Thermoregulation in multiple sclerosis

Abstract

Davis SL, Wilson TE, White AT, Frohman EM. Thermoregulation in multiple sclerosis. J Appl Physiol 109: 1531-1537. First published July 29, 2010 doi:10.1152/japplphysiol.00460.2010.-Multiple sclerosis (MS) is a progressive neurological disorder that disrupts axonal myelin in the central nervous system. Demyelination produces alterations in saltatory conduction, slowed conduction velocity, and a predisposition to conduction block. An estimated 60 -80% of MS patients experience temporary worsening of clinical signs and neurological symptoms with heat exposure. Additionally, MS may produce impaired neural control of autonomic and endocrine functions. This review focuses on five main themes regarding the current understanding of thermoregulatory dysfunction in MS: 1) heat sensitivity; 2) central regulation of body temperature; 3) thermoregulatory effector responses; 4) heat-induced fatigue; and 5) countermeasures to improve or maintain function during thermal stress. Heat sensitivity in MS is related to the detrimental effects of increased temperature on action potential propagation in demyelinated axons, resulting in conduction slowing and/or block, which can be quantitatively characterized using precise measurements of ocular movements. MS lesions can also occur in areas of the brain responsible for the control and regulation of body temperature and thermoregulatory effector responses, resulting in impaired neural control of sudomotor pathways or neural-induced changes in eccrine sweat glands, as evidenced by observations of reduced sweating responses in MS patients. Fatigue during thermal stress is common in MS and results in decreased motor function and increased symptomatology likely due to impairments in central conduction. Although not comprehensive, some evidence exists concerning treatments (cooling, precooling, and pharmacological) for the MS patient to preserve function and decrease symptom worsening during heat stress. demyelination; core temperature; sweating; skin blood flow; fatigue MULTIPLE SCLEROSIS (MS) is a disabling progressive neurological disorder affecting ϳ400,000 individuals in the United States. The pathophysiology of MS results in a disruption or loss of axonal myelin in the central nervous system (CNS), leading to the formation of scar tissue (sclerosis). MS is thought to involve a number of autoimmune injury cascades that appear to be dependent on the interaction of complex epigenetic and environmental factors. Immune responses in individuals with MS are skewed toward a proinflammatory state, resulting in inflammation, demyelination, and ultimately loss of axons and disorganization of normal tissue architecture within the CNS (23). Demyelination is associated with corresponding changes in axonal physiology, including a loss of saltatory properties of electrical conduction, reduction in conduction velocity, and a predisposition to conduction block. These pathophysiological mechanisms underlie the myriad of symptoms (Table 1) in individuals with MS and are contingent on the neuroanatomic l...

Warmer outdoor temperature is associated with worse cognitive status in multiple sclerosis

“…In addition, putative mechanisms underlying the effect of temperature on cognition remain to be explored in future research. That is, separate lines of research have shown that increased temperature is associated with increased lesion activity 3 and slowed or blocked conduction within demyelinated axons (for review, see 12 ), but it remains unclear whether these mechanisms or an as-yet unidentified mechanism is responsible for the heatrelated decrements in cognitive status observed among patients with MS in the current study. It may also be useful to examine individuals with secondary progressive MS, as we may expect to see exaggerated effects of slowed/blocked conduction as a result of demyelination in this more advanced disease subtype.…”

Neurophysiology of Skin Thermal Sensations

“…K+) ion channels in temperature transduction. In the context of human pathophysiology, increasing the knowledge on the function and interaction between TRP and K+ ion channels is of clinical significance for the study of those demyelinating diseases, amongst which multiple sclerosis, which present changes in membrane excitability and potassium channels function within the central nervous system (93), along with characteristics mechanisms of heat sensitivity resulting in temporary worsening of clinical symptoms (82,281).…”

Autonomic thermoregulatory dysfunction in neurofibromatosis type 1

“…For instance, after sympathectomy, local sweating responses to pilocarpine becomes exacerbated, but it subsequently decreases and, in some cases, ceases completely 22 . Decreased pharmacologically induced sweat production observed in type 1 diabetes and multiple sclerosis is an early sign of neuropathy, and it has been associated with reduced sympathetic nerve fiber density in the sweat glands 10,23,24 . In NF1, the development of large cutaneous and subcutaneous neurofibromas may cause dysfunctions in peripheral nerves leading to chronic pain, sensory loss, weakness or even palsy.…”

“…As an example, the neuropathy caused by progressive central demyelization in multiple sclerosis produces systemic failure in maintaining internal temperature during heat exposure due to decreased neural control of cardiovascular responses and impaired sweat function. As a result, most multiple sclerosis patients experience transient and temporary worsening of clinical signs and neurological symptoms during exposure to higher environmental temperatures and exercise 10 . Additionally, exercise intolerance and sweating dysfunction are considered common manifestations of diabetic autonomic neuropathy, even in the early stages of this disease, once the sweating response is diminished or completely suppressed, especially in lower limbs 11,12 .…”