Abnormal Input Research Articles

Geometrical visualisation of indirect space vector modulation for matrix converters operating with abnormal supplies

Matrix converters can be sensitive to abnormal supply conditions due to the absence of energy storage elements. This sensitivity can get worse when the matrix converters are modulated by a traditional indirect space vector modulation that assumes the input variables are sinusoidal and balanced. Therefore, this study proposes a methodology for the modulation of matrix converters without requiring any assumption of the input voltages. The method uses a geometric representation based on the singular value decomposition of the switch states to synthesise the rotating vectors of the target duty-cycle matrix. Furthermore, this study mathematically highlights the factors that regulate the amplitude of the output voltages and utilise them to compensate the adverse effect of the abnormal input voltages. Experimental results presented in this study validate that the proposed method can provide sinusoidal and balanced output currents in the presence of abnormal supply conditions.

Outlier Detection of Space Trilateration Localization Based on Geometric Inequalities

The three-dimensional positioning problem remains as a challenge in modern commercial communication networks. Yet conventional algorithms, such as the trilateration localization algorithm, are vulnerable to abnormal distance input values which are common in praxis. To address this problem, we introduced an outlier detection approach based on geometric reasoning prior to localization. This process detects and discards abnormal distance values and thus increase the robustness of conventional localization algorithms. Our main concern is the validity of geometry, for example, whether triangle or tetrahedron can be formed is valued in the spatial trilateration localization algorithm. This method is generally used to locate target on the ground, and the problem of ambiguity can be avoided. To this end, geometric reasoning based algorithms such as the triangle inequality and tetrahedral inequality are applied for detection. In this paper, we have mathematically validated the correctness of the proposed method. We have also demonstrated that the proposed method outperforms conventional methods using in silico simulation.

Voltage-Independent SK-Channel Dysfunction Causes Neuronal Hyperexcitability in the Hippocampus ofFmr1Knock-Out Mice

Neuronal hyperexcitability is one of the major characteristics of fragile X syndrome (FXS), yet the molecular mechanisms of this critical dysfunction remain poorly understood. Here we report a major role of voltage-independent potassium (K+)-channel dysfunction in hyperexcitability of CA3 pyramidal neurons in Fmr1 knock-out (KO) mice. We observed a reduction of voltage-independent small conductance calcium (Ca2+)-activated K+ (SK) currents in both male and female mice, leading to decreased action potential (AP) threshold and reduced medium afterhyperpolarization. These SK-channel-dependent deficits led to markedly increased AP firing and abnormal input-output signal transmission of CA3 pyramidal neurons. The SK-current defect was mediated, at least in part, by loss of FMRP interaction with the SK channels (specifically the SK2 isoform), without changes in channel expression. Intracellular application of selective SK-channel openers or a genetic reintroduction of an N-terminal FMRP fragment lacking the ability to associate with polyribosomes normalized all observed excitability defects in CA3 pyramidal neurons of Fmr1 KO mice. These results suggest that dysfunction of voltage-independent SK channels is the primary cause of CA3 neuronal hyperexcitability in Fmr1 KO mice and support the critical translation-independent role for the fragile X mental retardation protein as a regulator of neural excitability. Our findings may thus provide a new avenue to ameliorate hippocampal excitability defects in FXS.SIGNIFICANCE STATEMENT Despite two decades of research, no effective treatment is currently available for fragile X syndrome (FXS). Neuronal hyperexcitability is widely considered one of the hallmarks of FXS. Excitability research in the FXS field has thus far focused primarily on voltage-gated ion channels, while contributions from voltage-independent channels have been largely overlooked. Here we report that voltage-independent small conductance calcium-activated potassium (SK)-channel dysfunction causes hippocampal neuron hyperexcitability in the FXS mouse model. Our results support the idea that translation-independent function of fragile X mental retardation protein has a major role in regulating ion-channel activity, specifically the SK channels, in hyperexcitability defects in FXS. Our findings may thus open a new direction to ameliorate hippocampal excitability defects in FXS.

Imbalanced dataset-based echo state networks for anomaly detection

Anomaly detection is a very effective method to extract useful information from abundant data. Most existing anomaly detection methods are based on normal region or some specific algorithms, which ignore the fact that many actual datasets are mainly imbalanced, resulting in not function properly or effectively in practical, especially in the medical field. On the other hand, imbalanced dataset is also a frequently encountered problem in the learning of neural network because the lack of data in a minority class may lead to uneven classification accuracy. In this paper, inspired by these observations, a novel anomaly detection approach by using classical echo state network (ESN), a brain-inspired neural computing model, is presented. The entire dataset of the proposed method obeys an extremely imbalanced distribution, that is, anomalies are much rarer than normal data. And the training dataset has only the normal data. When the ESN is well trained, the parameters in ESN are the memory of normal data. If the normal data are added into the well-trained network, the error between the input data and the corresponding output is smaller compared with the error between abnormal input data and its corresponding output. Then anomaly behavior is detected if the error between the input data and the corresponding predictive value exceeds a certain threshold. Different from setting an invariable threshold arbitrarily for all of the data, the threshold value used in the proposed method is determined from the analysis of information theory and can be adjust adaptively according to different datasets. Experiments on abnormal heart rate detection are conducted to demonstrate and verify the effectiveness of the proposed detection algorithm and theory.

The role of Rac in tumor susceptibility and disease progression: from biochemistry to the clinic

The family of Rho GTPases are involved in the dynamic control of cytoskeleton reorganization and other fundamental cellular functions, including growth, motility, and survival. Rac1, one of the best characterized Rho GTPases, is an established effector of receptors and an important node in signaling networks crucial for tumorigenesis and metastasis. Rac1 hyperactivation is common in human cancer and could be the consequence of overexpression, abnormal upstream inputs, deregulated degradation, and/or anomalous intracellular localization. More recently, cancer-associated gain-of-function mutations in Rac1 have been identified which contribute to tumor phenotypes and confer resistance to targeted therapies. Deregulated expression/activity of Rac guanine nucleotide exchange factors responsible for Rac activation has been largely associated with a metastatic phenotype and drug resistance. Translating our extensive knowledge in Rac pathway biochemistry into a clinical setting still remains a major challenge; nonetheless, remarkable opportunities for cancer therapeutics arise from promising lead compounds targeting Rac and its effectors.

Research progress of functional magnetic resonance imaging in mechanism studies of tinnitus

Tinnitus is a subjective symptom of phantom sound in the ear or brain without sound or electrical stimulation in the environment. The mechanism of tinnitus is complicated and mostly unclear. Recent studies suggested that the abnormal peripheral auditory input lead to neuroplasticity changes in central nervous system followed by tinnitus. More research concerned on the tinnitus central mechanism. A rapid development of functional magnetic resonance imaging (fMRI) technique made it more widely used in tinnitus central mechanism research. fMRI brought new findings but also presented some shortages in technology and cognition in tinnitus study. This article summarized the outcomes of fMRI research on tinnitus in recent years, exploring its existing problems and application prospects.

Model predictive control for reduced matrix converter with transformer DC magnetic bias suppression

This study presents a model predictive control (MPC) considering transformer DC magnetic bias for a reduced matrix converter (RMC). The control scheme selects the switching state that minimises the error in the output current and input instantaneous reactive according to their reference values; furthermore, the pulse sequence in MPC has been re-distributed to suppress the DC magnetic bias in transformer for RMC. MPC also presents stronger immunity to the influence of abnormal input voltage than bipolar space vector modulation strategy. Moreover, the simple performance comparison between RMC and pulse-width modulated rectifier + dual active bridge was provided. The feasibility and validity of the proposed control scheme in an RMC has been verified by simulation results.

Typical sensory organization test findings and clinical implication in acute vestibular neuritis

ObjectiveSensory organization test (SOT) is used to evaluate postural instability. We wanted to characterize the SOT findings in patients with acute vestibular neuritis (VN). MethodsEighty-seven patients with VN were enrolled. The bithermal caloric and SOT were performed, and the results were compared with those from the dizziness handicap inventory (DHI). Abnormal SOT patterns were classified: severe, visual vestibular, vestibular, inconsistent, or normal patterns. The results were also analyzed by sensory analysis (somatosensory, visual, vestibular, and visual preference) and composite scores. ResultsSixty-one patients (70%) showed abnormal findings for conditions 5 and/or 6 (vestibular pattern), and half (30 of 61, 49%) of them showed additional abnormal results in more than conditions 5 and 6. In pattern analysis, the vestibular pattern (abnormal in conditions 5 and 6) was the most common pattern (36%), and the visual vestibular pattern (abnormal in conditions 4, 5, and 6) was the second most common (24%). In sensory analysis, vestibular dysfunction was observed in 59 patients (68%), visual dysfunction in 37 (43%), visual preference in 17 (20%), and somatosensory dysfunction in 5 (6%). Composite scores of SOT showed a significant correlation with the DHI scores, though no correlation was observed between DHI and caloric results (p<0.05). ConclusionVN can adversely influence on postural instability, with more severe patterns as well as classical vestibular patterns, indicating that abnormal vestibular inputs can influence postural stability in all SOT conditions and subjective symptom in patients with acute VN is more closely associated with the postural instability rather than canal dysfunction.

Stimulation of the mesencephalic locomotor region for gait recovery after stroke.

One-third of all stroke survivors are unable to walk, even after intensive physiotherapy. Thus, other concepts to restore walking are needed. Because electrical stimulation of the mesencephalic locomotor region (MLR) is known to elicit gait movements, this area might be a promising target for restorative neurostimulation in stroke patients with gait disability. The present study aims to delineate the effect of high-frequency stimulation of the MLR (MLR-HFS) on gait impairment in a rodent stroke model. Male Wistar rats underwent photothrombotic stroke of the right sensorimotor cortex and chronic implantation of a stimulating electrode into the right MLR. Gait was assessed using clinical scoring of the beam-walking test and video-kinematic analysis (CatWalk) at baseline and on days 3 and 4 after experimental stroke with and without MLR-HFS. Kinematic analysis revealed significant changes in several dynamic and static gait parameters resulting in overall reduced gait velocity. All rats exhibited major coordination deficits during the beam-walking challenge and were unable to cross the beam. Simultaneous to the onset of MLR-HFS, a significantly higher walking speed and improvements in several dynamic gait parameters were detected by the CatWalk system. Rats regained the ability to cross the beam unassisted, showing a reduced number of paw slips and misses. MLR-HFS can improve disordered locomotor function in a rodent stroke model. It may act by shielding brainstem and spinal locomotor centers from abnormal cortical input after stroke, thus allowing for compensatory and independent action of these circuits. Ann Neurol 2017;82:828-840.

Cervical Vertigo: Historical Reviews and Advances.

Vertigo is one of the most common presentations in adult patients. Among the various causes of vertigo, so-called cervical vertigo is still a controversial entity. Cervical vertigo was first thought to be due to abnormal input from cervical sympathetic nerves based on the work of Barré and Liéou in 1928. Later studies found that cerebral blood flow is not influenced by sympathetic stimulation. Ryan and Cope in 1955 proposed that abnormal sensory information from the damaged joint receptors of upper cervical regions may be related to pathologies of vertigo of cervical origin. Further studies found that cervical vertigo seems to originate from diseased cervical intervertebral discs. Recent research found that the ingrowth of a large number of Ruffini corpuscles into diseased cervical discs may be related to vertigo of cervical origin. Abnormal neck proprioceptive input integrated from the signals of Ruffini corpuscles in diseased cervical discs and muscle spindles in tense neck muscles secondary to neck pain is transmitted to the central nervous system and leads to a sensory mismatch with vestibular and other sensory information, resulting in a subjective feeling of vertigo and unsteadiness. Further studies are needed to illustrate the complex pathophysiologic mechanisms of cervical vertigo and to better understand and manage this perplexing entity.

Influence of neck torsion on near point convergence in subjects with idiopathic neck pain

BackgroundPeople with neck pain (NP) experience sensorimotor and oculomotor deficits thought to be due to abnormal cervical afferent input. Convergence insufficiency (CI) measured by near point convergence (NPC) may be a feature in NP and neck torsion might help to differentiate a cervical cause. ObjectivesThis study aimed to investigate repeatability and reliability of NPC in neutral and torsion and compare between idiopathic NP and controls along with correlation to the Convergence Insufficiency Symptom Survey (CISS). DesignComparative cross sectional observational study. MethodA Royal Airforce (RAF) Rule measured NPC with the neck in neutral and in 45° torsion to the left and right in 42 subjects. A revised 15 item CISS was also completed. The average of 3 trials in each position and torsion difference were calculated. Within one week, NPC inter-rater and test-retest reliability was evaluated in 10 subjects. ResultsA significant NPC torsion difference was demonstrated in participants with NP compared to controls (P = 0.01). No significant differences were seen for NPC values in neutral (P = 0.73). High inter-rater reliability (ICC = 0.95) and repeatability (ICC = 0.84) was obtained. No correlations were present between the CISS and NPC measures (r ≤ 0.18). ConclusionsNPC is impaired in neck torsion compared to neutral in NP supporting a cervical afferent cause. NPC, measured using the RAF Rule, is a reliable and repeatable measure and can be used to assess NPC and CI in those with NP. Objective rather than self-reported measures should be used to examine CI in NP.

Dizziness, Unsteadiness, Visual Disturbances, and Sensorimotor Control in Traumatic Neck Pain.

Synopsis There is considerable evidence to support the importance of cervical afferent dysfunction in the development of dizziness, unsteadiness, visual disturbances, altered balance, and altered eye and head movement control following neck trauma, especially in those with persistent symptoms. However, there are other possible causes for these symptoms, and secondary adaptive changes should also be considered in differential diagnosis. Understanding the nature of these symptoms and differential diagnosis of their potential origin is important for rehabilitation. In addition to symptoms, the evaluation of potential impairments (altered cervical joint position and movement sense, static and dynamic balance, and ocular mobility and coordination) should become an essential part of the routine assessment of those with traumatic neck pain, including those with concomitant injuries such as concussion and vestibular or visual pathology or deficits. Once adequately assessed, appropriate tailored management should be implemented. Research to further assist differential diagnosis and to understand the most important contributing factors associated with abnormal cervical afferent input and subsequent disturbances to the sensorimotor control system, as well as the most efficacious management of such symptoms and impairments, is important for the future. J Orthop Sports Phys Ther 2017;47(7):492-502. Epub 16 Jun 2017. doi:10.2519/jospt.2017.7052.

Intra-spinal microstimulation may alleviate chronic pain after spinal cord injury

Chronic pain after spinal cord injury (SCI) is a form of central neuropathic pain that is debilitating and often refractory to current pharmacological treatments. Neurostimulation pain therapies, such as epidural spinal cord stimulation, have only moderate success in reducing SCI pain. The pathogenesis of SCI pain may involve a state of central neuronal hyperexcitability, especially in the spinal cord dorsal horn, that develops after injury. We hypothesize that the neuronal structures near the spinal cord injury site may be an important pain generator, and intraspinal microstimulation (ISMS) may normalize dorsal horn neuronal hyperexcitability and hence alleviate SCI pain. Specifically, ISMS may induce frequency-dependent conduction block on axons of afferent sensory neurons, in the spinothalamic tract and Lissauer’s tract. ISMS may also facilitate primary afferent depolarization that elicits presynaptic inhibition of incoming afferent inputs. Together, these actions will reduce abnormal afferent inputs and ascending pain signals before they can reach the brain. Furthermore, ISMS may directly induce inhibitory postsynaptic potentials in dorsal horn neurons, and trigger the release of endogenous inhibitory neurotransmitters, opioids and serotonin to inhibit postsynaptic neurons and restore the compromised segmental pain inhibition after SCI. Finally, ISMS may alter the frequency and pattern of discharge such that the rostrally conducted impulses no longer code pain or activate brain areas concerned with pain signaling. Based on recent progress in understanding spinal learning and plasticity, we also postulate that repetitive or long-term ISMS may help the dorsal horn “reset” neuronal excitability and regain normal pain processing for a prolonged period. By finely tuning the stimulation parameters (e.g., intensity, pulse width, frequency), position, and geometry of ISMS electrode, multiple spinal structures (e.g., dorsal horn, dorsal column, spinothalamic tract) may be modulated to induce synergistic pain inhibition. Our hypothesis can be readily tested in preclinical models of SCI pain by using a combination of in vivo electrophysiological (neuronal activity) and animal behavioral (pain response) approaches. Since ISMS electrodes stimulate the spinal structures directly, we expect that the effective stimulus intensity and energy consumption can be lower than that for epidural spinal cord stimulation. The proposed hypothesis may provide insights and rationales for developing a novel neurostimulation pain therapy by directly inhibiting the pain generators in the spinal cord, and ISMS may be an alternative strategy to treat SCI pain.

The role of environmental stress on lower urinary tract symptoms.

Lower urinary tract symptoms (LUTS) have been associated with comorbid conditions such as anxiety and depression. In addition, stress appears to influence the development or exacerbation of LUTS. This article seeks to review literature regarding the role of environmental stress on LUTS, focusing on findings presented in the last year. Numerous authors have published on the impact early childhood experiences, acute and chronic stress, and psychiatric illness play in the development of LUTS. The exact nature of the association between bladder symptoms and psychosocial measures remains unknown and is likely due to a complex interplay between heritability, psychosocial factors, and environmental stress. The proposed pathophysiological pathways involved in emotional states such as anxiety and depression, stress, and bladder function include activation of the hypothalamic-pituitary axis, dysregulation of the serotonergic pathways, and central sensitization. Recent work has additionally suggested that urinary syndromes involving abnormal or augmented sensory input, such as overactive bladder and interstitial cystitis/bladder pain syndrome, may be a spectrum of the same disorder. There are numerous developments in our understanding of the role of environmental stress on the development and exacerbation of LUTS with new developments both clinically and in translational basic science work. Clinicians must acknowledge the high prevalence of affective disorders in patients with LUTS and realize their potential therapeutic influence. Simply addressing mechanisms at the level of the bladder alone may fail in a subpopulation of patients with LUTS who may have significant psychosocial drivers of their symptoms.

Use of neck torsion as a specific test of neck related postural instability

BackgroundDisturbed postural stability in neck pain (NP) is likely due to abnormal cervical afferent function. Several potential causes requires specific diagnostic tests. The neck torsion (head still body rotated) manoeuvre stimulates cervical but not vestibular receptors and identified abnormal cervical afferent input as the cause in patients with NP compared to healthy controls. Comparison between vestibular and NP subjects is now needed. AimsTo compare individuals with unilateral vestibular loss (UVL), persistent NP and asymptomatic controls. It was hypothesized that neck torsion will increase postural stability in NP compared to both the asymptomatic and UVL groups. MethodsTwenty UVL, 20 persistent NP and 20 asymptomatic control subjects underwent measurement of postural stability on a computerised force plate with eyes closed in comfortable stance under 5 conditions: neutral head, head rotated 45° (left and right) and neck torsion (left and right). Root mean square (rms) amplitude of sway was measured in the anterior posterior (AP) and medial lateral (ML) directions. Average torsion and torsion difference (average torsion – neutral neck) were calculated. ResultsNP subjects had significantly greater (p < 0.05) AP sway with average torsion and torsion difference compared to both control and UVL. There were no significant differences between control and UVL and no between group differences for neutral neck, rotation or rotation difference. ConclusionThe results of the study suggest that the torsion manouever may identify cervical afferent causes of disturbed postural stability. This is important for guiding assessment and management of balance disturbances in patients.

Pharmacological Modulation of the Sigma 1 Receptor and the Treatment of Pain.

There is a critical need for new analgesics acting through new mechanisms of action, which could increase the efficacy with respect to existing therapies and reduce their unwanted effects. Current preclinical evidence supports the modulatory role of sigma-1 receptors (σ1R) in nociception, mainly based on the pain-attenuated phenotype of σ1R knockout mice and on the antinociceptive effect exerted by σ1R antagonists on pains of different etiologies. σ1R is highly expressed in different pain areas of the CNS and the periphery (particularly dorsal root ganglia), and interacts and modulates the functionality of different receptors and ion channels . The antagonism of σ1R leads to decreased amplification of pain signaling within the spinal cord (central sensitization), but recent data also support a role at the periphery. σ1R antagonists have consistently demonstrated efficacy in neuropathic pain , but also in other types of pain including inflammatory, orofacial, visceral, and post-operative pain. Apart from acting alone, when combined with opioids, σ1R antagonists enhance opioid analgesia but not opioid-induced unwanted effects. Interestingly, unlike opioids, σ1R antagonists do not modify normal sensory mechanical and thermal sensitivity thresholds but they exert antihypersensitive effects in sensitizing conditions, enabling the reversal of nociceptive thresholds back to normal values. Accordingly, σ1R antagonists are not strictly analgesics; they are antiallodynic and antihyperalgesic drugs acting when the system is sensitized following prolonged noxious stimulation or persistent abnormal afferent input (e.g., secondary to nerve injury). These are distinctive features allowing σ1R antagonists to exert a modulatory effect specifically in pathophysiological conditions such as chronic pain .

66. Effects of cranio-spinal tDCS in the treatment of cognitive and motor symptoms in early Huntington’s Disease

Transcutaneous Direct Current Stimulation (tDCS) is a safe technique for modulating central nervous system excitability. We assessed clinical changes in early Huntington’s Disease (HD) following tDCS by evaluating Unified Huntington Disease Rating Scale (UHDRS). tDCS electrodes were applied over the thoracic spinal cord (T9–T11) and parietal cortex of right hemisphere, respectively as anode and cathode. We applied current at a density of 0.071 mA/cm2 and delivered a total charge density of 85.7 mC/cm2. The stimulation consisted in a daily session of treatment during 5 days, of 20 min (2.0 mA) each one. The clinical evaluation was performed before tDCS (T0), after 5 days of treatment (T1) and after 2 weeks from the last session (T2). After tDCS a significant improvement both in motor (T0 vs. T1: 17 vs. 12) and behavioral scores was found (T0 vs. T1 vs. T2: 25 vs. 18 vs. 13). We showed significant effects of tDCS on motor and behavioral symptoms in early HD. The configuration we used likely reduces the abnormal peripheral afferent input, possibly restoring at the same time the balance of interhemispheric communication by interfering with right parietal hyperactivity.

Cardiac Arrest-Induced Global Brain Hypoxia-Ischemia during Development Affects Spontaneous Activity Organization in Rat Sensory and Motor Thalamocortical Circuits during Adulthood.

Normal maturation of sensory information processing in the cortex requires patterned synaptic activity during developmentally regulated critical periods. During early development, spontaneous synaptic activity establishes required patterns of synaptic input, and during later development it influences patterns of sensory experience-dependent neuronal firing. Thalamocortical neurons occupy a critical position in regulating the flow of patterned sensory information from the periphery to the cortex. Abnormal thalamocortical inputs may permanently affect the organization and function of cortical neuronal circuits, especially if they occur during a critical developmental window. We examined the effect of cardiac arrest (CA)-associated global brain hypoxia-ischemia in developing rats on spontaneous and evoked firing of somatosensory thalamocortical neurons and on large-scale correlations in the motor thalamocortical circuit. The mean spontaneous and sensory-evoked firing rate activity and variability were higher in CA injured rats. Furthermore, spontaneous and sensory-evoked activity and variability were correlated in uninjured rats, but not correlated in neurons from CA rats. Abnormal activity patterns of ventroposterior medial nucleus (VPm) neurons persisted into adulthood. Additionally, we found that neurons in the entopeduncular nucleus (EPN) in the basal ganglia had lower firing rates yet had higher variability and higher levels of burst firing after injury. Correlated levels of power in local field potentials (LFPs) between the EPN and the motor cortex (MCx) were also disrupted by injury. Our findings indicate that hypoxic-ischemic injury during development leads to abnormal spontaneous and sensory stimulus-evoked input patterns from thalamus to cortex. Abnormal thalamic inputs likely permanently and detrimentally affect the organization of cortical circuitry and processing of sensory information. Hypoxic-ischemic injury also leads to abnormal single neuron and population level activity in the basal ganglia that may contribute to motor dysfunction after injury. Combination of deficits in sensory and motor thalamocortical circuit function may negatively impact sensorimotor integration in CA survivors. Modulation of abnormal activity patterns post-injury may represent a novel therapeutic target to improve neurologic function in survivors.

Not only amblyopic but also dominant eye in subjects with strabismus show increased saccadic latency.

Amblyopia is a developmental disorder of vision usually associated with the presence of strabismus and/or anisometropia during early childhood. Subject literature has shown that both the amblyopic and fellow eyes (especially in strabismic subjects) may manifest a variety of perceptual and oculomotor deficits. Previous studies using simple saccadic responses (pro-saccades) showed an increased saccadic latency only for the amblyopic eye viewing conditions. So far, there have appeared no saccadic latency studies in strabismic amblyopia for more complex volitional saccades. In order to maximize the contribution of the central retina in the process of saccade initiation, we decided to use delayed saccadic responses in order to test the hypothesis about saccadic latency increase in both eyes in strabismic amblyopes. The results from our study have shown that saccadic latency is increased both in the dominant and amblyopic eyes. In addition, the amblyopic eye in the strabismic group showed greater increase in saccadic latency compared to an amblyopic eye in the anisometropic group from our previous study. The observed increase in saccadic reaction time for the dominant eye is novel and provides further evidence that the visual pathway associated with the dominant eye might be also impaired in strabismic amblyopia. Since an abnormal binocular input during visual system development may affect gaze stability in both eyes, we speculate that unsteady fixation accompanied with subtle perceptual deficits contribute to an increase in saccadic latency that is observed in the dominant eye. Moreover, it appears that the cortical processes related to saccade decisions are delayed both for amblyopic and fellow eyes in strabismic subjects.

Atypical birdsong and artificial languages provide insights into how communication systems are shaped by learning, use, and transmission

In this article, I argue that a comparative approach focusing on the cognitive capacities and behavioral mechanisms that underlie vocal learning in songbirds and humans can provide valuable insights into the evolutionary origins of language. The experimental approaches I discuss use abnormal song and atypical linguistic input to study the processes of individual learning, social interaction, and cultural transmission. Atypical input places increased learning and communicative pressure on learners, so exploring how they respond to this type of input provides a particularly clear picture of the biases and constraints at work during learning and use. Furthermore, simulating the cultural transmission of these unnatural communication systems in the laboratory informs us about how learning and social biases influence the structure of communication systems in the long run. Findings based on these methods suggest fundamental similarities in the basic social–cognitive mechanisms underlying vocal learning in birds and humans, and continuing research promises insights into the uniquely human mechanisms and into how human cognition and social behavior interact, and ultimately impact on the evolution of language.