Anarthria represents the most profound manifestation of motor speech impairment, characterized by the absolute inability to articulate intelligible spoken language due to severe neuromuscular disruption. Far from being a cognitive or linguistic deficit in language formulation, this condition isolates an intact intellect behind an unresponsive vocal tract, standing at the complex crossroads of neurology, speech-language pathology, and neuropsychology. Understanding its pathophysiological substrates, clinical presentations, and diagnostic boundaries remains critical for clinician-scientists working to restore communicative agency to affected individuals.
Anarthria
1. Concise Definition
Anarthria is a severe neurogenic motor speech disorder characterized by the complete loss of the capacity to articulate speech sounds, phonemes, and words. It arises from severe neuromotor damage to the muscular systems responsible for respiration, phonation, resonance, and articulation, rendering the patient entirely mute or restricted to uncoordinated, non-communicative vocalizations.
Unlike linguistic impairments such as aphasia, individuals presenting with pure anarthria retain internal language formulation, grammatical comprehension, reading comprehension, and communicative intentionality. The disruption resides exclusively within the motor execution or motor planning pathways of the central or peripheral nervous systems. Clinically, it is conceptualized as the terminal, most severe grade on the spectrum of dysarthria, or alternatively as the complete presentation of severe apraxia of speech, leaving the vocal tract incapable of executing intelligible verbal motor programs.
2. Etymology & Linguistic Origin
The term anarthria derives from Ancient Greek linguistic roots. It is constructed from the privative prefix an- (ἀν-), denoting absence, negation, or privation, combined with the root noun arthron (ἄρθρον), meaning “joint” or “juncture.” In classic Hellenic linguistics, this root extended metaphorically to articulated, structured sound or distinct speech segments—hence arthroun (ἀρθροῦν), “to articulate or utter sounds distinctly.”
The suffix -ia (-ία) designates a pathological state or condition. The literal etymological meaning translates to “a condition of being without joints” or, in a phonetic context, “an absence of articulated speech.” The term entered the Western medical lexicon in the nineteenth century, formalized by French and German neurologists such as Pierre Marie, who sought a rigorous operational term to distinguish purely mechanical articulatory deficits from higher-order symbolic cognitive disturbances.
3. Pronunciation & Grammatical Form
The standard phonetic transcription of anarthria in the International Phonetic Alphabet (IPA) is /eɪnˈɑːr.θri.ə/ in British English and /ænˈɑːr.θri.ə/ or /eɪnˈɑːr.θri.ə/ in General American English. Grammatically, the term functions as an uncountable abstract noun (e.g., “The patient exhibited profound anarthria following the basilar artery thrombosis”).
Its adjectival form is anarthric (/eɪnˈɑːr.θrɪk/), frequently utilized in clinical phrases such as “anarthric patient” or “anarthric syndrome.” The condition can also appear in adverbial constructions as anarthrically, though this usage is rare in formal clinical literature. In historical texts, the variant spelling anarthrie appears in translations from the French and German neurological literature.
4. Detailed Conceptual Explanation
To fully grasp anarthria, one must dissect the intricate neurological hierarchy of human verbal communication. Human speech requires the coordinated execution of three major neurological domains: conceptual-linguistic processing (selecting words and constructing syntactic structures), motor planning and programming (translating linguistic symbols into spatiotemporal motor commands), and neuromuscular execution (transmitting nerve impulses to the vocal musculature to produce sound). Anarthria represents a breakdown at either the motor programming level or, far more commonly, the execution stage.
When neuromuscular execution fails entirely, every subsystem of speech production collapses. The respiratory system fails to generate the controlled subglottic air pressure needed to vibrate the vocal folds. The laryngeal subsystem cannot modulate vocal cord tension, causing aphonia or involuntary stridor. The velopharyngeal mechanism cannot seal the nasal cavity from the oral cavity, leading to total hypernasality. Finally, the oral articulators—including the tongue, lips, mandible, and soft palate—cannot assume the precise geometric configurations required to produce consonants and vowels. The outcome is absolute loss of articulate acoustic output.
A critical clinical distinction lies between pure anarthria and generalized mutism. While an anarthric individual cannot speak due to severe paralysis, paresis, or apraxia of the speech musculature, their cognitive desire to communicate, emotional responsiveness, and non-vocal language functions remain intact. Conversely, conditions such as akinetic mutism involve a fundamental defect in motivation, initiation, and drive to interact, rooted in frontal-subcortical or limbic circuit damage, despite an intact peripheral motor apparatus. In anarthria, the patient attempts to speak, but the vocal tract remains nonfunctional.
The anatomical substrates underlying anarthria are diverse yet concentrated along specific motor networks. The most common cause is severe bilateral damage to the corticobulbar tract, the primary descending pathway from the motor cortex to the cranial nerve nuclei in the brainstem (specifically cranial nerves V, VII, IX, X, and XII). Bilateral interruption of these upper motor neurons causes pseudobulbar palsy, precipitating spastic anarthria. Alternatively, extensive bilateral destruction of the lower motor neurons within the medulla oblongata and pons leads to bulbar palsy, resulting in flaccid anarthria marked by muscular atrophy and fasciculations.
Anarthria also occurs in non-paralytic forms, frequently referred to in neurological literature as “aphemic” or “pure cortical anarthria.” In these rare presentations, focal lesions affecting the dominant premotor cortex, supplementary motor area (SMA), or the anterior insula disrupt the feedforward and feedback motor models required to orchestrate speech movements, leaving the individual structurally and muscularly capable of reflexive movements (such as swallowing or coughing), yet completely unable to organize volitional articulatory gestures.
5. Historical Development
The clinical and conceptual formulation of anarthria emerged during the nineteenth-century golden age of European clinical neurology, amid intense scientific debates regarding the localization of cerebral function. In 1861, Paul Broca presented his seminal work on the loss of articulated speech, introducing the term aphemia to describe his patient Leborgne (popularly known as “Tan”). Broca conceptualized this condition as a loss of the specialized memory for motor speech coordination, preserving general intellect and language comprehension.
A profound epistemological shift occurred in 1906, when French neurologist Pierre Marie published his iconoclastic treatise, “Revision of the Question of Aphasia: The Third Left Frontal Convolution Plays No Special Role in Language Function.” Marie contested Broca’s claims, arguing that true aphasia was fundamentally a solitary cognitive-linguistic disorder linked to Wernicke’s sensory area, while Broca’s expressive disturbance was simply anarthria—a pure motor speech deficit. Marie localized this pure speech impairment to what he designated the “lenticular zone” (incorporating the lentiform nucleus, internal capsule, and external capsule), maintaining that lesions restricted to this quadrilateral space produced pure articulatory failure without intellectual deterioration.
Throughout the mid-twentieth century, the nomenclature became increasingly fractionated across international borders. British and American neurologists, influenced by John Hughlings Jackson and later by Russell Brain, favored separating expressive linguistic disturbances (aphasia/dysphasia) from mechanical motor execution disorders (dysarthria/anarthria). In the 1960s and 1970s, Darley, Aronson, and Brown at the Mayo Clinic established the modern classification of motor speech disorders, rigorously categorizing dysarthria subtypes and defining anarthria as the catastrophic, end-stage variant across all dysarthric classifications.
In modern cognitive neuroscience and neuroimaging, the advent of functional magnetic resonance imaging (fMRI), diffusion tensor tractography, and electrocorticography has clarified the neural architecture of speech motor execution. Investigators now map the specific functional connectivity among the ventral sensorimotor cortex, the basal ganglia loops, the cerebellum, and brainstem nuclei, revealing that historical “anarthria” encompasses distinct pathophysiological disruptions within highly specialized motor feedback and feedforward circuits.
6. Theoretical Foundations
The modern understanding of anarthria rests upon classical neurobiological and motor control frameworks, particularly the hierarchical models of motor speech production developed by James Abbs, Ronald Netsell, and Malcolm McNeil. In these paradigms, speech generation unfolds across distinct architectural strata: conceptualization, linguistic formulation, motor planning, motor programming, and motor execution. Anarthria represents a failure within the final two tiers—programming and execution.
From the perspective of computational motor control, anarthria can be analyzed through the lens of the DIVA (Directions into Velocities of Articulators) model, formulated by Frank Guenther and colleagues. The DIVA model posits that speech production relies on feedforward control subsystems operating alongside auditory and somatosensory feedback loops. Cortical planning maps send predictive motor commands to articulatory velocity position controllers. In pure motor execution anarthria, structural damage to corticobulbar projections interrupts the transmission of these velocity signals to the cranial motor nuclei, preventing mechanical output regardless of the integrity of internal forward models.
Neurologically, two primary theoretical frameworks explain execution failure: the Upper Motor Neuron (UMN) model and the Lower Motor Neuron (LMN) model. In bilateral UMN disease, the loss of cortical modulation leads to hypertonia, spasticity, hyperreflexia, and profound loss of individual motor unit control, causing antagonistic muscles to co-contract and locking the articulatory tract in fixed immobility. Conversely, LMN pathology severs the final common pathway; muscles undergo denervation, rapid atrophy, and flaccid paresis, depriving the speech apparatus of the contractile force necessary to produce sound.
At the network level, the basal ganglia and cerebellar circuits provide essential modulatory influence. Striatal-pallidal degradation, as seen in end-stage parkinsonian syndromes, causes profound akinesia and rigidity of the pharyngeal and lingual structures. Cerebellar destruction eliminates spatiotemporal coordination, rendering speech movements entirely dysmetric and erratic. When these regulatory circuits experience catastrophic bilateral disruption, coordinated articulatory movements collapse into profound, unresolvable mutism.
7. Key Components, Types & Dimensions
Anarthria is classified across several pathophysiological and neuroanatomical dimensions. Because it represents total failure of speech production, clinical typology mirrors underlying nervous system lesions:
- Spastic Anarthria: Results from catastrophic bilateral lesions of the upper motor neurons (corticobulbar tracts), frequently secondary to pseudobulbar palsy, bilateral strokes, or advanced motor neuron disease. It is characterized by severe muscular hypertonicity, hyperactive gag reflexes, clonus, emotional lability (pathological laughing and crying), and complete arrest of articulatory gestures.
- Flaccid Anarthria: Caused by bilateral destruction of the lower motor neurons within the cranial nerve motor nuclei (CN V, VII, IX, X, XII) or their peripheral axonal branches, common in progressive bulbar palsy or late-stage Guillain-Barré syndrome. Features include profound muscular flaccidity, extensive lingual atrophy, widespread fasciculations, absence of protective airway reflexes, and complete inability to sustain phonatory air pressure.
- Hypokinetic Anarthria: Typically observed in the terminal stages of progressive neurodegenerative basal ganglia disorders, such as Parkinson’s disease, progressive supranuclear palsy (PSP), or multiple system atrophy (MSA). The patient experiences extreme muscular rigidity, akinesia, and an absence of articulatory amplitude, reducing vocalization to an inaudible, motionless state.
- Hyperkinetic Anarthria: Arises from catastrophic, continuous involuntary movements that relentlessly interrupt and destabilize voluntary speech efforts. Seen in severe choreic or dystonic disorders (e.g., late-stage Huntington’s disease, generalized secondary dystonia), where violent, involuntary contractions of the diaphragm, laryngeal musculature, and tongue completely override voluntary motor control.
- Ataxic Anarthria: Caused by extensive bilateral cerebellar pathology. It involves total loss of motor coordination, dysmetria, and kinetic tremor across the respiratory and articulatory apparatus, rendering attempted verbal utterances entirely chaotic, fragmented, and acoustically uninterpretable.
- Apraxic Anarthria (Pure Cortical Anarthria / Aphemia): A high-level motor speech programming failure without neuromuscular weakness, spasticity, or sensory loss. It stems from localized lesions to the dominant inferior premotor cortex, left frontal operculum, or anterior insula. The individual cannot select, sequence, or initiate speech motor commands, yet exhibits preserved reflexive movements such as smiling, chewing, and swallowing.
- Mixed Anarthria: The most frequent clinical manifestation, resulting from combined neuromotor system pathology. Exemplified by amyotrophic lateral sclerosis (ALS), which combines spastic and flaccid disruptions, and severe traumatic brain injury, which often damages both cortical and subcortical pathways.
8. Examples & Illustrative Cases
To differentiate anarthria from related neurological syndromes, consider the clinical presentation of Locked-In Syndrome (LIS). A 58-year-old patient experiences an acute ischemic stroke resulting from occlusion of the basilar artery, leading to bilateral infarction of the ventral pons. The ascending reticular activating system and supratentorial cognitive networks remain undamaged, leaving the patient fully awake, oriented, and cognitively intact.
However, the descending corticospinal and corticobulbar tracts are entirely interrupted. The patient exhibits total quadriplegia and complete flaccid-spastic anarthria, unable to move the lips, tongue, palate, or pharynx, and incapable of producing voluntary phonation. Communication is restricted exclusively to preserved vertical eye movements and upper eyelid blinking, coordinated by the sparing of the midbrain tectum and oculomotor nerve nuclei (CN III). This presentation represents pure execution-level anarthria in its most dramatic form: profound physical mutism coupled with completely intact linguistic and cognitive processes.
A second illustrative example involves the progression of Bulbar Amyotrophic Lateral Sclerosis (ALS). A 64-year-old individual initially presents with mild hypernasality and imprecise lingual consonants. Over twelve months, neurodegeneration destroys both upper motor neurons in the primary motor strip and lower motor neurons within the hypoglossal, ambiguous, and facial motor nuclei.
Speech deterioration progresses from moderate mixed dysarthria to profound anarthria. In this final stage, the tongue lies completely motionless, atrophic, and covered in fasciculations along the floor of the mouth. The soft palate cannot elevate, the vocal cords cannot adduct to generate a voice, and respiratory vital capacity drops below one liter. The patient cannot generate intelligible sounds, yet can comprehend complex written prose and, prior to manual motor loss, type articulate messages on an eye-tracking computer interface.
9. Measurement & Assessment
Assessing anarthria requires a multidisciplinary evaluation combining neurology, speech-language pathology, and clinical neuropsychology. The primary diagnostic goals are establishing the motor etiology, documenting the absence of speech motor execution, ruling out cognitive-linguistic impairments, and determining whether non-verbal communication remains viable.
The evaluation protocol typically includes the following diagnostic steps:
- Structural and Reflexive Motor Examination: Detailed examination of the cranial nerves (V, VII, IX, X, XI, XII). The clinician evaluates resting posture, symmetry, range of motion, force, and tone of the facial, mandibular, lingual, and velopharyngeal musculature. Pathological reflexes, including the presence of a hyperactive jaw jerk, snout reflex, suck reflex, or absent gag reflex, are documented to differentiate upper from lower motor neuron pathology.
- Assessment of Non-Speech Oral Praxis: Differentiating between apraxic and dysarthric etiologies requires assessing non-verbal oral movements on command and imitation (e.g., coughing, blowing, puffing cheeks, whistling, clicking the tongue). Preserved reflexive and non-speech voluntary movements in the presence of complete speech mutism point toward apraxic anarthria.
- Acoustic and Physiological Instrumentation: Surface electromyography (sEMG) of the orofacial and laryngeal muscles, combined with kinematic tracking (e.g., electromagnetic articulography) and aerophonoscopic analysis, can confirm the absence of muscular contraction or reveal uncoordinated, sub-threshold motor unit firing during speech attempts.
- Language Comprehension and Cognitive Testing: Crucial for excluding global aphasia or cognitive dementia. Standardized aphasia batteries—such as the Western Aphasia Battery-Revised (WAB-R) or the Boston Diagnostic Aphasia Examination (BDAE-3)—are administered using adapted, motor-free protocols requiring only vertical eye movements, head nods, or eye-gaze selection to verify auditory comprehension, syntactic processing, and reading comprehension.
- Neuroimaging Protocols: High-resolution magnetic resonance imaging (MRI), incorporating diffusion-weighted imaging (DWI) and diffusion tensor imaging (DTI), identifies structural disruptions within the corticobulbar tracts, brainstem tegmentum, basal ganglia, and opercular white matter tracts.
10. Applications & Practical Significance
The diagnosis of anarthria carries profound clinical, ethical, and communicative implications. In critical care and neurorehabilitation units, accurately distinguishing between anarthria and receptive linguistic impairments (such as global aphasia) or altered consciousness (such as coma or vegetative states) determines patient management, autonomy, and medical decision-making.
Misdiagnosing an anarthric patient as cognitively non-responsive denies them medical agency. Once anarthria is recognized and receptive language confirmed intact, clinical teams can deploy augmentative and alternative communication (AAC) interventions. These systems range from low-tech visual eye-gaze boards and partner-assisted scanning to sophisticated high-tech solutions, including infrared eye-tracking communication devices, electromyographic switches, and brain-computer interfaces (BCIs).
Beyond communication, anarthria serves as a vital prognostic marker. In conditions such as traumatic brain injury, stroke, or Guillain-Barré syndrome, transitioning from complete anarthria to severe dysarthria signals emerging motor pathway recovery, guiding rehabilitation goals toward active phonatory shaping and articulatory placement. In progressive neurodegenerative disorders like ALS, monitoring the decline toward anarthria prompts timely discussions regarding nutritional support (such as gastrostomy tube placement), non-invasive ventilation, and voice banking before verbal abilities are lost entirely.
11. Research & Empirical Evidence
Contemporary clinical research into anarthria focuses on neuroplasticity, functional connectivity, and neurotechnological rehabilitation. Landmark studies conducted by neurosurgical teams and neural engineering laboratories, such as Edward Chang’s group at the University of California, San Francisco (UCSF), have transformed our understanding of how anarthric brains process speech intentions.
In a milestone 2021 study published in The New England Journal of Medicine, Chang and colleagues implanted a high-density subdural electrocorticography (ECoG) array directly over the speech-motor cortex of an anarthric individual who had lived with profound spastic anarthria following a brainstem stroke for over fifteen years. By employing deep learning algorithms to decode cortical activity intended for vocal tract movements, the researchers translated cortical signals directly into full words and sentences displayed on a digital screen in real time. This breakthrough provided empirical proof that the cortical representations of speech motor plans remain intact within the human cerebrum for years, even after descending motor pathways have been severed.
Neuroimaging research by Gorno-Tempini and colleagues into primary progressive aphasia (PPA), particularly the nonfluent/agrammatic variant, has demonstrated how targeted focal atrophy in the left inferior frontal gyrus and insula can begin as mild apraxia of speech and progress into pure anarthria. These structural MRI studies confirm that progressive degeneration of specific motor-programming networks can silence speech production while sparing non-verbal cognitive processing until late in the disease course.
Furthermore, physiological studies of pontine and bulbar strokes continue to clarify the precise lesion volumes required to cause anarthria. Clinical-pathological correlations demonstrate that unilateral lesions to the cortical motor strip typically cause transient dysarthria due to bilateral innervation of most motor cranial nerves (excluding the lower face and tongue). In contrast, sustained anarthria almost invariably requires bilateral disruption of upper motor neurons or catastrophic damage directly within the brainstem motor nuclei.
12. Cultural & Cross-Cultural Considerations
While anarthria represents a universal neurobiological impairment, its societal interpretation and the accessibility of compensatory interventions vary across cultures and healthcare environments. In high-income nations, anarthric individuals often access advanced assistive technologies, interdisciplinary neurorehabilitation teams, and legal protections that uphold the validity of non-verbal communication for legal and healthcare consent.
In contrast, in low-resource global contexts, severe motor speech disorders frequently remain underdiagnosed or misunderstood. Without adequate neuroimaging and specialized speech-language pathologists, anarthric individuals risk being miscategorized as intellectually impaired, leading to social isolation, institutionalization, or premature palliative withdrawal. The presence of pseudobulbar affect (uncontrolled laughing or crying), which often accompanies spastic anarthria, can further cause behavioral symptoms to be misread as psychiatric disorders in settings unfamiliar with central motor syndromes.
Cross-linguistic factors also influence how communication is reconstructed via augmentative platforms. Most high-tech assistive communication devices, predictive typing software, and speech-generating algorithms are built around English and other Indo-European linguistic frameworks. Patients whose primary languages rely on tonal systems (such as Mandarin or Vietnamese), agglutinative morphology (such as Turkish or Finnish), or non-Latin orthographies face additional systemic hurdles when adopting commercial communication systems, emphasizing the need for culturally and linguistically diverse assistive technology design.
13. Criticisms, Debates & Limitations
Despite centuries of study, the term anarthria remains subject to conceptual and taxonomic debate within neurology and aphasiology. The primary controversy involves whether the word should be reserved exclusively for mechanical, neuromuscular execution failure (the terminal endpoint of dysarthria) or include severe, total motor planning and programming deficits (terminal apraxia of speech).
Some European clinical traditions, following Pierre Marie and subsequent French schools, use “pure anarthria” to refer specifically to aphemia—an isolated, non-paralytic speech planning deficit caused by anterior cortical lesions. In contrast, the dominant Anglo-American framework, shaped by the Mayo Clinic classification, limits the diagnosis of anarthria to the severe, unphonated extreme of dysarthria. This taxonomy reserves the term severe apraxia of speech for pure motor programming failures, emphasizing that apraxic deficits lack true neuromuscular paresis, spasticity, or sensory denervation.
Another challenge involves clinical under-identification within intensive care settings. Distinguishing anarthria from akinetic mutism, cognitive abulia, catatonia, and severe receptive aphasia presents diagnostic difficulties, particularly when acute patients cannot complete standardized cognitive testing. Relying on simple bedside observations without neurophysiological monitoring can lead to diagnostic errors, underscoring the limitations of superficial clinical assessments in severe neurological crises.
14. Related Terms & Distinctions
Differential diagnosis requires distinguishing anarthria from several closely related clinical entities:
- Dysarthria: A group of motor speech disorders resulting from disturbances in muscular control over the speech mechanism due to central or peripheral nervous system damage. Distinction: Dysarthria presents with diminished intelligibility, altered resonance, and disrupted phonation, but articulated speech remains present. Anarthria represents the total absence of articulate speech (the zero point of the dysarthric continuum).
- Aphasia (Dysphasia): An impairment of language processing that affects the production or comprehension of speech, reading, and writing, caused by damage to language-dominant cortical networks. Distinction: In pure anarthria, internal linguistic competence remains intact; the individual can construct sentences, read, and understand speech, but cannot physically articulate sounds.
- Apraxia of Speech (AOS): A neurogenic disorder of speech motor planning and programming characterized by phonetic and phonemic speech sound errors, articulatory groping, and trial-and-error behaviors without neuromuscular weakness. Distinction: AOS features variable articulatory errors during sound production, whereas classic anarthria typically involves complete vocal tract immobility or severe paresis across all speech subsystems.
- Akinetic Mutism: A disorder of motivation, drive, and initiation characterized by profound reduction or absence of verbal output, spontaneous motor activity, and emotional expression, typically caused by bilateral frontal-subcortical or anterior cingulate lesions. Distinction: Patients with akinetic mutism lack the drive to communicate despite intact neuromuscular structures. Anarthric individuals actively attempt to communicate, demonstrating intact motivation and preserved emotional engagement.
- Aphonia: The loss of voice production secondary to structural, neurological, or functional pathology of the vocal folds, characterized by forced whispering. Distinction: Aphonic patients retain normal lingual, labial, and mandibular articulatory movements and can whisper words intelligibly; anarthric patients have lost both vocalization and oral articulation.
15. Summary / Key Takeaways
Anarthria represents the most profound motor speech disorder, marked by the complete loss of the ability to produce articulate speech sounds. It is caused by severe neurogenic disruption of the respiratory, phonatory, and articulatory systems. Arising from bilateral corticobulbar interruptions, brainstem infarctions, end-stage neurodegenerative diseases (such as ALS), or severe focal motor planning disorders, anarthria spares internal linguistic processing and cognitive comprehension.
Accurate clinical differentiation of anarthria from aphasia, akinetic mutism, and cognitive disorders remains vital for patient autonomy, ethical decision-making, and neurorehabilitation. Through modern augmentative communication platforms, eye-tracking technology, and advancing intracortical brain-computer interfaces, individuals with anarthria can bypass damaged motor pathways, regain communicative autonomy, and participate actively in social and clinical decisions.
References
- American Speech-Language-Hearing Association. (2023). Dysarthria in adults. American Speech-Language-Hearing Association. https://www.asha.org/practice-portal/clinical-topics/dysarthria-in-adults/
- Duffy, J. R. (2019). Motor speech disorders: Substrates, differential diagnosis, and management (4th ed.). Elsevier.
- Guenther, F. H. (2016). Neural control of speech. MIT Press.
- Moses, D. A., Metzger, S. L., Shenoy, K. V., & Chang, E. F. (2021). Neuroprosthesis for decoding speech in a person with anarthria. New England Journal of Medicine, 385(3), 217–227. https://doi.org/10.1056/NEJMoa2027540
- Smith, E., & Delargy, M. (2005). Clinical review: Locked-in syndrome. BMJ, 330(7488), 406–409. https://doi.org/10.1136/bmj.330.7488.406