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Editor: Rene Bermudez Updated: 6/21/2023 3:35:55 PM


Anhidrosis is the inability to sweat. It is important to recognize anhidrosis as it can be potentially life-threatening due to heat-related illnesses.[1] There are three main causes of anhidrosis, which are peripheral alterations in the eccrine gland itself, idiopathic, and central or neuropathic disease and/or medication that disrupts neural inputs from the anterior hypothalamus to the gland.[2]

Causes of central/neuropathic anhidrosis can occur at any level of innervation.[3] The disturbance can occur at the sweating center in the brain, the descending neural tract, or the sweat gland. A disruption will lead to an absence of sweating. Disruption in the neural input can be due to tumors or infarctions of the hypothalamus, pons, or medulla. Spinal cord tumors, injuries, or infarctions can disrupt the neural tract.[4] Other etiologies such as degenerative syndromes (Shy-Drager syndrome), autoimmune autonomic neuropathy, peripheral neuropathy (diabetes, alcohol use disorder, leprosy), and drugs have all been implicated in central/neuropathic anhidrosis.[5]

Peripheral alterations that cause anhidrosis can be congenital or acquired. In addition, forms of peripheral alterations can be due to genetic abnormalities such as incontinentia pigmenti, due to local destruction, for example, by a tumor, or obstruction by entities such as psoriasis.

As heat intolerance may be due to various underlying disorders, a detailed history is important in establishing the diagnosis. Heat intolerance can cause drowsiness, episodic inability to concentrate while in a hot environment, or fatigue, along with a decrease in the patient's normal sweating, which are clues to the diagnosis of anhidrosis. A detailed history should also include the addition of medications, medical events such as injuries, growths or radiation, alcohol consumption, the presence of autoimmune disease or diabetes mellitus, and family history.[2]


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Central and neuropathic causes of anhidrosis can occur anywhere along the neural track, as previously stated. There are diagnostic clues that will aid in locating the area of the lesion. If there is the involvement of the pons or medulla, the patient will have ipsilateral facial and neck anhidrosis.[6] Neural tracks in the spinal cord have both crossed and uncrossed fibers. Therefore, alterations in the spinal cord will result in anhidrosis of the skin that can be either ipsilateral or contralateral. Peripheral neuropathies tend to be symmetrical as in diabetes mellitus and alcohol use disorder.[7] However, there are cases of asymmetrical peripheral neuropathy leading to anhidrosis, such as in cases of leprosy. A patient with Horner syndrome will present after the disruption of the superior cervical ganglion. Regional anhidrosis can also occur due to the chemical blockade of a selected sympathetic ganglion. Congenital insensitivity to pain with anhidrosis is a rare entity that is autosomal and recessive. It presents with self-mutilation due to a lack of pain, intellectual disability, and recurrent fevers due to anhidrosis.[8][9]

Drugs that interfere with the synaptic transmission in the autonomic ganglia will lead to anhidrosis:[10]

  • Nicotinic acetylcholine receptor antagonists such as hexamethonium and trimethaphan
  • Muscarinic acetylcholine receptor antagonists such as atropine or scopolamine
  • Calcium channel blockers
  • Alpha-adrenergic blockers such as phentolamine
  • Alpha2-adrenergic agonists such as clonidine
  • 5-fluorouracil
  • Topiramate
  • Zonisamide
  • Quinacrine

There are numerous causes of abnormalities in the sweat gland that cause anhidrosis. Among the various causes are several hereditary and acquired systemic diseases that present with generalized or localized anhidrosis. Males with X-linked hypohidrotic ectodermal dysplasia will have an absence of sweat glands, whereas female carriers will have hypohidrosis or reduced sweating.[11][12] The other ectodermal dysplasias, such as Rapp-Hodgkin syndrome and Naegeli-Franceschetti-Jadassohn syndrome, can lead to sweat gland abnormalities.[13] Though not an exhaustive list, there are other rare inherited syndromes in which genetic errors result in sweat gland dysfunction such as Bazex-Dupre-Christol syndrome and Fabry disease.[14]

Local tissue destruction can be the culprit of acquired localized anhidrosis. Tumors, radiation therapy, systemic sclerosis, burns, graft-versus-host disease, acrodermatitis chronica atrophicans, and Sjögren syndrome can distort the normal architecture of the skin with subsequent anhidrosis. Entities that lead to obstruction of the glands are also implicated in anhidrosis. Psoriasis, lamellar ichthyosis, miliaria, eczematous dermatoses, porokeratosis, and bullous diseases are examples of obstruction.[15]


Anhidrosis is a clinical finding and not a distinct entity. The exact epidemiology will depend on the underlying etiology. In the majority of anhidrosis cases, men and women are equally affected, with a few exceptions. The age of presentation will vary based on the underlying etiology. Horner syndrome is one of the causes of anhidrosis and is an uncommon condition, occurring with a frequency of approximately 1 per 6,000. It may occur at any age or with any ethnic group.[16][17] 

Another cause of hypohidrosis/anhidrosis is hypohidrotic ectodermal dysplasia, in which patients either do not have eccrine sweat glands or are sparse and rudimentary. In the US, the prevalence of hypohidrotic ectodermal dysplasia is estimated to be 1 per 100,000 births. Internationally, the prevalence is reported at 7 cases per 10,000 births. 

Naegeli-Franceschetti-Jadassohn (NFJ) syndrome is also a rare cause of anhidrosis and is reported to have an international prevalence of around 1 case in 2-4 million population.[18][19] Fabry disease is another disorder where there is a lack of sweat glands, and its prevalence has been observed to be 1 per 40,000 people.[20] There are many other disorders that present with anhidrosis and have variable epidemiological indicators.


The pathophysiology of anhidrosis varies depending on the etiology, as anhidrosis is a clinical finding and not a distinct entity. For central and neuropathic anhidrosis, interruption of innervation at any level along the pathway from the sweating centers located in the brain to the sweat glands can result in absent sweating. Drugs that interfere with the synaptic transmission in the autonomic ganglia can inhibit sweating. Peripheral alterations can result in the absence of sweating. Peripheral alterations include genetic disorders, destruction, or obstruction. Genetic abnormalities underlie several types of anhidrosis, and the pathogenesis may be unknown. Other etiologies may have a known cause, such as local tissue destruction by prior radiation therapy. The clinical presentation and history can help delineate the pathophysiology.[21] 

As anhidrosis is a clinical presentation of an underlying disorder, it is beyond the scope to describe the pathophysiology of each disorder separately. However, for instance, Horner syndrome, which is a common cause of ipsilateral anhidrosis, depends on the level of interruption of the sympathetic supply. Anhidrosis with first-order neuron lesions affects the ipsilateral side of the body as the sympathetic supply from its central origin. The ipsilateral face is involved in lesions involving the second-order neurons. Postganglionic third-order neuron lesions occurring after the vasomotor and sudomotor fibers have branched off show very limited involvement of the face (area adjacent to the ipsilateral brow).[22]


The histopathology will vary depending on the etiology. Males with X-linked hypohidrotic ectodermal dysplasia will have an absence of sweat glands, whereas female carriers will have reduced glands. The clinical presentation and or a skin biopsy will help identify those with local destruction or obstruction.[23]

Light microscopy may not reveal marked morphological changes in sweat glands in patients with acquired idiopathic generalized anhidrosis (AIGA) due to idiopathic pure sudomotor failure (IPSF). Still, there may be lymphocytic infiltration around sweat glands.[24] Some cases of AIGA may reveal swollen secretory cells of the sweat glands and hyperkeratotic horny layer due to sweat gland failure.

History and Physical

History and physical exam findings for anhidrosis will differ between the various underlying etiologies. A thorough history should be obtained, including past medical history, medications, medical treatments (i.e., radiation therapy), and family history. A careful and detailed history will yield clues to a potential diagnosis.[9]

A patient may complain of heat intolerance, fatigue, drowsiness, or inability to concentrate in warm environments. A patient with central/neuropathic anhidrosis may have accompanying neurological symptoms such as ptosis and miosis in Horner syndrome. Although very rare, a patient with congenital insensitivity to pain with anhidrosis will present with self-mutilation.

Those with anhidrosis due to destruction will have the physical exam findings of the underlying etiology, such as scarring from a prior burn or sclerotic changes as in morphea.

Anhidrosis caused by obstruction will likewise have the physical exam findings associated with the underlying etiology, such as psoriatic plaques or lamellar ichthyosis.


Detailed patient history is paramount in determining the possible underlying etiology. The next step would be to determine any potential contributing factors, such as medications. Colorimetric and or gravimetric testing can demonstrate diminished or absent sweating. Injection of local, intradermal cholinergic drugs to promote sweating can be utilized. However, this should only be done in a small area as the side effect profile and its associated risks preclude injection into large areas. If a patient is suspected of having peripheral neuropathy, testing the axon reflex sweating by injecting an intradermal picrate or nicotine sulfate at an appropriate dose may be performed. A skin biopsy from an affected area should always be obtained in patients with suspected anhidrosis to identify abnormalities of the sweat glands.

A quantitative sudomotor axon reflex test (QSART) assesses the autonomic nerves that mediate sweating.[25] Mild electrical stimulation is applied to the skin via electrodes and acetylcholine enters the skin. Acetylcholine results in the stimulation of the sweat glands; and the sweat response is measured.

A silastic sweat imprint test also utilizes electrodes, however, pilocarpine is used to stimulate the sweat glands. indentations appear to mark the sweat droplets on a material formed of silicone rubber.[26]

A thermoregulatory sweat test utilizes the body's core temperature to assess a correlation to sweat production. It assesses the thermo-regulatory sudomotor mechanism of the body.[27]

Treatment / Management

Unfortunately, treatment options for anhidrosis can be limited unless an offending agent can be discontinued. Providers need to stress the importance of maintaining a cool environment for the patient. The use of water spray bottles for purposes of cooling can prove helpful. For those disorders due to clogged sweat glands, frequent and gentle exfoliation is useful. Those with disorders of cornification and overheating, such as lamellar ichthyosis, should be treated aggressively and monitored closely.

Although there is no remarkable evidence to support the use of corticosteroids, many case reports recommend the administration of corticosteroids in the early stages of AIGA.[28] However, if the treatment is delayed or when the destruction of sweat glands has already occurred, then corticosteroids may not be beneficial.(B3)

The cornerstone for the treatment of anhidrosis is the management of the underlying cause, such as treating lung carcinoma if that is causing Horner syndrome and resulting in anhidrosis.

Differential Diagnosis

When considering anhidrosis, a differential diagnosis will depend on the underlying etiology.

Central and Neuropathic Anhidrosis

  • Tumors, infarctions, or other alterations of the hypothalamus, pons, medulla, or spinal cord
  • Horner syndrome
  • Degenerative syndromes such as Ross syndrome or Shy-Drager syndrome
  • Autoimmune autonomic neuropathy
  • Congenital insensitivity to pain with anhidrosis
  • Peripheral neuropathy due to diabetes mellitus, alcoholism, leprosy, amyloidosis
  • Drugs


  • Nicotinic acetylcholine receptor antagonists such as hexamethonium and trimethaphan
  • Muscarinic acetylcholine receptor antagonists such as atropine or scopolamine
  • Calcium channel blockers
  • Alpha-adrenergic blockers such as phentolamine
  • Alpha2-adrenergic agonists such as clonidine
  • 5-fluorouracil
  • Topiramate
  • Zonisamide
  • Quinacrine

Peripheral Causes Due to Sweat Gland Abnormalities

  • Genetic disorders such as ectodermal dysplasias, incontinentia pigmenti, Bazex-Dupré-Christol syndrome, Fabry disease
  • Destruction from tumors, burns, radiation therapy, systemic sclerosis, morphea, Sjögren syndrome, graft-versus-host disease, acrodermatitis chronica atrophicans
  • Obstruction from miliaria, ichthyoses, psoriasis, eczematous dermatoses, bullous diseases


The prognosis of anhidrosis varies depending on the type of anhidrosis. Anhidrosis associated with a genetic syndrome is generally lifelong. In the setting of drug-induced anhidrosis, it is usually reversible with the discontinuation of the medication. Anhydrosis secondary to a treatable cause is generally reversible and has a favorable prognosis.


Complications will depend on the underlying etiology. Heat-related illnesses are the most grave complications of anhidrosis. Children are more vulnerable because their core body temperature rises faster than adults and their heat loss mechanism is less efficient. Heat-related illnesses are:

  • Heat cramps
  • Heat exhaustion
  • Heatstroke

The most feared complication, no matter the underlying etiology, is heatstroke.

Deterrence and Patient Education

Providers need to stress the importance of maintaining a cool environment for the patient. The use of water spray bottles for purposes of cooling can prove helpful. The patient is advised to wear loose and light clothing when it is warm and monitor their activity level not to overdo it. Frequent and gentle exfoliation is helpful for those disorders due to clogged sweat glands.

Enhancing Healthcare Team Outcomes

An interprofessional approach to anhidrosis is recommended. Anhidrosis and the underlying etiologies can cause severe emotional distress for patients. Quality of life may be low for patients of all ages secondary to societal scrutinization of their underlying condition (i.e., lamellar ichthyosis). Therefore, it is recommended to evaluate and arrange for mental health care in addition to the necessary medical care to address the underlying cause of the anhidrosis, if there is one. The outcome of patients with anhidrosis depends on the cause. There is no cure for those with inherited disorders, and it is a lifelong issue. The outcomes may improve for those with acquired anhidrosis by improving the primary condition or removing the offending medication. Most importantly, the patient should be actively involved in their care as the patient must maintain a cool environment and recognize the signs and symptoms of heat intolerance.



Gauer R, Meyers BK. Heat-Related Illnesses. American family physician. 2019 Apr 15:99(8):482-489     [PubMed PMID: 30990296]


Gagnon D, Crandall CG. Sweating as a heat loss thermoeffector. Handbook of clinical neurology. 2018:156():211-232. doi: 10.1016/B978-0-444-63912-7.00013-8. Epub     [PubMed PMID: 30454591]


Sato K, Kang WH, Saga K, Sato KT. Biology of sweat glands and their disorders. II. Disorders of sweat gland function. Journal of the American Academy of Dermatology. 1989 May:20(5 Pt 1):713-26     [PubMed PMID: 2654213]


Panda S, Verma D, Budania A, Bharti JN, Sharma RK. Clinical and laboratory correlates of selective autonomic dysfunction due to Ross syndrome. Journal of family medicine and primary care. 2019 Apr:8(4):1500-1503. doi: 10.4103/jfmpc.jfmpc_151_19. Epub     [PubMed PMID: 31143750]


Wenzel FG, Horn TD. Nonneoplastic disorders of the eccrine glands. Journal of the American Academy of Dermatology. 1998 Jan:38(1):1-17; quiz 18-20     [PubMed PMID: 9448199]


Yoo MY, Koong SS, Kim SW, Kim D. Ipsilateral Hyperhidrosis: Atypical Symptom of Small Lung Adenocarcinoma Evaluated by (18)F-FDG PET-CT. Nuclear medicine and molecular imaging. 2019 Jun:53(3):231-234. doi: 10.1007/s13139-019-00591-0. Epub 2019 Mar 26     [PubMed PMID: 31231444]


Fealey RD. Thermoregulation in neuropathies. Handbook of clinical neurology. 2018:157():777-787. doi: 10.1016/B978-0-444-64074-1.00048-3. Epub     [PubMed PMID: 30459040]


Schwartzlow C, Kazamel M. Hereditary Sensory and Autonomic Neuropathies: Adding More to the Classification. Current neurology and neuroscience reports. 2019 Jun 20:19(8):52. doi: 10.1007/s11910-019-0974-3. Epub 2019 Jun 20     [PubMed PMID: 31222456]


Li N, Sun J, Guo S, Liu Y, Wang C, Zhu C, Zhang X. Phenotypic and genotypic features of a pair of Chinese identical twins with congenital insensitivity to pain and anhidrosis: A case report. Medicine. 2018 Nov:97(47):e13209. doi: 10.1097/MD.0000000000013209. Epub     [PubMed PMID: 30461622]

Level 3 (low-level) evidence


Mack GW. A model for in vivo analysis of sudomotor sympathetic C-fiber activation and human sweat gland output. Journal of applied physiology (Bethesda, Md. : 1985). 2017 Aug 1:123(2):317-325. doi: 10.1152/japplphysiol.01070.2016. Epub 2017 May 18     [PubMed PMID: 28522768]


Okita T, Asano N, Yasuno S, Shimomura Y. Functional studies for a dominant mutation in the EDAR gene responsible for hypohidrotic ectodermal dysplasia. The Journal of dermatology. 2019 Aug:46(8):710-715. doi: 10.1111/1346-8138.14983. Epub 2019 Jun 27     [PubMed PMID: 31245878]


Gupta AA, Gotmare SS, Jain M, Pereira T, Khare P. Hypohydrotic Ectodermal Dysplasia in an Indian Family. Journal of the College of Physicians and Surgeons--Pakistan : JCPSP. 2019 Apr:29(4):381-383. doi: 10.29271/jcpsp.2019.04.381. Epub     [PubMed PMID: 30925967]


Papini M. Natural history of the Naegeli-Franceschetti-Jadassohn syndrome. Journal of the American Academy of Dermatology. 1994 Nov:31(5 Pt 1):830     [PubMed PMID: 7929942]

Level 3 (low-level) evidence


Siedler G, Káhn AK, Weidemann F, Wanner C, Sommer C, Üçeyler N. Dyshidrosis is associated with reduced amplitudes in electrically evoked pain-related potentials in women with Fabry disease. Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology. 2019 Apr:130(4):528-536. doi: 10.1016/j.clinph.2019.01.008. Epub 2019 Feb 4     [PubMed PMID: 30785009]


Guerra KC, Toncar A, Krishnamurthy K. Miliaria. StatPearls. 2023 Jan:():     [PubMed PMID: 30725861]


Smith SJ, Diehl N, Leavitt JA, Mohney BG. Incidence of pediatric Horner syndrome and the risk of neuroblastoma: a population-based study. Archives of ophthalmology (Chicago, Ill. : 1960). 2010 Mar:128(3):324-9. doi: 10.1001/archophthalmol.2010.6. Epub     [PubMed PMID: 20212203]

Level 2 (mid-level) evidence


Kucur C, Ozbay I, Oghan F, Yildirim N, Zeybek Sivas Z, Canbaz Kabay S. A Rare Complication of Radiofrequency Tonsil Ablation: Horner Syndrome. Case reports in otolaryngology. 2015:2015():570520. doi: 10.1155/2015/570520. Epub 2015 May 7     [PubMed PMID: 26064747]

Level 3 (low-level) evidence


Itin PH, Burger B. Spontaneous fading of reticular pigmentation in Naegeli-Franceschetti-Jadassohn syndrome. Dermatology (Basel, Switzerland). 2010:221(2):135-6. doi: 10.1159/000314693. Epub 2010 Jun 26     [PubMed PMID: 20587992]

Level 3 (low-level) evidence


Whittock NV, Coleman CM, McLean WH, Ashton GH, Acland KM, Eady RA, McGrath JA. The gene for Naegeli-Franceschetti-Jadassohn syndrome maps to 17q21. The Journal of investigative dermatology. 2000 Oct:115(4):694-8     [PubMed PMID: 10998145]


Mehta A, Beck M, Eyskens F, Feliciani C, Kantola I, Ramaswami U, Rolfs A, Rivera A, Waldek S, Germain DP. Fabry disease: a review of current management strategies. QJM : monthly journal of the Association of Physicians. 2010 Sep:103(9):641-59. doi: 10.1093/qjmed/hcq117. Epub 2010 Jul 21     [PubMed PMID: 20660166]


Saito H. The location and characteristics of the thermal sudomotor pathways in the human brainstem: A reappraisal. Autonomic neuroscience : basic & clinical. 2019 Mar:217():80-90. doi: 10.1016/j.autneu.2019.01.006. Epub 2019 Jan 28     [PubMed PMID: 30744906]


Reede DL, Garcon E, Smoker WR, Kardon R. Horner's syndrome: clinical and radiographic evaluation. Neuroimaging clinics of North America. 2008 May:18(2):369-85, xi. doi: 10.1016/j.nic.2007.11.003. Epub     [PubMed PMID: 18466837]


Sano K, Asahina M, Uehara T, Matsumoto K, Araki N, Okuyama R. Degranulation and shrinkage of dark cells in eccrine glands and elevated serum carcinoembryonic antigen in patients with acquired idiopathic generalized anhidrosis. Journal of the European Academy of Dermatology and Venereology : JEADV. 2017 Dec:31(12):2097-2103. doi: 10.1111/jdv.14443. Epub 2017 Jul 20     [PubMed PMID: 28662305]


Sawada Y, Nakamura M, Bito T, Sakabe JI, Kabashima-Kubo R, Hino R, Kobayashi M, Tokura Y. Decreased expression of acetylcholine esterase in cholinergic urticaria with hypohidrosis or anhidrosis. The Journal of investigative dermatology. 2014 Jan:134(1):276-279. doi: 10.1038/jid.2013.244. Epub 2013 Jun 7     [PubMed PMID: 23748235]

Level 3 (low-level) evidence


Illigens BM, Gibbons CH. Sweat testing to evaluate autonomic function. Clinical autonomic research : official journal of the Clinical Autonomic Research Society. 2009 Apr:19(2):79-87. doi: 10.1007/s10286-008-0506-8. Epub 2008 Nov 6     [PubMed PMID: 18989618]


Wolfe GI, Galetta SL, Teener JW, Katz JS, Bird SJ. Site of autonomic dysfunction in a patient with Ross' syndrome and postganglionic Horner's syndrome. Neurology. 1995 Nov:45(11):2094-6     [PubMed PMID: 7501165]

Level 3 (low-level) evidence


Loavenbruck A, Wendelschaefer-Crabbe G, Sandroni P, Kennedy WR. Quantification of sweat gland volume and innervation in neuropathy: Correlation with thermoregulatory sweat testing. Muscle & nerve. 2014 Oct:50(4):528-34. doi: 10.1002/mus.24185. Epub 2014 May 14     [PubMed PMID: 24449525]

Level 2 (mid-level) evidence


Ohshima Y, Yanagishita T, Ito K, Tamada Y, Nishimura N, Inukai Y, Iwase S, Sugenoya J, Watanabe D. Treatment of patients with acquired idiopathic generalized anhidrosis. The British journal of dermatology. 2013 Feb:168(2):430-2. doi: 10.1111/j.1365-2133.2012.11112.x. Epub 2012 Oct 5     [PubMed PMID: 22709381]

Level 3 (low-level) evidence