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Recovery from axial apraxia in the lateral hypothalamic labyrinthectomized rat reveals three elements of contact-righting: cephalocaudal dominance, axial rotation, and distal limb action.

In earlier work, we showed that in rats, proprioceptive-tactile information is sufficient for contact-righting on the ground (from lying on one side to prone). Thus, axial rotation, starting with the shoulders and followed by the pelvis, occurs normally in labyrinthectomized animals with eyes occluded. After damage to the lateral hypothalamus, even with labyrinths intact, contact-righting is at first abolished (1-2 days postoperatively), and when it reappears, involves pushing by the hindlegs. Rostrocaudal contact-righting, involving axial rotation, takes 3-4 days to recover. If labyrinthectomy is combined with lateral hypothalamic damage, the deficit is exaggerated and recovery is greatly slowed down, now requiring 2-3 weeks. The present paper shows that during this prolonged period of recovery several transitional forms of righting are present, each produced by a different combination of limb and body axis movements. At first, axial rotation is absent, and righting is achieved only by pushing with the limbs. This is followed by a transitional form in which, even though axial rotation cannot be triggered directly by contact with the ground, it can be triggered indirectly as an allied reflex when the paw places on the ground. Eventually the body axis actively initiates the rotation to proneness (at first, in the pelvis, later in recovery, in the shoulders), with the limbs being carried. Recovery of axial rotation overlaps with the recovery of cephalic dominance, yielding complex intermediate forms of righting.

Animals↗

Postural sway characteristics of the elderly under normal and altered visual and support surface conditions.

One of the most pervasive findings in the literature on the aged is the general slowing of cognitive-motor responses with advancing age. Hence, an increased slowness in the processing of information from vestibular, visual, and somatosensory systems could contribute greatly to a decline in postural stability. To examine this question, in a cross-sectional investigation, postural sway behavior of elderly (n = 18) and young (n = 10) adults was examined under conditions that stressed the slower integrative mechanisms rather than the reflexive mechanisms of postural control. The postural sway behavior of young and elderly subjects was examined for a prolonged duration (80 s), under altered visual and/or support surface (5 cm thick foam surface) conditions, and contrasted with normal stance. Results showed that the exclusion or disruption of one of the sensory inputs, alone, was not consistently sufficient to differentiate between elderly and young adults, because of compensation by the remaining sensory sources. Both alterations together (i.e., visual and surface), however, had a substantially greater effect upon the elderly than the young.

Adult↗

Rhythmic modulation of the responsiveness of locust sensory local interneurons by walking pattern generating networks.

1. Spiking local interneurons in the thoracic ganglia of the locust are known to process mechanosensory information from leg receptors and to contribute to postural reflexes. It is not clear, however, whether these interneurons are also involved in the control of leg movement during walking or whether their role in mediating local reflexes is phasically modulated by the walking pattern generating networks. To address these questions, intracellular recordings from spiking local interneurons in a midline population were made both in a "fictive walking" preparation reduced to isolated thoracic ganglia and in semi-intact locusts walking on a treadwheel. 2. In fictive walking (and therefore deafferented) preparations, rhythmic synaptic inputs were observed in 72% of the sampled local interneurons. These inputs resulted in a modulation of the interneurons' firing rate in phase with the centrally generated rhythm. A similar rhythmic drive was seen in spiking local interneurons recorded from semi-intact walking locusts. This drive persisted after amputation of the leg from which the interneurons received their sensory inputs. These results indicate that this population of interneurons receives inputs from central networks that participate in the generation of walking. 3. In fictive walking preparations where a hindleg was left attached to its segmental ganglion, individual local interneurons could be characterized physiologically by their receptive field properties. The central inputs were found to modulate the activity of members of all subclasses of interneurons (i.e., purely exteroceptive, purely proprioceptive, and with mixed receptive fields. The mode of modulation observed could oppose or assist the effect of sensory input expected to occur during normal walking.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

[Physiologic analysis of the effect of micropolarization on trace processes].

In chronic experiments on cats a conditioned reflex to time was elaborated by means of periodic passive liftings of one extremity during continuous subthreshold pressor stimulation of the same limb or during micropolarization of the contralateral sensorimotor cortical with a 0,2--1,8 mca current. In animals conditioned during pressor stimulation, trace motor reactions appeared in response to the stimulation or to micropolarization of the sensorimotor cortex and of several subcortical structures. In animals conditioned during micropolarization, trace motor responses were obtained both to sensorimotor cortex polarization and to pressor stimulation of the "conditioned" leg. The authors suggest a common physiological mechanism of the phenomena observed.

Animals↗

Presence of sensory nerve corpuscles in the human corpus and cervix uteri during pregnancy and labor as revealed by immunohistochemistry.

BACKGROUND: The uterus is exposed to changes such as enlargement and distension during pregnancy and labor. In these processes and in the process of cervical ripening, proprioceptive information is likely to be of great importance. Therefore, we wanted to study the possible existence of sensory nerve corpuscles in uterine corpus and cervix during pregnancy and labor. Studies on this aspect have not previously been perfomed. METHODS: Biopsies were taken from the upper edge of the hysterotomy during caesarean section at term (n = 8), in labor (n = 5) and from the corresponding area in the non-pregnant uterus after hysterectomy (n = 7). Cervical biopsies were obtained transvaginally from the anterior cervical lip. Serial cryostat sections were prepared for immunohistochemistry using polyclonal antibodies against nerve growth factor receptor p75, protein gene product 9.5 and S-100. RESULTS: Structures with the characteristics of sensory nerve corpuscles were observed in several specimens after staining for p75, PGP 9.5 and S-100. They were observed in specimens of the non-pregnant corpus and cervix and also in specimens of the pregnant cervix before onset of labor. However, they were absent in all specimens during labor. CONCLUSION: Sensory corpuscles have here for the first time been detected in the human corpus and cervix uteri. Studies on the importance of the corpuscles in relation to the protective reflex actions that occur in the uterus during pregnancy should be performed in the future.

Adult↗

A case of congenital non-progressive sensory neuropathy with tonic pupils.

One case of a non-progressive congenital neuropathy is reported. Clinical findings included subtotal analgesia, and diminished temperature, vibration and proprioceptive sense in arms and legs. The sensory nerve action potentials were absent. Autonomic dysfunctions were restricted to tonic pupils. Sural nerve biopsy taken at the age of 8 1/2 showed fascicular hypoplasia, subtotal loss of myelinated nerve fibers and severe loss of unmyelinated nerve fibers with a pathological size distribution. In the skin biopsy, including several cutaneous nerves, no myelinated nerve fibers were present, the unmyelinated nerve fibers were severely reduced and the collagen density was increased. Perivascular and periglandular innervation was significantly reduced. The findings in this case are suggestive of a malformative or fetally acquired lesion and further illustrate the difficulties in classification of the hereditary sensory neuropathies.

Child↗

Serotonergic/cholinergic muscle receptor cells in the crab stomatogastric nervous system. II. Rapid nicotinic and prolonged modulatory effects on neurons in the stomatogastric ganglion.

1. The gastropyloric receptor (GPR) cells, which are described in the preceding paper, are a set of proprioceptive cells in the crabs Cancer borealis and Cancer irroratus that contain serotonin (5-hydroxytryptamine, 5-HT) and choline acetyltransferase. These cells have a variety of synaptic effects on cells in the stomatogastric ganglion (STG). We used pharmacologic methods to distinguish the effects that were due to acetylcholine (ACh) from those that could be due to serotonin. 2. The GPR cells evoke excitatory postsynaptic potentials (EPSPs) in two gastric mill motor neurons [lateral and dorsal gastric (LG and DG)] in the stomatogastric ganglion. The EPSPs exhibit nicotinic pharmacology, indicating that they may be due to the release of ACh from the GPR cells. 3. A train of GPR action potentials induces plateau potential properties in the DG motor neuron. This plateau potential induction is not blocked by nicotinic or muscarinic antagonists, suggesting it might be due to serotonin released from the GPR cells. Bath-applied serotonin induces a tonic depolarization of DG with high-intensity spiking. 4. In the accompanying paper, it is shown that DG-evoked muscle contraction leads to the excitation of GPR2 through mechanical coupling of the muscles. Because GPR2 also excites DG, a positive feedback loop exists between GPR2 and DG. This reflex loop may be involved in the control of the medial tooth of the gastric mill. 5. GPR stimulation initiates or enhances rhythmic pyloric cycling. This is due at least in part to a direct enhancement of bursting in the pyloric dilator/anterior burster (PD/AB) pacemaker cell group and can outlast the period of GPR stimulation by up to 1 min. GPR-induced PD burst enhancement continues in the presence of nicotinic and muscarinic antagonists, indicating that the effect is probably not due to the release of ACh. Bath application of serotonin mimicks the neuromodulatory effect of GPR stimulation on the PD/AB group by inducing or enhancing bursting. 6. Thus the GPR cells elicit at least three different synaptic actions in the stomatogastric ganglion: 1) classical, fast nicotinic cholinergic EPSPs that may be important for reflex functions in the gastric mill; 2) noncholinergic, cycle-by-cycle plateau potential induction that might be critical for the timing and operation of the gastric mill, and 3) prolonged, noncholinergic burst enhancement in pyloric neurons that is mimicked by serotonin, lasts many cycles, and may act to assure that the pyloric central pattern generator (CPG) is activated and cycling strongly.

Animals↗

Edentulousness and neuroleptic-induced neck and trunk dyskinesia.

Edentulousness, by disrupting trigeminal propioceptive input from the oral cavity to the basal ganglia, may increase the risk for neuroleptic-induced orofacial dyskinesia. Since lesions of the globus pallidus alter trigeminal sensory-induced reflexive neck muscle activity in rats and the putamen-caudate complex regulates vestibular and propioceptive mechanisms, edentulousness could facilitate also the expression of neuroleptic-induced neck and trunk dyskinesias. In a sample of 131 neuroleptic-treated chronic schizophrenic patients, we found that edentulous patients exhibited significantly more neck and trunk dyskinesias as compared to nonedentulous patients (p less than 005). By contrast, dyskinesias of the face, tongue, and extremities did not differ between the two cohorts of patients. Our findings imply that edentulousness may increase the risk of neck and trunk dyskinesias and highlight the importance of the dental status in tardive dyskinesia.

Adolescent↗

The clinical significance of median occlusal position.

The harmony of the occlusal components of the teeth, mandibular joint and muscles, were investigated in 180 human subjects by clinical, dental articulator, radiographic and electrodiagnostic methods. Significant correlations were found between disharmony of these components at median occlusal position (MOP), and with pain-dysfunction of the masticatory system. Using the standardized stimuli of opening the jaw wide and snapping it shut automatically into MOP, temporalis and masseter muscle co-ordination and somesthetic reflex effects were quantified. The interval from tooth contact (s) to reinstitution of EMG activity (x), and the EMG silent-period duration (SP), were prolonged in the patients but returned to within the control range with elimination of the pain-dysfunction. Muscle incoordination with mandibular dysfunction was prevalent in the patients, and the incidence of osteoarthritis was greatest in those with persistent symptoms. The hypothesis was supported that disharmony of MOP exists in pain-dysfunction patients--while successful occlusal therapy leads to the restoration of the harmony within the biologic range. This implies physiological significance to this hitherto clinically neglected occlusal position.

Adult↗

Peripheral neuropathy in transgenic diabetic mice: restoration of C-fiber function with human recombinant nerve growth factor.

Mice (Ins.Dd1) with hypoinsulinemic diabetes were created by increased expression of syngeneic major histocompatibility complex (MHC) class I protein in pancreatic beta-cells. The diabetic state was characterized in these mice by high glucose concentrations and islet pathology. To determine whether a neuropathy would develop, motor and sensory conduction velocities (CV) were determined in the sciatic nerves of 2-, 4-, and 7-month-old control and diabetic littermate male mice. Recording bipolar electrodes were placed in the plantar muscles of the hind foot of anesthetized (ketamine/xylazine) mice. Bipolar stimulating electrodes were positioned near the sciatic nerve at the sciatic notch or near the tibial nerve at the ankle. Motor CV from alpha-motor fibers and sensory CV from proprioceptive Aalpha nerves were measured and expressed as meters per second (m/s). Group data are reported as mean +/- SE and compared by analysis of variance. The CVs from nondiabetic mice (controls) were not different across the three ages and averaged 41.3 +/- 1.7 m/s for motor and 38.7 +/- 1.7 m/s for sensory. The motor CVs from diabetic mice at 2 and 4 months were similar to controls. Sensory CVs were unchanged at 2 months but were lower at 4 months (18.9 +/- 2.4 m/s). Both sensory (23.9 +/- 2.1 m/s) and motor (18.9 +/- 1.8 m/s) CVs were significantly reduced at 7 months, which is indicative of a polyneuropathy. NGF has well-known trophic effects on sympathetic and small sensory neurons. To determine whether NGF could influence this neuropathy, 6-month-old control and diabetic mice were divided into the following groups: 1) control + vehicle, 2) diabetic + vehicle, and 3) diabetic + NGF (1 mg/kg, 3x week, s.c.). After 1 month of treatment, motor and sensory CVs were determined. In some mice, the branches of the sciatic nerve were exposed and in situ recordings from the sural nerve were performed to determine compound C-fiber CV, integral, and amplitude. Sensory CV, determined via Hoffmann's reflex (H-reflex) (A-fiber), was decreased in diabetic compared with control animals as expected (P < 0.05), and NGF did not alter this parameter. Continuing diabetes reduced the amplitude (0.9 +/- 0.2 vs. 3.2 +/- 0.7 mV x 10(-2); P < 0.05) and integral (6.9 +/- 1.9 mV/ms vs. 18.8 +/- 4.4 mV/ms; P < 0.05) of the C-fiber response versus control, suggesting fiber loss. NGF treatment normalized C-fiber amplitude (2.9 +/- 0.8 mV x 10(-2)) and integral (21.2 +/- 6.5 mV/ms) in animals with established diabetes, with no effect on blood glucose. The C-fiber CV was similar in all groups, indicating that the animals had some normally conducting small fiber sensory nerves. These studies characterized a motor and sensory polyneuropathy in transgenic diabetic mice and are the first to demonstrate directly that NGF treatment can protect or restore abnormal sensory C-fiber function.

Animals↗

Primary afferent synapses on developing and adult Renshaw cells.

The mechanisms that diversify adult interneurons from a few pools of embryonic neurons are unknown. Renshaw cells, Ia inhibitory interneurons (IaINs), and possibly other types of mammalian spinal interneurons have common embryonic origins within the V1 group. However, in contrast to IaINs and other V1-derived interneurons, adult Renshaw cells receive motor axon synapses and lack proprioceptive inputs. Here, we investigated how this specific pattern of connectivity emerges during the development of Renshaw cells. Tract tracing and immunocytochemical markers [parvalbumin and vesicular glutamate transporter 1 (VGLUT1)] showed that most embryonic (embryonic day 18) Renshaw cells lack dorsal root inputs, but more than half received dorsal root synapses by postnatal day 0 (P0) and this input spread to all Renshaw cells by P10-P15. Electrophysiological recordings in neonates indicated that this input is functional and evokes Renshaw cell firing. VGLUT1-IR bouton density on Renshaw cells increased until P15 but thereafter decreased because of limited synapse proliferation coupled with the enlargement of Renshaw cell dendrites. In parallel, Renshaw cell postsynaptic densities apposed to VGLUT1-IR synapses became smaller in adult compared with P15. In contrast, vesicular acetylcholine transporter-IR motor axon synapses contact embryonic Renshaw cells and proliferate postnatally matching Renshaw cell growth. Like other V1 neurons, Renshaw cells are thus competent to receive sensory synapses. However, after P15, these sensory inputs appear deselected through arrested proliferation and synapse weakening. Thus, Renshaw cells shift from integrating sensory and motor inputs in neonates to predominantly motor inputs in adult. Similar synaptic weight shifts on interneurons may be involved in the maturation of motor reflexes and locomotor circuitry.

Afferent Pathways↗

Spatiotemporal properties of eye position signals in the primate central thalamus.

Although both sensory and motor signals in multiple cortical areas are modulated by eye position, the origin of eye position signals for cortical neurons remains uncertain. One likely source is the central thalamus, which contains neurons sensitive to eye position. Because the central thalamus receives inputs from the brainstem, these neurons may transmit eye position signals arising from the neural integrator or from proprioceptive feedback. However, because the central thalamus also receives inputs from many cortical areas, eye position signals in the central thalamus could come from the cerebral cortex. To clarify these possibilities, spatial and temporal properties of eye position signals in the central thalamus were examined in trained monkeys. Data showed that eye position signals were decomposed into horizontal and vertical components, suggesting that the central thalamus lies within pathways that transmit brainstem eye position signals to the cortex. Further quantitative analyses suggested that 2 distinct groups of thalamic neurons mediate eye position signals from different subcortical origins, and that the signals are modified dynamically through ascending pathways. Eye position signals through the central thalamus may play essential roles in spatial transformation performed by cortical networks.

Adaptation, Physiological↗

Neurological, psychological and polygraphic findings in sleep drunkenness.

Eight patients suffering from idiopathic hypersomnia with sleep drunkenness were given neurological, psychological and polygraphic investigations, and that after 4, 8 and 12 hours of nocturnal sleep. Also examined and tested were 8 controls - after 4, 8 and 0 hours of sleep during the preceding night. The patients and the controls were awakened and tested in the afternoon hours 30-45 minutes after they had fallen asleep. Under those circumstances the state of sleep drunkenness was observed in the patients in 19 instances, but only once in the controls. While experiencing sleep drunkenness the subjects were found to have prominent cerebellar signs, proprioceptive hypo- or even areflexia, signs of vestibular and, rarely, pyramidal tract involvement. Psychological tests scores and scores for the fine and gross motricity tests were substantially worse in sleep drunkenness than in wakefulness. Sleep drunkenness manifested itself in the polygraphic recordings by signs of microsleep. Pathological predisposition to the development of sleep drunkenness in hypersomniacs was found to be the most significant factor responsible for the occurrence of this state. Attention is drawn to the analogy between states of sleep drunkenness and automatic behaviour in narcoleptics and hypersomniacs as a common feature of both states. The authors believe that sleep drunkenness in idiopathic hypersomnia develops as a result of chronic relative sleep deprivation in those patients whose sleep requirements are greater than conditions of normal life can permit.

Arousal↗

[Neurological symptoms in a-beta-lipoproteinemia (author's transl)].

Abetalipoproteinaemia (Bassen-Kornzweig syndrome), an autosomal recessive inherited disease, up to now has been described in 53 instances in the world literature. Neurological symptoms were reported in 34 of them. Ataxia, loss of proprioceptive sensation, and areflexia characterize this disorder, resembling Friedreich's ataxia. Other signs, which may be inconstantly found, are weakness, diminution of cutaneous sensation, and in the later course an atypical retinitis pigmentosa. Laboratory examinations show acanthocytosis, lowered concentrations of serum cholesterol, triglycerides and phospholipids and as the pathognomonic feature of this disease absence of beta-lipoproteins. Reduced serum concentrations of fat soluble vitamin are secondary effects of this metabolic disorder. In a few cases there are connections to familial hypobeta-lipoproteinaemia, which is autosomal dominantly inherited. Therapeutic trials with a controlled dietary intake of fat may cause an improvement of clinical symptoms, additional doses of fat-soluble vitamin, if given during the early stages of the disease are said to prevent from retinopathy but do not seem to influence the development and course of neuropathy.

Abetalipoproteinemia↗

Voluntary head stabilisation in space during oscillatory trunk movements in the frontal plane performed before, during and after a prolonged period of weightlessness.

The ability to voluntarily stabilise the head in space exhibited by two subjects during lateral rhythmic oscillations of the trunk has been investigated before, during and after a prolonged period of microgravity (microG) exposure. In flight acquisitions were performed onboard the Core Module of the Russian Space Station MIR as part of the T4 "Human Posture in Microgravity" experiment of the 179-days ESA-RKA mission EUROMIR-95. Data collection and kinematic analysis were performed by means of a space-qualified version of the automatic motion analyser ELITE. Head stabilisation in space strategy was estimated by means of the head anchoring index and cross-correlation analysis. Results show that head orientation may be well stabilised about the roll axis both with and without the presence of visual information. This was true despite the expected reduction in vestibular efficiency and muscular proprioception occurring in-flight. In one subject, however, vision was found to improve head stabilisation in space post-flight, presumably to recover from the postural deficiency induced by the long-term microG exposure. Head stability during trunk movements was achieved with either over-compensatory (out-of-phase), under-compensatory (in-phase) or mixed movement strategies, as was attested by the analysis of cross-correlation functions between head and shoulder movements. In weightlessness, vision occlusion seemed to influence the choice of the strategies to be used as well as the reduction of movement variability. The feedforward nature of compensatory head movements suggests that head stabilisation could be based in weightlessness on the internal postural body scheme, supposed to be adapted to the weightless environment within 5 months of microG exposure.

Adaptation, Biological↗

Specific adaptations of neuromuscular control and knee joint stiffness following sensorimotor training.

The aim of this study was to examine how fixations of the ankle joint during sensorimotor training (SMT) influence adaptations in mechanical stiffness and neuromuscular control of the knee joint. Sixty-three healthy subjects were randomly assigned to three training groups that differed in their degree of ankle joint fixation, which was either barefooted, with an ankle brace or with a ski boot. Mechanical knee joint stiffness and reflex control of m. vastus medialis, m. vastus lateralis, m. biceps femoris, and m. semitendinosus were tested during force controlled anterior tibial displacements. This force was applied as both a fast and a slow stimulus. After the training period the group that trained barefooted showed an increase in mechanical stiffness of the knee joint from 79 +/- 21 (Mean +/- SD) N/mm to 110 +/- 38 N/mm (p < 0.05) in the fast stimulus. The training group that trained with ski boots was able to improve knee joint stiffness from 67 +/- 26 N/mm to 96 +/- 47 N/mm (p < 0.05) in the slow stimulus. These improvements correspond with an enhanced activity of the hamstring muscles (m. biceps femoris and m. semitendinosus). From a more functional point of view, specific adaptations due to the fixation of the ankle joint may be helpful in the prevention and rehabilitation of knee joint injuries.

Adaptation, Physiological↗

[Specificity of nuclear elements of the motor region of the cortex in organizing a precise motor response].

After elaboration and consolidation of precise instrumental avoidance reflexes in dogs (lifting of a fore-leg to a 4-centimeters wide "safety zone"), a part of motor cortex in the area of moving leg was ablated. After the operation the search for "safety zone" i. e. the precision of estimating the position of the leg was irreversibly impaired, but the animal was still able to hold its extremity at the same level for a long period of time. Artifically elaborated motor coordination--antagonistic to the innate one--also showed irreversible impairment. However, in case of an extremely "drilled" reaction (5.000 pairings) the elaborated coordination persisted. Minimal amplitude of correction movements increased too (i. e. subtlety of movements decreased), but during retraining this parameter of the movement became compensated. The data obtained suggest that the specificity of central cellular elements of the cortical motor area consists in estimation of extremity position which is necessary for finding a given point in space.

Animals↗

Physiological tremor and control of limb position in 1 and 0 G.

Muscle and skeletal mechanoreceptors play an important role for the regulation of muscular tone and the genesis of normal Physiological Tremor (PT). For example if a big limb as the arm or leg is kept against the gravity vector, the la afferent spindle discharges continuously control the load bearing flexor in a negative feedback manner in order to compensate the gravity vector and to the stabilize arm position. This servo-like action, denoted as 'stretch reflex', not only increases static postural stability (tonic stretch reflex) but also counteracts against external disturbances by dynamically increasing the muscle tone. Muscle spindles are very sophisticated sensory organs. They have an own innervation and the endings of the nuclear bag fibres are highly sensitive for small microstretches. EMG and microneurografic studies showed their importance in the mechanism of the 8-12 Hz component for PT. In a 0 G a limb becomes position controlled. In contrast to 1g, where control of limb position is a subordinated function of force compensation in the load bearing muscle, an antagonistic control scheme is necessary in 0 G to compensate the arm against positional drifts. As a consequence there is a shift from load dependent (muscular) to position dependent (skeletal) mechanoreceptors that become involved in the neural control process. As the control process is reflected in the tremor pattern, we investigated arm tremor in a constant limb position in 1 and 0 G.

Arm↗