113 results about "Neuromuscular disease" patented technology

A method of treating a patient suffering from a disease, disorder or condition includes the administration to the patient of a therapeutically effective amount of botulinum toxin of a selected serotype until the patient experiences loss of clinical response to the administered botulinum toxin and thereafter administering to the patient a therapeutically effective amount of another botulinum toxin of a different serotype.

Modified and stabilized propeptides of Growth Differentiation Factor proteins, such as GDF-8 and Bone Morphogenetic Protein-11, are disclosed. Also disclosed are methods for making and using the modified propeptides to prevent or treat human or animal disorders in which an increase in muscle tissue would be therapeutically beneficial. Such disorders include muscle or neuromuscular disorders (such as amyotrophic lateral sclerosis, muscular dystrophy, muscle atrophy, congestive obstructive pulmonary disease, muscle wasting syndrome, sarcopenia, or cachexia), metabolic diseases or disorders (such as such as type 2 diabetes, noninsulin-dependent diabetes mellitus, hyperglycemia, or obesity), adipose tissue disorders (such as obesity), and bone degenerative diseases (such as osteoporosis).

The disclosure provides methods for treating neuromuscular disorders in mammals. The disclosed methods include administering therapeutically effective amounts of a GDF-8 inhibitor and a corticosteroid to a subject susceptible to, or having, a neuromuscular disorder, so as to maintain desirable levels of muscle function.

A method of providing rehabilitation movement training for a person suffering from nerve damage, stroke, spinal cord injury, neurological trauma or neuromuscular disorder in attempting to move a body part about a joint using a powered orthotic device includes sensing at least one electromyographic signal of a muscle associated with motion about the joint, applying in a first direction with respect to the joint a force having a magnitude that is a first function of the at least one sensed electromyographic signal, and applying in a second direction with respect to the joint a return force that is a second function of the at least one sensed electromyographic signal, wherein the second function differs from the first function.

This invention relates to drug delivery and specifically to the preparation and use of functionalized carriers such as nanopolymers and nanovesicles for improved delivery of nucleic acid agents (NAA) to tissues and cells. These compounds have broad applicability for treating numerous diseases and disorders, including neurodegenerative and neuromuscular disorders. The concept encompasses preferably polymeric carriers for delivery of a class of oligonucleotides that modulate RNA splicing.

Disclosed are methods of treating neuropsychiatric diseases, neuromuscular diseases, viral infections, neurodegenerative diseases and ricin poisoning using angiotensin II receptor blockers.

Botulinum toxin, a well know systemic poison, produces favorable therapeutic effect by virtue of regionally attaching to nerves within the myoneural junction and possibly other tissues in a target region of a particular tissue. The present invention provides compositions of botulinum toxin and a sequestration agent that increase sequestration and delivery of the botulinum toxin to neural and associated tissues, as compared with available formulations of botulinum toxins, and thereby produce a beneficial clinical effect. The sequestration agents of the present invention include proteins, lipids and carbohydrates. A preferred composition of the present invention comprises a botulinum toxin and an albumin. The present invention also provides methods of treating neuromuscular diseases and pain using the disclosed compositions and methods of making the disclosed compositions.

The disclosure provides improved neutralizing anti-GDF-8 antibodies capable of substantially higher levels of expression in host cells compared to previous anti-GDF-8 antibodies. Also provided are methods of using compositions comprising such antibodies to increase muscle mass or strength, and to treat or prevent muscular disorders, neuromuscular disorders, metabolic disorders, adipose tissue disorders or bone disorders.

A diaphragm pacing stimulatory method and a system to implement the method are provided to improve respiratory function and the quality of sleep in patients whose sleep is compromised by poor respiration. The diaphragm pacing method includes adaptations that make it particularly compatible with the onset of sleep and sustaining sleep. Embodiments of the method are operated independently of breathing effort the patient may make during sleep. Patients for whom the invention is appropriate include those with a neuromuscular disease, such as amyotrophic lateral sclerosis (ALS). System elements include an external electrical stimulator coupled to one or more implanted electrodes that stimulate diaphragm contraction. The system and method provide for a pacing of the diaphragm, improved breathing, and improved sleep. Features of improved sleep include longer sleep time, an increased amount of REM sleep, and fewer episodes of wakefulness and restlessness.

The invention relates to an antisense oligonucleotide targeted to the coding region of the human acetylcholinesterase (AChE), which selectively suppresses the AChE-R isoform of the enzyme. The antisense oligonucleotide is intended for use in the treatment and/or prevention of neuromuscular disorders, preferably myasthenia gravis. In addition, it can penetrate the blood-brain barrier (BBB) and destroy AChE-R within central nervous system neurons, while also serving as a carrier to transport molecules across the BBB.

A method and apparatus for assessing neuromuscular pathology in an individual, by (a) applying a plurality of stimuli to a peripheral nerve; (b) recording from the peripheral nerve, or from a muscle innervated by the peripheral nerve, at least one response to each stimulus; (c) processing each response into at least one response characteristic; (d) compiling the response characteristics from all of the responses into a plurality of descriptive parameters of the response characteristics; and (e) analyzing the plurality of descriptive parameters according to a function specific to the neuromuscular pathology so as to yield an indicator of the pathology.

A method and composition for treating a patient suffering from a disease, disorder or condition include the administration to the patient of a therapeutically effective amount of a combination of at least two neurotoxins selected from a group consisting of botulinum toxin types A, B, C, D, E, F and G. The amount of each selected neurotoxin administered is further selected to control a duration of therapeutic activity of the administered combination.

Treating human muscle tissue by the oral administration of a formulation of creatine derivative and in particular creatine esters and more particularly ethyl esters of creatine are described. The formulations comprise a phosphate such as dicalcium phosphate, a biodegradable polymer such as a polyvinyl pyrrolidine and a starch. The formulation may further comprise other excipients such as metal salt of a stearate, e.g. magnesium stearates. The formulation is produced as flowable particles with a sieve size of about 20 to 60 which particles are coated with a shellac to mask taste, avoid moisture uptake, and extend shelf life.

The invention provides conjugates, comprising an organ, tissue or tumor cell homing molecule linked to a moiety. Such a moiety can be, for example, an oligonucleotide, small interfering RNA, gene, virus, protein, pharmaceutical or detectable agent. In addition the invention provides methods to diagnose or treat neuronal or neuromuscular disease, or a pathology of the brain, or a tumor of neuronal or neuroectodermal origin, by administrating to a subject having or suspected of having a pathology a molecule or conjugate that homes to, binds to and is taken up by the brain cells or neuronal cells, or by the tumor cells of neuronal or neuroectodermal origin. The invention also provides a method of identifying and measuring neurite growth in neuronal cells.

The present invention relates to novel α-keto carbonyl calpain inhibitors for the treatment of neurodegenerative diseases and neuromuscular diseases including Duchenne Muscular Dystrophy, Becker Muscular Dystrophy and other muscular dystrophies. Disuse atrophy and general muscle wasting can also be treated. Diseases of the eye, in particular cataract, can be treated as well. Generally all conditions where elevated levels of calpains are involved can be treated. The compounds of the invention may also inhibit other thiol proteases such as cathepsin B, cathepsin H, cathepsin L, papain or the like. Multicatalytic Protease (MCP) also known as proteasome may also be inhibited and the compounds can therefore be used to treat cell proliferative diseases such as cancer, psoriasis, and restenosis. The compounds of the present invention are also inhibitors of cell damage by oxidative stress through free radicals and can be used to treat mitochondrial disorders and neurodegenerative diseases, where elevated levels of oxidative stress are involved.

The invention discloses a non-invasive neuromuscular disease inspection system based on an attached electrode, and belongs to the field of a medical apparatus. The system comprises a surface electrode collecting device, a surface electrical stimulation device and a control terminal, wherein the surface electrode collecting device comprises an attached electrode I, a signal processing module, a communication module I and a power supply I; the attached electrode I collects a human physiological signal and transmits the signal to the signal processing module; the signal processing module processes the signal and then transmits the signal to the control terminal through the communication module I; the surface electric simulation device comprises an attached electrode II, a stimulating signal generation module, a communication module II and a power supply II; and the stimulating signal generation module receives a control signal transmitted by the control terminal through the communication module II, then generates an electric stimulating signal, and carries out electric stimulation on the human surface through the attached electrode II. Great pain on a sufferer caused by a needle electrode is overcome by the system; and a portable non-invasive detection method is provided for neuromuscular diseases such as amyotrophy and motor neuron disease.

The invention provides methods and compositions for treating neuromuscular diseases including, but not limited to muscular dystrophies. It is demonstrated herein that statin drugs are therapeutic for neuromuscular disease, including, but not limited to muscular dystrophies.

The mdx mouse is a model of Duchenne muscular dystrophy. The present invention describes that mdx mice exhibited clinically relevant cardiac phenotypes. A non-invasive method of recording electrocardiograms (ECGs) was used to a study mdx mice (n=15) and control mice (n=15). The mdx mice had significant tachycardia, consistent with observations in patients with muscular dystrophy. Heart-rate was nearly 15% faster in mdx mice than control mice (P<0.01). ECGs revealed significant shortening of the rate-corrected QT interval duration (QTc) in mdx mice compared to control mice (P<0.05). PR interval duration were shorter at baseline in mdx compared to control mice (P<0.05). The muscarinic antagonist atropine significantly increased heart-rate and decreased PR interval duration in C57 mice. Paradoxically, atropine significantly decreased heart-rate and increased PR interval duration in all mdx mice. Pharmacological autonomic blockade and baroreflex sensitivity testing demonstrated an imbalance in autonomic nervous system modulation of heart-rate, with decreased parasympathetic activity and increased sympathetic activity in mdx mice. These electrocardiographic findings in dystrophin-deficient mice provide new bases for diagnosing, understanding, and treating patients with Duchenne muscular dystrophy.

A method of detecting neuromuscular pathology in an individual is disclosed comprising the steps of placing a detector on the skin surface of the individual substantially adjacent to a skeletal muscle; obtaining signals from the detector; processing the signals; and determining neuromuscular status in response to the signals. A system for detecting neuromuscular disease in an individual is disclosed, the system comprising at least one means for recording a first signal from a skeletal muscle; a filter in communication with the recording means to generate a second signal consisting substantially of spontaneous myoelectrical activity; and a processor in communication with the filter, wherein the first signal from the skeletal muscle is filtered so as to generate spontaneous myoelectrical signals, and further wherein the processor calculates the power spectral density of the filtered signals and determines the neuromuscular status in response to the power spectral density of the filtered signals.