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Heat Intolerance/Heat Stroke
Published in Charles Theisler, Adjuvant Medical Care, 2023
Heat intolerance includes symptoms of exhaustion, fatigue, nausea, vomiting, or dizziness in response to moderately warm temperatures. Certain disease symptoms (e.g., multiple sclerosis) typically worsen with increased body temperature. Other conditions such as diabetes, Parkinson’s, Grave’s disease, and Guillain-Barré syndrome as well as certain medications can cause heat intolerance.
Disorders of keratinization and other genodermatoses
Published in Rashmi Sarkar, Anupam Das, Sumit Sethi, Concise Dermatology, 2021
The disorder is characterized by large dark plate-like scales with minimal erythema of the skin (Figure 15.4). The scales are tightly adherent to the skin, and, in severe cases, cause scarring alopecia with loss of scalp hair, ear deformity, and ectropion and eclabium due to traction on eyelids and lips. Sweating may be impaired, leading to heat intolerance.
Pure Autonomic Failure
Published in David Robertson, Italo Biaggioni, Disorders of the Autonomic Nervous System, 2019
Disorders of sweating and thermoregulation are early symptoms of autonomic failure, although they usually do not lead patients to seek medical attention. Patients typically present with distal hypohidrosis or anhidrosis (Bradbury and Eggleston, 1925; Barker, 1933) that may gradually progress to total anhidrosis. Such patients can develop heat intolerance particularly in warmer climatic regions. Some patients report episodic unprovoked diaphoresis involving the whole body surface early in the course of their illness. This may be a consequence of denervation supersensitivity, although eccrine sweat glands are not customarily thought to obey Cannon’s law of denervation (Cannon, 1939). Some patients will sweat excessively in the proximal body regions as a compensatory response to the loss of distal sweating sites. Focal areas of increased sweating such as the face, a limb, or the hemibody have also been reported (Allen and Magee, 1934).
Physiology of sweat gland function: The roles of sweating and sweat composition in human health
Published in Temperature, 2019
As shown in Table 6, certain medical conditions and medications can impact sweating rate and sweat composition. As discussed in the Thermoregulation section above, evaporation of sweat is crucial for temperature regulation in warm conditions and this is evident in patients suffering from anhidroses. Diabetes mellitus, multiple sclerosis, spinal cord injury, and anhidrotic ectodermal dysplasia are associated with a significant reduction in sweating; which, in some cases, can severely impair one’s ability to dissipate heat during higher thermal loads [340–344]. In particular, heat intolerance is well documented in patients with anhidrotic ectodermal dysplasia, a genetic condition resulting in a paucity of sweat glands over the entire body surface [3,15]. In addition, the important function of salt conservation by the sweat gland is evident in patients with reduced ion reabsorptive capacities due to a genetic deficiency or absence of functioning CFTRs (cystic fibrosis) or impaired adrenal cortex function (Addison’s disease) [345,346]; who may be more susceptible to electrolyte imbalances [174–176,259,263,265,267].
Ross Syndrome
Published in Neuro-Ophthalmology, 2020
Manikanta Damagatla, Pratyusha Ganne, Rakesh Upparakadiyala, Prabhakaran N
The first case of Ross syndrome was described by Ross in 1958.2 Ever since there have been only a handful of cases reported worldwide. Some believe this to be a combination of two separate syndromes namely Harlequin syndrome and Holmes-Adie syndrome.3 Recent evidence suggests a decrease in sudomotor, vasomotor and pilomotor innervation in the skin of patients with Ross syndrome.4–6 Hence, there is a lack of sweating and cutaneous vasoregulation leading to heat intolerance. The iodine-starch test helps to demarcate areas of intact sweating and anhidrotic areas. Areas of intact sweating stain positive.7 Our patient showed no staining on the left side of her back and had patchy staining on the right side of her back (Figure 2). Tonic pupil results from damage to the ciliary ganglion or postganglionic parasympathetic nerve fibres.8 The exact cause of areflexia has not been found. Some postulate damage to the dorsal roots, sensory ganglia or the afferent fibres in the spinal cord.9,10 Tonic pupil may be present unilaterally or bilaterally and areflexia may be generalised. The tonic pupil shows a hypersensitivity response to dilute pilocarpine drops and this may be performed to confirm the diagnosis of postganglionic parasympathetic denervation hypersensitivity.11 The exact pathogenesis of the autonomic ganglion damage is uncertain but it is postulated that there is a congenital lack of factors that promote the survival of these neurons leading to their apoptosis. Some studies have suggested an autoimmune basis for the disease with some patients testing positive for different antibodies like anti-nuclear (ANA), SSA, SSB and anti-thyroid antibodies.12,13 Nolano et al. showed that this condition is progressive but benign.6
Use of the heat tolerance test to assess recovery from exertional heat stroke
Published in Temperature, 2019
Katherine M. Mitchell, Samuel N. Cheuvront, Michelle A. King, Thomas A. Mayer, Lisa R. Leon, Robert W. Kenefick
The IDF’s method of determining heat tolerance has changed over the years (see Table 2). The primary method of classifying heat intolerance is to assess Trec and HR values at the end of exercise (120 minute mark). Heat intolerance is classified when an individual has a rectal temperature greater than 38.5°C or HR above 145 bpm [52].