The Case of a Patient with Idiopathic Intracranial Hypertension Who Required Additional Stenting for Stent-Adjacent Stenosis.

Objective: We report the case of a patient with recurred idiopathic intracranial hypertension (IIH) with transverse sinus (TS) stenosis after initial stenting, which was treated with additional stent placed in tandem to the secondarily occurred stent-adjacent stenosis (SAS). Case Presentation: A 41-year-old woman complained of reduced visual acuity and blurred vision, and presented with papilledema. Lumbar puncture revealed an opening pressure of 36 cmH2O. MRI revealed no space-occupying lesions, and the patient was diagnosed with IIH based on the modified Dandy criteria. MR venography revealed stenosis in the right and hypoplastic left TS. The patient complained of headache and neck pain after each lumbar puncture for examination. Venous sinus stenting (VSS) was performed in the right TS. One month after stenting, follow-up angiography revealed stenosis in the remaining parts of TS. Five months after stenting, IIH recurred, and SAS was detected on angiography. An additional stenting procedure was performed. Three months after the second treatment, her symptoms disappeared and cerebrospinal fluid pressure was normalized. Conclusion: Patients with post-VSS recurrent IIH may develop restenosis in the remaining parts of TS at variable progression speeds. In this case, angiography revealed gradually advancing stenosis that seemed to form SAS at the time of recurrence. If the initial VSS is effective for IIH, SAS can also be treated effectively and less invasively with a second stent placement covering the entire TS length.

Effect of 35 degrees C hypothermia on intracranial pressure and clinical outcome in patients with severe traumatic brain injury.

BACKGROUND: From 1994, we have used therapeutic hypothermia in patients with severe traumatic brain injury (Glasgow Coma Scale scores of 5 or less). In 2000, we altered the target temperature to 35 degrees C from the former 33 degrees C, as our findings suggested that cooling to 35 degrees C is sufficient to control intracranial hypertension, and that hypothermia below 35 degrees C may predispose patients to persistent cumulative oxygen debt. We attempted to clarify whether 35 degrees C hypothermia has the same effect as 33 degrees C hypothermia in reducing intracranial hypertension and whether it is associated with fewer complications and improved outcomes. METHODS: We compared intracranial pressure (ICP) and biochemical parameters in the 30 patients treated with 35 degrees C hypothermia (January 2000 to June 2005) with those in the 31 patients treated with 33 degrees C hypothermia (July 1994 to December 1999). RESULTS: Patient characteristics were similar in the two groups. The mean temperature during hypothermia was 35.1 +/- 0.7 degrees C in the 35 degrees C hypothermia group and 33.4 +/- 0.8 degrees C in the 33 degrees C hypothermia group. Mean ICP was controlled under 20 mm Hg during hypothermia in both the 35 degrees C hypothermia and 33 degrees C hypothermia groups. The incidence of intracranial hypertension and low cerebral perfusion pressure did not differ between the two groups. The 35 degrees C hypothermic patients exhibited a significant improvement in the decline of serum potassium concentrations during hypothermia and in the increment of C-reactive protein after rewarming. The mortality rate and the incidence of systemic complications tended to be lower in the 35 degrees C group. CONCLUSIONS: Cooling patients to 35 degrees C is safe and the ICP reduction effects of 35 degrees C hypothermia are similar to those of 33 degrees C hypothermia.

[The influence of the primary management on the outcome of severe traumatic brain injury: role of neurosurgeons].

OBJECTIVE: To evaluate the influence of the primary management on the outcome in severe head-injured-patients, we retrospectively studied the patients transported to our hospital directly and the those referred from other hospitals. METHODS: The subjects include 83 patients with severe head injury with a Glasgow coma scale (GCS) score of 8 or lower at the time of arrival at the emergency room during the periods of between January, 2003 to March, 2006. Forty nine patients were transported directly (direct group) and 34 referred from other hospitals (transfer group). The patients in direct group was transported by a helicopter or an ambulance car, and the patients in transfer group were carried by an ambulance car. The variables analyzed in these 2 groups of patients were the initial GCS score, injury severity score (ISS), and the presence or absence of light reflex or shock at the time of transportation, the time periods from the injury and primary management, the time from the injury and operation in surgical patients, the type of primary managements and outcomes. RESULT: The number of patients with shock was significantly larger in the transfer group than that in the direct group. The shock was considered to be developed during the transportation. The outcomes were then significantly poorer in the transfer group than those in the direct group. There was no significant difference between the time from the injury and primary management in these 2 groups, but the primary management seemed to be more appropriate in the direct group compared to that in the transfer group. These findings suggested that outcomes of severe high-impact head injuries, such as injuries caused by a traffic accident, would be markedly affected by the primary treatment. CONCLUSION: The doctor-helicopter system, in which emergency physicians arrive at the site shortly after the occurrence of injury, and start primary examination, will influence outcomes of multiple injuries accompanying severe head injury. Severe head-injured patients by high-impact injury should be transported as early as possible to the emergency medical center, and neurosurgeons have an important role in the primary management.

[Clinical study of multiple traumas with severe facial injury undergoing emergency endovascular treatment: significance of emergency embolization of the external carotid artery].

The outcome of multiple injures freqently depends on the priority of treatments, and the decision as to the procedures and timing of primary care is extremely important. We studied the patients with multiple trauma whounderwent emergency endovascular treatment for facial hemorrhage related to external carotid arterial injury. The subjects are 5 patients who underwent embolization of the external carotid artery by an endovascular approach among patients with multiple traumas who were brought to our hospital by ambulance. In these patients, the vital signs on arrival, interval between injury and intravascular surgery, type of brain injury, type and grade of concurrent injury and outcome were studied. Three patients showed hemorrhagic shock on arrival, and 1 patient showed hemorrhagic shock immediately after arrival. The mean interval between injury and endovascular surgery was 3.9 hours. All patients had skull base fracture, and abnormal intracranial lesions on initial CT including 4 focal injuries and 1 diffuse injury. Moderate to severe thoracic/abdominal injuries were noted in 3 patients. In the remaining 2 patients, there was no trauma in the thoracic or abdominal regions. Intraperitoneal hemorrhage with splenic injury was observed in 3 patients. In 3 of 4 patients died by hemorrhagic shock because of the delay of endvascular treatments. In trauma patients with persistent hemorrhage, emergency endovascular treatment should be considered as a primary survey for initial treatment without delay under intensive conservative treatment.

[Simultaneous multiple hypertensive intracerebral hematoma].

Hypertensive intracerebral hemorrhage (HIH) occurring simultaneously in different locations is rare. We encountered 11 such cases between January 1990 and November 2002. The diagnosis of all 11 cases was established by computed tomography, and the location of the hematomas was: cerebellum and basal ganglia in 5 cases, pons and basal ganglia in 4, and subcortex and basal ganglia in 2. Our patients were analyzed with respect to clinical characteristics, pathogenesis of multiple hematomas, and indication of operation. These patients represented 1% of all 1,069 patients we encountered with HIH. As past history, there were no characteristic disorders except hypertension. There were no characteristic initial symptoms suggesting that hemorrhage had occurred simultaneously. Both supra- and infra-tentorial hematomas were observed in 80% of the patients, and the size of the multiple hematomas was proportional in principle. Cerebellar hematomas were often mild, and pontine hematomas were often severe. The outcome in those patients whose neurological grading was 1 to 3 was good with conservative therapy or surgical treatment. The severity, treatment methods, and outcomes in these patients were similar to those in patients with single HIH, which suggests only a slight influence of multiple lesions on outcome. As for the possible mechanism of simultaneous multiple hemorrhages, we speculated that bleeding occurred simultaneously in the different regions, or that the initial bleeding was followed after a short time by secondary bleeding due to high intracranial pressure and circulatory disturbance. In patients with cerebellar hematoma, initial symptoms suggested the development of secondary hemorrhage after primary hemorrhage. The surgical treatment for multiple hematomas should be determined by the location and maximum axis of the hematoma. We proposed that cerebellar hematomas should be removed if the supra-tentorial hematoma is small.

Effect of hypothermia on serum electrolyte, inflammation, coagulation, and nutritional parameters in patients with severe traumatic brain injury.

INTRODUCTION: We evaluated the effect of induced hypothermia on biochemical parameters in patients with severe traumatic brain injury. METHODS: We obtained hemoglobin, hematocrit, white blood count, lymphocyte count, platelet count, and serum concentrations of sodium, potassium, glucose, albumin, and C-reactive protein, and prothrombin time, hepaplastin test, activated partial thromboplastin time, antithrombin-III, alpha2PI, and nitrogen excretion on the day of admission, and on days 1, 3, 5, 7, 14, and 21 after the injury in 31 patients with severe head injury who were treated with hypothermia of 33 degrees ranging from 48 to 72 hours. We selected 33 normothermic patients as a control group; these patients were selected from patients who had been treated before hypothermia was used as a treatment modality, by the same criteria for hypothermia therapy. We compared the biochemical markers and rectal temperature and intracranial pressure in the hypothermia group with those in the normothermia group. Outcome was assessed using the Glasgow Outcome Scale at 6 months after injury. RESULTS: The demographic characteristics, severity, and outcome were similar in the hypothermia and normothermia group. Intracranial pressure was significantly decreased by hypothermia. Serum potassium concentration decreased significantly during hypothermia. White blood cell counts and C-reactive protein levels were higher after rewarming in the hypothermia group, and these were also higher in the patients with infectious complications, although the incidence of infectious complications did not differ between the hypothermia and normothermia groups. There were no statistically significant prolongations of activated partial thromboplastin time and no decline in prothrombin time with hypothermia. Platelet count, antithrombin-III, and alpha2PI did not differ significantly between the two groups. CONCLUSION: Hypothermia of 33 degrees for 48-72 hours does not appear to increase the risk for coagulopathy and infections, although hypothermic patients exhibited significant increments in inflammatory markers such as C-reactive protein and white blood counts after rewarming.