Study Prep PDF

 Connected to p Vestibulocerebellum (oldest)  helps control balance, posture and eye movements Connected to m  inputs from vestibular nuclei (sensory side) pedunc...

 Connected to p Vestibulocerebellum (oldest)  helps control balance, posture and eye movements Connected to m  inputs from vestibular nuclei (sensory side) peduncles Has 3 lobes: an  outputs to thalamus (to cortex) and vestibular nuclei which project to muscles (e.g. anti-gravity and trunk musculature, muscles controlling eyes) nodular  primarily is the flocculo-nodular lobe Has deep nucle  descending output from the vestibulocerebellum is relayed through brainstem reticular formation and vestibular nuclei (remember nin  postural stability Dentate nuc Spinocerebellum (middle aged)  functions to compare planned movement to actual movement and helps create an “error” signal to correct the movement if necessary  receives inputs from the spinal cord -the dorsal spinocerebellar tract (primarily sensory) -the ventral spinocerebellar tract (copy of motor drive to motoneurons)  Output from spinocerebellum is relayed through the interposed nuclei (=globose and eboliform nuclei) of cerebellum and projects to contralateral brainstem Red nucleus ( Rubrospinal tract) Cerebrocerebellum (newest) or ipsilateral to the side of unilateral cerebellar damage (e.g. when one limb affected). 1nystagmus (spontaneous eye movements) and vertigo (spinning sensation 'dizziness') 2ataxia (staggering gait); wide based stance ‐compensation for poor balance 3 failure of rapid alternating movements (“dysdiadochokinesia”) ‐(e.g. supination/pronation of the hand) 4intention tremor ‐worsening tremor during precise voluntary movements 5 Poor targeting of movements: Past‐pointing: inability to place a finger accurately on a selected point. Dysmetria: overshoot or undershoot of intended position (can be hand, eye or limb) ‐poor  Globus pallidus External segment Internal segment Subthalamic nucleus Substantia nigra There is a “direct pathway” that removes inhibition of the thalamus  enhanced activity in th motor cortices There is an “indirect pathway” that ends up inhibiting the thalamus  decreased activity in th motor cortices Increased activity in the indirect pathway, and reduced activity in the direct pathway,  Hypokinesia E.g. Parkinson’s disease Increased activity in the direct pathway, and reduced activity in the indirect pathway,  Hyperkinesia E.g. Huntington’s disease Basal Ganglia Dysfunction manifest in 3 ways: 1) Hypokinetic movement disorders e.g. Parkinson’s disease 2) Hyperkinetic movement disorders e.g.’s Huntington’s disease, Hemiballismus, Athetosis, Tourette syndrome (?)  neurodegenerative disease; idiopathic Parkinsonism: Symptoms: A syndrome of symptoms comparable to re  resting tremor (not intention tremor) Parkinson’s disease that are caused by loss  Rigidity (cogwheel rigidity) of dopaminergic neurons due to toxins,  slow movements (& difficulty initiating vascular damage, or inflammatory changes. movements)- bradykinesia May occur earlier in life  shuffling, slow gait, with stooped unsteady posture Parkinsonism (aka Secondary  masked facial expressions=muted Parkinsonism)causes: expression  Drugs (antipsychotics, large dopamine antagonists)-usually resolves after drug is It is a chronic and progressive disorder stopped produced by loss of dopaminergic neurons  Toxins (i.e MPTP cause irreversible damage to of Symptoms may have the substantia “ON” nigra. Alsoand “OFF” see Lewy dopaminergic neurons)- toxic b/c mitochondrial periods bodies whereaggregates (protein a patient fluctuates abnormal in dysfunction and free radical production between relatively symptom free (= on) cortex)  Infections (post encephalic syndrome, viral vs. incapacitated (=off). illness that causes degeneration of substantia nigra neurons)  Injury/trauma (vascular damage in basal ganglia, torsional damage, ventricular pressure Parkinson Tx: goal is to minimize symptoms on basal ganglia) 1. Pharmacological Treatment a) L-DOPA MOA: cross the BBB, increases dopamine release at remaining synapses Provides few years of therapeutic efficacy, not a cure because it relies on Disorder Features Due to Chorea Rapid, jerky, irregular involuntary movement Bilateral wasting of the often in the distal limbs or face putamen and caudate or choreoathetosis nucleus, cortical (athetosis = twisting, Seen in Huntington’s disease degeneration writhing movements) Hemiballism/ Involuntary proximal jerking, flinging limb Lesion of the Hemibalismus movement contralateral subthalamic nucleus Myoclonus Rapid, brief, irregular movements, usually multifocal Can occur spontaneously, in response to sensory stimuli or w/ voluntary movements can occur in a wide variety of metabolic and neurologic disorders (including BG dysfunction). can also occur in healthy people (e.g’s hiccups, twitching during sleep) Athetosis a constant succession of slow, writhing, usually caused by involuntary movements of flexion, extension, extrapyramidal lesions Disorder Features Due to Dystonia (general term Sustained muscle contractions Basal ganglia dysfunction encompassing the below with twisting, repetitive disorders) movements or abnormal postures Torticollis “wry neck” is an abnormal, Congenital or acquired asymmetrical head or neck position (twisted neck) Task-specific Dystonia (Focal A focal dystonia that appears Dystonia) during particular tasks; often tasks the person has spent a long time doing (i.e writing) Iatrogenic Movement Disorders: “Iatrogenic” = illness caused by a medical tx (often neuroleptic drugs, particularly antipsychotic meds (often block dopamine receptors so can  basal ganglia symptoms)) Disorder Features Due to Tardive Dyskinesia Involuntary movements of the can be a persistent late External Ear: Funneling/focusing of sound waves Temporal Lobe: is location of audi Important in localization of sounds Wernicke’s area: Middle Ear: Mechanical conversion of sound waves to pressure  Impt in understanding speech waves.  A pt with Wernicke’s aphasia is n 3 bones maleus, incus, stapes not understand language Input – vibration in tympanic membrane  They may speak a lot, but it does Output = movement of oval window (“word salad”) Inner Ear: Pressure waves converted to neural signal (i.e transduction) Location of sensory receptors on basilar membrane (hair cell mechanoreceptors- “organ or Corti” hair cells) CN 8  Vestibul ocochle “tonotopic” ar organization of nerve the basilar Types of Hearing Loss: Tests for Conductive vs Sensorineural  Conductive: failure in the transmission of Deafness: sound wave by the middle ear (mechanical Weber Test: problem)  Normal: vibration is ‘heard’ equally in both ears  Sensorineural: failure to transduction within  Conductive hearing loss: the vibration and/or transmission from the cochlear apparatus is louder in the ear with hearing loss Also, could be damage to CN 8  Sensorineural hearing loss: the often  tinnitus = 'ringing' in ears, or hearing other vibration is louder in the unaffected or sounds (pulsing, humming, clicking etc) that aren't opposite ear really there. caused by: aging (presbycusis = age related Rinne Test hearing loss),  Normal: air conductive (AC) is ~2x longer than bony conduction (BC)  Mixed Hearing Loss: combination of conductive  Conductive hearing loss: BC > AC (#1) and sensorineural (#2) hearing loss.  Sensorineural hearing loss: AC > BC, but the times of both are much  Central Deafness: when there is damage within the shorter central neural pathways (such as brainstem or cortex) Rare sometimes called 'deaf-hearing' because even though patients may not have sound awareness, they may have reflexive responses to sound.  Vestibulo-Ocular Reflex: works in horizon In the semicircular canals is endolymph 1.Head Moves → Inner Ear Detects Motion (movement detects rotational movement) 1. The vestibular system in your inner ear sen The bending of the stereocilia is done by 2.Signal Sent to Brain → Eyes Adjust Opposite movement of the endolymph 1. The brain processes the movement and tells Movement of the ampulla bending of the 2. Example: If your head turns left, your eyes m hair cell stereocilia 3.Result → Clear, Stable Vision Rotating the head  movement of endolymph 1. This happens automatically and very fast relative to the ampulla  increased firing in one CN VIII, and VOR is controlled by cerebellum. Coordination done b decreased in firing in the other CNVIII Ampulla-location of sensory receptors (mechanoreceptor) Bending them one way  depolarization Vertigo: sensation of whirling or spinning of th Bending them the other way  hyperpolarization Nystagmus: a repetitive movement of eyes left-right = horizontal nystagmus Utricle (horizontal orientation & Saccule up-down = vertical nystagmus (vertical orientation) (the otolith organs) all around = pendular nystagmus  Think of the otoliths like a tablecloth with marbles on top. It will be slow in one direction and fast in the ot If you tilt the table, the marbles roll, pulling So if you have slow moving left, and fas the cloth with them. To tell if it's right-beating or left-beating nysta Similarly, otoliths move and bend the Nystagmus can be evoked in healthy Nystagmus: individuals by: a healthy response to an unusual 1. Excessive rotational accelerate (i.e vestibular stimulus (e.g. a ride at an spinning) amusement park) 2. Caloric stimulation of the vestibular an unhealthy response to a normal apparatus (cool or warm water in ear canal vestibular stimulus (e.g. occurs COWS → Cold Opposite, Warm Same spontaneously) Warm water (44°C): Causes the endolymph to rise, mimicking a head turn toward the stimulated ear → Nystagmus to the same side. Cold water (30°C): Causes the endolymph to sink, mimicking a head Peripheral Vestibulocochlear Dysfunction: turn away from the stimulated ear vestibular apparatus damage or nerve damage → Nystagmus to the opposite side. So, loss of both auditory and vestibular function 3. Optokinetic stimulation of VOR (visually suggests damage to the end organ, or CN 8 following a moving pattern) You can get: sensorineural deafness, vertigo, 4. Toxicity (i.e alcohol) nystagmus, balance disturbance, tinnitus (=hearing ringing) Central Vestibulocochlear Dysfunction: since auditory is processed bilaterally in cortex, unilateral lesions of auditory cortex will not produce deafness (but they will have loss of auditory discriminatory capabilities) Oculocephalic reflex: Caloric Vestibulo-ocular reflex: Rotate the head in one direction, the eyes Elevate head to 30 degrees (brings semicircular should deviate in the opposite direction. The canal into a position to maximize the deviation should be smooth and conjugate response), infuse cold water into the ear canal. (both eyes move to same visual field) When cooled, semicircular canal apparatus normally this reflex is suppressed if we interprets this as movement (= rotation) in are conscious The oculocephalic reflex shows an intact the opposite direction. VOR system Eyes reflexively move towards the side being cooled. Note: if you do this in a conscious person, it causes slow eye movements to the side being cooled, but then a fast sacchade is produced to move the eyes back Corneal Reflex: = nystagmus. Wisp of cotton touched to cornea should  The Caloric activation provides a stronger bilateral eyelid closure. activation of the VOR than rotation of the head afferent sensory information in CN 5  activation of motor efferents in CN 7 1.Key Nerves Involved: 1. CN 3 (Oculomotor Nerve) in the midbrain: Controls the medial rectus, which moves the eye inward. 2. CN 6 (Abducens Nerve) in the pons: Controls the lateral rectus, which moves the eye outward. 2.Interconnections (MLF): 1. The medial longitudinal fasciculus (MLF) links CN 3 and CN 6, coordinating their actions to ensure both eyes move together. 3.Brainstem Pathways: 1. The pons and midbrain must work properly for smooth, coordinated horizontal eye movements. 4.In6 Coma: CN moves lateral rectus when we turn our heads to the left, this activates pontine gaze centre 1. If awhich (nuclei), comatose patient shows then activates CN 3 spontaneous through MLF tohorizontal move the righteye movements, medial rectus it someans both our their pons and eyes are midbrain gazing to thepathways left are still functional. Inter‐nuclear Opthalmoplegia (INO) demonstrates failure of this system of  conjugate eye movements Most commonly produced by damage to the MLF (X) The cortex can activate CN 6 via the pontine gaze center, and activate lateral rectus, but the activation of CN 3 for the contralateral eye is disrupted due to damage of the contralateral MLF INO can be unilateral equal actions of Left and Right cortex keeps the eyes centered a voluntary eye movement results from activating one cortex more than the other right cortex activates pontine gaze center on left side of brainstem and would  eyes to look left right cortex damage: Left paresis, & eyes deviate to the right (eyes look towards the damage side)  Accommodation-Convergence Reaction: Autonomic control of Pupil size: When you look at something close, 3 things happen simultaneously: PNS  constriction (miosis) of sphincter pupillae m. 1. Accommodation: From midbrain Edinger Westphal n. (CN3) lens is thickened to focus the near object on the retina (th SNS dilation (mydriasis) via dilator iridis m. “focal distance” of the system is adjusted. At rest, our pupil size is a balance of PNS and SNS 2. Convergence of the 2 eyes: there is activation of the medial rectus bilaterally (and relaxation of lateral rectus) Accommodation: in order to keep the this puts the image of the near object on the fovea of both image for close object in focus on the retina, retinas your eye needs to bend the light more (more refraction) 3. Pupillary constriction This done by contraction of the ciliary the pupils of both eyes constrict this limits stray light entering the eye muscle around the lens, which causes increases the depth of fi eld that is in focus it to become thicker  increased refraction “Round for Reading” “Flat for Far” Trying to get our vision to be: Far source: can see w/o accommodation Near source: can see w/ some accommodation Nearsightedness (me): use concave lens Farsightedness: use convex lens Photoreceptors:  Rods: Vitamin A deficiency: Have a very large outer segment = Carotene can be converted to Vitam particularly specialized to capture light. The retinal molecule of rhodops Are the primary photoreceptors conveying Vitamin A vision in dim/dark conditions Thus, deficiency in Vit A  lo  Cones: blue, red, green photoreceptors night blind There are 3 types of cones, each with a Severe dryness of the eye (xeropht different photo-pigment  colour vision and erosion of the cornea  blindne Are the primary photoreceptors conveying High incidence of Vit A deficiency in vision in bright conditions staple A leading cause of childhood blindn developing countries Transduction of Neural Signal Colour Blindness: Light hits retinal → Retinal changes shape caused by partial or total loss of 1 or mor Activates rhodopsin → Activates G protein true and complete “colour blindness” is very (transducin) o most commonly caused by congenital d Closes Na+ channels → Changes neurotransmitter 2 n d for the second (=green) class of con release  “red‐green” colour blindness (= deuteranop genes for opsin proteins are on X chrom Signal is sent to the brain → We see light! blindness is much more common in me 7‐10% of men have red – green colour b ***Rhodopsin is contained in the outer segments of rod cells and is a complex of a large protein “opsin” and The retina hassmall “retinal” other cells involvedmolecule in processing  Photoreceptors:  Rods: only 1 photopigment used “shades of grey” Have a very large outer segment = particularly specialized to capture light. Higher sensitivity to light than cones  better low light sensitivity ( = night vision “scotopic vision”) Are the primary photoreceptors conveying vision in dim/dark conditions Photopigment bleaches in bright conditions (this is why our night vision takes a while to improve after being in bright light) Disruption  night blindness  Cones: blue, red, green lower light sensitivity than rods There are 3 types of cones, each with a different photo-pigment/ wavelengths  colour vision Highly concentrated in fovea and macula  high resolution colour vision ( = “photopic” vision) in bright conditions light, but notDisruption --> colouryou truly dark conditions; blindness use “mesopic” vision (both rods and cones used) Melanopsin: newly discovered opsin respond to light, might be signal for alignment of circadian rhythm to day/night cycle may be preserved in most blind people and explain why they have preserved circadian Myopia = near sightedness dust or other health problems Far source: not focused on retina w/o accommodation severe in vitamin A deficiency Near source: focused on retina w/o accommodation Colour Blindness = usually poor red/green discrimi Hyperopia = far sightedness due to hereditary absence of red or green Far source: focused on retina w/ accommodation photoreceptors (more common in males) Near source: focused on retina w/ accommodation Night Blindness (Nyctalopia) = poor vision Presbyopia = stiffening of loss with aging loss of low light conditions accommodation can be caused by lots of things E.g. Longer and longer focal distance (year by year as lens nearsightedness, glaucoma, cataracts, cong gets stiffer) defects in rod system, retinitis pigmentosa, v Corrected with ‘reading glasses’ A deficiency (and others) Astigmatism = part of cornea or lens has a different Diplopia = double vision diffractive index, so part of the image is focused either eyes not targeted to the same location in front of or behind the retina can be  impaired neurological or mech the eyes Glaucoma = increased internal pressure in the eye Passages normally allowing draining of fluid in Strabismus = crossed eyes eyes becomes blocked both eyes not directed to same place May damage the nerve fibers exiting the eyeball usually from poor eye muscle control via the optic nerve  vision loss brain learns to ignore one image so may Scotoma = particular area of visual field ual Pathway: Retina  Lateral geniculate nucleus (LGN)  visual cortex (occipital lobe) Ganglion cells form CN 2 (optic nerve) Optic nerve projects to LGN in thalamus, pretectal area, and superior colliculus LGN projects to visual cortex (occipital lobe) via geniculocalcarine tract (aka the optic radiation) Visual Fields: those from the lateral side of the retina stay on the same side those from the medial (nasal) side of the retina cross at the optic chiasm Different Lesions  Different deficits Eye Movements: Extraocular Muscles: Sacchade: quick “darting” eye movements. (i.e scanning a face) Pursuit movements: slower movements used to CN 3: Oculomotor Nerve flow something moving in visual field Superior Rectus- elevate eye Medial Rectus- adducts eye Movements that stabilize the eye when the head Inferior Rectus- downward gaze moves: Inferior Oblique- elevate eye Vestibulo‐ocular use vestibular input to hold images stable on retina during brief / CN 4: Trochlear Nerve rapid head rotation (i.e. the VOR) Superior Oblique- wants to go down Optokinetic use visual input to hold images stable on retina during sustained or out slow head rotation CN 4 palsy-the SO is damage the IO is unopposed and so t Movements that keep the fovea on a visual target: moves up Sacchade Results in diplopia, so pe Quick jumps to bring new things into focus (i.e when reading) head to compensate, so t Pursuit movements (smooth pursuit) other eye when tilted will holds the image of a moving target on the fovea (i.e tracking a bird) to match the damaged ey Vergence (Convergence is a type of vergence) adjusts the eyes for viewing objects at diff erent distances CN 6: Abducens Nerve E.g. convergence while looking at a near object Lateral Rectus- abducts eye Consciousness: The state of being aware or perceiving Coma causes: Large areas of cortical dysfunction physical facts or mental concepts; a state of general Small lesions of the brainstem wakefulness and responsiveness to environment; a 4 lesions, all producing coma and e functioning sensorium. death: Cerebral hemisphere + thalamu Stupor: A state of impaired consciousness in which the Midbrain individual shows a marked diminution in reactivity to Pons environmental stimuli and can be aroused only by continual Medulla stimulation. How to differentiate between 1 & 2? C Coma: A state of profound unconsciousness from which one nerve exam helps identify different br cannot be roused; may be due to the action of an ingested lesions toxic substance or of one formed in the body, to trauma, or Sleep: two main stages to disease. Look at brainstem reflexes. If intact Non-REM: cortical dysfunction. Several stages from light sleep (Stage 1) to deep  E.g.’s of Brainstem reflexes: sleep (Stage 4) o pupillary light reflexe As you go 14: EEG activity slows, gets more syn o spontaneous and elicited eye m chromized and has larger spike activity o respiratory pattern REM: o Corneal reflex Limb and body motoneurons are inhibited so o Nociceptive reflex (i.e eyebrow) normally there are no movements and muscle o Gag reflex tone is very low. EXCEPT for extraocular Pupils in Coma: muscles ‐‐ one can observe rapid eye movements  Symmetrical and reactive round beneath the closed eyelids. pupils  usually exclude midbrain  Motor response to noxious stimulus: Respiration in Coma: resp system is a noxious stimulus (normally perceived as painful in brainstem, normally responds to evoke a motor reflex increasing blood CO2, by increasing RR “localizing response” vs flexion withdrawal vs othe and depth vs extension vs no response Better 1.Localizing Response: 1. The person moves their hand directly to the sit stimulus to try and remove it. 2. This shows higher brain function. 2.Flexion Withdrawal: 1. The person pulls their limb away from the stimulu aiming at it. 2. This is a reflexive action that involves the spina basic brain processing. 3.Other Postures: 1. Abnormal postures like decorticate (arms bent) Movements in Coma: tonic posture can occur decerebrate (arms straight and stiff) indicate seri spontaneously damage.  Deceberate posture: elbows extended; 4.Extension Response: wrists flexed 1. The limb extends instead of pulling away. This can Indicates damage to brainstem severe brainstem injury.  Decorticate posture: legs extended, 5.No Response: 1. No movement at all means severe damage or d elbows flexed, arms may move when head the nervous system. is rotated by examiner Summary: The more specific and purposeful the respons  Glasgow coma scale The Glasgow Coma Scale (GCS): is a neurological scale used to give a reliable, objective and repeatable recording of a person’s state of consciousness. It assesses 3 elements: Eye opening; Verbal response; Motor response (E,V,M) Each are rated on a numeric scale. Add together the scores: E + V + M lowest score possible is “3” score or 8 or less, considered comatose score of 3 or 4 has a very poor prognosis (~85% or more die or remain in vegetative state) is useful for tracking changes over time example here shows a deterioration! 13, 9, 7 Brain Herniation: is when a part of the brain moves from where it would normally be. i.e to a different area of the skull  Can be caused by: Brain Death: Increased intracranial pressure being permanent loss of cerebral and brain stem exerted on brain (from swelling, function, manifested by absence of intracranial bleeds, tumors, etc) responsiveness to external stimuli, absence of  Several types of brain herniation cephalic reflexes, and apnea. An isoelectric (flat o Supratentorial Herniation: the line) electroencephalogram (EEG) in the absence innermost part of temporal lobe of hypothermia and poisoning by CNS depressants (=“Uncus”) is pushed down along the margin of the tentorium 1. Uncal herniation/Transtentorial Persistent Vegetative State: herniation (same thing Complete unawareness of the self and environmen different word) ‐complete or partial preservation of hypothalamic an Pressure to be exerted on autonomic functions ‐no sustained, reproducible, purposeful or voluntary CN3 and brainstem you get responses to visual, auditory, tactile or noxious s oculomotor nerve palsy and ‐no evidence of language comprehension or express deteriorating brainstem But there are sleep / wake cycles. function A vegetative state is considered “persistent ” if > 4 Symptoms: down and out eye ptosis  tend to also exert influences on the contralateral side of the body Organized into 4 lobes:  Frontal  Parietal  Occipital  Temporal Frontal Lobe: movement and motor planning, Damage to Frontal Lobe: personality, decision making contralateral paralysis / paresis i. Primary motor cortex (= precentral gyrus) apraxia Location of “motor homunculus” ‐inability to perform complex motor tasks ii. Premotor corte and supplementary motor disturbances in micturition tern cortex (=motor association cortex) ‐incontinence, or inability to initiate micturition In front of primary motor cortex Broca’s aphasia Involved in programming complex ‐usually affecting both speech and writing (agraph personality changes movements Premotor area dedicated to speech formation ‐apathy, inappropriate behaviour iii. Broca’s area: impaired memory, declining intellect Lateral/inferior aspect of frontal lobe ‐frontal lobe degeneration common in dementia Involved in production of language (both written and spoken) iv. Prefrontal association cortex (prefrontal cortex=rostral poles of frontal lobe) Imparts our “personality”, drive/motivation, decision making Parietal Lobe: sensory processing Occipital Lobe: visual system proce i. Somatosensory cortex (=post central i. Primary visual cortex gyrus) At the caudal (tail) pole o Immediately behind the central sulcus occipital lobe (front of the parietal lobe) Processing visual info Location of “sensory homunculus” ii. Occipital association cortex (= ii. Posterior parietal cortex order visual cortex) Behind the somatosensory cortex Surrounding the primary v Integration of somatosensory and cortex visual inputs (NB for complex Involved in integration of movements) and controlling eye move iii. Parietal –temporal-occipital association cortex (=parietal association cortex) Occipital Lobe Damage: Behind the posterior parietal cortex  Visual field deficits: Integration of sensory info from E.g. Homonymous he temporal, Parietal Lobe parietal, and occipital lobes Damage: (if unilateral damage sensory (auditory, ”cortical blindness” if deficitsvisual, and sensory information)  Visual agnosia: failure of vi poor localization of sensation to a body area, deficits in proprioception and 2-point recognition. May have to touc discrimination to recognize it. agnosia (inability to recognize objects)  Altered eye movements-(l there are different types… e.g. visual optokinetic control) agnosia, or if they can’t recognize by touch, = Temporal Lobe: Auditory processing, language processing, loop of visual fibres. i) primary auditory cortex processing auditory information (with surrounding temporal cortex) ii) Wernicke’s area between primary auditory cortex and parietal lobe important for language comprehension iii)some ascending visual fibers (part of geniculocalcarine tract / optic radiation, = Meyer’s loop) Meyer’s loop is the portion of the optic radiation that passes through the Damage to Temporal temporal lobe Lobe: visual field deficits (b/c Meyer’s loop) Auditory deficits: usually not deafness, but more often complex deficits. e.g. can hear tones, but not recognize speech or music Wernicke’s aphasia: ‐speech disorder (aphasia) with a Aphasia = impairment of language Apraxia = impaired ability to performin can be impaired production of language, skilled motor task comprehension of speech or the ability to read or write But, consider all the steps involved: Executive functions: motivation Broca’s aphasia: “non-fluent aphasia” expressive aphasia reasoning. halting effortful speech and difficulty writing Praxis: making the movements c impaired vocabulary right sequence. but they understand speech and know what they Memory / experience with the t Object recognition. want to say! often this is very frustrating for them Visual and spatial integration. patient can have aphasia but may understand Attention: is focus on the task? Sensory feedback to help guide you perfectly (so be careful what you say!) Proprioception Wernicke’s aphasia: “fluent aphasia”, receptive Therefore, dysfunction (e.g. from stroke) aphasia cortical areas or levels of the brain can  lack of comprehension of language Can they understand what you’re asking often words can be spoken, but often strung motivated, can visually see what you’re together in a nonsensical way “word salad” Split Brain: the two sides of their brain are working in isolation from one another Corpus callosum is bundle of axons connecting the 2 cerebral hemispheres. this  surprisingly few functional deficits