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sleeping and awaken postural disorders etiology
sleeping and awaken postural disorders etiology
As probably not everybody knows, posture during sleep results from
involuntary muscular tonic activity aimed at granting survival
reflexive activity as breating, swallowing, digestive, joint
stabilization.... Sleeping position (prone, supine...) is the result,
that is why, for example, persons with big paunch only sleep
with stomach up, sholder instability let people
hardly sleep prone with hands under pillow and generally no one
suffocate accidentally sleeping mouth against the pillow.
The reason why apparently healty people wake up with painful back or
other muscular contractures is because, even if apparently
unmotivated, some strong reflexive activity is ongoing overnight,
question is: what goal, action and reflex might be involved ?
The goal is pharynx widening to guarantee airflow, the involuntary
action by which airflow is improved is cranio-cervical extension
(CCE) (yes, the same manoeuvre performed by medical
personnel to induce patient's pharynx widening ahead of a
mouth-to-mout respiration), the reflex that activetes CCE is the
Upper Airway Patency Maintenance Reflex (UAPMR) and is
elicited by pharyngeal vagal airflow receptors afferences, the
reason is that, in most of us, upper airway dilator muscles
(mostly tongue) are insufficient to grant good airflow (patency)
themselves, hence, POSTURAL MUSCLES COMPENSATE
KEEPING A CRANIO-CERVICAL FORCED RELATIONSHIP TO
RIDUCE AIRFLOW RESISTANCE THROUGH THE PHARYNX IN
AS ALTERNATIVE TO TONGUE MUSCLES.
Airway patency (pharyngeal widening) is physiologically achieved by
tongue muscles contraction (syncronous with respiration) to reduce
tongue size in order to maximize airway window, hence no reason to
CCE; when pathologic airway restriction arise the reason is likely to
deal with tongue muscles and airway patency has to be einforced
by CCE, next questions are: what's the cause to it and why
so common ?
Tongue muscles fail to clear pharyx because they are weak as a
neurologic direct consequence of hypoglossal nerve (tongue nerve)
compression in the intracranial area where it crosses the vertebral
artery. A physiologic vertebral artery (VA) is symmetric and lies
very close to hypoglossal nerve, hence, even a very slight VA
asymmetry (which is widely scientifically agreed to be present in
most of the population) may reasonably lead one VA branch to
touch/compress hypoglossus nerve (H/VA compression) inducing
unilateral tongue weakness.
Airway restrinction should be perceived as ad emergency,
nevertheless, in the awaken and non-REM sleep it is not, because
ongoing involuntary CCE fools pharynx into thinking airflow is ok,
whereas in REM sleep it displays it's whole harmfulness: the
reason why many of us suffer from snoring (OSA) is because
during REM sleep (only during REM we snore) postural muscular
tone ceases (except breath, and heartbeat fortunately), dropping
CCE as well (despite ongoing UAPMR), hence, collapsing
upper airway (tongue against the pharynx) and inducing snoring.
In the upright position CCE is active as well, it's action is well
identifiable by the "head forwarded posture" and by billion of
common symptoms most of wich we don't even relate to posture.
The mechanics of the postural syndromes is the same in most of
us, the hereby claimed cause (H/VA compression) is been
scientifically agreed to be present in most of us as well but the
relationship between them is surprisingly never been hypothesized
before.
Searching for this hypothesis in any existing literature will return
no matches, the effort to widespread is aimed at making this
matherial available to scientific society. UAPMR and
CCE whole-body mechanics are the core finding of my long
research and allows to relate postural causes and effects,
the theory is self-published (daily updated) and requires very little
effort to be validated but much more effort to be widespread
and taken in charge by clinical personnel.
This is my matherial:
* w w w .paoloplatania . it /engPosture theCaseStudy01.htm
Actually is no new fact to science, rather a new relationship between
well known and agreed scientific facts, some may ask: how come
that a patient gets to conclusion that no researcher has yet got to ?
I'ts much easier understanding single facts than their relationship,
by chance or by looking things in all possible way relationships
become evident, wheather chance may not be directed, the
patient's viewpoint is much different from the medical's,
moreover health is much more motivating than wage.
The following questions helps understanding:
1) Direct symptoms induced by H/VA compression (slightly
deviated tongue, swallowing difficulties, slight dysphagia,
maxillary arch asymmetry) are seldom perceived and never
reported as symptoms, whereas indirect H/VA compression
symptoms mediated by the postural disorder (back pain,
snoring, knee instability, sholuder instability, hip
degeneration, malocclusion..) are well perceivable and reported
as symptoms but unfortunately not relatable to H/VA
compression, hence, treated with symptomatic therapies...
how long will we wait for an orthopedist to "incidentally"
prospected a relationship between LCA rupture and
H/VA compression or for a dentist to relate overbyte to H/VA
compression ?
2) Despite scientific agreement on vertebral artery asymmetry,
unilateral blood flow restriction and closeness of H/VA
structures, no observation exists on likelihood of space conflict
between them.... how long may it still take for neurologists or
laryngologists or angiologist to "incidentally" report tongue
weakness as consequence of an overlooked H/VA
compression ? and how long more to hypothesize
it's postural ipacts ?
On the diagnostic side, the theory is completed but not yet relyably
validated, I'm curretly seeking neurologic measurements (EMG...) for
validation but for a patient it is hard to request a "custom
protocol" to be applyed by a professional neurologic lab
On the therapeutic side, two hypothesis exist, inveasive and non
invasive (I'm confident that much more may come out by
collaboration), but for both, health care specialists are unsuitable
interlocutors, this is why I'm currently oriented toward research
approch
Would anyone find sense please widespread, benefits may
come for all of us
Would anybody else require further details or want to
provide support and getting involved, feel free to thread-in or
contacting directly (by my site email please)
As probably not everybody knows, posture during sleep results from
involuntary muscular tonic activity aimed at granting survival
reflexive activity as breating, swallowing, digestive, joint
stabilization.... Sleeping position (prone, supine...) is the result,
that is why, for example, persons with big paunch only sleep
with stomach up, sholder instability let people
hardly sleep prone with hands under pillow and generally no one
suffocate accidentally sleeping mouth against the pillow.
The reason why apparently healty people wake up with painful back or
other muscular contractures is because, even if apparently
unmotivated, some strong reflexive activity is ongoing overnight,
question is: what goal, action and reflex might be involved ?
The goal is pharynx widening to guarantee airflow, the involuntary
action by which airflow is improved is cranio-cervical extension
(CCE) (yes, the same manoeuvre performed by medical
personnel to induce patient's pharynx widening ahead of a
mouth-to-mout respiration), the reflex that activetes CCE is the
Upper Airway Patency Maintenance Reflex (UAPMR) and is
elicited by pharyngeal vagal airflow receptors afferences, the
reason is that, in most of us, upper airway dilator muscles
(mostly tongue) are insufficient to grant good airflow (patency)
themselves, hence, POSTURAL MUSCLES COMPENSATE
KEEPING A CRANIO-CERVICAL FORCED RELATIONSHIP TO
RIDUCE AIRFLOW RESISTANCE THROUGH THE PHARYNX IN
AS ALTERNATIVE TO TONGUE MUSCLES.
Airway patency (pharyngeal widening) is physiologically achieved by
tongue muscles contraction (syncronous with respiration) to reduce
tongue size in order to maximize airway window, hence no reason to
CCE; when pathologic airway restriction arise the reason is likely to
deal with tongue muscles and airway patency has to be einforced
by CCE, next questions are: what's the cause to it and why
so common ?
Tongue muscles fail to clear pharyx because they are weak as a
neurologic direct consequence of hypoglossal nerve (tongue nerve)
compression in the intracranial area where it crosses the vertebral
artery. A physiologic vertebral artery (VA) is symmetric and lies
very close to hypoglossal nerve, hence, even a very slight VA
asymmetry (which is widely scientifically agreed to be present in
most of the population) may reasonably lead one VA branch to
touch/compress hypoglossus nerve (H/VA compression) inducing
unilateral tongue weakness.
Airway restrinction should be perceived as ad emergency,
nevertheless, in the awaken and non-REM sleep it is not, because
ongoing involuntary CCE fools pharynx into thinking airflow is ok,
whereas in REM sleep it displays it's whole harmfulness: the
reason why many of us suffer from snoring (OSA) is because
during REM sleep (only during REM we snore) postural muscular
tone ceases (except breath, and heartbeat fortunately), dropping
CCE as well (despite ongoing UAPMR), hence, collapsing
upper airway (tongue against the pharynx) and inducing snoring.
In the upright position CCE is active as well, it's action is well
identifiable by the "head forwarded posture" and by billion of
common symptoms most of wich we don't even relate to posture.
The mechanics of the postural syndromes is the same in most of
us, the hereby claimed cause (H/VA compression) is been
scientifically agreed to be present in most of us as well but the
relationship between them is surprisingly never been hypothesized
before.
Searching for this hypothesis in any existing literature will return
no matches, the effort to widespread is aimed at making this
matherial available to scientific society. UAPMR and
CCE whole-body mechanics are the core finding of my long
research and allows to relate postural causes and effects,
the theory is self-published (daily updated) and requires very little
effort to be validated but much more effort to be widespread
and taken in charge by clinical personnel.
This is my matherial:
* w w w .paoloplatania . it /engPosture theCaseStudy01.htm
Actually is no new fact to science, rather a new relationship between
well known and agreed scientific facts, some may ask: how come
that a patient gets to conclusion that no researcher has yet got to ?
I'ts much easier understanding single facts than their relationship,
by chance or by looking things in all possible way relationships
become evident, wheather chance may not be directed, the
patient's viewpoint is much different from the medical's,
moreover health is much more motivating than wage.
The following questions helps understanding:
1) Direct symptoms induced by H/VA compression (slightly
deviated tongue, swallowing difficulties, slight dysphagia,
maxillary arch asymmetry) are seldom perceived and never
reported as symptoms, whereas indirect H/VA compression
symptoms mediated by the postural disorder (back pain,
snoring, knee instability, sholuder instability, hip
degeneration, malocclusion..) are well perceivable and reported
as symptoms but unfortunately not relatable to H/VA
compression, hence, treated with symptomatic therapies...
how long will we wait for an orthopedist to "incidentally"
prospected a relationship between LCA rupture and
H/VA compression or for a dentist to relate overbyte to H/VA
compression ?
2) Despite scientific agreement on vertebral artery asymmetry,
unilateral blood flow restriction and closeness of H/VA
structures, no observation exists on likelihood of space conflict
between them.... how long may it still take for neurologists or
laryngologists or angiologist to "incidentally" report tongue
weakness as consequence of an overlooked H/VA
compression ? and how long more to hypothesize
it's postural ipacts ?
On the diagnostic side, the theory is completed but not yet relyably
validated, I'm curretly seeking neurologic measurements (EMG...) for
validation but for a patient it is hard to request a "custom
protocol" to be applyed by a professional neurologic lab
On the therapeutic side, two hypothesis exist, inveasive and non
invasive (I'm confident that much more may come out by
collaboration), but for both, health care specialists are unsuitable
interlocutors, this is why I'm currently oriented toward research
approch
Would anyone find sense please widespread, benefits may
come for all of us
Would anybody else require further details or want to
provide support and getting involved, feel free to thread-in or
contacting directly (by my site email please)
