Initial radiological findings utilizing titanium basket for cervical open door laminoplasty.

BACKGROUND: Cervical laminoplasty, utilizing different spacers to ''keep the door open,'' is the gold standard in Japan for treating ossification of the posterior longitudinal ligament (OPLL) and cervical spondylotic myelopathy (CSM). Here, we utilized a novel titanium ''basket'' spacer (Laminoplasty Basket: L-Basket; Ammtec, Tokyo) to perform open door cervical laminoplasty to keep the "door open" while also allowing for bony fusion across the open door. METHODS: Twenty-seven patients with/without OPLL were treated with open door laminoplasty utilizing the basket spacer. Patients were analyzed with preoperative/postoperative JOA scores, and X-rays/computed tomography (CT) at least 12 months (range, 12-19 months) postoperatively. RESULTS: Improvement from the preoperative JOA score of 10.3 points to the postoperative JOA of 14.8 points was noted 3 months postoperatively. There were no complications except one patient who had transient C5 palsy. Twelve months postoperatively, X-rays/CT documented fusion on both the open (62%) and hinge sides (90.2%); circumferential fusion was observed 59.8% of the time. CONCLUSION: This titanium "basket" spacer (Laminoplasty Basket: L-Basket; Ammtec, Tokyo) promoted bone union between the spacer and both lamina, lateral masses following cervical laminoplasty without undue complications.

[Case of intracerebral hemorrhage due to amphetamine abuse].

We report a case of intracranial hemorrhage due to amphetamine abuse in a young adult. A 34-year-old, confused woman was transferred to our emergency room with right hemiparesis and aphasia. CT at admission demonstrated intracerebral hemorrhage in the left frontal and parietal lobes, associated with subarachnoid hemorrhage. MRA shortly after admission revealed no intracerebral vascular anomaly. Cerebral angiography following admission showed irregularity of the vessel wall in the left anterior and middle cerebral arteries. Later, a toxicology screen test for urine was found to be positive for amphetamines and metamphetamines. These findings suggested that cerebral vasculitis and hypertensive surge induced by amphetamines caused intracranial and subarachnoid hemorrhage. Amphetamine abuse should always be considered as a cause of intracranial hemorrhage in young adults.

Secondary ischemia impairing the restoration of ion homeostasis following traumatic brain injury.

OBJECT: It is well established that posttraumatic secondary ischemia contributes to poor outcome. Ion dysfunction leading to cytotoxic edema is a primary force in the formation of ischemic brain edema and is a principal component of traumatic brain swelling. Because cell swelling is the result of net ion and water movement, it is crucial to have a thorough understanding of these transient phenomena. The purpose of this study was to characterize the effects of secondary ischemia following traumatic brain injury (TBI) on the ability to restore ion homeostasis. METHODS: Twenty-four Sprague-Dawley rats were divided into four groups of six animals each. The rats underwent transient forebrain ischemia via bilateral carotid artery occlusion combined with hypotension: 15 minutes of forebrain ischemia (Group 1); 60 minutes of forebrain ischemia (Group 2); impact acceleration/TBI (Group 3); and impact acceleration/TBI followed by 15 minutes of ischemia (Group 4). Ischemia resulted in a rapid accumulation of [K+]e:41.94 +/- 13.65 and 66.33 +/- 6.63 mM, respectively, in Groups 1 and 2, with a concomitant decrease of [Na+]e:64 +/- 18 mM and 72 +/- 11 mM in Groups 1 and 2. Traumatic brain injury resulted in a less severe although identical trend in ion dysfunction ([K+]e 30.42 +/- 11.67 mM and [Na+]e 63 +/- 33 mM). Secondary ischemia resulted in prolonged and sustained ion dysfunction with a concomitant elevation of intracranial pressure (ICP). CONCLUSIONS: Analysis of these results indicates that ischemia and TBI are sublethal in isolation; however, when TBI is associated with secondary ischemia, ion dysfunction is sustained and is associated with elevated ICP.

A new rat model of diffuse brain injury associated with acute subdural hematoma: assessment of varying hematoma volume, insult severity, and the presence of hypoxemia.

The aim of this study was to develop a new rat model of diffuse brain injury (DBI) associated with acute subdural hemorrhage (SDH). In order to make this model more clinically relevant, we determined whether the varying hematoma volume, severity of DBI, or the presence of hypoxemia could influence the physiological consequence. SDH was made by an autologous blood injection, while DBI was induced using the impact acceleration model (mild, 450 g/1 m, severe, 450 g/2 m). Physiological parameters measured included intracranial pressure (ICP), mean arterial blood pressure (MABP), cerebral blood flow (CBF), and brain tissue water content. In the first series, 23 rats were randomized into the five following groups: Group 1, sham; Group 2, 400 (microL SDH; Group 3, SDH400 + mild DBI; Group 4, SDH400 + severe DBI; and Group 5, SDH300 + severe DBI. Results suggested that SDH300 + severe DBI (Group 5) may be the most suitable model, in which the MABP and CBF temporarily decreased during the SDH induction, but thereafter recovered to the baseline. Conversely, ICP was persistently elevated throughout the experiment. The water content was also significantly higher in both hemispheres compared to that of sham. In the second series, the animal was exposed to a hypoxemic insult (10 or 30 min) in addition to SDH300 + severe DBI (Group 6). The prolonged hypoxemia caused both a severe CBF reduction without recovery and a bilateral brain swelling, whereas the brief hypoxemia showed a gradual CBF recovery from the transient reduction and an increased water content only in the SDH side. These results suggest that these models may be potentially useful to study the combination of DBI and SDH with or without hypoxemia.