Help for Hyperhidrosis
(11) Hyperhidrosis (excessive perspiration) frequently occurs between the second and the third week. (7) Hyperhidrosis (excessive perspiration) and cyanosis may appear between the fourth to tenth week after the injury and persist for months. This results in a prolonged, uncomfortable convalescence.
The clinical use of botulinum neurotoxin to effect a chemical denervation in a neuromuscular disorder was first described by Dr. Alan Scott who, in 1980, after a series of animal experiments, published the first report of the therapeutic use of BoNT A to treat strabismus in humans.54 Subsequently, through the 1980s, BoNT A was used to treat a range of focal dystonias including blepharospasm. BoNT A received U.S. Food and Drug Administration (FDA) approval as an orphan drug in December 1989, originally for the treatment of strabismus, blepharospasm, and hemifacial spasm. It was subsequently approved for the treatment of cervical dystonia and, more recently, for the treatment of glabellar wrinkles and hyperhidrosis. The use of botulinum neurotoxin preparations as treatments for the management of dystonia and spasticity is covered in more detail in Chapter 6.
(7) In very severe cases, deep aching pain, paresthesia (burning, prickling--a morbid sensation), cyanosis (blueness of the skin from imperfectly oxygenated blood), hyperhidrosis (excessive perspiration), and coldness of the injured part may appear two or three weeks after the injury has occurred and persist for many months. In milder cases, symptoms may persist for several hours, causing intense discomfort but gradually disappearing without serious consequences.
Heat cramps are painful cramps of the voluntary muscles, usually of the abdomen, legs, or arms. The cramps are caused by the inability of the muscles to relax once they have contracted. This inability to relax is caused by faulty nerve impulses to the muscles resulting from salt imbalance in the body. The condition occurs as a result of profuse sweating which removes water and sodium chloride from the body. Heat cramps normally result from excessive loss of salt after a person has been working in hot weather for a long period of time. The salt loss causes painful contractions of muscles the muscle contractions are referred to a heat cramps. A person with heat cramps will recover if the salt and water imbalance in the body is corrected and steps are taken to prevent heat cramps from developing into more serious injuries.
This systemic disease has an acute or insidious onset that may be very sudden. The patient experiences chills and fever, a severe headache, profuse sweating, generalized aching, malaise, arthralgia, weakness, and depression. His temperature increases as the disease progresses (104 F-106 F). Uncommon but characteristic features are orchitis and vertebral osteomyelitis. Although recovery is usual, there are pronounced disabilities, and the syndrome may reappear as relapses.
A number of treatment options have been described for the control of primary hyperhidrosis 8 . Specific therapies must be tailored to a patient's individual requirement, to gain maximum symptomatic improvement with minimum invasiveness and side-effects. Iontophoresis prevents sweat production within the gland. This treatment involves immersion of the sweating area in a solution, and the use of low-intensity electrical current from a D C generator to drive charged ions in the skin. Most patients find iontophoresis time-consuming and inefficient. Multiple weekly sessions are necessary and its application to body parts other than volar surfaces is very difficult. This method Cholinergic inhibitor (anticholinergic) therapy blocks neurotransmitter receptor sites on the sweat gland to stop sweat production. These drugs, such as glycopyr-rolate, may be administered orally and are the only systemic treatment in use in hyperhidrosis. The widespread anticholinergic side-effects limit patient...
The gold standard for treatment of palmar hyperhidrosis has long been recognized as thoracic sympathectomy (satisfactory control of sweating is up to 95 ) 15 . Though originally carried out as an open procedure (cervical or thoracic), a minimally invasive thoracoscopic approach is now used to interrupt the sympathetic chain (usually T2 and T3 ganglia). Transthoracic endoscopic sympathectomy (TES) is usually performed via one or two chest portals per hemithorax (usually 10 and 5 mm) and is associated with negligible scarring. Current technical controversies include anterolateral versus posterior approach in the prone position, diathermy coagulation of the sympathetic chain versus scissor dissection excision, and sympathetic chain transection versus surgical clip application 3 . The effects are usually instantaneous, with patients leaving the hospital within 24 h. TES is undoubtedly effective, with complete and durable improvement for palmar, axillary and facial hyperhidrosis. Curiously...
18.104.22.168 Focal Hyperhidrosis (Excessive Sweating) As many as 1 in 200 people may have focal hyperhidrosis and it can be extremely disabling both professionally and in private life 60 of these have excessive sweating in the palms or soles of the feet, 30 in the axillae, and 10 in the face. The cause is usually unknown so that treatment is symptomatic. In Ross syndrome, large areas of skin cannot sweat, and compensatory excessive sweating occurs in the residual areas with functioning sweat glands. In gustatory hyperhidrosis (Frey's syndrome), the cheeks sweat excessively in anticipation of food or when salivation occurs. The diagnosis is made on clinical grounds, and studies performed with indicator powder reveal the distribution and severity of resting hyperhidrosis and can document the integrity of normal thermoregulatory sweating. Clinicians can select from a range of treatments, depending on the severity of hyperhidrosis and the risks and benefits of therapy. In general, therapy...
In tinea cruris the predisposing factors, such as the use of synthetic and tight clothing and excessive sweating, should be avoided. In tinea pedis if secondary infection is present, it must be treated with topical antiseptics or topical and systemic antibiotics. Feet should be kept dry and patients should avoid the use of plastic, unventilated shoes. Antimycotic powders may help prevent relapse. Preventive measures should be taken as reinfection is observed.
The casual agent is Malassezia furfur (Pityrosporum). Three serotypes have been characterized A, B, and C, but the clinical presentation is identical for all serotypes (Br J Dermatol 1993 129 533-540). The micelial pathogenic form (M. furfur) is frequently seen associated with excessive sweating, increased sebum secretion, synthetic clothing, the application of oils, and topical or systemic glucocorticoids. Also constitutional factors such as genetic predisposition, Cushing's syndrome, diabetes and immunodeficiency are important. But it is not usually present in AIDS where seborrheic dermatitis is frequently seen. M. furfur is capable of inducing an inflammatory response with a mild lymphocytic CD4+ infiltrate. Specific antibodies and the capacity to activate complement have been demonstrated.
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