Transverse sinus stenting for idiopathic intracranial hypertension: a review of 52 patients and of model predictions.

BACKGROUND AND PURPOSE: Transverse sinus stenosis is common in patients with IIH. While the role of transverse sinus stenosis in IIH pathogenesis remains controversial, modeling studies suggest that stent placement within a transverse sinus stenosis with a significant pressure gradient should decrease cerebral venous pressure, improve CSF resorption in the venous system, and thereby reduce intracranial (CSF) pressure, improving the symptoms of IIH and reducing papilledema. We aimed to determine if IIH could be reliably treated by stent placement in transverse sinus stenosis. MATERIALS AND METHODS: We reviewed the clinical, venographic, and intracranial pressure data before and after stent placement in transverse sinus stenosis in 52 of our own patients with IIH unresponsive to maximum acceptable medical treatment, treated since 2001 and followed between 2 months and 9 years. RESULTS: Before stent placement, the mean superior sagittal sinus pressure was 34 mm Hg (462 mm H(2)0) with a mean transverse sinus stenosis gradient of 20 mm Hg. The mean lumbar CSF pressure before stent placement was 322 mm H(2)O. In all 52 patients, stent placement immediately eliminated the TSS pressure gradient, rapidly improved IIH symptoms, and abolished papilledema. In 6 patients, symptom relapse (headache) was associated with increased venous pressure and recurrent stenosis adjacent to the previous stent. In these cases, placement of another stent again removed the transverse sinus stenosis pressure gradient and improved symptoms. Of the 52 patients, 49 have been cured of all IIH symptoms. CONCLUSIONS: These findings indicate a role for transverse sinus stent placement in the management of selected patients with IIH.

Identification of patients at risk for ischaemic cerebral complications after carotid endarterectomy with TCD monitoring.

OBJECTIVES: Transcranial Doppler (TCD) monitoring for micro embolic signals (MES), directly after carotid endarterectomy (CEA) may identify patients at risk of developing ischaemic complications. In this retrospective multicentre study, this hypothesis was investigated. METHODS: Centres that monitored for MES after CEA were identified by searching Medline. Individual patient data were obtained from centres willing to collaborate. The number of emboli in 1h was computed. Uni- and multivariate logistic regression analyses were performed for the variables gender, age and number of MES. Discriminative ability of MES monitoring was investigated in a ROC curve. RESULTS: Nine hundred and ninety-one patients were monitored in the first 3h after CEA. Two percent developed ischaemic cerebral complications. Univariate analysis revealed statistically significant associations between ischaemic cerebral complications and both gender and MES, but not age. In a multivariate analysis, > or =8 MES/h showed a statistically significant relationship with cerebral complications (OR 8.1, 95% CI 1.8-36), in contrast to gender (OR 2.2, 95% CI 0.9-5.5). The ROC curve yielded an AUC of 0.83 for monitoring of MES. CONCLUSIONS: These results support the use of TCD monitoring for MES shortly after CEA in order to identify patients at risk of developing ischaemic cerebral complications.

Presynaptic failure of neuromuscular transmission and synaptic remodeling in EA2.

OBJECTIVE: To further investigate the basis of abnormal neuromuscular transmission in two patients with congenital myasthenic syndrome associated with episodic ataxia type 2 (EA2) using stimulated single fiber EMG (SFEMG) and in vitro microelectrode studies. METHODS: Two patients with genetically characterized EA2 previously shown to have abnormal neuromuscular transmission by voluntary SFEMG were studied with stimulated SFEMG and anconeus muscle biopsy with microelectrode studies and electron microscopy of the neuromuscular junction. RESULTS: In vivo stimulated SFEMG showed signs of presynaptic failure, with jitter and blocking that improved with increased stimulation frequency. Additional evidence of presynaptic failure was provided by the in vitro microelectrode studies, which showed marked reduction of the end plate potential quantal content in both patients. Of note, the end plate potentials showed high sensitivity to N-type blockade with omega-conotoxin not seen in controls. The ultrastructural studies revealed some evidence of small nerve terminals apposed to normal or mildly overdeveloped postsynaptic membranes, suggesting an ongoing degenerative process. CONCLUSIONS: The authors demonstrated presynaptic failure of neurotransmission in patients with heterozygous nonsense mutations in CACNA1A. The contribution of non-P-type calcium channels to the process of neurotransmitter release in these patients likely represents a compensatory mechanism, which is insufficient to restore normal neuromuscular transmission.

Transcranial Doppler in carotid endarterectomy.

PURPOSE: To evaluate the role of transcranial Doppler monitoring in reducing the complications of carotid endarterectomy, by analysing: (1) perioperative intracerebral blood flow velocity; (2) embolic load; and (3) effect of Dextran-40 therapy on patient outcome. DESIGN: Retrospective case series. METHODS: The study cohort consisted of 30 consecutive patients undergoing 32 carotid endarterectomy procedures. Continuous transcranial Doppler (TCD) monitoring of the ipsilateral middle cerebral artery (MCA) was performed to obtain flow velocities and embolic count. Flow velocity changes were analysed in relation to electroencephalographic (EEG) changes. A Dextran-40 infusion was instituted for patients who experienced a post-arteriotomy embolic load of >50 counts/hour. RESULTS: The average middle cerebral artery velocity (MCAvel) drop on cross clamping was 46+/-12.1%, expressed as a percentage of the individual's 24-hour pre-operative value. Clamping ischaemia developed in six cases (18.8%) of which three (9.4%) demonstrated TCD changes only, and three demonstrated both TCD and EEG changes (9.4%). The average increase in MCAvel at 60-120 minutes postarteriotomy, was 18+/-17.5%; six cases developed hyperaemia. Postoperative emboli were seen in 88% of cases with 31% of patients demonstrating embolic loads of >50/hour. CONCLUSIONS: Perioperative transcranial Doppler monitoring (1) is a useful adjunct to EEG assessment of cross clamping ischaemia, providing information in real time, on MCA blood velocity deterioration that may antecede irreversible change (2) detects postoperative hyperaemic response, and (3) allows quantification of microembolic loads that, when high, have been shown to be a precursor to localised cerebral ischaemia and can be effectively treated with Dextran-40 infusion.