Massive macroglossia developing fast and immediately after endotracheal extubation.

We report an unusual case of massive macroglossia that developed very rapidly after neurosurgery in the park bench position with neck flexion. A few minutes after endotracheal extubation, massive macroglossia was noticed with marked protrusion of the tongue from the oral cavity. The patient's hospital stay was prolonged due to difficulty in speaking and eating. Macroglossia is a rare complication; however, it may cause life-threatening airway obstruction. It is important to be prepared for managing post-operative macroglossia and keep in mind that it may develop rapidly, especially after prolonged surgery performed with sustained neck flexion. The patient should be informed of the risk of macroglossia and the associated problems prior to the operation.

Parent artery occlusion for posterior cerebral artery aneurysms.

SUMMARY: We review four cases of posterior cerebral artery (PCA) aneurysm, of which three showed intolerance of parent artery occlusion. In two, balloon test occlusion (BTO) indicated poor opacification of the PCA branches from the anastomoses, and therefore, permanent occlusion was not attempted.

Expression of smooth muscle proteins in cavernous and arteriovenous malformations.

Cavernous malformations (CVMs) and arteriovenous malformations (AVMs) were immunostained for three smooth muscle cell (SMC)-specific protein markers (smooth muscle alpha-actin, SM1 and SM2). Smooth muscle alpha-actin, a widely used marker of SMCs, is reportedly one of the earliest proteins expressed during differentiation of SMCs and expressed in some kinds of mesoderm-derived cells. In contrast, SM1, an isoform of myosin heavy chain (MHC), is detected only in SMCs. SM2 is another MHC isoform and expressed in the contractile phenotype of SMC. All 14 intraaxial CVMs were positive for smooth muscle alpha-actin, but SM1 was detected in only three of them and SM2 was not found. Their staining pattern resembled that of normal intraparenchymal and pial veins. All 15 cerebral AVMs and 5 out of 6 extraaxial CVMs from the cavernous sinus, orbit and scalp were positive for all three markers, as were the normal cerebral arteries. The venous components of AVMs, as well as the arterial components, expressed SM2, and were different from normal veins in the brain and intraaxial CVMs. This study shows that the histological analysis using the three markers for SMC is useful to differentiate intraaxial CVM from AVM and extraaxial CVMs.

Acute systemic inflammatory response syndrome in subarachnoid hemorrhage.

BACKGROUND AND PURPOSE: Systemic inflammatory response syndrome (SIRS) without infection is a well-known phenomenon that accompanies various acute cerebral insults. We sought to determine whether the initial SIRS score was associated with outcome in subarachnoid hemorrhage (SAH). METHODS: In 103 consecutive patients with SAH, the occurrence of SIRS was assessed according to the presence of >/=2 of the following: temperature of <36 degrees C or >38 degrees C, heart rate of >90 bpm, respiratory rate of >20 breaths/min, and white blood cell count of <4000/mm(3) or >12 000/mm(3). SIRS criteria and other prognostic parameters were evaluated as predictors of dichotomous Glasgow Outcome Scale score. RESULTS: SIRS was highly related to poor clinical grade (Hunt and Hess clinical grading scale), a large amount of SAH on CT (Fisher CT group), and high plasma glucose concentration on admission. By univariate analysis, the occurrence of SIRS was associated with higher mortality and morbidity rates than was the nonoccurrence (P<0.001). Among individual SIRS criteria, heart rate (P=0.003), respiration rate (P=0.003), and white blood cell count (P=0.03) were significant outcome predictors. By multivariate logistic regression analysis, the presence of SIRS independently predicted outcome. SIRS carried an increased risk of subsequent intracranial complications such as vasospasm and normal pressure hydrocephalus, as well as systemic complications. CONCLUSIONS: In SAH patients, SIRS on admission reflected the extent of tissue damage at onset and predicted further tissue disruption, producing clinical worsening and, ultimately, a poor outcome.

A novel intravascular drug delivery method using endothelial biotinylation and avidin-biotin binding.

In this study, a novel intravascular drug delivery system was developed in which a drug injected from a catheter was fixed to the vasculature of the targeted tissue. Cellular proteins of viable endothelial cells were first biotinylated directly by biotinylation reagents, and then bound by an avidinated drug or, using avidin as a linker, a biotinylated drug. In the initial experiments, we studied in vitro the biotinylation of cultured bovine aortic endothelial cells (BAECs) by applying biotinylation reagents (NHS-LC-biotin or sulfo-NHS-LC-biotin) onto the washed intact BAEC monolayers and showed that the amount of biotin bound to the cells depended on the concentration of the biotinylation reagents applied. The cell-bound biotin decreased with time after the biotinylation. When fluorescein-labeled avidin (FITC-avidin) was applied to the biotinylated BAEC monolayers, the FITC-avidin readily bound to the cells. An LDH-release assay showed that sulfo-NHS-LC-biotin was only slightly cytotoxic to the BAECs and a colony formation assay showed only slight adverse effects of the reagent. In vivo studies were carried out on the renal arteries of normal rabbits. A solution of NHS-LC-biotin was injected through a catheter to one kidney to biotinylate its vasculature and the vehicle to the other as control, followed by a perfusion with saline. Finally, a solution of FITC-avidin was injected to both kidneys that were then reperfused with the blood flow following the withdrawal of the catheters. In the histological sections, more than 85% of glomeruli was stained with fluorescein in the biotinylated kidney, whereas no glomeruli were stained in the control. In the kidneys harvested 2 days after the same procedure, most glomeruli were still brightly stained. In the final experiment, biotinylated kidneys were injected with a solution of avidin, followed by a solution of fluorescein-biotin. Control kidneys had no prior biotinylation but received the same injections of avidin and fluorescein-biotin as above. More than 80% of glomeruli were stained in the biotinylated kidneys but none in the controls. This indicated that biotinylated drugs can be anchored to the biotinylated vasculature through avidin without being flushed away by blood flows. No apparent adverse effect was found in the functions of biotinylated kidneys. We propose that this drug delivery system is feasible for the treatment of some pathological conditions of blood vessels such as microvascular proliferation in malignant tumors and for continuous drug delivery in certain target organs.

Traumatic trochlear nerve palsy following minor occipital impact--four case reports.

Four patients presented with transient trochlear nerve palsy following occipital impact. The impact was slight in all patients, and neuroimaging found no lesions of the nerve. Three patients had delayed onset. Two patients did not complain of diplopia, but were only aware of blurred vision. In such patients, the head tilting test was useful for diagnosis. Minor occipital impact can cause trochlear nerve palsy, which requires careful neurological examinations to identify.

Cranial fasciitis.

We report a case of cranial fasciitis in a 14-month-old boy. The lesion grew at the site of a previous head trauma, rapidly destroying the skull. Surgery disclosed that the lesion was highly vascular and adhered to the dura. Because histopathological study of a frozen section did not show malignancy, the authors decided not to perform dural excision after total removal of the lesion. No recurrence of the lesion was seen. The authors stress that this rate fibroblastic lesion must be included in the differential diagnosis of pediatric skull tumors and that careful histopathological observation is needed to avoid extensively invasive surgery.

Recurrent trigeminal neuralgia caused by an inserted prosthesis: report of two cases.

We report two cases of recurrent trigeminal neuralgia caused by an inserted prosthesis. Teflon material or polyurethane sponge inserted between the trigeminal nerve and the superior cerebellar artery became hardened and compressed the trigeminal nerve 17 months (Teflon) and 9 years (polyurethane sponge) respectively after the initial surgery. On the basis of these cases, it it suggested that actual decompression of the trigeminal nerve is important in surgery for trigeminal neuralgia, and that the prosthesis should not touch the trigeminal nerve.

Postsurgical development of dural arteriovenous malformations after transpetrosal and transtentorial operations: case report.

The authors present a case of mixed pial and dural arteriovenous malformations (AVMs) in the transverse and the sigmoid sinuses, which developed 2 years after the resection of a trigeminal neuroma via the transpetrosal and transtentorial approach. To the best of our knowledge, this is the first case of the delayed development of dural AVMs after transpetrosal and transtentorial surgery. The cause of acquired dural AVMs is discussed, and the potential risk of delayed development of dural AVMs after transpetrosal and transtentorial surgery is described.

Intracranial vertebral artery dissections: clinical, radiological features, and surgical considerations.

We reviewed 24 patients with intracranial vertebral artery dissections treated during the last 12 years. Sixteen patients were admitted with subarachnoid hemorrhage (SAH) and 8 did not have SAH. The mean age at the time of onset was 50.0 years. Male preponderance was noted. Among 21 patients with acute onset, 6 (29%) experienced prodromal neck pain and 3 (60%) of 5 SAH patients showed nuchal stiffness when examined within 6 hours of onset. The preoperative angiographical findings were uniform in SAH cases in contrast to the varied angiographical findings seen in non-SAH cases. So-called pearl and string sign was observed in most SAH cases, but the "string" was often so short and wide that the term "constriction" appeared more suitable. From intraoperative observations, the angiographical point of constriction seemed to represent the proximal or distal end of dissection. As for treatment, 19 patients underwent 20 surgeries. Trapping was performed in eight surgeries, base clipping was performed in five, and proximal clipping was performed in seven. Both trapping and base clipping prevented further bleeding, but trapping was associated with a high rate of postoperative lower cranial nerve palsy. Postoperative neurological complications were less frequent after proximal clipping, but subsequent postoperative bleeding occurred in one patient treated by this technique. The overall long-term outcome in the surgically treated cases in our series was favorable, but most patients suffered from various degrees of uncomfortable dysphagia or hoarseness for some period after surgery. It was also noted that, in half of the disabled cases, the major disability was attributable to lower cranial nerve palsy and respiratory troubles that developed postoperatively.

Vasospasm prevention with postoperative intrathecal thrombolytic therapy: a retrospective comparison of urokinase, tissue plasminogen activator, and cisternal drainage alone.

The authors report the results of a retrospective review, between January 1986 and December 1991, of the results of early surgery and intrathecal thrombolytic therapy in 111 patients with aneurysmal subarachnoid hemorrhage. Effects on clot lysis, angiographic and symptomatic vasospasm, cerebral infarction, and clinical outcome were compared in 60 patients treated with urokinase (UK) 60,000 IU/d for 7 days (UK group), 22 patients treated with 0.042 to 1 mg tissue plasminogen activator (tPA) every 6 to 8 hours for 5 days (tPA group), and 29 patients who did not receive treatment with either thrombolytic agent (no-treatment group). The no-treatment group consisted of all patients treated before July 1986 and of patients in whom thrombolytic therapy was attempted but failed to start or in whom the therapy was not used intentionally because of small subarachnoid clot. Treatment with UK was employed between July 1986 and March 1991, and tPA was employed during the remainder of the study for patients at a higher risk for vasospasm. The severity of angiographic vasospasm and the incidence of infarction in the UK and the tPA groups were less than those of the no-treatment group (P < 0.01), in spite of a larger amount of initial subarachnoid blood clot in both thrombolytic groups. This appears to be the result of the more rapid clearance of cisternal clot in the thrombolytic groups than the no-treatment group (P < 0.01). Only tPA therapy reduced the incidence of symptomatic vasospasm (P < 0.05). No serious complications were observed, although in the tPA group, asymptomatic intraventricular hemorrhage occurred in one patient, and transient confusion in another. Both received 4 mg tPA/d. Meningitis was suspected in 16 patients of the UK group. However, in this relatively small retrospective series, there were no differences among the three groups in overall outcome at 3 months. This study indicates that postoperative intrathecal thrombolytic therapies, especially with less than 4 mg/d of tPA, are effective in lysing subarachnoid clot and preventing vasospasm and infarction safely.