Summary

This document provides an overview of brain anatomy, including different regions, neuron structures, and action potentials. It also discusses different types of memory and areas and processes involved in memory storage and retrieval.

Full Transcript

Revision Topic 1 THE BRAIN Double Disociation = both areas have a distinct function and proven that other area does not have that function , no correlation Single Dissociation Directions Anterior/Rostral = Front Posterior/Caudal = End/Tail Dorsal = Top Ventral = Bottom/Feet Medial = towards the m...

Revision Topic 1 THE BRAIN Double Disociation = both areas have a distinct function and proven that other area does not have that function , no correlation Single Dissociation Directions Anterior/Rostral = Front Posterior/Caudal = End/Tail Dorsal = Top Ventral = Bottom/Feet Medial = towards the middle Lateral = away from the middle Inferior = below Superior = above Horizontal plate - both hemispheres cut open (view from top) Saggital - cut open in the middle , only one hemisphere visible (side view) Coronal - both hemispheres visible, (view from the back or front) Telencephalon = cerbral cortex, hippocampus , limbic system -> thinking, decision making, voluntray movement and sensory Diencephalon = thalamus, hippothalamus -> for the body homeostasis Mesencephalon = Midrain Metenencephalon = pons and cerebellum -> sleep, breating, balance, fine motor skills Mylencephalon = medulla -> basic life functions Central Sylcus = between frontal and parietal lobe Sylvanian Fissure/ Lateral sulcus = between temporal and frontal Parieto - Occipital Sulcus = between occciptal and parietal lobe Frontal Lobe -> complex thinking, emotions and voluntray moovement Precentral gyrus (primary motore cortex) = voluntary moovement Premotor cortex = plans & coordinates complex moovements supplementary motor area = plans & initiates moovemeny, muscle memory frontal eye field = voluntary eye moovements + visual attention Brocca's Area = motor speech area , speech production PFC = desciision making, social behavior, reasoning, logic Parietal Lobe -> sensory info, spacial info V5/htm = processes motion in visual info postcentral gyrus = primary somatosensory cortex ; touch, pressure, pain , temp secondary somatosensory cortex = more complex touch, texture and object regognition supramarginal gyrus = understaning spacial relations angular gyrus = language, math & spacial Occipital Lobe -> main areas fir visual processing primary V1 = light, edges and orientation, outlines secondary V2 = patterns and depth 3D V3 = motion and object shapes Temporal Lobe -> sound, language , object & face regocnition, memory and speech understanding superior temproal gyrus = processes sound + speech Wenickes Area = helps to understand speech (at the posterior, doral end of stg) middle tg = word & picture meaning inferior tg = complex visual processing, object & face regocnition V4 = color & visual details auditory tract = sound from ear to brain Basel Ganglia -> helps with voluntary moovement, motor leaning & coordination Caudte Nucleus = learning & moovement control; leaning how to catch a ball Thalamus = sends infro where it belongs Putamen = regulates moovemnt & influences motor skill (keyboard typing) Globus Padillus = maintaining smooth and balanced movement Subthalamic Nucleus = modulates output from basil ganglia to regulate movement Substancia Nigra = produces domapine - moovement and reward processing Limbic System -> emotion, memory and survival behaviors Fornix = connects diff parts of LS for memory formation Cingulate Gyrus = processng emotion , regulating behaviour - appropriate Thalamus = distributes info Olfactory Bulb = processes smell and links them to memory and emotion Septal Nuclei = pleasure, reward and social bonding Amygdale = processes fear and emotional reaction Hippocamus = forming and retrieving memory Mammilary Body = connects sensory info to memo for easier retrieval Cerebral Ventricles -> protect and support brain & spinal cord Lateral Ventricles = make and store brain fluid (CSF) to help protect the brain , soft padding inside head Third Ventricle = passes fluied from lateral to fourth Fourth Ventricle = near brainstem sends fluid around the brain and down the spine Neurons Structure Soma = cell body - produces protein, has cytoplamsa and cell membranes -> phospholipidic bilayer mebrane attracts water (hydrophilic) from outside and repells water from inside (Hydrophobic) , helps to keep the neurons charge stable Intercellular Membrane = inside cytoplasma high in K Extracellulat = outside cell high in Na + Nucleus = holds DNA Dendrites = recieve signals fromm other neurons Axons = carries electrical signal from dentrites to exon terminal Schwann Cell = Insulating Myelin sheets - no presence of ion channels Nodes of Ranvier = inbetween schwann cells and has ion channels Axon Terminal = connectst o other dentrites for signal transmission Ca+ Channels found at axon terminal for the synaptic trenmission Voltage Gated Ion Channels = open cdue to changes in membrane potential Ligand Gated Ion Channels = Channels that opens when neurotransmitter binds to them Action Potential 1) Resting State = -70 mV = sodium Na + outside cell more, potassium K inside (negative) 2) depolarizsation - cell becomes more positive, channels open and na+ flows in sodium channels potassium channels open and K flows out Threshold = -55, signals under that are failed attempts full depolarization until + 40 mV 3) Repolarization, getting ready for next action potention = resetting potassium channels open letting K in 4) Hyperpolarization - inner cell under -70 mV sodium potassium pump - restores the balance Types of Neurons Sensory - carry info from brain and spinal cord Motor Neurons - brain, spinal cord to muscle for movement Interneuron - connect senory & motor neuron with brain and spinal cord, can coordinate reflexes Mirror Neurons - when u do smt + when u observe smb else do smt Unipolar - like sensory neurons help transmit sensory signals, only one axon from cell body, no dentrites Bipolar - dendrite and axon, sesnory organs Multipolar - multiple extenisions - found in brain and spnal cord Pseudoneurons: similar to bipolar ones often found in sensory -> a neuron can fire up tp 200 action potentials per minute -> 40% of the brains energy ESPS = Exitatory , slight depolarisation, neuron is more likely to fire exmaple : glutamate binds to ligand gated channel Na+ flows inside IPSP = inhibitory, slight hyperpolarization , less likely to fire example : gaba bind to ligand gated channel K flows in simple diffusion = molecules moove inside and outside of the membrane without any help example oxygen facilitated diffusioon = ion channels help them to cross the lipide layer active transport ATP = sodium potassium pump , creates a defined concentration gradient Signal Transmission 1) Action potential reaches axon terminal 2) Volatge Gated Ca+ channel sopen, ca+ flows in and helps them to fuse with membrane aka exocitosis 3) Nt cross synaptic cleft 4) Nt bind to Ligand gated ion channels, ions flow in postsynaptic cell = Ionotropic G- Protein receptors -> Nt activates G protein inside cell -> slow but long lasting effect = Metabotropic 5) Cleanup - if Nt stays in synaptci cleft overstimulation can lead to cell death, or just rapid firing that can make u feel nervous Reuptake by presynaptic neuron & reuse -> endocytosis - Nt are put back into vescicles Enzymatic Breakdown Diffiusion - Nt drift away 6) Fine tuning - autoreceptors give feedback, when enough Nt hace been sent Agonsits -> mimic or engance natural body responses ex (insulin) they can also block neurotransmitters like antihistamines that block allergic reactions Partiial Agonist - partially activated receptor Depression: Reduced Receptor Sensitivity = neurotransmitter either less avilible or does not bond to receptor properly Receptor Downregulation = less receptors after lots of stress Excitotocity and Neuroplasticity = chronic stress can damage brain regions Addiction Overstimmulation of Dopamine Pathways = used to intense dopamine , beyond natural reward Tolerance: overstimmulation from drugs causes to downregulation of receptors Neurotransmitters: Glutamate = exhibitory Gaba = inhibitory Dopamine = Modulatory Serotonin = Modulatory Norepinephine = Modulatory Chemical Structrule of Neurotransmitters Aminoacids = Glutamate, GABA -> simple molecules directly influence Brain, usually exhitiory or ibhibitory Monoamines = Dopamine, Serotonin, Norapinephine, more complex -> involved in mood, motivation etc Neuroimaging Techniques CT - Computed Tomography xray based, radioactive light 3D pictures of brain can be built with computer not very detailed - spatial resolution shows no activity -> can be used to detect strokes, ischemic - blooc clumps white MRI - Magnetic Resonance Imaging produces 3D pic of every plane in the brain poor temporal resolution major fiber burdles can be seen DI - Diffusior Imaging looks at water diffusion in white matter visualisation of small fiber bundles FMRI - functional mri measures brain activity by detecting levels of oxygen in blood vessels low temporal resolution very high spatial rresolution BOLD SIgnal - no electrical activity single cell recording wire in brain with microelectrodes invasie high spatial and temporal resolution PET - Positron Emission tomography injection of radioactive particles -> when they come against other particles they travel other direction expensive, chemicals short lived colored maps of brain TMS - Transkranial Magnetic Stimulation wires placed above skull to stimulate a region brain - function relationship Lesions Brocca's Area etc Invasive EEG - Electrocephalogram electrodes on scalp non invasive what do they record low spatial resolution - only skull level high temporal alpha waves MEG - Magnetroncephalongraphy EEG with magnets detects magnetic field high temporal and better spacial resolution than eeg only signals near surface can be measured TES - Transcranial electrical stimulation activates cortex areas electrodes on scalp Opogenics inhibit and stimulate neurons proteins are introduced into genes - harmless viruses viruses are injected in brain and express proteins genes are modified will only exoress on particular neurons effects of turning on or off neurons can be observed Vision photons = light particles cornea = transparent outer layer of the eye that bends light lens = works together with cornea to form image on retina refraction = the bending of light clliary muscle = controlls the shap accomodation = ciliary muschle shapes lens to form pic on retina pupil = how much light enters the eye iris = around the pupil extrocellular muscke = muscle that controls eye movement choroid tissue = layer for blood supply retina = surface where light falls on inside eye fovea = sweet sport with most photoreceptors on retina aand clearer vision foveola = sweet spot inside fovea = clearest vision neural layer = layer that contains photoreceptors between retina and optic nerve photoreceptors = cells that resond to light rods = photoreceptors that are most active in low light, lot of the, per ganglion cell, hard to know where signal came from cones = for colors, blue, red, green = color and detail horizontal cells = connect photoreceptors and bipolar cells bipolar cells = interneurons that recieve infro from rhods and cones and pass them to ganglion cells ganglion cells = it's axons form optic nerve optic nerve = ganglion cells from this and it goes from retina to the optic chiasm amarcine cells = contact bipolar with ganglion cells important for inhibition -> Rhods and Cones do not produce full action potentials, signals do not go very far -> graded potential change in size of signal based on the strenght of signal recieved OPTIC ILLUSION Bright Images = cause photoreceptors to fire even after image Bright Color = same stimulus over and over and cones get tired - after blue green -> red fires Negative Photograph - rodes get same stimulus over and over so black turn white Process: When Light Rhodopsin in Rods changes shape and reduces cHMP -> closes sodium cahennel -> hyperpolarization -> less glutamate On Bipolar Cells are active when there's a decrease in glutamaten -> active when light Metabotropic Glutamate Receptors mGluR6 become inhibites (less likely to fire) by glutamate When Dark Photoreceptors become depolarized and release Glutamate OFF Bipolar Cels remain active when glutamate is released - ionotropic receptops like AMPA Neurotransmission -> Bipolare Cells djust their signalss to ganglion cells Off when dark and ON when light this dual system helps to detect increase and decrease of light Horizontal Cells enhance contrast from photoreceptors to bipolar receptors Gaba (inhibitory) released to modulate signal intensity when one bright light is detected by photo receptore horizontal cell, quiets down the photoreceptors next to it to make the brightness stand out Amarcine Cells -> helper cells that process signals before they get to Ganglion cells -> motion detection and fine tuning of signals Ganglion Cells collects signals from bipolar cels and transits them to the brain via the optic nerve turn electrical signals into action portentials Types: Midget GC = high resolution, color and fine detail Parasol GC = sensitivee to motion and low contrast Small Bistralfield GC = info about sprcific colors like blue / yellow contrast ON GC = have an On Centre, fires when light hits center of receptive field but background is dark OFF GC = have an OFF Centre fiires when light hits the center not the sourrounding Vision in the Brain contralateral = not same side ipsilateral = same side monocular zone = zone that can only be seen by one eye binocular zones = zone that is seen by both eyes LGN = Lateral geniculate nucleus LGN = structure in Thalamus that processes different aspects of vision from ganglion cells Parvovecular Pathway = processes fine detail, color and textures -> high resolution _> info from cones - color Magnocellular Pathway = broader shapes & low light levels , motion & spatial layout -> info from rods Parvocellular input from MIdget GC = P Cells Layer 3-6 in LGN - feeds into ventral stream Then Occiptal lobe V4 crucial for color and form fine detail and color , object regognition Ventral Stream - What pathway Inferior Temporal cortex Ventral Stram/Pathway - What Pathway damage here causes visual agnosia - problems with object regognition Magnocellular input from M Cells (parasol ganlion cells) Layer 1-2 LGN - feeds into Dorsal stream Then Ocipital Lobe -> V5 for detecting motion Motion Depth, Spatial Awareness Dorsal Stream - Where/How Parietal Cortex HIgh Motion sensitivity , low contrast Dorsal Stream/Pathway damage here causes optic ataxia - problems to combine motor actions with vision (grabbing a cup) Info from left eye -left optic nerve Info from right eye - right optic nerve Optic nerve - both eyes meet Both Right Visual field go right Both Left Visual fields go left Pretectal Nucleus gives feedback to pupils to adjust when too bright Then they go to LGN and then to primary visual cortex Then they go to Dorsal or Ventral Stream Organisation of V1 Left & Right Hemisphere with each 6 Layers Each processes coresponing visual fields Layer 1 = superficial ; communication between layers Layer 2/3 = visual info = sent to higher brain areas to help understand more complex visual details like color Layer 4a = input from LGN about visual environment Layer 4b = input from LGN about moovement and depth of visual field Layer 4c = 4ca for motion and 4cb for color and fine detail Layer 5/6 = send info to other brain region and provide feedback to LGN to refine processing Ocular Dominance Slabs -> some regions favor left or right eye Orientation Colums Neurons respind to edges or specific angels Simple Cells respond to specific orientations like vertical, horizontal or diagnoal lines if the line is in thr wrong direction or outside the area, the cell does not respond help detcet edges and orientations of objects, first step of regognizing shapes Complex Cells Response to line or edge moving trough a larger area they fire as long as it is mooving in the right direction good for detecting motion Hypercomplex Cells (End Stpped Cells) Stop responding if line or edge extends beyond a certain point detection of more complex shapes - the end of smt Hypercolum = functional unit that contains a complete set of orientation colums from 0 to 180 and color blobs Each hypercolumn represents a small unit of the visual field CO Blobs -> process color info In Layer 2/3 and 4C they distinguish colors, help separate color processing from other things like motion process color independent of orientation co blobs and orientation lines are often near eachother so the brain can easily integrate info Cortical magnification = fovea is dispropotionally represented in the brains visual cortex fovea is only a small part of visual field but has very detailed vision Lesions Optic Nerve damage - loss of vision in one eye (monocular blindness) Optic Chiasm - bitemporal hemianopia - loss of outer vision field (peripheral vision) Optic Tract and LGN - homonymous hemianopia - loss in common visual fields Attention attention is the cognitive process of selectively concentrating on one aspect of the environment and ignoring others voluntary attention (controlled) Top Down involuntary (uncontrolled) Bottom UP Process Selective Filtering (Frontal Lobes) Resource Allocation = enhanced performance for selected task (Thalamus) Enhanced processsing for chosen stimuli Shifting - attention is flexible (parietal lobe) Types Spatial Attention = attention to particular location Top Down SA = consciously looking for someone in a room Bottom up SA = a friend calls ur name -> posterior parietal cortex helps ro orient attention to spacial locations Feature Based Attention = ability to focus on specific charakteristics of a stimuli (looking for a red shirt) Object based attention = follow object Sustained Attention = maintaining focus over a longer period of time (right pfc and acc) Focused/ Selective Attention = concentrating on a single stimulus while ignoring others (pfc and parietal lobe and thalamnus) Divided Attention = essential in fast paced environments, reduces efficency (dlpfc) Executive Attention = Inhibiting distractions and managing conflict (acc) Temporal Attention = expect something at a certain time -> shortens reaction time covert - attention shift without eye moovement Overt = attention + eye/head shift Brain Areas Frontal Lobes (PFC) = maintain attention over time and set priorities, goal oriented attention Parietal Lobes (Posterior Parietal Cortex) = switching attention between diff stimuli - look towards sound or movement Superior Colliculus (Midbrain) = rapid shifts in attention bottom up Thalamus (Pulvinar Nucleus) = focusing on important stimuli while filtering out others Anterior Cingulate Cortex (ACC) = supresses background noise/ unimportant stimuli Visual Cortex = featuee vased attention Ventral Attention Network primarly right hemisphere stimulus directed attention - reacting to unexpected events Bottom Up = Exo vlpfc = evealuate and process unexpected syimuli Dorsol Attention Network goal directed -> choosing what to focus on top down = Endo Bilateral Frontal Eye Fields control eye movements and focus spatial attention when focusing on something we modulate neuron activity and have change blindness Cognitive Control the intentional selection of thoughts emotions and behaviors supression of inapropriate behavior acc -> conflict monitoring LPFC -> value of stimulus in current context Phinea"s Gage -> problems w emotional processing and rational descision making DLPFC = maintaining task relevant rules, controlling impulses and maintaining focus ACC = choosing correct behavior in real time, error detection VLPFC = supresses urges, inhibitation of automatic response MPFC = evaluates performance & accurate behavior - goal directed behavior Parietal Cortex = puts attention to relevant stimulus cerebellum = fine tuning of response, avoiding hesitation The MPFC has layers/Gradient Ventral Dorsal = maintenance (holding info - waitress) vs manipulation (working w info - math problem) Anterior Posterior = Abstract planning (front - general) vs detailed execution (back - specific plan steps) Lateral Medial = Lateral (out) focuses on external info like environment and medial on personal motivation Stroop Task Theories Processing speed = brain is trained to read a word quickly Selective Attention = reading the word does not require much effort Ultimate Theory = reading a word is an automatic habit Memory Linking Information makes it easier to remember Short Term Memory holds 5 +/- 2 items at a time and is limited by distraction and new stimuli Rehearsal helps retain memory longer Chunking = grouping items into chunks to improve retention (phonenumber) Forgetting Theories Proactive Interference = old memories block new ones Retroactive Interference = new memories overwrite old ones Displacement = New info pushes out out info in short term memo Retrival Failure = memory is stored but can't be accesed Memory Strategies = Mnemonics = chunking and repeated rehersal Practice mooved short term memo to long term incoming info -> short term -> working memo -> retrival -> shorterm Monkey Experiment -> monkey rembers a location of a cue (square) using working memory even when cue dissapear -> DLPFC plays a role in maintaining info aka holding on to infro temproraly, maipulating and goal directed behaviour -> retain, update and use info Memory Models Aktision-Shiffrin Model = Rehearsal moves memories from short term to long term storage Sensory Memory Model = Briefly holds sensory input Retrieval Recollection = Actively recalling details when answering questions Familiarity = recognizing something without detailed memory Wisconsing Card Sorting Test WCST diff crads with colors and shapes -> u need to figure out the sorting rule once you have figured it out, the rule changes WCST measures your brains ability to make that switch -> this tests cognitive flexibility = the ability to adapt to changing rules -> how well does ur brain handle goal directed behaviour, switching strategies and handling frustration PFC especially DLPFC is responsible for controlling attention, adapting and ihibitinh old habits connects to memory because you need to hold info temporarly, update working memory and monitor performance, rmbr last choice and if it was correct The Engram is a memory trace - where we store memories -> it is all over the brain Memory stores in Area's related to it's stiimulus - what fires together wires together aka synaptic plasticity and LTP dog + glasses -> we see glasses -> we think dog Long term memo - at least 1 day old Types: Declarative Memo = conscious recall of facts and events (medial temporal lobe) Episodic Memory = personal expirences, first day of school, autobiographical Semantic Memory = stores general knowledge and facts Implicit (non-declartive) Memo = skills, habits & conditioned responses Procedural Memory = how to perform tasks and actions - riding a bike - aquired trough practice and repititon ( Priming = unconscious influence of syimulus recalls another -> reading apple -> faster at regocnizing fruit (neocortex) Classic Conditioning -> Amygdala for fear Non Associative Memory = habituation -> reflex pathways Brain Regions of LTM Episodic = pfc,hippocampus,posterior parietal cortex, default mode network -> activates in autobiographical thought Semantic = temproal lobe, hippocampus - amygdalal for emo charged memo Procedural = Basal Ganglia, cerebellum, premotor cortex Priming = sensory corices, pfc Classical Conditioning = Amygdala (emotional) & cerebellum (motor reflex) Non - Associative Memory = Reflex Patheays, cerebellum Spatial Memory = hippocampus and cortex Hippocampus and Memory Consolidation -> hippocampus helps form new memos and later transfers them to the cortex for lonterm storage (semantic and episodic) -> once in longterm memory, the memory brcomrd motr and more independent of the hippocampus Organization of LTM Encoding = semantic encoding - storage based on meaning , but also visiual and auditory Storage = hippocampus for consolidation and cortex for LTM -> Schemeas related concepts REM Phase, deepest sleep, in sleep is crucial for consolidation LTP - Long Term Potentiation curcial for consolidation Neurotransmitters like glutamate and receptors like nmda Standart Consolidation Theory - does not take rebos into account Rebo's amnesia - old memos are better preserved than older ones - consolidation theory Habs law - what fires together wires together-> structural changes thanks to LTP Retrival - not perfect, memos can be reconstructed falsely Recall = actively retriving without cues free recal - no cues - most difficult cued recall Regocnition = identifying information in a list or environment - mpc - easiest influenced by cues - contextual or emotional triggers contextual cues = environment of recall matches encoding one emotional cues = emotion of recal matched emotion of encoding semanti cues = words or concepts related to target memo -> dog -> my dog Flashbub Memories have intense emotions and feel clear - but does not mean they are accurate memories are easier to retrieve when encoding and retrieval conditions match -> caffeine -> caffeie Memory Retrival Pathway Encoding = information is organized into neural networks based on associaton between concepts, related memos group together -> each piece of info = a node Activation of Pathways = a specific pathway is activated, typically witha retrival cue -> spreading activation, associates memos easier accesible Strenght of Pathways = frequently used pathways are easier to retrieve Weak Pathways = poor encoding - result in hard to retrieve memos Failures in retrival Cue Dependent Forgetting = memo is intact but can;t be accessed du to lack of efective cues Interference = older memories hinder retrival of new ones ; block retrival Weak Pathways = poor encoding, hard to remember Amnesia Anterogade Amnesia = inability to form new lonterm memories after onset ->damage to hippocampus - imapirs declarative memory Retrogade Amnesia = loss of memories formed before amnesia -> brain trauma - incomplete consolidation memo gone - declartive more than semantic affected Neuroplasticity = the brains ability to adapt and rewire when your young u have the most allowing for rapid learning and adaptation Structural Neuroplasticity = phisical change in the brains structure synaptogenesis = growth of new dendrites synaptic pruning = shrinkage or loss of unused connections Functional neuroplasticity = brain can take over functions after damage the older u get the less neuroplasticity u have chronic stress can also damage neurplasticiy LTP - happens when we learn process tha strenghtens connections between neurons the more ampa receptors there are the easier smt activates early LTP short term memo late LTP long term memo LTP and the novel protein syntheisis - axonal protein syntheis neuroplasticity and structural changes mostly studied in hippocampus at glutamate receptors Synaptic Placticiy = use it or loose it connection weak connection can turn into strong connection with LTP Actionpotention -> tini glutamate release -> glutamate binds to ampa and nmda - only ampa activates and lets na+ in -> sligh depolarisation - ndma remains closed blocked by mg + Strong or Repetitive Signal -> large amount of glutamate = glutamate bind to both receptors -> more na+, large depolarization and positive ions inside cell expell mg+, nmda activated and lets ca+ inside cell ca+ mediation of LTP induction Early phase - proteins make ampa more sensitive - easier depolarized -> short term memo Late phase - new proteins are made, connections are enhanced, new ampa receptors - more receptors and new connections Hippocampus Anatomy CA4 (inside) sends info to other regions CA3 memory retrival CA1 for Episodic and Anterogade Amnesia Subliculum under CA1 yellow = relay area for contextual processing Lateralization Contralateral Control = each hemisphere control the opposite side of the body - left - right Left Hemisphere = language, logic and detail - damage here causes asphasia Right Hemisphere = spatial ability emotions and holistic thinking - damage here causes neglect of left side Corpus Collasum = connects hemispheres ; split brain patients lose communication between sudes, revealing their unqiue roles Stoke = blood flow in brain is blocked or vessle burst, causing brain damage Ischemic = Blood Clot blocks flow - two types Hemoorrhagic = blood vessle burst - severe Transients Ischemic Attack TIA = temporary blockage no long lasting effect Brainstem = Affects breathing and heartbeat Damage Left Hemisphere = Speech issues (aphasia) Broca's Asphasia = trouble speeking Wernickes Asphasia = trouble understanding speech = dysartria Right Hemisphere = neglect of left side/ spacial issues = agnostic Contralateral neglect of left side Prosopagnosia = face blindness other symptoms weakness or numbness in one side (contralateral) memory, planning, descision making visual deficits and emotional changes Auditory Input = Ear - Auditory Area = pure word deafness Wernicke's Asphasia = trouble understanding speech Transcorical asphasia after WA - slight trouble understanding words betwen WA and BA = problem in processing = slow or inacurate answer Transcortical motor aphasia = lots of problems with speech Brocca's asphaisa = speech problems betwwen BA and Motor Output (mouth) = dysathria - difficulty pronouncing words Split Brain = no communication between hemisphere can name object in right visual field (processed by left hemisphere where language is cannot name object left visual field but can draw or regognize them Affected Brain Regions Middle Cerebral Artery MCA = lateral parts of frontal and parietal and temporal lobe Anterior Cerebral Artery ACA = medial part of frontal and parietal lobe Posterior Cerebral Arterie PCA = occipital lobe,temporal lobe Basilian Artery = brainstem and cerebellum CT Scan Ischemic stroke = dark - lack of bloodflow can be detected early - area less dense Hemorrhagic Stroke = light - bloodflow area more dense and bright Motor Brain Regions Motor Cortex M1 = voluntary movement ; precentral gyrus ; contains motor map Supplementary Motor Area SMA = plans movement ahead Premotor Cortex = plans movement based on sensory input PFC = plan scomplex movements Posterior Parietal Cortex = spatial / awareness of sourrounding Basel Ganglia = smooths and regulates moovement direct pathway = promotes movement by reducing inhibition of thalamus indirekt pathway = supresses unwanted moovements, more inhibition Caudate & Putamen (Striatum) = main imput areas Globus Pallidus = inhibits thalamus Subthalamic Nucleus = modulates basal ganglia output Substancia Nigra = produces dopamine to facilitate movement Cerebellum = cordinates movement. detects errors, improves movement cerebrocerebellum = plans and initiates movement Spinocerebellum = corrects limb positioning Vestibulocerebellum = balance and posture Cerebellar peduncles = bundles of fibers that connect cerebllum to brain and spinal cord for commmunication superior cerebellar peduncle SCP = cerebellum - midbrain, output pathway, fine tuning voluntary moveemnt middle cerebellar peduncle MCP = cerebellum to pons, input pathway, process planned movement vs execution Inferior cerebellat peduncle ICP = cerebellum - medulla - spinal cord, input sensory and output balance and posture Brainstem = relays sensory and motor signals, integrates mototr commands midbrain = motor contral pons = bakance medulla oblongate = reflexes for stability, posture and pain avoidance Levels of motor control = how complex is a task - need for high input -> this leads to efficiency so each part can focus on their part without disrupting other; individual focus -> backup = if higher levels are damages - basix stuff still works - peoples with mc damage still retain posture and reflex High = motor cortex, basel ganglia and cerebellum Intermediate = brainstem lower levels = spinal cord Voluntary Movements - initiated by higher levels (MC) and fine tuned by cerebellum and basel ganglia Invonluntary movement = manged by low levels (brainstem and spinal cord) = reflexes -> the levels ensure both can work together example walaking direction (voluntary) adjustments to maintain balance (unvoluntary) Adaptive Motor Control Feedback loops = higher levels adjust movement based on sensory input and error detection from cerebellum Feed Forward control = cerebellum predicts movement & adjust tgem before execution Spinal Cord Reflexes Spinal Cord = connects brain to body and connects to skeletal muscels for reflexes -> recieves sensory input znd generates approriate motor response to muschles - quick Agonist (primary muscle for movement) and Antagonist muscle (opposing muscle) = biceps and triceps when agonsit conrracts, antagonist relexes - spinal cord helps w this = rexiprocal innervation/inhibition Reflexes - involuntary movement triggered by sensory input strech reflex sends exitatory signals to agonist to strech and inhibiting to antagonist to relax happens when muscle spindel detects strech quick/fast -> spinal cord processes -> muscle contracts Motor Pathways Dorsolateral = Fine Movements Corticospinal Tract = directly controls limbs Corticorubrospinal Tract - idirect pathway via red nucleus - controls limb Ventromedial = Posture/Balance Corticospinal track = directly affects axial muscels Cortico - brainstem-apinal tract = indirectly affects posture via brainstem Pyramidial vs Extrapyramidial Systems Pyramidial (Corticospinal) = voluntray, fine control Extrapyramidial = involuntart, posture Motor Units = a motor neuron + the muscle fibers it controls Slow Units = fatige resistant = standing and maintaining posture Fast fatigue resistant = moderate = running fast fatigue units = powerful but short = jumping Disorders Parkinsons Disease = loss of dopamine in basal ganglia -> difficulty initating movements = tremorss and stiffness Huntington's Disease = neuronal death in the caudate/putamen -> results in involuntray movement Alcohol = impairs cerebellum - posture and coordination Epilepsy = seizures in motor cortex cause involuntairy movements Readiness Potention = electrical activity slowly building up in the brain before voluntary movemnt -> descision to moove may occure before consious awareness -> 500ms before movement vs aware 350 ms -> happens in supplementary motor cortex and later spreads to primary mc -> debates about free will - how much control do we really have about our brain? Cortical Homunculus Motor = represents body parts in mototr cortex and the regions that require the most precision - largest (hands and lips) sensory = similar map but reflects the amount of sensory receptors in a space Neuromodulation -> enhance or inhibit neural signals -. aiming to restore everything to its norm serotonin synthesis Tryptophan (TRP) - TRP/LNAAs ration in blood brain barrier TRP - Enzyme hydroxylase -> 5HT -> Enzyme AAAD -> Serotonin Serotonin = mood and sleep regulation, apetite and stress response ->cannot cross bbb Diet helps to keep us TRP/LNAA Plasms ratio protein has much trp - essential amio assid carbohydrates help with ratio bc insulin sends LNAA to muscle lowering competition Depression = low serotonin/low trp Omega 3 (walnut) enhances serotonin receptor funtion Fiber rich diets is gut for gut -> imost serotonin micronutients like b6, magnesium and zink are essential SSRI = chemical neuromodulation tms or dbs = electrical neuromodulation Homeostasis = normal state of the body

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