Neurological aspects of anhidrosis: differential diagnoses and diagnostic tools

Kee Hong Park; Ki-Jong Park

doi:10.14253/acn.2019.21.1.1

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Park and Park: Neurological aspects of anhidrosis: differential diagnoses and diagnostic tools

Review Article

Ann Clin Neurophysiol 2019;21(1):1-6.

Published online: 20 January 2019

DOI: https://doi.org/10.14253/acn.2019.21.1.1

Neurological aspects of anhidrosis: differential diagnoses and diagnostic tools

Kee Hong Park¹, Ki-Jong Park^2,^3,

¹Department of Neurology, Gyeongsang National University Hospital, Jinju, Korea

²Department of Neurology, Gyeongsang National University Changwon Hospital, Changwon, Korea

³Department of Neurology, Gyeongsang National University School of Medicine, Jinju, Korea

Correspondence to Ki-Jong Park Department of Neurology, Gyeongsang National University School of Medicine, 79 Gangnam-ro, Jinju 52727, Korea Tel: +82-55-214-3810 Fax: +82-55-214–3255 E-mail: pkjong@gnu.ac.kr

Received 21 June 2018 Revised 7 August 2018 Accepted 13 August 2018

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Anhidrosis refers to the condition in which the body does not respond appropriately to thermal stimuli by sweating. Sweating plays an important role in maintaining the body tem-perature, and its absence should not be overlooked since an elevated body temperature can cause various symptoms, even leading to death when uncontrolled. The various neurological disorders that can induce anhidrosis make a detailed neurological evaluation essential. The medication history of the patient should also be checked because anhidrosis can be caused by various drugs. The tests available for evaluating sweating include the quantitative sudo-motor axon reflex sweat test, thermoregulatory sweat test, sympathetic skin response, and electrochemical skin conductance. Pathological findings can also be checked directly in a skin biopsy. This review discusses the differential diagnosis and evaluation of anhidrosis.

Keywords: Anhidrosis, Sweating, Autonomic nervous system

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Fig. 1.

Thermoregulatory sweat test results for a patient with acquired idiopathic generalized anhidrosis. (A) Sweating was absent from the entire skin. (B) Systemic corticosteroid therapy induced partial improve-ment of sweating (area indicated in purple).

Fig. 2.

Example results from quantitative sudomotor axon reflex sweat tests. Forearm, sky blue; proximal leg, red; distal leg, purple; foot, blue. (A) Nor-mal results. (B) Diabetic neuropathy with length-dependent results. (C) Pure autonomic failure in the presence of generalized anhidrosis.

Table 1.

Drugs that can cause hypohidrosis⁶

Drug class	Drugs	Mechanism
Anticholinergics	Atropine, belladonna, dicycloverine, glycopyrrolate, hyoscyamine, propantheline	Antimuscarinic effect
Antidepressants (tricyclics)	Amitriptyline, clomipramine, desipramine, doxepin, imipramine, nortriptyline, protriptyline	Antimuscarinic effect
Antiepileptics	Topiramate, zonisamide, carbamazepine	Carbonic anhydrase inhibition (topiramate and zonisamide) Central anticholinergic effect (carbamazepine)
Antihistamines	Cyproheptadine, diphenhydramine, promethazine	Antimuscarinic effect
Antihypertensives	Clonidine	Central adrenergic effect
Antipsychotics and antiemetics	Chlorpromazine, clozapine, olanzapine, thioridazine, quetiapine	Antimuscarinic effect
Antivertigo drugs	Meclizine, scopolamine	Antimuscarinic effect
Bladder antispasmodics	Darifenacin, oxybutynin, solifenacin, tolterodine	Antimuscarinic effect
Gastric antisecretory drugs	Propantheline	Antimuscarinic effect
Muscle relaxants	Cyclobenzaprine, tizanidine	Uncertain, but possibly inhibition of spinal excitatory interneurons; possibly both central and peripheral antimuscarinic effects
Neuromuscular paralytics	Botulinum toxins	Cleavage of SNAP-25 inhibiting presynaptic release of acetylcholine
Opioids	Fentanyl, hydrocodone, methadone, morphine, oxycodone	Elevation of hypothalamic set point; calcium-channel antagonism

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