Intra-arterial thrombectomy versus standard intravenous thrombolysis in patients with anterior circulation stroke caused by intracranial arterial occlusions: a single-center experience.

Background: Severely impaired patients with persisting intracranial occlusion despite standard treatment with intravenous (IV) administration of recombinant tissue plasminogen activator (rtPA) or presenting beyond the therapeutic window for IV rtPA may be candidates for interventional neurothrombectomy (NT). The safety and efficacy of NT by the Penumbra System (PS) were compared with standard IV rtPA treatment in patients with severe acute ischemic stroke (AIS) caused by large intracranial vessel occlusion in the anterior circulation.

Methods: Consecutive AIS patients underwent a predefined treatment algorithm based on arrival time, stroke severity as measured by the National Institutes of Health Stroke Scale (NIHSS) score, and site of arterial occlusion on computed tomographic angiography (CTA).

Drugs and clinical trials in neurodegenerative diseases.

Neurodegenerative diseases are disabling conditions continuously increasing due to aging of population. A disease modifying therapy that slows or stops disease progression is therefore a major unmet medical need. Unfortunately, research for effective treatments is hampered by lack of knowledge on the pathologic processes underpinning these diseases and of reliable biomarkers.

Correlation between changes in CSF dopamine turnover and development of dyskinesia in Parkinson's disease.

To assess possible differences in dopamine metabolism that could parallel disease progression in Parkinson's disease (PD), we measured dopamine (DA) and its metabolites in the cerebrospinal fluid (CSF) in PD patients at different stages of disease: de novo (DEN), advanced not showing dyskinesias (ADV), and advanced with dyskinesias (DYS). DA, homovanillic acid (HVA) and dihydroxyphenylacetic acid (DOPAC) were significantly higher in DEN patients compared with other groups. A negative exponential correlation related DA level and disease duration.

Pedunculopontine nucleus deep brain stimulation changes spinal cord excitability in Parkinson's disease patients.

Bilateral peduncolopontine nucleus (PPN) and subthalamic nucleus (STN) deep brain stimulation (DBS) was performed in six-advanced Parkinson's disease (PD) patients. We report the effect of both PPN-DBS (25 Hz) and STN-DBS (185 Hz) on patient spinal reflex excitability by utilizing the soleus-Hoffman reflex (HR) threshold. Compared to controls (n = 9), patients showed an increase of HR-threshold, which was scarcely affected by levodopa, but significantly reduced by DBS.

Bilateral deep brain stimulation of the pedunculopontine and subthalamic nuclei in severe Parkinson's disease.

Gait disturbances and akinesia are extremely disabling in advanced Parkinson's disease. It has been suggested that modulation of the activity of the pedunculopontine nucleus (PPN) may be beneficial in the treatment of these symptoms. We report the clinical affects of deep brain stimulation (DBS) in the PPN and subthalamic nucleus (STN).

Biochemical and electrophysiological changes of substantia nigra pars reticulata driven by subthalamic stimulation in patients with Parkinson's disease.

To understand the events underlying the clinical efficacy of deep brain stimulation (DBS) of the subthalamic nucleus (STN), electrophysiological recordings and microdialysis evaluations were carried out in the substantia nigra pars reticulata (SNr), one of the two basal ganglia (BG) nuclei targeted by STN output, in patients with Parkinson's disease (PD). Clinically effective STN-DBS caused a significant increase of the SNr firing rate. The poststimulus histogram (PSTH) showed an excitation peak at 1.

Bilateral Implantation of Centromedian-Parafascicularis Complex and GPi: A New Combination of Unconventional Targets for Deep Brain Stimulation in Severe Parkinson Disease.

Objectives.  Traditional deep brain stimulation (DBS) at the subthalamic nucleus (STN) has proved to be efficacious on core Parkinsonian symptoms. However, very disabling l-dopa-induced abnormal involuntary movements (AIMs) and axial signs are slightly affected, suggesting that we target less conventional targets.

Kyphoplasty: a new opportunity for rehabilitation of neurologic disabilities.

Using percutaneous kyphoplasty, we treated a patient with a diagnosis of Guillain-Barré syndrome who complained of an unremitting pain in the spine, refractory to the conventional medical therapy, elicited by pressure over the spinous process, and in absence of neurologic deficits. The method provided swift midline back pain relief associated with an evident augmentation in the stability and in the vertebral body's height. The injection of polymethylmethacrylate was effective and safe, no cement leakages were observed, and no complications such as pulmonary embolism, toxicity, or infection were observed.

Induction of corticostriatal LTP by 3-nitropropionic acid requires the activation of mGluR1/PKC pathway.

Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder typically affecting individuals in midlife. HD is characterized by the selective loss of striatal spiny neurons, while large cholinergic interneurons are spared. An impaired mitochondrial complex II (succinate dehydrogenase, SD) activity is known as a prominent metabolic alteration in HD.

Neuronal vulnerability following inhibition of mitochondrial complex II: a possible ionic mechanism for Huntington's disease.

An impaired complex II (succinate dehydrogenase, SD) striatal mitochondrial activity is one of the prominent metabolic alterations in Huntington's disease (HD), and intoxication with 3-nitropropionic acid (3-NP), an inhibitor of mitochondrial complex II, mimics the motor abnormalities and the pathology of HD. We found that striatal spiny neurons responded to this toxin with an irreversible membrane depolarization/inward current, while cholinergic interneurons showed a hyperpolarization/outward current. Both these currents were sensitive to intracellular concentration of ATP.

Tissue plasminogen activator is required for striatal post-ischemic synaptic potentiation.

Recent experimental observations indicate that tPA plays a key role in the development of neuronal damage that follows cerebral ischemia and excitotoxicity. In an attempt to clarify how tPA favors ischemia-induced neuronal damage, we performed in vitro electrophysiological experiments in striatal slices by using mice selectively lacking this serine protease.We found that tPA ablation did not affect the membrane depolarization of striatal neurons exposed to combined oxygen and glucose deprivation but fully prevented the induction of NMDA-dependent post-ischemic long-term synaptic potentiation.