Russian DMSO Cerebral Palsy GHB DMSO Patent
This was challenging to translate, so I am posting it here for others who want to read it.
Here it is with clean paragraph breaks restored:
METHOD FOR REDUCING MUSCLE SPASTICITY
Abstract / Description
The invention relates to medicine and can be used in the restoration of motor functions in affected limbs.
The closest prior art in terms of technical essence and achievable result is a method for reducing muscle spasticity by intravenous administration of sodium oxybutyrate, followed by therapeutic gymnastics and electrical stimulation of the neuromuscular apparatus.
The disadvantage of the known method is that the reduction of pathologically increased muscle tone is achieved only for a short period of muscle relaxation.
The objective of the invention is to prolong the period of muscle relaxation.
This objective is achieved by the fact that the method for reducing muscle spasticity is carried out by intravenous administration of sodium oxybutyrate, followed by therapeutic gymnastics and electrical stimulation of the neuromuscular apparatus; additionally, the area of the spastic muscles is warmed, and into the same area an electrophoresis is performed with a mixture of 5–10% sodium oxybutyrate solution and dimexide in a 1:1 ratio; then, on the same area and on the spinal cord segments innervating these muscles, applications are applied consisting of a 5–10% solution of sodium oxybutyrate and dimexide and a 0.1–0.2% lidocaine solution in a ratio of 2:1:0.1.
Method of Implementation
The treatment begins with intravenous administration of sodium oxybutyrate to the patient.
A 20% solution of sodium oxybutyrate is used in a dosage of 10 to 20 mg of the substance per kg of the patient’s body weight (narcotic dose is 70–120 mg per kg, depending on the patient’s weight and individual reaction to the drug).
Administration of the indicated dose of the drug causes a partial myorelaxant effect, which occurs 30–40 minutes after administration and lasts for the subsequent 2–3 hours.
2.5–3 hours after the intravenous injection, the area of the spastic muscles and the corresponding spinal cord segments are warmed, and 5 ml of a mixture of 5–10% solutions of sodium oxybutyrate and dimexide is introduced into it by electrophoresis.
Warming is performed to increase the permeability for medicinal substances introduced by electrophoresis.
The inclusion of dimexide in the mixture promotes increased penetration of sodium oxybutyrate through the patient’s skin during electrophoresis and, consequently, its accumulation in the muscles.
The most pronounced myorelaxant effect is achieved when using sodium oxybutyrate at a concentration of 5–10% in a mixture with dimexide of the same concentration.
The use of solutions with higher concentrations for electrophoresis did not show correspondingly greater antispastic action.
Dimexide increases the skin permeability for sodium oxybutyrate compared to conventional electrophoresis and enhances the drug’s action.
In this case, small doses of sodium oxybutyrate exert an active effect, while the specific influence on spastic muscles is preserved without a pronounced general relaxing action.
Prolongation of the action of sodium oxybutyrate is ensured by its deposition in the skin during electrophoretic introduction and by the action of dimexide.
The electrode area is selected according to the size of the muscles, with mandatory localization in the area of the motor points.
Sodium oxybutyrate is introduced from the cathode, since in a weakly alkaline environment (pH 5.8) a positively charged sodium ion is detached from its molecule.
The duration of electrophoresis is 20 minutes.
After 2–2.5 hours, repeated warming of the muscles is performed using an electrobandage (skin temperature rises to 50°C), and after 10 minutes, an application of sodium oxybutyrate, lidocaine, and dimexide is applied to the area of the spastic muscles for 2 hours.
The indicated ingredients are used in the following proportions: sodium oxybutyrate 20% – 50.0 ml; lidocaine 2% – 10.0 ml; dimexide 20% – 50.0 ml, which corresponds to a 9% solution of sodium oxybutyrate, a 9.2% solution of lidocaine, and a 9% solution of dimexide.
1–2 layers of gauze, corresponding to the size of the spastic muscle, are moistened with 3–5 ml of the above mixture.
In this case, the application contains up to 400 mg of sodium oxybutyrate, 400 mg of dimexide, and 10 mg of lidocaine.
In low concentrations (0.5%), lidocaine solution in terms of toxicity does not significantly differ from novocaine. However, lidocaine acts faster, stronger, and more prolonged.
In the applications, a 0.1–0.2% solution of lidocaine is used.
The increase in the effectiveness of the action by these complexes of drugs is explained by their influence on various mechanisms of spasticity.
In this case, sodium oxybutyrate causes presynaptic inhibition in axodendritic synapses of afferent fibers, blocking the transmission of pathological impulses from spastic muscles to efferent structures.
Lidocaine reduces the formation of acetylcholine and lowers the excitability of peripheral cholinergic-reactive systems.
Dimexide increases the rate of absorption of medicinal substances through intact skin.
A compress paper is placed on top of the gauze, then a layer of cotton wool, and everything is bandaged.
Example
Patient G., 56 years old. Diagnosis: residual effects of arachnomyelitis in the thoracic spinal cord, pronounced spastic lower paraparesis.
Neurological status: cranial nerves without pathology. Pronounced spastic lower paraparesis with a marked increase in muscle tone of the spastic type in both extensors and flexors.
Walks with difficulty using a cane. Spastic-paretic gait. Notes sharp pains in the spastic muscles.
Hyperesthesia from the T1 level of conductive type, hypoalgesia in the segments on both sides.
Musculo-articular sense is not impaired. Patellar and Achilles reflexes are pathologically increased, elicited from expanded zones. Bilateral Babinski sign.
Treatment performed:
At 8:00 a.m., 10 ml of 20% sodium oxybutyrate solution was administered intravenously.
After 1 hour, the patient noted signs of reduced increased muscle tone, which became more pronounced after another half hour.
At the same time, subjective reduction in pain syndrome was noted.
For 40 minutes, the patient engaged in therapeutic gymnastics.
At 10:30 a.m., warming of the spastic muscles with a Sollux lamp was performed for 20 minutes.
At 11:00 a.m., electrophoresis with a mixture of sodium oxybutyrate and dimexide solution was performed for 20 minutes on the area of the quadriceps and gastrocnemius muscles, and then on the corresponding thoracic spinal segments.
At 12:30 p.m., warming of the paretic muscles was performed for 20 minutes using an electrobandage.
At 1:00 p.m., an application of a mixture of sodium oxybutyrate, lidocaine, and dimexide was applied to the area of the spastic muscles.
The total duration of action of the applications was 2 hours.
At 3:15–3:30 p.m., electrical stimulation of the paretic muscles of the lower limbs was performed.
In the complex of means reducing spasticity, during the day the patient noted significant muscle relaxation and disappearance of pain after electrophoresis, sodium oxybutyrate, and the application.
The described method increases the duration and effectiveness of the relaxing action on spastic muscles, significantly enhancing restorative treatment and allowing more productive therapeutic gymnastics and electrical stimulation.
After a course of treatment lasting 25 days, a significant reduction in spasticity, disappearance of pain, increased strength in paretic limbs, increased voluntary movement, and improved walking function were observed (the patient began to walk without a cane).
After discharge, the patient returned to work.
Electrophysiological Findings
Electromyography before and after treatment showed increased amplitudes and frequency of oscillations, indicating reduced reflex excitability of the spinal cord segmental apparatus.
The stretch reflex electromyogram showed disappearance of high-amplitude bursts.
Electrical activity of spastic muscles significantly decreased.
A decrease in H-reflex amplitude indicated reduced excitability of alpha-motoneurons.
Electrodiagnostic studies showed decreased electroexcitability (threshold increased by 2–2.5 mA).
Clinically, this corresponded to reduced spasticity and increased active movement.
Formula of the Invention
A method for reducing muscle spasticity by intravenous administration of sodium oxybutyrate followed by therapeutic gymnastics and electrical stimulation, characterized in that to prolong muscle relaxation, the spastic muscle area is additionally warmed, electrophoresis with a 5–10% sodium oxybutyrate and dimexide mixture (1:1) is applied, followed by applications of sodium oxybutyrate, dimexide, and lidocaine (2:1:0.1) to the same area and corresponding spinal segments.
Sources of Information
Zemskova I. F. Conservative methods of reducing spasticity in the complex of medical rehabilitation of patients with motor cerebral defects. Dissertation. Kiev, 1978.
Земскова И. Ф. Консервативные методы снижения спастичности в комплексе медицинской реабилитации больных с двигательным церебральным дефектом. Дисс. Киев, 1978.