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Neuroanatomy and Neurophysiology. Sensory Motor. Afferent Vision Kinesthesia Olfaction Hearing Taste Pain Temperature Touch Balance. Efferent Glands Muscle Organs Circulation Digestion Respiration Excretion Reproduction. , Viscera. Dendrite
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Sensory Motor • Afferent • Vision • Kinesthesia • Olfaction • Hearing • Taste • Pain • Temperature • Touch • Balance • Efferent • Glands • Muscle • Organs • Circulation • Digestion • Respiration • Excretion • Reproduction
Dendrite Cell Body Axon
Boutons contain: -neurotransmitters for excitation or inhibition of response -mitochondria for energy generation and protein development
Presynaptic neurons Postsynaptic neurons
Meningeal Lining protective and nutritive function
Cortex=Bark 6 layers of cells Pyramidal motor cells Non Pyramidal sensory cells
Broadman’s Map 1,2,3,4,6,8,17,18,22, 41,42,44,45
Fissure Gyri Sulci Frontal Lobe precentral gyrus supplemental motor area inf. frontal gyrus= pars operculum= Broca’s Area Parietal Lobe postcentral gyrus supramarginal gyrus angular gyrus Temporal Lobe superior temporal gyrusHeschl’s Gyrus Wernicke’s Area Occipital Lobe calcarine sulcus
Projectionto and from cortex to brain stem, spinal cord – Corona Radiata Association links regions of same hemisphereShort connect one gyrus to the next Long interconnect lobes of the brain of the same hemisphere- arcuate fasciculus Commissural from one location on one hemisphere to the corresponding location in the other –corpus callosum Myelinated Fibers Corona Radiata
Subcortical Structures Control of backgroundmovement initiation of movement patterns Lesions basal ganglia = extrapyramydal dysfunction including hypokenetic and hyperkenetic dysarthria Basal Ganglia
Cerebrovascular System Carotid Division ext&int carotid Int. carotid = Ant. Cerebral a. Mid. Cerebral a. Vertebral Division ant&post spinal a. basilar arteries = sup/ant cerebellar a. post cerebral a.
Cerebralvascular Obstruction • Thrombosis is a stationary obstruction • Embolus is a traveling clot that obstructs • Aneurysm is a dilation or ballooning of a vessel wall which can cause a rupture into surrounding space • Congenital, AVM • Trauma • CVA, TIA
Olfactory I Reaches the brain without going through thalamus Olfactory cortex in pyriform lobe and hippocampal formation
CN III oculomotor CN IV Trochlear CN VI Abducens
CN V TrigeminalSensory/motor 3 branches opthalmic: transmits sensory information from skin of the upper face maxillary: transmits sensory information from the middle face mandibular: sen/mot sensory from lower face, kinesthetic/proprioceptive sense of m. of mastication, sen. ant. 2/3 of tongue & floor of mouth (pain/temp), motor innervates m. of mastication, tensor tympani and veli palatini, mylohyoid, ant. belly of digastric
UMN Damage: increased jaw jerk reflex LMN Damage: atrophy/weakness of affected side, jaw pulls to unaffected side on closure bilateral-jaw hangs open TVP damage: hypernasality
Efferent for facial m. Afferent: -taste ant. 2/3 tongue -sublingual/submandibular glands UMN damage: no upper face paralysis LMN damage: upper/lower face paralysis on side of lesion VII CN S/M Facial Upper face innervated bilaterally Lower face contralateral
VIII CN S/M Vestibulocochlear
IX CN S/M Glossopharyngeal Part of Pharyngeal Plexus Efferent stylopharyngeus Afferent taste posterior 1/3 tongue, soft palate Pain, temp., touch posterior 1/3
X CN Vagus S/M Pharyngeal, superior, and laryngeal branches important in voice, speech, and swallowing Lesions can cause: Lack of sensation in pharynx Lack of muscle function: palate, pharynx, vocal fold, esophagus Large autonomic role
IX CN Accessory M Part of pharyngeal plexus for innervation of larynx, pharynx, and soft palate Sole innervation for trapezius and SCM
XII CN Hypoglossal M Innervation for the motor function of the tongue Each hypoglossal nucleus served by contralateral corticobulbar tract (L) UMN damage = (R) tongue weakness (L) LMN damage = (L) tongue weakness Fibers of the Corticobulbar Tract decussate prior to reaching the hypoglossal nucleus, therefore (L) UMN damage/ (R) LMN damage = (R) tongue weakness
Dorsal Root + Ventral Root = Spinal Nerve = Dorsal & Ventral Rami Branches of ventral rami go to sympathetic ganglia, nuclei of ANS Efferent neurons of dorsal and ventral rami go to motor end plates/muscle synapse Spinal Reflex Arc
UMN: commands from upper brain levels that activate or inhibit muscle function by synapsing with LMN LMN: dendrites and soma within the spinal cord,axons/components that communicate with muscle fiber Neuron within ventral gray matter is LMN or Final Common Pathway
UMN/LMN • LMN Damage: muscle weakness or complete paralysis, reflexes not intact • UMN Damage: muscle weakness or complete paralysis, reflexes intact because a spinal arc reflex is a LMN process
AST Tract: transmits info. On sense of light touch from spine to thalamus Ipsilateral: sensations on the same side as they enter the cord Contralateral: sensations on the opposite side as they enter the cord Decussate: cross the midline
Corticospinal Tract Pyramidal Tract Voluntary Movement Modification of Reflexes Visceral Activation Two neuron pathway consisting of an UMN and LMN
Corticobulbar Tract Arises from: cortical cells in lateral aspects of pre central gyrus premotor/somesthetic regions of parietal lobe Axons will: branch/decussate at different levels of brainstem synapse with nuclei of CN Sensory Information: facilitate/inhibit transmission to thalamus Serves: CN for speech
Higher Functioning • Primary activity areas: receive information from senses, extract info. • Adjacent higher order areas of processing (secondary, tertiary,quaterary): info. compared to other info. received and stored associated with modality • Association areas: highest level of cognitive processing
Motor Function • Identify target: tongue tip to alveolar ridge • Spacial orientation: integration of information of body parts in space • Posterior parietal lobe receives information from thalamus, cerebellum, basal ganglia • Develop plan to achieve target behavior • Premotor region, area 6, anterior to motor strip plans the action, receives info from areas 1,2,3 re location of muscles and joints • SMA, area 6 sup. & med., preparatory speech act, initiation of speech act • Execute plan: muscle movement with accurate timing force and rate • Area 4 execution of voluntary movement
Motor System Lesions • Dysarthria: speech disorder arising from paralysis, muscular weakness, and dyscoordination of speech musculature • Flaccid Dysarthria: LMN damage of CN, dysphonia due to VF paralysis, fasciculations, hypotonia, reflexive responses reduced or absent • Spastic Dysarthria: UMN bilateral damage to pyramidal or extrapyramidal tracts, hyper-reflexia, hypertonia • UUMN: less devastating than bilateral
Motor System Lesions • Ataxic Dysarthria: Damage to the cerebellum &/or brainstem vestibular nuclei • Loss of coordination, unable to achieve articulatory target, problems in coordination of rate, range, and movement • Dysdiadochokinesia • Dysprosody
Motor System Lesions • Hypokenetic Dysarthria: paucity of movement, inhibited initiation of movement, reduced ROM, rigidity, pill rolling hand tremor • Damage to BG &/or substantia nigra (SN) • SN produces Dopamine (DA) which balances acetylcholine (Ach), decreased DA results in inhibited initiation of motor function • Speech rushed, reduced duration of speech sounds, monopitch, monoloudness
Motor System Lesions • Hyperkenetic Dysarthria:Extraneous involuntary movement caused by BG circuit damage • Subthalamic N. damage: inhibition to GP is lost resulting in Ballism (uncontrolled flailing) • BG damage: if Ach is decreased and DA increased choreiform, involuntary twitching and movements, result • Tics: rapid movements of small groups of muscle fibers • Tremors: rhythmic contractions • Athetosis: slow, writhing movements • Dystonia: involuntary movement to a posture, posture held briefly
Motor System Lesions • Mixed Dysarthria: Damage to more than one of the controlling systems • S/F: found in ALS, disease of UMN & LMN • S/A: found in MS, UMN and cerebellum • S/A/hypo: Wilson’s disease (hepatolenticular degeneration)
Motor System Lesions • Apraxia/Dyspraxia: A dysfunction of motor planning in the absence of muscular weakness or dysfunction • SMA damage: difficulty in initiating speech • Dominant insular cortex damage: verbal dyspraxia (loss of fluency and groping behavior, ability to contract musculature voluntarily is impaired) • Oral apraxia: inability to perform non speech oral gestures • Supramarginal Gyrus damage: verbal apraxia affecting long and complex sentences
Hemispheric Specialization • Left Hemisphere • Lateral Fissure is longer • Planum Temporale (HG) is larger • Generally functional dominance for L/S • Processes consonant transitions and stop consonant bursts in (R) handed • Process of analysis, favored discrete, sequential, brief duration or rapidly changing information • Spoken/written language perception & production
Hemispheric Specialization • Right Hemisphere • Spatial and holistic elements • Face recognition • Speech intonation • Melody, tonal information • Perception of form • Intention of speaker
Lesion Studies • Speech and Language Areas • Wernicke’s Area (22): receptive or fluent aphasia • Relatively normal flow of speech • Has syntax • Does not understand what is said • Verbal paraphasias (substitution of words) • Neologisms (new word), jargon, word salad • Cannot repeat
Lesion Studies • Broca’s Aphasia: lesions to 44,45, operculum of frontal-parietal, insula, supramarginal gyrus of parietal lobe • Difficulty with the planning of speech • Non fluent aphasia • Expressive abilities severely limited • Usually retain auditory and visual input
Lesion Studies • Global Aphasia: Damage to both Wernicke’s and Broca’s Area and some sub cortical structures • Both receptive and expressive functions are severely impaired
Lesion Studies • Conduction Aphasia: lesion of arcuate fasiculus connecting Broca’s and Wernicke’s area • problem with repetition of words • Anomia: difficulty naming objects • Thalamic damage, cortical and subcortical structures