group GBI3+C), and day 90 after 10 min GBI (Group GBI10+C). The numbers of DCX-ir cells per unit area (mm2) were investigated in the anterior cingulate cortex (ACC) and retrosplenial cortex (RS). A two-way factorial analysis of variance regarding the time of GBI (sham, GBI3, GBI10) or the period after GBI (day 7, day 90) was employed in each area. Regarding the time of GBI, there were significant differences in both the ACC and the RS (p < 0.001, respectively). Regarding the period after GBI, there was no significant difference in the ACC, whereas a significant difference was found in the RS (p = 0.005). In each area and in each phase, the numbers did not change in GBI3 (one-way ANOVA followed by a Tukey test) and decreased in GBI10 (p < 0.005). The numbers in the RS from the acute phase to chronic phase did not change in the sham and GBI3, and decreased in GBI10 (independent t-test, p < 0.001). However, histochemical staining with Fluoro-Jade B suggested that neuronal cell death did not occur in both the ACC and the RS in all groups. The present findings indicate that the cortical remodeling potential in the Cg decreases in the acute phase after GBI, and continues to decrease until the chronic phase.

Acute stress exposure preceding transient global brain ischemia exacerbates the decrease in cortical remodeling potential in the rat retrosplenial cortex.

Doublecortin (DCX)-immunoreactive (-ir) cells are candidates that play key roles in adult cortical remodeling. We have previously reported that DCX-ir cells decrease after stress exposure or global brain ischemia (GBI) in the cingulate cortex (Cg) of rats. Herein, we investigate whether the decrease in DCX-ir cells is exacerbated after GBI due to acute stress exposure preconditioning. Twenty rats were divided into 3 groups: acute stress exposure before GBI (Group P), non-stress exposure before GBI (Group G), and controls (Group C). Acute stress or GBI was induced by a forced swim paradigm or by transient bilateral common carotid artery occlusion, respectively. DCX-ir cells were investigated in the anterior cingulate cortex (ACC) and retrosplenial cortex (RS). The number of DCX-ir cells per unit area (mm(2)) decreased after GBI with or without stress preconditioning in the ACC and in the RS (ANOVA followed by a Tukey-type test, P<0.001). Moreover, compared to Group G, the number in Group P decreased significantly in RS (P<0.05), though not significantly in ACC. Many of the DCX-ir cells were co-localized with the GABAergic neuronal marker parvalbumin. The present study indicates that cortical remodeling potential of GABAergic neurons of Cg decreases after GBI, and moreover, the ratio of the decrease is exacerbated by acute stress preconditioning in the RS.

Acute stress exposure preceding global brain ischemia accelerates decreased doublecortin expression in the rat retrosplenial cortex.

BACKGROUND: Psychological distress is a risk factor of stroke in humans and worsens the behavioral and neurological outcomes. In rats, acute stress exposure preceding ischemic events attenuates learning and memory. The retrosplenial cortex (RS) plays an important role in these functions, and global brain ischemia (GBI) or acute stress exposure can induce a decrease in expression of the immature neuronal marker, doublecortin (DCX), in the RS. However, little is known about the DCX expression in the RS after stress exposure prior to GBI. METHODS: Eighteen male Sprague-Dawley rats were used. Acute stress exposure was applied as the forced swim paradigm and GBI was induced by bilateral common carotid arterial occlusion for 10 min. The rats were divided into three groups: GBI model preconditioned by stress (n = 6, Group P), GBI model preconditioned by non-stress (n = 6, Group G), and controls (n = 6, Group C). We performed immunohistochemistry to observe and analyze the DCX-expressing cells and Fluoro-Jade B (FJB) staining to detect cell death in the RS after GBI in each group. RESULTS: The total number of DCX-expressing cells was 1,032, 1,219, and 1,904 in Group P, Group G, and Group C, respectively. The mean number of DCX-expressing cells per unit area was significantly lower in Group P and Group G than in Group C (P < 0.001). Moreover, the number was significantly lower in Group P than in Group G (P < 0.05). In each group, no FJB positive cells were observed. CONCLUSION: DCX plays an important role in various cytoskeletal changes. Preconditioning by acute stress exposure accelerated the decrease in DCX expression in the RS after GBI.

Endovascular treatment for ruptured vertebral artery dissecting aneurysms at the acute stage.

OBJECTIVE: Ruptured vertebral artery dissecting aneurysms (VADA) should be treated promptly because of the high risk of rebleeding. However, it is difficult to treat dissecting aneurysm during the acute stage using microsurgery because of high intracranial pressure or brain edema. Therefore, endovascular treatment of the ruptured VADA may be a better technique. We retrospectively studied the efficacy and outcome of endovascular treatment of ruptured VADA at the acute stage. METHODS: Ten patients with ruptured VADA received endovascular treatment at the acute stage. Eight patients who had dissecting aneurysms were treated by internal trapping of the dissected segment. We performed stent-assisted coiling (SAC) for a case of VADA in contralateral hypoplastic VA and a case of bilateral dissections, ruptured VADA of the right VA and VA dissection of the left VA. RESULTS: Four patients had good recovery, 3 patients had moderate disability, 2 patients had severe disability, and 1 patient died from initial severe SAH. There was no rebleeding or procedure-related complication. However, one patient who was treated by SAC had ischemic complications post-treatment. CONCLUSION: Endovascular treatment of ruptured VADA in the acute stage appears to be safe and effective.

DCX-expressing neurons decrease in the retrosplenial cortex after global brain ischemia.

Many studies have demonstrated cognitive function disorders including space learning disorders after global brain ischemia (GBI). Previous research on space perception and learning has indicated that the retrosplenial cortex (RS) is strongly involved. We performed immunostaining with doublecortin (DCX) for neurons with plasticity potential in the RS and investigated the neuronal numbers to assess the changes of plasticity in the RS following GBI. We employed male Sprague-Dawley rats and carried out bilateral carotid arterial occlusion for 10 min as a GBI model (control, n = 5; GBI model, n = 5). We counted the right and left hemispheres separately on two serial sections, for a total of four regions per animal to examine the differences in expression related to GBI. Additionally, we performed Fluoro-Jade B (FJB) staining to investigate the cause of any DCX-expressing neuron decrease. The total number of DCX-expressing neurons was 1,652 and 912 in the controls and GBI model, respectively. The mean number of DCX-expressing neurons per unit area was significantly lower in the GBI model than in the controls. FJB positive neurons were not found in the RS, while many were present in the -hippocampus CA1 after GBI. The decrease of DCX-expressing neurons in the RS indicated a plasticity decrease following GBI. The lack of FJB positive neurons in the RS after GBI suggested that the decrease of DCX-expressing neurons in the RS was not due to neuronal cell death in contrast to the hippocampus CA1, while the FJB positive neurons in the hippocampus indicated a delayed neuronal cell death as observed in many previous studies.

Decrease in doublecortin expression without neuronal cell death in rat retrosplenial cortex after stress exposure.

Exposure to acute stress by forced swim impairs spatial learning and memory in rats. The retrosplenial cortex plays an important role in spatial learning and memory. A cell population that expresses immature neuronal markers, including doublecortin (DCX), plays a key role in plasticity of the adult brain through formation of new neurons. Here, we aimed to determine whether rats exposed to acute stress showed changes in DCX expression in retrosplenial cortex cells. Twelve male Sprague-Dawley rats were used. Six were subjected to acute stress by forced swim (group S), and the remaining six served as controls (group C). Immunohistochemical staining was performed for DCX, neuron-specific nuclear protein, parvalbumin, calbindin, calretinin, and somatostatin. Newly generated cells were immunohistochemically detected by daily administration of 5-bromo-2'-deoxyuridine for 1 week. Fluoro-Jade B staining was performed to detect cell death. Group S showed lower number of DCX-expressing cells than group C (P<0.001). The proportion of DCX-expressing cells showing neuron-specific nuclear protein co-localization (24% in group S; 27% in group C) or parvalbumin co-localization (65% in group S; 61% in group C) remained unchanged after acute stress exposure. Neither 5-bromo-2'-deoxyuridine-positive nor Fluoro-Jade B-positive cells were found in the retrosplenial cortex of groups S and C. DCX-expressing cells in the retrosplenial cortex decreases markedly without cell death after acute stress exposure. Neuronal differentiation of these cells toward gamma aminobutyric acidergic interneurons appears to be unaltered. The decrease in DCX expression may reduce plasticity potential within the retrosplenial cortex and attenuate spatial learning and memory function.