Postural Muscle Tone Research Articles

Differentiating the Structural and Functional Instability of the Craniocervical Junction.

This paper presents the anatomical and biomechanical aspects of chronic instability of the craniocervical junction (CCJ) with a discussion on clinical diagnostics based on mobility tests and provocative tests related to ligamentous system injuries, as well as radiological criteria for CCJ instability. In addition to the structural instability of the CCJ, the hypothesis of its functional form resulting from cervical proprioceptive system (CPS) damage is discussed. Clinical and neurophysiological studies have shown that functional disorders or organic changes in the CPS cause symptoms similar to those of vestibular system diseases: dizziness, nystagmus, and balance disorders. The underlying cause of the functional form of CCJ instability may be the increased activity of mechanoreceptors, leading to "informational noise" which causes vestibular system disorientation. Due to the disharmony of mutual stimulation and the inhibition of impulses between the centers controlling eye movements, the cerebellum, spinal motoneurons, and the vestibular system, inadequate vestibulospinal and vestibulo-ocular reactions occur, manifesting as postural instability, dizziness, and nystagmus. The hyperactivity of craniocervical mechanoreceptors also leads to disturbances in the reflex regulation of postural muscle tone, manifesting as "general instability". Understanding this form of CCJ instability as a distinct clinical entity is important both diagnostically and therapeutically as it requires different management strategies compared to true instability. Chronic CCJ instability significantly impacts the quality of life (QOL) of affected patients, contributing to chronic pain, psychological distress, and functional impairments. Addressing both structural and functional instability is essential for improving patient outcomes and enhancing their overall QOL.

Pierre-Marie Gagey and the Evolution of Posturology: Unraveling the Complexity of the Fine Postural Control System.

The subtle sway of human standing posture began to be studied in the 19th century. Since then, numerous approaches - from the early statokinesiometers to the more advanced force platforms or 3D-posture recording systems - have been developed to understand human postural control physiology and its clinical implications. French physician Pierre-Marie Gagey made significant contributions to the field of posturology, a discipline focused on the intricacies of human postural control. From the 1950s, he advanced the field through observation and experimentation, particularly exploring the relationship between postural muscle tone and the fine postural control system. Gagey's collaboration with researchers of that time led to the refinement of stabilometry, a technique for measuring body sway in standing positions. Throughout his career, Gagey worked across multiple disciplines, including ophthalmology, podiatry, psychology, and the study of the vestibular and stomatognathic systems, to develop a comprehensive approach to postural assessment and treatment. His efforts culminated in the standardization of stabilometry, ensuring consistent and accurate measurements across different platforms. Gagey's work emphasized the complexity of postural control, highlighting the integration of peripheral and central nervous system inputs in maintaining balance. His research has left an enduring impact on the field of posturology, providing a framework for understanding and treating postural disorders. Pierre-Marie Gagey passed away in 2023, but his pioneering contributions continue to influence the study and clinical practice of human postural control. This narrative review aims to pay tribute to Dr. Gagey's career and research activity.

Dopamine release in the nucleus accumbens promotes REM sleep and cataplexy

Patients with the sleep disorder narcolepsy suffer from excessive daytime sleepiness, disrupted nighttime sleep, and cataplexy-the abrupt loss of postural muscle tone during wakefulness, often triggered by strong emotion. The dopamine (DA) system is implicated in both sleep-wake states and cataplexy, but little is known about the function of DA release in the striatum and sleep disorders. Recording DA release in the ventral striatum revealed orexin-independent changes across sleep-wake states as well as striking increases in DA release in the ventral, but not dorsal, striatum prior to cataplexy onset. Tonic low-frequency stimulation of ventral tegmental efferents in the ventral striatum suppressed both cataplexy and rapid eye movement (REM) sleep, while phasic high-frequency stimulation increased cataplexy propensity and decreased the latency to REM sleep. Together, our findings demonstrate a functional role of DA release in the striatum in regulating cataplexy and REM sleep.

Semaphorin7A: its role in the control of serotonergic circuits and functional recovery following spinal cord injury.

Serotonin is a monoamine neurotransmitter synthetized in various populations of brainstem neurons. In the spinal cord, descending serotonergic projections regulate postural muscle tone, locomotion and rhythm and coordination of movements via the Central Pattern Generator. Following a spinal cord injury, serotonergic projections to the lumbar spinal cord, where the Central Pattern Generators are located, are interrupted resulting in devastating locomotor impairments and changes in the expression and activation of serotonin and its spinal receptors. The molecular cues that control the precise patterning and targeting of serotonergic inputs onto Central Pattern Generator networks in healthy animals or after injury are still unknown. In our recent research work, we have been particularly interested in Semaphorin7A, which belongs to the Semaphorins family involved in guiding growing axons and controlling plasticity of synaptic connections. In this review, we discuss the role of Semaphorin7A signaling as an important molecular actor that instructs the patterning of serotonin inputs to spinal Central Pattern Generator networks. We show that Semaphorin7A controls the wiring of descending serotonin axons in the spinal cord. Our results reveal that mistargetting of serotonin fibers in the spinal cord is compensated in healthy uninjured Semaphorin7A deficient mice so that their gross locomotion proceeds accurately. We also demonstrate that when the system is challenged with a spinal lesion, the pattern of post-injury serotonin expression is significantly altered in Semaphorin7A deficient mice with specific ectopic targeting of serotonin fibers in the lumbar spinal cord. Compensatory mechanisms in place in uninjured Semaphorin7A deficient mice are lost and injured Semaphorin7A deficient mice exhibit a worsening of their post-injury locomotor abilities. Our findings identify Semaphorin7A as a critical determinant of serotonergic circuit formation in healthy or spinal cord injured mice.

The influence of anticoagulant and antiagregant therapy during pregnancy on clinical characteristics and outcomes of periventricular hemorrhages in newborns

To evaluate the characteristics of periventricular hemorrhages (PVH) in newborns of mothers receiving antiplatelet and anticoagulation therapy during pregnancy with hypercoagulation syndrome. One hundred and twelve newborns with PVH were evaluated: group 1 - 37 children, born after a pregnancy with hypercoagulation syndrome and antithrombotic therapy; group 2 - 55 children, born after a pregnancy without hypercoagulation syndrome and with preventive antithrombotic therapy; group 3 - 20 children, born after a pregnancy without hypercoagulation syndrome and without antithrombotic therapy. All newborns underwent clinical and neurologic examinations combined with assessment using special scales and intracranial ultrasound evaluation. Maternal anticoagulation therapy during pregnancy in groups I and 2 was associated with more severe condition of newborns with PVH (significantly prolonged artificial lung ventilation, more premature births, larger hemorrhage) compared to newborns in group 3. Follow-up of infants in groups I and 2 demonstrated a significantly slower progress of postural muscle tone, psychological and psychomotor development compared to infants in group 3. Hypercoagulation syndrome treatment during pregnancy significantly affects the severity of newborn's condition at birth and the development of severe neurological impairments in long-term period.

Pengaruh Terapi Integrasi Sensori Terhadap Tonus Anak Dengan Sensory Integration Disorder (SID) Berdasarkan Skor Clinical Observation Of Neuromotor Performance (CONP) Di Mitra Ananda Surakarta

Abstract: Sensory Integration Therapy-Muscle Tonus-Clinical Observation Of Neuromotor Performance. Special need children such as down syndrome, autism and intellectual disability suffered from Sensory Integration Disorder (SID) will have an impact on the weakness of postural muscle tone. Muscle tone measurement of children with SID is different from other children without SID. Clinical observation of neuromotor performance (CONP) is used as of one of criteria of muscle muscle tone in children with SID. The study aimed at finding theeffect of sensory integration therapy towards muscle tone based on Score of Clinical Observation of Neuromotor Performance (CONP) at Mitra Ananda Surakarta. The study was designed as quasi experiment one group pretest posttest design. population of this study is client with SID at Mitra Ananda Surakarta , by total sampling there are a number of 12 samples. Paired t-test is applied for analizing data with SPSS version 17.0. Paired t-test portrayed p-value > 0.05 it means that there are no significant difference in muscletone, before and after treatment. Sensory integration therapy doesn’t affect muscle tone for shildren with SID Based on Score of Clinical Observation of Neuromotor Performance (CONP) at Mitra Ananda Surakarta

Functional Neuroanatomy for Posture and Gait Control.

Here we argue functional neuroanatomy for posture-gait control. Multi-sensory information such as somatosensory, visual and vestibular sensation act on various areas of the brain so that adaptable posture-gait control can be achieved. Automatic process of gait, which is steady-state stepping movements associating with postural reflexes including headeye coordination accompanied by appropriate alignment of body segments and optimal level of postural muscle tone, is mediated by the descending pathways from the brainstem to the spinal cord. Particularly, reticulospinal pathways arising from the lateral part of the mesopontine tegmentum and spinal locomotor network contribute to this process. On the other hand, walking in unfamiliar circumstance requires cognitive process of postural control, which depends on knowledges of self-body, such as body schema and body motion in space. The cognitive information is produced at the temporoparietal association cortex, and is fundamental to sustention of vertical posture and construction of motor programs. The programs in the motor cortical areas run to execute anticipatory postural adjustment that is optimal for achievement of goal-directed movements. The basal ganglia and cerebellum may affect both the automatic and cognitive processes of posturegait control through reciprocal connections with the brainstem and cerebral cortex, respectively. Consequently, impairments in cognitive function by damages in the cerebral cortex, basal ganglia and cerebellum may disturb posture-gait control, resulting in falling.

Ventral medullary control of rapid eye movement sleep and atonia

Discrete populations of neurons at multiple levels of the brainstem control rapid eye movement (REM) sleep and the accompanying loss of postural muscle tone, or atonia. The specific contributions of these brainstem cell populations to REM sleep control remains incompletely understood. Here we show in rats that viral vector-based lesions of the ventromedial medulla at a level rostral to the inferior olive (pSOM) produced violent myoclonic twitches and abnormal electromyographic spikes, but not complete loss of tonic atonia, during REM sleep. Motor tone during non-REM (NREM) sleep was unaffected in these same animals. Acute chemogenetic activation of pSOM neurons in rats robustly and selectively suppressed REM sleep but not NREM sleep. Similar lesions targeting the more rostral ventromedial medulla (RVM) did not affect sleep or atonia, while chemogenetic stimulation of the RVM produced wakefulness and reduced sleep. Finally, selective activation of vesicular GABA transporter (VGAT) pSOM neurons in mice produced complete suppression of REM sleep whereas their loss increased EMG spikes during REM sleep. These results reveal a key contribution of the pSOM and specifically the VGAT+ neurons in this region in REM sleep and motor control.

A systematic approach to the neurological examination of llamas and alpacas

The clinical presentation of neurologic disorders in camelids varies widely depending on the underlying cause and localisation of the disease. Metabolic, cardiovascular and musculoskeletal conditions may also present with neurological signs and must thus be differentiated from those of true peripheral or central nervous system origin, through careful evaluation of history, clinical examination and diagnostic testing. Mentation and behaviour of camelids is generally evaluated from a distance, with subsequent assessment of cranial nerve function, gait, posture and postural reactions, spinal reflexes and muscle tone. Gait assessment often focuses on the differentiation between lower motor neuron weakness (LMN paresis) and general proprioceptive ataxia (with associated upper motor neuron weakness), in order to better localise spinal cord disorders. In this context, tail pull examinations may further aid in discerning upper versus lower motor neuron weakness. A thorough systematic neurological examination is thus paramount to achieve the following goals: determine the presence or absence of neurologic signs; localisation of the lesion (neuro-anatomic diagnosis); determine the etiology of a neurological condition.

The anatomical, cellular and synaptic basis of motor atonia during rapid eye movement sleep.

Rapid eye movement (REM) sleep is a recurring part of the sleep-wake cycle characterized by fast, desynchronized rhythms in the electroencephalogram (EEG), hippocampal theta activity, rapid eye movements, autonomic activation and loss of postural muscle tone (atonia). The brain circuitry governing REM sleep is located in the pontine and medullary brainstem and includes ascending and descending projections that regulate the EEG and motor components of REM sleep. The descending signal for postural muscle atonia during REM sleep is thought to originate from glutamatergic neurons of the sublaterodorsal nucleus (SLD), which in turn activate glycinergic pre-motor neurons in the spinal cord and/or ventromedial medulla to inhibit motor neurons. Despite work over the past two decades on many neurotransmitter systems that regulate the SLD, gaps remain in our knowledge of the synaptic basis by which SLD REM neurons are regulated and in turn produce REM sleep atonia. Elucidating the anatomical, cellular and synaptic basis of REM sleep atonia control is a critical step for treating many sleep-related disorders including obstructive sleep apnoea (apnea), REM sleep behaviour disorder (RBD) and narcolepsy with cataplexy.

Epilepsy and cataplexy in Angelman syndrome. Genotype-phenotype correlations

BackgroundAngelman syndrome (AS) is a neurogenetic disorder characterized by intellectual disability, epilepsy, and low threshold for laughter. AimsWe investigated the occurrence and severity of epilepsy and laughter-induced loss of postural muscle tone determined by the different genetic subtypes. MethodsThis study included 39 children with AS. Deletion breakpoints were determined by high resolution CGH microarray (1×1M Agilent). Clinical data were based on a parent interview and medical record review. ResultsAll patients with AS based on a deletion had epilepsy. Epilepsy was present in 3/4 children with UBE3A mutation, and 4/5 with pUPD. Onset of epilepsy occurred earlier in deletion cases compared to pUPD or UBE3A mutations cases. Laughter-induced postural muscle tone loss occurred only among deletion cases. We found no differences in severity of epilepsy between children with a larger Class I or a smaller Class II deletions, or between the total group with a deletion compared to children with pUPD or a UBE3A mutation. The drugs most frequently prescribed were benzodiazepines in monotherapy, or a combination of benzodiazepines and valproic acid. ConclusionEpilepsy is very common in patients with AS, especially in patients with a deletion. Postural muscle tone loss and collapsing during outbursts of laughter were seen in patients with a deletion only.

The influence of the deep muscle training on postural control and muscle tone among stroke patients. Preliminary observations

Abstract Introduction: An ischemic stroke is one of the most common causes of disability among adults. The results of a stroke incident are: abnormal muscle tension, free movement and postural control dysfunction, walking disturbances, body asymmetry. They contribute to the significant changes in the proper functioning in daily life. The aim of the project was to assess the influence of the exercises that activate deep body muscles on the postural control and muscle tension among people after ischemic stroke. Material and methods: The study included 18 patients (7 women and 11 men) after ischemic stroke with hemiparesis. Those patients was divided into two groups: research group (RG): 9 patients (average age 61,33), time from the stroke: 2 months to 4 years, control group (CG): 9 patients (average age 69,56), time from the stroke: 2 months to 4 years. RG was following the standard exercise program and additionally was performing exercises which activate deep body muscles. CG was following only the standard therapy program. PUM chair was used for deep muscles exercises. The posture control was assessed according to the Postural Assessment Scale for Stroke Patient and the muscle tension was assessed according to the Ashworth scale. Results: In the study group after deep muscle training reported a significant correlation between muscle spasticity of the lower and changes in body position. Conclusions: Obtained results indicate on the need to introduce deep muscles therapy in the reeducation of postural control among patients with hemiparesis and to continue research on more extensive group of patients.

Brainstem control of locomotion and muscle tone with special reference to the role of the mesopontine tegmentum and medullary reticulospinal systems.

The lateral part of the mesopontine tegmentum contains functionally important structures involved in the control of posture and gait. Specifically, the mesencephalic locomotor region, which may consist of the cuneiform nucleus and pedunculopontine tegmental nucleus (PPN), occupies the interest with respect to the pathophysiology of posture-gait disorders. The purpose of this article is to review the mechanisms involved in the control of postural muscle tone and locomotion by the mesopontine tegmentum and the pontomedullary reticulospinal system. To make interpretation and discussion more robust, the above issue is considered largely based on our findings in the experiments using decerebrate cat preparations in addition to the results in animal experimentations and clinical investigations in other laboratories. Our investigations revealed the presence of functional topographical organizations with respect to the regulation of postural muscle tone and locomotion in both the mesopontine tegmentum and the pontomedullary reticulospinal system. These organizations were modified by neurotransmitter systems, particularly the cholinergic PPN projection to the pontine reticular formation. Because efferents from the forebrain structures as well as the cerebellum converge to the mesencephalic and pontomedullary reticular formation, changes in these organizations may be involved in the appropriate regulation of posture-gait synergy depending on the behavioral context. On the other hand, abnormal signals from the higher motor centers may produce dysfunction of the mesencephalic-reticulospinal system. Here we highlight the significance of elucidating the mechanisms of the mesencephalic-reticulospinal control of posture and locomotion so that thorough understanding of the pathophysiological mechanisms of posture-gait disorders can be made.

The distinctive vertical heterophoria of dyslexics.

In this study, we looked for the presence of vertical heterophoria (VH) in 42 dyslexic children (22 males and 20 females) aged 118.5±12.9 months who were compared with a control group of 22 nondyslexic children (eleven males and eleven females) aged 112±9.8 months. Dyslexics presented a low-level (always <1 prism diopter) VH combined with torsion. This oculomotor feature clearly separates the dyslexic group from the normal readers group. It is independent of the type of dyslexia. The essential feature of this VH is a lability that appears during specific stimulation of sensory receptors involved in postural regulation. This lability is demonstrated using a vertical Maddox test conducted under very specific conditions in which postural sensors are successively stimulated in a predetermined order. A quantitative variation in this VH may be seen during the Bielchowsky Head Tilt Test, which reveals hypertonia of the lower or upper oblique muscles. Vertical orthophoria can be achieved by placing low-power prisms asymmetrically within the direction of action of the superior or inferior oblique muscles. The selection of power and axis is not only guided by elements of the eye examination but also from observation of postural muscle tone. All these elements suggest that the VH could be of postural origin and somehow related to the vertical action of the oblique muscles. VH and torsion are not harmful per se. There is no statistical relationship between their level and the various parameters used to assess the reading skills of dyslexic children. VH and torsion could be a clinical marker of global proprioceptive dysfunction responsible for high-level multisensory disturbances secondary to poor spatial localization of visual and auditory information. This dysfunction might also explain the motor disorders concomitant to dyslexia.

Revisión de los fundamentos teóricos de la gimnasia abdominal hipopresiva

Abdominal hypopressive gymnastics (AHG) is a means towards toning the abdominal muscles, muscles of the pelvic floor, and spine stabilizing musculature. As a differentiating trait, it is claimed that the practice of this method's moves does not cause intraabdominal pressure to increase.The objective of this study is to assess the validity of AHG's theoretical basis and to present arguments for its practice. A literature review is also presented.Discrepancies were found within the following theoretical grounds of AHG: (i)AHG causes stimulation of the expiratory area, and inhibition of the inspiratory area. (ii)AHG causes stimulation of the pneumotaxic center. (iii)Through AHG, postural relaxation of the diaphragm is achieved. (iv)The supraspinal respiratory centers regulate postural tension of the respiratory musculature. (v)Executing phasic abdominal exercises causes a decrease in postural muscle tone. (vi)In order to prevent stress urinary incontinence, training of typei fibers in the pelvic floor must be emphasized.

Walking pattern and neural control in incomplete spinal cord injury

Outdoor fallers differ from indoor fallers substantially in demographics, lifestyle, health condition and physical function. Biomechanical predictors of outdoor falls have not been well characterized. Current validated measures of postural deficits, which describe only the overall postural behavior, are predictive of indoor falls but not outdoor falls. We hypothesized that a model-based description of postural muscle tone and reflexes, particularly during dual tasking, would predict outdoor falls. We tested whether postural stiffness and damping from an inverted pendulum model were predictive of future indoor and outdoor falls among older adults from the MOBILIZE Boston Study. The center of pressure data during standing were obtained from 717 participants aged 77.9 ± 5.3 years. Participants stood barefoot with eyes open for 30 s per trial, in two sets of five standing trials. One set included a serial subtractions task. Postural stiffness and damping values were determined from the postural sway data. After the postural measurements, falls were monitored prospectively using a monthly mail-in calendar over 6–36 months. Associations of postural measures with fall rates were determined using negative binomial regressions. After covariate adjustments, postural stiffness (p = 0.02–0.05) and damping (p = 0.007–0.1) were associated with lower outdoor falls risk, but not with indoor falls. Results were invariant by direction (anteroposterior versus mediolateral) or by condition (quiet standing versus dual task). Outdoor fall risk may be tied to postural control more so than indoor falls. Dual tasking is likely related to fall risk among older and sicker older adults, but not those relatively healthy.

The effect of different breast support conditions on multiplanar breast kinematics and kinetics during running

Outdoor fallers differ from indoor fallers substantially in demographics, lifestyle, health condition and physical function. Biomechanical predictors of outdoor falls have not been well characterized. Current validated measures of postural deficits, which describe only the overall postural behavior, are predictive of indoor falls but not outdoor falls. We hypothesized that a model-based description of postural muscle tone and reflexes, particularly during dual tasking, would predict outdoor falls. We tested whether postural stiffness and damping from an inverted pendulum model were predictive of future indoor and outdoor falls among older adults from the MOBILIZE Boston Study. The center of pressure data during standing were obtained from 717 participants aged 77.9 ± 5.3 years. Participants stood barefoot with eyes open for 30 s per trial, in two sets of five standing trials. One set included a serial subtractions task. Postural stiffness and damping values were determined from the postural sway data. After the postural measurements, falls were monitored prospectively using a monthly mail-in calendar over 6–36 months. Associations of postural measures with fall rates were determined using negative binomial regressions. After covariate adjustments, postural stiffness (p = 0.02–0.05) and damping (p = 0.007–0.1) were associated with lower outdoor falls risk, but not with indoor falls. Results were invariant by direction (anteroposterior versus mediolateral) or by condition (quiet standing versus dual task). Outdoor fall risk may be tied to postural control more so than indoor falls. Dual tasking is likely related to fall risk among older and sicker older adults, but not those relatively healthy.

Neurophysiology of gait: From the spinal cord to the frontal lobe

Locomotion is a purposeful, goal-directed behavior initiated by signals arising from either volitional processing in the cerebral cortex or emotional processing in the limbic system. Regardless of whether the locomotion initiation is volitional or emotional, locomotion is accompanied by automatic controlled movement processes, such as the adjustment of postural muscle tone and rhythmic limb movements. Sensori-motor integration in the brainstem and the spinal cord plays crucial roles in this process. The basic locomotor motor pattern is generated by spinal interneuronal networks, termed central pattern generators (CPGs). Responding to signals in proprioceptive and skin afferents, the spinal interneuronal networks modify the locomotor pattern in cooperation with descending signals from the brainstem structures and the cerebral cortex. Information processing between the basal ganglia, the cerebellum, and the brainstem may enable automatic regulation of muscle tone and rhythmic limb movements in the absence of conscious awareness. However, when a locomoting subject encounters obstacles, the subject has to intentionally adjust bodily alignment to guide limb movements. Such an intentional gait modification requires motor programming in the premotor cortices. The motor programs utilize one's bodily information, such as the body schema, which is preserved and updated in the temporoparietal cortex. The motor programs are transmitted to the brainstem by the corticoreticulospinal system, so that one's posture is anticipatorily controlled. These processes enable the corticospinal system to generate limb trajectory and achieve accurate foot placement. Loops from the motor cortical areas to the basal ganglia and the cerebellum can serve this purpose.

Sleep Physiology: Setting the Right Tone

Humans prone to cataplexy experience sudden losses of postural muscle tone without a corresponding loss of conscious awareness. The brain mechanisms underlying this debilitating decoupling are now better understood, thanks to a new study using cataplectic mice.

A Noradrenergic Mechanism Functions to Couple Motor Behavior with Arousal State

Appropriate levels of skeletal muscle tone are needed to support routine motor behaviors. But, the brain mechanisms that function to couple muscle tone with waking behaviors are unknown. We addressed this question by studying mice with cataplexy--a condition caused by a decoupling of motor and arousal behaviors. Cataplexy is characterized by involuntary loss of muscle tone during wakefulness, which results in postural collapse during otherwise normal consciousness. Cataplexy is caused by loss of hypocretin (orexin) cells, but it is unknown how this loss triggers motor inactivity during cataplexy. Here, we used hypocretin knockout mice to identify the neurochemical cause of cataplexy and to determine the biochemical mechanisms that normally function to couple arousal and motor systems. Using genetic, behavioral, electrophysiological, and pharmacological approaches, we show that the noradrenergic system acts to synchronize motor and arousal systems. Specifically, we show that an excitatory noradrenergic drive maintains postural muscle tone during wakefulness by activating α1 receptors on skeletal motoneurons. Loss of this normal excitatory drive triggers motor inactivity during cataplexy by reducing motoneuron excitation. However, loss of this drive does not affect arousal since mice remain awake during cataplexy, suggesting the noradrenergic system is not required for maintaining wakefulness. Artificial restoration of noradrenergic drive to motoneurons prevents motor inactivity and rescues cataplexy. We conclude that hypocretin deficiency causes cataplexy by short-circuiting the noradrenergic drive to skeletal motoneurons. We suggest that the noradrenergic system functions to couple the brain systems that control postural muscle tone and behavioral arousal state.