Pressure and postural hyperhidrosis is the sweating response to pressure on one side of the body during position changes and lateral recumbency. It is a manifestation of hyperhidrosis. Hyperhidrosis is a disorder in which excessive sweat gland secretion is caused by sympathetic hyperexcitation. The sympathetic nerve governs sweating throughout the body. Under normal circumstances, the sympathetic nerve regulates body temperature by controlling sweating and heat dissipation. In hyperhidrosis, however, sweating and facial flushing are completely out of control. The excessive sweating and facial flushing leave the patient in a daily state of helplessness, agitation or panic. How is stress and postural hyperhidrosis diagnosed? Hyperhidrosis is usually not difficult to diagnose based primarily on a history of excessive sweating, typical clinical manifestations, and a combination of objective examinations. 1, according to the sweating situation is divided into: (1) limited hyperhidrosis: often begins in childhood or adolescence, can occur in both sexes, some have a family history, can last several years, to 25 years of age after a natural tendency to reduce. The most common sites of limited hyperhidrosis are the palmoplantar and friction surfaces, such as the axillae, groin, and perineum. This is followed by the forehead, tip of the nose, and chest. The palmoplantar hyperhidrosis can be persistent or transient, caused by mood swings, without seasonal differences, often with chills or even cyanosis of the hands and feet, which can be accompanied by keratinization of the hands and feet over time. Axillary sweating can be triggered by heat or mental activity. Axillary sweating is caused by excessive activity of the small sweat glands, unlike axillary odor which is mainly caused by the sweat glands. (2) Generalized hyperhidrosis: generalized hyperhidrosis caused mainly by other diseases, such as infectious hyperthermia, due to nervous system regulation or oral antipyretics to dissipate heat by sweating. Others like damage to the central nervous system including the cortex and basal ganglia, spinal cord or peripheral nerves can cause generalized hyperhidrosis. 2, according to the different reasons for producing excessive sweating is divided into: (1) neurological hyperhidrosis ① cortical hyperhidrosis: A. emotional hyperhidrosis: due to emotional stimulation, acetylcholine secretion increases and produces excessive sweating, cortical or emotional sweating that occurs after simultaneous sexual stimulation is a special type. B. palmar-plantar hyperhidrosis: seen in various ethnic groups, no significant gender differences, most patients have a positive family history. The onset of palmar-plantar hyperhidrosis often begins in infancy or childhood. Palmar-plantar hyperhidrosis does not occur during sleep or quiet and is not stimulated by heat sources. C. axillaryhyperhidrosis: axillary hyperhidrosis is not stimulated by heat sources, but by emotional stimuli and excessive sweating. otherdiseasewithcorticalhyperhidrosis): palmoplantar keratosis, congenital thick nail syndrome, recessive hereditary herpetic epidermolysis bullosa, congenital ichthyosis-like erythroderma, and nail-patellar syndrome can all present with cortical hyperhidrosis. It often occurs after excitement or eating, but can sometimes develop with heat stimuli, indicating that the subcortical centers are particularly hot (the hypothalamus also plays a role). Hypothalamic hyperhidrosis: The hypothalamus is the main autonomic center of the central nervous system and controls the regulation of sweating. Hypothalamic hyperhidrosis can be seen in the following diseases: A. Hodgkin’s disease (Hodgkinrsquo;disease): characterized by a triad of fever, night sweats and weight loss, with night sweats early in the disease, a sudden drop in body temperature during sleep with profuse night sweats, and fluctuating fever later. b. Diabetic hyperhidrosis (diabetesmellitus): there are three types; severe C. pressureandposturalhyperhidrosis: is a sweating response to pressure on one side of the body during postural changes and lateral recumbency. Idiopathicunilateralcircumscribedhyperhidrosis: is an episode of restricted sweating commonly found on the face or upper extremities. Heat, mental and gustatory stimuli can all contribute, but the former is more common, and the mechanism of sweating is unknown. The mechanism of sweating is unknown. ③ Medullary hyperhidrosis: Medullary hyperhidrosis (medullaryhyperhidrosis) is also known as gustatorysweating because the efferent stimuli often involve gustatory receptors. A. physiologic medullaryhyperhidrosis (physiologicmedullaryhyperhidrosis): many people have limited sweating after eating spicy and fragrant foods and beverages, mostly on the face, especially the upper lip and cheeks unilaterally or bilaterally, as well as the scalp and knees, usually within a few minutes. B. Pathologic medullary hyperhidrosis (pathologic medullaryhyperhidrosis): often involves the preauricular or subauricular region on one side, with varying degrees of involvement, and has three clinical types: local trauma or disease of the parotid gland; central neurological disease; such as spinal cavitation or encephalitis; and injury to the thoracic sympathetic trunk. The nucleus pulposus plays a role in all three types, but there is some variation in the afferent and efferent arcs, resulting in different clinical manifestations: a. auriculotemporal syndrome (auriculotemporalsyndrome): also known as Krey syndrome (Kreyrsquo;ssyndrome) in the parotid gland or preauricular region after surgery, trauma and cysts and other lesions that damage the auriculotemporal nerve 1 It occurs within 1 month to 5 years after the damage to the auriculotemporal nerve by surgery, trauma and cysts. The cause is the simultaneous involvement of the auricular nerve and the parotid gland, with regenerated parasympathetic fibers in the damaged parotid gland migrating distally to the nerve and innervating the sweat glands in the subauricular region. Surgical destruction of the tympanic plexus eliminates gustatory sweating in patients with this disease. b. Chordatympanicsyndrome: The clinical presentation is similar to auriculotemporal syndrome due to damage to the peripheral autonomic fibers near the submandibular gland, occurring at the chin and mandibular rim. c. Crocodile tear syndrome ( crocodiletearsyndrome: a lesion similar to gustatory hyperhidrosis, often following facial nerve injury, with the difference that the patient presents with gustatory tearing; originating from misdirection or short-circuiting of the peripheral autonomic pathways regulating tearing and salivation. d. Gustatory sweating due to spinal cavitation or encephalitis: probably due to stimulation of the vagus and glossopharyngeal nerves, causing destruction of the nucleus pulposus that controls sweating and salivation due to destruction of the medullary nucleus; the clinical presentation varies widely with a more extensive sweating response. e. Medullary hyperhidrosis following injury to the thoracic sympathetic trunk: seen in patients with sympathectomy, lung cancer, vertebral osteoma, subclavian aneurysm and thyroidectomy. Because the sympathetic chain in the upper mediastinum is adjacent to the vagus nerve, after sympathetic trunk injury, the vagus nerve sends cholinergic fibers to the adjacent sympathetic trunk preganglionic fibers, and patients often experience sweating reactions in the face, neck, trunk and upper extremities after eating or swallowing. (2) Non-neural hyperhidrosis (non-neuralhyperhidrosis) is not innervated by the sympathetic nervous system, but is a dominant sweating of glands sensitive to heat; and cholinergic and adrenergic drugs directly stimulate sweat glands and cause dominant sweating, as well as some organoidnevus and nevus-like hemangioma damage, Maffucci syndrome, actinomycosis, Hippdl-Trenaunay syndrome, hemangioblastoma, and blue rubber nevus syndrome, can present with localized sweating that may be related to the hemangioma at the site of involvement. In addition, colderythema occurs in patients with limited erythema of the skin after cold stimulation, severe pain and sweating in the central area, vascular atrophy and muscle atrophy, and the disease may be caused by the release of 5-hydroxytryptamine from platelets. (3) Compensatory hyperhidrosis (compensatoryhyperhidrosis) occurs when the sweat glands in one part of the body suffer from a certain factor and then compensate for the sweat glands in another part to maintain body temperature. The common diseases are as follows. (1) Diabetes mellitus: compensatory hyperhidrosis occurs in the lower body secondary to diabetic peripheral neuropathy with no or little sweating. Heat-stimulated hyperhidrosis of the upper body (trunk mainly), with nocturnal sweating common. Gustatory hyperhidrosis of the face and neck. (ii) Pathological, gustatory hyperhidrosis occurs after sympathectomy in the neck and thoracic sympathectomy. ③Nocturnal sweating, in addition to the above-mentioned causes that can lead to hyperhidrosis, can also occur due to cardiovascular endocarditis, lymphoma, hyperthyroidism, systemic vasculitis, pheochromocytoma, carcinoid syndrome, withdrawal reaction, uncontrolled autonomic function state, and other chronic infectious diseases.