Anhidrosis is the absence of sweating on the surface of the skin, also known as anhidrosis, and can be classified as limited or generalized anhidrosis. The causes of anhidrosis may include sweat gland dysfunction and neurological damage, and other disorders may also cause anhidrosis. The causes of anhidrosis include neurogenic anhidrosis, sweat gland dysfunctional anhidrosis, and idiopathic anhidrosis. The causes are: 1. neurophacic anhidrosis is caused by dysfunction of the neural pathways that activate the sweat glands. If medullary damage can cause ipsilateral segmental sweat closure or temporary anhidrosis in areas below the damage. Disease-induced generalized anhidrosis may be caused by increased cortical inhibition of the hypothalamus. Hypothalamic tumors or damage to the base of the third ventricle may also cause generalized anhidrosis and hyperthermia. Disorders of the lower brainstem may cause ipsilateral facial and cervical anhidrosis. Heat stroke and hyperthermia can also cause transient anhidrosis, which may be caused by a lack of central nerve impulses to the sweat glands due to hypothalamic inhibition by the disease. Leprosy, alcoholic neuritis, amyloidosis, diabetes mellitus, and gout can cause anhidrosis, and segmental anhidrosis may occur as a result of ganglionic blockade caused by these diseases. Autonomic neuropathy, ganglion block, Horner syndrome and type IV hereditary sensory neuropathy as well as cholinergic drug application can occur as anhidrosis. 2. anhidrosis due to disturbance of sudonriferous glands is seen in congenital ectodermal dysplasia, where the patient has underdeveloped sweat glands leading to pancytopenia. It is also associated with sebaceous gland, hair, and nail hypoplasia or mutilation in all areas. Acquired anhidrosis is seen in scleroderma, tumors, burns, skin grafts, radiation dermatitis, lymphoma, Sjogren’s syndrome, and chronic atrophic acrodermatitis, and can even lead to loss of sweating from small sweat glands. Certain drugs that cause destruction of sweat glands can also produce anhidrosis, such as anti-cholinergic drugs like miparin (Adipine), atropine and scopolamine, barbiturates and Valium cause anhidrosis due to necrosis of sweat glands. Anhidrosis occurs when sweat ducts are blocked and sweat is retained in the skin due to milia and inflammatory and keratotic skin diseases. The common clinical manifestations of milia are white prickly heat, red prickly heat, pus prickly heat, and deep insidious prickly heat. Ichthyosis, psoriasis, aspergillosis, sweat duct keratosis and atopic dermatitis, and seborrheic dermatitis can block the flow of sweat in the sweat ducts and cause anhidrosis. Zirconium salts, aluminum salts, formaldehyde, glutaraldehyde and iontophoresis can also cause local sweat hole occlusion. 3, idiopathic anhidrosis (idiopathic anhidrosis) neonates and premature infants with neurological imperfections and no sweating for several weeks after birth; patients with hypothyroidism, tumors, uremia, cirrhosis, endocrine diseases (e.g. Addison’s disease, diabetes mellitus, uremia) and rare genetic diseases (e.g. Fabry disease, Franceschetti- Jatassohn syndrome and Helweg-Larssen syndrome) can present with anhidrosis, and temporary anhidrosis can also be caused by radiation fever and compression of the plaster tube pattern.