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PubMed1993

Peripheral autonomic involvement in the carpal tunnel syndrome.

The sympathetic skin response (SSR), evoked from the middle finger of both hands by electrical stimuli to the median nerve (MN) at the wrist, was studied in 21 patients with bilateral carpal tunnel syndrome (CTS) and in 16 patients with monolateral CTS (14 at the right and 2 at the left side) without clinical signs of autonomic involvement. In monolateral and bilateral CTS there was a decrease in the SSR areas of both sides. In monolateral CTS the decrease was greater contralaterally to the lesion. A decrease in the SSR in CTS generally indicates a local blockade of sympathetic nerve excitability due to MN entrapment. Contralateral reduction of the sympathetic response suggests an involvement of the efferent pathway of the autonomic reflex far from the lesion at the wrist. However, dispersion of the excitement over a long distance and throughout numerous synaptic connections may affect contralateral more than homolateral SSR excitability. Finally, sympathetic damage in CTS is in accord with the anatomo-functional correlation (in the peripheral nerve and ganglia) between somatic sensory, which were most markedly involved in our patients, and sympathetic afferent nerve fibers.

Adolescent↗
PubMed2001

Afferent pathways of sympathetic skin response in spinal cord: a clinical and electrophysiological study.

BACKGROUND: Sympathetic skin response (SSR) recording is an established test of sudomotor autonomic functions. However, knowledge of its pathways in spinal cord is putative. OBJECTIVE: This study involved subjects with isolated spinal cord lesions to evaluate the afferent pathways of SSR. METHODS: Clinical examination was done according to standard neurological classification of spinal cord injury. Electrophysiological evaluation included: (1) conventional nerve conduction studies to exclude peripheral nerve lesions, (2) scalp somato-sensory-evoked potentials (SEP) with posterior tibial nerve (PTN) stimulation and (3) SSR recording from palm by stimulating supra orbital nerve (SON) at forehead, and PTN at ankle. Subjects with absent SSR in palm to SON stimulation were excluded. In such patients, the afferent tracts were considered abnormal when SSR was absent in palm on stimulation of PTN. RESULTS: Among 37 subjects (age-28.1+/-12.8 years), the afferent tracts of SSR were affected in 13. Sparing of afferent SSR tracts correlated with preservation of bladder sensations (P<0.01). There was no correlation between SSR and SEP. CONCLUSIONS: Spinal cord lesions frequently involve afferent tracts of SSR. Spinal afferents of SSR are closely related with tracts of bladder sensations and are different from pathways for SEP.

Adolescent↗
PubMed1988

Surgery for Wolff-Parkinson-White syndrome interrupts efferent vagal innervation to the left ventricle and to the atrioventricular node in the canine heart.

The hypothesis that cardiac surgery to interrupt accessory pathways also interrupts autonomic nerves to the canine ventricle and to the atrioventricular node was tested in four groups of dogs. Group 1 (n = 6) underwent dissection of the atrioventricular fat tissue and cryolesion created by application of a cryoprobe at -60 degrees C for 2 min along the lateral left atrioventricular groove, the same surgical procedure as carried out in patients with Wolff-Parkinson-White syndrome with accessory pathways located in the left ventricular free wall. Group 2 (n = 6) underwent dissection of the atrioventricular fat pad alone and group 3 (n = 6) dissection and cryolesion along the posterior left atrioventricular groove as performed in patients with Wolff-Parkinson-White syndrome with accessory pathways located in the posterior paraseptal area. Group 4 consisted of 11 non-operated control dogs. Four to 13 days after surgery the ventricular effective refractory period (ERP) was determined during bilateral ansae subclaviae stimulation (4 ms pulses, 2-3 Hz, and 2-3 mA), noradrenaline infusion (0.5 micrograms.kg-1.min-1), and bilateral vagal stimulation (4 ms pulses, 20 Hz, and current strength to induce asystole or complete atrioventricular block). Atrioventricular nodal conduction (AH interval) and spontaneous sinus cycle length were also determined in group 3 dogs. Ansae subclaviae stimulation and noradrenaline infusion shortened effective refractory period significantly at each left ventricular test site. The amount of effective refractory period shortening induced by ansae subclaviae stimulation did not differ among the test sites except for the posterior left ventricle in group 1 dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2006

Therapeutic effects of vagus nerve stimulation in epilepsy and implications for sudden unexpected death in epilepsy.

Vagus nerve stimulation (VNS) is a non-pharmacological therapy approved by the FDA for treatment of patients with partial-onset epilepsy. The most frequently encountered adverse effects typically occur during stimulation, are usually mild to moderate in severity, and resolve with reduction in current intensity or spontaneously over time. There are no apparent effects of VNS on vagally mediated visceral function. Though the precise mechanism of action of VNS remains unknown, available evidence suggests that central autonomic nervous system pathways are involved, which have also been implicated in sudden unexpected death in epilepsy (SUDEP). Studies to date of VNS and SUDEP are limited and do not conclusively show an association between VNS and SUDEP rates independent of other epilepsy-specific variables.

Anticonvulsants↗
PubMed1989

The C1 area of rostral ventrolateral medulla: a central site integrating autonomic responses to hemorrhage.

Activation of the sympathetic neurons and release of adrenomedullary catecholamines are the principal early reflex responses to hemorrhage. These are initiated by arterial baro- and chemoreceptors, from other cardiopulmonary receptors, and by intracerebral receptors responding to ischemia. A principal gateway for integrating the autonomic responses are a small collection of neurons in a region of the rostral ventrolateral medulla (RVL), containing a cluster of neurons of the C1 adrenergic cell group, the C1 area. Neurons in the C1 area of RVL project exclusively to autonomic nuclei of the spinal cord, are tonically active, and fire with a rhythm linked to the cardiac cycle. They are essential for maintaining resting discharge of sympathetic nerves and, consequently, arterial pressure (AP) and heart rate. They also are critical for reflex changes in AP in the baro- and chemoreceptor, somato-sympathetic (pain), and cerebral ischemic reflexes. Neurons of the C1 area are under tonic excitatory and inhibitory control by pathways from other autonomic centers. They are controlled by a range of neurotransmitters including, gamma aminobutyric acid (GABA), acetylcholine, catecholamines, enkephalin, and several neuropeptides. They also serve as a site of action for the hypotensive actions of several clinically important neurotransmitters. The C1-area of RVL may play a critical role in the autonomic responses to hemorrhage and may be an important target for drugs seeking to treat hemorrhagic shock.

Animals↗
PubMed1994

Vasopressin in the nucleus tractus solitarius: a modulator of baroreceptor reflex control of heart rate.

1. The main role of the nucleus tractus solitarius (NTS) as a relay center for viscerosensory fibers from the periphery and for pathways from modulatory autonomic centers is reviewed on the basis of its anatomical connections and neurotransmitter content. 2. Vasopressin is present in the entire neuroaxis and is of great importance in the control of cardiovascular function. The high endogenous content and receptor density, and the unique organization of vasopressin fibers projecting to the NTS are fundamental features for the modulatory effect exerted by vasopressin at the NTS on the baroreceptor reflex control of heart rate. 3. Vasopressinergic pathways from the paraventricular nucleus of the hypothalamus to the NTS constitute a physiological mechanism for the tonic maintenance of the baroreflex sensitivity and for displacing the heart rate response to higher values during increased activity, without changing the baroreflex sensitivity. This type of mechanism should play an important role in facilitating the tachycardic response during isotonic exercise.

Animals↗
PubMed2004

Induction and autoregulation of the anti-proneural gene Bar during retinal neurogenesis in Drosophila.

Neurogenesis in Drosophila eye imaginal disc is controlled by interactions of positive and negative regulatory genes. The basic helix-loop-helix (bHLH) transcription factor Atonal (Ato) plays an essential proneural function in the morphogenetic furrow to induce the formation of R8 founder neurons. Bar homeodomain proteins are required for transcriptional repression of ato in the basal undifferentiated retinal precursor cells to prevent ectopic neurogenesis posterior to the furrow of the eye disc. Thus, precise regulation of Bar expression in the basal undifferentiated cells is crucial for neural patterning in the eye. We show evidence that Bar expression in the basal undifferentiated cells is regulated by at least three different pathways, depending on the developmental time and the position in the eye disc. First, at the time of furrow initiation, Bar expression is induced independent of Ato by Hedgehog (Hh) signaling from the posterior margin of the disc. Second, during furrow progression, Bar expression is also induced by Ato-dependent EGFR (epidermal growth factor receptor) signaling from the migrating furrow. Finally, once initiated, Bar expression can be maintained by positive autoregulation. Therefore, we propose that the domain of Bar expression for Ato repression is established and maintained by a combination of non autonomous Hh/EGFR signaling pathways and autoregulation of Bar.

Animals↗
PubMed2000

Angiotensin peptides and baroreflex control of sympathetic outflow: pathways and mechanisms of the medulla oblongata.

The baroreceptor reflex is a relatively high gain control system that maintains arterial pressure within normal limits. To a large extent, this is accomplished through central neural pathways responsible for autonomic outflow residing in the medulla oblongata. The circulating renin-angiotensin system also contributes to the regulation of blood pressure, predominantly through its effects on the control of hydromineral balance and fluid volume. All the components of the renin-angiotensin system are also found in the brain. One of the principal products of the renin-angiotensin system cascade (brain or blood), angiotensin II, modulates the baroreceptor reflex by diminishing the sensitivity of the reflex and shifting the operating point for regulation of sympathetic outflow to higher blood pressures. This paper reviews our current knowledge about the neuronal pathways in the medulla oblongata through which angiotensin peptides alter the baroreceptor reflex control of sympathetic nerve activity. Emphasis is placed on the probable components and neural mechanisms of the medullary baroreflex arc that account for the ability of angiotensin peptides to change the sensitivity of the baroreceptor reflex and to shift the baroreceptor reflex control of sympathetic outflow to higher blood pressures in a pressure-independent manner.

Angiotensins↗
PubMed1995

Localization of NADPH-diaphorase activity in the salt gland of the saltwater-acclimated Pekin duck.

Exocrine secretion of the avian salt gland is controlled by the autonomic nervous system. NADPH-diaphorase histochemistry was employed at the light and electron microscopic level to provide the morphological basis for a putative nitrergic regulation of salt gland function. NADPH-diaphorase staining was localized in two cell populations of the parasympathetic secretory ganglion at high cell density and equal distribution throughout the ganglionic mass. In addition, salt gland-intrinsic neurons, arranged in small clusters and associated with major nitrergic fiber bundles, proved to be NADPH-diaphorase positive. These postganglionic nerve fibers innervated the secretory parenchyma in close proximity to the basal membrane of single secretory tubules as well as arterioles. The findings suggest participation of the nitrergic pathway in the autonomic control of avian salt gland function.

Adaptation, Physiological↗
PubMed2000

Neuronal propagation of HSV1 from the oral mucosa to the eye.

PURPOSE: To identify possible neuronal pathways leading to herpetic ocular disease after primary oral infection in mice. METHODS: The SC16 strain of herpes simplex virus (HSV)-1 (10(6) plaque-forming units) was injected into the mucocutaneous border of the left upper lip. Animals were killed 2 to 10 days postinoculation (DPI). Spread of the virus in neural structures was studied by immunochemistry. RESULTS: HSV1 first replicated at the site of inoculation and then at the superior cervical ganglion (at 2 DPI). The trigeminal ganglion and the facial nerve fibers were infected by 4 DPI. Infection of the ciliary body and iris occurred at 6 DPI, together with several brain stem nuclei belonging to the autonomic or sensory pathways. Between 8 and 10 DPI, the neural infection gradually cleared up, except for the ipsilateral sympathetic ganglion, and ipsilateral keratitis appeared in some animals. CONCLUSIONS: The pattern of viral dissemination in this mouse model suggests that infection of iris and ciliary body results from transfer of virus in the superior cervical ganglion from sympathetic neurons innervating the lip to neighboring neurons innervating the anterior uvea. Later, zosteriform spread of virus from the trigeminal system may have contributed to the clinical and histologic findings.

Animals↗
PubMed1998

Interaction between neuronal nitric oxide synthase and inhibitory G protein activity in heart rate regulation in conscious mice.

Nitric oxide (NO) synthesized within mammalian sinoatrial cells has been shown to participate in cholinergic control of heart rate (HR). However, it is not known whether NO synthesized within neurons plays a role in HR regulation. HR dynamics were measured in 24 wild-type (WT) mice and 24 mice in which the gene for neuronal NO synthase (nNOS) was absent (nNOS-/- mice). Mean HR and HR variability were compared in subsets of these animals at baseline, after parasympathetic blockade with atropine (0.5 mg/kg i.p.), after beta-adrenergic blockade with propranolol (1 mg/kg i.p.), and after combined autonomic blockade. Other animals underwent pressor challenge with phenylephrine (3 mg/kg i.p.) after beta-adrenergic blockade to test for a baroreflex-mediated cardioinhibitory response. The latter experiments were then repeated after inactivation of inhibitory G proteins with pertussis toxin (PTX) (30 microgram/kg i.p.). At baseline, nNOS-/- mice had higher mean HR (711+/-8 vs. 650+/-8 bpm, P = 0.0004) and lower HR variance (424+/-70 vs. 1,112+/-174 bpm2, P = 0.001) compared with WT mice. In nNOS-/- mice, atropine administration led to a much smaller change in mean HR (-2+/-9 vs. 49+/-5 bpm, P = 0.0008) and in HR variance (64+/-24 vs. -903+/-295 bpm2, P = 0.02) than in WT mice. In contrast, propranolol administration and combined autonomic blockade led to similar changes in mean HR between the two groups. After beta-adrenergic blockade, phenylephrine injection elicited a fall in mean HR and rise in HR variance in WT mice that was partially attenuated after treatment with PTX. The response to pressor challenge in nNOS-/- mice before PTX administration was similar to that in WT mice. However, PTX-treated nNOS-/- mice had a dramatically attenuated response to phenylephrine. These findings suggest that the absence of nNOS activity leads to reduced baseline parasympathetic tone, but does not prevent baroreflex-mediated cardioinhibition unless inhibitory G proteins are also inactivated. Thus, neuronally derived NO and cardiac inhibitory G protein activity serve as parallel pathways to mediate autonomic slowing of heart rate in the mouse.

Animals↗
PubMed2005

TWIN SISTER OF FT (TSF) acts as a floral pathway integrator redundantly with FT.

In Arabidopsis, several genetic pathways controlling the floral transition (flowering) are integrated at the transcriptional regulation of FT, LFY and SOC1. TSF is the closest homolog of FT in Arabidopsis. TSF expression was induced rapidly upon activation of CONSTANS (CO). The mRNA levels of TSF and FT showed similar patterns of diurnal oscillation and response to photoperiods: an evening peak, higher levels in long day (LD) than in short day (SD) conditions, and immediate up-regulation upon day-length extension. These observations suggest that TSF is a direct regulatory target of CO. tsf mutation delayed flowering in SD conditions and enhanced the phenotype of ft in both LD and SD conditions. TSF and FT also shared similar modes of regulation by FLC, an integrator of autonomous and vernalization pathways, and other factors such as EBS and PHYB. Consistently, TSF overexpression caused a precocious flowering phenotype independent of photoperiods or CO, or FLC. These observations suggest that TSF is a new member of the floral pathway integrators and promotes flowering largely redundantly with FT but makes a distinct contribution in SD conditions. TSF and FT seem to act independently of each other and of LFY, and partially upstream of SOC1. Interestingly, the expression patterns of TSF and FT in seedlings did not overlap, although both were expressed in the phloem tissues. Our work revealed additional complexity and spatial aspects of the regulatory network at the pathway integration level. We propose that the phloem is the site where multiple regulatory pathways are integrated at the transcriptional regulation of FT and TSF.

Arabidopsis↗
PubMed2002

Effects of a startle on heart rate in patients with multiple system atrophy.

The patient cooperation usually required for neurophysiological assessment of autonomic cardioregulatory function is difficult to obtain from patients with bradykinesia. A particularly interesting condition occurs in multiple system atrophy (MSA), which features both bradykinesia and autonomic dysfunction. Another characteristic of patients with MSA is their normal motor reaction to a startling stimulus. We used startle as a stimulus for testing autonomic cardioregulatory function in patients with MSA, thus avoiding the need for patient cooperation. In 10 healthy volunteers and 8 MSA patients, we recorded the electrocardiographic QRS complex with surface electrodes attached over the chest and delivered an acoustic startle stimulus after 8 seconds of baseline recording. We calculated the ratio between the pre-stimulus and the post-stimulus heart beat intervals (R-R ratio) by dividing the mean prestimulus R-R interval by the shortest R-R interval obtained within 10 seconds poststimulus. Healthy volunteers had a significant shortening of the R-R interval. The peak of the effect occurred after 2 to 5 seconds, with a mean R-R ratio of 1.14 (S.D. = 0.09). In contrast, R-R shortening was markedly reduced in patients, even though they had a normal motor response. The mean R-R ratio in patients was 1.03 (S.D. = 0.03), significantly lower than in healthy volunteers (P < 0.01). Our results demonstrate an abnormally reduced modulation of the heart beat frequency in patients with MSA, compatible with a dysfunction on pathways responsible for autonomic regulation. The method described here may be useful in the assessment of cardioregulatory function in poorly cooperative patients with normal startle responses.

Acoustic Stimulation↗
PubMed1992

Projections from the commissural subnucleus of the nucleus of the solitary tract: an anterograde tracing study in the cat.

The commissural subnucleus (COM) of the nucleus of the solitary tract (NTS) is known to receive primary afferents from the lungs and other viscera innervated by the vagus nerve, and thus to participate in central autonomic and respiratory control. The aim of the present study was to identify the areas of terminal arborizations of COM neurons in order to examine brainstem sites which may be involved in reflex responses mediated by these neurons. The projections were studied in cats, using biocytin as an anterograde tracer. Labeled fibers and terminal boutons were visualized by horseradish-peroxidase histochemistry, 2-3 days after microinjection of the tracers into the COM 1-2 mm caudal to the obex. Labeled axons were examined in the brainstem from the rostral pons to the caudal medulla and were found bilaterally, with an ipsilateral predominance, mainly in the following regions: (1) The dorsolateral rostral pons. Terminal boutons were observed in the lateral and medial parabrachial nuclei, Kölliker-Fuse nucleus, and around the mesencephalic trigeminal tract. This area corresponds to the pontine respiratory group also known as the "pneumotaxic center." (2) The pontine area dorsolateral to the superior olivary nucleus. This region contains the A5 noradrenergic cell group; (3) Near the ventral surface, below the facial nucleus. This area overlaps with the 'retrotrapezoid nucleus.' (4) Respiration-related areas of the medulla, including the dorsal and ventral respiratory groups, and the Bötzinger complex. (5) The dorsal motor nucleus of the vagus. These results suggest that the COM is involved in reflex arcs, which have both respiratory functions and autonomic functions. The pathway to the dorsolateral pons, which has been identified in our recent electrophysiological study is likely to play a role in mediating respiratory responses from pulmonary rapidly adapting receptors. Other pathways may represent additional projections from second-order neurons receiving input from this group of lung receptors, or projections from as yet unidentified neurons that relay information from different afferents terminating in the COM.

Animals↗
PubMed2001

A case of primitive floor of the mouth paraganglioma in a child: an embryological theory unifying viscerocranium appended paragangliomas.

BACKGROUND: Paragangliomas are unusual tumors in the head and neck originating from the paraganglia or glomus cells of neural crest origin. METHODS: We describe the first case of a primitive paraganglioma of the floor of the mouth presenting in childhood. RESULTS: Complete surgical removal was performed after embolization of the left lingual artery. There was no evidence of either persistent or recurrent disease 5 years after surgery. The embryologic and anatomic origins of head and neck paragangliomas are reviewed. CONCLUSIONS: An embryologic theory based on the common neural crest origin and migration pathways of both autonomic viscerocranium appended ganglias and paragangliomas is proposed that unifies the topographically heterogeneous group of viscerocranium-appended paragangliomas.

Child↗
PubMed1998

[Pain syndromes with causal participation of the sympathetic nervous system].

The efferent sympathetic nervous system is organized into subsystems that innervate and regulate via separate peripheral sympathic pathways the different autonomic target organs. This review discusses mechanisms through which this efferent system may be causally involved in the generation of pain. Clinical pain syndromes in which this may be the case are "complex regional pain syndromes" (CRPS) type I (previously reflex sympathetic dystrophy) and type II (recently causalgia). The "sympathetically maintained pain" (SMP) is a symptom (and not a clinical entity) that can principally also be present in other pain syndromes. An explanatory hypothesis, which may explain the clinical phenomenology of CRPS (different types of pain, swelling, autonomic, motor and trophic changes) and the mechanisms involved, is described and discussed. This hypothesis consists of different components that either have been tested and verified experimentally or which are still hypothetical. The hypothesis consists of changes in the primary afferent (nociceptive and non-nociceptive) neurones (sensitization, ectopic impulse generation) and of the neurones in the spinal cord (preferentially in the dorsal horn) which are secondary consequences of the changes in the primary afferent neurones ("central sensitization"). These changes are not specific for SMP. The centerpiece of the hypothesis is a positive feedback circuit that consists of the primary afferent neurones, spinal cord neurones, sympathic neurones and the pathologic sympathetic-afferent coupling. This coupling can occur directly via noradrenaline (or possibly another substance) at different sites of the afferent neurone (at the lesion site, remote from the lesion site in the periphery and in the spinal ganglion). The direct coupling requires that the afferent neurone expresses adrenoceptors. Indirect coupling can occur via the vascular bed or otherwise, e.g. by changes of the neurovascular transmission. The activity in the sympathetic neurones to the affected extremity can change. This change does not consist of a generalized increase of sympathetic activity but of a change of the reflexes (e.g., thermoregulatory and nociceptive reflexes). From this follows that the pathophysiologal processes operating in CRPS may occur at four levels of integration that interact with each other: effector organ, peripheral afferent and sympathetic neurone, spinal cord, supraspinal centres. Recent experimental investigations on rats show that the sympathetic nervous system is possibly also causally involved in the generation of inflammation and inflammatory pain. The mechanisms by which this occurs are different from those operating in SMP during CRPS.

Animals↗