Severe Calcification of Femoral Arteries Causes Tourniquet Failure Accompanied by Massive Bleeding.

Tourniquet failure is attributed to inadequate tourniquet pressure, inadequate exsanguination, failure to compress medullary vessels within the bone, and incompressible calcified arteries. We herein report a case of massive bleeding using a properly functioning tourniquet in a patient who had bilateral calcified femoral arteries. When incompressible calcified arteries are present, the inflated tourniquet cuff fails to adequately compress the underlying artery, yet acts as an efficient venous tourniquet, which leads to an increase in bleeding. It is therefore critical to preoperatively confirm the effectiveness of the tourniquet in arterial occlusion in patients with severe arterial calcification.

Propofol, an Anesthetic Agent, Inhibits HCN Channels through the Allosteric Modulation of the cAMP-Dependent Gating Mechanism.

Propofol is a broadly used intravenous anesthetic agent that can cause cardiovascular effects, including bradycardia and asystole. A possible mechanism for these effects is slowing cardiac pacemaker activity due to inhibition of the hyperpolarization-activated, cyclic nucleotide-gated (HCN) channels. However, it remains unclear how propofol affects the allosteric nature of the voltage- and cAMP-dependent gating mechanism in HCN channels. To address this aim, we investigated the effect of propofol on HCN channels (HCN4 and HCN2) in heterologous expression systems using a whole-cell patch clamp technique. The extracellular application of propofol substantially suppressed the maximum current at clinical concentrations. This was accompanied by a hyperpolarizing shift in the voltage dependence of channel opening. These effects were significantly attenuated by intracellular loading of cAMP, even after considering the current modification by cAMP in opposite directions. The differential degree of propofol effects in the presence and absence of cAMP was rationalized by an allosteric gating model for HCN channels, where we assumed that propofol affects allosteric couplings between the pore, voltage-sensor, and cyclic nucleotide-binding domain (CNBD). The model predicted that propofol enhanced autoinhibition of pore opening by unliganded CNBD, which was relieved by the activation of CNBD by cAMP. Taken together, these findings reveal that propofol acts as an allosteric modulator of cAMP-dependent gating in HCN channels, which may help us to better understand the clinical action of this anesthetic drug.

A Pure Acute Subdural Hematoma Presenting with a Diploic Arteriovenous Fistula: Case Report and Literature Review.

Objective: We report a case of pure acute subdural hematoma (SDH) caused by a diploic arteriovenous fistula (AVF) and it is a first case report as far as we researched it. Case Presentation: A 19-year-old man was admitted as an emergency to our hospital with headache and nausea. CT scan on hospital admission showed a right acute SDH. Because there was no history of head trauma, MRI, MRA, and DSA were performed to identify a source of bleeding. DSA disclosed an AVF. The shunt was located between a frontotemporal branch of the middle meningeal artery (MMA) and a diploic vein, and its shunting point formed an aneurysmal sac, which was considered to have ruptured. Endovascular treatment was administered rather than surgical treatment to prevent re-bleeding because the patient was conscious and alert, CT showed a small SDH, and the left MMA near the shunting point was accessible for catheterization. A diluted mixture of 25% n-butyl-2-cyanoacrilate was injected into a left frontoparietal branch just before the shunting point and the shunt, including the aneurysmal sac, was obliterated. The patient's postoperative course was uneventful and he was discharged without neurological deficits. Conclusion: We experienced a patient with a pure acute SDH caused by diploic AVF. In patients with non-traumatic acute SDH, DSA is recommended to determine its underlying cause. Our review of published reports yielded few instances of non-traumatic pure acute SDH in young people. Possible causative factors should be investigated promptly and appropriate treatment provided immediately.

Positive Inotropic Effects of ATP Released via the Maxi-Anion Channel in Langendorff-Perfused Mouse Hearts Subjected to Ischemia-Reperfusion.

The organic anion transporter SLCO2A1 constitutes an essential core component of the ATP-conductive large-conductance anion (Maxi-Cl) channel. Our previous experiments using Langendorff-perfused mouse hearts showed that the Maxi-Cl channel contributes largely to the release of ATP into the coronary effluent observed during 10-min reperfusion following a short period (6 min) of oxygen-glucose deprivation. The present study examined the effect of endogenous ATP released via Maxi-Cl channels on the left ventricular contractile function of Langendorff-perfused mouse hearts, using a fluid-filled balloon connected to a pressure transducer. After the initial 30-min stabilization period, the heart was then perfused with oxygen-glucose-deprived Tyrode solution for 6 min, which was followed by a 10-min perfusion with oxygenated normal Tyrode solution in the absence and presence of an ATP-hydrolyzing enzyme, apyrase, and/or an adenosine A1 receptor antagonist, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX). In the absence of apyrase and DPCPX, the left ventricular developed pressure (LVDP) decreased from a baseline value of 72.3 ± 7.1 to 57.5 ± 5.5 mmHg (n = 4) at the end of 6-min perfusion with oxygen-glucose-deprived Tyrode solution, which was followed by a transient increase to 108.5 ± 16.5 mmHg during subsequent perfusion with oxygenated normal Tyrode solution. However, in the presence of apyrase and DPCPX, the LVDP decreased to the same degree during 6-min perfusion with oxygen-glucose-deprived Tyrode solution, but failed to exhibit a transient increase during a subsequent perfusion with oxygenated normal Tyrode solution. These results strongly suggest that endogenous ATP released through Maxi-Cl channels contributes to the development of transient positive inotropy observed during reperfusion after short-period hypoxia/ischemia in the heart.

A computational analysis of the effect of sevoflurane in a human ventricular cell model of long QT syndrome: Importance of repolarization reserve in the QT-prolonging effect of sevoflurane.

The slowly and rapidly activating delayed rectifier K+ channels (IKs and IKr, respectively) contribute to the repolarization of ventricular action potential in human heart and thereby determine QT interval on an electrocardiogram. Loss-of-function mutations in genes encoding IKs and IKr cause type 1 and type 2 long QT syndrome (LQT1 and LQT2, respectively), accompanied by a high risk of malignant ventricular arrhythmias and sudden cardiac death. This study was designed to investigate which cardiac electrophysiological conditions exaggerate QT-prolonging and arrhythmogenic effects of sevoflurane. We used the O'Hara-Rudy dynamic model to reconstruct human ventricular action potential and a pseudo-electrocardiogram, and simulated LQT1 and LQT2 phenotypes by decreasing conductances of IKs and IKr, respectively. Sevoflurane, but not propofol, prolonged ventricular action potential duration and QT interval in wild-type, LQT1 and LQT2 models. The QT-prolonging effect of sevoflurane was more profound in LQT2 than in wild-type and LQT1 models. The potent inhibitory effect of sevoflurane on IKs was primarily responsible for its QT-prolonging effect. In LQT2 model, IKs was considerably enhanced during excessive prolongation of ventricular action potential duration by reduction of IKr and relative contribution of IKs to ventricular repolarization was markedly elevated, which appears to underlie more pronounced QT-prolonging effect of sevoflurane in LQT2 model, compared with wild-type and LQT1 models. This simulation study clearly elucidates the electrophysiological basis underlying the difference in QT-prolonging effect of sevoflurane among wild-type, LQT1 and LQT2 models, and may provide important information for developing anesthetic strategies for patients with long QT syndrome in clinical settings.

[Ruptured Dissecting Aneurysm of M2 Portion of the Middle Cerebral Artery:A Case Report].

A 71-year-old woman presented with a sudden onset of headache and vomiting. Computed tomography(CT)showed diffuse subarachnoid hemorrhage(SAH)that was more severe on the right side. Three-dimensional CT angiography and right carotid angiography(CAG)demonstrated 2-mm microaneurysms at the middle cerebral artery(MCA)bifurcation and anterior communicating artery, with slight narrowing and dilatation of the M2 inferior trunk. Each microaneurysm was smooth, making it difficult to identify the bleeding source. Thus, surgery was postponed at the acute stage, and further investigation was planned. Repeated CAG was diagnostically unsuccessful, finding no source of the bleeding. On day 45 after the onset, exploratory craniotomy was performed to confirm the cause of the SAH. During the operation, both microaneurysms were found to be unruptured. However, the distal portion of the M2 inferior trunk was dark purplish and red and enlarged in a fusiform shape, suggesting a dissecting aneurysm. Residue of the SAH observed near the enlarged vessel identified it as the bleeding source. The enlarged vessel was wrapped with Bemsheets, and the Bemsheets was clipped to secure it. A dissecting aneurysm of the distal MCA is rare, as is the onset of bleeding. Based on a review of the literature related to dissecting aneurysms of the distal MCA, we recommend exploratory craniotomy if CT demonstrates laterality of the sylvian fissure on the SAH and CAG reveals stenosis or occlusion of the distal MCA in cases of SAH for which no bleeding source is detected.

[A case of ganglioglioma extended to the lateral ventricle and associated with neurofibromatosis type 1].

We encountered a rare case of intraventricular ganglioglioma associated with neurofibromatosis type 1. A 42-year-old woman presented with a feeling of heaviness of the head and dizziness. She was diagnosed with neurofibromatosis type 1 because she had multiple subcutaneous neurofibromas and café au lait spots. On admission, she deteriorated slightly(Japan Coma Scale 1)and suffered from cognitive dysfunction and right hemiparesis. A computed tomography(CT)scan showed that she had an obstructed hydrocephalus with a long and circular mass lesion, 2cm in diameter, in the anterior horn of the left lateral ventricle. The mass showed low signal intensity(SI)on the T1-weighted image(WI), heterogeneous high SI on the T2-WI, and dense enhancement on a Gd-DTPA contrast MRI, extending from the head of the left caudate nucleus to the lateral ventricle. The patient underwent an urgent operation via an anterior transcallosal approach because of an obstructed hydrocephalus. The tumor was removed in its entirety, including its origin at the caudate head. The pathological diagnosis was a ganglioglioma grade 1 according with the classification of the World Health Organization. Here we describe this case and discuss the rare association between gangliogliomas and neurofibromatosis type 1.

Surgical strategy for intracranial endodermal cyst--case report.

Two cases of endodermal cyst of the posterior fossa are reported. A 12-year-old girl presented with severe headache and vomiting caused by increased intracranial pressure. Computed tomography and magnetic resonance (MR) imaging showed a cystic mass occupying the ambient and quadrigeminal cisterns. A 65-year-old woman presented with dizziness, and MR imaging revealed a cystic mass in the posterior fossa. The two patients underwent surgery for decompression and resection of the cyst. Surgical specimens of the cyst walls consisted of a single layer of ciliated columnar epithelium. The diagnoses were endodermal cyst. The optimal surgical goal is total resection of the cyst wall, but the cyst wall sometimes tightly adheres to the adjacent nerves, vessels, and vital structures. The cyst must communicate adequately with the surrounding cerebrospinal fluid space, and a newly closed cyst space must be avoided, by the widest possible resection of the cyst wall.

[A case of herpetic meningoencephalitis associated with massive intracerebral hemorrhage during acyclovir treatment: a rare complication].

We report a case of a 35-year-old female with herpetic meningoencephalitis confirmed by polymerase chain reaction and immunohistochemical study for herpes simplex virus-1 accompanied with a massive intracerebral hematoma as a complication. A hematoma localized at the medial temporal lobe and the medial frontal lobe occurred on the 11th day after initiation of acyclovir treatment. She subsequently required emergency surgery for temporal lobectomy, as well as hematoma and external decompression. Intracerebral hematoma with MR imaging showed gyral pattern along the cortex of the medial temporal lobe and the base of the medial frontal lobe. We speculate that the hemorrhage occurred by rupture of small vessels affected by vasculitis in addition to hypertension caused by increased intracranial pressure. We therefore emphasize the risk of intracerebral hemorrhage at an early stage or during acyclovir treatment, especially during one or two weeks after initiation of the treatment, and the necessity of careful observation during these periods.

The course of the lesser petrosal nerve on the middle cranial fossa.

OBJECTIVE: The course of the lesser petrosal nerve is not well understood and may be confused with the course of the greater petrosal nerve during middle fossa surgery. The objective was to examine the course of the lesser petrosal nerve along the floor of the middle cranial fossa from the region of the geniculate ganglion to its outlet from the skull base. There are no studies focused on the course of this nerve in relationship to the floor of the middle cranial fossa. METHODS: Twenty middle fossae from adult cadaveric specimens were examined using 3 to 40x magnification. RESULTS: The lesser petrosal nerve was partially exposed on the floor of the middle fossa without drilling in 75% of the middle fossae and totally covered by thin bone in 25%. It crossed the floor anterior to the greater petrosal nerve and exited the middle fossa through the canaliculus innominatus in 14 cases, foramen spinosum in 3 cases, and the sphenopetrosal suture in 3 cases. The course of the lesser petrosal nerve has been shown in textbooks to be parallel to the greater petrosal nerve. However, the lesser and greater petrosal nerves diverged in the area medial to the geniculate ganglion in 90% of middle fossae with the angle of divergence averaging 11.6 degrees. The course of the lesser petrosal nerve was divided into three patterns based on the site of confluence of the three bundles of fibers forming the nerve. CONCLUSION: The relationships of the lesser petrosal nerve in the middle cranial fossa have been described. An understanding of these relationships will reduce the likelihood of it being confused with the greater petrosal nerve during surgical approaches to the middle fossa.

[Superior sagittal sinus thrombosis caused by Crohn's disease and macrocytic anemia : a case report].

A 32-years-old man with a past history of hemorrhoids presenting with hemiparesis was diagnosed as having sagittal sinus thrombosis with hemorrtagic infarction. Laboratory data revealed macrocytic anemia (Hb 11.2 g/d/) with hypoproteinernia (5.5 g/d). After discharge the patient developed abdominal pain, diarrhea, edema in the leg and sustained anemia. Final diagnosis through colon fiberscope findings was Crohn's disease Macrocytic anemia seemed to be induced by Vit. B12 deficiency due to malabsorption. The mechanism and causal relationship between Crohn's disease and sinus thrombosis is discussed.

Can proximity of the occipital artery to the greater occipital nerve act as a cause of idiopathic greater occipital neuralgia? An anatomical and histological evaluation of the artery-nerve relationship.

BACKGROUND: The purpose of this study was to clarify whether proximity of the occipital artery to the greater occipital nerve can act as a cause of occipital neuralgia, analogous to the contribution of intracranial vessels due to compression in cranial nerve neuralgias, represented by trigeminal neuralgias due to compression of the trigeminal nerve root by adjacent arterial loops. METHODS: Twenty-four suboccipital areas in cadaver heads were studied for anatomical relationships between the occipital artery and the greater occipital nerve, with histopathological assessment of the greater occipital nerve for signs of mechanical damage. RESULTS: The occipital artery and greater occipital nerve were found to cross each other in the nuchal subcutaneous layer, and the latter was constantly situated superficial to the former at the cross point. An indentation of the greater occipital nerve due to the occipital artery was observed at the cross point in all specimens. However, histopathological examination did not reveal any findings of damage to nerves, even in specimens with atherosclerosis of the occipital artery. CONCLUSIONS: Although the present study did not provide direct evidence that the occipital artery contributes to occipital neuralgia at the point of contact with the greater occipital nerve, the possibility still cannot be precluded, because the occipital artery may be palpable in areas corresponding to tenderness of the greater occipital nerve. Further studies, including clinical cases, are needed to clarify this issue.

Anesthetic management of an extremely obese patient.

We present the case of a morbidly obese woman, with a body mass index (BMI) of 73.7 kg.m(-2), who had a gynecological operation under combined general and epidural anesthesia. The patient's trachea was intubated, using a fiberscope, while she was breathing spontaneously after the intravenous injection of fentanyl and propofol as sedatives. Anesthesia was maintained with intravenous propofol and epidural mepivacaine. When the gynecologist placed a sponge in the abdominal cavity to retract the bowel, the patient experienced severe arterial deoxygenation and mild hypotension, due to massive atelectasis of the left lung. Both oxygenation and perfusion were corrected by the removal of the sponge and with the placement of a pillow under the patient's left shoulder. The atelectasis resulted from compression of the left lung by the fatty mediastinum and by the diaphragm being pushed up by the sponge. The hypotension resulted from impaired venous return and hypoxia. The patient suffered no perioperative complications other than atelectasis and a surgical-site infection. Key factors that contributed to the favorable outcome of this patient included a careful tracheal intubation technique, the choice and dose of anesthetic agents, immediate correction of the factors leading to atelectasis, early ambulation, and prophylaxis for deep vein thrombosis.

Anatomic dissection and classic three-dimensional documentation: a unit of education for neurosurgical anatomy revisited.

OBJECTIVE AND IMPORTANCE: Despite development of computer-assisted neurosurgical navigation, learning by dissecting anatomic specimens is still important. CLINICAL PRESENTATION: We describe the processes from preparation of specimens for cranial dissection to documentation of three-dimensional (3-D) stereoscopic pictures, particularly focusing on the latter, which has been initiated in the Microneuroanatomy Laboratory, Department of Neurological Surgery, University of Florida. INTERVENTION: Preparation consists of irrigation of the major vessels and injection of colored silicone. The 3-D documentation, obtaining two pictures corresponding to each eye's view, is obtained by the shoot-shift-shoot method using a single camera mounted on a slide bar. The key of this method is correct shifting of the camera without alignment error to get exact 3-D effects. Observation of 3-D image can be made with free viewing, a 3-D viewer, or projection. Tips concerning all of the processes involved are described. CONCLUSION: The presented method of dissection and obtaining 3-D images is beneficial for accomplishing studies of anatomy and for providing teaching method.

Nevoid Basal cell carcinoma syndrome with medulloblastoma and meningioma--case report.

A 35-year-old man presented with a rare case of nevoid basal cell carcinoma syndrome, or Gorlin's syndrome, associated with both medulloblastoma and meningioma, manifesting as visual field constriction due to multiple parasellar tumors. He had undergone resection of a medulloblastoma at the age of 1 year 9 months, followed by adjunctive irradiation with a total dose of 40 Gy. He presented with multiple subcutaneous nodules on his face and neck. Histological examination of biopsy specimens established the diagnosis of nevoid basal cell carcinoma syndrome. Tuberculum sellae meningioma was removed through a craniotomy, and his symptoms improved. Meningioma is known to occur in the field of therapeutic irradiation, so chemotherapy may be a better option for medulloblastoma associated with nevoid basal cell carcinoma syndrome.

Pineal parenchymal tumor with marked retinoblastic differentiation: case report.

A 53-year-old woman was found to have a tumor in the pineal region. Histologically, Homer-Wright rosettes were sporadically distributed in a diffuse proliferation of round tumor cells that were immunoreactive for synaptophysin and chromogranin. A few perivascular pseudorosettes were also present, and the perivascular tumor cells were immunoreactive for glial fibrillary acidic protein and vimentin. By electron microscopy, well-developed junctions and pronounced interdigitation of abutting plasma membranes were noted in many tumor cells, as well as abundant intracytoplasmic microtubules. These findings indicated that the tumor was a pineal parenchymal tumor accompanied by an extraordinary epithelial-like differentiation, suggesting retinoblastic photoreceptor cell differentiation.