pilocarpine/stroke

The discovery and validation of biomarkers in neurological and neurodegenerative diseases is an important challenge for early diagnosis of disease and for the development of therapeutics. Epilepsy is often a consequence of brain insults such as traumatic brain injury or stroke, but as yet no

A woman with spastic hemiparesis from a stroke was injected with botulinum toxin type B (BoNTB) at a dose of 10,000 U. Although this had the desired effect of a reduction in her spasticity, she also developed severe dry mouth, which became refractory to local remedies such as moist towels, lip

MicroRNAs regulate protein synthesis by binding non-translated regions of mRNAs and suppressing translation and/or increasing mRNA degradation. MicroRNAs play an important role in the nervous system including controlling synaptic plasticity. Their expression is altered in disease states including

A 2-year-old mentally retarded boy with frontal lobe epilepsy presented with an episode that resembled heat stroke during the administration of zonisamide. He developed hyperpyrexia with oligohidrosis and central neurological symptoms, including, chorea-like involuntary movements, resting tremor,

Citicoline (CDP-choline; cytidine 5'-diphosphocholine) is an important intermediate in the biosynthesis of cell membrane phospholipids. Citicoline serves as a choline donor in the biosynthetic pathways of acetylcholine and neuronal membrane phospholipids, mainly phosphatidylcholine. The ability of

UNASSIGNED Temporal lobe epilepsy (TLE) is one of the most drug-resistant types of epilepsy with about 80% of TLE patients falling into this category. Increasing evidence suggests that neuroinflammation, which has a critical role in the epileptogenesis of TLE, is associated with microglial

OBJECTIVE It has been proven that extracellular HMGB1 is involved in progression of neurologic disorders, such as stroke, traumatic brain injury, meningitis and epilepsy. Glycyrrhizin (GL) is a direct inhibitor of HMGB1, and blocks HMGB1 release into the extracellular. We aim in this study to

Parasympathetic activity is often reduced in hypertension and can elicit anti-inflammatory mechanisms. Thus we hypothesized that chronic vagal nerve stimulation (VNS) may alleviate cardiovascular end-organ damage in stroke-prone spontaneously hypertensive rats. Vagal nerve stimulators were

BACKGROUND Choline alfoscerate (α-GPC) and Cytidine 5'-diphosphocholine (CDPCholine) are both acetylcholine precursors and are considered to act as pro-cholinergic nootropic agents. Acetylcholine precursors have also recently found frequent use in the neurology clinic. Stroke and many types of

OBJECTIVE Diseases such as temporal lobe epilepsy, brain trauma and stroke can induce endothelial cell proliferation and angiogenesis in specific brain areas. During status epilepticus (SE), bone marrow-derived cells are able to infiltrate and proliferate, dramatically increasing at the site of

1. Gradients of excitation in the swimmeret system were created by applying either pilocarpine or carbachol to selected ganglia in isolated abdominal nerve cords. The state of the system was monitored in each segment with extracellular electrodes on nerves that innervated swimmerets. In preparations

Detrended fluctuation analysis (DFA) is a new technique used to characterize the long-range temporal correlation (LRTC) structure of non-stationary time series, which has been applied in electroencephalographic (EEG) oscillations and diseases such as Alzheimer and stroke. In this paper, DFA is used

Apart from stroke, epilepsy is the most common neurological disorder with 0.5% of prevalence. The present study was performed in order to determine the monoamine levels, (M(1)-like) muscarinic and (D(1)- and D(2)-like) dopaminergic receptor changes in frontal cortex of adult rats after

Status Epilepticus (SE) is a major neurological emergency and is considered a leading cause of Acquired Epilepsy (AE). We have shown that SE produces neuronal injury and prolonged alterations in hippocampal calcium levels ([Ca2+]i) that may underlie the development of AE. Interventions preventing