61 results about "Neurological deficit" patented technology

A system and method that facilitates stimulating neural pathways, e.g., muscles and/or associated nerves, of a patient's body for the purpose of therapeutic medical treatment by rehabilitating weakened muscles and using neuroplasticity to retrain sequential muscle movements and/or to provide the ability to directly deliver functional motor movements. Use of the present invention is of particular value for treating a patient following a stroke. More particularly, such systems are characterized by a plurality of discrete devices, preferably battery powered but may alternatively include RF-powered devices as well or in combination, configured for implanting within a patient's body via injection, each device being configured to affect a parameter, e.g., via nerve and/or muscle stimulation and/or to sense a body parameter, e.g., temperature, O₂ content, physical position, electrical potential, etc., that operate under control of a system controller that coordinates the sequential stimulation via wireless commands to the implanted devices.

The invention relates to a novel nerve duct bracket and a preparation method and application thereof. Three-dimensional graphene or graphene derivative multichannel active nanofiber sponge is used asa stuffing inner core, and nanofibers in an axial direction are used as an outer pipe. The preparation method comprises the steps of performing ultrasonic dispersion on graphene or a graphene derivative into spinning liquid, performing electrostatic spinning, and performing drying so as to obtain a nanofiber film; performing shearing, and performing homogenization and crushing so as to obtain broken fiber mixed liquid; pouring the broken fiber mixed liquid into a multichannel mold, and performing freeze drying; performing cross-linked shaping; performing drying and shaping so as to obtain thethree-dimensional graphene or graphene derivative multichannel nanofiber sponge; and performing fixing in an axial direction spinning receiver, and performing axial direction spinning on an outer layer so as to obtain the novel nerve duct bracket. The novel nerve duct bracket is used for inducing repair and regeneration of nerve tissue. The novel nerve duct bracket disclosed by the invention is simple to operate and good in repeatability, and a new thinking is provided for repairing neurological deficits.

The invention discloses an external thoracolumbar vertebra distraction repositor which comprises a fixed support, two hollow screws, a distracter, a pressurizer and a T-shaped socket spanner; the fixed support comprises a beam and two sets of clamps; the distracter comprises a body and two distraction rods, and one end of the distraction rod is provided with a C-shaped foot hook which is vertical to the distraction rod; the pressurizer comprises a thread rod, a connector and an extension rod; the connector comprises a nut which is connected with the thread rod and a lantern ring which is sleeved on the extension rod, and the lantern ring and the extension rod as well as the lantern ring and the nut are respectively connected with each other rotatably in two intersected planes. The distraction repository can spread the vertebral body to the maximum height according to the practical conditions, and through utilizing the self restrictive tensile forces of the anterior and the posterior longitudinal ligaments of the vertebral body, the vertebral body can be effectively corrected to be backwards protruded for an angle of 2-8 degrees; and moreover, the heights of the anterior, the center and the posteriors can also be effectively reposed. In addition, the distraction repository is also suitable for spreading, restoring and reposing the burst fractures without symptoms of stressed spinal cord and neurological deficit when vertebral body paries posterior fracture is burst in the spinal canal.

Medical compositions and methods of treating or preventing neurodegeneration in a human suffering from or that is at risk of or susceptible to neurodegeneration or cellular dysfunction associated with expression or impaired cellular function of a neuronal protein encoded by one or more genes that code for alpha-synuclein (SNCA), Parkin RBR E3 ubiquitin protein ligase, (PARK2), Leucine-rich repeat kinase 2 (LRRK2), PTEN-induced putative kinase/(PINK1), Daisuke-Junko 1, (DJ-1) and ATPase type 13A2 (ATP13A2), are disclosed. Methods of treatment for these disorders is also provided, comprising administering a vector into a cell, wherein the vector facilitates expression of a molecular component that alters one of the aforementioned genes in the cell or expression of the gene in the cell, the gene being implicated in an etiology of the neurological deficit.

A neuroprotective pharmacological method in cerebral ischemic insult comprising administration of L- or DL-threo-DOPS or a pharmaceutically acceptable acid addition salt thereof to a patient. Threo-DOPS directly acts on neurons to exert an effect to protect against neuronal death due to brain ischemia, an antilethal effect, and an anti-edema effect due to excessive polarization of neuronal membrane potential caused by an increase in Na-K-ATPase activity. renaline.

The present invention is directed to methods of treating neurological deficits resulting from injury or disease to the striatum or substanta nigra pars compacta of a human by administering BMP7 to the striatum or substanta nigra pars compacta of a human in amounts effective to induce cell populations having the capacity to differentiate towards a dopaminergic phenotype to in fact differentiate towards a dopaminergic phenotype, and to neurotrophic compositions and matrices suitable for use in such treatments.

Methods and apparatuses for sensory electrical stimulation of the peripheral nervous system to improve human motor function and performance are described. Methods and devices may be used to enhance physical performance of athletes, professionals, and gamers or improve motor function (hand, finger and limb movement) in patients rehabilitating from neurological deficits and impairments caused by stroke, traumatic brain injury and other neurologic or non-neurologic conditions. These apparatuses and methods may be used for physical training and mental training (to improve memory and functional performance including motor coordination, limb-eye coordination, occupational and recreational skills) through periodic or sustained sensory electrical stimulation. Treatment plans may be based on biomarkers and may be used alone or in combination with other apparatuses. Learning and feedback techniques individualize treatment parameters depending on the subject's neurologic and motor function in diseased patients and healthy users.

A system, method and apparatus for diagnosis and therapy. Preferably, the system, method and apparatus is provided for diagnosis and therapy of neurological and/or neuromuscular deficits by using a computational device. Optionally and preferably, the system, method and apparatus track one or more physical movements of the user, which are then analyzed to determine whether the user has one or more neurological and/or neuromuscular deficits. Additionally or alternatively, the system, method and apparatus induce the user to perform one or more physical movements, whether to diagnose such one or more neurological and/or neuromuscular deficits, to treat such one or more neurological and/or neuromuscular deficits, or a combination thereof.

The present invention relates to methods of controlling neurological deficits in patients who have undergone cardiopulmonary bypass (CPB) by administering xenon to said patients.

The present invention relates to analysis of image data, e.g. brain image data, where regions of interest are identified in patient specific image data based on non-image data. The brain image data is analyzed by correlating non-image data (20) in the form of data indicative of a neurological deficit and an object model (21) to identify one or more regions of interest (22) in the brain model, mapping the brain model to patient specific brain image data to obtain target image data (24), and identifying the one or more regions of interest in the target image data.

An object of the present invention is to provide a medicine for general anesthesia which can prevent and/or alleviate an anesthetic-induced neurological deficit in the brain (preferably in the developing brain). The present invention relates to a medicine which comprises a combination of a general anesthetic and hydrogen and can prevent and/or alleviate an anesthetic-induced neurological deficit in the brain (preferably in the developing brain).

The invention provides methods of treatment or prophylaxis of damaging effects of penetrative injury to the brain or other part of the central nervous system. The methods are based in part on results in a rodent model of penetrative ballistic injury showing that an inhibitor of PDF-95 NMDAR interaction is effective in inhibiting neurological deficits resulting from such injury. The methods are useful for treating subjects having or at risk of penetrative brain injury, including subjects who have been shot in the head or at risk of such injury (e.g., military or law enforcement personnel).

A method for treating a central nervous system or peripheral nervous system dopaminergic deficit state or other neurological deficit state in a mammalian organism in need of such treatment, said method comprising administering to said mammal an amount of thalidomide effective in the treatment of a dopaminergic deficit state or other neurological deficit state and for a time sufficient to achieve a suitable blood level to treat said dopaminergic deficit state or other neurological deficit state.

The invention discloses a medicine for treating ischemic cerebral arterial thrombosis, of which the active component is Z-octadecyl-9-alkenyl-propylsulfamide being 80-250 mg/kg in effective dose. The medicine is used in an oral manner. The active component of the medicine is the Z-octadecyl-9-alkenyl-propylsulfamide so that the medicine has a significant effect of treating the ischemic cerebral arterial thrombosis, can improve neurological deficit of mice, can reduce cerebral infarction volume and can alleviate the degree of encephaledema.

The invention discloses a flexible peripheral neurological deficit repairing duct. The flexible peripheral neurological deficit repairing duct is a flexible threaded pipe prepared from high molecularmaterials and extracellular matrices through electrospinning. The invention also discloses a preparation method of the flexible peripheral neurological deficit repairing duct. The preparation method comprises the following steps of adding the high molecular materials and the extracellular matrices into an organic solvent under room-temperature condition, so as to obtain an electrospinning stock solution of 4%-16%(w/v, mg/ml); preparing soluble or non-soluble materials into a thread model containing thread-shaped side walls; uniformly spraying the electrospinning stock solution onto the threadmodel, and forming the threaded pipe from electrospinning on the thread model; and removing the threaded model so as to obtain the threaded pipe shaped flexible peripheral neurological deficit repairing duct.

The present invention features methods and compositions for treating a patient who has a neurological deficit. The method can be carried out, for example, by contacting (in vivo or in culture) a neural progenitor cell of the patient's central nervous system (CNS) with a polypeptide that binds the epidermal growth factor (EGF) receptor and directing progeny of the proliferating progenitor cells to migrate en masse to a region of the CNS in which they will reside and function in a manner sufficient to reduce the neurological deficit. The method may include a further step in which the progeny of the neural precursor cells are contacted with a compound that stimulates differentiation.

The invention relates, inter alia, to methods of treating stroke, e.g., ischemic stroke, e.g., acute ischemic stroke, and methods of reducing infarct size and/or other neurological deficits associated with stroke, e.g., ischemic stroke, e.g., acute ischemic stroke, using a VLA-4 antagonist such as natalizumab. It was discovered that VLA-4 antagonists such as natalizumab can effectively reduce the infarct size and other associated neurological deficits of a stroke, e.g., an ischemic stroke; e.g., an acute ischemic stroke, e.g., when administered within a specified time period after the onset of the stroke. Also disclosed herein are articles of manufacture and kits for the treatment of stroke, e.g., ischemic stroke, e.g., acute ischemic stroke.