This document discusses various types of excessive sweating conditions (hyperhidrosis) including their causes, presentations, and treatments. It describes primary cortical (emotional) hyperhidrosis which commonly affects the axillae and palms. Secondary causes include hyperhidrosis related to the hypothalamus or gustatory system. Treatment options mentioned are topical antiperspirants, oral medications like glycopyrrolate, and botulinum toxin injections for select cases.

1. Done by: Zainab Nasser
Dermatology resident

3. Excessive production
of eccrine sweat

4.  primary cortical (emotional) hyperhidrosis:
favoret sites: are the axillae or palms and soles >
face.
 involvement is bilateral and symmetric.
Sweating only during waking hours points the
diagnosis.

6. Secondary hypothalamic (thermoregulatory)
Hyperhidrosis:

7. Secondary medullary (gustatory) hyperhidrosis:
physiologic as exemplified by the facial sweating that
occurs with spicy foods (taste receptors send afferent
impulses).
or pathologic as occurs in Frey’s syndrome ( disrupted
nerves for sweat aberrantly connect with nerves for
salivation).
Frey’s syndrome:
• injury to auriculotemporal branch of CN V in parotid
region (carries sympathetic fibers to sweat glands in
scalp and parasympathetic fibers to parotid gland).
•haphazard regeneration leads to redness
(vasodilation) and hyperhidrosis of ipsilateral
cheek when eating

9. consideration of possible underlying etiologies
 topical antiperspirants containing aluminum chloride
or aluminum chloride hexahydrate can be applied.
 if necessary, initially preceded by oral glycopyrrolate
or oxybutynin.
 Injection of botulinum toxin type A every ~6 months is
very effective for primary cortical (emotional)
hyperhidrosis.

10. Delineation of area for injections of botulinum
toxin A for axillary hyperhidrosis (starch–iodine
technique).
Blue-black areas represent foci of sweating. In
the case of onabotulinumtoxin A, a total of 50–
100 U is injected, utilizing 10–15 injection sites.

12.  A side effect of medications with anticholinergic
properties (e.g. atropine, tricyclic antidepressants,
glycopyrrolate).
 Manifestation of inherited disorders, in particular
ectodermal dysplasias , as well as acquired disorders
such as Sjögren’s syndrome.
 Neurologic disorders, from tumors or infarcts of the
hypothalamus, pons, or medulla to peripheral
neuropathies.

13. Increased risk of developing
hyperthermia.
 Evaluation includes colorimetric testing
and biopsy of affected skin.

15.  Eccrine variant:
associated with degradation of sweat by resident
microflora; most commonly involves the feet.
 Apocrine variant:
associated with degradation of odiferous substances
(e.g. triglycerides) by skin flora.
 Rarely, it is a sign of an inherited metabolic disorder.

16. The smell can be rancid (Corynebacterium)
or sweaty (Micrococcus).

18. Colored sweat
 classification:
• intrinsic:
due to the lipofuscin content of apocrine sweat (yellow,
green, black) .
• extrinsic :
staining of sweat by clothing or chromogenic bacteria (e.g.
Corynebacterium) or fungi.

20. Excessive sweating leads to maceration
and blockage of eccrine ducts; can be
exacerbated by occlusion, e.g.
clothing, athletic equipment,
prolonged bed rest.

21. Classically divided into three major types:
(1) crystallina – tiny, superficial, short-lived, clear
vesicles.
• reflect ductal occlusion within the stratum
corneum.
(2) rubra (prickly heat) – pruritic erythematous
papulovesicles and occasionally pustules that favor
the upper trunk .
•reflect ductal occlusion within mid-epidermis.
(3) profunda – white papules due to excessive
sweating in a hot climate (rare)
• reflect ductal occlusion at dermal–epidermal
junction.

22.  DDx:
miliaria rubra needs to be distinguished from:
1.Folliculitis
2. Grover’s disease
3.neutrophilic eccrine hidradenitis
4. cutaneous candidiasis.
 management:
cool environment.

23. Miliaria crystallina. Multiple small
superficial vesicles with clear fluid
Miliaria rubra. Multiple erythematous
nonfollicular papules and papulovesicles
on the back.

24.  pathogenesis:
Occlusion then rupture of apocrine sweat gland ducts
 site:
axillae > anogenital or periareolar region > periumbilical
or presternal area
 epidemiology:
seen primarily in women ages 15–35 years.

25.  presentation:
Multiple skin-colored papules that are follicular,
dome-shaped, and often pruritic .
 management:
• May improve with oral contraceptive pills (OCPs)
or pregnancy.
• topical CS or calcineurin inhibitors .

28. Most commonly related to administration of chemotherapy (e.g.
cytarabine) and is thought to result from excretion of the
drug(s) into the eccrine sweat, leading to a toxic insult.
 presentation:
Erythematous papules and plaques that may have clinical
overlap with Sweet’s syndrome

29.  management:
•spontaneously resolves
•sometimes a short course of systemic CS is prescribed
once an infectious process such as cellulitis or septic
emboli is excluded.

30.  pathogensis:
•Occurs following vigorous physical activity.
•primarily in healthy children.
• Thought to be precipitated by rupture of eccrine glands.

31.  presentation:
Erythematous, tender nodules appear suddenly,
most often on the soles ,and then spontaneously
resolve over days to weeks.

33. Common disorder in healthy individuals
 affects the palms >> soles.
Presentation:
• Multiple annular and semi-annular collarettes of white
scale that usually measure <5 mm, but may be larger;
no preceding vesicles or inflammation clinically.
• Recurrent and sometimes associated with
hyperhidrosis.

35.  management:
nonspecific; effectiveness of topical agents, e.g.
12% ammonium lactate, 20% urea, is limited.