The Brain: Anatomy & Function PDF

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 Íhe Broin : centra Sulcus Fronłql Porietal ccipita) S c p iefo scipitq emporai Brain stem cer ebellum 0b SciG 1A higher Mental functions. dam ag riSk taking /impuse 1 distracti0 behaviour /emotion proble ms. motor WeokneS Porietol lobe Sensory info, Visuo - Spatial langu ge dom age 0 imgey , negiee of side. 9 Freod , wsite, Sowve motns. Occipital lobe Visual Corte info from ye front l0b respond to what se. dom og e hallucinations,homonymo 5 hemianopia - Hemporar Iobe - Hearing , Spee ch , comprehension , memory , perception + recognitie dam ge anterograde amnesią Braun Stem Cerebellum ontro1S vital functions motor (ont rolBaI ce eye mouement , near ing, Spcech , coordination, precision ,timing - chewing + S Gilo w ing -  Gr vs h f MG er tissue regions of the CNs aY on tracts Carry Grey matter - neuron Semg s.— white matter - y elinate df ons info- Mosily inside. Surrsunded by white mo Her.(Spinal (ord) hosty outsi de... loy er of CorHx (broin) Grey mattei deep = Nu ce i A vs S S Grey neuron Somas Whi e myetin ated ons Puronomic Nervbus Sysem processing highér fun ction5 info high way brauns Comm uni Catior branch of PNs.— emoti 0 , conS n Kon t(Gc Reguiates: functions of internal rg "ga cerebrgl Coite rau buik beneath bro Con tr 1S SMuoth + Cordicc m " utside loy er — grey mater. Monitors homeo SFasis g|nds. |Nuçiei 6G deep in bidin subCon Scious. PD ms Sympathetic * amp up exóitefor Fight or fright. Stress. activity Parosympathetic = resting t dig esfing. Es Exerúse Excitement , Emeg en ey, D mai n tain body, Con serue energy Embarra SS ment Digestion, Defecation , Diuresis. 1| wl orgon. pri gte communiCa ti on horacol mbar▇ Cranio Sacral. (aboue + belo ) Sympothetic G nglio - near Spinal Cord. Nor adrenelin ParoSympatheti c gongia - near e ffocror orgns. Acetylcholine ( ch) Somatic NerVouS SyS R Control vO ntary m " acetyicho|i e (Ach) Sen Sory neuron fferent info IN motor neurons efferentinfo ouT.  Neuron nerve cew body and all of its process. Roles recieve integrate Communicate axon terminals nucleys Axon hillock & myelio sheaths cell body Cchwann (Soma) axon Dendrites receive Signals from other ceus Axon hillock - enerate impvises. Nucleus controis entire neuron Soma - organizes and Keeps cell functional. Axon Koodway to transfer signais along Myelin Sheath increase speed of signal Insulation Noge of Ranvier di ffusion of ions Schwann cen - produce myelio Sheath Axon terminals formsjunctions with other cels. Seasory Motor lnter afferent effecent Process info in the Transfer info from Transfer info from CNS CNS and transter external envico ment to external enviroment From one neuroo *c another within the CNS to e ffector CNS. to organ (muctle / glond).  Motor Control How different Systems in interact the NS ability to direct or regulate the mechanisrs essential for moue ment. understanding nature of movement + how movement is controiled 0 Enviromentat result of movement ? movement pattern 3 Neuro metor processes underlying mouement Refiex Theory Sherring ton ( 190 6 ) Stimulus - response Refiexes combined actions that Create behaviser into Hier archial Theorg Adams (19a1) cortical centers Cootcol. Top- down mamer in nS closed 100p Rredboct Motor program theorg Schmidt (qq 6)adaptive 1fexible sensory open loop pieprogiamad. mp's, ge neneralised mp Eloiogical theoryg Gibson Pick (2000) persop/tast/envisment infiuentes Systems theory motor behaviour leanning Schumwoy Cook (2001) body systems owerico to actiuate Synergies Functionql goqis. person t enviroment, Central pattern generator CpG genetically predetermined mouement pattein. neural networks in ouvs Produce thythmic patterend outputs resembling ( wio sensory Feedback inpurs or descending normal movement. motor iopurs). Repitition of rhythmic movements + System returns to its Starting condition when process ceases. Moror programs prestruchtured sers of commads in Cns Execution of Cocidinated mquements wo requiring Continuous Control. = open 1∞op movemect pre progrommed fexecuted wis need Poc Sensory Reeolback. closed 100p5 Sensony kedback bled to adjost moGement in (cttino. neurofocilitation therapeutic approach Bobath. facilitate normal movement. lohibit abnot nal ones Nturodevelopment treatmant Tmotor Controi move meat pa therns + functisnality. address abnurmal tone mouement pafferos + PoSture. Normolize m' rone Motor Sensory inputs motor Outouts.  use H or lose Newropiasticing Individual - task enviroment. Ly enrichmant a mouldable brain Rewire How the braun can chonge to adopt leam + vecover from brain injury Cortical maps Con be modified. How the ns changes in vesponse to ^ Repition and Intensity induces neural experience changes. early intervention time sensrtive. Ability to Focilitate functional Combine functional Changes w/ training and use gaun / gaal w pt. and sensory feedback from it. Synapse communication w neurorrans used mitters. frequeotly Strengthened Tempory changes can becoma permonent with reptition + Intensity Perdorc activity - blood flow to brain Engage in problem Soluing Motivation etc Feedback. motor learning permanent chonges un motor behaviour Sensoty practice , learning Feedback , Skill acquisition Theories Denervation Supersensitivity- hyper actwe neurons More receptors to copture Synapse ^. Neural neurotronsmitters. regeneration Brains Can regenerate /regrows new Oxons injured axons Conateral Sprouting - Ntighbour 0 Xons beqiun Sprouting. Sprout to innervate injued Oxons unmasking of Silent Synpses. Synopses unused Synopses accessed to Form pothways to take over new Cortical reorganisation damaged ones Bloodflow T to areos of Cortex involved tosk Excibility of neurons weeks of practice cortical mops eniage to include previous uninvolued areas.  h lo Rule s7 t) t us e it or lose i 2 t al use i + imp roue it Dnatt Specficity uhe al a Repitition maters t L h i Intensity materS eeh e Time maters t a Sali e ce ma erS ubz Age matjers t Írans ferenc at a Interferen ce ,o0 e i h 1  Rered VoWfonel Mouemen : p fa , env wd orhes (or) - disrupted ability to conscio sy + inten tiona liy contral body oue ments. Neurgl im poiremenrs.— hemipiegi spas tcity ataxia Synergistic Movemen t CNus StroKe ,ms „PD TBI Stroke m° w Motul (o0H 1une pa Hern ms w ▇ ata ▇ S0aStt X motor con (Ol Ki nesig higidi y clskinesiq P rad kinesia Speed , Contro1, cOo d. rem (s x fyncti ón ity a† Xia | )W 0 T Spasticity J( 0 5 te e pa xi Aon (ma| Mou ement oterns. S nso on how SenSory input is percieued S enso1y pathways c rebtal Cor e x (height ened / reduced | obS ent) Spinal cor dl +br ain SHem perip heral nerves Hyperesthesiq (Strokel - damage to Somoto Sen5 y Cortex, thal mus Hypo esthesia (hyp esthesia, anesthesu porąesthesio). *n egi Anesthesi Paresthesi ms - se sor y Sign ) tranSmi SSi on disrup d. ( resthesio) Allodynig PDl - basa gongl dystunction ( pores thesi ). B domoge to Somoto Sen S ry cor x, bra n Stem, perpheral nerues. ( hyrec/hypoesthesia , poresthesia , oliody nia).  a Stroke Ms U TB hemi — w q 0 esS fotigue X paresis e Sposticity X i hal t intetion resting tcEhE (eor S X in ntion 0 aE festin fion it froP Scis 6r unstab e g Shu ffie foot ElLeat ) p stura Seuere b h instabilit mod mod mo of 2 ttiln iaL Qtaxiq X X il Free 2ing X X i G u ia) pda a a  Post ral Contre) Abi lity to adopt posture for functional +aSKs.— Balance equilibrium 1. Stabi lity * Ccontral Centre of moss over bose of support -— 2. Orent aton : Opproptia te telotionship betu en body + en roment. Stro Ke hemiparesi.X m° Confrol. X balance. asymmetrical ms asticity fatig e. Mofor 1 sen S y. Coord. ba lonce. Stab i y S pa PD Po$tur al instGbilty. X communi Cation B6 t cortiat areos. Fo wGrd fiex. TB Xx Moto pionning m " weakne sS. Balon ce. Co (dl. Fon Normal State of tensión / Contraction / resitance in m * e rest or duting passiue mauement. Support posture Stabii)ation alio efici ent Mouement hyper tonia -fo kne. t.Bgid. Sposticity * velocty -de pendent in ton e hy potonia - J m° tone resis fenie. up▇ fiexor patern S hotten ing exten Sor patern ;: lengthenig Domaged umt... X inhibi tory Control of e o sTive contractiodescending Damaged BG.— ns. (cerebraltrectsGu (erCoruhic broin S ii ) Sco spinę1). Cerebel ar dy function Aegu ation of TOn e rqnsmisSion of Mot or i9nc|S0ltered.— Inhi bito y vs eritetory Sy e on 5 PoermS of mouCmem efecte ol. Specife woys m's + jsénts wek tog ether o produe courdinated , froctional achon1. |earned ł Stored os moto ( prog1ams. Strok e : iex 1| ex ten Sor syoe(. Compe nSo T0 Po: Bradykinesia , higidity. festin ating. freezing - ns: Ataii. fatigue 161 : Abnomc po imp rl ę mof p chnug  Sensory Systems modqlity Pick Up in fo location where Stim IS inten Sity thow much Stim timing Cralt 1 srop f 3fim Somatosensonu So/. fouth piestue, temp, poun , propmioception. motor controt, bciante Toord Vestibular SyStem 201. head poSition movement, balonce, posture contiol gort Stability Visugi System 10/. SPatial awateness balance coned Auditory 10:/. cues Fot matol actility graviception 10 /. CNS damage Stioke affecting Somatosensory demyetio ation of Sensory pathuseys. Neurotrasmission distuption dopamine deficitc impair Seasaty-mstor integiation  Neural INen Neutel impairements 0 Neural :demege in the Ns ( Motor Control ISensation / c re ). CNS impairements. PNS imp Qir ements Neuromusculor jun ction StroKe impair ements. ms adicuio athy Po p neuro a thy T Non - neurąl : (mus tuloSketetal Cy Non - neu muscuioSKe Ctal cv/ uimono1y other System c OA Co PD imp irements fractu es hear failur D iabo tendin othies PAD Obes'i y Ca (VechGn IC lI ICTI0N S, Rigiding ^ m° tone that persists throughout Rom. Cog wheel thythmic jerky resistence lead pipe hypertonia Stealy Consistent T resistente to possive Roc. Stroke ( Bosal genglia dysPunction). Stif(ness resistence prolonged Static Stretching Slow thythmic mouements Fatigve management. breathing + relaxation heat therapy Freczing A Sudden temporary mnobility to initiate or continue movement. PO - during gait fransitions ( turning , initiating) ^ visk of Folls. dopamune Substantiq nigra. Communication 4 motor control X PT management motor Cortex pie motor Coltex Rhythmic Continubes waiking patterns. Circuts (onnecting to Falls education BG distupred obstacle navigation Cueing Cocing technique to improve movement initiation continuity + Coord int stimuti (porietal Cotten theimus). Over ride the System - Provides non - automatic drive for ome t timing weight Sh.ft method ( proprioception) Activate alt Motor * Circoits to bypass impaired pathweys Auditory metronome , music counting cadence , Stride. Khyfhmic auditory Stim ViSual Flash lights to rhython targets lasor pointer. Tactile touch or guidance. proprioceptive feedback. Verbal prompis reminders. Conscious movement planning  Techneleg in NR i i a Robotic va wearable devic es. E StimAntigrey t(eaoaaf. Eiecttical w)h eeichoi LitobahuSucassithered opymmaoy thtis ta imgvse mater rewwey of the aim os on odjinch epehtiue pretise Contro lled moveh ens. Ex Siketeton Elai VR Stim ul ie recl w01id scenorios ingog g,to Specifie_ mogi gi ss. hifror thet opy. oh la wear bve devices. m nitol ti (k ) e M on ts. recoid Muscle achi vi (en(outages tontinu us vehob C home ). C getch. Functronvu iechri ccl G ąt M "s ICF Intern ationq Clori fitetian of funttioning , disability heaHhs creotes Stan datol languoz e + frone wo For the desctiption of heaHth -relcte d Clini Cal Tea Son ing. Vi cr pictule. Coh erent vie ) States. focuser on fun Ction (other thon olisabi lity heolth Condition (impai(ements)body funchon ach uity Stru u es (Timi ta fioą ) participorion ((restictions). Contextuc fo envi(onmenta foche |peSonç/ factoi  5 0 al inclusive interuention ta Accessibily un h0 Acceptobility i iLa) Adopt obiity Affor dobiity 9hab A Account ob lily 1 lä ) s hiti  Traumatic Braio Injoors Acquired Broun Inury Traum atic Broun Injury Insuits to the brain that are most frequent cause of nor adults + odolescents. Congenital o( Perinatal 10 young nature. distinct raumatic injory Insuit to the braun caused by ?xternal Subarachnind haemert hoge Force. Cerebral abscess. PREV 2000 un NI per yeor dimnished or gltered State of consciousness RTA's Falls ossaults impaired cognitive abilities t Phyiscal Function. - behaviour and emations disturbed. Sports Skul fractuies. (depressed ) penetrating wourds Dicect Impact On Skcuil high momentum Penetratioo through Skul into brawn substace Sudden decelerations on Collision between braun Substance and interncl Skull 1mpact. Structure. ujury to extracranial bbload focat specific location contusion, Swelling pressure. Vessels. haematoma(a), in farct. Gbcess angular acceteration (tissues diffuse widespread (division of axons throughout axongi injury grey or white motter). bounce ground inskun wiins diffuse vascclar ischaemia fat embolismn protecting) (threwn) meningitis Subarachnoid haemmhorage Intracranial mechs Extracranial mechs plimary hypoxia diffuse axonai injury lacelations contusions hypotension ' Secondaru ischemia haemorrhage bram Swelting infection  Primory Mild C0 CUS5| 0 imp ct Some brai tisSue damaged by grey ma tter contusions or a onai distuphin. Accelerotion | dece leration | o tational fo ces produte diAuse a ona nju y. cerebra ContuSion Ond cor tica bruiS ung * e Se ondory aem rh ge res uit of laceration.ii ad Sub Qrachnoid (in brai or on Surface) Sub dulal extrq du a/ - it Q Ce e ( T Brain Steting - veno0s congestion (tan Cause ischoemia Gn d (ouse domoge to "inact neurons ) + Struchtu es, I fection From open fractuies cSF rhin otrh o a con caufe futh or d amage. ICp manitoring Gp▇ ebr a ▇ fusion ▇ donage) frima1y and Secondary T6 rebeomi ng lesS eosy to difler entiate. Pa Herns of Chong. fatients lose (nsciwusness or develep oter nue footues time of injwy. Condition imp ue s with time 2. losS ofcon soCi 05 nesS time of injury but Condition deterio Qtes. IF lost Con Sciou Sness.e. then gets worse 3. Features of broin unjsy /domogo dev p e mument of unjity ond persis t w/o ch onge -— muuF au0 y en a10n | p 0u(1eVe (O sCi( S esS Im Q 1 0 IYuSKU▇ K ▇ e I▇ Fiexibitty  arkinSons ged Go - omoles nd most commoncauS of neur di sability *— e most Common disease to offec the boso gonglia. Si progression.— excessive movement or dimini Shed moue ment. motor disturbences. Ba Sal gangliq : prOcess of cenI death Our ow ceuIs Kill our ow ceus (unknoLon why). Pr gra mm e o qU n Cel degra ded death remo al (a ptosis). neuro chemi Cql Chnges. Dopamine déple tio 1idiopathic ParKinSoni sm. 857. Sym ptom atic Par Kinsonis m. tumar in 66. compression of aideroin z AEnCeteiio SCIerotit Porki0Son phali tic Parki nseniS m. 1S m. vostul a r thange. Atheroma of 66 t i n tei nal neurofrophic vir us / head inju y *— copSule. (Some drugs that block dopamine con couse Parkinsons) e T positton emiss ion tomogro hy dererue depa ine corcentrotion  ParkinSon DiSPa se pr gresSiue degen ofdepominergie neura s P in suo Stontio nigro por s copacto l d omioergic neurons. altered mste msuement Signs * Sypton 1RFP gaitShuffle T ren ofS rest (pillLcol) R igidity (cogwheel WS eadpipe ) A KineSia (nomvmnt ) Bradlykinesio(stru9 i t6 move ) osturaliostability(hunched) (as) m sk PGce xpre ssion les o grey mcter uclei grop f ceIl bedlier (o )e gguia gr p f Ceul_boolies 10 PNS. Subs tantia nigta (in midbroio). (eurons) iRE CT fDR MesS age_Sent from Cortex _putomen (glutamete) me ssage_fro putaenen –globus pallidus int (gab9) 0messcge from G tha lamus then to m 0 me s ageback toCortez Stimulate iN D EcT ß nhib it 0fro0m Cortex putamen (giutsmote) 0 utom en GPE (gab ).IesS Oction po tential 0 GPE Subtha Imisa gah 0 0subthalmı GPI(glute mate_ 0 GPI thalamus O.  D am ne defici en c Da age to dopaminergic neu(onsiaSubstaofia nigr _pos Com pc cta mbalGcebetwen dopamiae 1auSe ? Co Unk o cye yLch▇ Genetics ? Levad a nc)Mor conce Aeuto disabi ity y > Mcl e  most Common disabitity in young pespie. unkn causC Femaie > male. Oes tle'is us tiplPSclerosis progres iue ne uro1 gicai diseose Demyetinating diseose peg ener 0tive dis ease that at acks CNS. How ms a qck s W 6CSUT CKneUrOnS mye lin affect ed aro nd the ner ve fibres in broin t Seterosis = scorring Sping/ cord Nerve signqIs Sio e ol or biocked. DeMyelination of ner ve Fibres losS of myelin e los5 of action potential Sp eed.— dlestructio0 of Oligo den dro cy tos Ayon intact. DiStributien of pi ques white dots Shown on Scon fimaging Axon al domoge exposed ner ve Fibre (iesions.) RelopSing lremiting ms : Symproms come + 9o. Gool heg Ith fo lowed by Sudden rel pSe (80 7. Secondary progressive 1s Gradua/ wors en ng of Symptos w| fewer remiss ion $ (deuelop in lo y) (5 |.) Priary progresiv aI Si s d Symptoms From begining. Symptoms groduatly devel worsen ov er time (1o-IS /) fatigue bal an e lesion in.. ert o sensqtiD Cerbum + Cerebe lium : balnce + (14 - 39/.) emotional biadder | bow l impairemenfS co - or el tremors. pai Motor nerve tract S to zone m" weak es , Spasticity poralysis, vi ión probi em5, bladder bowe l weoknes pas ticty isSves -— VIS ual dsturbanæ Sençory ner ve: ai ered Sen sation , spas m) Numb Ness. prickling 4 Inrenfion 1remor dysarthria burning Sensati on htax a (80/) ate dy phagia  hateg tom o koisy: StroKg 2nd leading Cause of death giob. CvA Cerebro vascular accid ent Clinicq Syn dt ome of pres umed Vascular origi charae tériSed by ropidiy deveoping Sigos of focal or ghobal disturban ce of (ere br al function reduced bioo Flow to port of bro a— brain tissue d epr ived of 0ª + nutrients. broin ceus die ropidly Weq esS Sign ficont broin clamoge , disobihły , death compi e te paralysis on | -side f bo ey C on Q) side of broi ffects 0 Side of body = R - Sided hemi plegi / hemi - CVA on 0 side f brain f ecs0 side of body aresis. L- Side d (sch mie Heorrth agie Common - 80/ f stro kes. 1ess Comm n 20 1 of all Stro kes. Blockoge of biood Supply to braun throm botit. Clot Weak biood vess els rupture on d biee d into bioin, emlbo (iC cio eISewhere trGveir. Intr qterebrai haemorrho9 pidural , subdura or Subarachn oid qthero Scerosis- pi que Cl gged areries. Anterior | hae m rrh C 9e (erebrGI CIasS i Ficqtion S : ar. |nternals Totai Ant erior Circu atio Inforct ThCI Mi ddi e d1łe Cerebtal Corotioart entire ant circu lation supply ing i si de oSterior tereb ral Ort. Parti | PACI porł of ünt cir cul at on Sup y g Si de. B9silar orter LQ Cunor InfarctLACI one of Sma1l Qitenies deep in braun vertebral Posterior Circulation InfardPoc rery ,Ci cul q ion t bockof bi Circle ofWilliS