Aphasia/Neurology Test 1 – Flashcards
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Aphasia
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An acquired communication disorder caused by brain damage, characterized by an impairment of language modalities: speaking, listening, reading, and writing; it is not the result of a sensory or motor deficit, a general intellectual deficit, confusion, or a psychiatric disorder.
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Cognitive-linguistic processes
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aphasia, right hemisphere disorders, TBI, language of confusion, language of generalized intellectual impairment
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Motor speech programming
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apraxia of speech
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Neuromuscular exectuion of motor speech
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dysarthria
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Family of disorders involved with Aphasia
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spoken language expression, spoken language comprehension, written expression, and reading comprehension
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Aphasia
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Relatively intact nonlinguistic cognitive skills but possibly has sensory deficits such as auditory and visual agnosia and visual field deficits
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Etiology of aphasia
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Cerebrovascular accident (stroke), TBI, brain tumor growth (neuroplasms), surgical removal of brain tissue, infection, progressive processes; ALWAYS ACQUIRED
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Incidence of aphasia
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25-40% of people who survive a stroke have aphasia (about 55% L hemisphere)
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Role of SLP
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Providing prevention for at risk groups Educating professionals on needs of person with aphasia Screening people who show a language difficulty and determining further assessment and/or referrel Assess, diagnose, develop treatment plan Counsel patient and family Remaining informed of new research on aphasia Advocating for individuals with aphasia
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Role of neurons
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Receive signals, conduct signals, transmit signals
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Types of neurons
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sensory, motor, inter
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Synapse
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Space between 2 nerve cells used for transmission of impulse
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Action potential
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Neuron fires below threshold, reaches a stimulus and depolarizes until it reaches this. It is then repolarized, goes into a refractory period and reaches a resting state before firing again.
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Axo-dendritic synapse
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Most common synapse
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Axo-somatic synapse
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Less common synapse
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Axo-axonic synapse
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Rare, presynaptic inhibition
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Dendro-dendritic synapse
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Rare, local inhibitory feedback circuits
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Myelin
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Insulation surrounding axons, promote impulse, Node of Ranvier in between (CNS=oligodendrocytes, PNS= schwann cells)
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Central Nervous System
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Brain and spinal cord (tract, pathways, between neurons = neuron groups)
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Peripheral nervous system
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Cranial nerves and spinal nerves (nerve, between CNS and end organs (muscle, etc.) =neuron groups)
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Transverse plane
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Superior/inferior
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Coronal plane
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Anterior/posterior
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Sagittal plane
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Medial/transverse
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Prosencephalon
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Forebrain
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Forebrain
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Telencephalon (cerebral hemispheres/basal ganglia) and diencephalon (thalamus/hypothalamus)
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Cerebrum
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L/R hemispheres, basal ganglia, limbic lobe, cortex (outermost layer)
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Frontal lobe
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Pre-central gyrus (primary motor cortex/motor strip and contralateral control of muscles), pre-motor cortex and supplementary motor areas, pre-frontal cortex
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Precentral gyrus
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Area of representation depends upon complexity of movement (lower 1/3 represents part of face/throat, legs go down into the longitudinal fissure)
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Broca's area
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Responsible for the fluent production of speech (44/45)
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Parietal lobe
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Post-central gyrus (primary sensory cortex/sensory strip and contralateal sensory input), association areas for sensory and visual processing, VERY LATERALIZED (R hemisphere= attention and spatial processing)
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Supramarginal gyrus
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Around posterior end of sylvian fissure (40); damage could lead to problems in reading, writing and math
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Angular gyrus
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Posterior to supramarginal gyrus (39); damage could lead to problems in reading, writing, and math
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Primary sensory strip
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1, 2, 3
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Temporal lobe
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Auditory processing, superior/middle/inferior gyri, Heschl's gyrus (primary auditory cortex, transverse (41/42))
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Wernicke's area
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Posterior portion of superior temporal gyrus, auditory association area, important in development and use of language (22)
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Occipital lobe
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Concerned with vision, primary visual cortex (17)
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Insula
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Role is less understood, insults can impact language, activated during attention, language, speech, and working memory, damage can induce aphasia, has 4 distinct regions: social emotional, sensorimotor, olfactory, and gustatory
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Commissural connection
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Across 2 hemispheres
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Association connection
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Within one hemisphere (short= within lobes/ long= between lobes)
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Projection connection
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Between different areas (ex: cortex and lower brain or spinal cord)
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Basal ganglia
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Collection of cell bodies at the base of cortex, associated with motor control of tone and posture
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Cerebrospinal fluid
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Produced by the choroid plexus, drainage occurs in subarachnoid space
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Hydrocephalus
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Abnormal collection of cerebrospinal fluid
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Pyramidal tract of motor control
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Voluntary control, upper motor neurons (corticospinal/corticobulbar tracts), lower motor neurons
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Extrapyramidal tract of motor control
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Involuntary control (selective activation of movements and suppression of others, initiation of movements, setting rates/force of movements, coordination of movements), damage can result in tremor, tics, chorea, or other uncontrolled body movements
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Midbrain
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Mesencephalon, with hindbrain = brain stem
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Hindbrain
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Metencephalon (pons, cerebellum), myelencephalon (medulla oblongata), with midbrain = brain stem
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Medulla
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Base function of life (i.e. heart rate, breathing, etc.)
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Limbic lobe
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Fear responses, making memories, etc.
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Brain stem
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Midbrain and hindbrain
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Diencepalon
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Thalamus (sensory info. goes through and funnels to te right places), hypothalamus (link between nervous and endocrine system), epithalamus (sleep cycles), subthalamus
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Cerebellum
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2 hemispheres, postural stability, motor learning/coordination
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Meninges
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Layers surrounding brain tat protect it and remove waste (Medial to transverse: pia mater, subarachnoid space, arachnoid mater, dura mater, skull (bone), skin
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Ventricular system
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Extracts cerebrospinal fluid from blood and circulates only products of CNF, (lateral ventricles, third ventricle, fourth ventricle, subarachnoid space, choroid plexus)
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Choroid plexus
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Produces cerebrospinal fluid
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Upper motor neurons
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Damage will show to be the same initially and then move to hyperflexibility, spasms, and neuron firing with out inhibition
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Lower motor neurons
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Brain stem muscles, damage causes weakness, flacidity, and atrophy
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Risk factors for aphasia
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Medical (hypertension, heart disease, diabetes, high cholesterol) Lifestyle factors (smoking, stress, inactivity, alcohol, etc.) Demographic (sex differences, handedness, age) Regional difference ("stroke belt") Race/ethnicity/SES/cultural factors
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FAST
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Face drooping, Arm weakness, Speech difficulty, Time to call 911 (sudden numbness, sudden confusion, sudden trouble seeing, sudden trouble walking, sudden severe headache)
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Infarct
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Area of dead tissue
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Ischemic/Occlusive stroke
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Thrombotic, embolic, or temporary (TIA)
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Thrombotic stroke
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A local accumulation of cells along the wall of a blood vessel, blood clumps in specific place
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Embolic stroke
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Plaque, bacteria, etc. travel from elsewhere and get lodged and block blood flow
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Temporary stroke
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"Warning/mini stroke", temporary occlusion that resolves within 24 hours
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Hemorrhagic stroke
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Rupture of a blood vessel and applies pressure on the brain (aneurysm, arteriovenous malformation, trauma)
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Aneurysm
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Weakening of vessel wall, usually affects internal corotids
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Arteriovenous malformation
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2% of hemorrhagic strokes, absent capillaries, tangled arteries/veins, weak walls with high internal blood pressure
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Trauma causing hemorrhagic stroke
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Often results in diffuse damage
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Location of hemorrhage
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Epidural (not w/in tissue, not as common), subdura (not w/in tissue, not as common), subarachnoid (blood in space), intracerebral (bleed w/in body of brain)
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Neoplasms
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Benign (won't spread), malignant (will spread), primary (starts in the brain; gliomas/meningiomas), metastatic (start elsewhere and end up in the brain; lung/breast/melanoma)
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Mechanisms of CNS symptoms
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Tumor invades, irritates and replaces normal tissue Tumor and subsequent edema compress normal tissue and its blood vessels, causing ischemia Tumors in the 3rd or 4th ventricle obstruct CSF pathways, causing hydrocephalus (ventricles enlarge by excess of CNF)
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TBI
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Penetrating (may cause aphasia depending on where) Closed head (cognitive/communicative disorders, language impact tends to be more related to discourse/pragmatics)
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Language basics
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Information stored in patterns of neuronal activation, learning = strengthening, graceful degradation, thought and language are not synonymous (there's ambiguity)
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Lemma
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Lexical item to represent a concept (could be a phrase vs. a word)
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Syntax
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Language input (ex: the dog bit the man vs. the man bit the dog)
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Phonemes
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Output (sounds)
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Hickok and Poeppel
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Attempts to synthesize what is known about the anatomy of language into a comprehensive model, only describes single word comprehension/single word repetition
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Dual stream model
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Ventral stream (comprehension) and dorsal stream (repetition)
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Processing sounds
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Auditory cortices bilaterally (41/42), not symmetrical
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Ventral stream (comprehension)
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Bilaterally organized but weak left bias, lexical interface (links a phonological sound and distributes semantic info.) and higher level interface (syntax, combination network), NOT FOR SINGLE WORD
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Dorsal stream (repetition)
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Left hemisphere dominant, articulatory network, auditory motor interface
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Trigeminal nerve
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CN V, mastication and sensation to the face, teeth, gums and anterior 2/3 of tongue
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Facial nerve
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CN VII, all movements of facial expression: eyes, nose, mouth, external auditory
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Acoustic nerve
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CN VIII, equilibrium/hearing
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Glossopharyngeal nerve
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CN IX, taste, swallowing, elevation of pharynx, larynx, sensation to posterior tongue, upper pharynx
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Vagus nerve
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CN X, taste, swallowing, elevation of palate, phonation, parasympathetic outflow to viscera organs
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Accessory nerve
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CN XI, turning of head/shrugging shoulders
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Hypoglossal nerve
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CN XII, movement of tongue
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Aphasia info
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Onset is sudden, it involves multiple language modalities, results from damage to the CNS, motor, sensory, and cognitive impairment may coexist but do not explain language deficit
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Classifying aphasia
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Fluency, auditory comprehension, auditory comprehension, repetition, and naming
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Fluency
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Quality of speech, thematic elaboration, articulatory agility, prosody, adequacy and variety of grammatical morphology and syntax
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Paraphasia
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The production of unintended syllables, words, or phrases during the effort to speak
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Phonemic paraphasia
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Speech sound substitution; the error sounds like the target (e.g. "powel" for towel), usually number of syllables and vowel sounds remain the same
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Neologistic paraphasia
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When less than half of the target word is achieved
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Semantic/verbal paraphasia
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Substitution of one word for a semantically-related word (e.g. dog for cat)
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Broca's apashia
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Non-fluent, agrammatic (substantive words, some overlearned phrases, effortful articulation/disrupted prosody, phonemic paraphasias), naming difficulties, impaired repetition, relatively intact auditory comprehension, often co-occurring dysarthria or apraxia of speech Lesion to Broca's area
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Transcortical motor aphasia
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Non-fluent (better than Broca's, short phrase length,short/incomplete sentences, some grammatical words, impairment seen in narrative), deficits in initiating speech, impaired naming, preserved repetition, relatively intact auditory comprehension Lesion anterior to Broca's area (subcortical frontal), medial frontal involving the supplementary motor cortex
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Global aphasia
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Non-fluent/mute (minmal speech output, stereotypic utterances), impaired naming, impaired repetition (poor), impaired comprehension (poor) Large infarction that destroys areas like Broca's, Wernicke's, supramarginal/angular gyri, and white matter
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Mixed transcortical aphasia
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Non-fluent (not as limited as global), impaired naming, echolalic, impaired comprehension, articulatory effort, phonemic paraphasias, perseverations Lesions to the anterior and posterior brain, left frontal love infarct (Broca's area/ prefrontal regions)
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Wernicke's aphasia
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Fluent/paraphasic (well-articulated, prosodic speech, paraphasias common, info. empty words/phrases, perseveration), impaired naming, impaired repetition, impaired comprehension Lesions to superior temporal gyrus, Wernicke's area, left temporal/parietal lobes
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Transcortical sensory aphasia
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Fluent verbal expression (good articulation, decent phrase length, some empty content words, some syntax, adequate prosody), auditory comprehension is poor, relatively intact repetition, semantic paraphasias more than phonemic paraphasias, perseveration Lesions in the temporo-occipital region, inferior Wernicke's, posterior 2nd/3rd temporal gyri, temporal-parietal-occipital junction
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Conduction aphasia
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Fluent/phonemic paraphasias (average phrase length, disruptions, word retrieval errors, phonemic/literal paraphasias, circumlocutions), relatively intact naming, impaired repetition, intact comprehension, conduit d'approche Lesion sight not really known, maybe arcuate fasciculus
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Conduit d'approche
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Refers to the tendency, most evident in conduction aphasics, to make repeated attempts at a word (e.g., for pretzel, "trep . . . tretzle . . . trethle . . . tredfles . . . ki")
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Anomic aphasia
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Fluent spontaneous speech w/ good articulation, syntax, phrase length and prosody (occasional semantic paraphasias), word-finding difficulty, auditory comprehension and repetition may be mildly impaired Lesions are variable, typically scattered through left hemisphere
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Subcortical aphasia
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A language disorder associated with damage to subcortical brain structures such as the basal ganglia, the thalamus, or white matter pathways in the general vicinity of these structures, usually caused by ischemic strokes, "borderline fluent"
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Thalamic aphasias
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Impaired naming, variable phrase length, hypophonic, paraphasic, and perseverative language, fluency interrupted by word-finding/stopping mid-message, variable comprehension, repetition relatively intact
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Non-thalamic subcortical aphasia
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Typically involves the structures of the basal ganglia (caudate nucleus, globus pallidus, putamen), potentialy due to associated hypoperfusion of cortices
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Hypoperfusion
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The inadequate perfusion of body tissues, resulting inadequate supply of oxygen and nutrients to the tissue
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Anterior capsular-putaminal aphasia
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Impaired naming, variable phrase length, paraphasias, hypophonia, dysarthria, relatively intact comprehension and repetition
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Posterior capsular-putaminal aphasia
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Impaired naming, variable phrase length, hypophonic, well-articulated, intact grammar, paraphasias, poor comprehension and repetition
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Gray matter
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The grayish substance of brain and spinal cord composed of neuronal and glial cell bodies, un-myelinated nerve fibers, and synapes
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White matter
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Substance of the brain and spinal cord consisting of myelinated fibers and containing no neuronal cell bodies or synapses; in a freshly sectioned brain it glistens white because of the high content of lip-rich myelin
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Description of the Circle of Willis
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Begins with 2 vertebral arteries that meet and become basilar arteries. The basilar artery then separates into 2 posterior cerebral arteries (L/R). Those go foward and then stop and split in to the middle cerebral arteries and then anterior cerebral arteries. The 2 anterior cerebral arteries are connected with 1 anterior communicator artery.
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Description of the Ventricular System
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CSF flows from the lateral ventricles into the third ventricle, and then the fourth ventricle via the cerebral aqueduct in the brainstem. From the fourth ventricle it can pass into the central canal of the spinal cord or into the cisterns of the subarachnoid space The fluid then flows around the superior sagittal sinus to be reabsorbed via the arachnoid villi.
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Description of neuron firing
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At rest, on the inside of a nerve cell there is more Potassium (K+), and on the outside there is more Sodium (Na+) and Calcium. Therefore, inside is negative in relation to the outside. 1. Neurotransmitters are sent out by the adjoining neuron. 2. This prompts the ligin gate to open, which lets sodium into the cell. The ligin gate is sensitive to chemicals. 3. The influx of sodium encourage the first sodium channel on the axon to open, allowing more sodium into the cell. There is now positivity within the cell. 4. The positivity within the cell prompts the potassium gate to open, which allows potassium out of the axon. 5. MEANWHILE, the sodium encourages the next sodium gate to open. 6. Then potassium and sodium reset to their original state, which requires ATP, and is done through the potassium sodium pump. 7. This process propagates its way down the axon. 8. When it gets to the end, there is an ion gated calcium channel which allows calcium into the cell, because this will bring it closer to equilibrium. 9. The influx of calcium triggers proteins to send neurotransmitters from the axon to the adjoining dendrite, via the synapse. 10. A calcium pump, which uses ATP, sends calcium back out, ready to be used for the next signal. 11. The process repeats as neurotransmitters prompt it to.
