It's the same toxin that causes a deadly type. Botulinum toxin (abbreviated as BTX or BoNT) is produced by Clostridium botulinum, an anaerobic gram-positive bacteria. Clinical botulism syndrome may appear after ingestion of contaminated food, colonization of the baby's gastrointestinal tract, or infection in a wound. The active component of BOTOX is a derivative protein complex of Clostridium botulinum.
The protein consists of a type A neurotoxin and several other proteins. Under physiological conditions, the complex is presumed to dissociate and release the pure neurotoxin. The formation of neutralizing antibodies against botulinum toxin type A may reduce the effectiveness of botox treatment by inactivating the biological activity of the toxin. Patients treated with BOTOX achieved a statistically significant benefit in the primary efficacy endpoint compared to placebo a 30 days after your first active treatment.
The median paralysis unit (MPU) is believed to be a more pharmacologically relevant unit of biological activity. Muscle activation patterns can change spontaneously in cervical dystonia without changing the clinical presentation of the dystonia. The GAS performed by the physician for active and passive functional objectives was a secondary endpoint at weeks 8 and 12. Improvements were also observed in the self-assessment of the subject's age and attractiveness with BOTOX (24 units and 44 units) compared to placebo using the Facial Line Outcomes questionnaire (FLO-1), at the main time of day 30 (p.) Because of the anticholinergic activity of botulinum toxin, care must be taken when treating patients at risk of angle-closure glaucoma, including patients with anatomically narrow angles. D In fundamental studies, the pre-specified least important difference (MID) for the total I-QOL score was 8 points, based on MID estimates of 4 to 11 points reported in patients with neurogenic detrusor hyperactivity. To identify the location of the appropriate injection sites in the frontal muscle, the overall relationship between the size of the subject's forehead and the distribution of frontal muscle activity must be evaluated.
Therapeutic effects of detrusor botulinum toxin A injection on neurogenic detrusor hyperactivity in patients with different levels of spinal cord injury and types of detrusor sphincter dyssynergy. Classical absorption, distribution, biotransformation and elimination studies have not been performed of the active substance due to the extreme toxicity of botulinum toxin type A. There are no data available on the concomitant use of anticholinergics with BOTOX injections in the treatment of overactive bladder. The light chain (~50 kD, amino acids 1-44) acts as a zinc endopeptidase (Zn2+) similar to tetanus toxin, with proteolytic activity located at the N-terminus (see the following image).
Patients with laterocolis had ipsilateral sternocleidomastoid, splenius capitis and trapezium involvement, while retrocolis was caused by bilateral splenius capitis activity. After approval, a double-blind, placebo-controlled study was conducted in patients with multiple sclerosis (MS) with urinary incontinence due to neurogenic detrusor hyperactivity who were not adequately treated with at least one anticholinergic and without catheterization at the start of the study. Botulinum toxin is also used to treat overactive bladders in patients who do not respond to or cannot tolerate the side effects of other medications.
