It becomes the own story of experiencing the impairment of two basic sides of neurobiological functions, one related with the chemical acquired deshinibition for the cortical abstract area motor and cognitive pattern pathways, and the other consists in the same sponsor of one pharmacological regulation mandatory for control the these pathways.

1. The exciting and the control of neuron cognitive pathway
It becomesthe ownstoryof experiencingthe impairmentof twobasicsidesof neurobiological
functions,one relatedwith the chemical acquired deshinibition forthe cortical abstract area
motor andcognitive patternpathways,andthe otherconsistsin the same sponsorof one
pharmacological regulationmandatoryforcontrol the these pathways.
One consistsin the profuse generationof signalsfromsome point ( maybe raphe nuclei of
brainstem) intothe pathwaysthatrealease the thalamus fromthe basal ganglia,striatumand
pallidum, profusion originated since some externalextrastimuluson the psycological chilhood
learningprocess like some habitsrepetitive recorded betweenthesestructures, aswe studied
on Motor ModulationUnit .
The origins:Those extrastimuluswere competingamongextra-attentionfromsome other
external strictpatterns througharoundthe learningmodelsbasedprimaryover the areaof the
comprehensiontemporal neocortexincludingsome abstractfunction perceptionsexcited
increasingly originatedbasicallyinthe basicreceptorslike visual,auditoryorvestibularcells
intothat learningprocess,provoquingextrasignalsfromfrontal abstractandtemporal
comprehensioncortex,exciting fromthe inhibitionof the striatum onthiswaythe
desinhibitionof the inhibitionof the pallidumneurons( dompaminreceptors ) andalsotring
the thalamusbutsince otherabstract inputpathways.
In the normal consecutionof learninglife asaconsequence of those cyclingexigenciasof that
pathway, an occilatinginitiationof signalsfromthatthalamusorbasal ganglia( relatedwith
motor regulations) intrusive onthe voluntaryabstractfrontal areanormal signals,developed
these extrastimulations,resulting repetitive goingandbackwave of signals between Frontal,
Wernickand Basal gangliaareas. Thisimpairmentis expressedinthe obssesive tendencefor
incidence of workingortolike stayingcaptionsfrommuscles, vestibular,auditionand eyes (
the same sensationof stresswhenwe are pressedforculminatingsomething experiencingthe
desire fordrinkor to eatsearchingcalm).
The secondfunctionis chemical:the consequence of helpingdosis of treatmentforconvulsive
obssesive syndrome whichin thiscase istreatedwith aninhibatorof the receptorsof central
nervoussystem:dopamineandserotonine neurotransmitters, presentedonthe Motor
Modulation pathwaydescriptedbefore, avoidingbothto reachto interactwiththe receptors
of the dendrites ( Neuron-transmission andNeuroanatomy Units) of the followingneurons of
basal gangliaand the thalamuswhere those pathwaysubstances workselon ,whenthe
pathwayfromfrontal and motorareas of the neocortex produce andreceivesignals
respectevely.
It resultsan interuptionof the desinhibition of thalamusand specially the inhibitionof basal
gangliaenchargedof the developof chunksinitiatedby certainsignalsfromfrontal neocortex
and the voluntarytemporal motorneocortex around Wernick´sárea( Abstract Unit) whichin
thiscase theyare compulsive; resultingalsothistreatmentthe desirablecontrol of the back
and go stimuluspathwayof those abstractandmotor pathways,exprressedinimpaired
thoughtsthat can produce some imsomniaatnight,helpingcontinueconstantthougts
The chemical notwantedeffect wouldbe anextrastimulusonthe receptorsof musclessince
the heart , the tongue andotherfinal muscle fiberswhere the temporal motorneocortex

2. signalsend,when the complex of the motorareasignals canexcitate, because the
pharmacologyanthagonistof the receptorsonthe motorpathwaymakesthe basal ganglia
regulators remaininginhibitedacause of the same descartof theirneurotransmitters;then,
whenthe effectof thatprimarytreatmentevoluates insome hours,the excitatorysignalon
theirfollowingmotorneuronsorthe sympatheticnerves ( throughthe muscles) becomes
increased afterthatinhibitiondecreases andmakestostay the muscles a little spasmodic
because those neurotransmittersrelease withtheir neuron receptors onmuscleseachtime
theyreach to endtheirinhibitory pathwaythatcouldreachalsothe forebrainonfrontal or
temporal areaswhere the desirableeffectalsoapply.
This isthus the suministrationof complementarytreatmentforthe excitationonthe
sympatheticmetabotropicneuronsterminals thatcausesspasmodicmuscles,reduces the
nervousextrapiramidal sympatheticsignals,expressing the calmagainstspasmodicmuscles
excitedbythe clearreturnof the recpetionof the signalsreceptorsof the abstract, motor
thalamusandbasal gangliarespectevely.
Summary:Thiscase describesenterilytwoprocessthatjoinedwork functionsof the
coordinatedreaction whenthe MotorModulationishelpedbythe actionof some antagonist
of the neuroncommunication;presented inthose referencesfromthe same course;hoping
we couldcontinue trustinthe medicine science asacontributorof our selhhelp. Thank you.
External reference: Wikipedia
The raphe nuclei (Greek: ῥαφή, "seam")[1]
are a moderate-size cluster of nuclei found in
the brain stem. They have 5-HT1 receptors which are coupled with Gi/Go-protein-
inhibiting adenyl cyclase. They function as autoreceptors in the brain and decrease the
release of serotonin. The anxiolytic drug Buspirone acts as partial agonist against these
receptors.[2]
Selective serotonin reuptake inhibitor (SSRI) antidepressants are believed to
act in these nuclei, as well as at their targets