324 results about "Peripheral nervous system" patented technology

The present invention relates to a neural stimulation delivery device to deliver electrical and/or chemical stimulation to target sites in the central and peripheral nervous system. The device generally includes a tubular body defining a plurality of ports along the longitudinal axis thereof, a plurality of delivery structures insertable in the body, and a control mechanism in communication with the plurality of delivery structures to independently move each of the plurality of delivery structures through a respective one of the plurality of ports with respect to each other of the plurality of delivery structures. The ability of each delivery structure to be independently moveable through a respective port allows each delivery structure to be selectively advanced or retracted independent of the movement of another delivery structure.

A universal closed-loop functional electrical stimulation system comprising at least one electrode assembly adapted to deliver an electrical stimulation signal to the central nervous system, peripheral nervous system, or muscles of a user, a sensor system adapted to detect a mechanical response to a muscle stimulation signal of at least one muscle associated with a muscle group stimulated through the nervous system or proximate to the electrode assembly. An electrical stimulation device operably coupled to at least one electrode assembly and the sensor system, the electrical stimulation device including a control system to automatically receive feedback from at least one characteristic of the muscle from the detected muscle response and adjust at least one parameter of the muscle stimulation signal in real-time and in response thereto and a programmed microprocessor for controlling said electrical stimulation and receiving input from said sensor system.

The instant disclosure describes methods for treating diseases and conditions of the central and peripheral nervous system by stimulating or increasing neurogenesis. The disclosure includes compositions and methods based on muscarinic receptor modulation, such as via inhibition of acetylcholine esterase (AChE) activity, alone or in combination with another neurogenic agent to stimulate or activate the formation of new nerve cells.

Substituted piperidine compounds represented by the structure I are provided,

wherein each of R_1a, R_1b, R_1c, R_1d, R_1e, R_1f, R_1g, R_1h, R₂, R_2A, R₃, R₄, A, X, a, x and n is as defined in the specification. Substituted piperidine compounds of structure I may permeate or penetrate across a nerve cell membrane into the interior of a nerve cell, may inhibit intracellular Rho kinase enzyme found in nerve cells in mammals, and may find utility in repair of damaged nerves in the central and peripheral nervous system of such mammals. These compounds may induce the regeneration or growth of neurites in mammalian nerve cells and may thereby induce regeneration of damaged or diseased nerve tissue. These compounds also find additional utility as antagonists of the enzyme Rho kinase in treatment of disease states in which Rho kinase is implicated. Pharmaceutical compositions containing these substituted piperidine compounds may be useful to promote neurite growth and in the treatment of diseases in which Rho kinase inhibition is indicated.

Apparatus and method for making and using devices that generate optical signals, and optionally also electrical signals in combination with one or more such optical signals, to stimulate (i.e., trigger) and/or simulate a sensory-nerve signal in nerve and/or brain tissue of a living animal (e.g., a human), for example to treat nerve damage in the peripheral nervous system (PNS) or the central nervous system (CNS) and provide sensations to stimulate and/or simulate “sensory” signals in nerves and/or brain tissue of a living animal (e.g., a human) to treat other sensory deficiencies (e.g., touch, feel, balance, visual, taste, or olfactory) and provide sensations related to those sensory deficiencies, and/or to stimulate (i.e., trigger) and/or simulate a motor-nerve signal in nerve and/or brain tissue of a living animal (e.g., a human), for example to control a muscle or a robotic prosthesis.

The present invention relates to compositions and methods for the treatment and diagnosis of conditions, disorders, or diseases involving cell death. The invention encompasses protective nucleic acids which, when introduced into a cell predisposed to undergo cell death or in the process of undergoing cell death, prevent, delay, or rescue the cell from death relative to a corresponding cell into which no exogenous nucleic acids have been introduced. The invention encompasses nucleic acids of the protective sequence, host cell expression systems of the protective sequence, and hosts that have been transformed by these expression systems, including transgenic animals. The invention also encompasses novel protective sequence products, including proteins, polypeptides and peptides containing amino acid sequences of the proteins, fusion proteins of proteins, polypeptides and peptides, and antibodies directed against such gene products. The invention further relates to target sequences, including upstream and downstream regulatory sequences or complete gene sequences, antibodies, antisense molecules or sequences, ribozyme molecules, and other inhibitors or modulators directed against such protective sequences, protective sequence products, genes, gene products, and/or their regulatory elements involved in cell death. The present invention also relates to methods and compositions for the diagnosis and treatment of conditions, disorders, or diseases, involving cell death, including, but not limited to, treatment of the types of conditions, disorders, or diseases, which can be prevented, delayed or rescued from cell death and include, but are not limited to, those associated with the central nervous system, including neurological and psychiatric conditions, disorders, or diseases, and those of the peripheral nervous system. Further, the invention relates to methods of using the protective sequence, protective sequence products, and/or their regulatory elements for the identification of compounds that modulate the expression of the protective sequence and/or the activity of the protective sequence product. Such compounds can be useful as therapeutic agents in the treatment of various conditions, disorders, or diseases involving cell death.

An intravascular lead is used to deliver energy for stimulating nervous system targets using energy delivery elements (e.g. electrodes) that are in direct contact with the nervous system targets. The lead may be positioned within the internal jugular vein and the nervous system targets may include the carotid artery/carotid sinus bulb and/or associated baroreceptor afferents, and/or surrounding nervous system targets in the region of the internal jugular vein, such as the carotid sinus nerve and/or associated nerve branches and/or the vagus nerve and/or associated nerve branches. Stimulation energy travels along a conductive bridge that extends from the intravascular lead to the nervous system target, or is relayed from the intravascular lead to another device disposed within or surrounding the target structure.

The present invention pertains to a process for production of recombinant arylsulfatase A in a cell culture system, the process comprising culturing a mammalian cell capable of producing rASA in liquid medium in a system comprising one or more bio-reactors; and concentrating, purifying and formulating the rASA by a purification process comprising one or more steps of chromatography. Other aspects of the invention provides a pharmaceutical composition comprising rASA, which is efficiently endocytosed via the mannose-6-phosphate receptor pathway in vivo as well as a rhASA a medicament and use of a rhASA for the manufacture of a medicament for reducing the galactosyl sulphatide levels within target cells in the peripheral nervous system and/or within the central nervous system in a subject. A final aspect of the invention provides a method of treating a subject in need thereof, said method comprising administering to said subject a pharmaceutical composition comprising a rhASA and thereby obtaining a reduction in the galactosyl sulphatide levels in target cells within said subject.

The present invention relates to novel compounds of Formula I, their pharmaceutically acceptable derivatives, tautomeric forms, isomers, polymorphs, prodrugs, metabolites, salts or solvates thereof. The invention also relates to processes for the synthesis of novel compounds of Formula I, their pharmaceutically acceptable derivatives, tautomeric forms, isomers, polymorphs, prodrugs, metabolites, salts or solvates thereof. The present invention further provides pharmaceutical compositions comprising compounds of Formula I and methods of treating or preventing one or more disorders of the central and/or peripheral nervous system, preferably by modulating neurological and/or psychiatric targets (GPCR and/or non-GPCR).

Apparatus and method for making and using devices that generate optical signals, and optionally also electrical signals in combination with one or more such optical signals, to stimulate (i.e., trigger) and/or simulate a sensory-nerve signal in nerve and/or brain tissue of a living animal (e.g., a human), for example to treat nerve damage in the peripheral nervous system (PNS) or the central nervous system (CNS) and provide sensations to stimulate and/or simulate “sensory” signals in nerves and/or brain tissue of a living animal (e.g., a human) to treat other sensory deficiencies (e.g., touch, feel, balance, visual, taste, or olfactory) and provide sensations related to those sensory deficiencies, and/or to stimulate (i.e., trigger) and/or simulate a motor-nerve signal in nerve and/or brain tissue of a living animal (e.g., a human), for example to control a muscle or a robotic prosthesis.

The present invention provides a self anchoring electrode for recording, measuring and/or stimulating nerve activity in nerves and/or nerve fascicles of the peripheral nervous system, and methods for using such a self anchoring electrode.

Methods are provided for reducing copper values for, by way of example, treating, preventing or ameliorating tissue damage such as, for example, tissue damage that may be caused by (i) disorders of the heart muscle (for example, cardiomyopathy or myocarditis) such as idiopathic cardiomyopathy, metabolic cardiomyopathy which includes diabetic cardiomyopathy, alcoholic cardiomyopathy, drug-induced cardiomyopathy, ischemic cardiomyopathy, and hypertensive cardiomyopathy, (ii) atheromatous disorders of the major blood vessels (macrovascular disease) such as the aorta, the coronary arteries, the carotid arteries, the cerebrovascular arteries, the renal arteries, the iliac arteries, the femoral arteries, and the popliteal arteries, (iii) toxic, drug-induced, and metabolic (including hypertensive and/or diabetic disorders of small blood vessels (microvascular disease) such as the retinal arterioles, the glomerular arterioles, the vasa nervorum, cardiac arterioles, and associated capillary beds of the eye, the kidney, the heart, and the central and peripheral nervous systems, (iv) plaque rupture of atheromatous lesions of major blood vessels such as the aorta, the coronary arteries, the carotid arteries, the cerebrovascular arteries, the renal arteries, the iliac arteries, the fermoral arteries and the popliteal arteries, (v) diabetes or the complications of diabetes.

Compounds, compositions and methods are provided which are useful in the treatment of conditions such as central or peripheral nervous system disorders through the modulation of potassium ion flux through voltage-dependent potassium channels and/or depressing cortical and/or peripheral neuron activity are disclosed. Novel derivatives of N-phenylanthranilic acid are also disclosed.

The invention relates to the use of agmatine, in the treatment of acute neurotrauma (such as stroke) and degenerative disorders of the central and peripheral nervous system (such as dementia). The invention further provides novel compounds of general formula I (which are quinuclidine derivatives), formula II (which are norbornane derivatives), formula III (which are adamantane derivatives), and formula IV (which are phenothiazine derivatives): wherein R1, R2 and R3 are each independently hydrogen, hydroxy, substituted or unsubstituted C1-4 alkyl, substituted or unsubstituted C1-4 alkoxy, halogeno, amino, phenyl, or R4NR5; R4 and R5 are each independently hydrogen, or (CH2)n-[NH(CH2)x]y-NHR6, or (CH2)n-[NH(CH2)x]y-NH-NHR6, or (CH2)n-[NH(CH2)x]y-(NR7=)CNHR6, or (CH2)n-[NH(CH2)x]y-NH(NR7=)CNHR6 wherein n is from 0-5, y is from 0-5 and each x is independently from 1-5; R6, and R7 are each independently hydrogen, hydroxy, substituted or unsubstituted C1-4 alkyl, substituted or unsubstituted C1-4 alkoxy, or halogeno; and pharmaceutically acceptable salts and optically active isomers thereof.

The present invention is directed to a combination of therapeutic compounds and treatment methods and kits using the combination. In particular, one of the combination affects the NCca-ATP channel of neural tissue, including neurons, glia and blood vessels within the nervous system. Exemplary SUR1 and/or TRPM4 antagonists that inhibit the NCca-ATP channel may be employed in the combination. The combination therapy also employs one or more of a non-selective cation channel blocker and/or an antagonist of VEFG, NOS, MMP, or thrombin. Exemplary indications for the combination therapy includes the prevention, diminution, and/or treatment of injured or diseased neural tissue, including astrocytes, neurons and capillary endothelial cells, that is due to ischemia, tissue trauma, brain swelling and increased tissue pressure, or other forms of brain or spinal cord disease or injury, for example. In other embodiments, there are methods and compositions directed to antagonists of TRPM4, including at least for therapeutic treatment of traumatic brain injury, cerebral ischemia, central nervous system (CNS) damage, peripheral nervous system (PNS) damage, cerebral hypoxia, or edema, for example.