Sweating Disorders

Drug class

Common examples

Mechanism

Anticholinesterases

Pyridostigmine

Cholinesterase inhibition

Antidepressants: selective serotonin reuptake inhibitors

Citalopram

Serotonergic effect on the hypothalamus or spinal cord

Duloxetine

Escitalopram

Fluoxetine

Fluvoxamine

Mirtazapine

Paroxetine

Trazodone

Venlafaxine

Antidepressants: tricyclics

Amitriptyline

Norepinephrine reuptake inhibition with stimulation of peripheral adrenergic receptors

Desipramine

Doxepin

Imipramine

Nortriptyline

Protriptyline

Antiglaucoma agents

Physostigmine

Physostigmine = cholinesterase inhibition

Pilocarpine

Pilocarpine = muscarinic receptor agonism

Bladder stimulants

Bethanechol

Muscarinic receptor agonism

Opioids

Fentanyl

Histamine release

Hydrocodone

Methadone

Morphine

Oxycodone

Sialogogues

Cevimeline

Muscarinic receptor agonism

Pilocarpine

From Cheshire and Freeman [13]; Cheshire and Fealey [12]

Important questions comprise duration of the disorder, diseases and conditions before onset, progression to other body regions, areas of increased or decreased sweating, symmetry, triggers (increased ambient temperature, physical activity, stress), diurnal sweating and comparison to sweating before the onset of disease. Night sweat can be a real distressing symptom with many different reasons. To investigate if the disorder occurs isolated or as part of a generalised autonomic dysfunction, the other autonomic subsystems should be interrogated (s. Chap. 2). The diligent interrogation of a patient suspected of autonomic dysfunction occasionally reveals the phenomenon of gustatory sweating, that is, profuse sweating associated with the ingestion of food. In Table 4.2, we have listed some questions that may help.

Table 4.2

Questions that may help

Do you sweat in the feet? Are your socks drenched after sports?

Do you sweat in intimate area?

Is there excessive sweating in your armpits?

Did you let things fall down because of sweating in your hands?

Do you feel embarrassed when shaking hands because of sweat sometimes?

For physiology see Sect. 1.2.2, for history taking see Sect. 2.2.2.1.

4.4 Physical Examination

Complete physical and neurological examinations are mandatory, looking for signs of PNP, myelopathy or Horner’s syndrome, plexus brachialis lesion, brain stem affection and/or central lesions. To investigate focal sweating dysfunction at bedside, it is valuable to investigate the patient undressed in a quiet room with comfortable ambient temperature and watch for sweat droplets and areas of skin discoloration. Hairiness and tropical changes of the skin and nails hint to peripheral nerve involvement. Distribution of sweat droplets shall be documented, particularly in regions of increased sweating: the face, dorsal neck, axillae, palms and soles and inguinal region. Measurement of skin temperature in different body regions, lateralisation and distal versus proximal distribution by infrared surface method are recommended. The investigator feels changes in skin moisture and texture by touching. It is notable if there are obvious sweat stains on the clothing. For total absence of sweating, patients should be observed in hot environment, the absence of sweating in isolated areas or restriction of profuse sweating to the upper body, while sweating in the lower body areas is absent (may hint at ANP in diabetes mellitus). Documentation by a standardised sketch or photography may help for follow-up.

4.5 Horner’s Syndrome

Horner’s syndrome (HS) is a central or peripheral sympathetic denervation of the eye. Denervation of the M. tarsalis superior results in ptosis; sympathetic denervation of the inner eye results in parasympathetic predominance causing myosis. HS is best diagnosed in a darkened room. HS is placed in this chapter, because depending on the location of the sympathetic lesion, hypohidrosis occurs to the skin of the forehead/face or ipsilateral arm (Fig. 4.1). Enophthalmus is considered part of the trias. However, enophthalmus per se is only rarely present, being mimicked by ptosis. Therefore a more correct description of HS is:

1.

Ptosis
2.

Myosis
3.

Hypohidrosis

Fig. 4.1

Schematic sketch and table helping to diagnose the location of a sympathetic lesion often including Horner’s syndrome (Adapted from Wasner et al. [14]); DF areas of disturbed facial flushing, Arm sympathetic arm innervation, hf hemifacial, * medial forehead and nose

HS is an important hint that – accompanied by other signs – may already help to establish the diagnosis. Clinical evaluation is mandatory along the route of the sympathetic fibres guided by clinical presentation (Fig. 4.1).

HS is also one of the leading signs of harlequin syndrome. It is in fact the name of two very different conditions. Here we describe the harlequin syndrome caused by sympathetic lesion; the other condition with this very same name is a skin disorder of congenital ichthyosis.

The name is derived from loss of flushing on one side of the face by ipsilateral sympathetic lesion, which prevents sympathetic facial vasodilatation and sweating. The site of the lesion might as well be identified by Fig. 4.1. In rare cases, symptoms of harlequin syndrome are seen in Adie’s syndrome (tonic pupils with hyporeflexia) or Ross syndrome (tonic pupils with hyporeflexia and segmental anhidrosis). The latter two are usually accompanied with a more widespread involvement of the autonomic nervous system.

4.6 General Considerations for Diagnostic Work-Up

Specific laboratory work-up is necessary only in rare cases and laboratory tests are not widely available [7]. Diagnosis of patients suffering sweating dysfunctions should not depend on the presence of a specialised autonomic laboratory Table 4.1.

4.6.1 Generalised Hyperhidrosis

A carefully taken history should already reveal the generalised character of sweating. In many cases, the patient will tell that “his whole body is soaked wet all the time”. It can be time consuming to find out if increased sweating always affects the whole body or only specific areas. What are the exact circumstances and situations when profuse sweating occurs (physical activity, emotional stress, hot environment, night sweat)? How was sweating before the patient noticed the changes, and was there increased focal sweating before? Concomitant diseases, medication and drug abuse have to be evaluated carefully. According to the obtained information, further diagnostic work-up and management have to be planned.

4.6.2 Generalised Hypohidrosis

This is a rare and sometimes life-threatening condition, because of hyperthermia or heat-related illness, as body core temperature homeostasis cannot be maintained. Most patients remain unaware of hypohidrosis and may report on heat intolerance with dizziness, vertigo, dyspnoea and even fainting. It has to be differentiated if the condition increased gradually, maybe as a severe form of progressive hypohidrosis beginning in the extremities, or if it had sudden onset. In the latter case, drugs may play a causal role including antimuscarinic anticholinergic agents, carbonic anhydrase inhibitors and tricyclic antidepressants [12]. These drugs are quite often found to cause sudomotor side effects in elderly patients. Other neurological side effects such as overactive bladder, neuropathic pain, irritable bowel syndrome, reactive airway disease, Parkinson’s disease, dizziness, depression, nausea and headache may contribute to heat-associated illness in this population (for a detailed description of the route of action of different drugs, see Cheshire and Fealey [12]). Further factors include decline in sweating responses with ageing and fluid restriction. As acetylcholine is the principal neurocrine mediator, anhidrosis is one of the clinical hallmarks by which acute anticholinergic toxicity may be recognised. The symptom of drymouth often accompanies the less apparent symptom of hypohidrosis. In any case, drug screening may be valuable including a drug history, eventually also drug abuse.

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