急性脑梗塞与单侧多汗症

出汗异常是自主神经功能障碍中最常见的症状之一。本文报道５例脑梗塞伴对侧躯体出汗异常患者。３例为大脑中动脉区梗塞、２例为脑岛皮层区梗塞。出汗部位以额和前臂明显，持续１～４天，未发现其它自主神经功能障碍。本文就５例患者并结合有关文献对其预防、临床特征、发病机理及临床意义作一讨论。     

Unilateral hyperhidrosis after cerebral infarction

Unilateral hyperhidrosis occurred contralateral to acute cerebral infarctions in six patients. Two patients had localized infarctions of opercular cortex, while the other four had large strokes involving both superficial cortical and deep subcortical structures. The unilateral hyperhidrosis typically involved the face and arm and was transient, lasting 1 to 3 days. No other autonomic dysfunction occurred. One patient died, and the others had significant residual neurologic disability, thus indicating poor prognosis when this sign is present. Disruption of a pathway of cortical origin, inhibitory to contralateral sweating, is a proposed mechanism for the hyperhidrosis seen contralateral to acute cerebral infarction in these patients.     

Autonomic failure after stroke – is it indicative for pathophysiology of complex regional pain syndrome?

In order to find pieces of evidence for a central origin of autonomic failure in complex regional pain syndrome I (CRPS I), the pattern of autonomic symptoms in CRPS I patients was compared to patients a few days after stroke. Autonomic failure in the latter group is assumed to represent definite CNS origin. Seventeen stroke patients, 21 patients in the acute and late stage of CRPS I and a control group of 23 healthy subjects were investigated. Detailed neurological examination was performed, sweating was induced centrally (thermoregulatory sweating, TST) and peripherally by carbachol iontophoresis (QSART) and quantified by evaporation hygrometry. Skin temperature was assessed by infrared thermography. The incidence of motor-sensory dysfunction (without pain) and the incidence of edema was strikingly similar in stroke and CRPS patients. Furthermore, stroke patients had increased TST but not QSART responses on the contralesional limb (P < 0.05) and skin temperature was decreased (P < 0.001). The same pattern of autonomic failure was found in late CRPS (TST: P < 0.02, skin temperature: P < 0.01) whereas in acute CRPS additional, presumably peripheral mechanisms, contribute to sympathetic symptoms. In conclusion, our investigation suggests that many clinical symptoms and the main features of sympathetic dysfunction in CRPS could be explained by a CNS pathophysiology.     

Pontine hemorrhage presenting with Foville syndrome and transient contralateral hyperhidrosis]

This report concerns a 88-year-old diabetic and hypertensive woman with pontine hemorrhage who presented with Foville syndrome and contralateral hyperhidrosis. She was admitted to our hospital for sudden onset of headaches and disturbed consciousness. Neurologic examination revealed bilateral miosis, Foville syndrome and superficial hemianesthesia on the right side of the face and body. No associated Horner syndrome and other autonomic dysfunction were observed. Laboratory data were normal except for diabetic findings. Brain CT and MRI revealed a hematoma in the left side at the lower pons. One month after the onset, hemihyperhidrosis on the face, arm and upper trunk contralateral side of the lesion appeared abruptly, and gradually disappeared a week later. Sweating on the ipsilateral side was normal and no new lesion was seen on the brain CT then. Only a few cases of contralateral hyperhidrosis due to pontine lesion have been reported. We suggest that the contralateral inhibitory sweating pathway was disrupted though the ipsilateral excitatory one was intact. Contralateral hyperhidrosis attributed to imbalance of the perspiratory control can be observed in the subacute or late phase after pontine hemorrhage.     

Autonomic nervous system disorders in stroke

Disturbances of the autonomic nervous system are common in patients with various cerebrovascular diseases. They are attributed to damage of the central autonomic network, particularly in the frontoparietal cortical areas and in the brain stem, or to a disruption of the autonomic pathways descending from the hypothalamus via the mesencephalon, pons, and medulla to the spinal cord. The most common clinical problems include abnormalities in heart rate and blood pressure regulation, reflecting cardiovascular autonomic dysfunction, and asymmetric sweating with cold hemiplegic limbs, reflecting changes in the sudomotor and vasomotor regulatory systems. Bladder and bowel dysfunction and impotence are also frequent complaints after stroke, but the present knowledge concerning their prevalence and clinical significance is still limited. Cardiovascular autonomic dysfunction, which is mainly related to increased sympathetic activity, is most evident in the acute phase of stroke, whereas other autonomic disorders, such as abnormal sweating, are long-standing or even irreversible. In addition to the well-established sympathetic hyperfunction, abnormalities of the parasympathetic nervous system may also contribute to the autonomic imbalance after stroke. Reliable recognition of autonomic dysfunction using quantitative analysis methods is important, because these disturbances are not only subjectively disabling and uncomfortable, but they may also be prognostically unfavorable. Moreover, quantitative measurements also form the ground for successive treatment of various stroke-related autonomic disorders.     

脑梗死患者交感神经皮肤反应分析

交感神经皮肤反应（sympathetic skin response,SSR）是由内源或外源性刺激所诱发的皮肤 瞬时电位变化,属于脑和脊髓参与的交感催汗运动。本文主要概述近年来SSR在脑梗死患者中应用 价值,阐述其对脑梗死患者自主神经功能紊乱的临床诊断作用,与脑梗死患者运动功能的相关性, 以及SSR在推断交感神经可能的中枢传导通路中的价值。     

Sweating dysfunction in Parkinson's disease.

We sought to determine the prevalence and nature of sweating disturbances in patients with Parkinson's disease (PD), and investigated their correlation with other clinical features and with Quality of Life (QoL) measures. A questionnaire on symptoms and consequences of sweating dysfunction was completed by 77 consecutive outpatients, from three movement disorder clinics, and 40 controls. QoL was assessed using the disease-specific Parkinson's Disease Questionnaire (PDQ)-39 and generic EuroQoL (EQ)-5D rating scales. Patients also underwent a clinical examination, including assessment with the Unified Parkinson's Disease Rating Scale and the Hoehn and Yahr staging system. Sweating disturbances, either hypohidrosis or in particular, hyperhidrosis, were reported by 64% of patients and by 12.5% of controls (P < 0.005) and were often localised or asymmetric. Complaints of sweating disturbances were not correlated with disease severity, but did correlate with other symptoms of autonomic dysfunction. Sweating problems occurred predominantly in off periods and in on periods with dyskinesias. Sweating disturbances were not correlated with overall QoL scores, but we did observe a significant correlation with the pain dimension of the PDQ-39 and the visual analogue scale of the EQ-5D. Furthermore, many patients reported physical, social, and emotional impairment due to sweating. Sweating disturbances are common and distressing symptoms of PD that are related mainly to autonomic dysfunction, off periods, and dyskinesias.     

Disorders of sweating

The clinical spectrum of sweating disorders includes sudomotor excess and deficiency. Hyperhidrosis is characterized by sweating beyond that required to maintain a constant internal body temperature. Hypohidrosis and anhidrosis are distinguished by a reduced or absent ability to generate sweat for the purpose of evaporative heat dissipation. Whereas hyperhidrosis is usually benign, anhidrosis may predispose to hyperthermia. Either hyperhidrosis or anhidrosis may accompany a more serious underlying disorder. Correct diagnosis depends on determining the anatomical pattern of sweating and localizing the lesion within the autonomic nervous system. Sudomotor deficits may involve the frontal operculum, hypothalamus, brain stem, spinal cord, sympathetic chain ganglia, peripheral nerve, or eccrine sweat glands. Treatments for hyperhidrosis include topical aluminum chloride, oral anticholinergic agents, intradermal botulinum toxin for some localized syndromes, and thoracic ganglionic sympathotomy or sympathectomy for refractory palmar hyperhidrosis.     

Alterations in cardiovascular autonomic function tests in idiopathic hyperhidrosis

We performed cardiovascular autonomic function tests to assess sympathetic and parasympathetic functions in patients with idiopathic hyperhidrosis. We studied 35 patients with idiopathic hyperhidrosis and 35 age- and sex-matched controls. A thermoregulatory sweat test (TST) was performed in all subjects. Sweating was qualitatively (Minor's test at 22°C) and quantitatively (skin conductance) evaluated. Orthostatism, tilt to 65°, cold pressor test, deep breathing, Valsalva maneuver and hyperventilation were performed in patients and controls. A greater fall in blood pressure values was observed in patients than in controls in the upright tests (p<0.05). In particular, postural hypotension was present in a subgroup of patients (34%), in whom changes in lying-to-standing blood pressure and heart rate were greater (p<0.001) than those of the remaining patients. The TST revealed that the total body sweat rate (ml/cm(2)/min) was more pronounced in patients with postural hypotension (p<0.001) than in the other patients and controls. The skin conductance values of patients with postural hypotension were higher (p<0.001) than those of the remaining patients. A positive correlation was found between skin conductance values and postural hypotension. Dehydration and poor water intake may play a role in postural hypotension in patients with severe hyperhidrosis and pronounced thermoregulatory sweating. A significantly marked increase in parasympathetic function was observed in patients. Responses to deep breathing, Valsalva maneuver and hyperventilation were significantly greater in patients (p<0.001) than in controls. Idiopathic hyperhidrosis seems to be a complex dysfunction that involves autonomic pathways other than those related to sweating.     

Botulinum toxin type A in primary palmar hyperhidrosis: randomized, single-blind, two-dose study.

BACKGROUND: Primary palmar hyperhidrosis is characterized by excessive sweating due to increased sympathetic cholinergic sudomotor nerve traffic to the palmar surface of the hands. Clinical studies suggest that intradermal injections of botulinum toxin are effective in the treatment of palmar hyperhidrosis. OBJECTIVES: To establish the effectiveness of intradermal botulinum toxin in reducing hyperhidrosis, to determine the most effective dose of toxin, and to examine its effect on muscle strength. METHODS: In a prospective, single blind, randomized trial, 24 patients with severe palmar hyperhidrosis received either a low (50 U) or a high dose (100 U) of botulinum toxin type A (Botox, Allergan) injected intradermally in 20 sites in each palm. RESULTS: Following injection with either dose, iodine starch test revealed a significant decrease in sweating within the first month. Six months after injection, the anhidrotic effect was still evident in two thirds of the patients in both groups. Handgrip strength was not affected with either dose but finger pinch strength, 2 weeks after the injection, decreased 23 +/- 27% with 50 U (p < 0.05) and 40 +/- 21% with 100 U (p < 0.001). Pinch strength improved gradually but 6 months after treatment it was still 7-11% lower than at baseline. CONCLUSIONS: Both 50 and 100 U of botulinum toxin type A, injected intradermally in each hand, decreased sweating in patients with primary hyperhidrosis for at least 2 months in all the patients, and 6 months in most patients. Weakness in the intrinsic muscles of the hand was observed.     

Cardiovascular and sweating dysfunction in patients with Holmes-Adie syndrome.

A cross-sectional study is reported in which 53 patients with Holmes-Adie syndrome have been subjected to a battery of tests of autonomic nervous function referable to the cardiovascular system, to two objective tests of sweating function, and to subjective assessment of sweating by application of quinizarin powder followed by body heating. The majority of patients were consecutive referrals; none was selected because of clinical indications of autonomic dysfunction. Eighty three per cent of these patients had at least one, 57% at least two, and 40% at least three objective test abnormalities, as defined by values lying outside 95 percentiles of healthy subjects who were matched for age and subjected to the same tests. In the context of multiple testing, the probability of finding outside values was such that a minimum of 3 was required to define abnormality. On this basis 40% of patients were found to have significant evidence of autonomic dysfunction. The most frequent abnormalities were impaired digital vasoconstriction to cold (23%), a reduced heart rate response to the Valsalva manoeuvre (17%), and excessive variability in sweating between test sites (in one of the tests, 43%) which is consistent with patchy loss. Abnormal quinizarin test appearances were seen in 10 patients and in a further five patients the appearances were thought to be suggestive of abnormality. Though assessment of the results of this test are subjective, the observations are consistent with the findings obtained from the objective tests which were applied. Cardiovascular and sweating abnormality did not concur significantly and only the former was found to increase progressively with known duration of the pupillotonia. It is concluded that Holmes-Adie syndrome is commonly accompanied by progressive mild but widespread autonomic involvement but rarely is this symptomatic. If symptoms suggestive of autonomic neuropathy are found in a patient with tonic pupils, a careful search for some other generalised disorder is recommended.     

Social anxiety and functional impairment in patients seeking surgical evaluation for hyperhidrosis

Primary hyperhidrosis is characterized by excessive sweating and often accompanied by social avoidance. Social anxiety disorder (SAD) is characterized by fear and avoidance of social situations, often partly related to fears of showing signs of excessive autonomic nervous system activation, such as sweating. To clarify the relationship of hyperhidrosis and SAD, this study assessed severity of sweating, overall social anxiety and social anxiety due to sweating, and disability in 2 groups: patients seeking surgical treatment for hyperhidrosis (n = 40) and patients seeking treatment for SAD (n = 64).     

Unilateral persistent hyperhidrosis after ischemic stroke]

A 64-year-old right hemiplegic woman, who had been treated for hypertension for 15 years, was admitted to our hospital. Neurologic examination on admission disclosed right hemiplegia and motor aphasia; however, ophthalmoparesis, pupillary abnormality, and blepharoptosis were not evident. Excessive sweating on the right side of the body, which was most marked on the face, was observed. Amount of sweating on the left side of the body was normal. Unilateral hyperhidrosis persisted for more than 2 months. MRI revealed hemorrhagic infarctions in the left basal ganglia, internal capsule, thalamus, hypothalamus, and medial part of the cerebral peduncle. 123I-IMP SPECT disclosed hypoperfusion in the left striatum, thalamus, occipital cortex, and right cerebellar hemisphere. Cerebral angiography revealed arteriosclerotic changes in the basilar artery, but that the left posterior cerebral artery and its branches were not occluded. Unilateral persistent hyperhidrosis is rare after ischemic stroke. Hypothalamic lesion was thought to be responsible for the hyperhidrosis in this patient. As the hypothalamus receives its blood supply from the posterior cerebral artery, unilateral persistent hyperhidrosis may be an important sign of cerebral infarction in the posterior cerebral artery region.     

Clinical use of non-a botulinum toxins: botulinum toxin type B

Botulinum neurotoxin type B (BT, BT-B) has been used as NeuroBloc/MyoBloc since 1999 for treatment of cervical dystonia, hyperhidrosis, spastic conditions, cerebral palsy, hemifacial spasm, bladder dysfunction, spasmodic dysphonia, sialorrhoea, anal fissures, piriformis syndrome, various pain conditions and cosmetic applications. Generally, its therapeutic effects are comparable to BT type A (BT-A). The adverse effect profiles of BT-B and BT-A, however, differ considerably. BT-B has been found to produce more regional as well as systemic anticholinergic adverse effects, such as dryness of mouth, accommodation difficulties, conjunctival irritation, reduced sweating, dysphagia, heartburn, constipation, bladder voiding difficulties and dryness of nasal mucosa. In BT-B the relationship between autonomic and motor effects known from BT-A is substantially shifted towards autonomic effects. BT-B, therefore, should be used carefully in patients with autonomic disorders and in patients with concomitant anticholinergic therapy. If NeuroBloc/MyoBloc is used to treat cervical dystonia patients with antibody-induced failure of BT-A therapy, 86% of those will develop complete secondary therapy failure after five applications. If NeuroBloc/MyoBloc used to treat cervical dystonia patients without prior exposure to BT, 44% of those will develop complete secondary therapy failure after nine applications. NeuroBloc/MyoBloc, therefore, is associated with substantial antigenicity problems originating from a particular low specific biological potency. Systemic anticholinergic adverse effects and high antigenicity limits the clinical use of NeuroBloc/MyoBloc considerably.     

Hyperhidrosis in social anxiety disorder

Purpose: Excessive sweating (hyperhidrosis) is an overlooked and potentially disabling symptom, which is often seen in social anxiety disorder (SAD). We conducted a retrospective review of data acquired in patients with SAD who had participated in placebo-controlled clinical trials of fluoxetine, cognitive behavior therapy, clonazepam and gabapentin. Four specific topics were addressed: (1) overall levels of sweating; (2) characteristics of those with hyperhidrosis; (3) a comparison of active treatments relative to placebo on hyperhidrosis; and (4) an examination of baseline sweating severity as a predictor of treatment outcome. Methods: Using the Brief Social Phobia Scale (BSPS) and Social Phobia Inventory (SPIN), we examined the above questions. Results: Hyperhidrosis was found in 24.8–32.3% of 375 subjects assessed, depending upon the scale used. Hyperhidrosis was associated with higher levels of disability, fear, avoidance, and other physiologic symptoms. While treatment in general was associated with a reduction in the rate of hyperhidrosis from 23.7% to 9.7% (BSPS), and 34.0% to 15.5% (SPIN), only fluoxetine differed significantly from placebo in respect of change in sweating score from baseline to endpoint. In an ANCOVA, gabapentin differed from placebo on the SPIN. Conclusion: We conclude that hyperhidrosis is frequently seen in patients with SAD, and that its response to treatment is variable. Further attention should be paid to the possible importance of this symptom in social anxiety.     

Hyperhidrosis in Parkinson's disease.

We studied the sudomotor skin response (SSR) in patients with Parkinson's disease with and without symptomatic hyperhidrosis. The study was carried out in 13 patients who complained of excessive sweating and in 37 patients who did not have excessive sweating. Patients were matched for age, sex, degree of impairment, duration of the disease, and number and severity of autonomic disturbances. Excessive sweating involved mainly the face, head, and trunk. The SSR was recorded from the palm of the hands to electrical stimulation of the median nerve at the wrist. We analyzed onset latency, peak to peak amplitude, and waveform. Patients with hyperhidrosis had more often absent responses (chi(2) = 5.292; P = 0.021), their responses were of lower mean amplitude (analysis of variance [ANOVA]; F[2,101] = 11.678; P < 0.001), and they had a reduced number of responses with a predominantly negative component (chi(2) = 8.493; P = 0.004) than patients who did not complain of sweating disturbances. Our results indicate that excessive sweating in Parkinson's disease concurs with decreased activation of sweat glands in the palms of the hands and suggests that axial hyperhidrosis could be a compensatory phenomenon for reduced sympathetic function in the extremities.     

The effects of water ingestion on orthostatic hypotension in two groups of chronic autonomic failure: multiple system atrophy and pure autonomic failure

BACKGROUND: Oral ingestion of water increases seated blood pressure in patients with chronic autonomic failure by mechanisms that remain unclear. As orthostatic hypotension is common in chronic autonomic failure, and is not always adequately controlled by medication, the potential benefits of water ingestion on standing blood pressure were studied in two types of autonomic failure: multiple system atrophy (MSA), in which the lesion is central and pre-ganglionic, and pure autonomic failure (PAF), in which the lesion is post-ganglionic. METHODS: In 14 patients with autonomic failure (seven PAF and seven MSA) standing blood pressure and heart rate were measured before, and 15 and 35 minutes after ingestion of 480 ml distilled water. Patients remained seated for 15 minutes after water ingestion, with beat to beat cardiovascular indices measured with the Portapres II device with subsequent Modelflow analysis. RESULTS: Standing prior to water ingestion caused a significant fall in blood pressure in all patients. After water ingestion there was a rise in seated blood pressure. Seated and standing blood pressure at 15 and 35 minutes after water ingestion was significantly higher than before water, with an improvement in orthostatic symptoms. The time to first significant rise in seated blood pressure occurred at 5 minutes post water ingestion in PAF and at 13 minutes in MSA. These increases were accompanied by increases in total peripheral resistance, reaching significance by 5 minutes in PAF and 13 minutes in MSA. There were no significant changes in cardiac output, stroke volume, or ejection fraction. CONCLUSIONS: Water is thus beneficial in improving standing BP in AF, acting within 15 minutes in both MSA and PAF. The earlier onset of the pressor effect in PAF may reflect the differing lesion site and underlying pathophysiology between these conditions.     

Preliminary findings of the effects of autonomic dysfunction on functional outcome after acute ischemic stroke

Background and purpose

Impaired autonomic function is common in the acute poststroke phase but little is known about its effects on functional outcome after acute ischemic stroke. This study sought to investigate the impact of autonomic dysfunction by Ewing's classification on functional outcome 2 months after acute ischemic stroke.

Methods

34 consecutive acute ischemic stroke patients within 7 days after onset were enrolled. On admission, autonomic function was assessed by Ewing's battery tests. Stroke severity was assessed by the National Institutes of Health Stroke Scale (NIHSS), autonomy in activities of daily living by the Barthel Index (BI), and global disability by the modified Rankin Scale (mRS). BI and mRS were also evaluated 2 months after ischemic stroke onset.

Results

On admission, eight patients were diagnosed as minor autonomic dysfunction and 26 patients as relatively severe autonomic dysfunction. The prevalence of relatively severe autonomic dysfunction in ischemic stroke patients was 76.5%. There were no significant differences in baseline characteristics between the minor and severe autonomic dysfunction groups. 2 months after stroke onset, the mean BI score of patients with minor autonomic dysfunction and severe autonomic dysfunction increased from 76.3 ± 15.3 on admission to 95.0 ± 7.1, 66.5 ± 15.2 on admission to 74.8 ± 15.9 respectively. The mean BI score after 2-month stroke onset and the change in BI from admission to 2-month outcome (delta BI) in patients with severe autonomic dysfunction were lower than those in patients with minor autonomic dysfunction (all P < 0.05).

Conclusions

Autonomic dysfunction occurs in acute stroke patients. Relatively severe autonomic dysfunction is related to an unfavorable functional outcome in patients with acute ischemic stroke.     

Lateralization in autonomic dysfunction in ischemic stroke involving the insular cortex

Autonomic nervous system dysfunction is a common complication of ischemic stroke. Clinical and experimental data indicate hemispheric lateralization in the control of autonomic activity. The insular cortex has also been shown to play a crucial role in the central autonomic network. The aim of this study was to assess cardio-autonomic dysfunction in patients with ischemic insular versus non-insular cortex infarction, and to demonstrate a possible lateralization in autonomic activity mediated by the insular cortex. Sympathetic function was prospectively assessed by determining plasma norepinephrine and epinephrine in 15 patients with left-hemisphere (LH; four insular infarction), and 14 with right-hemisphere (RH) middle cerebral artery (MCA) stroke (five insular infarction). Systolic and diastolic blood pressure and heart rate were recorded during the first 5 days after stroke. Sympathetic activity was significantly higher in insular than in non-insular infarction (p < 0.05) with concomitantly elevated cardiovascular parameters in insular stroke patients. The pathological activation of the sympathetic nervous system was most excessive in RH-stroke involving the insular cortex (p < 0.05). Our data indicate a hemispheric lateralization in autonomic activity which is mediated by the right-sided insular cortex. Patients with RH stroke involving the insular cortex are most susceptible to develop cardio-autonomic dysfunction.     

Treatment of gustatory sweating with botulinum toxin

Gustatory sweating is an autonomic disorder that frequently occurs after parotid gland surgery. We investigated the action of intracutaneous injections of botulinum toxin (BTX) (1.0–2.0 mouse units/2.25-cm² skin area) in 45 patients (mean age, 52 years) with gustatory sweating. The area of hyperhidrosis was determined by Minor's iodine test before and up to 24 weeks after the injection. The effect of BTX was assessed by measuring the hyperhidrotic area. The maximum BTX-induced reduction of gustatory sweating was seen at 7.4 · 4.5 days after injection. The area of sweating decreased from 17.6 · 8.6 cm² before BTX to 1.3 · 1.6 cm² after BTX (p < 0.0001). Half the patients rated gustatory sweating subjectively as completely abolished, and the remainder felt pronounced improvement. No toxic effects were observed. In none of the patients did hyperhidrosis recur over a 6-month follow-up. We conclude that BTX is a safe and effective treatment that can be recommended as the therapy of choice in gustatory sweating.