Effect of cognitive and motor tasks on postural stability in Parkinson's disease: a posturographic study.

To analyse the effect of concomitant cognitive or motor task performance on balance control in Parkinson's disease (PD), we performed a posturographic study in 24 PD patients and in 20 sex- and age-matched control subjects. Postural sway was measured with eyes open (EO) and eyes closed (EC) during quiet stance and during performance of calculation or motor sequence of thumb opposition to the other fingers. No difference of centre of foot pressure (COP) parameters was observed during quiet standing (either EO or EC) between patients and controls, but visual deprivation induced in both groups a worsening of postural stability. COP area was significantly increased in PD patients during dual task performance, whereas no difference of COP path and x-y axes was observed. The effects induced by the performance of cognitive or motor task were significantly more evident in PD patients with clinical evidence of postural instability (presence of prior falls in the history). This study demonstrates that dual task interference on postural control can be observed in PD patients during performance of cognitive as well as motor tasks. The balance deterioration during dual task performance was significantly enhanced in patients with history of prior falls. These findings have some implications for the strategies to be used in reducing the risk of fall in PD.     

Autonomic dysfunction in chronic liver disease

Chronic liver disease is accompanied by a number of circulatory changes including impairment of cardiovascular autonomic reflexes. This occurs irrespective of the aetiology of liver disease, increases in prevalence and severity with worsening hepatic function, and is related at least in part to an autonomic neuropathy. Parasympathetic abnormalities predominate and, although largely subclinical, they may play a role in the altered fluid homeostasis and neurohumoral disturbances associated with cirrhosis. On prospective follow up, the presence of autonomic impairment was associated with a five-fold increased mortality, largely from sepsis and variceal haemorrhage. Defective responses to such stressful events as a result of an afferent defect could possibly explain these findings. Further studies are required to evaluate the natural history of this complication, and determine if it is reversible with improvement in hepatic function or after liver transplantation.Professor Triger passed away on 13 March 1993. His obituary appears on page 283.     

Sympathetic skin response and R–R interval variation in chronic uremic patients

Sympathetic skin response (SSR) and R–R interval variation (RRIV) were studied in 36 chronic, nondiabetic uremics to compare with their nerve conduction studies (NCS) and clinical dysautonomia. Abnormal SSR was noted in 5 (13.9%) patients, abnormal RRIV in 14 (38.9%), and abnormal NCS in 26 (72.2%). The patients were classified into three groups: group (GP) 1: “normal,” n = 21 (58.3%), normal RRIV and SSR; GP 2: “isolated parasympathetic dysfunction,” n = 10 (27.8%), abnormal RRIV and normal SSR; and GP 3: “sympathetic sudomotor dysfunction,” n = 5 (13.9%), abnormal SSR. A significant difference in age was found among the three groups (GP 3 > GP 2 > GP 1; P < 0.0001, ANOVA). After controlling the age factor, we still noted a tendency toward increasing NCS disturbances (distal latency and nerve conduction velocity of peroneal nerve; P < 0.05, multiple regression analysis) and frequencies of clinical autonomic symptoms (postural dizziness and impotence; P < 0.05, Mantel–Hanszel test) from GP 1 to GP 3. Patients with abnormal SSR (GP 3) displayed significantly higher frequencies of postural dizziness and impotence, indicating the relationship between an absence of SSR and clinical dysautonomia. © 1994 John Wiley & Sons, Inc.     

轮状病毒中枢神经及肺部感染

研究背景 轮状病毒性胃肠炎是婴幼儿期最常见腹泻疾病之一。国内外对轮状病毒中枢神经及肺部感染告道甚少。 研究方法 用电镜、免疫电镜、酶联免疫吸附与阻断试验确诊轮状病毒中枢神经及肺部感染。 研究结果 200例轮状病毒性胃肠炎患儿中,并发轮状病毒性脑膜炎一例,轮状病毒性肺炎2例,其中1例同时合并胸膜炎、胸腔积液。 结论 轮状病毒中枢神经及肺部感染预后良好。     

Effects of Pharmacological Autonomic Blockade on Dual Atrioventricular Nodal Pathways Physiology in Patients with Slow-Fast Atrioventricular Nodal Reentrant Tachycardia

The purpose of this study was to investigate the atrioventricular AV nodal physiology and the inducibility of AV nodal reentrant tachycardia (AVNRT) under pharmacological autonomic blockade (AB). Seventeen consecutive patients (6 men and 11 women, mean age 39 ± 17 years) with clinical recurrent slow-fast AVNRT received electrophysiological study before and after pharmacological AB with atropine (0.04 mg/kg) and propranolol (0.2 mg/kg). In baseline, all 17 patients could be induced with AVNRT, 5 were isoproterenol-dependent. After pharmacological AB, 12 (71 %) of 17 patients still demonstrated AV nodal duality. AVNRT became noninducible in 7 of 12 nonisoproterenol dependent patients and remained noninducible in all 5 isoproterenol dependent patients. The sinus cycle length (801 ± 105 ms vs 630 ± 80 ms, P < 0.005) and AV blocking cycle length (365 ± 64 ms vs 338 ± 61 ms, P < 0.005) became shorter after AB. The antegrade effective refractory period and functional refractory period of the fast pathway (369 ± 67 ms vs 305 ± 73 ms, P < 0.005; 408 ± 56 ms vs 350 ± 62 ms, P < 0.005) and the slow pathway (271 ± 30 ms vs 258 ± 27 ms, P < 0.01; 344 ± 60 ms vs 295 ± 50 ms, P < 0.005) likewise became significantly shortened. However, the ventriculoatrial blocking cycle length (349 ± 94 ms vs 326 ± 89 ms, NS) and effective refractory period of retrograde fast pathway (228 ± 38 ms vs 240 ± 80 ms, NS) remained unchanged after autonomic blockade. Pharmacological AB unveiling the intrinsic AV nodal physiology could result in the masking of AV nodal duality and the decreased inducibility of clinical AVNRT.     

An atypical case of mononeuritis multiplex in primary Sjogren's syndrome

We present an atypical case of peripheral nervous system (PNS) involvement in Sjogren's syndrome in a 63 year-old woman. Symptoms of an entrapment neuropathy were the first manifestation of the systemic disease and they were subsequently coupled to those of a mononeuritis multiplex. Clinical and laboratory signs for the diagnosis of Sjogren's syndrome became subsequently overt. The mononeuritis multiplex remained clinically limited to the upper limbs and characterized by unusually severe motor symptoms which progressed up to the development of a final complete deplegia. By contrast, sensory symptoms at the upper limbs remained mild over the entire course of the disease and the lower limbs revealed a subclinical sensory-motor damage only during the late stage.     

EFFECTS OF ANGIOTENSINS II AND III ON GLOMERULOTUBULAR BALANCE IN RATS

1. The role of angiotensin as a modulator of proximal glomerulotubular (GT) balance was investigated in anaesthetized rats by examining the relationship between glomerular filtration rate (GFR) and absolute proximal reabsorption (APR) during removal of endogenous angiotensin II (AII) and III (AIII) with enalaprilat (CEI) and then during their subsequent replacement by intravenous infusions. 2. Enalaprilat lowered mean arterial blood pressure (MABP) and increased renal blood flow (RBF), GFR, urine flow rate and sodium excretion. Filtration fraction (FF) was not altered. Absolute proximal reabsorption, derived from fractional lithium clearance, increased by only 48% of the change expected for 'perfect' GT balance. 3. Angiotensin II replacement corrected MABP, GFR and plasma renin level, but reduced RBF and increased FF; APR was decreased and GT balance was restored. Urine flow and sodium excretion remained above control values with AII. 4. Replacement with AIII did not correct the hypotension but completely reversed the renal and renin responses to enalaprilat and restored GT balance without affecting FF. 5. It was concluded that the relation between proximal reabsorption and GFR is considerably modified by the intrarenal angiotensin concentration. The findings are best explained by a direct stimulation of proximal tubular sodium transport by angiotensin at the concentrations existing in anaesthetized rats.     

Effect of electric and chemical stimulation of the raphe obscurus on phrenic nerve activity in the cat

The effect of electrical and chemical (l-glutamate) stimulation of the raphe obscurus on phrenic nerve activity was examined in the cat. Phrenic nerve activity was recorded from a C5 nerve root in anesthetized, paralyzed and artificially ventilated cats. Neural discharge was quantitated by integrating the phrenic nerve activity. The respiratory frequency was determined from the integrated nerve signal. Focal electrical stimulation (18–144 μA; 5–40 Hz; 100 μs pulse duration) resulted in significant (P < 0.05) increases in both integrated phrenic nerve (IPN) amplitude and respiratory frequency. These changes were dependent upon current intensity and frequency of stimulation. The largest increases in IPN amplitude and respiratory frequency were47 ± 17%and146 ± 8%, respectively. To insure that the changes in integrated phrenic nerve activity (IPNA) were the result of stimulation of cell bodies and not axons of passage,l-glutamate (100, 200 nmol) was microinjected (100 nl) into the raphe obscurus. Significant (P < 0.05) dose-related changes occurred in integrated phrenic nerve amplitude with an increase of44 ± 13% at 100 nmol and80 ± 13% at 200 nmoll-glutamate. No significant increase in respiratory frequency was observed withl-glutamate microinjection. The results suggest that the raphe obscurus may be involved in respiratory control.     

Short and long term effects of exercise training on the tonic autonomic modulation of heart rate variability after myocardial infarction

We studied the effects of cardiac rehabilitation on the sympathovagalcontrol of heart rate variability in 30 patients after a first,uncomplicated myocardial infarction. Twenty-two patients completed8 weeks of endurance training (trained), while eight decidednot to engage in the rehabilitation programme for logisticalreasons, and were taken as untrained controls. Age, site ofinfarction, ejection fraction, ventricular diameter and stresstest duration were similar in the two groups at baseline. Heartrate variability was evaluated 4 weeks after infarction beforestarting rehabilitation, and repeated 8 weeks and one year laterin both trained and untrained patients. Measures of heart ratevariability, obtained from both time- and frequency- domainanalysis of a 15 min ECG recording in resting conditions, wereas follows: mean RR interval and its standard deviation (RRSD),the mean square successive differences (MSSD), the percent ofRR intervals differing >50 ms from the preceding RR (pNTN50),the low and high frequency components of the autoregressivepower spectrum of the RR intervals and their ratio (LF/HF).At baseline, heart rate variability was similar in trained anduntrained patients. In the short term (8 weeks after infarction),training increased RRSD by 25% (P<0·01), MSSD by 69%(P<0·01), pNN50 by 120% (P<0·01), and reducedLF/HF ratio by 30% (P<0·01). The effects persistedafter one year in trained patients. In untrained patients, theautonomic control of heart rate variability did not change 8weeks after myocardial infarction and was only slightly modifiedby time. Thus, exercise training, performed for 8 weeks aftera myocardial infarction, modifies the sympathovagal controlof heart rate variability toward a persistent increase in parasympathetictone, known to be associated with a better prognosis. This maypartly account for the favourable outcome of patients who undergorehabilitation.     

Interleukin-6 production by astrocytes: Induction by the neurotransmitter norepinephrine

Astrocytes contribute to the immunocompetence of the central nervous system (CNS) via their expression of class II major histocompatibility complex (MHC) antigens and the production of inflammatory cytokines such as interleukin-1 beta (IL-1β), tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6). Of these cytokines, IL-6 is of particular interest because one of its many immune and inflammatory actions is the promotion of immunoglobulin synthesis, and it is thought that IL-6 expression within the brain exacerbates autoimmune diseases of the CNS, which are marked by local immunoglobulin production. Several stimuli induce astrocyte IL-6 expression, including such inducible endogenous factors as IL-1β and TNF-α. We have investigated the possibility that a constitutively present endogenous factor, the neurotransmitter norepinephrine (NE), can induce astrocyte IL-6 production. We report that NE induces both IL-6 mRNA and protein in primary neonatal rat astrocytes, with optimal induction at 10 μM. IL-6 protein induction by NE is comparable to that seen with IL-1β or TNF-α, and NE synergizes with these cytokines for a ten-fold enhanced effect. In contrast to astrocytes, microglia are relatively unresponsive to NE, IL-1β and TNF-α for IL-6 production. Experiments with the β-adrenergic receptor agonist isoproterenol, and α and β-adrenergic receptor antagonists (propranolol, phentolamine, atenolol, and yohimbine) indicate that β₂ and α₁-adrenergic receptors are involved in NE induction of astrocyte IL-6 expression. These results help to further the understanding of neuron-glial interactions, and the role of astrocytes and adrenergic activity in immune responses within the CNS.