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Cranial Nerves I.Olfactory II.Optic III.Oculomotor IV.Trochlear V.Trigeminal VI.Abducens VII.Facial VIII.Vestibulocochlear IX.Glossopharyngeal X.Vagus XI.Accessory XII.Hypoglossal Fall 2012
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Cranial Nerves CN IOlfactory----------- CN IIOptic----------- CN IIIOculomotorMidbrain CN IVTrochlearMidbrain CN VTrigeminalPons CN VIAbducensPons CN VIIFacialPons CN VIIIVestibulocochlearPons CN IXGlossopharyngealMedulla CN XVagusMedulla CN XISpinal accessoryMedulla CN XIIHypoglossalMedulla
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Spinal Cord / BS Changes Spinal Cord Brainstem
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CN Functional Components
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CN Functional Columns S.L. 4th VENTRICLE GSE GVE SVE GVA SVA SSA GSA
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CN Nuclei
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Cranial Nerves CN IOlfactorySSA CN IIOpticSSA CN IIIOculomotorGSE, GVE CN IVTrochlearGSE CN VTrigeminalSVE, GSA CN VIAbducensGSE CN VIIFacialSVE, GVE, GSA, SVA CN VIIIVestibulocochlearSSA CN IXGlossopharyngealSVE, GVE, GSA, SVA CN XVagusSVE, GVE, GSA, GVA, SVA CN XISpinal accessorySVE CN XIIHypoglossalGSE
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Cranial Nerves CN IOlfactorySSA CN IIOpticSSA CN IIIOculomotorGSE, GVE CN IVTrochlearGSE CN VTrigeminalSVE, GSA CN VIAbducensGSE CN VIIFacialSVE, GVE, GSA, SVA CN VIIIVestibulocochlearSSA CN IXGlossopharyngealSVE, GVE, GSA, SVA CN XVagusSVE, GVE, GSA, GVA, SVA CN XISpinal accessorySVE CN XIIHypoglossalGSE
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No CBs for CN III, IV or VI - through PPRF in pons Corticobulbar Projections
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CN I Olfactory Epithelium Lifespan 2 months Mitosis of basal cells replace lost receptors Direct access to stimuli Unmyelinated axons form CN I – through cribriform plate
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Specialized dendrites – olfactory vesicles/knobs CN I
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As many as 10 3 afferent fibers may synapse with one mitral or tufted cell Odorant dissolved in aqueous phase of mucus interacts with specific receptor Often many odorants in one “smell” CN I
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Olfactory Cortices Pyriform area Olfactory bulb Olfactory tract Area subcallosal Medial olfactory stria Intermediate olfactory stria Lateral olfactory stria Anterior commissure Optic tract (cut) Uncus Amygdaloid body Entorhinal area
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Anosmia = loss of sense of smell Result of head injury, chronic nasal infection, or tumor in inferior frontal lobes Olfactory hallucinations can be the result of temporal lobe seizures They are often part of the “aura” that precedes a seizure Olfactory System
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CN II Visual field = part of visual world seen by each eye Image is inverted and reversed Left Right Binocular Monocular Cresent
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CN II
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Extra- Geniculate Pathways 20% not to LGN Superior colliculus Suprachiasmatic nucleus Pretectum
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Pupillary Light Reflex
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Lesions always named for visual field deficit, not the physical entity damaged Think upside down and backwards Scotoma = small deficit Anopsia (Anopia) = large deficit Visual Lesions Definitions
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Homonymous Deficits the same for both eyes Heteronymous Deficits different for both eyes Hemianopsia One half of visual field is lost Quadrantanopsia One quarter of visual field is lost Visual Lesionsc Definitions
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Visual Lesions
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Functions to keep object in focus as it moves from far to near distance Pathway poorly understood Three events occur Medial recti contract Lens thicken Pupils constrict Accommodation Reflex
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Involves lesion of pretectum Pupil is small and irregular Accommodation reflex present Pupillary light reflex absent Mnemonic is ARP - PRA Argyll Robertson Pupil
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CN III GSE LR 6 (SO 4 ) 3 GVE Sphincter pupillae, ciliary muscles No direct CBs EW III Nucleus
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Pupillary Light Reflex
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CN III Lesion Right CN III nerve or nucleus lesion
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CN IV GSE LR 6 (SO 4 ) 3 No direct CBs IV Nucleus
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CN IV Lesion Right CN IV nerve or left nucleus lesion
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CN V GSA Face, scalp, nasal/oral cavities, dura SVE Muscles of mastication No direct CBs Motor Main S
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Trigeminal Nuclei GSASVE
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Trigeminal Dermatomal Distribution Non-overlapping dermatomes, unlike spinal nerves
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CN V
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Trigeminal Corticobulbars
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Trigeminal Corticobulbars Lesion MOTOR CORTEX (FACE AREA) MOTOR V NUC. MOTOR V NUC. MOTOR CORTEX (FACE AREA) Corticobulbar projections lost
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Corneal Reflex
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Lacrimal Reflex
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Trigeminal System Lesions Peripheral nerve lesions All sensations lost in distribution of division involved Unilateral motor nucleus lesion Ipsilateral loss of muscles of mastication (LMN)
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Trigeminal System Lesions Unilateral spinal V nucleus lesion Ipsilateral loss of pain and temperature sense Unilateral chief V nucleus lesion Ipsilateral loss of discriminative senses (touch, 2-pt, vibration, proprioception ) Unilateral VTTT, VPM, internal capsule or Area 3,1,2 lesion Contralateral loss of all modalities
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CN VI GSE LR 6 (SO 4 ) 3 No direct CBs VI Nucleus
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CN VI Lesion Right CN VI nucleus lesion Right CN VI nerve lesion
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CN VII GSA Skin around ear, EAM SVA Anterior 2/3 tongue SVE Muscles facial expression GVE Lacrimal, submandibular, sublingual glands, nasal/oral mucosa FacialMotorNucleus
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Facial Nerve Corticobulbars Bilateral CBs Upper Contralateral CBs Lower
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CN VII Lesions b c
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CN VIII SSA Hearing CochlearNuclei
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CN VIII – Auditory Pathways
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Unilateral lesions of cochlea, cochlear nerve or cochlear nuclei Profound ipsilateral hearing loss Unilateral lesions above cochlear nuclei No significant hearing loss Bilateral central lesions Profound hearing loss SON lesions Difficulty localizing sounds in space; Not deaf Auditory Lesions
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Presbycusis Hearing loss associated with age Gradual, bilateral Most common cause of hearing loss Hypacusis Reduction in hearing Anacusis Absent hearing Auditory Lesions - Definitions
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Problem in external or middle ear Sound wave energy does not reach oval window Causes Excess cerumen Foreign matter in external auditory canal Otosclerosis which fixes the footplate of the stapes Otitis media May be reversible Hearing aids may be helpful Conduction Deafness
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Problem in inner ear Disease of cochlea, CN VIII, or cochlear nuclei Causes Toxic drugs Long exposure to loud noises Rubella, cytomegalovirus, syphilis Diabetes Ménière’s disease Acoustic neuroma Sensorineural Deafness
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Will localize hearing loss 256 Hz tuning fork on vertex of skull Ask patient to localize sound Sound in both ears if patient is normal Louder in ear with conduction deafness Louder in normal ear in patient with sensorineural deafness Weber Test
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Compares air vs. bone conduction Tuning fork on mastoid process, then next to ear Air > bone conduction in normal patient Bone > air in conduction deafness Air > bone in sensorineural deafness Rinne Test
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Weber vs RinneTests Weber TestRinne Test NormalSound perceived as coming from midline Air conduction > bone conduction Conduction Deafness Sound perceived as coming from affected ear Bone conduction > air conduction on affected side Sensorineural Deafness Sound perceived as coming from normal ear Air conduction > bone conduction
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CN VIII SSA Balance, equilibrium VestibularNuclei
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CN VIII – Vestibular Pathways
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VOR
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Light Reflex
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Optokinetic Reflex Track an object while head is stationary Railroad Nystagmus Slow component first Fast component second
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Voluntary FEF = saccades OEF = smooth pursuit
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Consists of slow and fast components Always named for direction of fast component Physiologic Seen after head rotations Activation of vestibular system Slow component opposite direction of head turn - VOR Fast component in direction of head turn - cortex Pathologic / Clinical When it occurs spontaneously Most common finding in vestibular disorders Nystagmus
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COWS
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Oculocephalic Reflex Test integrity of vestibular system in comatose patient Rotate head side-to-side; Activate VOR If brainstem is intact Eyes slowly opposite direction of head movement Positive / Present (normal) doll’s eye reflex If brainstem is not intact Eyes in same direction of head movement Negative / Absent (abnormal) doll’s eye reflex
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Peripheral 75 % of all cases Occurs intermittently More distressing than central vertigo Nystagmus always present Central 25 % of all cases Nystagmus may or may not be present Other deficits often seen due to brainstem involvement Vertigo
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Cortical Lesions FEF = gaze preference to side of lesion OEF = no smooth pursuit ability to side opposite lesion
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CN IX GSA Misc ear, pharynx SVA Posterior 1/3 tongue SVE Stylopharyngeus GVE Parotid gland Bilateral CBs Nucleus of Solitary Tract (NTS) NucleusAmbiguus
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CN X GVA Thorax / abdomen viscera SVA Epiglottis GSA Ear, TM, dura GVE Paras to thorax / abdomen viscera SVE Pharynx, larynx Bilateral CBs Dorsal Motor Nucleus of Vagus NucleusAmbiguus NTS
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CN XI SVE Trapezius and SCM Bilateral CBs
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CN XII GSE Intrinsic and all extrinsic tongue muscles except palatoglossus Contralateral CBs HypoglossalNucleus
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CN XII Corticobulbars Contralateral CBs
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CN XII Lesions Contralateral CBs Contra UMN lesion OR Ipsi LMN lesion NORMAL
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Alternating Hemiplegias
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Alternating Hemiplegias Contra UMN Signs Paresis (generalized) Increased DTRs Increased muscle tone Spasticity Babinski sign present Clonus may be present Disuse atrophy
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Alternating Hemiplegias Contra UMN Signs Paresis (generalized) Increased DTRs Increased muscle tone Spasticity Babinski sign present Clonus may be present Disuse atrophy
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Alternating Hemiplegias Contra UMN Signs Paresis (generalized) Increased DTRs Increased muscle tone Spasticity Babinski sign present Clonus may be present Disuse atrophy
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