943 results about "Traumatic brain injury" patented technology

A user-friendly reliable process is provided to help diagnose (assess) and treat (rehabilitate) impairment or deficiencies in a person (subject or patient) caused by a traumatic brain injury (TBI) or other neurocognitive disorders. The economical, safe, effective process can include: generating and electronically displaying a virtual reality environment (VRE) with moveable images; identifying and letting the TBI person perform a task in the VRE; electronically inputting and recording the performance data with an electronic interactive communications device; electronically evaluating the person's performance and assessing the person's impairment by electronically determining a deficiency in the person's cognitive function (e.g. memory, recall, recognition, attention, spatial awareness) and/or motor function (i.e. motor skills, e.g. balance) as a result of the TBI or other neurocognitive disorder.

A method of treating shoulder dysfunction involves the use of a percutaneous, intramuscular stimulation system. A plurality of intramuscular stimulation electrodes are implanted directly into select shoulder muscles of a patient who has suffered a disruption of the central nervous system such as a stroke, traumatic brain injury, spinal cord injury or cerebral palsy. An external microprocessor based multi-channel stimulation pulse train generator is used for generating select electrical stimulation pulse train signals. A plurality of insulated electrode leads percutaneously, electrically interconnect the plurality of intramuscular stimulation electrodes to the external stimulation pulse train generator, respectively. Stimulation pulse train parameters for each of the stimulation pulse train output channels are selected independently of the other channels. The shoulder is evaluated for subluxation in more than one dimension. More than one muscle or muscle group is simultaneously subjected to a pulse train dosage. Preferably, the at least two dosages are delivered asynchronously to two muscle groups comprising the supraspinatus in combination with the middle deltoid, and the trapezious in combination with the posterior deltoid.

A method of inhibiting the binding between N-methyl-D-aspartate receptors and neuronal proteins in a neuron is disclosed. The method comprises administering to the neuron an effective inhibiting amount of a peptide replacement agent for the NMDA receptor or neuronal protein interaction domain that effect said inhibition of the NMDA receptor—neuronal protein interaction. The method is of value in reducing the damaging effect of injury to mammalian cells. Postsynaptic density-95 protein (PSD-95) couples neuronal N-methyl-D-aspartate receptors (NMDARs) to pathways mediating excitotoxicity, ischemic and traumatic brain damage. This coupling was disrupted by transducing neurons with peptides that bind to modular domains on either side of the PSD-95/NMDAR interaction complex. This treatment attenuated downstream NMDAR signaling without blocking NMDAR activity, protected cultured cortical neurons from excitotoxic insults, dramatically reduced cerebral infarction volume in rats subjected to transient focal cerebral ischemia, and traumatic brain injury (TBI) in rats.

A portable virtual reality device is disclosed that will facilitate the effective and efficient screening for TBI in military personnel in forward deployed military settings or remote locations using minimally trained staff. This includes the establishment of a protocol that will provide cost effective pre-screening of military personnel prior to deployment to establish a baseline of brain function prior to possible future injury. The efficiency of the device will promote subsequent follow-up screening to assess the effectiveness of prescribed TBI treatment. Further protocols for diagnosis and rehabilitation applications using the same virtual reality portable device will allow more advanced usage for clinicians providing ongoing evaluation and treatment.

This technology relates generally to compounds and methods for stimulating neurogenesis (e.g., post-natal neurogenesis, including post-natal hippocampal and hypothalamic neurogenesis) and/or protecting neuronal cell from cell death. Various compounds are disclosed herein. In vivo activity tests suggest that these compounds may have therapeutic benefits in neuropsychiatric and/or neurodegenerative diseases such as schizophrenia, major depression, bipolar disorder, normal aging, epilepsy, traumatic brain injury, post-traumatic stress disorder, Parkinson's disease, Alzheimer's disease, Down syndrome, spinocerebellar ataxia, amyotrophic lateral sclerosis, Huntington's disease, stroke, radiation therapy, chronic stress, abuse of a neuro-active drug, retinal degeneration, spinal cord injury, peripheral nerve injury, physiological weight loss associated with various conditions, as well as cognitive decline associated with normal aging, chemotherapy, and the like.

A system and method for providing therapy and assessment utilizing vibrotactile feedback is disclosed. Such treatment is useful for the assessment and treatment of disequilibrium, movement and balance disorders. The system and method measures a subject's performance of predetermined tasks with respect to expected parameters using sensors such as force plates, inertial sensors, and three dimensional cameras. Predetermined motions are motions such as stand, sit-to-stand, reach, bend, functional gait, functional gait plus headshake, and other functional tasks. Vibrotactile stimulation may be applied during the subject's performance as disruptive input. Variance and rate of change of variance between measured and expected parameters is used as a tool for assessment of said subject, and is also used for providing real-time vibrotactile training to said subject. The invention is useful in the treatment of Traumatic Brain Injury (TBI), neurologic disorders causing disequilibrium and balance disorders, and the like.

Provided are methods for ameliorating a symptom of a neuropsychiatric disorder in a subject. Also provided are methods for ameliorating at least one physical symptom or at least one psychological symptom resulting from tobacco cessation in a subject, methods for ameliorating a symptom of Alzheimer's disease or other cognitive disorder in a subject, methods for ameliorating a symptom of schizophrenia, schizoaffective disorder, or other psychotic disorder in a subject, methods for ameliorating a symptom of a depressive disorder in a subject, methods for ameliorating a symptom of bipolar disorder in a subject, methods for ameliorating a symptom of post-traumatic stress disorder or other anxiety disorder in a subject, methods for predicting a predisposition to suicide, suicidal ideation, suicidal behavior, or a combination thereof in a subject, methods for ameliorating a symptom of a pain disorder in a subject, methods for ameliorating a neurodegenerative disorder in a subject, methods for ameliorating a symptom of traumatic brain injury in a subject, methods for ameliorating a sleep disorder in a subject, and methods for improving cognitive functioning in a subject. In some embodiments, the methods include administering to a subject in need thereof an effective amount of a neuroactive steroid composition comprising pregnenolone (PG), allopregnanolone (ALLO), dehydroepiandrosterone (DHEA), progesterone (PROG), precursors thereof, metabolites thereof, pharmaceutically acceptable salts thereof, derivatives thereof, or combinations thereof.

The OculoKinetic Device is used to test an individual to evaluate brain functions and to identify the presence of a traumatic brain injury or disease which manifests itself through abnormal ocular responses to stimuli by using the high-speed tracking of an individual's eye movements, pupil size and reactivity, eye lid position and blink parameters and optionally along with other ocular elements, i.e., eyeball pressure, temperature, blood flow, etc. The eye movement stimulus protocol uses a target that moves in any direction of the two-dimensional plane and may use a color display or geometric shapes. In addition, the stimuli can be used in conjunction with cognitive testing, balance assessment, and other non-eye tests.

Embodiments of the present invention comprises apparatuses and methods of measuring levels of neurological impairment. Certain embodiments of the invention comprise a headset that emits light into the user's eyes and the system tracks the pupils' orientation, movement, contraction and dilation. In specific embodiments, the headset can run a battery of tests and calculate a score indicating the user's level of neurological impairment.

Provided herein are 3,3-disubstituted 19-nor-steroidal compounds according to Formula (I) and (III): where R¹, R², R³, R^3′, R₄, R^6a, R^6a, R^11a, and R^11b are as defined herein. Compounds of the present invention are contemplated useful for the prevention and treatment of a variety of CNS-related conditions, for example, treatment of sleep disorders, mood disorders, insomnia, anxiety, depression, traumatic brain injury (TBI), stress, and epilepsy.

The present invention provides methods and systems for conditioning cerebrospinal fluid (CSF). The methods provide for efficiently removing target compounds from CSF. The systems provide for a multilumen flow path and exchange of a majority volume portion of CSF in the CSF space. The removal and/or delivery of specific compounds can be tailored to the pathology of the specific disease. The removal is targeted and specific, for example, through the use of specific size-exclusion thresholds, antibodies against specific toxins, and other chromatographic techniques, as well as delivery and/or removal of targeted therapeutic agents. The invention finds use as a diagnostic, therapeutic and drug delivery platform for a variety of diseases affecting the CNS by accessing the CSF space. Exemplified disease conditions treatable by the present CSF processing systems and methods include, but are not limited to: Cerebral Vasospasm, Guillain Bane Syndrome, illustrating multi-lumen lumbar approach Alzheimer's, Parkinson's, Huntington's, Multiple Sclerosis, Amyotrophic Lateral Sclerosis, Spinal Cord Injury, Traumatic Brain Injury, Stroke, Cancer affecting the brain or spinal cord, Prion disease, Encephalitis from various causes, Meningitis from various causes, diseases secondary to enzymatic or metabolic imbalances, Biological Warfare, etc. For the first time, the present invention offers patients a disease-modifying, disruptive technology treatment platform that addresses the known disease pathogenesis of a number of neurologic conditions to which there are presently limited and ineffective treatment options.

A pharmaceutical composition containing a magnesium salt and an osmotic hypertonic agent, like a mannitol, is disclosed. Also disclosed are methods of treating individuals who have suffered a neurological insult, such as traumatic brain injury.

The OculoKinetic Device is used to test an individual to evaluate brain function including, but not limited to, identifying the presence of a traumatic brain injury or central nervous system disease which manifests itself through abnormal ocular responses to stimuli by using the high-speed tracking of an individual's eye movements (monocular or binocular, and either conjugate or disconjugate in horizontal, vertical, or torsional directions or combinations thereof), pupil size and reactivity, eyelid position, and blink parameters, and optionally along with other ocular elements, i.e., eyeball pressure, temperature, blood flow, etc. The eye movement stimulus protocol uses a target that moves in any direction of a two- or three-dimensional plane and may use a color display or geometric shapes. In addition, the stimuli can be used in conjunction with cognitive testing, balance assessment, and other non-eye tests.

The invention provides methods for reducing traumatic injury through the use of ischemic conditioning.

The invention relates to a rheumatalgia-relieving plaster for treating trauma and process for preparation, wherein the plaster is prepared from 108 kinds of Chinese herbs including Sichuan aconite root, Kusnezoff monkshood root, jack-in-the-pulpit tuber, pinellia tuber, seed of nuxvomica, momordica seed, chaulmoogra seed, stinkweed root, pricklyash peel, pangolin scales, sargentgloryvine, root bark of chinese wolf berry, zedoary, shiny pricklyash, achyranthes and cyathula root, spicebush root and burred tuber.

This technology relates generally to compounds and methods for stimulating neurogenesis (e.g., post-natal neurogenesis, including post-natal hippocampal and hypothalamic neurogenesis) and/or protecting neuronal cell from cell death. Various compounds are disclosed herein. In vivo activity tests suggest that these compounds may have therapeutic benefits in neuropsychiatric and/or neurodegenerative diseases such as schizophrenia, major depression, bipolar disorder, normal aging, epilepsy, traumatic brain injury, post-traumatic stress disorder, Parkinson's disease, Alzheimer's disease, Down syndrome, spinocerebellar ataxia, amyotrophic lateral sclerosis, Huntington's disease, stroke, radiation therapy, chronic stress, abuse of a neuro-active drug, retinal degeneration, spinal cord injury, peripheral nerve injury, physiological weight loss associated with various conditions, as well as cognitive decline associated with normal aging, chemotherapy, and the like.

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.