Internal carotid and vertebral artery dissections - a comparison of clinical, radiological and prognostic characteristics.

AIM OF STUDY: To examine whether baseline characteristics, potential risk factors, clinical symptoms, radiological presentation, and long-term outcomes differ between internal carotid artery dissection (ICAD) and vertebral artery dissection (VAD). CLINICAL RATIONALE FOR STUDY: Cervical artery dissection (CeAD) is a major cause of cerebral ischaemia in young adults. Its clinical course is highly variable, resulting in challenges in making a proper diagnosis. METHODS: We performed a retrospective analysis of 31 patients (mean age 42.2 years) with CeAD (18 with ICAD, 13 with VAD) treated in our neurology department from 2008 to 2018. Appropriate imaging confirmed the diagnosis of CeAD. RESULTS: Patients with ICAD presented Horner syndrome significantly more often (44.4% vs 7.6%; p = 0.04). Patients with VAD more often had ischaemic events (ischaemic stroke, TIA or transient blindness) (84.6% vs 44.6%; p = 0.0032). Ischaemic stroke was more severe in patients with ICAD [(median NIHSS 6, interquartile range 4-12) vs VAD (median NIHSS 4, interquartile range 1.5-5.5), p = 0,03]. Occlusion occurred more often in patients with VAD (69.2% vs 22.2%; p = 0.013). Most patients had a favourable outcome (mRS 0-2). CONCLUSIONS AND CLINICAL IMPLICATIONS: In a series of patients with CeAD, we observed significant differences between VAD and ICAD in terms of clinical symptoms and radiological features.

[Management of ureteric sticture via a percutaneous double J stent implantation--description of 2 cases]. / Leczenie zwezenia moczowodu za pomoca przezskórnej implantacji cewnika Double J--opis 2 przypadków.

Ureteric stricture is the cause of urinary retention above the stricture level and obstructive nephropathy development with progressive renal parenchyma destruction leading to the renal failure. In the management of ureteric stricture, apart from surgery, less-invasive methods of recanalization are applied: transurethral (retrograde) double J stent implantation or, if the above method is unsuccessful, percutaneous (antegrade) double J stent implantation. In this paper we present 2 cases of percutaneous double J stent implantation: in patient after cystoprostatectomy with ureteric stricture at the level of uretero-ileostomy and in patient after renal transplantation with ureteric stricture at the level of ureterovesicostomy.

[Endovascular treatment of a subclavian fistula as a complication after cardiac pacemaker implantation]. / Przetoka podobojczykowa jako powiklanie po implantacji stymulatora serca leczona na drodze wewnatrznaczyniowej--opis przypadku.

Increasing number of complications of cardiac pacemaker implantations is related to increasing number of this procedures due to the aging of the population. A rare complication after pacemaker implantation is subclavian fistula. We present endovascular treatment of subclavian fistula with a covered stent after implantation of cardiac pacemaker.

Wernicke-Korsakoff syndrome as a rare phenotype of sporadic Creutzfeldt-Jakob disease.

We reported the case of a patient with Wernicke-Korsakoff syndrome (WKs) as an early clinical manifestation of sporadic Creutzfeld-Jakob disease (sCJD). The 66-year-old female complained of dizziness and imbalance which mostly occurred while walking. A neurological examination revealed a triad of symptoms characteristic for WKs such as gaze paresis, ataxia of limbs and trunk as well as memory disturbances with confabulations. The disturbances increased during the course of the disease, which led to the death of the patient four months after the appearance of the signs. The patient was finally diagnosed with sCJD disease. The most useful ancillary examination results supporting sCJD diagnosis were brain diffusion DWI MRI (diffusion weighted magnetic resonance imaging) and the presence of 14-3-3 protein in CSF (cerebrospinal fluid). Since that manifestation of sCJD is very unique other causes should be taken into consideration while making a final diagnosis.

Dynamic perfusion CT: optimizing the temporal resolution for the calculation of perfusion CT parameters in stroke patients.

PURPOSE: To assess the influence of different temporal sampling rates on the accuracy of the results from cerebral perfusion CTs in patients with an acute ischemic stroke. MATERIAL AND METHODS: Thirty consecutive patients with acute stroke symptoms received a dynamic perfusion CT (LightSpeed 16, GE). Forty millilitres of iomeprol (Imeron 400) were administered at an injection rate of 4 ml/s. After a scan delay of 7s, two adjacent 10mm slices at 80 kV and 190 mA were acquired in a cine mode technique with a cine duration of 49 s. Parametric maps for the blood flow (BF), blood volume (BV) and mean transit time (MTT) were calculated for temporal sampling intervals of 0.5, 1, 2, 3 and 4s using GE's Perfusion 3 software package. In addition to the quantitative ROI data analysis, a visual perfusion map analysis was performed. RESULTS: The perfusion analysis proved to be technically feasible with all patients. The calculated perfusion values revealed significant differences with regard to the BF, BV and MTT, depending on the employed temporal resolution. The perfusion contrast between ischemic lesions and healthy brain tissue decreased continuously at the lower temporal resolutions. The visual analysis revealed that ischemic lesions were best depicted with sampling intervals of 0.5 and 1s. CONCLUSION: We recommend a temporal scan resolution of two images per second for the best detection and depiction of ischemic areas.

Endogenous neuroprotective factors: neurosteroids.

Neurosteroids are a group of steroid hormones synthesized by the brain in the presence of steroidogenic enzymes. Specific neurosteroids modulate function of several receptors, and also regulate growth of neurons, myelinization and synaptogenesis in the central nervous system. Some neurosteroids have been shown to display neuroprotective properties, which may have important implications for their potential use in the treatment of various neuropathologies such as: age-dependent dementia, stroke, epilepsy, spinal cord injury, Alzheimer's disease (AD), Parkinson's disease (PD) and Niemann-Pick type C disease (NP-C). This paper focuses on neuroprotection afforded by neurosteroids.

Stiripentol. A novel antiepileptic drug.

Epilepsy is one of the most widespread pathologies of human brain, affecting approximately 1% of world population. Despite the development of new methods of seizure control, chronic administration of antiepileptic drugs (AEDs) remains the treatment of choice. Nevertheless, pharmacotherapy is not always effective. In the case of single drug treatment, the number of non-responding patients is as high as 30%. Moreover, chronic medication with currently available AEDs may result in severe side-effects and undesired drug interactions. That is why in recent years intensive research has been carried out aiming at the development of new therapeutic strategies in epilepsy. The goal of this review is to assemble current literature data on stiripentol (STP), a novel anticonvulsant unrelated to any other AEDs. STP potentiates central gamma-aminobutyric acid (GABA) transmission and is characterized by nonlinear pharmacokinetics and inhibition of liver microsomal enzymes. STP has proved its anticonvulsant potency in different types of animal seizures, as well as in clinical trials. The drug seems a good candidate for adjunctive therapy in intractable epilepsy.

Agmatine enhances the anticonvulsant action of phenobarbital and valproate in the mouse maximal electroshock seizure model.

Accumulating evidence indicates that agmatine (AGM--an endogenous neuromodulator/neurotransmitter in the brain) exerts the anticonvulsant action in various in vivo experiments. Therefore, the aim of this study was to assess the influence of AGM on the protective action of numerous conventional and newer antiepileptic drugs [carbamazepine (CBZ), lamotrigine (LTG), oxcarbazepine (OXC), phenobarbital (PB), phenytoin (PHT), topiramate (TPM) and valproate (VPA)] in the mouse maximal electroshock seizure (MES) model. Results indicate that AGM (up to 100 mg/kg, i.p., 45 min before the test) neither altered the threshold for electroconvulsions nor protected the animals against MES-induced seizures in mice. Moreover, AGM (100 mg/kg, i.p.) significantly enhanced the anticonvulsant effects of PB and VPA in the MES test by reducing their ED50 values from 22.54 to 16.82 mg/kg (P < 0.01) for PB, and from 256.1 to 210.6 mg/kg (P < 0.05) for VPA, respectively. In contrast, AGM at 100 mg/kg (i.p.) had no significant effect on the antielectroshock action of the remaining drugs tested (CBZ, LTG, OXC, PHT, and TPM) in mice. Estimation of total brain PB and VPA concentrations revealed that the observed interactions between AGM and PB or VPA in the MES test were pharmacodynamic in nature because neither total brain PB, nor total brain VPA concentrations were altered after i.p. administration of AGM at 100 mg/kg. Moreover, none of the examined combinations of AGM (100 mg/kg) with CBZ, LTG, OXC, PB, PHT, TPM, and VPA (at their ED50 values from the MES test) affected motor coordination in the chimney test, long-term memory in the passive avoidance task, and muscular strength in the grip-strength test in mice, indicating no acute adverse effects in animals. In conclusion, one can ascertain that the selective potentiation of the antielectroshock action of PB and VPA by AGM, lack of any pharmacokinetic interactions between drugs and no acute adverse effects, make the combinations of AGM with PB or VPA of pivotal importance for epileptic patients. It seems that modulation of AGM concentration in the brain may occur favorable in further clinical practice.

Is nitric oxide involved in the anticonvulsant action of antiepileptic drugs?

Experimental data indicate that nitric oxide (NO) may play a role in the pathophysiology of epilepsy. It is also possible that NO-mediated events are involved in the expression of the anticonvulsant action of some antiepileptics. The aim of this review was to assemble current literature data on the role of NO in the anticonvulsant action of antiepileptic drugs (AEDs). The influence of various NO synthase inhibitors (NOSI) on antiseizure activity of AEDs was tested in many animal experimental models of epilepsy (electrically and pharmacologically evoked seizures, sound-induced convulsions, amygdala-kindled seizures). Although some NOSI were able to modify the anticonvulsive properties of AEDs, the involvement of NO pathway in the mechanisms of action of AEDs in most cases does not seem probable, since the effects of NOSI were not reversed by L-arginine, a NO precursor.

Calcium modulation in epilepsy.

The ideal antiepileptic drug (AED) should correct the aberrant pathophysiology of epileptogenesis without interfering with normal neurotransmission A new group of drugs with antiepileptic efficacy, without sedative properties, would be an exciting prospect. Theoretical considerations and results from experimental animal models of epilepsy have put forward the possibility that calcium (Ca2+) antagonists may form such a group. The initiation of epileptogenic activity in the neuron is thought to be connected with the phenomenon known as "intrinsic burst firing", which is activated by an inward Ca2+ current. Ca2+ is described as the primary mediator of "excitotoxic" neuronal damage. Both necrotic and apoptotic cell death is associated with Ca2+ entry into the cells during status epilepticus. The Ca2+ channel blockers depressed epileptic depolarizations of neurons. In this review, we present anticonvulsant effects of cinnarizine, flunarizine, nifedipine, nimodipine, nicardipine, amlodipine, isradipine, niguldipine, diltiazem, verapamil and dantrolene in animal models of seizures. Also, a detailed analysis of interactions between Ca2+ blockers and AEDs was performed. Clinical trials in intractable epilepsy support to a certain degree antiepileptic properties of Ca2+ antagonists.