Psych 301 Midterm 2

Difference between secondary and primary motor cortexes?

secondary: planning, preparation and coordination of movement primary: neural impulses

Disconnecting animals brain from spinal cord

- Many behaviours are happening at level of spine/brain stem - we can disconnect an animals brain from spinal cord and put it on a treadmill holding it up in harness and if treadmill moves the animals feet will walk - animal can do walking pattern without brain output -Walking just based on feedback

Cerebellar damage and prism goggles

- Under standard conditions, many tasks we have learned we are pretty good at: individual throwing dart at board trying to hit center (hitting 0). -Individuals normally pretty good at this, but then we place prism goggles on them that changes angle of their vision (15-35 degree) to the left - they start to hit darts too far to left but over time they begin to adjust and get back to normal. -Taking goggles off - throw way to far to the right but eventually adjust to normal again. - Individual with cerebellar damage: to begin with, they throw okay, and when you put prism goggles on them they do not adapt or adjust, they continue to throw too far to the left. When we take prism goggles off them they go back to having good accuracy - no adjustment. - Shows that cerebellum is important to learning and adapting to ongoing fluid situations

Lead poisoning

-"Crackpots" -Toxic psychosis seen in people who steeped tea in cracked ceramic pots -Our entire environment is contaminated with lead - push to remove lead from paint and fuel -Some toys are painted with lead paint - makes it look nice -Many communities in N.A living in constant lead exposure in water like Lake Michigan -Toxic psychosis: produces cognitive impairments, at extreme levels - paralysis, insanity, lack of touch with reality -Many non-specific situations/issues

Secondary motor cortex - 8 areas

-2 areas of premotor cortex -3 supplemental motor areas -3 cingulate motor areas -Many different cortices and have slightly different behavioural effects of damage but don't know many differences yet

Meningiomas

-20% of all tumours we get -Growing in meninges so we can remove it and not effect brain function as much since not in the brain itself -Encapsulated and benign

Secondary effects of brain damage - diaschisis

-A brain lesion can cause dysfunction in an area remote to it because of its strong connections with that area - functionally connected -Recovery may occur because of a spontaneous reduction of diaschisis (metabolic depression in cerebral areas remote to the lesion) -Example: severe stroke, lost tissue in cortex, also led to hypoactivity in cerebellum due to diaschisis -Every area has a number of inputs and outputs and if one area receives many inputs from an area that has been lost or damaged, it'll now be hypoactive -Cells eventually increase activity and will adjust to a new baseline so we see diaschisis go away

Compensatory strategies

-A mainstay of rehabilitation of patients with brain dysfunction -Recovery may not represent true restitution of function, but substitution of a new behaviour -A patient learns strategies to adapt to his/her new motor, sensory, or cognitive impairments -Example: brian area controlilng movement that died from stroke - not getting function back from that specific area but other areas around it are picking up slack - substitution of function -Seen at brain and behavioural level -In rat: give large lesions to motor related areas - animal can nice and easily walk across bar/high vertical space without lesion, and after lesion initially they have a lot of trouble walking along the bar but eventually they learn to do it again. However, the way in which they walk on bar is different from how they used to do so - using other parts of brain to get across - neuroplasticity in action

What is a neurological examination

-A series of tests conducted by a neurologist in order to evaluate the integrity of the nervous system for many reasons including but not limited to: -Following a trauma or stroke -When there are suspected neurodegenerative changes -Following exposure to a neurotoxic agent -Aging -Detective work -Example: someone cannot speak - this may be an issue of attention, motor control of face and mouth, or an issue with CNS - we need to figure out what is causing it -Brain region damage can happen at many levels: could be muscle atrophy, cranial nerves/spinal cord, NMJ, brainstem, internal capsule (white matter that travels in telencephalon and traeels from cortex), damage to connections that cause damage, ceerebral hemisphere (telencephalon)

Anticipatory hemodynamics

-A statistical issue with fMRI studies, where if an area is repeatedly active with little spaces in between, the hemodynamic response starts preceding the activity, shunting oxygen to that brain area before the task even begins -When you make someone do task over and over again or when we get really good at it - hemodynamic response will start beforee wee actually do thee task or have brain activity

Reliability of fMRI study

-A statistical issue with fMRI studies, where something that seems statistically significant the first time may not be statistically significant the second time -Test-reetest: make someeone do something in a scan then make them do it again in another scan: only 30% of the voxels active in the first scan actually show up in the second scan - we don't really get a lot of overlap -fMRI is only measuring fractions in percent difference of oxygenated blood - there's lots of statistical noise -Between different labs/scanners, data doesn't line up super well

Gaze palsy

-A term used to indicate a symmetric limitation of the movements of both eyes in the same direction

Minamata disease

-A type of mercury poisoning that came to prominence in the 1960s after decades of industrial pollution in the city of Minamata, Japan. -Caused by severe methylmercury poisoning -Ataxia, numbness, muscle weakness, damage to vision/hearing/speech, paralysis, coma, death; congenital effects -Water run-off from industrial zone

Awareness Intervention program for anosognosia

-AIP group showed improved self awareness but not associated with improved functional outcome

Testing Vestibulocochlear nerve (VIII)

-Auditory perception and vestibular information/balance -Auditory: test hearing at a number of different locations and intensities -Close one ear, whisper to another ear, ask patient: Can you tell me what you heard? -Balance: Due to combo of vestibular information, visual, and proprioception so wee . want to minimize input from other things to check vestibular system alone - ask individual to close eyes and march in place and if there's a problem they'll usually turn to side of lesion

What haapepns when doapmine transmission increased - drugs

-ALl drugs of addiction directly or indirectly increase dopamine transmission from the SNc and other main dopaminergic region, the VTA -These paths are somewhat related to reward and motivation, learning, and habit formation in addition to movement -Drugs like cocaine increase goal directed behaviours (purposeful behaviour at low doses), impulsivity, and at higher doses causes reptitive behaviours - streotypy -In animal model if we give them too much cocaine or stimulant we see animal shows species-specific behaviours over and over again like continuous grooming - known as stereotypy - excessive amount of species-specific behaviour due to use of psychostimulant drugs -Human version of stereotypy: excessive picking at our own skin or picking, clenching our jaw, grinding our teeth - often called punding or tweaking -When we take these psychostimulants - we are greatly potentiating the dopamine signal - massive increase in dopamine function in the brain which has changes in cognition and basic changes at level of sensorimotor processes -Potentiate direct pathway (D1R) and inhibit indirect pathway (D2R) - lots of go and little stop so purposeless behaviours are released

Cranial Nerve VI

-Abducens -Motor -Eye movement

Cranial Nerve XI

-Accessory -Motor -Movement of muscles of head rotation and shoulder shrug

Article: Lohse et al. What is the dose-response relationship for rehabilitative therapy following stroke?

-Across studies, there wa a benefit . for treatment groups receiving more therapy -Forest plot showing effect sizes and 95% confidence intervals for each study. -Positive values show a difference in favor of increased time scheduled for therapy -Along middle line is "0" null effect. Some therapies error bar so large we seee no effeect. - When we take them all together we clearly land on side on the right/positive - more therapies = more improvement. -Increased scheduled therapy = greater effect size/more recovery (small effect size but positive, g = 0.35) -Positive relationship between dose and . response

What is Alexia, Dyslexia, and Agraphia

-Alexia = problem with reading -Dyslexia = problem with written language -Agraphia = problems with writing

Primary motor cortex

-Also known as precentural gyrus, M1 -Somatotopic organization: motor homunculus (Penfield). Specific parts of motor cortex control specific parts of body >may be further divided to not just controlling muscle but also type of movement - turn left hand right vs. turn it left -Receives feedback from the muscle and joints -Controls our muscles

Contralateral neglect

-Also known as: Hemispatial neglect, unilateral neglect, or neglect syndrome -Failure to respond to visual, auditory, or somatosensory stimuli -Produced by very large right posterior parietal lesions -Individuals only attend to right side of body or items in environment -Patients are typically unable to respond to stimuli to the left of their body (viewer-centered/egocentric left). -Individuals may be capable of UNCONSCIOUSLY perceiving objects on their left -Prism goggles: will helf individuals pay attention to left sidee of world - this is not deficits in sensory/eye problems, but deficits in ATTENTION

Tumours

-Also referred to as a neoplasm = new growth -Cluster of cells that aren't supposed to be there -Growth is independent of rest of bodies growth -Not folloiwng standard developmental trajectory

Parasites

-An since cell organism that lives in or on another organism, deriving nourishment at the expense of its host, usually without killing it

Environmental factors in functional recovery, constraint induced therapy

-Animals in enriched environments: same damage in 2 different animal groups - some in low stimulus in environment and some in intermediate, and some in very enriched. Best enrichment is social interactions in rats, we see recovery is poorer in social isolation -In animal and humans enriched environments lead to better recovery - therapy may reflect a form of environmental enrichment -Monkeys with focal strokes to the motor cortex that were retrained in skilled hand use >Restrain good arm and make them only use bad arm, better recovery of bad arm - this is known as CONSTRAINT-INDUCED THERAPY -In strokes: social isolation critical factor in recovery

How we can test anosognosia - Ramachandran

-Anosognosia is lack of knowledge of one's own dyfunction - Usually anosognosia we see complete recovery after a few days usually week or two -A brain dysfunctional patient does not appear to be aware of impaired neurological or neurospychological functioning which is obvious to the clinician -Patient: right hemisphere stroke, left side paralyzed - could converse fluently, intelligent, normal in most aspects, mentally capable, can hold a conversation. Asking her why did you come to hospital: I had a stroke, fell down in my bathroom and my sister brought me to hospital and they did a brain scan and they told me they had a stroke. Ask: Can you walk? She said of course I can walk - despite fact that she spent so long in hospital. Ask can you use both your hands? She said yes I can, even though clearly her left hand has not moved at all. -Confront patient - "are both arms equally strong" - yes doctor. Then say "touch my nose with your right hand" and then "touch my nose with your left arm" - patient cannot do it. Ask "are you touching my nose?" - "yes" can you see yourself touching my nose? - patient says "yes" >Not denial of paralysis, but patient asserts the paralyzed arm does not belong to her raise paralyzed arm and ask patient "what is this" - they will say "it's my brothers hand/someone elses hand" -More commonly, patient will resort to all kinds of tricks to avoid confronting the paralysis - these are Freudian defense mechanisms e.g. "Touch my nose with your right hand, touch my nose with your left hand" - Patient will do with right hand but when asked to do with paralyzed hand say "No, I don't want to touch your nose - I'm very tired" - provide some rationalization or "I have severe arthritis in my left arm" or "I'm not accustomed to taking orders from anybody" -Repression, threatening to ego and self esteem -Even after patient recovers from anosognosia, if you ask them why they didn't know they were paralyzed before they deny their denial "I told you it was paralyzed yesterday" 2 possibilities: Is knowledge of paralysis available somewhere in brain but access to it is blocked, or does knowledge simply not exist? -Cocktail trail with glasses of champange on it, say "pick up the tray" - normal person would use 2 hands >Patient with left arm paralyzed - would go to middle of tray and pick it up >Patient will go straight to right side with right hand and doesn't notice left arm fails to do the job - they truly don't know they are paralyzed -Reward patient for telling you truth: 2 tasks - if you put lightbulb on lamp I'll give you 5 dollars. If you tie these shoelaces I'll give you 10 dollars. >Normal: pick larger reward >If paralyzed and know it: go for lightbulb becaues they know they cannot tie shoelace with one hand >If anosognosia: goes straight to the shoe and starts to try to tie it with no sign of frustration - even after many trials goes for shoe over and over again - repressing failed attempts (Freudian repression) -Knowledge, if there is deeply embedded in brain and not accessible in an easy manner -Give patient a choice: 5 dollars to carry a glass in one hand or 25 to carry a two handed tray -If individual that has one hand paralyzed doesn't know it's paralyzed they will choose 2 handed tray test because they want 25 dollars -If individual is just in denial they will choose 5 dollar task because they know they will fail at carrying the 2 handed tray -"I'm going to inject this anesthetic to paralyze your left arm to completely paralyze it for a few minutes is that okay" >Patient says "but Doctor is that fair" >Take salilne and inject it and ask "Can you move your arm?" >Patient says "no it's paralyzed" - now made paralysis more acceptable so patient willing to admit they are paralyzed >Go back next day and say "I'm going to inject your right arm with this anesthetic" (right arm not actually paralyzed) "Can you move your arm?" -Yeah of course it's moving "your anesthetic doesn't work"

Language problems

-Aphasia: problems with language production and/or comprehension. Understanding words you're hearing or speaking words out loud -Alexia: problems with reading -Agraphia: problems with writing

Posterior parietal cortex damage

-Apraxia -Contralateral neglect

Spatial averaging

-At best, our voxels are 1mm^3 but we are encompassing tens of thousands of neurons in that one voxel. Different circuits of activity will be showing up as the same voxel in an image. -We get an epiphenomenon: when we see something that doesn't reflect the true activity - we see effects that don't reflect any one type of activity -If we average across a space we run across an epiphenomenon - when averaging includes outliers this happens - we get some weird average -Depending on method of analysis, what you get is the middle that doesn't exist, Ex: average of all books in Jay's office are on chair, but none there -A problem that occurs in interpreting fMRI studies, where the average doesn't represent either of two participants

Mental Status Exam (MSE) - What does it test

-Attention and orientation -Language -Memory -Visuospatial function -Executive functions -This cheecks in on cognitive processese needed to function in the world -Targeted to people in risk of neurodegenerative disorders, strokes, traumatic brain injuries

Testing attention and orientation

-Attention: if impaired, it's going to effect all the other tests so we start with this test because what we get here influences all other tests we have - Keep track of persons alertness and if they seem like they are in touch with the world -Spelling world backwards -Counting backwards from 20 - Auditory vigilance = paying attention to something you say then give some information about it - An individual can seem remarkably capable of holding a conversation but if you ask the person where they are right now and what day of the week it is - they have lapses in these basic pieces of knowledge: current ewhereabouts, time - If we see problems in these sort of things it's hard to say where the problem is: problems with attention may suggest parietal lobe but we don't know for sure -Usually cortical or immediately subcortical -Reegions involved: focal cortical or subcortical regions, but origin may also may be diffuse if due to a toxin

Testing Hypoglossal nerve (XII)

-Back or bottom of tongue -Important for movemnets -Lateral moveement: push tongue against cheek and then other -Palpate and asseess for strength -Stick out tongue -If there is problem with one of the cranial nerves with either left or right side, we see that the tongue doesn't sit symmetrically: asymmetries in the tongue

Meningitis

-Bacteria often attack the meninges, producing an inflammation known as meningitis -1/4 of all people with bacterial meningitis will die - fatal -Common cause is streptococci -Starts with dizziness, confusion, headache, fever, trouble staying awake -In kids, hard to identify and symptoms include irritability and drowsiness and not knowing what's going on -Many antibiotics cross BBB so we can treat -Case of son that got sick - had bacterial meningitis and was drowsy, couldn't stay awake, fever, headache - didn't take child to doctor and administered naturopathic medicines - didn't cure the meninges and it got much worse. Friend that was a nurse said the child had bacterial meningitis and should take them to the doctor but they didn't - they didn't call anyone until the child had a seizure but by this time it was too late - child died and charged with negligence

Aneurysm

-Ballooning of a weakened portion of an arterial wall - accumulates blood and gets larger and larger and if it exceeds the structural integrity of tissue it'll rupture and you get a stroke -Could be present at birth or develop over time -Likelihood of having them increase with agee -In 40s: 3.5% have aneurysm in head and in 60s-70s, 6% have them -Not necessarily a problem at first but major problem if they do rupture - blood is toxic to th ebrain, it has things in it we normally want to keep out of the brain and when aneurysms rupture we will have high pressure fluid flowing into soft tissue so it can actual cause strctural damage

Posterior-Dorsal region of Broca's critically involved in...

-Basic phonological components of langauge - sound processing/production

Spatial resolution of fMRI

-Better than PET -1mm^3 voxel still not sufficient to be lookin at one neuron vs. anothre -Roughly ~100k neurons running through that area, still very large

Nonfluent aphasias

-Broca's aphasia or expressive aphasia -Can understand speech, comprehension in tact or not impaired much -Labors hard to produce speech -Can be mild or severe - often can produce some speech and ways different patients produce speech vary -Vocabularly there, but not syntax (like what we see in species other than humans) -Good cognition, but very hard to produce good speech -Automatized phrases more eeasily said

Subdivision of Broca's Area

-Broca's area isn't just one area - it is several nuclei -When we look at this area with mapping/staining brain, there are many discrete subunits within Broca's area -We have a dorsal-posterior, and ventral-anterior

Transcortical aphasia/isolation syndrome

-Can repeat (echolalia) words -Cannot speak spontaneously -Often poor comprehension -Sits in middle of Wernicke and Broca's -Nature of damage is messy, often see large lesions

Damage to ceerebellum

-Cannot adjust movements -Issues with coordination, timing, sequence -Loss of ability to precisely control the direction, force, velocity, and amplitude of movements -Loss of ability to adapt patterns of motor output to changing conditions -Cannot maintain steady postures like standing, disturbances in balance, gait, and control of eye movements -Impairments in measures of attention and executive control, procedural memory, working memory, language, and visual-spatial processing - cognitive impairments *Individuals born without cerebellum or loses it early in life may not show obvious emotion or cognitive impairment but will show deficits in movement* -Impairments in learning new motor sequenes

Effects of repeated mild closed head injuries

-Cases of chronic traumatic encephalopathy (CTE) suggests that there is long-term damage associated with concussion, even if it isn't visible after a single episode -CTE used to be called punch-drunk syndrome, dementia pugilistica -You can get CTE without even being diagnosed with concussion at any time -CTE often looks somewhere between Parkinson's and Alzheimere's: memory and motor impairments - problem emotional regulation, impulsivity, pathological level of jealousy and problems in domestic lives, confusion, paranoisa, errors in good judgement -Seen in many athletes, epilepsy, individuals with ASD, domestic abuse victims

Epilepsy

-Characterizeed by recurrent unprovoked seizures - due to atypical, eexcessivee, or synchronous neuronal activity in the brain -Must have at least 2 unprovoked seizures on seperate days, generally greater than 24 hours after -In reality, epilepsy is probably result of many different types of brain dysfunction that are related manifesting as same thing - multiple dysfunctions caused by ifferent mechanisms but manifesting inn same outcome -Usually result of brain becoming hyperexcitable -No anti-epilepsy drug, but there are drugs to help with seizures

Most common place aneurysms form

-Circle of willis -Where vertebral and c arotid arteries meet

Basal ganglia

-Classical view is that it modulates motor OUTPUT -Critical to habit formation -Many cognitive roles -Promotes skill learning -Caudate and putamen = striatum -Globus pallidus - internal and external -Striatum and Globus pallidus are strictly the basal ganglia but also has other things it works with such as subthalamic nuclei and substantia nigra (part of midbrain, important dopamine area of brain) which are sometimes referred to as part of the basal ganglia -Thalamus sometimes thrown into basal ganglia

Contusion

-Closed-head injuries that involve damage to the cerebral circulatory system - produces internal hemorrhaging and a hematoma (pool of blood outside blood vessels) -Comes in many forms: car aaccident, accident from sport -Occurs wheen brain slams against skull -Frequently contrecoup injuries: blow causes brain to strike inside of skull on other side of the head - due to fact that brain is a semi-floating object

Encapsulated tumours

-Cluster of cells contained as a seperate structure -Growing within own membrane - seperate piece of tissue on its own so when we remove it wee don't lose too much good tissue and it's usually all gone -Genereally BENIGN: growing a little slower and if we remove it, the likelihood of it growing back is very low

Lexicon

-Collection of all words in a given laguage

What is Language

-Comes from the word for "tongue" -The combination of sounds for communication -Many components - most basic are sounds

Junior Seau: Case study of CTE

-Concussion is a subset of mild TBI, although mild TBI can include subconcussive impacts as well Seau complained of headaches, episodes of dizziness, and insomnia since as early as the 1990s After his retirement, he drank heavily, made reckless business and financial decisions, became more aggressive and violent Had CTE NFL has now published a protocol dealing the protective measures a player must follow after a concussion -Concussion defined as "a complex pathophysiological process affecting brain, induced by biomechamincal force" - CTE, a neurodegenerative disease pathologically confirmed by the presence of a unique pattern of hyperphosphorylated tau neurofibrillary and astrocytic tangles in the brain. -Junior Seau = Hall of Fame Football League linebaker - had CTE -Autopsy confirmed diagnosis of CTE -Early symptoms CTE: headache, aggression, mood swings, suicidality, cognitive impairment, motor defecits that can manifest after period of latency after mild TBI -Incidence of CTE unkown since can only be diagnosed postmotem -CTE differs from Alzheimers in that they have tau-reactive astrocytese and lack beta amyloid and tau deposition in CTE predominantly localized to superficial cortical layers, sulcal depths -4 stages of CTE based on severity

Contralateral neglect

-Contralateral neglect = we see this after severe strokes in the parietal lobe, unable to pay attention to half of the world - usually the left half - Problem in the right parietal lobe - Ask patient to copy an image, and we see a failure to complete the left half - Egocentric neglect - ignore everything that's left according to themselves - They understand there is a conceptual issue that doesn't line up with their thoughts but they cannot attend the left half of things (e.g. drawing a clock, won't fill up left half of the clock but will know there's something off about the clock they drew since 11 isn't beside the 12) - Not really a visual or cognitive problem but issue of attending to the world -Individual often doesn't know they have an impairment

Testing Acessory nerve (XI)

-Controls muscles of neck and shoulders -Either palpating, providing resistance, or both - make sure they can use the muscles -Shrugging of shoulders -Head resistancee -Ask patient to turn head to the leeft, then ask to turn to right while you try to reesist it -Ask patient to shrug shoulders while you try to resist it

Bonferroni correection

-Correcting for multiple comparisons -Every voxel is a t-test, so since we're doing so many t-tests we need to correct for thaat

How is CTE related to Tau and neurofibrillary tanges

-Cytoskeleton is bound together by Tau molecules - it keeps the structural integrity of the cytoskeleton -In cases of CTE, we see post-mortem hyperphosphorylated tau proteins - unusual state that causes it to aggregate with itself so we have tau clumps due to this and they are no longer bound to cytoskeleton - cytoskeleton breaks apart. -Tau tangles are also seen in Alzheimer's -It's not clear if Tau is cause or effect: examining different brains postmortem: normal, mild CTE, severe CTE - when we stain for tau-tangles we see that tangles start in CTE deep in the sulci (in folds of cortex) - in neocortex and as disease progresses the tau proteins/hyperphosphorylated tau are more present all across the cortex -In Alzheimer's: tau tangles don't begin in the same way, they aren't deep in the sulci, they begin in brainstem, and we find them earliest in the disease in the temporal lobes - there's a different disease progression but final stages of CTE and Alzheimer's are more similar

Damage to primary motor cortex

-Damage isn't disruptive as we might think -Some damage seems sensory in origins due to fact that it gets lots of input from somatosensory areas - feedback 1) Independent movement: moving 1 finger vs. all of them together 2) Astereognosia: issue with recognizing something with touch 3) Reduced speed/accuracy/force -Lack of severe impairments suggests that what's probably happening is the secondary motor cortex has some input that can go to lower brain areas that do not pass through primary motor cortex

Damage to supplemental and cigulate motor areas

-Damage just decreases the overall level of voluntary behaviour that animal performs -Less top-down movement

Damage to dorsal language pathway vs. ventral language pathway

-Damage to dorsal language pathway: issues with speech production, cannot do movments we need (no interaction with motor area), phonetics, sound aspects -Damage to ventral language pathway: issues with semantics and comprehension, seperating homnyms

Case study of patient G.O

-Damage to somatosensory nerves of his arms -He had numerous problems with movement -Cannot feel things with hands or fingers - cannot pick up coin from ground, cannot button buttons, cannot correct processes/adjust movements in relation to somatosensory sensations -Example: If someone bumps into you while you are holding coffee you will adjust yourself so that you do not spill it based on your somatosensations - without this you won't correct movements -Many movements we do have to do with maintaining a certain amount of pressure/grip -Carrying a briefcase: reequires consistent amount of carrying - tugging on the hand by briefcase is driving a lot of moveement completely absent of any conscious thinking - G.O not able to correct his grip

Fasano and Lozano paper: key points

-Deep brain stimulation has become widely accepted as a treatment for Parkinson's disease, dystonia, and tremor and as an off-label treatment for many other movement disorders -DBS field is expanding exponentially along two not mutually exclusive directions: clinical and technological -Clinically, we have achieved a deeper understanding of outcomes, thus facilitating the process of target and patient's selection -The recent technological advantages have opened new avenues toward new targets and indications

Comorbidities with epilepsy

-Diabetes, Major Depressive Disorder, Anxiety, Migraine, stroke, heart disease, asthma, arthritis -Suicide - especially when epilepsy is intractable >Medication not working, not willing to get surgery - high rates of suicide >Major crisis >Cannot have drivers license, cannot maintain job - anxiety/social stigma

EEG and epilepsy

-Diagnosis relies heavily on EEG -Preictal, ictal aand interictal patterns -When seizure comes on: synchronized and massive amounts of activity - excessive, all lining up with one another -Different epilepsies will have different characteristic patterns on EEG

Praxis/apraxia

-Difficulty performing certain actions on commnd especially when something is novel or weird -Often has to do with parietal lobe

Memory test in MSE

-Digit span: create an increasing number of digits that a person has to remember. 7 +/- 2 is typical digit span - relatively normal. Less than this suggests working memory deficits -Pointing span: "point to picture of duck, then dog, then cat" - sequence of working memory and holding that on -Verbal, visual object laerning -Past public/personal events -Factual knowleedge

2 pathways of basal ganglia

-Direct and Indirect pathway -Various parts of cortex involved to combine sensory information and . body and atteention information to initiate movement -Essentially leads to thalaamus that effects frontal cortex - which is the primary and secondary motor cortex causing us to move -Baseline: to be at rest/still - default in the brain known as tonic inhibition - constant lack of movement. Motor/premotor areas in frontal cortex are normally tonically inhibited - Tonic inhibition is due to signal from Gpe + Gpi to the thalamus (Globus pallidus internal + external) - Output from basal ganglia is usually there (default output = GABA signal) - usually have very strong GABA signal travelling from globus pallidus to the thalamus - inhibits the thalamus, which means very little glutamate going to frontal cortex/motor cortex so little stimulation to motor cortex. - Tonic inhibition

Effect of Lesion Size and Location on recovery

-Direct relationship between size and extent of recovery -Larger lesions = more functional impairments, less likely it will r ecover -More focal = less impairments -Patients with bilateral lesions show less recovery than patients with unilateral lesions. E.g. bilateral hippocampal lesions results in profound anterograde amnesia and unilateral lesions result in less severe impairments and better recovery

Primary Progressive MS

-Disease progression from onset, without plateaus or remissions or with occasional plateaus and tempory minor improvements -Symptoms stick around all the time

Ischemic stroke

-Disruption of blood supply to some area of the brain -Main reaeson why we don't want a lot of cholesterol and why we monitor our blood ressure 3 main causes: 1) Thrombosis - a plug blocks blood flow t hat could be fatty tissue, oil, blood clot, bubblees of air, bits of tumour 2) Embolism - thrombus that is travelling around - starts somewhere, often on larger piece and then breaks off and floats down and forms a plug somewhere else 3) Arteriosclerosis: fatty material deposited in vessel wall - channels get narrower and narrower and increases likelihood that an embolism will get stuck in that narrow passageway, or it could get so narrow that it causes the plug itself - cholesterol levels

Problems with Wernicke-Geschwind Model

-Doesn't take into account any other brain regions involved - we see a lot of bilateral activity, axons move in both directions -Ventral part of cortex probably also involved (noun) -Overly simplistic when it comes to regions of Broca's & Wernicke's area, and directionality of flow -Relied mostly on diffuse loss-of-function studies: in these studies, nature of stroke they have can cause vastly many different areas to be damaged.

Progression of disease: relapsing-remitting form - inside-out theory

-Dotted line = threshold for showing symptoms - above threshold = symptomatic -Disease is combination between immune system function and cytodegeneration -Inside-out: cells are dying and that's represented by the long diagonal line = cytodegeneration, loss of cells - this is starting really early before anyone is symptomatic -Argument: in addition to cytodegeneration we have an immune system response (orange) - whether you are symptomatic or not is a combo of degree of degeneration and if you're having an immune response -Dotted orange + blue part = combination of immune activity and cytodegeneration -When we see combo of immune system activity and degeneration and it crosses the threshold - the individual is symptomatic and we have relapse of MS symptoms, but when immune activity decreases a bit then you show no symptoms - below the threshold. -Your degeneration is getting worse and worse - more cells dying, so it takes less and less immune activity in order to be symptomatic - over time, remissions get shorter and shorter until one day -cytodegneration is so severe that the extent of dying cells is enough to produce symptoms - doesn't matter if you have an immune response over time - Over time, we see tapering off of immune responses - maybe because immune system will have reduced response if problems are too big -Larger immune system response when there is more to save - when stronger chance of preserving these cells - Bright spots may be the astrocytes -Secondary progressive stage: cytodegeneration enough to produce symptoms, no more relapse-remitting

Ptsosis

-Droopy eye, means oculomotor nerves (III) probably not working

Bell's Palsy

-Droopy eyelid, dry eye, excessive tears -Facial paralysis, twitching, or weakness -Drooping corner of mouth, dry mouth, impaired taste -Can come out of nowhere: wake up one day and half of your face is paralyzed -Usually very severe and on one side - spontaneously resolves - muscle tone of face lost

Drugs and fMRI studies

-Drugs: everyone is consumers of psychoactive drugs, different drugs that have an effect on brain function

Toxolasma gondii

-Eukaryotic parasite that thrives best in cats -Interesting life cycle and will travel in different hosts in different parts of its life cycle -Diff hosts in breeding and reproduction stage: have to leave the cat and have life stages outside of cats and then back to the cat - From cat, to another host, back to cat - Soposky: studied rats. Found that it infects rats, and you see a loss of fear specifically for cats. - It is Protozoan: rat will ingest it via feces or food, this eukaryote gets into the brain and damages the brain - and causes cysts but it doesn't damage the brain in all the same way. It uniquely effects the hippocampus and specific circuits of the hippocampus - damage amygdala, don't lose all sense of fear, but rats lose sense of fear for CATS -Circuit for mating is increased. - Rats are relatively normal but now they lose their fear of cats - if they smelt. Cat urine it wouldn't scare them or it might acutally attract them - Cat eats them and gets it - the parasite returns to cat -1/3 of humans will be affected with toxoplasma gondi - may be related to certain personalities: schizoaffective personality traits but we don't know about this for sure -Brought to humans by cat feces or urine.

Infiltrating tumours

-Grows diffusely through surrounding brain tissue -Malignant tumours -Thread in with our heealthy tissues -Majority of brain tumours are infiltrating -Hard to remove and destroy completely

Executive function in MSE

-Executive function = ability to organize, plan, make judgements, inhibit inappropriate responses -Judgement: find letter on ground and has stamp on it, do you pick it up and put in mailbox or open it? -Verbal fluency: say 10 cities, 10 countries, 10 vegetables, 10 colours: making lists in categories, saying 10 words that start with S Test of peerservative behaviour: -Luria 3-step: classic figure in neurological test. Fist, palm, edge, do this oveer and oveer and as fast as you can. You are showing perservative behaviour if you get stuck on one thing -Drawing loops, alternating patterns -Oral trail making test -Regions involved: prefrontal cortex and/or associated projections

Cranial Nerve VII

-Facial -Both Motor and Sensory -Taste from anteerior tongue, a little facial sensation, all muscles of facial expression

Facial Nerve Test (VII)

-Facial nerve controls most of the muscles of our face- most of our facial expressions come from it -Ask patient to look up and wrinkle forehead --Observing patients nasolabial fold -Ask patient to smile -Ask patient to close eyelids -See if Face is symmetrical -Facial asymmetries: Bell's Palsy - Even at rest, our facial nerve sends important information to our muscles which is why we want to palpitate the muscle to make sure muscle is not wasting/atrophic - losing muscle tone is problematic

Anosognosia

-Failure of individual to self-reflect that they have a disorder -Critical predictor of recovery - Do they secretly know they have a problem or just don't want to admit it or do they actually not know?

Problems with statistics in fMRI

-False positives occur roughly 5% of the time if you set your p-value at 0.05 -P value at 0.05 means that if theree is a 95% chance it's right, we will say it is a significant difference - this is true for a single analysis but in an f MRI eeach voxel is an analysis so it's a huge number of analysees -At minimum, we will be doing statistical tests of 60,000 voxels - 1 million, so this 5% chance of being wrong increases when we do many t-tests -In a substantial proportion of voxels we see as p values less than 0.05 will bee false positivese (1/20) -We need to correct for this issue: make p . value smaller -Salmon example: dead salmon found to have more brain activity in emotional pictures - many false positives in fmRI .

Ballistic responses

-Fast, not enough time to use feedback -No time for corrections e.g. throwing a punch -Exception to flowchart

Epileptic Aura

-Feelings that happen before the seizure occurs -Can take many forms - feeeling of epiphany, bad smell, sense of fear/anxiety, a memory -Often consistent that this feeling will happen every time you have a seizure Important for 2 reasons: 1) Nature of aura/what kind of stimulus it is, is predictive of the epileptic focus - where problem brain structures are. Epileptic focus = where seizure is most likely to start, related to type of aura. Bad smell before seizure indicative of olfactory area of cortex = focus Fear/anxiety may be in/near amygdala or temporal lobe around it 2) Warn epileptic of an impending seizure

Testing for Language in MSE

-Fluency: repeat lines and sentence -Naming -Reptition -Prosody: pattern of stress and intonation in a persons language: being able to differ "No. Dogs are here", or "No dogs are here" - often critically involved in right half of our cortex -Comprehension -Reading -Writing -Praxis: asking someone to repeat something in the context of language. Describe something with language or ask them to describe something with language and then ask them to perform that section. Being able to follow commands according to a request and move in a meaningful way "hold out your hand and pretend it is a saw". Often related to parietal lobe

2 types of aphasia

-Fluent and non-fluent

Regions involved in language problems

-Focal or diffuse damage to left hemisphere language network usually -What's going on is a mess

Article: Funnel plot

-Funnel plot showing effect sizes (g) as a function of precision (SE) - asymmetry not significant - Funnel plot: point isn't to show the effect, but it is to check the existing literature and make sure it is legit - scientists have a habit of publishing results when positive and holding them when they are negative so we spot this using a funnel plot -As standard error gets smaller and smaller - sample size gets larger and larger - better study -Y axis = standard error -X axis = effect size of the outcome/observed outcome -Many false positives on bottom right, and false negative on bottom left -As studies get better and better we have less standard error (closer to top)  -Often right side of funnel plot is very well-represented, many positive results published -Often find that the left half of funnel plot is missing since less studies want to publish negative results -In Lohse paper we see relatively good representation on left and right as we go up we see true effect

2 types of focal seizures

-Generally have smaller impact on life 1) Simple partial seizure: Jacksonian seizures. Symptoms are primarily sensory or motor or both. -Weird, not immediately identifiable as seizures - may be like uncontrollable laughing or crying fit, jerk/spasm of single part of body, short-term problem with languge or comprehension. -Not diffuse effects - one body part, movement, cognitive domain. Tend to last 30s - 1 min. -Typically no loss of consciousneses, but what's happening is outside of their conscious control. -Sometimes only effect subjective experience like out of no where intense panic. -Only diagnosed via EEG. 2) Complex partial seizure: -Sometimes lose consciousness but not always, may just have altered consciousness. Lip smackingm, picking at clothes, sense of being unaware of surroundings - loss of touch with reality. -50% of all epilepsy cases -Engage in compulsive, reptitive, simple behaviours (automatisms), and more complex behaviours that can appear perfectly normal -Temporal lobe epilepsy - originate in the MEDIAL TEMPORAL LOBE -Aura we get in these is often intense deja vu - usually means the focus is partially in hippocampus (learning and memory) -These individuals are most resistant to treatment - doesn't benefit as much as other epilepsies, most intractable

Cranial Nerve IX

-Glossopharyngeal -Both Motor and Sensory -Taste and sensation from posterior tongue, muscles of pharynx (speech, swallowing)

Planning out movements

-Goals start as a vague thing - doesn't include what body parts we need to use and what muscles -From here, we start selecting sensorimotor programs

Key features to examine when testing motor function

-Gross appearance of muscle -Muscle tone -Muscle strength -Effect on reflexes (upper vs. lower motor lesions)

Top-down/ventral language pathway

-Has to do with semantics, meaning of our language -Ventral part in Broca's is important for top-down aspects -Important for seperating homnyms - Trying to differentiate meaningful words that have same sounds (eight vs. ate) -Interacts with our long-term memory like our vocabulary

Early vs. later seizure

-Head injuries and brain dysfunction in general cana predispose some individuals to having seizure but we do not know whaat/why - small correlations -Different types of TBI/damage can cause early vs. later seizure

Genetics and MS

-Higher concordance rate in monozygotic (25%) than dizygotic (5%) twins -Three times higher incidence in females than in males -Substantially higher incidence in Caucasians (0.15%) than in other ethnic groups -Some relationship with inheritance - monozygotic twins if one develops MS, other is more likely to develop MS - tapers off -Genetics isn't huge - more environmental factors

Geography of MS

-Highest incident of MS is in Canada -More women than men have this 3:2 -One of biggest predictors of developing MS is where you live geographically, especially true for first 15 years of your life -Even in a country itself we see northern states have more than southern states -Less common if ancestors from Africa

Chopping onion sensorimotor program

-Highest level programs (cortical programs): Chop onion -Lower-levels = brain-stem "Pick up onion, pick up knife" -Lowest levels = spinal motor circuits - all various elements of motor sequence to complete picking up onion and knife -Intention activates right programs - smaller programs concerned with more specific movements

Cranial Nerve XII

-Hypoglossal -Motor -Movement of tongue musclees (speech, swallowing)

Hemorrhagic stroke

-Iccurs when a blood vessel in the brain leaks or ruptures; also known as a bleed -Rupturing aneurysm major causee of it

Wilder Penfield

-Identified and mapped neocortical language zones during surgery

Age as a predictor of functional recovery

-If it happens early enough in life we have a better chance of other brain areas substituting function and taking over roles -Removal of an infant monkey's primary motor cortex results in a less dramatic impairment than in an adult monkey -Brain injury resulting in aphasia before age 1 is associated with the best recovery; recovery diminishes as age increases

Stimulating posterior parietal cortex - low level vs. high level

-If we stimulate neurons of posterior parietal cortex at a low level you will generate an urge/intention to do something/perform some specific movement - e.g. I want to touch my ear -If we stimulate neurons of posterior parietal cortex at a high level you generate the sensation that an action was actually performed, even though no movement was elicited

Immediate seizures, Early seizures, Late seizures, Latent period

-Immediate - 24 h after injury -Early - less than 1 week after injury -Late - more than 1 week after injury -Latent period - time between injury and onset of late seizures -In subset of people with head . traume will develop epilepsy later on in life, but often a very long latent period (15-20+ years)

Why MS is not primarily an autoimmune disease

-Immune system seems to be attacking its own cells, but this theory may not be totally true  i) When we examine myelin itself, if it was an autoimmune disorder it would be attacked. In MS we see that the innermost layers are what are showing dysfunction first. Layers that are being damaged/dysfunctional first are the inside layers. If it was actually autoimmune the outside layers would be damaged first ii) In many individuals neurodegeneration is accompanied with immune system responses but some individuals with MS don't show much inflammation or immune response at all - not immediately apparent iii) Prescription given is often something that helps immune function -immune modulator: helps in some individuals but doesn't slow the progression: relapsing-remitting period gets smaller and smaller still and we still see later stages of disease progressing

Fluent aphasia

-Impairment in input or reception of language, but not production -Speaking is effortless, but the content of it is greatly impaired -Also known as Wernicke's Aphasia or Sensory aphasia -Deficits in classifying sounds or comprehending words -Word salad: intelligble words strung together randomly - patient confuses phonetic characteristics -Often the patient cannot write (agraphia) because cannot discern phonemic characteristics -Syntax often relatively in place - verbs and nouns where they are supposed to be but content still doesn't make sense -When things become more and moree automatized - get easier to say so individual can say certain phrases well like "Have a good day" -Issue with phonemes and comprehending language, so leads to deficits in language individual is producing

Huntingtons and basal ganglia

-In Huntingtons, neurons across the brain area affected, especially the striatal neurons that project to the GPe (part of indirect paathway) - gets rid of STOP signal so we have all go and no stop - constant movement -Due to mutation of Huntingtin gene -Not many treatments

Parkinsons and basal ganglia

-In Parkinsons, most dopaminergic neurons of substantia nigra die meaning it's no longer sending dopamne to the striatum -Result is decreased transmission in the GO pathway (normally increased by dopamine) and increased transmission in STOP pathway -Less go, more stop --> diminished movement

Phonemes

-In language, the smallest distinctive sound unit -Fundamental language sounds that form a word

Primary progressive inside-out theory

-In primary progressive, you have same cytodegeneration -Exact same diagonal line -In these individuals they don't have a strong immune response to the degeneration -For many years of their life - no symptoms at all then one day, degeneration gets so bad it crosses clinical threshold and they exhibit those symptoms - suddenly they have MS and they have MS all the time - present all the time -Primary progressive usually much later in life

Regional hemodynamics

-In some studies, we can see a decrease in blood flow to the hippocampus rather than an increase during behvaiours where the hippocampus should be active -We make the assumption that increase in blood = increase in activity -Quality of our result is dependent on quality of our algorithm -A statistical issue with fMRI studies, where blood flow is not consistent across the brain

Fasano and Lozano paper: explain when deep brain stimulation (DBS) should be offered as a treatment for Parkinson's disease

-In the past, DBS was offered only in late phase of the disease (13-14 years after diagnoses) - considerations has moved the time for surgery earlier -DBS produces motor improvement of signs responding to dopaminergic drugs, whereas unresponsive features often predominate in late stages of the disease -Older patients are more likely to develop surgical complication and/or worsening of motor functions -DBS at advanced stages of illness can alleviate certain aspects of motor dysfunction without addressing ongoing difficulties in well-being and social relations with others in the environment -Earlystim trial: examined patients with early occurence of motor fluctuation (mean disease duration around 7 years) .- found early and sustained improvment of quality of life in patients reeceiving DBS -Proposal for using STN DBS in patients without motor fluctuation (disease duration less than 4 years) less compelling since it may expose patients to potentially dangeerous side effects without improving motor function and quality of life and unclear impact over long term

Apraxia

-Inability to perform movements on command, with no simple motor deficits or deficits in comprehension or motivation -Associated with LEFT posterior parietal cortex damage but symptoms are usually bilateral -Great difficulty making specific movements when requested to do so particularly when those movements are outside context within which they would usually perform them - Movements themselves may not be impaired but if you ask someone to do something on command they have problems with it, or if you ask them to use tools, or just spontaneously using tools might be impaired - If asked to do something outside of normal range to interact with world - trouble to do - Someone who is painter and can paint on canvas with no problem if they have apraxia but if you ask them to pain on a piece of wood or weird surface they show troubles doing so -Show trouble with weird movements/novel movements: "Pretend this pen is a knife and chop this piece of wood"

Infection and encephalitis

-Infection is invasion of the brain by microorganisms or some foreing body -Encephalitis = inflammation we get when something infects the brain

Secondary progressive MS

-Initial relapsing-remitting MS that suddenly begins to have decline without periods of remission -Symptpoms present all the time, after that period of relapse and remitting

Heavy metal brain

-Investigated spontaneous neural activity and functional connectivity in Heavy metal music lovers compared to classical music loveers during resting states -Assumption: classical muscic lovers are normal, control leevels and and there is psychopathology associated with liking heavy metal -Look at differences in functional connectivity between the 2 groups - substantial changes -Said "the results may partly explain disorders of behavioural and emotional cognition in HMML compared with CML) -Problems: Didn't check assumptions or control for a bunch of different things. Assumed disordered, Assumed personal traits, Random speculations

Right hemisphere contributions to language - what happens when we remove left vs. right hemisphere

-Involved in good auditory comprehension of language -Hemispherectomy (removal of a hemisphere): >If left hemisphere is removed early, the RIGHT hemisphere can acquire language >If left hemisphere is removed in adults, severe deficits in speech occur, but still good auditory comprehension IN SOME CASES >Removal of right hemisphere produces subtle changes in language comprehension -Right hemisphere seen more in melody and timbre of language, and visual meaning, but not involved at all in syntactical language -Left hemisphere totally involved in syntax

Recovery trajectory and anosognosia

-It is a critical predictor of the recovery trajectory - in general, with anosognosia there is a worse functional recovery trajectory - our ability to recovery will be slower/more impaired than individuals without anosognosia -Those with initial anosognosia found to have poorer functional outcomes -Anosognosia not forever in time - it may disappear rapidly on order of weeks -Found that rehabilitation progress is not as strong when anosognosia is present

Treating Parkinsons

-L-dopa: converted to dopamine by our brain, allows us to restore dopamine levels in our brain and restore healthy movement -Deep brain stimulation of STN: inhibits the STN: no longer stimulating the GPi, so GPi sends less GABA/inhibition to the thalamus - reduces tonic inhibition, so thalamus can excite the motor cortex and allow for movement -Decreases activity in the indirect pathway - less STOP -benefits often outweight the cost

Aphasia

-Language disorder - Inability or difficulty in producing COHERENT SPEECH. -Aphasia is an acquired communication disorder that impairs a person's ability to process language, but does not affect intelligence. Aphasia impairs the ability to speak and understand others. -A person with aphasia may have trouble understanding, speaking, reading, or writing. -Common after stroke/damage to left hemisphere - typically due to very distributed/diffuse strokes so not just damage to language areas, but also other areas concerned with other functions -When we deal with an individual with aphasia, they ahve language impairments - problems with comprehension/production but will also have other issues such as damage to motor cortex that may be controlling your arm -Hard to disentagle if it is strictly a motor or cognitive disorder

Dual Language Pathway Theory

-Language is moving in multiple directions -Area 6 (motor cortex) and 47 (semantics) are often targets of flow of information -Instead of thinking of Broca's as production and Wernicke's as comprehension, each actually has components of both production and comprehension -There is ventral and dorsal part - Top-down and Bottom-up

Global aphasia

-Language issues all across the board -Labored speech and poor comprehension -Where this cut off occurs is blurred - don't know when it's broca's and when it turns into global

Bottom-up/Dorsal language pathway

-Language production pathway -Only pathway used when someone is asked to repeat nonsense words (speech sounds with no linguistic content) -Related to short-term memory/working memory -Phonetics - turning basic sounds into more complex stimulus into brain - words, etc.

Visuospatial function in MSE

-Line cancellation -Copy of geometric designs -Judgement of line orientation -Object/face/colour . recognition

Morphemes

-Smallest meaningful units of words - little collections of sounds that mean something -Example: pre-

Contralateral neglect and line cancellation

-Line cancellation test can test contralateral neglect; draw second line through all the lines on the page - If individual has normal, standard, visuospatial function they are able to cancel all the lines -Contralateral neglect: doesn't cancel out lines on the left

Anatomical areas associated with Language

-Many areas associated with language -Fissures and gyri, Brodmann's areas, insula and medial superior temporal gyrus -Inferior frontal gyrus - included in Broca's area -Superior temporal gyrus - included in Wernicke's -When these areas are damaged we see impairment in linguistic abilities -The vast majority of our brain will get involved in linguistic procressing in some way - whether it's vocab, prosody, syntax, etc. -The left hemisphere seems to be dominant for language but in fMRI . studies we will see bilateral activation (BOLD signals) - areas in the right hemisphere play a role in language but if lost, we can substitute their functions

Wakfield - MMR vaccine and autism

-Many complications that result with measles -Wakefield published paper in Lancet - popular journal that showed a case study with small number of participants (around 20) and showed in crude statistical terms that all of those individuals with ASD had also been vaccinated with MMR - problem: no good control group  -Wakefield wanted to make MMR vaccine look bad to make the vaccine he was currently creating look better -By 2010, medical council of UK convicted him of medical misconduct -Paper was retracted -No relation between vaccines and autism

Fasano and Lozano paper: explain the current state of the research on whether it is better to administer DBS to the subthalamic nucleus or the globus pallidus when treating Parkinson's disease

-Many randomized trials compare STN and GPi Deep Brain Stimulation -Motor benefits can be similar with each target -Quality of life similar, tremor similar , motor fluctuations similar -STN stimulation shows greater benefit in severity of off symptoms (rigidity, braykinesia) and cost-efficacy -Dyskinesias supression and long term effects on stability and cognition (axial motor symptoms, speech and swallowing, cognition, mood and apathy) favor GPi >Post-op management better in GPi

Chronic vs. acute dysfunction

-Massive tumour, littile impariment vs. sudden stroke with associated damage (of a comparable size) leaves individual functionally devestated -You can have exactly same size of brain dysfunction, but if it comes on slowly (chronic) you will have less impairment than if it is acute and sudden -Often, our tumours are slowly growing and many years later someone will report headaches or dizziness - we assume that slow growth allows neighbouring regions to compensate f or loss of . tissue but if it happens all at once it is worse

What are prefrontal lesions before 16 months associated with? (Related to age and recovery)

-May be associated with an inability to learn social and moral rules later in life -Dysfunction that occurs early in life related to impairment later in life -If you have damage later in life you may not see same impairments and may be less than earlier for prefrontal lesions

Semantics

-Meaning of words and sentences that correspond to all lexical terms

Regions involveed in memory

-Medial temporal structures (hippocampus), thalamus, basal forebrain, prefrontal cortex -Digit + Pointing = prefrontal cortex, basal ganglia: -Details about whose the president = longer term memory structures seen in medial temporal structures (cortex around hippocampus and hippocampus)

Heavy Metals - Mercury

-Mercury can accumulate in the brain and it can permanently damage it - producing toxic psychosis -English hatmakers using mercury in preparation of felt for hat -Liquid and solid mercury not that bed - evaporated mercury is the problem - inhalation very dangerous -Currently, mercury vapourant is seen from amalgam tooth fillings but there are no known case studiees of people with the fillings with toxic psychosis -Mercury and lead us in Japan getting into water supply - affected fish they were eating - people born with birth defects and general cognitive impairments -Small amounts of ethylmercury are present in vaccines as a preservative, but there is no evidence to suggest harmful neurological effects

Article: Lohse et al. - What were their goals

-Meta-analysis that explored relationship between time scheduled for therapy and improvement in motor therapy for adults after stroke . by comparing high doses to low doses, and using metagression to quantify the dose-response relationship further -Objective: quantify magnitude of functional improvement gained by increasing therapeutic time after stroke -Population: adults after stroke. -Dose = total time scheduled for therapy (e.g. 3 hours/10 days = 30 hours) - which may not accurately . reflect actual practice time or number of movement reptitions but it's the only consistently reported metric in rehabilitation research studies -Response = defined as a standardized effect size , Hedges' g which shows improved function or reduced impairment on a standardized, validated behavioural test -Used randomized controlled trials that were not dosage matched for total time scheduled for therapy. Used articles with different types of therapy interventions since it's currently unclear how type of therapy provided affects responses. -Regression models used to predict improvement during therapy as a function of total time scheduled for therapy and years after stroke

Relapsing-remitting MS

-Most common form -Go through pereiods where you're symptomatic and showing muscle numbness, confusion, etc. and then times of remission where you feel totally normal -Then go through stage of secondary progressive

What is the most common type of malignant brain tumour in adults

-Most common version is the GLIOBLASTOMA: infiltrating, malignant, prognosis is a year and a half at the offset (1-1.5 year immediate survival rate

Olfactory Test - Cranial Nerve I test

-Most commonly damaged in individuals -Ethmoid ridge, cribiform plate, and TBI -"Can you smell this?" -Cover one nostril, ask person with eyes closed to identify some smell - someething characteristic like coffee or mint or clothing - Main reason why damage to cranial nerve 1 (olfactory) is common because olfactory axons come through many porous holes in the bone: cribriform plate (porous region), it is very easy for these brains to shear and cut the axons if we have a blow to the head -Anosmia = loss of smell Very common even in small head injuries

Metastatic tumours

-Some infiltrating brain tumours grow from tumour fragments carried to the brain from another body part via the bloodstream -Commonly originate from a breast or lung cancer

Cranial Nerves

-Most of our efferent nerves and afferent nerves come out of spinal cord -Other information coming of brain stem/areas near it -Cranial nerves: extention of CNS -Twelve pairs of nerves—the cranial nerves—lead directly from the brain to various parts of the head, neck, and trunk. -Cranial nereves are listed from anterior to furthest down brain stem (1--> 12) -White matter sticking out of brain

Human impact epilepsy has - Stigma

-Negative consequences especially when untreated -Idea of being posseessed and spirits

Lohse et al.: What does the paper indicate is the relationship between time-since stroke and benefits of increases in therapy time?

-Neither linear nor quadratic effects of time after stroke were significant -There was a significant positive effect of time scheduled for therapy on outcomes even when controlling for time after stroke -There was no interaction between time since stroke and time scheduled for therapy -The lack of interaction suggests that the benefit of large increases in therapy is similar across a range of post stroke times regardless of w hether client is several months or several years after stroke (which ranged from 0.003 to 5.38 years) -Importantly, there are complications to this effect. -For instance, if started too early, intensive therapy may hinder the rate of recoveryor have no benefit over less intense therapies. -Also, too many hours of therapy may not be tolerable for participants, leading to dropouts. -These nonlinearities are important considerations for clinicians, which are not captured in the current analysis. -As more data is added at different time points, these complexities in the dose-response relationship can be modeled more reliably.

Common treatments for epilepsy

-No cure but we treat seizures - try to reduce overall activity of brain -Either change levels of glutamate or GABA 1) Anticonvulsants: reduces the likelihood, duration, and severity of seizure -Side effects: 30-50% of people do not respond to first drug they take, with every subsequent drug you try, the rate/lack of success likelihood will get bigger -Once a day therapy to keep brain activities lower -Changes in mood, likelihood of psychosis, memory issues, issues with cognition or movement 2) Vagus nerve stimulation -Stimualte vagus nerve (travel to visceral organs and up into brain) via. electrial stimulation -Not great efficacy 3) Ketogenic diet -Higher level of ketones in body, may help in epilepsy 4) Cannabidiol (CBD) -Psychoactive ingredient in cannabis -Can help with frequency and severity of seizures -Small subjective effects on you

Seizure

-Occasional, excessive, and disorderly discharge of nerve tissue on muscles -Seizures can alter consciousness, sensation, and behaviour -Seizures: spontaneous and unprovoked activity - brain activity that is generated on it's own and very excessive

Cranial Nerve III

-Oculomotor -Motor -Most eye movement, eyelid movement

Testing Oculomotor, Trochlear, and Abducens - Cranial nerves III, IV, and XI

-Oculomotor muscles: control our eye - in charge of most eye movement and eyelid movement. -Trochleaer and Abducens - both in charge of eye movement, control only a single muscle -Test: -Follow an object/light without moving their head: ask patient to fix their eyes on pen and follow its movement - look for gaze restrictions >Search for problems with areas they cannot look - could be due to oculomotor problems or something else in brain - Cortical issues would be associated with hindered voluntary eye movement

Cranial nerve I

-Olfactory -Sensory -Smell

What to do when someone has seizure

-Only call 911 if you know they've never had seizure -Put them on side to avoid choking, put pillow under heada -Do not stuff mouth with anything -Loosen clothing

Cranial Nerve II

-Optic -Sensory -Vision

Key features to examine when testing somatosensory function

-Pain - pinch -Light touch and propriocpetion (knowing where body is in space, driven by reeceptors in muscles) -Testing for asterognosis - ability to recognize an object by touching it with hands -Testing for agraphethesia - close eyes and write something on hand and ask them to identify what you wrote on their skin

Patient History

-Past medical history -Age, education, handedness -Education= good predictor at bieng resilient to neurocognitivee deecline -Handedness = good way of telling where problems may be centrally - where they might be in the brain (most individuals are left brain dominant) as most are right handed (90%), and of these right handed individuals most have left hemisphere dominant for language . -Left handers: majority of them also left hemisphere dominant for language as well (75%), remaining 25% are eithere right hemisphere dominant and other half havee a weird split in which both left and right hemisphere are critically involved -Use of medication and/or reecreational drugs -Family medical history -Disease processes: make predictions about what will happen in ensuing years -Temporal profile: suddent vs. gradual, acute vs. chronic -Changee over time: static, improvement, worsening -Identify triggers/relieveers of symptoms -Gauge severity of symptoms

What are the components of language

-Phonemes -Morphemes -Lexicon -Syntax -Semantics -Prosody -Discourse

Damage to premotor cortex

-Problems with sequencing motor behavior - putting them together -Problems with imitating someone elses behaviour -Problem with following along with external stimulus in environment: following screen with dot on it that zig zags and follow dot with finger - cannot do this -No outright paralysis, but disorderliness to movement.

Multiple Sclerosis

-Progressive disorder that primarily attacks myelin of axons in the CNS, but there is also cell loss -Common symptoms in advanced cases: visual disturbances, muscular weaknesses, numbness, treemor, loss of motor coordination -Immune system appears to attack CNS myelin as if it were a foreign substances -Loss of myelin causes signal to disappear - signals don't reach muscles at all -Progressive disorder and most common form is relapsing-remitting version 2 types: Relapsing-remitting, and secondary-progressive -Bright spots in scan: indicates where there may be cortical damage, in MS we see there is cell loss and tissue damage

Secondary motor cortex projections and role

-Projects to primary motor cortex, each other, and brain steme -Related to movement - motor patten -Programs specific patterns of movement after taking instruction from association cortices -Ability to write signature with hand and toe is due to secondary cortex -Stimulation produces complex movements (before and during voluntary movements) -Premotor areas encode spatial relations and program movements -Select specific muscles to carry out motor program

Visuospatial problems

-Prosapagnosia = failure to reecognize faces -See all the features of the face but can't put all those features together into a face - Often damage in ventral surface of brain: fusiform gyrus, also know as fusiform face area - Fusiform gyrus is good at helping us detect subtle differences -Constructional apraxia = difficulty putting pieces of an object together -Dressing apraxia = difficulty getting dressed

Posterior parietal cortex

-Provides information on where our body parts are in relation to the external world - we need to know where we are in the world and what's around us before we take an action -Not a single region, activity across it reflects specific areas of the body - some regions specified for different parts of the body (arms, head, etc.) -Receives input from visual, auditory, and somatosensory systems -Most output goes to secondary motor cortex, also goes to frontal eyefield and dorsolateral prefrontal association cortex -Involved in contralateral neglect

What inherent problems do we encounter in neuroscience when we use terms like "psychological" vs "biological"?

-Psychogenic = due to psychic, mental, or emotional factors and not to detectable/organic factors -We try to reduce psychiatric illness to brain processes since it comforts patients as it confirms the "physical" reality of their ilnesses -We still categorize ilnesses as "organic" or "functional/psychogenic" meaning physical/nonphysical -We may still view a "psychological" ilness as less "real" than a brain lesion -We fail to recognize that things like emotion and stress are also organic processes even if they aren't connceted to brain damage -Disorders seen as all in the head = not treated with respect and properly taken care of since there is not "physiological" basis to them -Many psychological processes have a biological basis

How does a "psychogenic" diagnosis negatively affect a person?

-Psychogenic seizures/non-epileptic seizures = functional disorder since no physical site of injury can be found - electrical activity of brain is normal. Often due to some traumatic emotional event. - -Every illness is different, dynamic, and not a static phenomenon that exists in time so static, mehchanistics models like organic vs. psychogenic distort the chacter of any illness -Psychogenic diagnosis may devalue a persons illness and see it as less legit since there's no physilogical basis . -Philosophy matter in "brain matters" - arugment over mind-body still exists today and can be harmful for certain diganoses

Key features to examine when testing coordination

-Quick, alternating movements -Point-to-point movement -Heel-to-shin test -Standing/sitting -Gait - posture, way you walk (problems with cerebellum cause changes in gait) -Romberg test

Cerebellum

-Receives input from primary and secondary motor cortex, information about descending motor signals from brain stem nuclei, and feedback from motor responses via somatosensory and vestibular systems -It compares our intended movements to our actual movements, and then corrects our behavioru -Critical for motor and cognitive timing and sequence -Has Purkinje cells - very branched cells, getting a lot of input from sensory ststems, and signals coming down from motor areas -Corollary discharge: second signal from motor cortex/secondary motor cortex that goes to the cerebellum - when we send signal from motor cortex to muscles to tell body to move, a mirror image of this goes to the cerebellum -Doesn't send information directly to muscles - sends some to brain stem, some to motor system in order to correct and adjust behaviours, usually happens 7 times a second -Not related to ballistic movements

Dorsolateral preefrontal cortex

-Receives projections from the posterior parietal cortex - main input. But highly innervated by many other areas including visual and auditory -Projects to secondary motor cortex, primary motor cortex, and frontal eye field -Involved in assessments of external stimuli -May work with posterior parietal cortex in decision regarding voluntary response initiation -Builds a model in order to get to some goal -Involved in decision making and voluntary movement -Its neurons fire EARLIEST in entire sensorimotor hierarchy before a movement happens - first part of thinking you want to do something -Called a motor cortex but also involved in many things - problem solving, math, learning, working memory, linguistics) -Neurons in here fire for many different aspects - type of food presented, what room animal is in, specific movements, combination of both objects and movement - many aspects of situations represented in this area -Damage here will affect many sophisticated cognitive functions since involved in so many other things

Aphasia and recovery

-Recovery varies -Therapy may help, and groups have added benefits -Social network benefits -Aphasia groups ran by speech language pathologists: Fraser Health Aphasia Group -Augmentative and alternative communication (AAC) devices - iPad with imagery built into it, can go through categories and choose nouns or verys, especially helpful in nonfluent aphasia

Preictal, ictal, and postictal

-Refers to different parts of EEG -Preictal - EEG prior to seizure -Ictal - EEG during seizure -Postictal - EEG anytime after seizure and prior to other one, usually refers to immediately post -Interictal - when you are not in seizure zone at all

Regions involved in visuospatial problems

-Regions involved: right hemisphere's attention network

Syntax

-Rules of grammar -Phrases and sentences

Seizures vs. convulsion

-Seizure itself doesn't have to have any behavioural output - doesn't have to change muscle rigidity -Seizure refers specifically to brain activity -In some cases we see convulsion: increase in muscle rigidity and tone - shaking, tonus -Seizures are not convulsions but can cause them

Anterior-Ventral region of Broca's critically involved in...

-Semantic processing - meaning of words

Surgical method of using auras

-Since nature of aura can predict focus, we can stimulate parts of brian to try to produce the aura and this area of brian thata creates aura will be whata we want to remove -Burnt toast = aura, stimulate brain until patient says they smell toast

Default mode network

-Some regions of our brain are more active at rest than during the task -To find these regions wee define a seed region: such as prefrontal cortex, and see whenever this region is active, what othere regions of the brain area also active, and what regions become less active - positive and negative correlations -Resting statee functional connectivity MRI: comparing activity in any one region and see what other regions go up or down with it. -During mind wandering, one particular network activity comes up again and again: the default modee network -There are 3 regions: medial prefrontal cortex, lateral parietal cortex, and posterior cingulate - functionally, not structurally connected

What did Binder & colleagues find with speech? - What are the different Brain areas activated by language tasks?

-Speech zones aree widespread throughout the brain -If we have tight controls, we see distinct areas are active according to the type of task you are doing -Noun type activates different area along ventral zone of brain. -Selecting a word for animal, tool, vs. person we see activity in different regions -Premotor cortex is active in a task requiring matching a noun to one of four target words -Speaking words, hearing words, viewing words, and generating views activates distinct set of areas in the brain -Premotor cortex & temporal cortex are active with nouns for tools.

Effects of cortical stimulation by TMS

-Stimulating certain areas of brain we see various outcomes. These apply to modern stimulation (e.g. TMS) - TMS = Transcranial magnetic stimulation, a brief radiofrequency pulse is administered -Total arrest of speech -Hesitation and slurring of speech -Speech distortion and repitition of speech -Number confusion while counting -Naming difficulties -Misnaming and perseveration (repitition)

Indirect pathway -STOP

-Stops movement -End result: lots of GABA going to the thalamus which inhibits it -Parts of cortex sends glutamate to indirect neurons of striatum, which will inhibit the globus pallidus external -Globus pallidus external normally inhibits 2 things: globus pallidus internal and the subthalamic nuclei -Inhibiting GPe means that means that it is no longer inhibiting Gpi and inhibiting it - we have disinhibited this signal so now the Gpi is free to send a strong GABA signal to the thalamus and inhibit it so no information is going to motor cortex -Inhibiting GPe means it no longer inhibits the subthalamic nuclei, so now subthalamic nuclei is disinhibited and it is free to send an excitatory/glutamatee signal to Gpi so stimulates it to send a strong inhibitory signal to the thalamus and prevent it from activating the motor cortex

Discourse

-Stringing sentences together to form a meaningful narrative -Pragmatics is meaning in context of discource

What region of the brain is anosognosia associated with?

-Stroke that causes damage to right hemisphere, especially right frontal parietal stroke where you have complete paralysis of left side of body because of damge to internal capsule >Most know they have paralysis >Some deny their own paralysis even when patient is mentally normal in all other respects - perfectly intelligent and can carry out a fluid conversation -Not seen as much with left hemisphere stroke

Article: CTE

-Study found evidence linking hits to the head rather than concussions to onset of CTE -Examined brains of 4 teenagers with head injuries and and found signs of CTE -Used mice to recreate head trauma, to reveal more about origins of CTE and relationship to TBI, concussions, and subconcussive head injuries -Found that brain pathology was unrelated to signs of concussion, including altered arousal and impaired balance -These findings provided a strong causal evidence linking head impact to TBI and early CTE, independent of concussion -The results may explain why approx 20% of athletes with CTE never suffered diagnosis of concussion -Concussion, TBI, and CTE is being jumbled together as categories - Concussion is based on signs and symptoms of neurological syndrome, what happens after you get a hit to the head -TBI is an injury/event, not a syndromee - it's an event and it involves damage to tissue. If you don't have a concussion you can have a brain injury, and if you have a concussion you may not have TBI -CTE = bona fide neurodegenerative disease - it'll progress independently of whether you have future hits -Focus on concussion doesn't prevent development of CTE -"So concussion may or may not be a TBI and equally important not having a concussion may or may not be associated with a TBI. A concussion doesn't tell you anything about a TBI. Nor does it tell you anything about CTE." -"Bobblehead effect" - cumulative effect of smalleer hits - concussion is a minor subset of all hits, vast majority are subconcussive (where brain is shaken but not so violently that damage to brain cells is severe)

Dopmine role in movement

-Substantia Nigra (SNc) - critical area, one of 2 major dopamine areas in brain, releases dopamine to primary target - which is striatum -Striatum = major dopamine target of the brain -Within the striatum, there are 2 different families of dopamine receptors: i) Dopamine D1 receptors (D1R) --> positive modulatory role, activates cells/increases activity. Most are in the DIRECT pathway/excitatory pathway. ii) Dopamine D2 receptors (D2R) --> when dopamine binds to these cells it inhibits these cells - has a negative modulatory role. Are in the INDIRECT pathway/inhbitory pathway -SNc releases dopamine onto striatum - activates D1R receptors in the direct pathway which increases activity in this pathway -Activation of D2R receptors in the indirect pathway inhibit the cells in that pathway so it decreases transmission in the indirect pathway -Result: More go, less stop --> movement

What is a stroke, infarct, penumbra

-Sudden-onset cerebrovascular disorder that causes brain damage -If one area of brain not getting enough blood, after 3-4 minutes those cells will die -Infarct = area of dead or dying tissue. Immeediate damage - wheere strokee was, would have died 3-4 minutes after onset. -Penumbra = dysfunctional area surrounding infarct, tissue in this area may either recover or die. Usually isn't functioning properly but we can save it. -Stroke is 3rd leading cause of death in Canada, top 5 cause of adult disability - leads to many problems like eneeglect, aphasia, and motor control issues

Secondary effects of brain damage - edema

-Swelling/edema after stroke may mask or distort functions in essentially intact regions of the brain -Disipation of these effects may account for substantial early recovery -When you have an injury, especially TBI, we see a loss of many functions all at once and then the doctor reports based on that what recovery will look like. A week later, many functions will spontaneously come back and these rapid recoveries are probably related to edema going away

Neurocysticerosis

-Tape worm in the brain -Normally we ingest tape worms and they are in their guts - But in some points of their life cycle they're more likely to reach the brain if ingested - Once they get in the brain they form cysts - which at first look like a tumour in an MRI or some sort of benign growth and upon sugery we find out what's going on -Doesn't change behaviour in any way - Presence of these parasites causes an immune response - and as these immune cells show up, the parasites eat them - take advantage of this immune reaction -Can be spread just by someone who has the parasite in their body and doesn't wash their hands

Motor equivalence

-The ability of the sensorimotor system to carry out the same basic movement in different ways that involve different muscles -Example: signature is something characteristic of you, you can sign it with your left or right hand, or even toe -You can apply sensorimotor program from one part of body to another -In a study ., finger and toe zig zag and signature . movements cause similar activity in some areas of brain (motor regions) - overlapping activity is primarily seen in the secondary motor cortex, not primary

Rabies

-The rabies virus has an affinity for the nervous system -Only 15% of us that get bitten by a rabid animal actually develop rabies ourselves -Spread involves a bite -virus has . to take advantage of a protein that travels along axon back to cell body - retrograde transport into the cell -In order to get rabies it has to infect your motor neurons and take over machinery to travel up the axon into cell bodies and spread - to get to motor neurons you must break the skin -The affects are lethal but it takes a while to get there: weeks-month till you will die from rabies -Symptoms: headache, general discomfort and unhappiness, malaise, irritability, fever, fogginess -Later stages: persistent problem with SWALLOWING: often called hydrophobia (old name) - frothing, pain, uncontrollable movements and jerking, lose full touch with reality, mania, lethargy, problems with movement death - problems with breathing

Hierarchial control of movement

-There are lower levels and higher levels -Lower levels are concerned . with controlling muscles -Higher levels are concerned about abstract intentions/goals and what we're thinking about some concept "I need to get from here to the bus stop" - higher levels are areas such as the prefrontal cortex -Association cortex - goal/plan -Secondary motor cortex - thinking about where we are in the world, what muscles we can use, where our hand is relative to where we want it to be -Primary motor cortex - getting more specific as what to do with muscles - contract/relax this muscle -Brain stem motor nuclei -Spinal motor circuits -Cerebellum and Basal ganglia are critically involved in movement but don't fall into the standard hierarchy - they are outside of it

Fluent aphasia subcategories

-There are subcategeories including conduction aphasia and anomic/amnesic aphasia -Conduction aphasia - not as severe, some sort of break in path between phonological loop and actual semantic loop - disconnection between motor systems producing words and perceptual word image >Cannot REPEAT words but can speak, name objects, and understand speech -Anomic aphasia/amnesic aphasia: Cannot NAME objects. Know some picture is an anchor and can describe it but cannot access it as a noun

Direct pathway - GO

-To activate motor cortex, we have to inhibit the inhibition: known as DISINHIBITION -Shorter route for information to travel -In striatum there are many neurons and some are part of direct path and some are part of indirect -Cortex sends signal to direct pathway neurons of the striatum, which will inhibit the globus pallidus internal, which means it no longer sends GABA to the thalamus (DISINHIBITION) - no more tonic inhibition going from basal ganglia to the thalamus, so that thalamus is now free to send glutamate/excitatory signal to morter cortices and allow for movement -Critical role in determining strength, velocity, and learning skills -Basal ganglia sends information to motor cortex to tell you what to move

Cranial Nerve V

-Trigeminal -Both Sensory and Motor -Facial sensation, moveement of biting/chewing/swallowing jaw muscles

Testing Trigeminal nerve (V)

-Trigeminal nerve, largest of our cranial nerves, gets most of sensory information from our face -Facial somatoseensation: test multiple points along face since many different branches of trigeminal nerve/different divisions. Test with different types of touches: soft (cotton), prickly since wee have different . typees . of sensory receptors for touch -Asking patients if he/she can feel the examiner touching their forehead, cheek, and jaw -Motor function: -Chewing, mandibular functions --> puffing face, resistance, ask patient to move face and jaw -Place finger of muscle and ask patient to clench their teeth and feel jaw muscles contracting -Reflex: - Seeing if placing cotton on cornea will cause patient to blink -Use tendon hammer to demonstrate jaw jerk

Cranial Nerve IV

-Trochlear -Motor -Eye movement

Syphilis

-Type of bacteria that can attack brain -General paresis: syndrome of psychosis/dementia that results from a syphilitic infection of the brain -Syphilis is a very common sexually transmitted disease - it is most commonly passed by genital contact, a bacterial infection - you can be infected but it will get into a dormant stage before it affects you -During dormant stage if you have a skin test you would find the bacteria syphilis but no other symptoms would be there - you would seem healthy -Eventually looks like general paresis: hallucinations, delusions, dementia -Give antibiotics to treat it - easily treated, earlier we're treated the more likely there will be no likely life issues in future -Later cases: give high doses of IV antibiotics

Wernicke-Geschwind Model

-Unidirectional model based on lesion theories -Word sounds are sent to the primary auditory cortex, and word meaning is represented in Wernicke's area (comprehension) -Word meaning is sent to Broca's area via the arcuate fasiculus -Broca's area sends instructions for speech articulation to the motor cortex -To read, visual areas send information to the angular gyrus and to Wernicke's or Broca's area -Comprehension is extracted from sounds in the Wernicke's area Passed over the arcuate fasciculus sent to Broca's area. Instructions created there of what you want to say and then sent to your motor cortex so you can say it.

Cortical language components of nonfluent aphasia: -Apraxia of speech due to.. -Deficits in sentence comprehension due to.... -Reptition ofspeech due to.... -Working memory and articulation impairment due to....

-Usually damage to Broca's area, presumably the dorsal pathways/posterior region of Broca (production) -Semantics intact, not phonemes -Various area of cortex being damaged - on one side of Broca's area is prefrontal cortex, and just below is the temporal lobe, insula, etc. -Apraxia of speech due to damage of insula -Deficits in sentence comprehension due to damage to superior temporal gyrus (auditory cortex) -Reptition of speech (Tan) due to damage to arcuate fasiculus -Articulation impairment and working memory = damage to Broca's -Often with nonfluent aphasia even if person can only say one thing "Tono" they are expressive and can change intonation and use gestures to epxlain themselves, and can even count (automatized)

Cortical language components of fluent

-Usually damage to Wernicke's area - ventral pathways/anterior regions of Broca -Lack of speech comprehension and other core difficulties with language - damage to medial temporal lobe and underlying white matter often seen (long term memory) -Damge to temporal cortex contributes to deficits in holding sentences in meory until can be repeated - working memory impairments as well

Cranial Nerve X

-Vagus -Both Motor and Sensory -Outer ear canal sensation, motor control of heart, lungs, viscera, larynx (speech), more

Preictal activity

-Valuable since may provide hints that seizure will come -If we had electrode on our head, we could predict that a seizure is likely to happen soon based on the EEG -Preictal spikes in some kinds of epilepsies may predict oncoming of seizure (but not seen in ALL types of epilepsies)

Risks that come to increase likelihood of having epilepsy

-Vascular disorder/circulatory system issues, running in family. trauma, tumour: only small amount -Vast majority = cryptogenic/idiopathic: we do not know why these individuals have epilepsy -Risk factors caan include: family history, CNS infections, tumours, trauma, congenital/developmental, strokes -By large, we do not know what is causing epilepsy, we presume it has something to do with an early damage that feeds forewards -Head injuries often provoke seizure

Cranial Nerve VIII

-Vestibulocochlear -Sensory -Sound, sense of balance

Prosody

-Vocal inontations "tone of voice" -Goverened by seperate regions that handle syntax

Focusing on incraesing activity: problem with fMRI

-We are predisposed to looking at increasing in activity, when we see heat maps we see increase in activity in a given region -Some parts of the brain may just be active all the time, and playing an essential role -Example: hippocampus doesn't show up on fMRI in experiments wee think hippocampal activity is important, this is because the hippocampus is active all the time, so it will be active in both control and active behaviour condition -Our brain is actually often much more active at rest than during mental activity

Taupathies

-We can refer to Alzheimer's CTE, and Parkinson's as being a Taupathy - pathologies in many different diseases that centre around Tau -Tau may not be a cause of CTE but a by-product of the main problem - just because it's seen in post-mortem studies doesn't mean it's the problem killing the cells -100% diagnoses is post-mortem for CTE - so we can never be sure until post-mortem if someone has it

fMRI: how it's not necessarily necessity

-We can see activity that isn't strictly necessary to the acutal function - even when we subtract out control conditions -For example: language usually left hemisphere of our brain is dominant but when we do fMRI we always see bilateral activity in linguitic based tasks -Don't need activity for something to actually show up in MRI - correlation doesn't mean causation!

Temporal resolution of fMRI

-We havee activity in a giveen reegion of the brain and then around 6 seconds later we geet a surge of blood: we deal with changes on the order of SECONDS not MILLISECONDS, there is a constant delay built in -Time doesn't line up in a really good way, (fMRI: BOLD response), on a "second" scale, and APs are on a scale of milliseconds - thus too slow -Many fast changse will not bee captured in the fMRI but it's still betteer than PET (which could be 45 minutes long)

Removing a tumour

-We need to think about where it is in the brain, if it's agressive, if it's infiltrating or encapsulated -We want to remove it without damaging other regions too much -In general, if at front of the brain we can remove without too many problems -If tumour is growing on base of skull or near brain stem, doctor won't want to perform surgery since brain stem is where vital life functions are regulated

Vitmain D and MS

-Weak link between Vitamin D and MS -Vitamin D promotes calcium absorption and phosphate - which can modulate immune system function sometimes -We see correlations but no actual reasons why vitamin D deficiency may cause MS -Vitamin D supplements seem to reduce MS -Anywhere north of northern California and southern Ontario in winter months we don't get levels of vitamin D we need from the sun

Secondary generalization

-When a focal seizure evolves into a generalized seizure

Bacterial infections

-When bacteria attack the brain they often lead to the formation of cerebral abscesses = pus pockets -Bacteria are cells, living organisms

Concussion

-When there is a blow to the head but no evidence of a contusion or other structural damage -Loss of consciousness often occurs -Form of Mild Traumatic Brain Injury (MTBI) -When diagnosing someone we do so by seeing symptoms of nausea, vomiting, headache

How is Language human-specific

-While many animals demonstrate a rudimentary language, syntax is human specific - grammar rules are an essential part of understanding language in humans -We can train apes to learn a rich vocabularly and convey information using sign language or pressing buttons but they cannot differentiate "Bob hits Jay" vs. "Jay his Bob" -In parrots we say they can have amazing cognitive abilities like categorizing things, understanding concept of zero, knowing how many green blocks there are vs. balls on some plate, neologism - coining a new word to solve a problem you have -Thing that is critically missing is syntax

Arcuate Fascilculus

-White matter tracts that travel between Broca and Wernicke's area - communication in both directions

2 types of generalized seizures

1) Absence seizures: also known as petite mal seizure. Loss of consciousness, cessation of ongoing behaviour, vacant look, fluttering eyelids. -Very common in childhood -Behavioural manifestation - no actual noticeable changes in muscle . tone -See loss/dream-like state -No information you say to them will reach their consciousness -Even though we count them as being generalized, they often do have a focus, but usually we see activity change across entire brain -Individuals can have absence seizure for most of child and will just spontaneously resolve/disappear for rest of your life -Could predict different epilepsy later on in life -Don't fall over, usually maintain posture - continue to sit -Primary cortical tissue rather than deeper -Characteristic spiking pattern: bilaterally symmetrical, 3-per-second spike-and-wave discharge -Often goes undiagnosed since completely resolves 2) Tonic-clonic seizures: Also known as grand mal -Devestating =, make your day-day life unpleasant -Muscles becoming so tight that you are taaking up less oxygen - hypoxive state/low oxygen state and excessive activity- this can cause you to have damage to brain -Most likely to have damage to brain with this type of epilepsy -Loss of connsciousness, equilibirum, really high/strong signals in brian, tongue bitinng, urination, cyanosis, problem with blood -Tonic = tonus, go rigid -Clonic = clonus, shaking -May see this not only in epilepsy, but can happen after brain damage (like within 24 hour hours of car crash)

Threats of open-head injury

1) Actual damage itself (gunshot wound, Phineas gage rod in his brain) 2) Secondary injury - an infection, exposing brain to atmopshere

2 areas involved in language

1) Broca's Area: -Language production -Discovered by patient who had stroke and only could say "Tan" over and over again but had good comprehension of language - cannot produce language. -Tan had localize brain damage around one area near the premotor-prefrontal border, this area became known as Broca's area 2) Wernicke's Area -Parieto-temporal-occipital junction -Comprehension of language -Patients with aphasia that could speak and grammar/syntax relatively in tact, but what was coming out of their mouths didn't make sense - impaired comprehension -Damage here also results in damage to superior temporal gyrus at times - which is auditory cortex, so problems with hearing lead to problems with language

2 ways to deal with aneurysms

1) Clipping: clip the neck of aneurysm so the blood cannot flow into it - we can either remove or leave it there - usually we remove the tissue -In order to clip the aneurysm it requires open-skull surgery -We don't want air in our brain, that's why we have meninges so open-skull surgery isn't reccomended unless absolutely necessary -Longer lasting results 2) Coiling: Not open-skull surgery, relatively minor. Have surgery in feemoral artery and insert catheter that travels into brain and create a coil into anuerysm made of platinum - induces blood clotting and causes it to become solid rather than liquid. Complications from these surgeries are minimal but it's not as effective - won't stop it from growing.

2 types of seizures

1) Focal seizure: most seizures, have point in brain from which they arise. Doesn't involve entire brain, usually localized to a single brain area - won't spread to other regions. 2) Generalized seizure: Involves entire brian *Caution: when it comes to generalized, it involves whole brain but we can see secondary generalizations

3 domains of action clasically considered susceptible to apraxic errors

1) Imitation of gestures (especially meaningless ones) 2) Performance of meaningful gestures on command 3) Real or pantomime use of tools and objects - use in weird way

Behaviours that cannot be expained by sensorimotor hierarchy

1) Individuals with damage to cerebellum - display odd behaviours such as strange gait and problems with coordination 2) Alcohol effects 3) Parkinson's - rigid muscles, tremor, loss of voluntary movement 4) Huntingtons - inability to stop compulsively moving body - reptitive movements, high muscle tone in some parts, cleching jaw very hard, strain on neck muscles - cannot sleep because cannot stop moving 5) Psychostimulants - at high doses lead to purposeless behaviours such as excessive grooming in rats and in humans picking at ourselves and grinding at our teeth -Not all diseases to hierarchy, but still lead to profound changes in motor ability

Steps involved in carrying out a movement

1) Intention/decision/goal 2) Motor plan: often irrespective of body, we can apply a motor plan to numerous areas of the body. "I need a drink of water". 3) Motor signal: what muscles you need to move . to carry out motor plan . 4) Movement 5) Sensory information: gives us feedback - as we move we have stretch receptors - in the skin and hands, that give us a sense of where we are in space (proprioception) >On the way to picking up a cup, there are many corrections we can do to aim our arms in the right way

3 main assertions of the central sensorimotor program theory

1) Lower levels of sensorimotor system hierarchy possess "sensorimotor programs" and those programs represent particular patterns of activity. Contracting certain muscles/sets of . them. 2) A particular movement is produced by activating the appropriate combination of . the sensorimotor programs 3) Once a particular level of sensorimotor hierarchy is activated, it is capable of operating on the basis of sensory feedback without . direct control by the higher levels -Don't have to constantly think about it - do it relatively automatically -Goals: things that start higher level get offloaded into loewr parts of hierarchy so free up parts of higher areas

Why is studying neural basis of language complex?

1) Most of the brain takes part in language one way or another 2) Most patients who add information to studies of language have had strokes, usually of the middle cerebral artery - diffuse affects 3) Immediately following stroke, symptoms are generally severe but improve considerably as time passes 4) Aphasia syndromes described as nonfluent (Broca's) or fluent (Wernicke's) have many varied symptoms, each of which may have different neural basis 5) Normally, when we have a complex, complicated syndrome that we normally only study with brain damage we want to create an animal model so we can understand it better - problem: no other species have language so we cannot create an animal model of aphasia. Most studies are limited to humans and where damage is due to larger, diffuse problems

Forms of dysfunction anosognosia is linked to (4)

1) Movement disorders 2) Contralateral neglect 3) Memory disorders 4) Dysexecutive syndrome (frontal lobe syndrome): disinhibition, impulsiveness, disruptions in planning and certain types of memory (i.e., working memory)

Common components of a neurological exam

1) Patient history 2) Cranial nerve function 3) Motor function (reflexes) 4) Somatosensory function 5) Coordination 6) Mental status

Common misconceptions about brain dysfunction

1) People believe recovery from brain dysfunction depends in large part on injured person's efforts. - You need to maintain a positive attitudee and push through 2) People believe a person with even severe brain dysfunction can recover completely (always limitation on how much you can recover). Brain tissue isn't same as arm, leg tissue and when we lose brain cells they are gone forever - no such thing as full recovery 3) Many misattribute a behaviour (aggression, tired) that is the result of brain dysfunction to the person's personality or life stage. In reality, there are personality changes that can be caused by injury itself. 4) Social psychologists have shown people are more forgiving of person behaviour if have bandage on head because its visible, more visibility of injury=more sympathy. If there's no visible injury we minimize that persons function. 5) Many people believe that emotional problems after brain injury are usually not related to brain dysfunction. Especially if injury is to front of head like prefrontal cortex we will have emotional dysregulation. 6) Many people falsely believe that a second brain injury can restore lost memories in individuals with amnesia. In reality, nature of injury is different so manifestation will be different. 7) Many people believe that people with amnesia are totally normal in every other respect 8) Many people believe that people with amnesia have no trouble learning new info (amnesia is entirely retrograde-loss of memory for events prior to the injury). In reality, we can have anterograde and retrograde amnesia.

Theories of pathogenesis of MS

1) Primarily an autoimmune disease ("outside-in" theory) - immune system attacking cells 2) Primarily a neurodegenerative disease with inflammation in some patients ("inside-out theory) - immune system response may be the result of other neurodegeneration. Cells are dying (neurodegeneration) and with this neurodegenerative part, we see some immune function - not all individuals with MS have this immune response

2 processes that influence learning of sensorimotor programs

1) Response chunking -With practice we carry out motor programs as chunks instead of individual units. -Chunks can be combined into LARGER chunks. -Frees up areas that were involved before -Kid learning to play guitar: must independently think wheree each finger goes and after a while don't have to think about each finger independently, and can automatically play c chord, e tc. -As more things get automatizied/practiced - it gets loewr in hierarchy 2) Shifting control to lower levels -At first when we learn things it involves a lot of conscious thought and planning -Newely learned sequences of finger movements - dorsolateral prefrontal cortexand posterior parietal highly active -After practice, total maount of cortex required gets smaller and eventually don't even need dorsolateral prefrontal cortex - Frees up higher levels of sensory motor system hierarchy to deal with more complex activities of performance such as expression of musical piece rather than performance of each individual note -Allows greater speed. -Different circuits of lower levels can act simultaneously without interfering with one another.

3 principles to think about when testing cranial nerves

1) Sensory: test that sensation (somatosensation - touch skin, vision - test vision) 2) Motor/movmeent ability - can eye move, does musclee still work (provide resistanceo n muscle) 3) Palpating muscle to make sure no atrophy of wasting

DIscuss the challenges involved in interpreting functional brain imaging data

1) Spatial averaging 2) Spatial resolution 3) Temporal resolution 4) Not neceessarily necessity 5) Focus on increases in activity 6) Regional hemodynamics 7) Confound: anxiety 8) Drugs 9) Anticipatory hemodynamics 10) Reliability 11) Statistics

Optic Nerve - Cranial Nerve II test

1) Standard visual acuity tests for each eye: snellen chart: useful for most conditions but under some pathological conditions we may need to use other techniques 2) Visual field confrontation: funduscopy exam. In the fundus we look for unusual shapes such as lots of intracranial pressure that causes fundus to swell. Fundus = part in eyeball opposite to pupil, back of the inside of the eye, including the retina and optic nerve -Macula = larger area around fovea responsible for acute vision -Papilledema and Intracranial pressure: Papilledema is what we get when the optic disk swells, blurred disk margins vs. sharp disk margins in normal optic disk - due to increased intracranial pressure

3 important properties of ischemia-produced brain damage

1) Takes a while to develop - takes one or two days for it to manifest. If we can predict it before that day or two we could prevent some brain injury 2) Damage is more likely in some parts of the brain than in others (e.g. neurons in some parts of the hippocampus since it's a highly active region doing lots of work so very sesnitive to changes like amount of glucose) - srtoke isn't more likely in some parts of brain, it's just that some areas of brain are more sensitive to insult. 3) Mechanisms of ischemia-induced damage vary between brain structures

Treatment for MS

1) Vitamin D supplements - some benefits 2) Corticosteroids - some benefits but comes with many side effects (insomnia, BP) 3) Immune system Modulators some benefit but doesn't stop progression - not beneficial if not having strong immune response 4) Cannabis - helps with muscle tone and rigidity, spasms, using CBD not THC - sativex sometimes prescribed in MS - mix of 50/50 THC and CBD 5) Physical therapy 6) Muscle relaxants 7) Liberation treatment of veins (NO) - italian doctor thought MS problem is reduction of blood going to brain and if we liberate the veins it can help MS - early studies found it helped but after this no evidence. Seems to be no point to liberation treatment. -None are cures :(

Sensorimotor association cortex: 2 areas

2 specific regions: 1) Dorsolateral prefrontal association cortex 2) Posterior parieetal association cortex -Top-most level of what action we want to do - these are the earliest regions/topmost in our hierarchy -Dorsolateral and posterior parietal are actually clusters of nuclei in reality

Viral infections

2 types: 1) Those with particular affinity for neural tissue 2) Those that attack all tissues indiscriminately, include nervous tissue -Virus = cluster of proteins with RNA/DNA inside that takes advantage of cellular machinery to reproduce

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Confound of anxiety in fMRI

Confound: anxiety, claustrophobia - need to use a cage that keeps your head still. -Falling asleep, boredom -A statistical issue with fMRI studies, where the baseline level of arousal goes up when you put someone in a scanner, which makes studies difficult

Testing Glossopharyngeal nerve (IX) and Vagus neerve (X)

Glosspharyngeal: -The tongue -First 2/3 of tongue -Gets taste information and important for pharynx (using our speech) Vagus: -Swallowing and voice -Gag reflex -Hard to test its control on viscera -Ask patient to cough -Ask patient to open his mouth and say "AAA" upon instruction - palate should move upwards -Observe uvula position - should be in centre

Top-down vs. Bottom-up causes of movement

Top-down: process is being generated in brain first and makes sense of that idea - "I'm looking for my friend" - this is the idea, and your movements will be voluntarily driven and conscious -In fMRI: frontal eye field and supplementary eye field are active when we are trying to look for someone Bottom-up: taking basic features of the world and putting it together into a more complicated thing. Blinky flashy TV drawing your attention non-voluntarily - can try to suppress but still incliniation to look there. -Driven by superior colliculus of midbrain - visual stimuli