Deep brain stimulation (DBS) is used to treat symptoms by modulating the cortico-striato-thalamo-cortical (CSTC) loop in the central nervous system (CNS), and attempts to research loop circuit disorders have been globally initiated among the intractable neurological and psychiatric disorders. DBS treatment has been evaluated for all these newly found CNS loop circuit disorders. In 2011, neurosurgical treatments for psychiatric disorders were renamed from “psychosurgery” to “neurosurgery for psychiatric disorders (NPD)” by the World Society for Stereotactic and Functional Neurosurgery (WSSFN). Moreover, in 2014, “Consensus on guidelines for stereotactic neurosurgery for psychiatric disorders” was published by the WSSFN to address the differences in correspondence of stereotactic NPD. Globally, two multicenter prospective randomized control trials regarding DBS of the subcallosal cingulated gyrus and ventral anterior internal capsule/ventral striatum for intractable depression have been terminated after futility analysis. However, DBS for intractable obsessive-compulsive disorder (OCD), unlike for intractable depression, is showing steady development. In Japan, NPDs have not been performed since 1975 following the adoption of “Resolution of total denial for psychosurgery” by the Japanese Society of Psychiatry and Neurology. Nevertheless, a trend to adopt new neuro-modulation techniques for psychiatric disorders, including DBS, are emerging. We have created a clinical research protocol for the use of DBS in intractable OCD, which has been approved by the ethical committee of Hamamatsu University School of Medicine, with the hope of commencing DBS treatment for intractable OCD patients in the near future.
The amygdala and uncus are located close to important neurovascular structures. We describe a safe technique for resection of amygdala and uncus. Under general anesthesia, the patient is positioned supine, with the head rotated approximately 20 degrees to the unoperated side and slightly extended. By using a trans-anterior T1 subpial approach, the inferior horn of the lateral ventricle is opened, and hippocampectomy is performed. We treat an imaginary plane formed by the inferior circular sulcus of the insula, the endorhinal sulcus, and the inferior choroidal point as the upper border of amygdalar resection. After confirming the position of the inferior choroidal point, the border between the temporal stem and uncus is exposed from anterior to posterior. This border is continuous with the endorhinal sulcus. By exposing the endorhinal sulcus, the anterior choroidal artery and optic tract can be visualized. The amygdala is disconnected through complete exposure of the endorhinal sulcus to the inferior choroidal point. After the lateral side of the uncus is disconnected, the amygdala and uncus are removed en bloc. Since April 2014, we have used the described procedure to remove amygdalar–uncal lesions in 15 patients. The lesion was completely removed in all cases without complications. Histological specimens were obtained in all cases. Our procedure enables safe and complete removal of amygdalar–uncal lesions. Imagining the plane formed by the inferior circular sulcus, inferior choroidal point, and endorhinal sulcus is essential for complete removal of the lesion and for preserving important structures.
We performed metabolomic analyses of mouse brain using a transient middle cerebral artery occlusion (tMCAO) model with Matrix Assisted Laser Desorption/Ionization (MALDI)-mass spectrometry imaging (MSI) to reveal metabolite changes after cerebral ischemia. We selected and analyzed three metabolites, namely creatine (Cr), phosphocreatine (P-Cr), and ceramides (Cer), because these metabolites contribute to cell life and death. Eight-week-old male C57BL/6J mice were subjected to tMCAO via the intraluminal blockade of the middle cerebral artery (MCA) and reperfusion 60 min after the induction of ischemia. Each mouse was randomly assigned to one of the three groups; the groups were defined by the survival period after reperfusion: control, 1 h, and 24 h. Corrected samples were analyzed using MALDI-MSI. Results of MSI analysis showed the presence of several ionized substances and revealed spatial changes in some metabolites identified as precise substances, including Cr, P-Cr, Cer d18:1/18:0, phosphatidylcholine, L-glutamine, and L-histidine. Cr, P-Cr, and Cer d18:1/18:0 were changed after tMCAO, and P-Cr and Cer d18:1/18:0 accumulated over time in ischemic cores and surrounding areas following ischemia onset. The upregulation of P-Cr and Cer d18:1/18:0 was detected 1 h after tMCAO when no changes were evident on hematoxylin and eosin staining and immunofluorescence assay. P-Cr and Cer d18:1/18:0 can serve as neuroprotective therapies because they are biomarker candidates for cerebral ischemia.
Traumatic brain injury (TBI) is a leading cause of death and disability in trauma patients. Patients with TBI frequently sustain concomitant injuries in extracranial regions. The effect of severe extracranial injury (SEI) on the outcome of TBI is controversial. For 8 years, we retrospectively enrolled 485 patients with the blunt head injury with head abbreviated injury scale (AIS) ≧ 3. SEI was defined as AIS ≧ 3 injuries in the face, chest, abdomen, and pelvis/extremities. Vital signs and coagulation parameter values were also extracted from the database. Total patients were dichotomized into isolated TBI (n = 343) and TBI associated with SEI (n = 142). The differences in severity and outcome between these two groups were analyzed. To assess the relation between outcome and any variables showing significant differences in univariate analysis, we included the parameters in univariable and multivariable logistic regression analyses. Mortality was 17.8% in the isolated TBI group and 21.8% in TBI with SEI group (P = 0.38), but the Glasgow Outcome Scale (GOS) in the TBI with SEI group was unfavorable compared to the isolated TBI group (P = 0.002). Patients with SBP ≦ 90 mmHg were frequent in the TBI with SEI group. Adjusting for age, GCS, and length of hospital stay, SEI was a strong prognostic factor for mortality with adjusted ORs of 2.30. Hypotension and coagulopathy caused by SEI are considerable factors underlying the secondary insults to TBI. It is important to manage not only the brain but the whole body in the treatment of TBI patients with SEI.
Metronidazole induced encephalopathy (MIE), an encephalopathy brought by an antibiotic, is characterized with cerebellar dysfunction, altered mental status and extrapyramidal symptoms. MIE can result in an acute manifestation, but MIE has not been reported as a stroke mimic. An 86-year-old patient undergoing metronidazole therapy for Clostridium difficile enteritis presented to our hospital with sudden disoriented status and motor weakness of the left extremities. Computed tomography (CT) was unrevealing of intracranial hemorrhagic change, and CT angiography did not show any apparent major occlusion or stenosis of the intracranial vessels. However, CT perfusion (CTP) revealed a decrease in peripheral blood flow in the right cerebral hemisphere, and tissue plasminogen activator was administrated for a possible acute ischemic stroke. The findings of follow-up magnetic resonance imaging (MRI) were typical for MIE, revealing areas of hyperintensity on fluid attenuated inversion recovery (FLAIR) signal intensity in the dentate nuclei, the splenium of the corpus callosum, and in the dorsal midbrain. The degree of hyperintensity was stronger in the left dentate nucleus than in the right left dentate on FLAIR and the apparent diffusion coefficient map. The asymmetric findings of the left dentate nucleus on MRI were considered to be responsible for the clinical symptoms and the findings of CTP. We report a rare case of MIE mimicking an acute ischemic stroke, and hypothesize the relationship between the findings of CTP and that of MRI based on the anatomical connection of the dentate nucleus and the cerebral hemisphere.