Posture, etiology of a syndrome - The case study

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Preface

Posture

Posturology

The case study

The backstage

Bibliography

Etiopathogenesis

This section presents the etiological hypothesis to both components of platania's syndrome:

Hypoglossal Nerve Neuropathy (HNN): as first primary etiopathogenesis of either Tongue motor insufficiency (TMI) and Dental Conflict (DC) pathomechanics,
Pharyngeal Afferences Disorder (PAD): although uncovered by the rest of the case study, this hypothesis is under investigation as possible concurrent first primary etiopathogenesis of Tongue motor insufficiency (TMI),
Maxillary Arch Insufficiency: as second primary etiopathogenesis of Dental Conflict (DC) only.

Evidences suggesting a congenit and inheritabile nature of the etiopathogenetic factor

Inheritability: the presence of Maxillary Arch Insufficiency in patient's mother, affecting left emiarch as well, suggests inheritability and predisposition;

Congenit origin: the following symptoms and indicators are present since early childhood and are ascribable to Tongue Motor Insufficiency (TMI) or Dental Conflict (DC) pathomechanics

deciduous teeth extractions due to development disorder suggests early presence of Maxillary Arch Insufficiency;
first oral orthotics (failed attempt) appliance at age 6 due to teeth development disorder suggests early presence of Maxillary Arch Insufficiency as well;
first memories of left side motor disorder (Head Forwarding Postural Strategy (HFPS)) are dated age 17 and may be described as easiness in stumbling on the left stride;
ingrown toe nails on the left foot since age 7 witness the left side motor disorder (Ese01).

ETIOPATHOGENESIS: Hypoglossal Nerve Neuropathy (HNN) (first primary)

Hypoglossal Nerve Neuropathy (HNN) is the term to generally describe the neurogenic origin of tongue weakness , its exact diagnosis is hereby theorized.
The evidences collected reasonably entitle Tongue Motor Insufficiency (TMI) as pathogenetic factor of Platania's Syndrome, this section gathers clues of its neurogenic origin (Ecl20 and Ese08), of lesion localization (Ethn01, Ethn03) and of broad diffusion of the same lesion in the population (Ethn02).

Description

Ethn01

Hypoglossal Rootlets Emergence Entrapment (HREE)
(This hypothesis is currently submitted to validation protocol (STAGE 4) to get more precise and instrumental clues.)

Clue of HREE in the patient MRI (Ddo09).
vertebral artery coronal view

click to enlarge

Intracranial neurovascular conflict: Hypoglossal Nerve (HN) / Vertebral Artery (VA) conflict seems to be a recurrent condition [19]. Hypoglossal rootlets, at their emergence from medulla oblongata, often appear crossed, entrapped and compressed by a branch of Vertebral Artery (VA).

The likelyhood of conflict between Hypoglossal Nerve (HN) and Vertebral Artery (VA) is enforced by their anatomical shape and relationship:

Either branches of the Vertebral Artery (VA) lies contiguous to the ventral side of the medulla oblongata,
Hypoglossal nerve's are the most ventral rootlets emerging from medulla oblongata,
Symmetric vertebrobasilar junction and narrowly angled Vertebral Artery (VA) branches minimizes risk of conflict with Hypoglossal Rootlets
Whereas asymmetric vertebrobasilar junction and/or widely angled Vertebral Artery (VA) branches are higly likely to conflict with Hypoglossal Rootlets

Below are presented some samples of conflictual HN/VA relationship and some anatomical higlights, the collection is a random selection of images returned by google internet search engine (with keywords like "vertebral artery", "medulla oblongata", "brainstem") and witness that this neurovascular conflict is as diffused as overlooked.

Wide VA left branch (ventral view)	Wide VA left branch (frontal view)	Wide VA left branch (ventral view)	Hypoglossal Rootlets Emergenge (lateral view)	Hypoglossal Rootlets Emergenge (dorsal view)
click to enlarge	click to enlarge	click to enlarge	click to enlarge	click to enlarge
Courtesy of: Medical University of Warsaw, Poland see it in the original context	Courtesy of: Timothy C. Hain, MD see it in the original context	Reference missing	Courtesy of: Henry Grey "Anatomy of the human body"

Although no literature ascribes neurogenic symptoms to this recurrent finding, it's opionon of the author that such an apparently asymptomatic neurovascular lesion may instead yield a sufficient amount of tongue weakness to provoke the reaction described in Platania's syndrome, together with vertebro-basilar vascular insufficiency and vessel sufferance and their higly harmful potential. Given the relevance of this hypothesis to Platania's syndrome, for easyness of reference this neurovascular conflict lesion is hereby baptized Hypoglossal Rootlets Emergence Entrapment (HREE).

Ethn02

HREE Diffusion in the population

Ethn03

Other neurogenic etiologies
(The following etiopathogenetical option are not under current investigation)

Neuro-Vascular extracranial lesion:

Internal Carotid Artery (ICA) Entrapment [17, 19],
Occipital Artery Entrapment [19, 20],

Neuro-Structural lesion:

foramen compression,
condilar fossa compression,

Anatomic variations inducing lesion: whatever vein / artery / vertebra / gland (parotid).

Lower motor neuron disease

Upper motor neuron

Neuromuscular surgical complications

Post surgical aberrant innervation [9] after childhood's tonsillectomy

Other surgical complications

ETIOPATHOGENESIS: Pharyngeal Afferences Disorder (PAD) (first primary)
This hypothesis may concur in Cranio-Cervical Extension (CCE), although may not explain Tongue Motor Insufficiency (TMI), it deserves full consideration because it is wise to exclude its partial involvement in the etiopathogenesis. Pharyngeal Afferences Disorder (PAD) may explain AUCCE but not PUCCE and SBCCE, furthermore, regression events may be ascribed to temporary pharyngeal mucosa sensory loss due to contextual factors.
#	Description
Etph01	Pharyngeal over sensitivity (Although untreated by the rest of the case study, this hypothesis requires to be explicitly excluded) This condition may be induced by vagal nerve over sensitivity or pharyngeal airflow receptors exaggerated afferent signal and may mimic airflow insufficiency to central nervous system, thus eliciting Upper Airway Patency Maintenance Reflex (UAPMR) to induce AUCCE.

ETIOPATHOGENESIS: Maxillary Arch Insufficiency (MAI) (second primary)
To be completed
#	Description
Etmi01	To be completed

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