Download Heading: Sensory Deprivation in Humans, Mice, and History Caleb B. Carson Running Head: Sensory Deprivation

Running Head: Sensory Deprivation
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Heading:SensoryDeprivationinHumans,Mice,andHistory
CalebB.Carson
Running Head: Sensory Deprivation
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Abstract
Thispaperwillhighlightastudydoneinlabmice,toobservetheeffectsofsensory
deprivationonspinaldendrites.Lightwillbegiventothehistoryofsensorydeprivation
chambers,focusingonJohnC.Lillyandhiswork,aswellashisfindingsintheeffectsof
thesechambersonpeople.Thewriter’sowntheorywillbeproposed,basedoffofan
analyzedcasestudy,centeredaroundthehearinglossofanolderwoman.Thiscasestudy
involvestheobservationandtreatmentofawomanwhoclaimedtohearvoicesafter
hearinglossduetoacaraccident.Timeisgiventodefiningtheuseandstructureof
vibrissae,inordertohighlighttheirimportanceinthespinaldendritestudy.
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HistoryofSensoryDeprivationChambers
Littlewasdoneinthestudyofsensorydeprivation,throughthemeansofactual
testsinhumansubjects,untilameansinwhichtotestpeople,andtheories,wasdeveloped
byJohnCLilly.Foralongtime,peopletheorisedoutlandishpossibilitiesofwhatwould
happenwhensomeonewasdeprivedofnearlyalltheirsenses.Somebelievedyoucould
contactotherworlds,whilemoregroundedthinkersassumedyouwouldsimplybeputinto
ahigherstateofconcentration,abletotheorize,think,andpondermoreefficiently.Many
peopleweretested,andwhilefewspokeoftravelingtootherworlds,moststated
experiencingwhatmanyknowasan,“outofbodyexperience”.Feelingdisconnectedfrom
theirbodiesduetoanabsenceofsensoryinputtoletthebrainknowweareevenstillalive,
webegintofeeldetached.StudiesdonebyLillyresultedinfindingsthatshowedjust15
minutesofnear-totalsensorydeprivationwasenoughtotriggervividhallucinationsin
manyofitstestsubjects.
"Somewhere,deepwithinthebrain,wasamechanismcapableofgeneratinginternal
experiencescompletelyindependentoftheoutsideworld,andthissettledtheissueofwhat
happensinprofoundphysicalisolation.Theminddoesnotpassintounconsciousness,the
braindoesnotshutdown.Instead,itconstructsexperienceoutofstoredimpressionsand
memories.Theisolatedmindbecomeshighlyactiveandcreative.Thiswastheprincipal
discoverythatDr.Lillyreportedinhisfirstthreescientificpapersontheisolationtank
research,publishedin1956,1957,and1958."
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DefiningSensorydeprivation
Itisnecessary,thatwhendiscussingorreadingatopicofinterest,apersonshould
beginwithabasicandconcreteunderstandingregardingthefoundationsofthesubject
matter.SensorydeprivationisdefinedbyDictionairy.comas,“Theexperimentalornatural
reductionofenvironmentalstimuli,asbyphysicalisolationorlossofeyesight,often
leadingtocognitive,perceptual,orbehavioralchanges,asdisorientation,delusions,or
panic.”Thisdefinitionwouldnotbefoundtobeallinclusive,however,onewoulddowell
touseitasacornerstonefromwhichtobuildoff.Firstly,whenreconstructingthis
definitionforpurposesofapplication,Iwouldliketostartoffontheabsenceofrecognition
inregardstoauditorydeprivation.Inthispaperyouwilllearnaboutawomanwho
experiencedsomeeffectsofwhatispresumedtobesensorydeprivation,duetothelossof
herhearing.
Followingthissamepathofdefinitoryreasoning,theothersensesneedtobe
includedinafullyworkingdefinitionaswell,asthisis“sensory”deprivation;sensorybeing
anallinclusiveword.Inastudythatwillbeincludedinthispaper,andwillcomprisean
extensiveamountofthiswriting,micewereforcedintoaformofsensorydeprivationby
theremovingoftheirwhiskersor,“feelers.”Withthisinmind,thedefinitionshouldalsobe
suretoinclude,whetherdirectlyorindirectly,thelossoftactilesensory.
TheVibrissae
Theaforementionedwhiskersarealsoknownas“vibrissae”,andareatypeof
mammalianhairthataretypicallycharacterisedanatomically,bytheirlargesize,asawell-
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innervatedhairfollicle,andbyhavinganidentifiablerepresentationinthesomatosensory
cortexofthebrain.
Theyarespecializedfortactilesensingactingmuchlikeskinorfeelers.What
howevermakesthemdifferentfromotherhairsandaretheydifferentatall?Thereare
numerousdifferences.Thevibrissalhairisusuallythickerandstifferthanothertypesof
pelagichair,but,likeotherhairs,theshaftconsistsofaninertmaterialcalledkeratin,and
containsnonerves.Contrastly,ifthesevibrissaehavenonerves,howcantheybeusedfor
tactilesensory?Theansweristhattheygrowfromaspecialhairfollicle,incorporatinga
capsuleofbloodcalleda“bloodsinus,”whichisheavilyinnervatedbysensorynerves.
VibrissaeinApplicationStudies.
Nowthatweknowtheirfunction,letuslookatwhythesewhiskersaresopivotal.It
isfoundthatratsandmicehaveapproximately30macrovibrissaeoneachsideoftheface,
withwhiskerlengthsuptoaround50mminlaboratoryrats,30mminlaboratorymice.
Thus,anestimateforthetotalnumberofsensorynervecellsservingthemystacialvibrissal
arrayonthefaceofaratormousemightbe25,000.Thisnumberinrelationtothenumber
ofsensoryneuronsinthebodyofamouseorratisastonishing.Inordertobetter
understandtheextentofthedeprivationthemicewereputunder,youcanimaginethisas
theequivalenttocuttingoffbothofyourhands.Nowwithamorecomprehensiveand
operationalunderstandingofthepremiseoftheresearchportrayedthroughthismedium
ofwriting,wewillbeginlookingdeeperintosensorydeprivationinlabratsandmice,and
eventually,inpeople.
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PreventionofDendriticSpineLossinMiceviaSensoryDeprivation
Tobegin,anunderstandingmustbehadofthespinaldendrite,andtherebytheloss
ofsynapsesthatisexperiencedbymiceastheyage.Experienceplaysakeyroleinthe
modificationofsynapticactivity,however,itisnotcurrentlyunderstoodhowitrelatesto
thenearlylifelongsynapselossinmice(thecontinuedlossofsynapsesoccurringnaturally
throughouttheagingprocess.).Whatisknownforsurebyscientistshowever,isthat
synapticlossisapparentthroughoutthelifeoflaboratorymice.Ithasbeendiscoveredthat
sensorydeprivationthroughthemediumofwhiskertrimming,decreasesthenumberof
synapseslostthroughoutthelifeofthemouse,aninquisitiveandseeminglycontradictory
discovery.
Thetypicalpercentageofspinalsynapseslostinhumansandmostmammalsison
average50%,andtakesplacethroughouttheentirelifespanoftheanimal,primaryinthe
adolescentstages.Whenthevibrissaearetrimmed,causingnearcompletetactilesense
deprivation,thelossofsynapsesisgreatlydecreased,almosttoastop.However,ifamouse
isputthroughadolescenceinadeprivedstate,andthenhasitssensesrestoredin
adulthood,thesynapticlossisspedupincredibly.Thisindicatesthattheroleofexperience
insynapselossisoneofimportance,butnotyetclearlydefined.Itisalsofoundthat
Piaget'sideaoflearningreboundisfoundtobepresent,andseeminglyrelatedtothe
occurrenceofarapidlossindendriticspines,soonaftersensoryrecover.
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ExperimentResultsandFindings
Itisfoundintheexperiment,Long-termsensorydeprivationpreventsdendriticspine
lossinprimarysomatosensorycortex,incontrolmiceonemonthofage,thatthenumberof
spineseliminatedoveratwoweekperiodwassignificantlyhigherthanthepercentage
formed.Todeterminetheeffectsofthesensorydeprivationonthisspinaldendriteloss
rate,micefromfourweeksofagetosixweeksofagehadtheirwhiskerstrimmedonone
sideofthefacialpad.Thenumberofspinesgeneratedandeliminatedcomparedtothe
“non-deprivedconstantgrowthvs,non-depriveddendritelossratio”,wasfardifferent;not
speedingupthegrowth,butsimplyslowingtheloss.Therewasnosignificantchangeinthe
numberofspinesformed.Asmentionedpreviously,onceadulthoodisreached,(whichin
thiscaseisdefinedas4monthsandbeyond),thelossofdendriticspinesissignificantly
reduced.However,whentestsonadultswentfromonlytwoweekswithlittleresultsand
werebumpedupto2months,asignificantreductioninspinereductionwasfound.
Todeterminewhetherspinelosswouldreboundafterreintroductiontotactile
sensory,whiskersoftwomontholdmiceweretrimmedfortwoweeks,andallowedto
regrowthenexttwoweeks.Itwasfoundthatduringthesetwoweeks,dendriticspineloss
exceededthatofthecontrolgrouprate(naturalspinallossrate).Similarresultswere
foundwhentrimmingwaslengthenedtofourweeks,andgrownandtestedoverthenext
two.
-Belowarethreecharts,twoconcerningtheeliminationoftheFilopodia,whichwill
notbeincludedinthispaper,whilethefirstshowstheratiobetweensensorydeprived
miceandnon-deprived,andtheirpercentageofspineloss.
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EffectsofSensoryDeprivationinHumans
TheCase
A63yearoldwomancomplainedthatshewashearingvoicesforthepast11⁄2,to
2years,andthatthepresenceofvoiceshavebeenincreasingrecently,especiallyatnight.
Initially,thevoicesfrightenedher,andshethoughtshewasgoingmad;thensherealized
theywerenotreal.Shehadhearinglossinherleftearfollowingacaraccident5yearsago,
anditwasrecommendedthatsheuseahearingaid.Duetothefactthattheaiddisturbed
herear,sheuseditirregularlyfor3yearsandnotatallthereafter.
Fivetosixmonthslater,shestartedtohearvoices.Everythingwasnormalinthe
patient'spsychiatricexaminationexceptforauditoryhallucinationsandanxiousmood.
Therewasnosubstanceuseorpsychiatricillnessinherhistory,andacompleteblood
count,biochemicaltests,thyroidfunctiontest,EEG,cranialcomputedtomographyscan,
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andneurologicalexaminationsofthepatientwereallnormal.The,“MinnesotaMultiphasic
PersonalityInventoryandBeierSentenceCompletion”testswereevaluatedasnormal.
TreatmentandProcedure
“Treatmentwasstartedwitholanzapine10mgdailyanddiazepam10mgdaily.
Later,diazepamwasstoppedandcontinuedbyolanzapine5mgdailyonly.Onthetenth
dayoftreatment,theauditoryhallucinationsdisappeared.Thepatientwasobservedfor10
monthsatregularintervals;shetookolanzapine5mgdailyandusedahearingaidfor7
months.Duringthistime,nopsychopathologyhadbeendetected.”(CanadianJournalof
Psychiatrypg.3)
PhantomExtremityPhenomenon
Animportantquestionmustbeaskedhere.Howdoesalossofhearinginonlyone
ear,createsuchacaseashearingvoices?Therehavebeencountlesscaseslikethisone,and
themajoritydonotleadtosomethingasfantasylikeashearingvoices.Thereishowever,
anotherphenomenoninconcurrencewithsensorydeprivation,andthatisknownasthe,
“PhantomExtremityPhenomenon.”Manyhaveheardofphantompains,leftbehindwith
thelossofalimbeitherthroughamputationorothermeans.Damagetothesensorynerve
canaffectreuptake,andothercomponentsofthesensoryneurons,creatingafeelingthat
thelimbisstillthere,throbbinginpain.Thisoperationissimilartowhatishappeningin
thiscaseoflostsenseofhearinginoneear.Inbothcasesthestimuligoingtothecortexis
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blocked,butitisstillunknownastohowthisperceptualdisorderoccurs.Thereisatheory
thatthisiscausedbyreceptorhypersensitivity.
“Thiscouldbeexplainedbyexaminingtheeffectivemechanismsofhallucinogens
andatypicalantipsychotics.Hallucinogensandserotonin-dopamineantagonists(SDAs)act
throughthesamereceptorsbutcreatedifferenteffects.Hallucinogensactivate5HT^sub
2A^,5HT^sub2C^,and5HT^sub6^receptorsandcausehallucinations.Incontrast,SDAs
blockthesereceptorsandpreventtheformationofhallucinations.”Theparametersforthe
CharlesBonnetSyndromeareallmetwiththisspecificcasestudy.However,itwasinitially
discardedasapossibleanswer,simplybecauseCBSdeals,orhasonlydealtinthepast,
withvisualhallucinations,notauditory.However,becauseitwasproventhroughmultiple
teststhatthewomanwaspsychologicallysound,carriednodisorders,andrecognizedthe
hallucinationsasimaginaryamongotherpivotalcriteria,thecasemayprovetobewhatis
neededtoexpandtheworkingdefinitionofCBS,toincludeauditoryhallucinationsaswell,
andpotentiallyevenothersensicallybasedhallucinations.
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BringingitBacktoLilly
Whenwelookatthiscase,aswelookedattheresultsproducedfromsensory
deprivationchambertestsdonebyLilly,wecanbegintotheoriseonourown,usingLillys
dataasabasis.Itcanbereasonablyinferred,thoughnotscientificallyprove,thatperhaps
thecauseofthewoman'simaginaryvoiceswasmuchlikethehallucinationshavingbeen
reportedinS.D.Ctests.Duetoalackofsensoryinputtothecortexforanextendedlengthof
timefromthedamagedear,thebraincreatedit’sownsensoryinputinanattempttofillthe
void.Muchlikehallucinationscausedinthedeprivationchambers,broughtonbyalackof
sensorystimulus,themindcouldthencreateitsownstimulus,causingvoicestobe,
“heard,”inthedamagedear,
Itisisscientificknowledgethatthebrainisthecontrolcenterofthebody,making
sureallsystemsoperateefficiently,andevensacrificingorganstosaveitself.Thebraincan
becalledacontrolfreak,asitdominatesallotherorgans,assuringthebodyrunstheway
thebrainintendsitto;mendingerrorswhenneeded,andmaintaininghomeostasis.For
thesereasons,inanattemptto,“restorebalance”tothewoman'sdamagedbody,thebrain
createdauditorystimulusthatseemedtocomefromthedamagedear,inorderto,as
stated,“fillthevoid”.
Thisis,ofcourse,merelyapersonalhypothesisonlylooselysupportedbycasestudy
evidence.However,onecouldfindtheretobemerittothistheory,andtheremayalready
beresearchavailabletosubstantiatethisclaim.Manyopposingfactsarepresent,oneofthe
mostloomingbeingcasesoftheblind.Ifthereweretobeacaseofhallucinationduetothe
sensorydeprived,itcertainlywouldhavebeenheardmoreofinthosewhoareblind.This
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howeverdoesnotincludethosebornblind,norperhapseventhosewhowentblindata
youngageasthespinalstudyinmicemaysupport;butthosewholosttheireyesightlater
intheirlifewillbeaninterestingplacetostartinsearchforvalidation,ordestructionof
saidtheory.
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