Possible compensatory mechanisms of segmental and unilateral hyperhidrosis
● 第 70 回日本自律神経学会総会 / シンポジウム 9 / 分節性／半側性多汗症：臨床的特徴と病態 司会：犬飼洋子・齋藤 博 Possible compensatory mechanisms of segmental and unilateral hyperhidrosis: estimation based on the efferent phase of the physiological mechanism of the skin pressure-sweating reflex
Yoko Inukai
Kew words: segmental hyperhidrosis, unilateral hyperhidrosis, skin pressure-sweating reflex, compensatory hyperhidro- sis, sweating
Abstract: Segmental and unilateral hyperhidrosis are forms of sweating disorder. In some cases, these are accompanied by anhidrosis/hypohidrosis in other skin areas. The pathogenesis of these hyperhidrosis may be compensatory and is likely caused by underlying lesions in anhidrosis/hypohidrosis areas, but the precise mechanism remains unclear. Hyperhidrosis is often located horizontally contralateral same myelomere skin areas as the anhidrosis/hypohidrosis, whereas vertically ipsilateral adjacent to other rostral and caudal my- elomere with anhidrosis/hypohidrosis. The similar efferent phase of the physiological “skin pressure-sweating reflex” might be associated with these mechanisms. This horizontal reflex is primarily due to inhibitionof ipsilateral sweating by unilateral skin pressure, secondarily contralateral sweating increases. Microneurog- raphy indicates that this phenomenon occurs because unilateral skin pressure reduces the amplitude of ipsilateral sudomotor nerve activity and increases contralateral activity. Vertically, studies using the ventilated capsule method during heating, show that pressure on the bilateral skin of the back by supination decreases sweating on the upper body and increases sweating on the underbody. Central sudomotor sympathetic outflow (frequency of sweat expulsion) in response to body temperature is simultaneously hyperactivated, indicating that sweating is increased compensatorily to maintain a constant total sweating rate. In conclusion, segmental hyperhidrosis in segments other than those directly affected may be compensatory. （The Autonomic Nervous System, 56: 25 ～ 32, 2019）
causes of segmental hyperhidrosis brought by spinal Introduction cord lesions: (1) disinhibition of preganglionic sympathetic Segmental and unilateral hyperhidrosis are the forms neurons due to interruption of the inhibitory descending of sweating disorders. These hyperhidrosis are reported pathway by, for example, Chiari-type malformation18), sporadically and are often uncomfortable for patients. (2) overactivity of relatively intact19) preganglionic The mechanism underlying this condition is unknown. sympathetic neurons due to spinal cord lesions such Previous reports about this condition and its etiology are as syringomyelia with Chiari malformation20), and (3) summarized below. autonomic hyperreflexia due to cutaneous stimulation, such as postural change, or bladder and intestine stimu- Reported segmental hyperhidrosis by overactivity of lation1). It is also reported that segmental hyperhidrosis sympathetic neurons is usually associated with irritation or infiltration of pre- Segmental hyperhidrosis is an uncommon finding. ganglionic sympathetic fibers or the sympathetic chain30) Three mechanisms have been hypothesized as possible by mesothelioma, a thoracic central disc herniation, chickenpox13), herpes zoster30), nonsystemic vasculitic Department of Physiology, Aichi Medical University School neuropathy28), or eccrine angiomatous hamartoma27). of Medicine, 1-1 Yazakokarimata, Nagakute, Aichi 480-1195, Japan
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Reported unilateral hyperhidrosis by excitation due to the lesions of affected body sides 3UHVV Most cases with localized unilateral hyperhidrosis reported were considered to be idiopathic. Secondary localized unilateral hyperhidrosis is usually attributed to neurological factors such as intracranial tumor, cerebral infarction or hematoma, encephalitis, spinal cord injuries including syringomyelia, neuritis, osteoma also of the cervical rib, chickenpox, bronchial carcinoma14) or pleural malignancy7), e.g., mesothelioma29), or trauma to the 6) autonomic nervous system of the affected body side . Excision of cervical ribs, which may cause hyperhidro- sis by excitation of autonomic efferent fibers abolished this hyperhidrosis26). Thus, direct infiltration of the sympathetic chain is also postulated to cause unilateral hyperhidrosis. The possibility of compensatory hyperhidrosis due to 7DNDJL anhidrotic areas on other area Fig. 1 Sweating the whole body while the left axilla and the In most cases, sweating is localized to the ipsilateral)LJ right iliac crest are pressed (areas of sweat are stained with side as a tumor, although cases of contralateral sweating iodostarch reaction using Minor’s method). Hemihidrosis have been reported8). Since 2007, I and my co-authors occurs on the upper body caused by pressure at a contralateral upper-body site, in particular, the side of the reported many cases of segmental and unilateral chest. Hemihidrosis occurs on the underbody due to pressure 2)4) hyperhidrosis accompanied by anhidrosis/hypohidrosis . at a contralateral underbody site, e.g., the side buttocks.24) In some cases of segmental hyperhidrosis, anhidrosic/ hypohidrotic areas occurred ipsilateral to superior or in- ferior adjacent dermatomes. In other cases, anhydrotic/ What is the mechanisms of compensatory segmental or hypohidrotic areas occurred in the same dermatomes unilateral hyperhidrosis?: similar to the efferent phase of contralateral to hyperhidrotic areas. These cases “skin pressure-sweating reflex” included patients with harlequin syndrome, Ross syn- Presumed segmental or unilateral compensatory drome15), cervical disc herniation, and lung cancer (cases hyperhidrosis is similar to phenomena seen in the are described below). Anhidrosis can likely be attributed efferent phase of the physiological “skin pressure- to underlying lesions. We were unable to confirm such a sweating reflex”. In this reflex, unilateral sweating is lesion, however, in some cases. suppressed segmentally primarily by ipsilateral skin The pathogenesis of these sweating disorders may be pressure, and thereby, sweating in the contralateral compensatory but remains unknown. In one case, hyper- same spinal segment is secondarily enhanced (Ogata et hidrosis that presented on the left side of the face and al., 1935)9) (Fig. 1)24). It is suggested that the pressure- anhidrosis that presented on the right hand started at sweating reflex is a somato-sympathetic reflex involving the same time. Hyperhidrosis of the left hand developed spinal segments where afferent impulses produced by
2.5 years later, and thus may have been compensatory5). skin pressure modify central sudomotor volleys. The Ross syndrome is a neurological disorder with progres - contralateral sweating increase is may response to the sive unilateral or bilateral segmental anhidrosis with ipsilateral sweating decrease. It is estimated that this a unilateral segmental compensatory hyperhidrotic latter efferent phase is compensation24). The mechanism band. The most disturbing symptom in these patients for this reflex may help to elucidate the hyperhidrotic is compensatory segmental hyperhidrosis, and often mechanism which is caused by the anhidrosis on the hypohidrosis or anhidrosis is not noticed. Yet, lesions contralateral same spinal segments or ipsilateral different that need to be treated would be exist at the sudomotor segments due to lesions. level in the anhidrotic area. First, cases of segmental or unilateral hyperhidrosis
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Possible compensatory mechanisms of segmental and unilateral hyperhidrosis that are accompanied by anhidrotic areas will be dis- cussed, along with possible mechanisms for case observa- / 5 tions using results of studies that elucidate mechanisms 5 underlying the skin pressure-sweating reflex. &㻌
Cases Case 1: Unilateral hyperhidrosis A 45-year-old man presented with a chief complaint
(CC) of hyperhidrosis since 30 years old. Findings from a thermoregulatory sweat test (TST) are provided in
Fig. 2A. Sweat was identified by a change in color to dark purple (by an iodostarch reaction) in the indicator, 6ZHDWLQJDUHD 㻌 which was made up of the liquid mixture of povidone &RPSHQVDWLRQ 0HGLDOVDJLWWDOSODQH
$ % iodine solution, absolute ethanol and castor oil painted )LJ Fig. 2 Case 1. A: Findings of the thermoregulatory sweat test. on the skin over the entire body, and the dispersed Sweat was identified by a change in color to dark purple (by potato starch powder (Minor’s method). The patient an iodostarch reaction) in the indicator, which was made up of was exposed at rest to an ambient temperature of the liquid mixture of povidone iodine solution, absolute ethanol 40°C and 50% relative humidity in an artificial climate and castor oil painted on the skin over the entire body, and chamber. Unilateral hyperhidrosis on the left side and the dispersed potato starch powder (Minor’s method). The unilateral anhidrosis in the right side occurred over the photographs and the sketch are shown. The patient was sitting at rest at an ambient temperature of 40°C and 50% whole body. Increased sweating on the left seemed to relative humidity in an artificial climate chamber. Unilateral be compensatory for anhidrosis on the right side, which hyperhidrosis on the left side and contralateral anhidrosis is horizontally contralateral in the same myelomere in occurred over the whole body. The horizontally increase in which hyperhidrosis is observed. sweating on the left side seemed to compensate for anhidrosis
The presumed etiology of this abnormal sweating on the right, which is contralateral in the same myelomere as hyperhidrosis. B: Magnetic resonance imaging (MRI) image distribution is maybe cervical disk herniation shown in showing cervical disk herniation. The largest disk protrusion the magnetic resonance imaging (MRI) (Fig. 2B). The is observed in the medial sagittal plane. greatest disk protrusion is seen in the medial sagittal plane. The protruding cervical disk, which is slightly area (Area c). to the right at C5/6, might press the same side of the The presumed etiology of this distribution of abnormal spinal sulcal artery (Fig. 3C, Case 1) and cause unilateral sweating is cervical spondylosis shown in the MRI (Fig. insufficient peripheral perfusion of the sudomotor 3B). The most prominent spicule at C5/6 is seen in the pathway around the anterior horn, resulting in ipsilateral left paramedial sagittal plane, and might press the ipsi- and unilateral anhidrosis without motor or sensory lateral sympathetic premotor neuron in the dorsolateral disturbances4). Therefore, the lesion might be on the funiculus at the C7 level (Fig. 3C, Case 2). This finding anhidrotic side. was ipsilateral to the anhidrotic side and corresponded to the hypohidrotic segment4). Therefore, the lesion might Case 2: Segmental unilateral hyperhidrosis be in the anhidrotic site (segment). A 37-year-old woman presented with a CC of left unilateral hyperhidrosis of the face and the upper body. Case 3: Segmental unilateral hyperhidrosis, harlequin Findings of TST are provided in (Fig. 3A). Hyperhidrosis syndrome extended from the left half of the face, neck and shoulder A one-year and nine-month-old boy presented with to the cervical (C) 6 area of the left upper extremity (Area right hemifacial flushing (Fig. 4A) and anhidrosis a). Anhidrosis was observed from the ipsilateral C7 area from the contralateral (left) half of the face (harlequin on the left arm to the left half of the trunk, subjacent syndrome) to the C4 level. Higher skin temperature and vertical to the hyperhidrotic area (Area b). Other was measured on the right arm. Findings of TST are hypohidrosis area was observed on the right side of the illustrated in Fig. 4B. Anhidrosis was seen on the left same myelomere areas horizontal to the hyperhidrotic half of the face to the left T1 dermatome. The lesion
（27） 自律神経 56 巻 1 号 2019 年
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$QWHULRU VSLQDODUWHU\ &DVH & Fig. 3 Case 2. A: Findings of the thermoregulatory sweat test. Area a) Hyperhidrosis: from the left half of the face, neck and shoulder to the C6 area of the left upper extremity. Area
)LJb) Anhidrosis: ipsilateral to the hyperhidrotic area, from C7 on the left arm to the left half of the trunk, and vertically subjacent to the hyperhidrotic area. Area c) Hypohidrosis: horizontal right side of the same myelomere level of the hyperhidrotic area. B: MRI image shows cervical spondylosis. The left paramedial sagittal plane showed the largest protruding spicule at C5/6. This site matches the left anhidrotic myelomere4). C: The involved lesion is assumed to be in the spinal cord. Case 1: The most protruding cervical disk in the medial sagittal plane, which is slightly to the right side at C5/6, might press the same side of the spinal sulcal artery. Case 2: The left paramedial sagittal plane showing the most protruding spicule at C5/6, which may press the ipsilateral sympathetic sudomotor tract in the dorsolateral funiculus at C7 level. may be in this location (Area a). Hyperhidrosis was seen anhidrosis) in the same myelomere with the anhidrosis on the left (ipsilateral to the anhidrosis) from T2 to the (Area c). Hyperhidrosis seemed to occur vertically and trunk (Area b), and on the right (contralateral to the horizontally because of anhidrosis.
（28） Possible compensatory mechanisms of segmental and unilateral hyperhidrosis
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'LUHFWLRQRI FRPSHQVDWLRQ F)LJig. 4 Case 3. A: Right hemifacial flushing at bathing (harlequin syndrome). B: Findings of the thermoregulatory sweat test. a) Anhidrosis: from the left half of the face to the left T1 dermatome. The lesion may be in this location. Hyperhidrosis: b) from the left (ipsilateral of
the anhidrosis above-mentioned) T2 to the trunk and, c) in the same right (contralateral of the anhidrosis) myelomere as the anhidrosis.
The lesion is assumed to be in the left cervical Takagi et al. clarified that: 1) hemihidrosis is a reflex sympathetic trunk depending on the distribution of the effect by contra-unilateral skin pressure; 2) between the anhidrotic area. sweating area of the inhibited side and the facilitated contralateral area, the border is almost clear on the Discussion midline (Fig. A), but the border of the top and bottom Anhidrosis may induce compensatory hyperhidrosis is unclear; 3) hemihidrosis is induced by contralateral horizontally on the contralateral side in the same sweating inhibition as a result of skin pressure. The dermatomes (Fig 2A, Fig 4) and vertically on rostral and cause of increased sweating on the non-pressure side caudal dermatomes ipsilateral adjacent to the areas of may be reciprocal innervation of bilateral sudomotor anhidrosis (Fig. 3A, Fig. 4). nerves or compensation; 4) when the chest is pressed The physiological phenomenon of “the skin pressure- bilaterally, sweating on the upper body is bilaterally sweating reflex” is due to segmental inhibition of inhibited and sweating in the lower body increases, i.e., unilateral sweating primarily by ipsilateral skin pressure, the vertical effect is observed. thereby contralateral sweating in the same segment Skin pressure might not affect human central ther- as skin pressure is secondarily enhanced, a horizontal moregulatory activity but may exert a sweat-inhibitory direction effect. The efferent phase of this phenomenon effect, primarily through the interaction of sudomotor is similar to unilateral hyperhidrosis caused by contra- impulses somewhere along efferent pathways, possibly at lateral possible disease. This process was reported by the spinal segmental level10). Ogata et al. (1935)9) and the mechanism was elucidated by Takagi (1950) (Fig. 1)23)–25).
（29） 自律神経 56 巻 1 号 2019 年
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5RRPWHPSHUDWXUH 䒾㽅& PRGLILHG 6XJL\DPDHWDO źLQGLFDWHVXGRPRWRUQHUYHEXUVWV㻌 ۃ Fig. 5 Bilateral integrated skin sympathetic nerve activity (SSNA) assessed by )LJ microneurography and determining the sweat rates using the ventilated capsule method
before and during pressure application in a healthy young adult. During pressure application on the right side at the level of the spina iliaca anterior superior, sweat rate on the pressure side (right) was diminished. Skin pressure reduces the amplitude of ipsilateral (right) sudomotor nerve activity ( ▼ ), and increases contralateral amplitude of sudomotor nerve activity. In spite of these amplitude asymmetries, bilateral SSNA bursts appeared in synchrony in the presence as well as in the absence of pressure stimuli. Further, reflex latency of sudomotor nerve activity was not changed by pressure application. These
results may indicate that unilateral skin pressure may not influence the central rhythm generating the SSNA22).
Horizontal compensatory hemihyperhidrosis mechanism patients with hemihidrosis is necessary to elucidate Asymmetries in skin sympathetic nerve activity mechanisms accurately. corresponding to pressure hemihidrosis were clarified in humans22). Skin sympathetic nerve activities (SSNAs) Vertical compensatory hyperhidrosis mechanism from bilateral peroneal nerves were simultaneously In an upright or a sitting position, sweating starts recorded ( ▽ & ▼ in Fig. 5) with measurements of sweat nearly simultaneously in all body regions; in the supine rate using the ventilated capsule method to identify su- position, sweat onset is delayed on the arms and chest; domotor nerve activity in healthy young adults. Stimulus therefore, sweating starts earlier on the legs when 3)11) by mechanical pressure was applied on the skin on the exposed to constant heat (this is the vertical effect). right hip at the level of the spina iliaca anterior superior Such a delay of onset at specific skin sites has been at room temperature 28–32ºC. Sweat rate on the pres- ascribed largely to skin pressure11). To assess this effect sure side (right) was diminished. Skin pressure reduces on sudomotor function, we measured sweat rates in the amplitude of ipsilateral sudomotor nerve activity healthy young males on the forearm, chest and thigh by ( ▼ ), and increases amplitude of contralateral sudomotor capsules with bottom of 8 cm2 (Fig. 6A) and frequency nerve activity. In spite of these asymmetries, bilateral of sweat expulsion (Fsw) by capsules with bottom of 1.13 SSNA bursts appeared in synchrony in the presence as cm2 (Fig. 6B-1) as an index of sudomotor outflow12)21) using well as in the absence of pressure stimuli. Further, reflex the ventilated capsule method. Tympanic (Tty) and skin latency of sudomotor nerve activity was not changed temperatures in upright sitting and supine positions by pressure application. These results may indicate that were also recorded for 60 min in a hot environment unilateral skin pressure stimulus may not influence the (40°C) with relative humidity of 40%3). In the supine posi- central rhythm generating the SSNA. tion, sweat rate in response to mean body temperature These findings indicate that a purpose of the was suppressed in the upper bodies (forearm and chest) compensatory sweating facilitation for the contralateral and increased in the lower body (thigh) (Fig. 6A)3). This anhidrosis will be to maintain total sweat rate in a semi- phenomenon is caused by pressure on the skin of the hot environment. Nevertheless, monitoring SSNAs in back due to the supine position. These findings suggest
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Possible compensatory mechanisms of segmental and unilateral hyperhidrosis
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Fig. 6 A: The linear relationship of the sweat rate and mean body temperature. Thick
lines and filled circles ( ● ) indicate sitting and dashed lines and open circles ( ○ ) supine positions. Mean ± SE. For the forearm and the chest, the slope of the regression line was significantly shallower. In contrast, for the thigh, a steeper line was found for the supine position than in the sitting position. That is, in the supine position, a sweating response to
)LJmean body temperature was suppressed on the upper bodies and was enhanced on the lower body. B-1: Identification of sweat expulsion. Sweat rate curves from the right and left forearms obtained from a subject. Fine bulges on the curves marked by open arrows ( ▽ ) are sweat expulsions. The sweat expulsions were synchronous at the two recording sites
indicating that sudomotor activity is discharged from the thermoregulatory center. B-2: The relationship of the frequency of sweat expulsion (Fsw) and mean body temperature (Tmb). The regression line was steeper and Fsw are significantly more in the supine than in the sitting position (ANCOVA, interaction: P=0.016), suggesting that the gain of central integration and rhythm-generation reaction to body temperature was enhanced in the supine position in a hot environment.3) (Reprinted from Auton Neurosc, 119, Inukai Y, Sugenoya J, Kato M, et al., Effects of body posture on local sweating and sudomotor outflow as estimated using sweat expulsion. 48–55, Copyright 2005, with permission from Elsevier.) that the skin pressure-sweating reflex effect might Conclusions also be induced to the caudal i.e. vertical direction. During heating, central sudomotor sympathetic outflow The mechanism of the efferent phase of the skin (indicated by Fsw) in response to body temperature was pressure-sweating reflex is similar to pathologic hyperactivated due to skin pressure to upper body (Fig. segmental or unilateral hyperhidrosis that may help to 6B-2)3), suggesting that sweating, except for the area elucidate pathophysiology. Suppression of some sudomo- where pressure is applied, is compensatorily increased to tor functions due to a lesion may cause compensatory maintain a constant total sweat rate. increased sweating of ipsilateral other adjacent spinal
（31） 自律神経 56 巻 1 号 2019 年 segment area in the vertical direction and in the 805–816. contralateral same spinal segment area in the horizontal 11) Ogawa T, Ito M, Miyagawa T, et al. Regional differences in occurrence of thermal sweating. Jpn J Biom 1979; 16: 22–29. direction. Nevertheless, for clear assessment of patho- 12) Ogawa T, Sugenoya J. Pulsatile sweating and sympathetic physiology, research using SSNA or sweat expulsion in sudomotor activity. Jpn J Physiol 1993; 43: 275–289. hyperhidrotic and anhidrotic areas of the patients with 13) Plyler ET, Gross TL, Chillag S. Segmental hyperhidrosis segmental or unilateral hyperhidrosis are necessary. preceding chickenpox. J S C Med Assoc 1984; 80: 504–505. 14) Poh SC. Bronchial carcinoma with hemilateral hyperhidro- sis. Singapore Med J 1978; 19: 59–60. The conclusions above were presented at the sympo- 15) Ross AT. Progressive selective sudomotor denervation; a sium “Segmental and/or Unilateral Hyperhidrosis: Clini- case with coexisting Adie’s syndrome. Neurology 1958; 8: cal Characteristics and Etiologies” in ISAN (International 809–817. Society for Autonomic Neuroscience) 2017/ JSNR (Japan 16) 齋藤 博，金原禎子．限局性脊髄障害例における温熱性発汗 機能：視床下部脊髄路の脊髄内下行部位に関する研究．自律 Society of Neurovegetative Research) 2017. 神経 2006；43：277–283. 17) Schulz V, Ward D, Moulin DE. Segmental hyperhidrosis Acknowledgments: I appreciate honorary professor Tokuo as a manifestation of spinal and paraspinal disease. Can J Ogawa, Aichi Medical University and professor Satoshi Neurol Sci 1998; 25: 325–327. Iwase, Aichi Medical University for the inspection of this 18) Stovner LJ, Sjaastad O. Segmental hyperhidrosis in two siblings with Chiari type malformation. Eur Neurol 1995; 35: abstract and advice. I also appreciate honorary professor 149–155. Junichi Sugenoya, Aichi Medical University for the 19) Sudo K, Fujiki N, Tsuji S, et al. Focal (segmental) dyshidro- advice on the logic of this article. sis in syringomyelia. J Neurol Neurosurg Psychiatry 1999; 67: 106–108. 20) Sudo K, Tashiro K. Segmental hyperhidrosis in syringomy- Con ict of Interest: Author Yoko Inukai has no financial elia with Chiari malformation. J Neurol 1993; 240: 75–78. relationships to disclose. 21) Sugenoya J, Ogawa T. Characteristics of central sudomotor mechanism estimated by frequency of sweat expulsions. References Jpn J Physiol 1985; 35: 783–794. 1) Glasauer FE, Czyrny JJ. Hyperhidrosis as the presenting 22) Sugiyama Y, Watanabe T, Takeuchi S, et al. Asymmetric symptom in post traumatic syringomyelia. Paraplegia 1994; discharges of skin sympathetic nerve in humans with 32: 423–429. special reference to pressure hemihidrosis. Environmental 2) 犬飼洋子，岩瀬 敏，菅屋潤壹ら．発汗障害の 2 乳幼児例． Medicine 1992; 36: 207–210. 第 119 回日本神経学会東海北陸地方会．2007 年 10 月 27 日． 23) 高木健太郎．半側発汗の動機について．日本生理誌 1949； 臨床神経学 2008；48：287. 11：137–141. 3) Inukai Y, Sugenoya J, Kato M, et al. Effects of body posture 24) Takagi K. Influences of skin pressure on temperature on local sweating and sudomotor outflow as estimated using regulation. In: Essential Problems in Climatic Physiology. sweat expulsion. Auton Neurosci: 2005; 119: 48–55. Yoshimura H, Ogata K, Itoh S, edi. Nankodo: Kyoto: 1960. p. 4) Iwase S, Inukai Y, Nishimura N, et al. Hemifacial hyper- 212–249. hidrosis associated with ipsilateral/contralateral cervical 25) Takagi K, Sakurai T. A sweat reflex due to pressure on the disc herniation myelopathy. Functional considerations on body surface. Jpn J Physiol 1950; 1: 22–28. how compression pattern determines the laterality. Funct 26) Telford ED. Cervical rib and hyperhidrosis. Br Med J 1942; Neurol 2014; 29: 67–73. 2: 96. 5) Kocyigit P, Akay BN, Saral S, et al. Unilateral hyperhidrosis 27) Toll A, Gallardo F, Jucglà A, et al. Multifocal segmental with accompanying contralateral anhidrosis. Clin Exp hyperthermic and hyperhidrotic naevus flammeus: a Dermatol 2009; 34:e544–546. peculiar variant of eccrine angiomatous hamartoma? Clin 6) Kreyden O, Schmid-Grendelmeier P, Burg G. Idiopathic Exp Dermatol 2007; 32: 696–698. localized unilateral hyperhidrosis. Arch Dermatol 2001; 137: 28) Tsunemi T, Yokota T, Kikyo H, et al. Nonsystemic 1622–1625. vasculitic neuropathy presenting with truncal segmental 7) Lindsay DC, Freeman JG, Record CO. Unilateral hyperhi- sensory disturbance and hyperhidrosis. Muscle Nerve 1999; drosis associated with underlying intrathoracic neoplasia. 22: 646–647. Thorax 1986; 41: 814–815. 29) Waran E. Doctor, I am sweating on just one side of my 8) McCoy BP. Apical pulmonary adenocarcinoma with contra- body: unilateral hyperhidrosis associated with mesothe- lateral hyperhidrosis. Arch Dermatol 1981; 117: 659–661. lioma. Clin Case Rep 2016; 4: 533–534. 9) 緒方維弘，市橋貞三．発汗ニ及ボス體位ノ影響．満州醫 30) Wu JJ, Murase JE, Huang DB, et al. A unique pattern of 誌 1935；23：1127. hyperhidrosis and herpes zoster. Arch Dermatol 2006; 142: 10) Ogawa T, Asayama M, Ito M, et al. Significance of Skin 1069. Pressure in Body Heat Balance. Jpn J Physiol 1979; 29:
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