Background Excessive sweating from cerebral infarction has been reported rarely in the available stroke literature, and its pathophysiological mechanisms and clinical significance have remained obscure. In addition, there have been no reports that medullary infarction results in only contralateral hemihyperhidrosis without ipsilateral Horner’s syndrome. In the hope of increasing recognition of this phenomenon, we describe five patients with hyperhidrosis, including two patients with medullary infarction, and discuss the clinicoanatomic correlations.
Case Descriptions Contralateral hyperhidrosis occurred in two patients with large strokes involving both superficial cortical and deep subcortical structures of the middle cerebral artery territory and in two patients with medullary infarctions. Bilateral hyperhidrosis of the face was noted in one patient with basilar artery thrombosis and bilateral cerebellar and pontine infarctions. The hyperhidrosis typically involved the face and arm and was transient, lasting from 2 days to 2 months. No associated Horner’s syndrome, hypothalamic dysfunction, or other autonomic dysfunction was observed.
Conclusions The phenomenon of hyperhidrosis might be attributed to a lesion of a putative sympathoinhibitory pathway that controls sweating. This pathway might originate in the cortex, possibly in the operculum, and make terminal connections with the contralateral thoracic spinal cord. Our observations suggest that the fibers of this putative pathway may be very close to the corticospinal tract.
Recently it was reported that the phenomenon of hyperhidrosis, as determined by a quantitative hydrotic analysis, is a common manifestation in patients with hemispheric brain infarction.1 2 However, unilateral hyperhidrosis contralateral to lesions after stroke seems to be observed infrequently in practice because sweating has been assessed by examination only under basal conditions or because sweating dysfunction has received little attention in cerebrovascular disease. Sweating dysfunction was recorded in only 3 of 633 consecutive strokes by Labar et al,3 and we found it in only 5 of 350 patients with acute stroke observed during a 40-month period. Lesions of the cerebral hemisphere,1 2 3 4 hypothalamus,5 and pons6 7 8 have been implicated in the literature in the phenomenon of hyperhidrosis, but a correlation between medullary lesions and hyperhidrosis has not been reported. In this report we describe 5 patients with hemihyperhidrosis contralateral to cerebral infarction, including 2 patients with medullary infarction. MRI allowed relatively precise clinicoanatomic correlations in these patients.
A 62-year-old man presented with global aphasia, right homonymous hemianopia, and severe paralysis of the right arm and leg with mild right facial weakness. MRI indicated a left middle cerebral artery (MCA) infarction (Fig 1⇓). On admission profuse unilateral hyperhidrosis was noted over the right face, neck, distal arm, and palm of the hand. No ptosis, anisocoria, fever, or abnormal electrolytes were observed. A mild electrocardiographic (ECG) abnormality attributable to preexisting ischemia was present. The patient’s history revealed aortic regurgitation and congestive heart failure. One month later aspiration pneumonia with congestive heart failure developed, and the patient died 2 days later. The unilateral hyperhidrosis had persisted for 1 month.
A 61-year-old man presented with global aphasia, right homonymous hemianopia, mild left gaze preference, and right hemiplegia. MRI revealed a left MCA infarct. On admission he was treated in the intensive care unit with a diagnosis of brain herniation and aspiration pneumonia due to deep stuporous mentality and high fever. After 30 days of hospitalization the patient was transferred to the general ward because his mentality improved and his fever subsided. Five days later he experienced profuse unilateral hyperhidrosis over the right side of the face. We noted no ptosis, anisocoria, or fever. Serum electrolytes were normal, and the ECG showed only left ventricular hypertrophy. Two months later sweating was symmetrically normal.
A 54-year-old man presented with ataxic gait and alteration of mental state. Two days later he worsened, responding only to noxious stimulation. Changes in his respiration pattern, bilateral facial weakness, and tetraplegia with bilateral Babinski’s sign developed. We observed a pinpoint pupil with sluggish light reflex, without corneal reflex and oculocephalic reflex. An endotracheal tube was then inserted, after which time excessive bilateral sweating of the face was noted, with large drops of sweat dripping continuously from his forehead, nose, and orbit. MRI revealed a basilar artery thrombosis, bilateral cerebellar infarct with swelling, bilateral pontine infarct, and a right posterior cerebral artery (PCA) infarct (Fig 2⇓). The patient was afebrile, electrolytes were normal, and cardiac arrhythmia was not observed. Respiratory arrest developed 2 days later. The bilateral hyperhidrosis of the face persisted until his death 2 days after the aggravation of stroke.
A 60-year-old man presented with vertigo, ataxic gait, horizontal nystagmus, left-sided hypesthesia, left-sided weakness with Babinski’s sign, and left-sided cerebellar dysfunction. Two days later unilateral hyperhidrosis was prominent on the forehead, face, palm of the hand, and sole of the foot on the left. The patient had no ptosis, anisocoria, or fever. MRI revealed a small infarct of the right medulla oblongata (Fig 3⇓). No ECG or electrolyte abnormalities were reported. The unilateral hyperhidrosis gradually disappeared over the next 7 days.
A 64-year-old man presented with right-sided hypesthesia, right hemihyperhidrosis, and difficulty in swallowing. Four days before admission he had suddenly developed right-sided hypesthesia. One day later he observed right-sided hyperhidrosis with large beads of sweat on the face, arm, and leg. He was admitted because of difficulty in swallowing, which developed the day before admission. The patient had no ptosis, anisocoria, or fever. Serum electrolytes and ECG were normal. MRI showed an infarct of the left medulla oblongata (Fig 4⇓). The right-sided hyperhidrosis resolved itself in 1 month.
Excessive sweating (hyperhidrosis) after stroke has been reported in many lesions of the cerebral hemisphere,1 2 3 4 hypothalamus,5 pons,6 7 8 and spinal cord.9 Appenzeller4 described a patient with a pathologically demonstrated opercular infarction who had unilateral hyperhidrosis, ptosis, miosis, and hemiplegia on the side contralateral to the infarction. Labar et al3 observed profuse unilateral hyperhidrosis not only in patients with large infarctions involving both superficial and deep structures but also in those with smaller infarctions of the opercular cortex. In our series, two patients (cases 1 and 2), both with a large MCA infarction, showed this phenomenon. Sakashita et al5 reported that a patient with hemorrhagic infarctions in the left basal ganglia, internal capsule, thalamus, hypothalamus, and medial part of the cerebral peduncle had contralateral persistent hyperhidrosis for more than 2 months. We found three reported cases of excessive sweating associated with brain stem infarction that involved the basis pontis6 7 or the inner part of the pontine tegmentum extending to the basis pontis.8 In one of our patients (case 3), the infarction demonstrated by MRI involved the bilateral pons and cerebellum and the right PCA territory as a result of basilar artery thrombosis. We observed contralateral hemihyperhidrosis in two patients (cases 4 and 5) with medullary infarction. One patient with hemiparesis had a lesion of the anterior portion of the upper medulla and the lateral-superficial portion of middle medulla; the other without hemiparesis had a lesion of the posterolateral and anterior portions of the middle medulla. Severe constant symmetrical hyperhidrosis below the ninth thoracic dermatome was reported in a patient with a spinal cord lesion caused by a bilateral pyramidal tract lesion.9
Although the pathophysiological mechanisms of unilateral hyperhidrosis associated with cerebral infarction are still uncertain, this phenomenon could be explained by the disruption of a putative inhibitory neural pathway that controls sweating of the contralateral face and body. The aforementioned clinicoanatomic correlations through MRI or pathology suggest that this putative pathway might originate in the cortex, possibly in the operculum, project to the hypothalamus, descend to the brain stem, cross in the medulla, and make terminal connections with the contralateral thoracic spinal cord. At the level of the pons and the medulla, the fibers of this pathway seem to descend in very close proximity to the corticospinal tract and along the inner side of facilitory fibers, which are speculated to travel through the dorsolateral part of the pontine tegmentum and the lateral reticular formation in the medulla.
Our observations contradict the notion that unilateral hyperhidrosis after cerebral infarction is due to diminished sweating ipsilateral to the infarction (ie, partial Horner’s syndrome without ptosis or miosis), making the contralateral side appear hyperhidrotic. No patient developed a complete oculosympathetic paresis. Keane10 found that only 7 of 100 patients with Horner’s syndrome had miosis and anhidrosis without ptosis. None of these 7 patients had contralateral hemihyperhidrosis. Unilateral anhidrosis, without ptosis or miosis, has not been reported as presentation of a partial Horner’s syndrome.
Recently Korpelainen et al11 demonstrated ipsilateral hypohidrosis by means of a quantitative stimulated (thermal) sweat test in 18 patients with pontine and medullary infarctions. However, this finding seems to differ from unilateral sweating dysfunction associated with previous studies1 2 3 4 5 6 7 8 and our cases. Further study is required to demonstrate this difference.
In previous studies3 4 6 7 8 including our series, it has been reported that hyperhidrosis typically involved the face and arm. Korpelainen et al1 2 also revealed that excessive sweating at all registration sites (forehead, chest, forearm, hand, leg, and foot) occurred, but it was most obvious on the forehead and hand because of the high absolute evaporation rates at the baseline. Accordingly, the forehead and hand seemed to be the most common sites of hyperhidrosis.
The phenomenon of hyperhidrosis has been reported to be associated with severe neurological deficit and poor prognosis by Labar et al,3 but it was not associated with a poor prognosis in the series of Korpelainen et al1 2 and in our patients. Further study is needed to determine its clinical significance.
Finally, the signs and symptoms of Wallenberg’s lateral medullary syndrome (LMS) have often been described in the literature.12 13 14 15 16 Kim et al15 described the wide spectrum of LMS and the correlation between clinical findings and MRI in 33 subjects. Our two patients with medullary infarction seemed to exhibit a variation of LMS rather than the typical syndrome according to clinical findings and MRI. However, because there have been no reports that only contralateral hyperhidrosis without ipsilateral Horner’s syndrome is one of the manifestations of LMS, our patients may not have had LMS. Therefore, further clinical observations and experiences may be needed to delineate this phenomenon.
- Received November 4, 1994.
- Revision received January 31, 1995.
- Accepted February 16, 1995.
- Copyright © 1995 by American Heart Association
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