Posture, etiology of a syndrome

• Active: Tongue Motor Insufficiency (TMI) provokes an effort to gain Cranio-Cervical Extension (CCE) even when against gravity,
• Unilateral: Cranio-Cervical Extension (CCE) is induced only on the Tongue Motor Insufficiency (TMI) affected side.

Extrinsic tongue muscles (genioglossus (GG), hyoglossus (HG) and styloglossus (SG)) are responsible for pharyngeal airway patency [1, 2, 3, 4, 6, 8] as their co-contraction optimises tongue shape and position to reduce airflow resistance, this goal is achieved by rhythmic co-contractions [3, 4] reflex, synchronized with the respiratory muscles, and triggered by the same chemo receptors eliciting the respiratory reflex.

• head position [14, 15]: in the supine position, gravity requires an over effort for weak GG muscle to sustain the tongue weight in addition to provide airway patency, resulting in further limitation due to airway increased collapsibility;
• oxygen demand: in panting breathing during physical efforts, airway cross sectional area requirement is higher then in normal airflow demand, resulting in further limited airflow capability.

Cranio-Cervical Extension (CCE) role in upper airway patency improvement (as to say airflow resistance reduction) is widely known [16] and accepted (employed even in first aid procedures), hence, is not by chance that human physiology has developed air resistance vagal receptors which are there to elicit a permanent pharyngeal reflex to improve airway patency as soon as an airflow resistance is detected, engaging Head Forwarding Postural Strategy (HFPS) to implement Cranio-Cervical Extension (CCE).

This hypothesis highlights an Upper Airway Patency Maintenance Reflex (UAPMR) elicited by unilateral upper airway patency loss owed to Tongue Motor Insufficiency (TMI) and triggering itself the AUCCE spasm featured in Head Forwarding Postural Strategy (HFPS) fully justifying Head Forwarding Postural Strategy (HFPS) presence in the prone and supine positions, moreover, the contralateral physiologic tongue contraction is suspected to further limit airflow by moving the tongue according to the following model:

Tongue dislocation model

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Legend:
Blu tongue: physiologic tongue contraction, Cian tongue: weak tongue contraction, Arrow: airway patency indicator, imaging: 1 (tongue motor physiology (TMP) + basal airflow demand), 2 (TMP + augmented airflow demand), 3 and 4 (same as 1, 2 but Tongue Motor Insufficiency (TMI) instead of TMP).

Tongue dislocation model: the model describes the suspected increased airflow resistance due to increased oxygen demand, the background MRI image is a general (not patient's image) cranial section just above the mandibular arch:

• 1 blue arrow / 2 blue arrow ratio is the airflow resistance variation by TMP bilateral co-contraction inducing bilateral protrusion and depression,
• 3 cyan arrow / 4 red arrow ratio is the airflow resistance variation by Tongue Motor Insufficiency (TMI) muscular co-contraction inducing unilateral protrusion and depression along with dislocation toward the unaffected side.

With Tongue Motor Insufficiency (TMI), a unilateral tongue contraction, is neither able to provide the required airway patency with basal respiration (3 vs 1) nor in case of augmented airflow demand (4 vs 2), moreover, unilateral extrinsic muscles contraction induces tongue displacement decreasing the distance between tongue and posterior pharynx wall (red arrow), thus, further stimulating air resistance pharyngeal receptors of the vagus nerve, enforcing the afferent signals inducing a stronger Upper Airway Patency Maintenance Reflex (UAPMR), augmenting AUCCE and worsening Head Forwarding Postural Strategy (HFPS).

Please note that extrinsic tongue muscles not only provide tongue intraoral volume regulation (Genioglossus) and vertical elevation (Styloglossus and Hyoglossus), but also cuncur in giving shape to pharynx as Styloglossus lies behind pharynx mucosa and superior pharyngeal constrictor muscle, as such, unilateral tongue weakness may either increase emitongue volume, displace tongue within pharynx and give asymmetric shape to oro-pharyinx, resulting in pharyngeal airflow irregular and asymmetric resistance.

Upper Airway Patency Maintenance Reflex (UAPMR) is implemented by a firing pattern that mimics other well known vagal ejective reflexes: the cough reflex and the gag reflex. It is not by chance that these reflexes share the same base firing pattern, given Cranio-Cervical Extension (CCE) is the key condition to provide upper airway patency to maximise either ejection and intake. Since Upper Airway Patency Maintenance Reflex (UAPMR) goal is not to maximize emergency peak ejection but to maximise regular intake, it is implemented as a light Cranio-Cervical Extension (CCE) chronic spasm instead of an abrupt acute Cranio-Cervical Extension (CCE) spasm with ejective feature.

Evidence of the existence of Upper Airway Patency Maintenance Reflex (UAPMR) and of its complex firing pattern is provided by the postural reaction of a Head Forwarding Postural Strategy (HFPS) patient to pharyngeal vagal receptors reset done by pharyngeal local appliance of lidocaine 2%, as shown below.

Pharyngeal vagal receptors reset

This experiment describes cranio-cervical-thorax relationship in normal (Habitual) Head Forwarding Postural Strategy (HFPS) context and under a "faked" (Lidocaine) and a "true" (Regress+1) context of Head Forwarding Postural Strategy (HFPS) regress.

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• Habitual:ordinary posture, this context is reproducible, Cranio-Cervical Extension (CCE) degree is constant, duration, except regression event, is chronic,
• Lidocaine: posture under the effect of lidocaine 2%, this context has demonstrated to be reproducible, Cranio-Cervical Extension (CCE) regress is light but systematic, duration is matter of minutes, after that, Habitual context is restored,
• Regress+1: posture under the effect of an index 1 regression event, this context is not yet reproducible, this particular event has been triggered by atlas manipulation technique, which appliance has unfortunately revealed not to provide reproducible effects, Cranio-Cervical Extension (CCE) regress is similar to other index 1 regression event, duration has been 1 day, after that, Habitual context is restored.

• Habitual vs Lidocaine: immediate postural reorganization after abrupt and short term pathologic stimulus interruption, evidence of chin-ear-sterno angle reduction is visually confirmed, Head Forwarding Postural Strategy (HFPS) index 0 regression event has been reported by the patient. This is a "faked" context as there is no Tongue Motor Insufficiency (TMI) improvement.
• Habitual vs Regress+1: longer term adaptation after 1 day absence of pathologic stimulus, evidence of chin-ear-sterno angle reduction, cervical spine forward inclination decrease, increased chest expansion and decreased shoulder girdle forwarding are visually confirmed, Head Forwarding Postural Strategy (HFPS) index 1 regression event has been reported by the patient. This is a "true" context as the patient reports Tongue Motor Insufficiency (TMI) improvement as well.
• Lidocaine vs Regress+1: significant analysis, same cranial-horizon inclination, clue of scalenus contraction release in regress+1 context.

Pharyngeal vagal receptor reset procedure has already been successfully employed [21, 22, 23] in demonstrating the relationship between upper airway receptors and airflow resistance but has never concerned any motor reaction (eg. postural) other than upper airway dimension variation, whereas, the author hereby indeed does.

It is author's opinion that airflow resistance increase after vagal receptor reset, occurs as main consequence of the subsidence of the Cranio-Cervical Extension (CCE) spasm in ongoing Head Forwarding Postural Strategy (HFPS) subject, as such, it should NOT occur (or should be much lighter) in healthy posture subjects who fully entrust airway patency maintenance to tongue physiologic rhythmic respiratory contractions [3, 4].

Although apparently denying literature conclusions, the author's claim is not contradictable by existing studies as none of them has been carried out with adequate protocol: "healthy" control subjects have not been sampled according to Head Forwarding Postural Strategy (HFPS) features. According to the undeniably high incidence of Head Forwarding Postural Strategy (HFPS) clues in the population and Head Forwarding Postural Strategy (HFPS) hereby claimed relationship with upper airway patency (TMI), healthy control subjects, without explicit specification, are likely to be HFPS ongoing subjects, as such, the result of these studies on healthy posture subjects is unpredictable and requires further research to be described.

• obstructive sleep apnoea (OSA) studies disclose augmented pharyngeal collapsibility (snoring) during REM sleep as well as recursive presence of Cranio-Cervical Extension (CCE) in OSA patients [24, 6],
• neurological bibliography describe postural muscle tone drop during REM sleep [25],
• otorhinolaryngology focus on airflow resistance increase after vagal receptor reset [21, 22, 23],
• present study describes Head Forwarding Postural Strategy (HFPS) subsidence after vagal receptor reset,

The above findings are relatable by the hypothesis of Upper Airway Patency Maintenance Reflex (UAPMR) triggering Head Forwarding Postural Strategy (HFPS) to implement AUCCE in response to increased airflow resistance introduced by Tongue Motor Insufficiency (TMI) (hence, preventing snoring during non REM sleep), confirming the consequences of Head Forwarding Postural Strategy (HFPS) loss on airflow (snoring when Cranio-Cervical Extension (CCE) muscular tone drops during REM sleep).

• From self evaluation: Head Forwarding Postural Strategy (HFPS) is present in the prone as well as the supine position (not interested by cranial weight bearing unbalance), evidence is provided by anterior scalenus (AS) and tensor fascia lata (TFL) pathologic contraction undeniably present at night before sleep and since morning arousal confirming active cervical spine forward inclination, furthermore, left sub occipital muscles are overactive in the prone and supine positions providing additional Atlanto-Occipital Joint (AOJ) extension;
• From Self evaluation: oxygen demand dependence of some unilateral motor unbalance (Ese05, Ese07) supports airway adaptation insufficiency;
• From Regression events: oxygen demand dependence of some unilateral symptoms (Ere02) supports airway adaptation insufficiency.

Airflow asymmetric afferences localization

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Legend:
Blu: Upper airway in physiologic head position,
Red : Upper airway in Cranio-Cervical Extension (CCE),
dummy A:comparative PHP/CCE upper airway,
dummy B:Upper airway areas classification according to airflow receptor features,
cyan: Receptors sensitive to only-nasal airflow,
orange: Receptors sensitive to CCE airway widening and to tongue weakness airway narrowing,
green: Receptors sensitive to vagal reset,
area A: nasopharynx (only cyan receptors),
area B: oropharynx (orange and green receptors),
area C: laryngopharynx (only green receptors).

• Only-mouth breathing (with held nose) does not improve Cranio-Cervical Extension (CCE) confirming that Upper Airway Patency Maintenance Reflex (UAPMR) is constantly elicited, even in the absence of nose airflow afferences and, therefore, excludes nasopharynx;
• Although laryngopharynx is sensitive to vagal reset it is unlikely responsible of the improvement of CCE induced by it. If the hypothesis that tongue weakness induces an airflow window reduction is true, then only the receptors detecting this asymmetric restriction are capable of elicting asymmetric afferentces (hence, only oropharynx), moreover, even if laryngopharynx would be capable of detecting airway restriction it would be senseless to elicit a CCE reflex to widen another area (the oropharynx). This analysis suggests to exlude laryngopharynx;
• Oropharynx is subject to either mouth and nose airflow, is exposed to airway narrowing in case of tongue weakness, benefits from CCE airflow window widening and is sensitive to vagal reset, hence, oropharynx receptors are eligible as the most likely to produce asymmetric afferent signal that triggers Upper Airway Patency Maintenance Reflex (UAPMR).

• Passive:Tongue Motor Insufficiency (TMI) requires gravity (upright position) to induce cranial extensors-flexors unbalance,
• Unilateral: Cranio-Cervical Extension (CCE) is induced only on the patient left side.

Tongue muscles pulling on the styloid process and on the mandible (behind chin) feature a cranial flexion moment arm and, given the continuous and strong tonic contraction for pharyngeal airways patency [8], exert direct hyoid-cranial flexion force. These literature overlooked features is hardly escaped to physiology which may rely on GG, HG, SG, stylohyoid (SH) and infrahyoid muscular chain for AOJ flexion, undeniable healthy posture indicator. The following models provide explanation of the theory.

• temporomandibular joint (TMJ) is considered "locked" (teeth clenching) resulting in non deformable mi-ccr, mi-si, si-ccr relationship,
• cranial centre of rotation (ccr) is simplified to be a single point, thus, considering occipital condyles to move on a round atlas track concentric with ccr,
• cranial centre of rotation (ccr) is the fixed point of observation.

• hcf is a fixed pulley system,
• tcf represent the resultant point of application of extrinsic tongue muscles force exerted by co-contraction of GG (mi-tcf), HG (hcf-tcf) and SG (si-tcf).

Mandible depressors are also capable of Atlanto Occipital Joint (AOJ) flexion, the action is provided by geniohyoid (GH), digastric (DG), stylohyoid (SH) and Milohyoid (MH) complex, the model is not presented as it's out of the scope of the present analysis.

Although AUCCE plays the key role in Head Forwarding Postural Strategy (HFPS), PUCCE seems to be reasonably involved as impairment in tongue muscles may introduce cranial flexion weakness, but, without proper measurements, it is not possible to quantify the extent of Cranio-Cervical Extension (CCE) induced by PUCCE.

Moreover, Head Forwarding Postural Strategy (HFPS) is present regardless from head position, whereas PUCCE is only triggered head upright, as such, PUCCE may not be responsible for provoking Cranio-Cervical Extension (CCE) in the prone and supine position.

These findings allow to state that GG, HG and SG actively participate in cranial inclination tuning and that a Tongue Motor Insufficiency (TMI) might result in cranial displacement (PUCCE)

Tongue muscles pressure against palate is reasonably suspected [11, 13] to have a plastic function over the maxillary alveolar process and maxillary teeth axis orientation. The daily amount (about 2000 x 3 kg) of swallowing induced force pulses [11] and continuous tongue elevation pressure [8] (to hold the tongue high against the nasopharynx during nose breathing) is transferred to the palate and teeth and counterbalances cheeks and lips opposite forces, hence, being SG equipped with enviable palatal lateral expansion moment arm and being GG able to frontally expand the arch, tongue muscles are suspected to have a primary role in expansion.

Based on the patient's finding examination (Ecl19, Ecl20, Ecl22, Ese08, Eot05), a relationship between Tongue Motor Insufficiency (TMI) and maxillary insufficiency seems more then suspect, the next step is to determine which is primary on which other:

• Can arch asymmetry be primary over Tongue Motor Insufficiency (TMI) ? To answer this question an oral splint (Ddo07a) designed to produce palatal arch symmetry (buccal side remains asymmetric) has been applied for 1 month with the goal of "fooling" the tongue into making it "think" that maxillary arch is symmetric for observing body reaction to restored arch symmetry. Mastication, swallowing and postural disorders persist despite palate symmetry, hence, palatal asymmetry is unlikely primary over Tongue Motor Insufficiency (TMI),
• Can Tongue Motor Insufficiency (TMI) be primary over arch asymmetry ? Although there is no direct clue to this hypothesis, the unlikelihood of the opposite, the concurrence of left Tongue Motor Insufficiency (TMI) with ipsilateral maxillary insufficiency and the orthodontic treatment outcome enforce the suspect of Tongue Motor Insufficiency (TMI) being primary over maxillary insufficiency.

Maxillary arch insufficiency is an irreversible structural under development (at least not spontaneously reversible within acceptable times) of the maxillary arch and, given its etiopathogenetic role in Mandible Retruding Postural Strategy (MRPS), is considered a second primary pathomechanics and requires a dedicate diagnostic/therapeutic process but only after first primary process is successfully terminated. Refer to section maxillary arch insufficiency for thorough mechanics exploration.

These findings allow to state that GG, HG and SG actively participate in maxillary arch expansion and that a Tongue Motor Insufficiency (TMI) may result in maxillary arch insufficiency, hereby theorized to be primary over Mandible Retruding Postural Strategy (MRPS).

• Critical functionality: among all Head Forwarding Postural Strategy (HFPS) involved muscles, tongue accomplishes the highest priority tasks, a higher priority function then respiration is barely imaginable;
• Clinically reliably diagnosed: Tongue Motor Insufficiency (TMI) is diagnosed by clinical evaluations, presence is chronic and the neurological indicator has never disappeared to any evaluation;
• Not secondary to other function unbalance: no evidence of muscular disorder to which Tongue Motor Insufficiency (TMI) may be secondary to;
• Not secondary to structure unbalance: no evidence of anatomical degeneration to which Tongue Motor Insufficiency (TMI) may be secondary to.

Despite some clinical literature proposes these functions to be involved in posture, their pathomechanics is still controverse. Although the disorder of these functions is part of platania's syndrome and is secondary to Tongue Motor Insufficiency (TMI), it is NOT considered to be primary to Head Forwarding Postural Strategy (HFPS) and Mandible Retruding Postural Strategy (MRPS) for the following reasons:

• both Mandible Retruding Postural Strategy (MRPS) and Head Forwarding Postural Strategy (HFPS) neither worsen nor subside during swallowing, phonation or mastication;
• after orthodontic treatment Mandible Retruding Postural Strategy (MRPS) greatly improves but neither swallowing nor phonation nor mastication does, furthermore Head Forwarding Postural Strategy (HFPS) persists;

• Structural: Dental Conflict (DC) is a consequence of a structural (maxillary arch) disorder,
• Bilateral: Cranio-Cervical Extension (CCE) is induced symmetrically.

Dental Conflict (DC) mechanics over TMJ disorder eliciting condition is as follows: neurological afferences (trigeminal nerve) produced by pathologic teeth contacts generate inhibitory reflexes directed to the responsible muscles aimed to avoiding every type of harmful motion, these reflexes successfully grant teeth safety but on the other side generate pathologic torques on mandible provoking the TMJ disorder.

TMJ disorders are widely suspected to induce, among several other symptoms, postural unbalances. Although Mandible Retruding Postural Strategy (MRPS) seems reasonably related to TMJ disorder, the pathomechanics of its impairing capabilities over posture is unclear. Although several symptoms are ascribable to TMJ disorder (condile dislocation, mastication disorder and temporal muscles painful contractures), postural disorder doesn't appear to be mediated by these conditions, the author in spite proposes the following hypothesis to justify Cranio-Cervical relationship modification (CCE) consequent to TMJ disorder:

• Vagal mediated: Cranio-Cervical Extension (CCE) compensates airway patency loss (tongue backward motion) due to mandible retrusion;
• Neck internal proprioception mediated: Cranio-Cervical Extension (CCE) is induced by internal neck proprioceptive afferences triggered by organs (arteries, nerves, glands) compressed by the retruded mandible;
• Trigeminal mediated: Cranio-Cervical Extension (CCE) is meant to optimise Cranio-Cervical-Mandibular relationship, in response to pathologic mandible retrusion, to grant functionality (mastication, swallowing);

Physiologic maxillary and mandibular arches get together (centric occlusion) when molar and pre molar teeth on one arch contact the opposite molar and pre molar teeth on the opposite arch in normocclusion TMJ position. Normocclusion TMJ is not functional to the patient's bite as it would cause upper and lower incisors to contact (due to upper incisors crowding, Ecl19) preventing molar and pre molar contact. Molar occlusion, in context of incisor teeth crowding, is achievable with mandible retrusion.

Mandible retrusion is not the only TMJ displacement, nevertheless is considered the main responsible for Mandible Retruding Postural Strategy (MRPS) for the following reasons:

• left condile further backward motion is suspected (Esy11) but is thought to be derived by unilateral Cranio-Cervical Extension (CCE) component, thus, the consequent postural disorders pertain to Head Forwarding Postural Strategy (HFPS)
• slight unilateral lack of vertical dimension is present (also kinesiologically diagnosed) as consequence of maxillary alveolar process asymmetric development (Ecl22,Eot05) but its extent is supposed to be negligible (better say tolerable) according to quite symmetric facial mimic muscles, reliable TMJ displacement indicators.