Depressed Reflexes Research Articles

Depression of cough reflex by microinjections of antitussive agents into caudal ventral respiratory group of the rabbit

We have previously shown that the caudal nucleus tractus solitarii is a site of action of some antitussive drugs and that the caudal ventral respiratory group (cVRG) region has a crucial role in determining both the expiratory and inspiratory components of the cough motor pattern. These findings led us to suggest that the cVRG region, and possibly other neural substrates involved in cough regulation, may be sites of action of antitussive drugs. To address this issue, we investigated changes in baseline respiratory activity and cough responses to tracheobronchial mechanical stimulation following microinjections (30-50 nl) of some antitussive drugs into the cVRG of pentobarbital-anesthetized, spontaneously breathing rabbits. [D-Ala(2),N-Me-Phe(4),Gly(5)-ol]-enkephalin (DAMGO) and baclofen at the lower concentrations (0.5 mM and 0.1 mM, respectively) decreased cough number, peak abdominal activity, and peak tracheal pressure and increased cough-related total cycle duration (Tt). At the higher concentrations (5 mM and 1 mM, respectively), both drugs abolished the cough reflex. DAMGO and baclofen also affected baseline respiratory activity. Both drugs reduced peak abdominal activity, while only DAMGO increased Tt, owing to increases in expiratory time. The neurokinin-1 (NK(1)) receptor antagonist CP-99,994 (10 mM) decreased cough number, peak abdominal activity, and peak tracheal pressure, without affecting baseline respiration. The NK(2) receptor antagonist MEN 10376 (5 mM) had no effect. The results indicate that the cVRG is a site of action of some antitussive agents and support the hypothesis that several neural substrates involved in cough regulation may share this characteristic.

Involvement of 5-hydroxytryptaminergic transmission for the Mesobuthus tamulus venom-induced depression of spinal reflexes in neonatal rat in vitro

Mesobuthus tamulus (MBT) venom is shown to depress the spinal reflexes through a mechanism unrelated to the NMDA receptors. 5-Hydroxytryptamine (5-HT) is another excitatory transmitter in the spinal cord therefore, the present study was undertaken to examine the involvement of 5-HT in the venom-induced depression of reflexes. The experiments were performed on isolated hemisected spinal cords from 4 to 6-day-old rats. Stimulation of a dorsal root with supramaximal strength evoked monosynaptic reflex (MSR) and polysynaptic reflex (PSR) potentials in the corresponding segmental ventral root. MBT venom (0.3 μg/ml) depressed the spinal reflexes in a time-dependent manner and the maximal depression was seen at 10 min. The time to produce 50% depression (T-50) of MSR and PSR was 8.1 ± 1.41 and 6.8 ± 0.5 min, respectively. Pretreatment with pindolol (1 μM; 5-HT 1A/1B receptor antagonist) blocked the reflexes up to 15 min. On the other hand, ketanserin (10 μM; 5-HT 2A/2C receptor antagonist) or ondansetron (0.1 μM; 5-HT 3 receptor antagonist) blocked the venom-induced depression of MSR and PSR during entire exposure time (30 min). The 5-HT concentration of the cords exposed to venom (1.6 ± 0.04 μg/g tissue) was significantly greater than the control group (0.98 ± 0.08 μg/g tissue). The results indicate that venom-induced depression of spinal reflexes is mediated via 5-HTergic transmission involving 5-HT 1A/1B, 5-HT 2A/2C and 5-HT 3 receptors.

E-036 Hemodynamic stability during carotid artery stenting under general anesthesia in elderly patients with a high grade carotid artery stenosis

Purpose of studyDuring carotid artery stenting (CAS) under local anesthesia, hemodynamic instability (hypotension, bradycardia, etc) has been reported to occur. Hemodynamic instability during CAS under local anesthesia, especially in elderly...

HYPOXIC ISCHAEMIC ENCEPHALOPATHY IN NEWBORN INFANTS

Neonatal encephalopathy has been defined as “a clinically defined syndrome of disturbed neurological function in the earliest days of life in the term infant, manifested by difficulty with initiating and maintaining respiration, depression of tone and reflexes, sub normal level of consciousness and often seizures”. It occurs in about 2–3 per 1000 births in developed countries. In developing countries, neonatal encephalopathy accounts for the largest number of deaths in infancy and childhood – approximately 1 million per year worldwide. Neonatal encephalopathy is associated with significant morbidity and mortality and is an important predictor of long term neurodevelopmental disability in near- and full-term newborn infants. Fifteen to 20 percent of infants with neonatal encephalopathy die in the neonatal period, and a further 25 percent have permanent neurologic deficits.

Somatosensory Evoked Potential for Detection of Subclinical Neuropathy in Egyptian Children with Acute Lymphoblastic Leukaemia

To evaluate neurological changes developing during paediatric Acute Lymphoblastic Leukaemia (ALL) therapy clinically and through electrophysiological Study of Somatosensory Evoked Potentials (SSEPs) changes in different phases of therapy. Thirty five-ALL patients with age range from 3-14 years were included compared to 30 healthy controls. History, neurological examination, complete blood counts, cytological examination of bone marrow aspirate and cerebrospinal fluid with Measurement of Serum Methotrexate (MTX) were done. The SSEPs were performed and patients subjected to another SSEP with measurement of serum MTX level before and 10 days after intra-thecal injection (IMTX). Clinical neurological findings in patients after induction were depressed deep tendon reflexes (43.3%), hypotonia (28.6%), lost pain sensation (28.6%), muscle weakness (17.1%) and movement disorders (17.1%). Percentage of delayed SSEPs after induction were at levels of brachial plexus (28.6%), spinal cord (68.6%), cortical conduction (31.4%), ERB-N13 Inter Peak Latency (IPL) (74.3%) and N13-N20 IPL (17.1%) in the studied patients. Significant prolonged latency of N13 (p = 0.005), N20 (p = 0.04) and IPL of ERB-N 13 (p = 0.005), N13-N20 (p = 0.01), Inter-Side Difference (ISD) of N13 (p = 0.01), ERB-N13 (p = 0.02) and N13-N20 (p = 0.03) after induction compared to values at diagnosis. Significant positive correlation were found between serum MTX after IMTX with N13-N20 IPL (p = 0.01), N20 ISD (p = 0.03) with significant prolongation in N20 latency, N13-N20 IPL and ISD of N20 compared to values before injection. ALL patients have prolonged latency of SSEPs at cervical cord and cortical levels which increased after IMTX due to axonal injury throughout the cord. SSEPs could be an early diagnostic tool for subclinical neuropathy.

1-Nitro-2-phenylethane, the main constituent of the essential oil of Aniba canelilla, elicits a vago-vagal bradycardiac and depressor reflex in normotensive rats

Previously, it was shown that intravenous (i.v.) treatment with the essential oil of Aniba canelilla (EOAC) elicited a hypotensive response that is due to active vascular relaxation rather than to the withdrawal of sympathetic tone. The present study investigated mechanisms underlying the cardiovascular responses to 1-nitro-2-phenylethane, the main constituent of the EOAC. In pentobarbital-anesthetized normotensive rats, 1-nitro-2-phenylethane (1–10 mg/kg, i.v.) elicited dose-dependent hypotensive and bradycardiac effects which were characterized in two periods (phases 1 and 2). The first rapid component (phase 1) evoked by 1-nitro-2-phenylethane (10 mg/kg) was fully abolished by bilateral vagotomy, perineural treatment of both cervical vagus nerves with capsaicin (250 µg/ml) and was absent after left ventricle injection. However, pretreatment with capsazepine (1 mg/kg, i.v.) or ondansetron (30 µg/kg, i.v.) did not alter phase 1 of the cardiovascular responses to 1-nitro-2-phenylethane (10 mg/kg, i.v.). In conscious rats, 1-nitro-2-phenylethane (1–10 mg/kg, i.v.) evoked rapid hypotensive and bradycardiac (phase 1) effects that were fully abolished by methylatropine (1 mg/kg, i.v.). It is concluded that 1-nitro-2-phenylethane induces a vago-vagal bradycardiac and depressor reflex (phase 1) that apparently results from the stimulation of vagal pulmonary rather than cardiac C-fiber afferents. The transduction mechanism of the 1-nitro-2-phenylethane excitation of C-fiber endings is not fully understood and does not appear to involve activation of either Vanilloid TPRV 1 or 5-HT 3 receptors. The phase 2 hypotensive response to 1-nitro-2-phenylethane seems to result, at least in part, from a direct vasodilatory effect since 1-nitro-2-phenylethane (1–300 µg/ml) induced a concentration-dependent reduction of phenylephrine-induced contraction in rat endothelium-containing aorta preparations.

Indian red scorpion venom depresses spinal synaptic transmission without involving NMDA receptors

Stings of Indian red scorpion (Mesobuthus tamulus, MBT) produce neurological abnormalities such as convulsions and paralysis. These parameters indicate the activity at alpha-motoneuron. The present study was therefore, undertaken to evaluate the effect of MBT-venom on spinal reflexes and the involvement of N-methyl-d-aspartate (NMDA) receptors. The experiments were performed on isolated hemisected spinal cords from 4 to 6 days old rats. Stimulation of a dorsal root with supramaximal strength at 0.1Hz evoked monosynaptic (MSR) and polysynaptic reflex (PSR) potentials in the corresponding segmental ventral root. Superfusion of MBT-venom depressed the spinal reflexes in a time- and a concentration-dependent (0.1-1microg/ml) manner. MBT-venom at 0.1, 0.3 and 1.0microg/ml produced maximal depression of 55, 75 and 90% at 30, 10 and 7min, respectively. The time required to produce 50% depression (T-50) of MSR was 19.0, 8.0, and 3.6min and for PSR was 15.0, 5.6, and 2.9min at 0.1, 0.3 and 1microg/ml of venom, respectively. Pre-treatment with DL-alpha-2-amino-5-phosphonovaleric acid (APV) decreased MSR by 26% and abolished PSR. In the presence of APV, the MBT-venom-induced depression of MSR was not different from the venom only group. The results indicate that venom-induced depression of spinal reflexes did not involve NMDA receptors.

Atypical, perhaps under-recognized? An unusual phenotype of Friedreich ataxia

Friedreich ataxia (FRDA) is typically characterized by slowly progressive ataxia, depressed tendon reflexes, dysarthria, pyramidal signs, and loss of position and vibration sense with onset before 25 years. While several atypical forms of FRDA are recognized, profound vision deficit is rare. We describe here a 41-year-old man with profound vision deficit and episodic complete blindness associated with marked optic atrophy, spastic paraparesis, and sensory neuropathy without ataxia whose diagnostic evaluation revealed compound heterozygosity for two frataxin mutations, a 994 GAA repeat intronic expansion and c.389G > T (p.G130V) missense mutation. This case emphasizes that FRDA should be considered for individuals with significant vision deficit with optic atrophy and sensory neuropathy, even in the absence of ataxia. This case also raises the additional, related concern that prior studies may underestimate the frequency and varieties of variant forms of FRDA.

Effect of sensory inputs on the soleus H-reflex amplitude during robotic passive stepping in humans

We investigated the modulation of the soleus (Sol) Hoffmann (H-) reflex excitability by peripheral sensory inputs during passive stepping using a robotic-driven gait orthosis in healthy subjects and spinal cord-injured patients. The Sol H-reflex was evoked at standing and at six phases during passive stepping in 40 and 100% body weight unloaded conditions. The Sol H-reflex excitability was significantly inhibited during passive stepping when compared with standing posture at each unloaded condition. During passive stepping, the H-reflex amplitude was significantly smaller in the early- and mid-swing phases than in the stance phase, which was similar to the modulation pattern previously reported for normal walking. No significant differences were observed in the H-reflex amplitude between the two unloaded conditions during passive stepping. The reflex depression observed at the early part of the swing phase during passive stepping might be attributed to the sensory inputs elicited by flexion of the hip and knee joints. The present study provides evidence that peripheral sensory inputs have a significant role in phase-dependent modulation of the Sol H-reflex during walking, and that the Sol H-reflex excitability might be less affected by load-related afferents during walking.

Soleus H-reflex graded depression by contralateral hip afferent feedback in humans

The aim of this study was to establish the effects of contralateral hip oscillations on the ipsilateral soleus H-reflex. A servomotor system was utilized to impose bilateral hip oscillations at 0.5 Hz, while braces stabilized the joint position of both legs. The soleus H-reflex was evoked every 4 s during bilateral synchronous and asynchronous hip movements and during unilateral hip oscillations with the contralateral leg hyperextended or flexed. In all experimental conditions, a stimulus was delivered to the posterior tibial nerve while the ipsilateral leg was moving either into extension or flexion. Torques at the hip and ankle joints and activity from six muscles were recorded from both legs. The ipsilateral soleus H-reflex was profoundly depressed in all conditions. The reflex depression was less during asynchronous than synchronous hip oscillations. Further, the soleus H-reflex depression did not vary with the contralateral hip flexed or extended, but it was larger when the ipsilateral hip was moving in flexion. These findings demonstrate that sensory afferent feedback from the contralateral hip adjusts the amount of inhibition acting on the ipsilateral soleus H-reflex, supporting cross-leg reflex and heteronymous muscle afferents interactions in humans.

Homotopic long-term depression of trigeminal pain and blink reflex within one side of the human face

Electrical low-frequency stimulation (LFS) of cutaneous afferents elicits long-term depression (LTD) of craniofacial nociception and pain. The study addresses spatial organization of LTD within one side of the face. The blink reflex was evoked by electrical test stimulation in the supraorbital nerve area before and after conditioning LFS in 10 healthy volunteers. Noxious LFS (1Hz) was applied to skin afferents of supraorbital (sLFS), infraorbital (iLFS), or mental (mLFS) nerves. All stimuli were applied to the same side of the face with intensities of three times pain threshold. Volunteers rated the test stimulus intensity. Each volunteer participated in four sessions with sLFS, iLFS, mLFS, or without LFS (control). Pain ratings of electrical test stimulation were differently affected in experimental sessions (p<0.01) with strongest reduction by -19.6% after sLFS. The reflex integral decreased by -34.7% significantly stronger after sLFS than in all other experimental conditions (p<0.001). Electrical pain thresholds increased significantly stronger in sLFS than in iLFS, mLFS, and control (p<0.001). Trigeminal nociception and pain were inhibited by homotopic LFS at the forehead but not after heterotopic LFS of infraorbital and mental nerve skin afferents. Homotopic organization of ipsilateral trigeminal LTD in man may have implications for future neuromodulatory treatment of chronic craniofacial pain.

Inhibitory mechanisms following electrical stimulation of tendon and cutaneous afferents in the lower limb

Electrical stimulation of the Achilles tendon (TES) produced strong reflex depression (duration>250 ms) of a small background contraction in both heads of gastrocnemius (GA) via large diameter electrodes localized to the tendon. The inhibitory responses were produced without electrical (M wave) or mechanical (muscle twitch) signs of direct muscle stimulation. In this study, the contribution of presynaptic and postsynaptic mechanisms to the depression was investigated by studying conditioning effects of tendon afferent stimulation on the mechanical tendon reflex (TR) and magnetic motor evoked potential (MEP). TES completely inhibited the TR over an ISI of 300 ms that commenced before and continued during and after the period of voluntary EMG depression. Tendon afferent conditioning stimuli also partially inhibited the MEP, but over a short time course confined to the period of voluntary EMG depression. The strength and extended time course of tendon afferent conditioning of the TR and its failure to produce a similar depression of the MEP are consistent with a mechanism involving presynaptic inhibition of Ia terminals. Cutaneous (sural nerve) afferent conditioning partially inhibited the TR and MEP over a short time course (ISI <100 ms) resembling the inhibition seen in the voluntary EMG. This was consistent with the postsynaptic origin of cutaneous inhibition of the motoneurons.

Miller Fisher syndrome

The annual incidence of Miller Fisher syndrome is about 0.1 per 100 000 population in the UK.1 According to the World Health Organization, there are about 20 000 neurologists in...

Vagal stimulation for heart failure: Background and first in-man study

This article reviews the background and rationale that have led to the first in-man study of the effects of direct chronic vagal stimulation for the management of heart failure. Following a brief discussion of the concept of "autonomic imbalance," the focus shifts to the wealth of pathophysiologic information gathered over the years by the in-depth study of an animal model for sudden cardiac death. These data, on the bleak prognostic outcome associated with the presence of depressed vagal reflexes in both animals and men and on the striking reversal in outcome produced in high-risk dogs by direct vagal stimulation, made logical the move toward a human study. The data of the first pilot trial in man are presented and reviewed. The study population consisted of eight patients with advanced heart failure who underwent implantation of a neurostimulator system capable of delivering low-current electrical pulses to stimulate the right vagus nerve. These initial data suggest that chronic vagal stimulation in man is feasible and safe. Furthermore, in this pilot study, the treatment appears to be associated with beneficial effects.

Flexor reflex decreases during sympathetic stimulation in chronic human spinal cord injury

A better understanding of autonomic influence on motor reflex pathways in spinal cord injury is important to the clinical management of autonomic dysreflexia and spasticity in spinal cord injured patients. The purpose of this study was to examine the modulation of flexor reflex windup during episodes of induced sympathetic activity in chronic human spinal cord injury (SCI). We simultaneously measured peripheral vascular conductance and the windup of the flexor reflex in response to conditioning stimuli of electrocutaneous stimulation to the opposite leg and bladder percussion. Flexor reflexes were quantified using torque measurements of the response to a noxious electrical stimulus applied to the skin of the medial arch of the foot. Both bladder percussion and skin conditioning stimuli produced a reduction (43–67%) in the ankle and hip flexor torques ( p < 0.05) of the flexor reflex. This reduction was accompanied by a simultaneous reduction in vascular conductance, measured using venous plethysmography, with a time course that matched the flexor reflex depression. While there was an overall attenuation of the flexor reflex, windup of the flexor reflex to repeated stimuli was maintained during periods of increased sympathetic activity. This paradoxical depression of flexor reflexes and minimal effect on windup is consistent with inhibition of afferent feedback within the superficial dorsal horn. The results of this study bring attention to the possible interaction of motor and sympathetic reflexes in SCI above and below the T5 spinal level, and have implications for clinicians in spasticity management and for researchers investigating motor reflexes post SCI.

Extracellular magnesium enhances the damage to locomotor networks produced by metabolic perturbation mimicking spinal injury in the neonatal rat spinal cord in vitro

An acute injury to brain or spinal cord produces profound metabolic perturbation that extends and exacerbates tissue damage. Recent clinical interventions to treat this condition with i.v. Mg 2+ to stabilize its extracellular concentration provided disappointing results. The present study used an in vitro spinal cord model from the neonatal rat to investigate the role of extracellular Mg 2+ in the lesion evoked by a pathological medium mimicking the metabolic perturbation (hypoxia, aglycemia, oxidative stress, and acid pH) occurring in vivo. Damage was measured by taking as outcome locomotor network activity for up to 24 h after the primary insult. Pathological medium in 1 mM Mg 2+ solution (1 h) largely depressed spinal reflexes and suppressed fictive locomotion on the same and the following day. Conversely, pathological medium in either Mg 2+-free or 5 mM Mg 2+ solution evoked temporary network depression and enabled fictive locomotion the day after. While global cell death was similar regardless of extracellular Mg 2+ solution, white matter was particularly affected. In ventral horn the number of surviving neurons was the highest in Mg 2+ free solution and the lowest in 1 mM Mg 2+, while motoneurons were unaffected. Although the excitotoxic damage elicited by kainate was insensitive to extracellular Mg 2+, 1 mM Mg 2+ potentiated the effect of combining pathological medium with kainate at low concentrations. These results indicate that preserving Mg 2+ homeostasis rendered experimental spinal injury more severe. Furthermore, analyzing ventral horn neuron numbers in relation to fictive locomotion expression might provide a first estimate of the minimal size of the functional locomotor network.

Involvement of nitric oxide in 3-nitropropionic acid-induced depression of spinal reflexes in neonatal rat spinal cord in vitro

The objective of the present investigation is to study the involvement of nitric oxide (NO) in 3-nitropropionic acid (3-NPA)-induced depression of spinal reflexes. Experiments were conducted on preparations of hemisected spinal cord isolated from 4 to 8 day old rats. Stimulation of a dorsal root evoked reflex potentials (monosynaptic, MSR; polysynaptic, PSR) in the corresponding segmental ventral root. Superfusion of 3-NPA (3.4 mM) depressed the spinal reflexes in a time-dependent manner and the reflexes were abolished after 35 min. The time required to produce 50% depression of the reflexes (T-50) was 17.8 ± 5.3 min for MSR and 17.5 ± 2.1 min for PSR. L-NAME (Nω-nitro- l-arginine methyl ester; 100 µM), a nitric oxide synthase inhibitor, antagonized the 3-NPA (3.4 mM)-induced depression of reflexes and increased the T-50 values (34 and 30 min for MSR and PSR, respectively) significantly ( P < 0.05). In addition, hemoglobin (Hb, 100 µM), a NO scavenger, blocked the 3-NPA-induced depression of reflexes significantly ( P < 0.05). T-50 values in Hb pretreated cords were 57 and 45 min for MSR and PSR, respectively which were greater than the cords pretreated with L-NAME. The nitrite (NO 2 −) content of the 3-NPA exposed cords was 84 µM/g of tissue which was significantly greater than the control (13 µM/g; P < 0.05). Pretreatment of cords with L-NAME or Hb antagonized the 3-NPA-induced increase in NO 2 −. The results indicate that NO produced by 3-NPA is involved in the 3-NPA-induced depression of spinal reflexes.

Flexion reflex modulation during stepping in human spinal cord injury

The flexion reflex modulation pattern was investigated in nine people with a chronic spinal cord injury during stepping using body weight support on a treadmill and manual assistance by therapists. Body weight support was provided by an upper body harness and was adjusted for each subject to promote the best stepping pattern with the least manual assistance required by the therapists. The flexion reflex was elicited by sural nerve stimulation with a 30 ms pulse train at 1.2-2 times the tibialis anterior reflex threshold. During stepping, stimuli were randomly dispersed across the gait cycle which was divided into 16 equal bins. A long latency (>110 ms) flexion reflex was present in all subjects, while a short (>30 ms) and a medium latency (>70 ms) flexion reflex were present only in three subjects. For each response, the non-stimulated EMG was subtracted from the stimulated EMG at identical time windows and bins, normalized to the maximal corresponding EMG, and significant differences were established with a Wilcoxon rank-sum test. The long latency flexion reflex was facilitated at late stance and during the swing-to-stance transition phase. A reflex depression was present from heel strike until mid-stance and during the swing-to-stance transition phase. The short and medium latency flexion reflexes were depressed during mid-stance followed by facilitation during the stance-to-swing transition phase. Regardless of the latency, facilitatory flexion responses during the swing phase coincided with decreased activity of ipsilateral ankle extensors. The flexion reflex was modulated in a phase dependent manner, a behavior that was absent for the soleus H-reflex in most of these patients (Knikou et al. in Exp Brain Res 193:397-407, 2009). We propose that training should selectively target spinal reflex circuits in which extensor muscles and reflexes are involved in order to maximize sensorimotor recovery in these patients.

Aortic baroreceptor function and depressed baroreflex sensitivity following myocardial infarction

Depressed sinoaortic baroreflex control of heart rate following myocardial infarction (MI) is associated with increased morbidity and mortality. The etiology of this autonomic disturbance is unknown but could potentially occur at several levels of the reflex arc. The purpose of this study was to assess whether depressed baroreflex sensitivity (BRS) post-MI is associated with aortic baroreceptor dysfunction.BRS was measured before and 4–8 weeks after anterior MI in 17 chronically-instrumented, trained, conscious dogs. BRS (ms/mm Hg) was defined as the slope of the relationship between changes in systolic blood pressure (SBP) and heart period in response to a bolus dose of phenylephrine (PE). After the effects of MI on BRS were determined, the animals were anesthetized and the aortic depressor nerves (ADN) were isolated from the cervical vagi. Aortic baroreceptor function was measured by direct recording of ADN activity during gradual elevation of SBP induced by PE infusion.BRS was depressed following MI in 7 of these dogs and preserved in the remaining 10. Aortic baroreceptor sensitivity (ABS) defined as the slope of the relationship between changes in ADN activity and SBP was not significantly different between the dogs with depressed BRS compared to the dogs with preserved BRS post-MI.In conclusion, the response of the aortic baroreceptors to an increase in SBP is similar in dogs with and without depressed BRS post-MI. Based on these data, we conclude that depressed reflex control of heart rate following MI is not related to dysfunction of the afferent limb of the sinoaortic baroreflex.

Sensorimotor function as a predictor of chronic ankle instability

Background Recurrent ankle injury occurs in 70% of individuals experiencing a lateral ankle sprain. The cause of this high level of recurrence is currently unknown. Researchers have begun to investigate sensorimotor deficits as one possible cause with inconclusive and often conflicting results. The purpose of this study was to further the understanding of the role of sensorimotor deficits in the chronically unstable ankle by establishing which specific measures best distinguish between chronically unstable and healthy ankles. Methods Twenty-two participants with chronic ankle instability and 21 healthy matched controls volunteered. Twenty-five variables were measured within four sensorimotor constructs: joint kinesthesia (isokinetic dynamometer), static balance (force plate), dynamic balance (Star Excursion Balance Test) and motoneuron pool excitability (electromyography). Findings The above variables were evaluated using a discriminant function analysis [Wilks’ Λ = 0.536 χ 2(7, N = 43) = 22.118, P = 0.002; canonical correlation = 0.681]. The variables found to be significant were then used to assess group discrimination. This study revealed that seven separate variables from the static balance (anterior/posterior and medial/lateral displacement and velocity) and motoneuron pool excitability constructs (single-legged recurrent inhibition and single- and double-legged paired reflex depression) accurately classified over 86% of participants with unstable ankles. Interpretation These results suggest that a multivariate approach may be necessary to understand the role of sensorimotor function in chronic ankle instability, and to the development of appropriate rehabilitation and prevention programs. Out of the four overall constructs, only two were needed to accurately classify the participants into two groups. This indicates that static balance and motoneuron pool excitability may be more clinically important in treatment and rehabilitation of chronic ankle instability than functional balance or joint kinesthesia.