Botulinum toxin is a protein product of the gram-negative anaerobic bacterium, Clostridium botulinum, it also contains the same toxin found in food poisoning. After purification, botulinum toxin became the first bacterial toxin to be used in medical treatments. (5 Vangelova) After being injected into the body, the toxin attaches itself to nerve endings at the point where the nerves join muscles. The chemical acetylcholine is released which then signals the muscles to contract resulting in weakness and paralysis. Extra contractions are blocked by the injections into the muscle but leave enough strength for normal use. (Vangelova) This botulism toxin is categorized into 7 serotypes (A though G). Type A of botulism toxin is most commonly known as Botox. The Botox toxin is recognized as the most potent and has been studied the most for clinical use. Although botulinum toxin is a lethal toxin, it can be used as an effective and powerful medication by injecting minimum quantities of the toxin into overactive muscles. (Shipla) In 2002, Botulinum type A was approved and has since become a popular cosmetic treatment to help minimize the appearance of facial lines and wrinkles, along with the smoothing of skin for a younger appearance. (Botox: Beyond Cosmetic Fixes) The use of this type A Botulinum toxin is rapidly expanding to include a variety of treatments including ophthalmological disorders, gastrointestinal, urological, orthopedic, dermatological, secretory, painful and cosmetic disorders. (Jankovic)
Botulinum toxin first gained clinical acceptance as a result of marked benefits it produced in patients with dystonia. This neurological disease involves chronic abnormal muscle posture and tension. (5 Vangelova) Dystonias are clas...
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...eda, Juan, and Joseph Jankovic. "Long-Term Efficacy and Safety of Botulinum Toxin Injections in Dystonia." National Center for Biotechnology Information. U.S. National Library of Medicine, 04 Feb. 2013. Web. 13 Apr. 2014. .
9. Karp, Barbara Illowsky. "Botulinum Toxin Physiology in Focal Hand and Cranial Dystonia." National Center for Biotechnology Information. U.S. National Library of Medicine, 20 Nov. 2012. Web. 13 Apr. 2014. .
10. Lakraj, Amanda-Amrita D., Narges Moghimi, and Bahman Jabbari. "Hyperhidrosis: Anatomy, Pathophysiology and Treatment with Emphasis on the Role of Botulinum Toxins." National Center for Biotechnology Information. U.S. National Library of Medicine, 23 Apr. 2013. Web. 13 Apr. 2014.
National Institute of Arthritis and Musculoskeletal and Skin Diseases. "Hidradenitis Suppurativa: MedlinePlus." Nlm.nih.gov/. U.S. National Library of Medicine, n.d. Web. .
Rowland, Lewis P. (ed.): Merritt's Textbook of Neurology, eighth edition. Lea and Febiger. Philadelphia, 1959, pp. 630--631.
Guided by fabulous results in preventing permanent damage from stroke and other injuries to the central nervous system in rats and other animals, researchers around the world have launched scores of trials in humans (12). However, many promising new therapies are sitting on the shelf because of a lack of money and other resources necessary to conduct large, lengthy, and expensive studies to conclusively show that a new drug or treatment really works in people. The requirement for safety and efficacy can be frustrating, especially for badly needed treatments that are very promising, but such caution is necessary.
Around the world, many people are living with neurologically debilitating disorders like multiple sclerosis. Multiple sclerosis is best described as a pathological “inflammatory-mediated demyelinating disease of the human central nervous system,” and affects more than 2.5 million people globally (Trapp & Nave, 2008).
With more than 200,000 US cases per year, Parkinson’s disease has become a major part
Amyotrophic lateral sclerosis, also known as ALS or Lou Gehrig's disease, is a disease of the nerve cells in the brain and spinal cord that control voluntary muscle movement (Dugdale, Koch, and Zieve 2010). In ALS, nerve c...
Introduction: This report is to discuss an experiment to assess the sensory and motor functions of the facial nerve in humans. The facial nerve is one of twelve cranial nerves that innervates the head and neck. These nerves serve a variety of functions, both sensory and motor, and are responsible for moving the muscles in the face, head and neck, and receiving information the brain can interpret into all five sense. Appendix A outlines each cranial nerve, it’s sensory and/or motor function, and the foramen in the bones of the skull it passes through.
The path physiology of Parkinson’s disease is the pathogenesis if Parkinson disease is unknown. Epidemiologic data suggest genetic, viral, and environmental toxins as possible causes. Nigral and basal loss of neurons with depletion of dopamine, an inhibitory neurotransmitter, is the principal biochemical alteration in Parkinson disease. Symptoms in basal ganglia disorders result from an imbalance of dopaminergic (inhibitory) and cholinergic (excitatory) activity in the caudate and putamen of the basal ganglia.
Shabat, S., Leitner, Y., David, R., & Folman, Y. (2012). The correlation between Spurling test and imaging studies in detecting cervical radiculopathy. Journal Of Neuroimaging: Official Journal Of The American Society Of Neuroimaging, 22(4), 375-378. doi: 10.1111/j.1522-6569.2011.00644.x
...of minutes but can reoccure many times a day. The group inculeds paroxysmal paresthesia, trigeminal neuralgia, painful tonic spasms, paroxysmal dysatrias and ataxias, paroxysmal diplopia, paroxusmal dyskinesia, facial myokymia. Here we can also include the symptom of Lhermitte.
Multiple sclerosis is a chronic disease of the central nervous system. It is understood as an autoimmune disease, a condition where the body’s immune system mistakenly attacks normal tissues. In Multiple Sclerosis, the patient’s own cells & antibodies attack the fatty myelin sheath that protects and insulates nerve fibres in the brain and spinal cord, the two components of the CNS. This ultimately causes damage to the nerve cells and without the insulation the myelin sheath provides, nerve communication is disrupted. Hence, Multiple Sclerosis is characterized by symptoms that reflect central nervous system involvement (Luzzio, 2014).
Dyck, P., Feldman, E., & Vinick, A. (2013, November 26). Diabetic Neuropathy: The Nerve Damage of Diabetes. Retrieved from http://diabetes.niddk.nih.gov/dm/pubs/neuropathies/#types
Bushby RF, Birnkrant DJ, Case LE, Clemens PR, Cripe L, Kaul a, et.al Diagnosis and management of Duchenne Muscular Dystrophy. Lancet Neurol. 2010;9:77-93.(PubMed:19945913)
Multiple sclerosis (MS) is an acquired demyelinating disease of the central nervous system (CNS) that typically is diagnosed in the second or third decade of life. Normally, nerves are enclosed in myelin sheaths that help facilitate transmission of nerve impulses within the CNS and the peripheral nervous system throughout the body. In patients with MS, the myelin sheath is damaged and eventually degenerates, causing patches of scar tissue called plaques or lesions to occur anywhere randomly on the myelin sheath (Ruto, 2013). This results in impaired nerve conductivity, which interferes with message transmission between the brain and the other parts of the body. As a result, impulse transmission is altered, distorted, short-circuited, or completely absent. This interference in impulse transmission creates muscle weakness, muscle imbalance, and possibly muscle spasms with partial or complete paralysis. Multiple sclerosis also can result in visual impairment and alteration of cognitive abilities, as well as pain, numbness, or tingling sensations (Ruto, 2013).
National Institute of Neurological Disorders and Stroke (2011). National Institutes of Health. Retrieved [18th April 2011] from http://www.ninds.nih.gov/disorders/picks/picks.htm.