Unit 3_fall2011 - KIN 3E03/Life Sciences 3K03 Neural...

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Unformatted text preview: KIN 3E03/Life Sciences 3K03 Neural control of human movement Dr Ramesh Balasubramaniam Fall 2011 NOTES Unit 3 Neural plasticity How development, learning and memory change the brain? Strengthening synapses Synapses used often are strengthened (A) Those not used are weakened and can become ineffective (B) Used lots A B Not Used Production of structural changes as a result of reverberation of activity (memories, experiences) in synapses. This helps facilitate transmission over the pathway. A memory held around long enough in the short term will eventually be put into long term memory as a result of strengthened synaptic connections. Synaptic changes over in Organism Development Over the first few years of life, the brain grows rapidly. As each neuron matures, it sends out multiple branches (axons, which send information out, and dendrites, which take in information), increasing the number of synaptic contacts At birth, each neuron in the cerebral cortex has approximately 2,500 synapses. By the time an infant is two or three years old, the number of synapses is approximately 15,000 synapses per neuron (Gopnick, et al., 1999). 6-fold increase As we age, old connections are deleted through a process called synaptic pruning. Pruning is common because life expectancy 100+ years ago used to be very low (mid-40s); the brain fine-tuned itself to this timeline/lifetime in order to facilitate learning in shorter periods. MEDIAL temporal lobe not the same as MT area Amnesia Amnesia Partial or total loss of memory, usually resulting from shock, psychological disturbance, brain injury, or illness.# # Organic caused by shock, brain injury, illness # hypoxic episode, herpes encephalitis # epilepsy, brain injury, Alzheimer's disease# # Psychogenic caused by psychological trauma # dissociative disorders # psychogenic fugue # multiple personality or bipolar disorder# Amnesia Amnesia can be global or material-specific! # Global any kind of information is affected# Material-specific certain kinds of material #(e.g., faces)# after before # Amnesia can be anterograde or retrograde# # Anterograde amnesia inability to learn anything new since the time of the trauma (usually organic)# # Retrograde amnesia loss of memory for events prior to the time of the trauma (psychogenic or organic)# GLOBAL Anterograde Amnesia (can learn nothing new after the time of trauma) HM Can retrieve early memories but it drops off after a certain point (mild retrograde, too) Most famous case reported by Scoville & Milner (1957)! # Scoville did the surgeries for psychosis but didn't work, so tried it for epilepsy on about 30 patients. Patients studied by removal of lesion on Brenda Milner# both sides of brain at medial temporal lobe # HM: bilateral medial temporal lobe lesion for status epilepticus in 1953# HM's lesion: bilateral medial temporal lobe removal HM = no hippocampus, amygdala, overlying (rhinal) cortex HM's amnesic syndrome Severe deficit (global anterograde amnesia) show word or face, ask later, doesn't know reads newspapers repeatedly doesn't remember own physician# see on formal tests or everyday life # word lists # faces and objects # recall or recognition# # Only mild retrograde amnesia loss of memories that are a up to 2-3 years old at the time of the lesion, but childhood memories in tact known as a time-limited or #temporally-graded retrograde amnesia# Retrograde vs. anterograde amnesia normal memory for remote events (childhood, etc) for HM, retrograde amnesia is approx. 2 yrs Retrograde and anterograde amnesia can occur together or separately (HM has both) HM also has this Remote versus Recent Memory: HM, Loss of Recent memory temporally-graded retrograde amnesia Rey-Osterrieth Figure Other forms of amnesia Unilateral hippocampal damage results in material-specific deficits #left = words, names, etc. (language) #right = faces, objects, etc.! ! Korsakoff's psychosis results in similar amnesia plus confabulation (fill in memory gaps with fabricated stories)! Some have problems with Wernicke's area (rapid, fluent, ! but non-sensical output) Frontal lobes STM, working memory, temporal order, confabulation! Electroconvulsive Therapy (ECT,ECS)# Location of the hippocampus Emotions Suffers most due to aging (dementia) Amyloid placques = Alzheimer's Patient with damage to the hippocampus. Focal lesion to his hippocampus, he can't tell the difference between categories of information presented to him. Capgras Delusion `Mme M.' believed that her husband, children, neighbours and others had been replaced by doubles (Capgras 19thC). Ramachandran's patient in San Diego called PK (2001). He believed that his mother has been replaced by an impostor. Cases have been described where the delusion that pets or even inanimate objects have been replaced by replicas. - Hippocampus is intact - Amygdala is intact - The connection between the hippocampus and the amygdala is severed - Use of a galvanic skin response test to see if they have any response (emotional - limbic) to faces Face recognition Ventral (who? what?) stream is busted in capgras delusion Analysis of visual form Capgras? Identification Somatic / Emotional response MEMORY STRATEGIES Ml K TPUXC GYI OSFP SH DFKUXC RWJF MY MEMORY FOR WORDS IS RATHER GOOD Better encoding hence better retrieval Memory is also quite sequence specific ALPHABET EXAMPLE. . Structural changes in the brain are seen as a consequence of long-term activity. What about skills like sport? Do they cause changes in the brain? London cabbies have more hippocampal gray matter (better encoding of specific categories geographical maps) - New cells grow in the area of increased activity and create more synapses Learning to juggle Juggling Group: 12 subjects learned a three-ball cascade juggling routine. They were considered to be skilled jugglers when they could juggle for 60 seconds. Non-Juggling Group: 12 subjects had no juggling practice. Synapses form Synapses have weakened, myelination decreased Changes were seen in the: Visual Cortex Parietal Lobe Increased Synapses with practice The brain of a juggler These data suggest that learning new skills can alter brain structure. However, it is unclear what exactly caused the brain changes. The expansion in the two brain areas may have been caused by an increase in the number of nerve cells, glial cells or synapses. Processes motor actions Where visual information is transformed into coordinates of motor activity One more time... Memory & consolidation Amnesia and localization of memory Learning: changes in the brain Learning, consolidation and memory Changes in the brain as a function of learning London cabbies and jugglers NEXT: plasticity Strengthening synapses Synapses used often are strengthened (A) Those not used are weakened and can become ineffective (B) Used lots A B Not Used Cross-modal plasticity in congenitally deaf These PET/MR images show increased neural activity in the superior temporal gyrus in congenitally deaf subjects when they viewed signs or sign-like movements, suggesting that auditory cortical regions may contribute to the processing of visual information in the deaf Optic nerve hypoplasia Sometimes referred to as ONH autism Or DeMorsier's syndrome Congenital blindness (optic nerve to one or both eyes impaired before birth) Extremely sensitive to sound; for example have perfect pitch. Musical savants can have ONH. Theory is that the visual cortex switches over to process sound Also have left motor cortex damage resulting in right side paralysis IQ generally around 60 (pretty retarded) William's Syndrome: - Congenital chromosomal defect - Generally brought about by incestual pregnancy - Blind, Downs Syndrome-y - Extremely developed pitch (savant-esque) VIDEO OF A MUSICAL SAVANT Auditory Motion Perception Early blind subjects show activation of the visual cortex during an auditory motion tracking task Visual areas become involved in auditory processing Functional Re-mapping of the cortex Domain specific changes can occur when we specialize in a skill over extended periods of time - this can result in overlap of neurons in different domains. Poirier et. al. (2006) Re-Writing the Cortical Map Primary Sensory Cortex (S1) Located posterior to the central gyrus (behind M1) (postcentral gyrus) Arranged in a somatotopic map the sensory homunculus Similar to but not the same as somatotopic map involved in movement. ** Not the same as plasticity - re-mapping can change with injury and learning ** Cortical Re-Mapping Motor cortical areas for each digit mapped Digits 3 and 4 are sewn together (now functionally act as one digit) Months later, the cortical areas for D3 and D4 have merged Plasticity and phantom limbs Re-mapping and Rewiring of the cortex seems to occur under many circumstances Imaging studies have shown massive cortical reorganization Somatotopic map can redraw itself in response to new circumstances This is called Plasticity of the brain or Neuroplasticity What are Phantom Limbs? Phantom limbs the vivid impression that a lost limb is present; can be painful and distressing Clinical Phenomena Phantom limbs have been observed throughout history (Moby Dick Capt. Ahab) 1st clinical description during the American Civil War -The case of George Dedlow by Dr. Silas Weir Mitchell Clinical Phenomena Incidence: 90 - 98% of patients who lose a limb experience phantom sensations Less prevalent in early childhood (perhaps because brain topography is changing) Onset: Immediate in 75% of cases Duration: Few days to decades (57 yrs!) Body Part: Arm, leg, breast, face, organs Posture: "habitual" posture, can change Experimental Studies Primate Amputation When middle finger was amputated, motor cortex for that finger started responding to adjacent finger stimulation within months (Merzenich et al., 1984) After 12 years of arm amputation, the "hand cortex" responded to stimulation on the face (Pons et al., 1991) Experimental Studies Human Brain Imaging Patients with arm amputations demonstrated activation of the "hand cortex" when the face and upper arm were stimulated (Ramachandran, 1993) L R MEG scans from a patient whose right arm was amputated. Right hemisphere activity is normal, while left activity shows reorganization. Red = face, Green = hand, = upper arm Blue Referred Sensation Ramachandran was able to elicit sensation in the amputated arm (the phantom limb) by stroking the patient's face Experimental Studies Referred sensations of phantom fingers map onto the face (Ramachandran, 1993) Left face regions elicited localized sensations in the phantom fingers. P = pinkie, I = index finger, T = thumb, B = ball of thumb Experimental Studies Referred sensations also map onto upper limbs (shoulder) Mapping onto adjacent cortical areas Phantom Limb Treatment Painful sensations (e.g. clenched fists, spasms) can be treated with a mirror box With treatment, the phantom limb can change its posture or disappear entirely Phantom Limb Implications Brain topography is dynamic and neural organization can be altered (Neuroplasticity) Phantom limb sensations are real, they have identifiable neural correlates Phantom Limb Implications Painful and distressing phantom limbs can be treated with visual feedback (mirror box) Increasingly studied in the USA as a result of Afghanistan and Iraq wars Body image is a transitory internal construct Anatomy of the Frontal Lobes Dorsolateral PFC Ventral/Medial Orbital PFC Some symptoms associated with frontal lobe damage Working memory deficits Temporal memory / Source memory Perseveration not able to change a rule quickly (multiply to divide) Loss of spontaneous behavior Apathy Planning deficits/impaired goal-directed behavior Disinhibition/impulsive behavior Impaired attention Depression Elevated mood short term task oriented memory Memory-related deficits Working memory: delayed response tasks Temporal memory: when did the event occur? Source memory: where did I get this information from? which memory came first? Recognition (asked if they saw a watch, lock) seems to be fine Recency (asked which came first) poor in patients with frontal lobe damage/lesions Temporal memory example Recalling where an object is is processed in the PFAA Activity in the prefrontal cortex continues even when the stimulus is removed, implying that there is residual tonic activity holding the memory in place (spatial memory) THE STROOP EFFECT RED BLUE GREEN RED BLUE YELLOW BLUE GREEN RED YELLOW RED BLUE GREEN RED BLUE YELLOW BLUE GREEN RED YELLOW Inhibition-Related Deficits Stroop task (unable to do this task). Delayed reaction to stroop task Perseveration Cannot return to the task after being distracted Wisconsin Card Sorting Task Impaired planning in the PFC of frontal lobe Social Disinhibition/Impulsivity ... lack of restraint (social, sexual, etc.) Loss of spontaneous behavior Poor planning/goal-directed behavior Bad prioritization Attentional deficits Personality Changes in FL Dementias Impairments in social skills - example of social disinhibition inappropriate or bizarre social behavior "loosening" of normal social restraints (e.g., using obscene language or making inappropriate remarks) Change in motivation apathy, withdrawal, lack of interest, and initiative which may appear to be depression but the patient does not experience sad feelings. Personality Changes in Anterior Strokes (2000, Neurology) Depression In 75% of anterior CVA pts In 50% of TL CVA pts CVA = cerebrovascular accident = stroke Emotional Problems Apathetic behaviour, mood swings Present in 18% of stroke pts In 100% of anterior CVA pts In 0% of pts with TL or OL CVA Presence of post-stroke depression and emotional ability is greatly influenced by lesion location Phineous Gage Railroad foreman Well-respected, hard-working 1848: tamping iron accident He never lost consciousness, and had no obvious neurological symptoms But he was "no longer Gage" BOOM, HEADSHOT! Totally owned his left frontal lobe, but left his right frontal lobe intact. Dorsolateral PFC Had no affect on optical nerve or senses Phineous Gage Gage's Doctor described Gage's post accident social disinhibition personality as Fitful, irreverent, indulging at times in the greatest profanity which was not previously his custom, manifesting but little deference for his fellows, impatient of restraint and advice when it conflicts with his desires, at times pertinaciously obstinate, yet capricious and vacillating, devising many plans of future operation, which are no sooner arranged than they are abandoned ... a child in his intellectual capacity and manifestations, he has the animal passions of a strong man. After his accident he lacked emotional restraint, was easily seemingly depressed and lacked the ability to plan ahead (perservation - e.g. wisconsin task) Anatomical Subdivisions of Frontal Cortex went in here came out here Two Broad Frontal Syndromes 1. Dorsolateral prefrontal syndrome Lowered general arousal Impaired attention/distractable Apathy, depressed mood Perseverative behavior Working memory deficits Diminished spontaneous behavior Difficulty with goal-directed behavior Two Broad Frontal Syndromes 2. Ventromedial prefrontal syndrome Disinhibition of drives Impulsivity Elevated mood Hyperactive Impaired attention lacks decision making *** PHINEAS GAGE WAS A MIXTURE OF #1 AND #2 *** Theories of Prefrontal Function There have been many Attentional function, reasoning and planning, inhibition/ selection, "personality", working memory, temporal integration None capture the full range of deficits But clearly, prefrontal cortex, sitting between sensory and limbic systems on the one hand and motor systems on the other, is in a position to integrate information in the sensory environment, with internal motivations, goals, previous experience, etc. Mediates sensory information and thoughts, etc. Causes of FL Dysfunction Traumatic Brain Injury (TBI) Tumors Vascular Lesions Neuropsychiatric Diseases Schizophrenia Frontal lobe dementias (Pick's Disease) neurodegenerative; loss of speech and dementia FL Injury in TBI The frontal lobes are extremely vulnerable to injury due to thinner their location at the front of the cranium, proximity to the skull sphenoid wing and their large size. MRI studies have shown that the frontal area is the most common region of injury following mild to moderate TBI (Levin et al., 1987). 2 main types of TB injuries resulting in "FL" dysfunction Injury at the site of impact ("coup") or where the brain hits the cranium on the opposite side ("contrecoup"). Diffuse axonal shearing (white matter connections w/FL) tissues sliding ('shearing') over one another during acceleration or decelleration of brain matter Frontal Lobe Dysfunction in CVA Anterior Cerebral Arteries Anterior Communicating Artery 70% of all ischemic strokes occur in the anterior circulation. 70% of 88% (total ischemias) Common Symptoms of TBI (Mild to Moderate) Behavior problems aggression and violence, impulsivity, disinhibition, acting out, noncompliance, social inappropriateness, emotional outbursts, childish behavior, impaired self-control, impaired self-awareness, inability to take responsibility or accept criticism, inappropriate sexual activity Emotional problems depression, apathy, anxiety, irritability, anger, paranoia, confusion, frustration, agitation, and mood swings Executive/Cognitive problems such as problems with planning, organizing, abstract reasoning, problem solving, and making judgments, may make it difficult to resume pre-injury work-related activities Anosmia (inability to discriminate odors) caused by lesions at the bottom of the ventromedial FL (close to olfactory lobe/bulb) Vascular Lesions and Frontal Lobe Dysfunction Large vessel strokes (unilateral damage) one side/hemisphere LH: speech/language (Broca's), right-sided motor deficits, and depression RH: spatial deficits, left-sided motor deficits, elevated mood Ruptured aneurysm of the ACoA (anterior communication artery) Personality changes Small Vessel/Microvascular Disease Variable presentation of symptoms unable to process stimulu in one hemisphere Frontal Lobe Dysfunction in Tumors Intrinsic tumors (e.g., gliomas tumors arising from glia) are most common and typically begin unilaterally and spread through corpus callosum. Can cause gradual or abrupt changes in personality/ mood with or without cognitive changes Symptoms determined by tumor features: Size Rate Location One more time.... Frontal lobe function Damage to Frontal lobe How is this related to emotions and high-level cognition? The sense of time How does the CNS know time? Are there circuits in the brain for the perception of time? Neural event counters. Long range rhythms vs time in the short range. Supplementary motor area Frontal lobe (planning) Basal Ganglia Cerebellum 1-1000 theory of timing: hypothesis involving a structure that tells you how much time has elapsed in NEURAL units CORTICAL KEYBOARD METAPHOR Event times Time time series Paced; 250 - 2000 ms 30 - 50 free responses kymograph Time Index number The Cerebellum and Timing Cerebellum is thought be involved in the timing of movements because cerebellum lights up in fMRI study of complex/novel timing tasks (Penhune et al. 1998) cerebellar patients are imparied at tasks like tapping along to a metronome beat Cerebellum also lit up when IMAGINING metronome beat Two basic models: Clock counter model Pacemaker produces output to counter Longer intervals represented by more pacemaker outputs in counter Interval model Different intervals represented by distinct elements Each corresponds to a specific duration Pacemaker 40 Hz 25 ms 10 pulses = 250 ms 20 pulses = 500 ms 30 pulses = 750 ms Clock counter cells reset every 25 ms, fire 40 times in a second 250 ms 500 ms 750 ms Spencer et al (2003): Cerebellum is only responsible for stopstart movements, not continuous mot...
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