[Postoperative dissection of the vertebral artery in two steps]. / Dissection postopératoire de l'artère vertébrale en deux temps.

The diagnosis of perioperative vertebral artery dissection can be difficult because of non-specific clinical signs. We report a case revealed by a tegmento-thalamic stroke after an abdominal second surgical look. The interest of this observation is related to a particular evolution in two steps separated by a 2-month-interval and an intercurrent cervical manipulation. After the second anesthesia, neck pain associated with a third cranial nerve palsy and a supranuclear ophtalmoplegia revealed a tegmento-thalamic ischemic stroke due to vertebral artery dissection. We discuss here the different factors possibly involved in the pathophysiology of postoperative vertebral artery dissection: positioning, cervical manipulation, subclavian central venous access and cisplatin toxicity. Vertebral artery dissection should be discussed in case of postoperative neck pain, especially with non-typical symptomatology.

[Impact of a stroke-unit on rtPA use in a community hospital: a 3-year prospective study]. / Impact de la création d'une unité neurovasculaire sur l'utilisation du rtPA dans l'infarctus cérébral en centre hospitalier général : étude prospective sur trois ans.

INTRODUCTION: Although intravenous thrombolysis has been used for ischemic strokes since 2004 in our community hospital located in Pau (southwest of France), a specifically dedicated stroke-unit (SU) was created only recently in June 2010. We decided to collect prospective data to compare the use and efficacy of intravenous thrombolysis before and after the opening of this dedicated stroke unit. METHODS: Stroke patients with internal carotid artery territory involvement treated with intravenous thrombolysis were compared between two similar periods. The first period (called pre-SU period) stretched from January 2009 to June 2010. The second period (called SU period) stretched from June 2010 to October 2011. We collected prospectively all morbidity/mortality data as well as a modified Rankin score (mRS) three months later. RESULTS: During the pre-SU period, 21 strokes were treated with a mean NIHSS score of 15. Three months later, the mRS score was less than or equal to 2 for five patients, and greater than or equal to 3 for 12. A total of four patients died. In addition, two-thirds of patients (14 of 21) had suffered from notable complications at the initial phase of their stroke. During the SU period, 27 strokes were treated with a mean NIHSS score of 14. At 3 months, the mRS score less than or equal to 2 for 15 patients, and greater than or equal to 3 for nine other patients. A total of three patients died. During this second period, less than 50% of the patients (13 of 27) were not affected by any complication at the initial phase. Statistically, the results also show a better short-term (24 hours with NIHSS) and medium-term (3 months with NIHSS and mRS) clinical outcome for patients treated during the SU period. CONCLUSIONS: Instituting a dedicated stroke-unit helped improve outcome after ischemic strokes treated by intravenous thrombolysis. It also increased the number of patients and reduced the complications at the initial phase.

[Mutism and acute behavioral disorders revealing MELAS syndrome]. / Mutisme et troubles du comportement aigus révélant un syndrome MELAS.

INTRODUCTION: MELAS syndrome (mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes) is a rare genetic mitochondrial disease which can cause cerebral (cerebrovascular accident, migraine, mental deterioration..), sensorial (bilateral symmetrical deafness) and peripheral (muscular involvement, neuropathy) disorders potentially associated with diabetes, renal or cardiac disorders, or growth retardation. Eighty percent of the patients have the 3243 A>G mutation in the leucine RNA transfer gene. Clinical manifestations leading to discovery of the mutation can be extremely varied, affecting patients of different age groups. CLINICAL CASE: We report the case of a 49-year-old man who presented acute fits of confusion followed by mutism and praxic disorders. History taking revealed recently diagnosed type 2 diabetes, axonal neuropathy, and bilateral symmetrical deafness requiring hearing aids. The initial MRI showed FLAIR sequences with bi-parietal abnormalities, no signs of recent stroke on the DW/B10000 sequences, and basal ganglia calcifications. Blood tests and morphological findings ruled out a vascular origin. Search for lactic acidosis remained constantly negative in blood samples despite positive cerebrospinal fluid samples (N×3). The 3243 A>G mitochondrial DNA mutation was identified. The neuropsychological evaluation revealed a serious dysexecutive syndrome with a major impact on the patient's self sufficiency. CONCLUSION: Neurocognitive disorders are not common in MELAS syndrome. Brain MRI results and the presence of extra-neurological signs can be helpful for diagnosis.

Investigation of PK-PD drug-drug interaction between acenocoumarol and amoxicillin plus clavulanic acid.

A pharmacokinetic-pharmacodynamic (PK-PD) drug-drug interaction between acenocoumarol and amoxicillin + clavulanic acid antibiotic was assessed in eight healthy volunteers, using a population PK-PD) model. Each subject received at day 1 a single dose of 8 mg of acenocoumarol. Then 1 g of amoxicillin + 250 mg of clavulanic acid was given from days 3 to 9. On day 8, each subject received a single dose of 8 mg of acenocoumarol concomitantly with the antibiotic combination. Eleven blood samples were taken during 48 h following each acenocoumarol administration. Acenocoumarol plasma concentrations and prothrombin time were measured at each sampling time. We first identified the structural PK model by pooling data from this trial with individual data from other acenocoumarol PK trials. An indirect response model was used to fit PD data. Models were built using a non-linear mixed effect modelling approach with nonmem software. Covariates were tested on PK and PD parameters, including antibiotic treatment. Acenocoumarol PK data were fitted by a two-compartment, first-order input model with log normal inter-individual variability. Weight and antibiotic treatment were found to improve significantly the fit of PK data with a 15% decrease in acenocoumarol clearance with concomitant antibiotics (P < 0.05). An indirect response model was successfully applied to the PK-PD data of acenocoumarol. No covariate, including antibiotic treatment effect, significantly affected PT. Drug-drug interaction was demonstrated at the PK level, without any PD corollary.

[Central post-stroke pain]. / Les douleurs centrales post-AVC.

Central post-stroke pain (CPSP) is known since the famous Dejerine-Roussy syndrome and its description has not improved. The subject has however been revived over the last decade thanks to advances in central nervous system imaging with magnetic resonance imaging (MRI), the description of allodynia functional phenomena with fMRI, the study of opioid receptors, and above all, the analysis of pain pathways by laser-evoked potentials. Progress has also occurred in CPSP treatment with motor cortex stimulation, which probably opens a period of neuromodulation of the cortical areas controlling pain. The thalamus plays a prominent role in this disorder of central control of pain.

[Intracranial extension of extracranial vertebral artery dissections. A review of 16 cases]. / Débord intracrânien des dissections de l'artère vertébrale extracrânienne. Etude de 16 patients (17 cas de dissections).

INTRODUCTION: Vertebral artery (VA) dissections can involve both the extracranial and intracranial portions of the VA. Intradural extension explains the occurrence of subarachnoid hemorrage (SAH). We have studied the rate of this extension, the risk of associated SAH and the therapeutic repercussions at the acute stage. METHODS: From 1985 to 2001, 42 patients with a recent extracranial VA dissection were admitted to our department of neurology. When the diagnosis of extracranial VA dissection (involving the first, second or third segment of the VA) was established, we looked for an ipsilateral intracranial extension (involving the fourth segment of the VA and/or the basilar artery). VA dissections strictly located at the intracranial level were excluded. RESULTS: Among 42 patients with angiographically diagnosed extracranial VA dissections, 16 patients (38 percent) had an ipsilateral intradural extension. Two of them developed an inaugural and spontaneous SAH. After a mean follow-up of 4 Months under antithrombotic treatment, none of the patients has developed SAH or recurrent SAH. CONCLUSIONS: Because of the potential risk for spontaneous SAH at the acute stage, it seems important to exclude an intracranial extension. Lumbar puncture should be undertaken to exclude SAH before consideration of antithrombotic therapy.