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Bulbocavernosus reflex in patients with conus medullaris and cauda equina lesions.

The clinical value and practical application of the electrically induced BC reflex was investigated in 40 patients with traumatic or compressive lesions of the conus medullaris or cauda equina. It was shown that the BC reflex was either absent or delayed depending upon the invovlement of the sacral 2--4 spinal and radicular segments. The latency of the BC reflex was normal in patients with mainly epiconus and lumbar cord involvement. The loss of the BC reflex in the acute period of traumatic lesions was an adverse prognostic sign while the presence of the reflex whether or not delayed, indicated a more benign final outcome of sphincter and sexual reflex disturbances. In chronic progressive compression, the latency of BC reflex was often delayed.

Cauda Equina↗

Differential age-dependent attenuation of reflex tachycardia by verapamil in rats.

To determine if verapamil alters baroreflex function differently depending on age, reflex heart rate responses to intravenous infusions of phenylephrine or sodium nitroprusside were compared in conscious 5- and 14-month-old rats before and after daily oral administration of verapamil (100 mg/kg) for 6 days. The effects of verapamil on parasympathetic and sympathetic mediation of heart rate were also assessed by repeating baroreflex tests after treatment with either propranolol or atropine. All reflex heart rate responses were initially smaller in 14- than in 5-month-old rats. Regardless of age, magnitude of reflex bradycardia or the effects on it of either cholinergic or beta-adrenergic blockade, were unaffected by verapamil. By contrast, reflex tachycardia which was attenuated in both age groups, was decreased further by subsequent cholinergic or beta-adrenergic blockade in 5-month-old rats, but only by cholinergic blockade in 14-month-old rats. These findings suggest that while verapamil did not affect autonomic mediation of reflex bradycardia, it reduced that of reflex tachycardia differently depending on age. Whereas it attenuated both sympathetic and parasympathetic mediation of reflex tachycardia in 5-month-old rats, it attenuated only sympathetic mediation in 14-month-old rats.

Aging↗

Sympathetic responses evoked by vestibular stimulation and their interactions with somato-sympathetic reflexes.

In chloralose anesthetized cats mass reflex discharges of the renal sympathetic nerve were recorded following stimulations of low threshold, large myelinated afferents in vestibular and superficial peroneal nerves. Reflex responses caused by stimuli applied to both nerves were quite similar; a brief excitatory phase was followed by a long inhibitory phase or "silent-period'. Decerebration did not have any appreciable effects on either reflex but decerebellation (in addition to decerebration) greatly increased the excitatory response and shortened the inhibitory phase or "silent period' of the vestibulo-sympathetic reflex. The somato-sympathetic reflex response however, was not much altered by this procedure. When a vestibular nerve stimulus, given as a conditioning shock, preceded a testing stimulus applied to the cutaneous nerve by less than 300 msec, the test response was completely inhibited. The "recovery curve' of this conditioning--testing response showed that after decerebellation the inhibitory effect of vestibular conditioning stimulus on testing response was much reduced. The autonomic effector responses, blood pressure, heart rate and galvanic skin reflex (GSR) following low intensity stimulation of vestibular and cutaneous nerves were also studied. Repetitive stimulations applied to either nerves evoked a depressor response kand augmented GSRs but caused no significant changes in heart rate. Decerebellation reduced the depressor response produced by repetitive stimulation of vestibular nerves. The study indicates that vestibular nerves, as well as cutaneous afferents, which are powerful imputs for evoking somatic reactions, also elicit autonomic reflexes and that similarity and interactions between sympathetic reactions evoked by these two inputs suggest a common central mechanism.

Animals↗

Effects of dopaminergic agonists on somato-autonomic reflexes.

In cats lightly anesthetized with urethane (600 mg/kg, i.p.) reflexes of the blood pressure (BP) and of the nictitating membrane (NM) were elicited by stimulation of the sciatic nerve (16 V, 0.3 ms, 1-128 Hz, 2 s or 2 min) prior to and after the administration of apomorphine (0.05-0.2 mg/kg, i.v.) or piribedil (0.4-1.0 mg/kg, i.v.). In case of short-train (2 s) stimulation, both dopaminergic agonists shifted the frequency-response curves of NM contractions to the right, i.e. depressed NM reflexes in the entire range of the stimulation frequencies applied. At the same time, BP reflexes were depressed only in the range of lower frequencies (1-4 Hz). At higher rates (32-128 Hz) BP reflexes were potentiated. The reactions of BP to sustained (2 min) stimulations displayed a flat pressor plateau in response to lower-frequency stimulation, and a two-component pattern (an initial pressor peak followed by a plateau) to the higher-frequency one. Compatibility with the effects seen to short-train stimulations, the dopaminergic agonists prolonged the rise-time and augmented the amplitude of the initial pressor peak to sustained stimulations with lower and higher frequencies, respectively. The plateau of the pressor response to higher frequencies was depressed by higher doses (greater than 0.4 mg/kg) of piribedil. Administration of haloperidol (0.05-0.2 mg/kg, i.v.) resulted only in a partial restoration of the reflexes of BP and NM. The manifold effects of dopaminergic agonists on the somato-autonomic reflexes studied support the thought than NM and BP reflexes are organized, at least partially, in different ways.

Animals↗

The aortic nerve-sympathetic reflex in the rat.

The effects of stimulation of aortic nerve A- and C-fibers on the renal and cardiac sympathetic nerve activities in anesthetized and immobilized Sprague-Dawley rats were investigated. A separate aortic nerve was found in 46 rats (90%) out of 51. Activation of A- and C-fiber groups, alone or in combination, resulted in an inhibition of renal and cardiac nerve activities. However, an excitatory component preceding the inhibitory component, representing the reflex response to stimulation of non-barosensory afferent fibers contained in the carotid sinus or aortic nerve, was never observed. This result provides electrophysiological evidence supporting the view that the rat's aortic nerve does not contain a significant amount of functionally active non-barosensory afferents. As with the aortic nerve reflex in the rabbit and cat, the sympatho-inhibitory action of C-fibers was more powerful and longer-lasting than that of A-fibers. Furthermore, the C-fiber reflex was elicited at stimulus frequencies as low as 2 Hz. No significant difference was found between the reflex response of cardiac and renal nerves. On the other hand, stimulation of the superior laryngeal nerve, which constitutes an important pathway carrying arterial baroreceptor fibers, caused a reflex sympathetic response typically consisting of excitatory and inhibitory components. Thus, the rat's aortic nerve provides a useful experimental means to activate selectively central neural structures associated with barosensory afferents and to elicit the reflex response homologous to that in the arterial baroreceptor reflex in rabbits and cats.

Animals↗

Effect of spontaneous exercise on reflex slowing of the heart in decerebrate cats.

Exercise has been shown to reduce the ability of the baroreflex to slow the heart, and signals arising from cerebral cortex may cause this reduction. To test whether signals arising from the cerebral cortex are required to cause this inhibition, reflex slowing of the heart was assessed in decerebrate cats during rest and spontaneous walking. This reflex was quantified by the relation between systolic blood pressure and the subsequent heart beat interval or its inverse, beat to beat heart rate, during transient rises in pressure caused by injections of phenylephrine. Reflex slowing of the heart was reduced during spontaneous exercise compared to rest. Exercise may inhibit reflex cardiac slowing by activating beta-adrenoceptors that inhibit vagal effects on the heart. To test whether activation of beta-adrenoceptors caused the inhibition of reflex cardiac slowing produced by spontaneous walking in these decerebrate cats, the ability of the baroreflex to slow the heart during blockade of beta-receptors by propranolol was tested in 3 cats. Propranolol did not abolish the inhibitory effect of spontaneous walking on this reflex. These data indicate that the cerebral cortex and beta-adrenoceptors are not required for exercise to inhibit reflex cardiac slowing.

Animals↗

Viscero-sympathetic reflex responses to mechanical stimulation of pelvic viscera in the cat.

Viscero-sympathetic reflex responses to mechanical stimulation of urinary bladder and colon were studied in cutaneous vasoconstrictor (CVC) neurones supplying hairy skin, in muscle vasoconstrictor (MVC) neurones supplying skeletal muscle and in sudomotor (SM) neurones supplying the sweat glands of the central paw pad of the cat hindlimb. The cats were anaesthetized, paralysed and artificially ventilated. The vasoconstrictor activity was recorded from the axons of the postganglionic fibres that were isolated in filaments from the respective peripheral hindlimb nerves. The activity in the sudomotor neurones was monitored by recording the fast skin potential changes occurring on the surface of the central paw pad. Afferents from the urinary bladder and from the colon were stimulated by isotonic distension and isovolumetric contraction of the organs. Most CVC neurones with ongoing activity were inhibited by these stimuli; only a few CVC neurones were excited. The MVC and SM neurones were generally excited by the visceral stimuli, yet the size of the evoked skin potential changes was variable. The reflex responses elicited in the sympathetic outflow to the cat hindlimb by stimulation of visceral afferents from the pelvic organs are uniform with respect to the different types of afferent input system but differentiated with respect to the efferent output systems. Graded stimulation of the visceral afferents from the urinary bladder by isotonic pressure steps elicited graded reflex responses in CVC (threshold less than 30 mmHg) and MVC neurones (threshold less than 20 mmHg) and a graded increase of the arterial blood pressure (threshold less than 20 mmHg). These graded reflex responses are closely related to the quantitative activation of sacral afferent neurones with thin myelinated axons innervating the urinary bladder that are also responsible for eliciting the micturition reflex, but not to the quantitative activation of sacral afferent neurones with unmyelinated axons. The latter have thresholds of 40-50 mmHg intravesical pressure at which the size of the vesico-sympathetic reflexes in the vasoconstrictor neurones was about 50% of maximal size. This does not exclude the fact that activation of unmyelinated vesical afferents contributes to the vesico-sympathetic reflexes.

Animals↗

Reflex interaction from the urinary bladder and the rectum on anal motility in the cat.

The intrinsic recto-anal inhibitory reflex (RAIR) and the extrinsic vesico-anal excitatory reflex were studied in anaesthetized cats in order to explore the nervous components of anal pressure regulation. The magnitude of the RAIR was documented at varying levels of anal pressure. Minimal anal pressure during RAIR was positively correlated to anal pressure immediately prior to rectal distension. It was possible to elicit the vesico-anal excitatory reflex concomitantly with an ongoing RAIR. It was also possible to elicit a RAIR during the vesico-anal excitatory reflex. The magnitude of the pressor reflex response was not changed by concomitant activation of the inhibitory reflex and vice versa. This suggests an independent action on the internal anal sphincter (IAS) of the two reflexes. Spontaneous detrusor contractions were abolished by rectal distension. However, an escape phenomenon from this inhibition was observed, suggesting a spinal, associative, connection. The results support the concept of a direct action of both extrinsic and intrinsic nervous mechanisms on the smooth muscle of the IAS.

Anal Canal↗

Influences of the sympathetic and parasympathetic nerve transection on cardiovascular reflexes induced by volleys in the IXth nerve fibers of rat.

The effect of vagotomy and sympathectomy on cardio-acceleratory and arterial hypertensive reflexes evoked by electrical stimulation of the rat glossopharyngeal (IXth) nerve was studied in relation to changes in baseline heart rate and arterial blood pressure. Uni- and bi-lateral transection of the cervical vagal trunk brought about augmentation of baseline heart rate, accompanied by a depression in reflex tachycardia; the amount of depression being inversely related to that of an increase in baseline heart rate. The latter increased more after a right vagotomy than after a left vagotomy. No appreciable change in reflex hypertension as well as in baseline blood pressure was observed by different types of vagotomy. For unilateral sympathectomy, semilunar cordotomy caudal to the obex was performed. It was found that right semilunar cordotomy significantly depressed the magnitude of cardio-acceleratory and arterial hypertensive reflexes in association with a significant decrease in baseline heart rate, though there was a less pronounced decrease in baseline blood pressure. The result obtained by a left semilunar cordotomy was similar to that of a right semilunar cordotomy, except that the decrease in reflex tachycardia was very small and statistically insignificant. Thus, the efferent activities in vagus and sympathetic nerves were more effective on the right than on the left side, in modifying reflex tachycardia and baseline heart rate, whereas, right and left sympathetic efferent outflows were equally effective in depressing the reflex increase in blood pressure.

Animals↗

Asymmetry and time-course of cutaneous sympathetic reflex responses following sustained excitation of chemosensitive nociceptors in humans.

Sympathetic reflex responses were elicited in human volunteers by sustained selective excitation of nociceptors by noxious chemicals, namely topical application of mustard oil which elicited burning pain, or histamine which induced itching in a skin area of 5 cm2 on the volar aspect of one forearm. Stimulus-related sympathetic reflex responses were studied by means of computer-assisted infrared thermography of the palmar aspects of both hands. Nociceptive stimulation induced a decrease of skin surface temperature in both hands interpreted as vasoconstriction. The magnitude of the reflex cooling was correlated with the magnitude of the sensation (r = 0.49), but independent of the quality of sensation (itch or pain). The temperature reduction was maintained for more than 30 min and its time-course matched the time-courses of pain or itch sensations. It is concluded that the sustained and selective excitation of nociceptors elicits a sustained sympathetic reflex response, which adapts very slowly. The time-course of the reflexes suggests that these are not arousal responses, but may be indicators of nociceptive processing in conscious humans. Contralateral temperature decreases were consistently smaller than ipsilateral ones. Thus, sustained nociceptive-specific vasoconstrictor reflexes may be somatotopically organised with an emphasis on areas close to the painful stimulus (homotopic), which has so far only been shown in animals. The study thus demonstrates for the first time in humans the presence of a sympathetic reflex asymmetry, which is specific for nociceptive afferent input.

Adult↗

Analysis of the forelimb crossed extension reflex in thalamic cats during stepping.

Forelimb crossed extension reflexes were examined in 22 thalamic cats. These reflexes were elicited either by backward passive movement or by repetitive electrical stimulation of cutaneous and joint afferent nerves in the contralateral forelimb. Single stimulation of the superficial radial nerve evoked two types of reflex responses--early (ER) and late (LR)--from the triceps brachii muscle on the contralateral side. The latencies were about 7 and 16-25 ms, corresponding to the propriospinal (PSR) and spino-bulbo-spinal (SBS) reflexes of the ipsilateral flexor, respectively. Repetitive stimulation of the superficial radial nerve evoked the LR but not the ER. The crossed extension reflex and LR were abolished by lesions of the dorsolateral funiculus of the cervical cord on the side opposite to the recording. The tonic EMG activity, crossed extension reflex and LR in the extensor on the side of lesions were abolished by lesions of the ventrolateral funiculus of the cervical cord. During forelimb stepping, the amplitudes of both ER and LR fluctuated depending on the phase of the step cycle. The ER appeared during a narrow period in the early phase of the stance, whereas the LR was observed during a wide period from the middle of the swing to the middle of the stance. Both responses were absent from the middle of the stance to the middle of the swing. These observations suggest that forelimb crossed extension reflexes involve both spinal and supraspinal (SBS) loop mechanisms, and that these are utilized during stepping, with the latter mechanism in particular playing an important part in the extension phase of the forelimb forward movement.

Afferent Pathways↗

Impaired scaling of long latency postural reflexes in patients with Parkinson's disease.

Young normal subjects adapt the size of posturally stabilizing reflexes in the lower extremity to predictable and unpredictable perturbations through shifts in cognitive set. It is unknown whether limitations in this ability to shift cognitive set may contribute to impaired scaling of postural reflexes in patients with Parkinson's disease. In this study, we have addressed this issue in 12 posturally unstable Parkinson patients and 13 age- and sex-matched controls. Postural stability was disturbed by sudden toe-up rotations of a supporting platform upon which subjects were standing. Subjects' cognitive set was altered by varying the perturbation amplitude either predictably (serial 4 degrees versus serial 10 degrees) or unpredictably (random mixture of 4 degrees and 10 degrees). Posturally stabilizing long latency (LL) reflexes were recorded from the shortened tibialis anterior muscle of both legs. We found that Parkinson patients, unlike some control subjects, were unable to scale the size of their LL reflex in response to variations in perturbation amplitude during predictable conditions. In addition, we observed that Parkinson patients could not modify the amplitude of the LL reflex through alterations in cognitive set during random conditions. We conclude that Parkinson patients have a fundamental difficulty in modifying the size of posturally stabilizing LL reflexes, as reflected by both problems with amplitude scaling and difficulties with changes in cognitive set. It is possible that this inability to modify LL reflexes may be a factor contributing to postural instability in Parkinson's disease.

Adult↗

Analgesic-antiinflammatory drugs inhibit orbicularis oculi reflexes in humans via a central mode of action.

1. A cross-over single blind study examined the possible central effects of non-opioid analgesic drugs on the trigeminal reflexes. 2. The corneal reflex and blink reflex (R1, R2) were recorded electromyographically and response areas measured in healthy volunteers before and after intramuscular injection of piroxicam (40 mg); and after intravenous injection of lysine acetylsalicylate (500 mg). After the last drug recording the subjects received intravenous naloxone (2 mg) followed 5 minutes later by further reflex testing. Saline was used as a placebo in control experiments. 3. Both analgesics reduced the corneal reflex: piroxicam induced a 27% and lysine acetylsalicylate a 21% a reduction that naloxone did not reverse. Neither drug reduced the early or the late component of the blink reflex. 4. The marked inhibitory changes that the two non-narcotic analgesics produced on the corneal reflex--a nociceptive response--indicate a centrally-mediated action. 5. Naloxone's failure to reverse the induced analgesia argues against opiate receptor mediation.

Adult↗

The effects of age and attention upon reflex inhibition.

Previous research has suggested that reflex amplitude may be influenced by the direction of attention. The purpose of this investigation was to evaluate the effects of an attention-demanding visual reaction time task upon the elicitation of reflexes and modification of reflexes by an antecedent prestimulus in young and elderly adults. In young subjects, eyeblink inhibition was augmented by the task, yet there was no effect upon overall reflex amplitude. Elderly subjects showed no effect upon reflex inhibition while overall reflex amplitude was diminished by the task, independent of the amount of inhibition. In young subjects, the prestimulus also accentuated the initial decelerative component of a biphasic heart rate response. The reaction time task also served to augment this deceleration. The elderly heart rate response was not affected by the experimental conditions. These results provide evidence that reflex inhibition is modulated by attention. However, the relationship is complex, developmentally sensitive, and involves generalized attentive processes as well as selective attention toward specific stimuli or sensory modalities.

Adolescent↗

Types of afferents from the knee joint evoking sympathetic reflexes in cat inferior cardiac nerves.

In anesthetized cats electrical stimulation of the medial articular nerve of the knee joint evoked sympathetic reflex discharges in inferior cardiac nerves. Low intensity single stimuli elicited early reflex discharges (A-reflexes, latency 70-90 ms, duration 110-200 ms) whereas short tetanic stimulation at higher intensities evoked, in addition, late reflexes (C-reflexes, latency 390-480 ms, duration 230-400 ms). An analysis of the relation between the conduction velocity and the electrical threshold of 231 single medial articular nerve fibers revealed that the A-reflex is mainly due to activation of Group II units, whereas the C-reflex is evoked by activity in unmyelinated Group IV fibers.

Animals↗

Memory traces in spinal cord produced by H-reflex conditioning: effects of post-tetanic potentiation.

Operant conditioning of the wholly spinal, largely monosynaptic triceps surae H-reflex in monkeys causes changes in lumbosacral spinal cord that persist after removal of supraspinal influence. We evaluated the interaction between post-tetanic potentiation and these memory traces. Animals in which the triceps surae H-reflex in one leg had been increased or decreased by conditioning were deeply anesthetized, and monosynaptic reflexes to L6-S1 dorsal root stimulation were recorded before and after tetanization from both legs for 3 days after thoracic cord transection. Animals remained anesthetized throughout and were sacrificed by overdose. Reflex asymmetries consistent with the effect of H-reflex conditioning were present after transection and persisted through the 3 days of study. Tetanization affected conditioned leg and control leg reflexes similarly. This finding suggests that, while post-tetanic potentiation and probably H-reflex conditioning alter Ia synaptic transmission, the two phenomena have different mechanisms.

Animals↗

Relation between electromyogram and torque of isometric reflex contractions in man.

Human subjects maintained isometric plantar or dorsal flexions of the ankle in a matching task. H-reflexes of different sizes were superimposed on the steady activity. The peak-to-peak amplitude of the reflexes was measured on the electromyogram (EMG) of the soleus muscle. The size of the corresponding muscle contractions was determined on the isometric torque signal in relation to the maintained flexion force. The EMG-torque relation which was defined as the reflex muscle contraction as a function of the EMG reflex signal approximated a square root function for a given steady contraction level. It was not modulated by steady dorsal flexions, but it decreased continuously with stronger plantar steady torques. This dependence was caused by the silent period following the reflex discharge. Since the reflex discharge and the silent period were near in time to the duration of the contraction, the silent period had a direct effect on the reflex contraction amplitude.

Electromyography↗

Excitatory and inhibitory A- and C-reflexes in pelvic parasympathetic efferent nerves elicited by single shock to A and C afferent fibers of perineal and limb somatic nerves in anesthetized rats.

The effects of single electrical shocks to myelinated A and unmyelinated C afferent fibers of perineal and limb somatic nerves on the reflex discharges in pelvic parasympathetic (L6/S1) efferent nerves to the bladder were examined in anesthetized central nervous system (CNS)-intact and acute spinal rats. When the bladder was empty, stimulation of perineal somatic inputs to the L6 and S1 segments from the perineo-femoral branch of a pudendal nerve produced excitatory A- and C-reflex discharge components in postganglionic parasympathetic efferent nerve branches on the bladder surface. When the bladder was expanded and pelvic efferent neurons were rhythmically active, additional inhibitory A- and C-reflex components could be seen. After acute spinal transection, the same stimuli elicited excitatory A- and C-reflex discharges of similar latency as those observed before the spinal transection, but were of larger amplitude and longer duration; resting activity in the pelvic nerve was low, and no evoked inhibitory reflex components could be observed. Electrical stimulation of afferents in the tibial nerve had no effect when the bladder pressure was low, but when the bladder was distended, early and late components of reflex inhibition and excitation of parasympathetic activity were visible in CNS-intact rats; these reflex responses were abolished following spinalization.

Anesthesia↗