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SENSORY STIMULUS CODING 4 aspects that are encoded every time the body receives a sensation
1. Modality
· 4 Main Types Touch Thermal Nociceptive Proprioceptive
· 2 Principles Specific Receptor Energies Receptors are specialized to transmit information about a specific type of stimulus Receptor specificity: Receptors are maximally sensitive to a single stimulus energy
Labeled Line Code Modalities are segregated on Peripheral afferents Central pathways
· \ Excitation of a particular receptor always elicits the same sensation
2. Intensity
· Frequency code: stimulus intensity is directly proportional to: Receptor potential Frequency of firing
· Population code: stimulus intensity is directly proportional to: Number of excited receptors and afferents (recruitment of sensory units)
3. Duration
· signaled by duration of firing on afferent fiber · mainly due to Slowly adapting recptors Slower conducting afferent fibers
4. Location
· Receptive fields of peripheral afferents · Dermatomes of dorsal roots · Somatotopic organization of pathways maintained throughout Spinal cord Brainstem Thalamus Cortex
Directionality (some receptors) Some receptors respond only when stimuli are presented from and to a particular location Firing patterns different depending on direction of stimulus Mainly due to rapidly adapting receptors Important for proprioception RECEPTIVE FIELDS
Receptive fields can be Excitatory or Inhibitory Inhibitory interneurons sharpen the signal by inhibiting the fields adjacent to the stimulus Lateral inhibition: responsible for two point discrimination One neuron’s excitatory receptive field may be another neuron’s inhibitory receptive field Different sizes on different parts of the body Spatial discrimination is highest were receptive fields are numerous and small 2-point discrimination threshold: used to test the dorsal column medial lemniscal system
Review Relay points: dorsal horn, nuclei, thalamus, reticular formation, and 10 and 20 sensory cortex
Each relay point can modulate via 1. Intrinsic (interneurons) 2. Extrinsic (descending fibers)
Peripheral receptive field Area of body that contains all receptor endings of a single afferent fiber (first order neuron)
Central receptive field Area of body represented by a cell body in the dorsal column of the spinal cord (second order neuron) A central cell body can have input from several receptors \ Its receptor field is a composite of the contributing peripheral receptor fields
FINE DISCRIMINATIVE TOUCH AND PROPRIOCEPTION
DORSAL COLUMN / MEDIAL LEMNISCAL SYSTEM
Rapidly Adapting Receptors Indicate changes Located in: Muscles Hair Joints Skin (touch receptors)
Primary Afferents Aa (group I) Proprioception
Ab (group II): most rapidly conducting and heavily myelinated Proprioception Vibration Fine touch
Major Tracts of Spinal Cord Dorsal Columns: Fasciculus gracilis: lower thoracic dermatomes and lower Fasciculus cuneatus: mid to upper thoracic dermatomes and higher Spinocervical tract: small fiber tract in lateral funiculus
Large diameter primary afferents enter DORSAL HORN more medially and do one of the three things:
1. Make no synaptic contacts, 10 afferents join the dorsal columns (the majority do this) 2. Synapse in dorsal horn nucleus proprius (lamina’s III – VI), 20 afferents join the dorsal columns 3. Synapse in dorsal horn nucleus proprius (lamina’s III – VI), 20 afferents join the spinocervical tract
Fibers ascend on ipsilateral side until the spinomedullary junction Nucleus gracilis Nucleus cuneatus Lateral cervical nucleus (C1 – C5)
Decussation Gracilis and Cuneatus: Internal Arcuate Fibers Lateral cervical: Anterior Commissure of Spinal Cord
Medial Lemniscus On contralateral side Terminates on: ventral posterior lateral nucleus of thalamus (VPL)
Fibers continue Posterior Limb of Internal Capsule Postcentral gyrus
Descending control (extrinsic) at relay points · Higher areas of brain control input and output of: VPL Dorsal column nuclei Spinal cord dorsal horn · Modifies neural code to enhance quality and fidelity of relevant input · Contrasts: suppresses irrelevant input (Intrinsic control at relay points = interneurons) TRIGEMINAL LEMNISCAL SYSTEM (Counter part of DC/ML for the face)
Rapidly Adapting Receptors
Primary Afferents Aa (group I): proprioception (chewing) Ab (group II): proprioception, vibration, and fine touch (most rapidly conducting and heavily myelinated)
Nuclei 1. Mesencephalic nucleus of CN V (rostral pons, rostral to the entrance of CN V) 2. Chief sensory nucleus of CN V (mid- pons) 3. Descending rostral spinal nucleus of CN V (mid-pons) 4. Motor nucleus of CN V
Large diameter primary afferents of CN V enter the PONS
1. Make direct synaptic contact with motorneurons in the motor nucleus of V - Cell bodies of these primary afferents reside in the mesencephalic nucleus 2. Synapse with neurons in the chief sensory nucleus 3. Descend a short distance in the spinal tract of CN V and synapse in rostral 1/3 of spinal nucleus of CN V
Secondary afferents cross the midline of the pons and group together on the contralateral side Caudal to pons: ipsilateral Rostral to pons: contralateral
Trigeminal lemnicus travels with medial lemniscus Terminates on: ventral posterior medial nucleus of thalamus (VPM)
Fibers continue: Posterior limb of internal capsule Postcentral gyrus (lateral bank)
Descending control VPM Chief sensory nucleus Spinal nucleus
SIGNS OF LESIONS OF DC/ML AND TRIGEMINAL LEMNISCUS
Increased two point threshold Loss of texture discrimination Loss of vibration sense (use tuning forks: 40 – 50 Hz flutter test for meissner’s / 300 Hz vibratory test for pacinian) Loss of limb position and movement sense *Loss of directional sensibility (# drawing) *Loss of dexterity of distal extremities *Astereoagnosis (lost ability to tell the shape of an object in hand) *Ataxia (inability to stand without swaying and walking with an unstable gait)
SITE OF LESION DETERMINES LATERALITY OF DEFICIT DC/ML Ipsilateral in spinal cord Contralateral in medulla and rostrally Trigeminal Lemniscal Ipsilateral at level of entrance of CN V and caudally (below mid-pons) Contralateral rostral to entrance of CN V (above mid-pons) CRUDE TOUCH PAIN (NOCICEPTION) AND THERMAL SENSATIONS
ANTEROLATERAL SYSTEM
Slowly adapting receptors Indicate duration Touch, pain, thermal
Primary afferents Ad (group III) Crude touch Pain Warm and cold C (group IV) Pain Warm
Major tracts of spinal cord Spinothalamic tract (STT) Spinoreticular tract (SRT) Spinomesencephalic tract (SMT)
Small diameter primary afferents enter DORSAL HORN more medially and do one of the three things:
1. synapse in dorsal horn in lamina I, or V & VI 20 afferents cross via anterior white commissure to form STT on contralateral side (lamina I – marginal layer: all secondary afferents are nociceptor specific)
2. travel 2-3 segments up or down Lissauer’s tract synapse in lamina I, or V & VI 20 afferents cross to form STT on contralateral side
3. synapse in dorsal horn in lamina II (substantia gelatinosa) 20 afferents join Lissauer’s tract, travel up or down 2-3 segments re-enter dorsal horn, synapse on 30 afferents in lamina I or V 30 afferents cross to form STT on contralateral side
Significance of lissauer’s tract
- Distributes crude touch, pain and thermal sensations in spinal segments on ipsilateral side - Interruption or lesion of the STT on the contralateral side produces diminished sensations several segments below the lesion (because sensations are distributed rostrally and caudally)
Direct terminations of STT Ventral posterior lateral nucleus (VPL) Collaterals to reticular formation periaqueductal gray intralaminar thalamus Posterior limb of internal capsule Postcentral gyrus
Spinothalamic tract = neospinothalamic system Good localization and quantitation Conveys fast pain Pain that happens immediately after injury Other components of anterolateral system · spinoreticular tract crossed and uncrossed 20 or 30 afferents or collaterals ending in reticular formation
· spinomesencephalic tract crossed and uncrossed 20 or 30 afferents or collaterals ending in PAG
· spinotectal tract crossed and uncrossed 20 or 30 afferents or collaterals ending in superior colliculus (here bang to left, look left)
Terminations of SRT and SMT - Reticular formation (alerting and arousal) - PAG (activation of descending control & pain suppression) - Intralaminar nuclei (arousal, behavioral activation) - Cortical association areas (recognition and appreciation: recognize as hot, sharp . . .) - Limbic system and hypothalamus – via intralaminar nuclei and directly (mood and behavior changes)
SRT and SMT = Paleospinothalamic system Slow, persistant annoying pain Poor localization and quantitation Elicits affetive and motivational aspects of pain
VENTRAL TRIGEMINAL SYSTEM (counterpart of ALS for face)
Slowly adapting receptors
Primary afferents Ad (group III): crude touch, pain, warm and cold C (group IV): pain, warm
Descending tract of CN V Caudal spinal nucleus of CN V
Small diameter primary afferents of CN V enter the PONS - Descend in the spinal tract of CN V - Synapse in most caudal subdivision of the spinal nucleus of CN V (nucleus caudalis) - 20 afferents cross the midline of the medulla - group together on the contralateral side as the VTT – ventral trigeminal thalamic
Ventral trigeminal tract (VTT) - Travels with spinothalamic tract - Substantially grouped rostral to mid-pons Ipsilateral below caudal pons Contralateral above caudal pons - Terminates on ventral posterior medial nucleus (VPM) Good localization and quantitation Fast pain
Fibers continue - posterior limb of internal capsule - postcentral gyrus, lateral bank
Other VTT terminations: slow, lingering pain, poor localization and quantitation - Reticular formation - PAG - Intralaminar Nuclei - Cortical association areas - Limbic system and hypothalamus
Descending control – originates primarily from PAG (5-HT from raphe, NE from locus coeruleus) / suppresses pain - spinal cord dorsal horn - spinal nucleus of CN V - VPM
SIGNS OF LESIONS OF ALS AND VENTRAL TRIGEMINAL TRACT
STT unilaterally (rostral to medulla SRT and SMT are intact and convey some poorly localized sensations) ¯ pain, thermal, crude touch on contralateral side
STT, SRT, SMT unilaterally ¯¯ pain, thermal, crude touch on contralateral side
STT, SRT, snd SMT bilaterally ¯¯¯ (including total loss) pain, thermal, crude touch bilaterally
Spinal tract and caudal nuclues of CN V unilaterally ¯¯¯ (including total loss) pain, thermal, crude touch from ipsilateral face (10 afferents no synapse or cross yet)
VTT unilaterally ¯¯ pain, thermal, crude touch from contralateral face
Summary
· ALS = contralateral all the way
· VTT
contralateral
caudal pons
¯ ipsilateral ENDOGENOUS PAIN SUPRESSION MECHANISMS
Gate Control Theory Activity on large diameter afferents can inhibit activity of pain transmission neurons - Occurs in dorsal horn - Requires inhibitory neurons
Basis for counter-irritants - TENS (transcutaneous electrical nerve stimulation)
Descending Pain Control Mechanisms · Periaqeductal Gray Primary structure of origin Receives input from SMT (STT and SRT also) Electrical stimulation elicits analgesia High density of opiate receptors
Sends output to monoaminergic nuclei Raphe nuclei (5-HT) – more prominent Locus coeruleus (NE)
· Monoaminergic fibers Descend in dorsolateral region of spinal cord Terminate in substantia gelatinosa of dorsal horn
· Dorsal horn Synapse on interneurons Excited interneurons release enkephalins Inhibition of pain transmission neurons Or Synapse directly on pain transmission fibers Inhibition of impulse transmission of pain neurons
Endogenous pain suppression systems also activtated by initially non-painful conditions Examples: Anticipatory/preparatory (stress) –soilders Physical exertion –athletes
Via: Hypothalamus Limbic system
Opiate and non-opiate mechanisms
NEUROPHYSIOLOGY OF CLINICAL AND CHRONIC PAIN
Stages of Pain
1. Brief - superficial injury - fast and well localized - transient - stimulation of nociceptors
2. Persisting - greater injury - inflammation - slow and generally localized - emotional and motivational - altered receptor sensitivity, peripheral nerve or facilitated CNS transmission
3. Abnormal and chronic - result of even greater injury - slow and poorly localized - inflammation - emotional and motivational - altered receptor, nerve or CNS pathways
Hyperalgesia = enhanced pain response to noxious stimuli after injury Primary: at site of injury Secondary: surrounding site of injury
Allodynia = sensitization to the extent that normally non-noxious stimuli are painful Primary: at site of injury Secondary: surrounding site of injury
Mechanisms of Altered Pain Transmission 1. Sensitized peripheral receptors - chemical mediators substance P elicits release of many other chemicals making nerve ending hyperalgesic or alodenic
2. Sensitized peripheral nerves - damage or demyelination ectopic impulse generation via pseudoreceptors and/or short circuits reverberation: recurrent excitation
3. Damage to CNS pathways - ascending and descending ex. Thalamic syndrome: vascular lesion in thalamus is perceived as pain coming from body
Referred Pain Convergence Superficial receptive field onto visceral receptive field Facilitated by Lissauer’s tract Brain interpets input as coming from most familiar region (skin instead of visceral)
Phantom Limb Pain Brain remembers limb in somatotopic map
Pain, Tickle, Itch, and Sex Carried on same central pathways, so how do we tell the difference?
2 theories 1. Pattern coding Pattern 1 = Itch Pattern 2 = Pain
2. Population coding Few = Itch Many = Pain PAIN MANAGEMENT
Pain = an unpleasant sensory and emotional experience associated with actual or potential tissue damage (always subjective)
Pain ® fear and helplessness ® sleep deprivation ® anxiety ® Pain
3 classes of analgesic drugs 1. NSAIDs: non steroidal anti inflammatory drugs (aspirin & other salicylates)
2. Opioid Analgesics: (do not say narcotic)
3. Analgesic adjuvants: tricyclic antidepressants, anticonvulsants, antihistamines, benzodiazepines, sedative hypnotics, steroids, caffeine, dextroamphetamines, phenothiazines
Principles of pain treatment - Identify source of pain. - Start with the weakest analgesic that can effect the pain - Give each drug an adequate trial - Do not use analgesics on an as needed basis (PRN) in acute pain states - Know side effects of drugs used and treat prophylactically where possible - Avoid excessive sedation - Do not use placebo response as an indicator of non-organic or predominately psychological pain - Use combination s of drugs only when specific effects are desired (be wary of synergistic affects) - Be aware of development of dependenceing drugs, not always clear cut
Acute pain vs. Chronic pain Acute Symptom of a disease Self limiting Provoked by a noxious stimulus Evokes an autonomic response (ex. HR) Has biological function Chronic Pain itself is the disease Provoked by a pathological process Psychological and behavioral aspects predominate Autonomic responses are normal No biological function
Forms of Pain - sensation - symptom - disease
Varying degrees of sympathetic maintained pain May relieve sympathetically maintained pain, but leaving the sympathetically independent pain Patient may state that pain has changed focus or even become worse
Levels of Pain Pain Level 1 Nociception Pain Level 2 Specific Spinal Cord Systems
CELL DEATH
ISCHEMIA = insufficiency of blood Blood flow to brain must deliver nutrients (O2 & glucose) and remove wastes Blood supply to brain is separated into arterial territories If severe and prolonged can result in neuronal cell death and stroke
Stroke - Occulsive –due to atherosclerosis and thrombosis - Hemorragic – due to hypertension and aneurysms
CELL DEATH
Necrosis - associated with non-phsiological circumstances that disrupt homeostasis - disruption of cell membrane - influx of Ca++ ions and water: disruption of ionic grandient - mitochondria swell and become disfunctional - lysosomal enzymes activated - cell swells and lyses - local inflammatory response
Apoptosis: Programmed Cell Death (PCD) - regulated cellular self destruciton - functions in normal development and tissue homeostasis - requires new RNA and protein synthesis (inhibitors of transcription or translation prevent apoptosis) - requires activity of specific genes - endonucleolytic cleavage and cellular DNA fragmentation into pieces - membrane blebbing - intracellular compaction of nuclear chromatin - deposition of electron dense chromatin along inner margin of nucleus - apoptotic bodies: pinching off of cell membrane - contents sealed until phagocytized by macrophages: \ no inflammatory response
Apoptosis is triggered by
Glutamate excitotoxicity ® activation of phospholipases ® activate NO ® radical formation ¯ sustained levels of intracellular Ca++ ¯ activation of proteases and promoting formation of free radicals ¯ damage to cellular proteins and membranes
b - amyloid peptide -Alzheimer’s plaques
AUDITORY SYSTEM
SOUND
· Longitudinal pressure wave · Produced by vibrating bodies · Properties Frequency Pitch (Hz) Can hear 20 – 20000 Hz Ear is differentially sensitive to 1200 – 4000 Hz Intensity Loudness (dBs) dB = 20 log (test pressure / reference pressure) sensitive to 0 – 120 dBs 1,000,000 x the threshold = 120dBs 160 ruptures eardrum
PRESBYCUSIS – sensorineural loss in aged Slow progressive degradation Loss of: Auditory and vestibular hair cells Ganglion cells Hearing and balance (particularly at high frequencies) 20 – 30 dB difference at 2000 Hz
ACOUSTIC APPARATUS
External ear Pinna External auditory canal Tympanic membrane
Middle ear (air filled) Ossicles Middle ear muscles Eustachian tube: middle ear ® nasopharynx / maintains = air pressure on both sides of tympanic membrane
Inner ear (fluid filled) Oval window Round window Cochlea Vestibular apparatus
Sound waves initiate 1. movement of ear drum in cadence 2. rocking action of ossicles (malleus ® incus ® stapes) which ampiflies the sound waves 3. fluid wave in the inner ear 4. movement of basilar membrane 5. excitation of hair cells
MIDDLE EAR
Amplification of sound wave by increasing the pressure of the vibration Lever action of ossicles ( force) Small size of oval window relative to tympanic membrane (¯ area) P = F / ¯A
Middle ear muscles Muscle Ossicle Nerve Tensor tympani Malleus Trigeminal Stapedius Stapes Seventh
Function: Sharpen reception of around 2000 Hz (selective filter for speech) Protect ossicles from jarring during bodily movements Attenuate sound vibrations reaching inner ear (anticipate loud sounds and contract to protect) Hyperacusis ® over sensitive to sound because of loss or damage of MEM function
INNER EAR Bony labyrinth of the temporal bone– contains perilymph ( Na+, ¯ K+) Vestibular apparatus Cochlea Divided into 2 chambers by membranous labyrinth 1. Scala vestibuli – oval window
membranous labyrinth Scala media –organ of corti (contains endolymph: K +, ¯ Na+) Roof = vestibular (Reissner’s) membrane Floor = basilar membrane 2. Scala tympani –round window
Helicotrema – is at the apex where the scala vestibuli and scala tympani chambers meet Spiral ganglia – auditory cell body processes Peripheral (hair cells) Central (innervate cochlear nuclei) Tectorial membrane - covers hair cells Stria vascularis
HAIR CELLS In general: Mechanorecptor Transducers (transduce vibration into bioelectrical signal) amplifiers frequency filters
Outer Hair cells: 3 rows 1 auditory fiber innervates 10 OHC’s measure Hz
Inner Hair cells: 1 row 1 IHC connected to 10 auditory fibers primary sensory cells
Stapes oscillation ¯ pressure wave in fluid of 3 chambers ¯ traveling wave in basilar membrane whose shape and peak matches the frequency of the sound ¯ stimulation of the Organ of Corti in a particular region (point of highest amplitude creates standing wave) ¯ motion of particular set of hair cells ¯ cilia of hair cells (embedded into the tectorial membrane) are sheared due to movement of membrane ¯ Hyperpolarization and depolarization ¯ Sum to equal Receptor potential (graded) ¯ Net depolarization causes Ca++ entry, release of transmitter (glutamate) ¯ CN 8 excitation
Frequencies of sound are differentially distrubuted along the basilar membrane which acts as a frequency analyzer High frequency = base of cochlea (stiff fibers) Lower frequency = near apex of cochlea (flexible fibers)
Frequency encoded by Where along the basilar membrane the maxium peak occurs Patterns of the CN8 firing Theories One to one correlation Only at low frequencies Each cycle discharges an 8th nerve action potential Volley principle Assumes that auditory fibers work in concert Phase locking Several fibers respond to different phases of cycles Inputs converge centrally and collectively convey cycle input Place Principle Place along the basilar membrane where the 8th nerve fiber innervates determines pitch Tonotopic organization (fibers from apex – low innervate superficial levels) Ordered connections between nerve and CNS
Intensity encoded by Degree of movement of the basilar membrane (amplitude of traveling wave) & \degree of movement of hairs cells & \ amplitude of receptor potential & \ amount of transmitter released Firing rate and recruitment of CN 8 fibers
OLIVOCOCHLEAR INPUT - near superior olivary nucleus - terminate on the hair cells directly or on afferent fibers of CN 8 - allow us to focus our attention on particular sounds - raises auditory thresholds - involves inhibitory (GABA) transmission CENTRAL AUDITORY PATHWAY
Dorsal and intermediate acoustic stria Medulla – cochlear nuclei (8th nerve branches into dorsal, anteroventral & posteroventral)
¯ trapezoid body
Pons – superior olive (at level of facial colliculus)
¯ lateral lemniscus
Midbrain – inferior colliculus
¯ brachium of inferior colliculus
Diencephalon – medial geniculate
¯ auditory radiations
Telencephalon – superior temporal gyrus and transverse temporal (Heschl’s gyrus) / Brodmann’s 41 & 42
SOUND LOCALIZATION - Superior Olivary Nucleus – coincidence detectors - Utilizes interaural time differences Time difference (lag time) of the ear that is further away from the sound - Utilizes interaural intensity differences
Right ear ® left hemisphere ® responds best to verbal tests Left ear ® right hemisphere ® responds best to musical passages
**Only lesions at cochlear nucleus cause monaural disability** (CNS receives extensively crossed input) Lesions of the cortex affect ability to localize sound on contralateral side
Conduction Deafness Problem: outer or middle ear Air conduction impaired / bone conduction is okay Use Rinne’s test hold tuninig fork near ear and when no longer heard place on mastoid process if hearing commences positive for conduction deafness Examples: Otosclerosis: the footplate of the stapes binds to the oval window due to growth of the bone Wax accumulation and adhesion of ossicles to bony wall Otitis media – inflammation of middle ear
Sensorineural Deafness Problem: inner ear or CNS pathway Air and bone conduction are impaired Examples: Degeneration of Hair cells: loud sounds – shearing cilia antibiotics – over broad frequency range Tumors of the auditory nerve Diseases Meningitis Meiner’s – rupture of endolympatic (membranous) chamber VESTIBULAR SYSTEM
I. Static A. Functions 1. Balance 2. Posture (keeps you upright) 3. Detects linear acceleration (acceleration = change in velocity)
B. Reflexes 1. Vestibulocollic Reflexes – head and trunk · Tonic Labyrinth Reflex - Keeps head upright on shoulders - Keeps trunk upright and centered over pelvis - Constant tone in muscles of neck and axial muscles of trunk
· Labyrinth Righting Reflex - As head falls down, jerks it back upright - Ex. falling asleep in class
· Ocular Torsion Reflex - Maintains horizontal visual field by rotating eyes when tilting head
2. Vestibulospinal Reflex – limbs - Acts on muscles of limbs particularly the extensors of the legs - Keeps body upright against gravity - Adjusts for changes in platform stance
C. Anatomy and Physiology Vestibules Two types: 4 total (one of each on each side) Utricle – horizontal Saccule – vertical
Detect linear acceleration
Hair cells located in Macula Kinocilium and stereocilia are covered by otolithic membrane Calcium carbonate crystals in otolithic membrane increase inertial mass
D. Pathways
Utricle or Saccule (Macular hair cell) Utricle or Saccule (Macular hair cell) ¯ ¯ CN VIII CN VIII ¯ ¯ Inferior vestibular nucleus Lateral vestibular nucleus Caudal Medial vestibular nucleus ¯ ¯ Medial vestibulospinal tract Lateral vestibulospinal tract (located in descending MLF bilaterally) (ipsilaterally) ¯ ¯ Head upright / thoracic spinal cord Body Posture and Extensors
D. Other Postrual Control Reflexes NOT of vestibular system origin, but work with vestibular system Cervicocollic and Cervicospinal Reflexes Bending neck generates proprioceptive signal Compensatory actions are elicited in neck, back, and limb extensor muscles Keeps head upright and maintains balance
II. Dynamic A. Functions Detects angular acceleration
B. Reflex Vestibulo-ocular reflex - Acts on extrinsic muscles of eye - Produces eye movements that are compensatory to head movements - Stabilizes the visual field on the retina during movement of the head
C. Anatomy and Physiology Semicircular Canals –dynamic functions 2 sets of three on each side: 6 total Anterior (Superior) Horizontal (Lateral) Posterior (Inferior)
Detect angular acceleration
Establishes 3-D (x, y, z) coordinate system Vector analysis of activity on 6 canals computes position of head in space **Maximum response in canals which are in PARALLEL planes Anterior right with posterior left Anterior left with posterior right Left and right horizontal canals Utriclepedal (toward utricle) = depolarization Utriclefugal (away from utricle) = hyperpolarization
Hair cells located in Cristae ampullaris Found in ampulla of each canal Kinocilium and stereocilia are encapsulated by cupula
D. Pathway
Semicircular canal (cristae ampullaris hair cell) ¯ CN VIII ¯ Superior vestibular nucleus Rostral Medial Nucleus ¯ Ascending MLF (bilaterally) ¯ Nuclei of CN III, IV, and VI (LR6 SO4 all others by 3) ¯ Maintains visual fixation as head rotates
Hair Cells · Specialized sensory receptor · One Kinocilium and many Stereocilia Bend toward Kinocilium = depolarization Bend away from Kinocilium = hyperpolarization · Innervated by peripheral processes of CN VIII, vestibular division Cell bodies reside in Scarpa’s ganglion Central processes terminate vestibular nuclei of medulla and in cerebellum Tonically active because hair cells are in a constant field of acceleration (gravity) Rate of firing encodes status of vestibular system · Receive efferent innervation from brainstem area
NYSTAGMUS (Named for fast phase) Slow Phase Active Driven by Vestibular system Opposite to direction of head rotation
Fast Phase Passive Reflex return of eye to middle position Same direction as head rotation
POST-ROTARY NYSTAGMUS Slow Phase is in SAME direction of original head rotation Fast Phase is in OPPOSITE direction
SUMMARY In The Direction Of The Original Rotation 1. slow phase of post rotary nystagmus 2. tendency to fall 3. past pointing
In The Opposite Direction Of The Original Rotation 1. vertigo (world is spinning in opposite direction of original rotation) 2. slow phase of regular nystagus
Caloric testing of vestibular function - patient reclines head 60o so that horizontal canal is now vertical - irrigate external auditory canal with hot or cold water - convection currents established in endolymph of semicircular canals - causes deflection of the cupula and stimulation of hair cells - Fast Phase will be in the direction of COWS: Cold = Opposite side Warm = Same side
Doll’s eyes test - passive movement of head from side to side - normal response is for eyes to move oppositely to head - pathological response: eyes move with head
Irritative lesions: eyes move slowly to opposite side of lesion, fast return (it’s irritating you so you have a hard time looking away from it)
Destructive lesions: eyes move slowly to same side of lesion, fast return (it’s to emotionally painful to look at it since its missing) VISUAL PATHWAY: CN 2
CENTRAL VISUAL PATHWAY 1. Retina Choroid layer Pigmented layer Rods and Cones electrical signal Horizontal cells ¯ Bipolar cells Amacrine Cells Ganglion cells Light
2. Optic nerve (axons of ganglion cells)
3. Optic chiasm
4. Optic tract
5. Lateral Geniculate Nucleus 6 Layers - 1, 4 and 6 – contralateral eye - 2,3 and 5 – ipsilateral eye
6. Optic Radiations = geniculocalcarine = geniculostriate Path from lateral geniculate body to visual cortex Found within retrolenticular part of internal capsule Loop of Meyer – axons from inferior retina (upper visual field) follow contours of inferior horn of lateral ventricle \ can be involved in pathology of temporal lobe
7. Visual Cortex Occipital lobe along calcarine fissure Left visual field = right hemisphere Right visual field = left hemisphere Lower visual field = above calcarine fissure Upper visual field = below calcarine fissure Primary cortex = Brodman area 17 Accessory cortex= Brodman areas 18 & 19 50% of cortex represents macular projections Stripe of Genari – layer that is unique to visual cortex
MAIN BLOOD SUPPLY Central retinal artery enters in CN 2 No direct supply to layers of retina by capillaries – only through diffusion
TERMINOLOGY · Macula lutea – yellow spot that is devoid of blood vessels (contains fovea)
· Fovea centralis – site of greatest visual acuity
· Optic disc – site where optic nerve exits eye (blind spot)
· Ora serrata – edge of neural retina (at the anterior aspect of eye)
VISUAL FIELDS AND DEFICITS Lens inverts and reverses the image on retina
Homonymous – deficit in same visual fields in both eyes Heteronymous – deficit in different visual fields
Hemianopsia – loss of half of visual field Quadranopsia – loss of one quarter of visual field
Lesions · Optic nerve Blind in right or left eye O.S. – oculus sinister = left eye O.D. – oculus dexter = right eye
· Compression at optic chiasm (usually pituitary related) Lose temporal visual fields (nasal retinal fields) Heteronymous hemianopsia (left visual field lost on left eye & right visual field lost on right eye)
· Behind optic chiasm but before lateral geniculate body Homonymous hemianopsia, including area of macula
· After lateral geniculate body Homonymous hemianopsia with macula sparing
· Temporal Cortex lesion Involved in object recognition, no problem with visual acuity
· Parietal Cortex lesion Involved in visual guided behavior (ex. trouble drawing)
OTHER DISEASES Macular degeneration – peripheral visual field intact (can see everything except what you are trying to look at)
Diabetic retinopathy – damage to the small blood vessels
Detached Retina – photoreceptors become disengaged from pigmented epithelium
Glaucoma – results from prolonged increased intraocular pressure
Cataract – age related, lens becomes opaque
Papilledema – since retina is an extension of diencephalon and is surrounded by dura, an increase in intracranial pressure compomises flow of the retinal vein causing engorgement of the veins on the posterior surface of the eye
VISION I
Photoreceptors - 4 types 1 type of rod 3 types of cones - Parts synaptic terminal inner segment (cell nucleus, mitochondria, and other biosynthetic machinery) outer segment (site of phototransduction) - Light goes past synaptic terminal and inner segment to get to outer segment - Light is absorbed by visual pigment embedded in discs located in outer segment Light rays enter the outer segment, encounters first disc If not absorbed by first disc’s pigment it goes on to second disc or the next one if needed This is an efficient way of capturing photons of light - Each photoreceptor only has one type of pigment
Visual Pigments - composed of 2 parts that do not absorb light when separated 1. vitamin A (retinal) 2. opsin protein loops across membrane 7 times 4 kinds - blue cone opsin - green cone opsin - red cone opsin - rhodopsin - retinal + opsin = pigment Blue pigment = S pigment for short l (few in number) Green pigment = M pigment for medium l Red pigment = L pigment for long l - Red-Green Color Deficiency: red & green cone pigments are similar to each other neighbors to each other on the X chromosome - embedded across entire surface of disc in outer segment of photoreceptor - absorbs light
Phototransduction 1. visual pigment absorbs a photon 2. Isomerization of visual pigment: 11-cis retinal (bent) ® all trans retinal (straight) 3. retinal breaks away from opsin (no longer light sensitive) 4. G-protein activates cGMP phosphodiesterase (¯ cGMP) 5. cGMP gated Na+ channels close 6. photoreceptor hyperpolarizes 7. decrease in inhibitory transmitter released
Retinal Pigment epithelium -3 funtions 1. optical function - contains melanin - absorbs extra light preventing scattering 2. metabolic function - All-trans retinal in converted back to 11-cis retinal so that it can reattach to opsin - Regenerates a light sensitive pigment (pigment regeneration) 3. Renewal of outer segment - The oldest disc is at the tip near the epithelium - Phagocytoses outer segment tips Retinal neurons 1. Photoreceptors (vertical) 2. Horizontal cell (major contributor of horizontal flow) 3. Bipolar cell (vertical) 4. Amacrine cell (horizontal) 5. Ganglion cell (vertical)
Ganglion Cells - output neurons of retina (1 million ganglion cells from each eye) - transmit information as trains of action potentials (not graded like photoreceptors) - combine signals from several photoreceptors via horizontal, bipolar, and amacrine cells - electrical response depends on precise pattern of light on retina and how pattern changes with time
Ganglion Receptive Fields –portion of visual field to which the neuron responds (part of retina it monitors) 1. Ganglion cells have circular receptive fields that vary in size (small ones in fovea) 2. Ganglion cell receptive fields have a center and an antagonistic surround 3. Ganglion cells process information in 2 parallel pathways On-center ganglion cells Provide information for incremental contrast Fire few action potentials in darkness Light directed at center of receptive field increases their firing rate Light directed at surround decreases firing rate Diffuse light gives only small response Off-center ganglion cells Provide information for decremental contrast Light directed at center decreases firing rate Light directed at surround increases firing rate Firing rate is highest for a short time after light is removed Diffuse light gives only small response
What do ganglion cells tell the brain? - report principally on contrast in visual input rather than absolute intensity - report on rapid changes in visual image or illumination - begin to process information on color, form, and movement via M and P type ganglion cells (within M and P type subsets of ganglion cells are both on and off center ganglion cells)
M type ganglion cells - Gross features & Motion - large receptive fields / large dendritic arbors / large cell bodies - projects to the magnocellular layers of LGN (layers 1 & 2) - Makes up 10% of what is going to LGN
P type ganglion cells - fine details & color vision (wavelength specific) - small receptive fields / small dendritic arbors / small cell bodies - project to the parvocellular layers of the LGN (layers 3-6) - make up 90% of what is going to the LGN
Night and Day vision - rods mediate night vision & cones mediate day vision - rod and cone signals travel though different pathways in the retina Rods innervate rod bipolar cells Cones innervate two types of cone bipolar cells (on and off center) - rods - higher convergence onto ganglion cells allowing for summation and \ sensitivity - cones - lower convergence onto ganglion cells [1cone : 1 bipolar : 1 ganglion (in fovea)] allowing for acuity VISION II
Magnocelluar and parvocellular systems - Parallel pathways - Extend throughout the visual pathway (ganglion cells ® LGN ® striate cortex ® extrastriate cortex) - Synapse to specific layers of LGN
Receptive Field -portion of visual field or retina to which a cell responds when stimulated by light 1. Ganglion cells Concentric and circular Central area and surrounding antagonistic areas 2. LGN cell Same as ganglion cell receptive field in structure and function 3. Simple Cortical cell Located in visual cortex Rectangular or ovoid shaped Responds to a line or bar of light with a specific axis Light in specific axis produces a stimulatory response / light outside of axis produces an inhibitory one 4. Complex Cortical cell Located in visual cortex Receives input from several simple cortical cells Responds to orientation and movement of light
Primary Visual Cortex Hypercolumn –cube containing: - Orientation columns Collections of simple cortical cells All cells in a column have the same axis of orientation Axis changes slightly when moving one orientation column to the next in line - Blobs Function in color perception Cylindrical shape Partially extend through gray matter - Ocular dominance columns I & C columns -refer to visual information from the ipsilateral & contralateral eye
Retinotopic Map - fovea is represented on cortex more superficially - visual cortex is larger than motor, somatosensory, and auditory cortexes put together
Visual Agnosias -Patient may see 20/20 but be unable to detect one of the aspects of vision - prosopagnosia – inablility to recognize faces (infants are born with this ability) - object agnosia – incorrect naming, using, and recognition of real objects
Depth Perception - Monocular cues –refinements of our ability to see depth with one eye Previous familiarity –know the relative sizes of objects \ tall object that looks short is further away Familiarity interposition –when one object blocks the view of another Shadows and illuminations –closer objects are closer Perspective –parallel objects seem to come together in the distance Motion parallax –moving objects that are closer move across field more quickly than objects farther away - Stereoscopic / Binocular cue (binocular disparity) Since our eyes are 6 cm apart, objects are seen from a slightly different angle from each eye Resulting in two slightly different pictures from each eye which the brain fuses to get a 3D sense Used to distinguish two objects that are relatively close Gives a more refined sense of depth perception oculomotor system
I. Gaze Stabilization A. Vestibulo-ocular - Vestibular input keeps images fixed on retina during head movement - Continuous input from semicircular canals - Nystagmus resets eyes when they reach limit of the orbit - Reflex conjugate movements (both eyes move in same direction) - Commands originate in vestibular nuclei
B. Opticokinetic - visual input keeps images fixed on retina during head movement - requires visual image on retina (does not work in the dark) - can override the vestibulo-ocular reflex - reflex conjugate movements - commands originate in occipital cortex
II. Gaze Shifting mechanisms A. Smooth pursuit movements - fovea fixes on moving object and pursues it - requires moving object - this movement can occur when head is stationary or moving - voluntary conjugate movement - commands originate in occipital cortex (and temporal lobes)
B. Saccadic movements - rapid ballistic movement - does not require visual input (sounds or tactile stimulation can elicit) - cannot control velocity of saccade - voluntary conjugate movement - commands originate from frontal cortex (contra-lateral frontal eye fields #8)
C. Vergence movements - when object moves toward face ® convergence eye movements - when object moves away from face ® divergence eye movements - linked with pupillary contriction and accommodation of lens - keeps image in focus - voluntary disconjugate movement - commands originate from occipital cortex
Nerves and Muscles
LR6 SO4 (all others are by 3) CNS areas involved in eye movements
· Oculomotor nuclei (III, IV, & VI) Saccade and pursuit Recruitement order of neurons is based on position of eye rather than load Neurons do not respond to muscle stretch
· Vestibular nuclei Signals originating in the semicircular canals drive the vestibular input Vestibular input is directly on neurons in the abducens, trochlear, and oculomotor nuclei
· Superior colliculus
· Lateral gaze center = Paramedian pontine reticular formation (PPRF) Important for control in saccades and pursuit conjugate eye movements Stimulation of PPRF drives eyes to the ipsilateral side Destruciton of PPRF results in paralysis of ipsilateral gaze
· Vertical Gaze center Important for control in saccades and pursuit conjugate eye movements Mesencephalic reticular formation organizes the vertical component of conjugate eye movements Vertical eye movements require activity on both sides of midbrain Communication is through the posterior commissure
· Medial longitudinal fasciculus -required for conjugate gaze mechanisms · Cerebral cortex · Cerebellum -Participates in control of eye movement through vestibular neurons · Sensory input (II, V, VIII, auditory
Saccades and pursuit chain of command Contra-lateral frontal lobe (primarily in frontal eye fields) Pursuit movement is organized in the occipital and temporal lobes Cortex ® superior colliculus ® gaze centers
Vergence Organized in midbrain, near oculomotor nucleus Accomodation and pupillary constriction accomplished through Retinal input to optic tectum (superior colliculus) Edinger-Westphal nucleus (parasympathetics)
Strabismus = misaligment of eyes Results in diplopia (double vision) External – weakness of medial rectus Internal – weakness of lateral rectus
Amblyopia Result of constant diplopia Brain ignores input from one eye Does not focus or orient the eye
Pupillary Light Reflexes - Direct and consensual reflexes to light in one eye - Pupil size is determined by balance of parasympathetic and sympathetic systems - Argyll-Robertson’s pupil = pupil constricts when bring something closer, but unresponsive to light Result of tertiary syphilis, alcoholism, or encephalitis
SMELL
Vomeronasal organ – responsible for detection of pheromones no topographical organization for smell cortex
receptors located in olfactory epithelium odorants are absorbed into the mucus odorants may bind to olfactory binding proteins olfactory binding proteins transport odorant molecules to the particular receptor receptor is coupled with Golf adenylate cyclase , cAMP , Na+ depolarizes cell nerve transmitters released into synaptic site of glomerulus
at the glomeruli the olfactory nerves synapse on mitral and tufted cells neurons that provide horizontal inhibition are: periglomerular and granule cells
two olfactory tracts communicate through the anterior commissure anterior olfactory nucleus (located in optic tract) allow communication between the 2 olfactory bulbs
olfactory tract ® uncus entorhinal cortex and pyriform cortex (adjacent to anterior perforated substance) also see synapses in amygdaloid complex projections from entorhinal cortex to hippocampus (influence limbic system) stria terminalis ® medial dorsal nucleus of thalamus ® prefrontal cortex
TASTE
3 papillae Circumvallate and Foliate From posterior 1/3 and edge of tongue Transmit through CN IX Responsible for bitter and sour Fungiform From anterior 2/3 of tongue Transmitted through CN VII Responsible for sweet and salty
4 taste sensations 1. Sweet Located: fungiform papillae G-coupled receptor, AC, cAMP, closes K+ channel, cell becomes depolarized 2. Salty Located: fungiform papillae Associated with Na+ leak channel 3. Bitter Located: foliate and circumvallate papillae Inositol triphosphate/calcium pathway: intracellular Ca++ leads to transmitter release 4. Sour Located: mixture of papillae Related to pH: H+ occlude a voltage dependent K+ channel
Primary synapse for taste is at solitary nucleus ® VPM ® cortex (insula and postcentral gyrus)
Taste is coded: label line code, cross talk system, cross fiber pattern coding MOTOR UNIT
Injury to Motor Pathways Cortical motor pathway - distal muscle paresis
Brain stem pathways – weakness in axial, proximal, and girdle muscles
Basal Ganglia and cerebellum – changes in rate, rhythm, amplitude, and initiation of motor responses
Spinal cord to muscle – paralysis and loss of reflexes
Final common pathway Projection of alpha motor neuron from spinal cord to a muscle When this pathway is cut there is no way to stimulate muscle contraction Ends in neuromuscular junction (release of Ach to activate nicotinic Ach receptors)
Pathologies at NMJ Myasthenia gravis ® kills receptors (IgG mediated autoimmune destruction of nicotinic receptors) Botulism ® blocks release of Ach Curare ® blocks Ach receptor Succinylcholine ® inactivates receptors
Motor Unit – a single alpha motor neuron and all the muscle fibers that it innervates
Types of Motor Units
1. slow, fatigue-resistant primarily for muscles which are activated constantly anti-gravity, axial, and girdle muscles red fatigue resistant muscles neurons: smaller axon diameters and lower thresholds
2. fast, fatigue-resistant – intermediate mixed
3. fast-twitch, fatigable finger muscles white fast twitch muscles
Graded force of Muscle Contraction 1. Size principle Neurons are recruited according to size Slow,fatigue resitant alpha motor neurons first (have lower thresholds and produce less force) More stimulation progressively larger neurons reach threshold
2. Rate Modulation The greater the frequency of stimulation in a motor axon the greater force of contraction Smooth movements due to asynchronous firing of motor units
Somatotopic arrangement of motor neurons Motor neuron pools located more laterally project to more distal muscles Motor neuron pools located more medially project to more proximal muscles Motor neuron pools located dorsally innervate flexors Motor neuron pools located ventrally innervate extensors
Lower Motor Neuron Lesion Peripheral nerve lesion or lesion at nuclei
1. period of hyperexcitability fibrillations fasciculations 2. flaccid paralysis – no muscle tone and atrophy 3. hyporeflexia 4. giant motor units – reinnervation by adjacent motor units resulting in rougher movements
Brown-Sequard Syndrome – hemi-section of spinal cord
1. Ipsilateral flaccid paralysis at level of lesion and spastic paralysis below lesion (corticospinal tract) 2. Ipsilateral loss of fine touch and proprioception (dorsal columns) 3. Contralateral loss of pain and temperature (spinothalamic) 4. Band of analgesia at level of lesion (anterior white commissure)
Alpha motor neurons are in lamina 9 Muscle tone – contraction of muscle resulting from sensory feedback of muscle length
2 sensory receptors for muscle 1. Muscle spindle Primary sensory ending Sensitive to velocity of stretch Activate Ia afferents Monosynaptic contact to motor neurons Basis of myotactic (stretch reflex) Secondary sensory ending Sensitive to chronic muscle stretch Activate II afferents Polysynaptic contact to motor neurons
2. Golgi Tendon Organ Naked sensory ending inside tendon Sensitive to tension / force (when tendon is pulled, endings stretch channels open) Activate Ib afferents Inhibits alpha motor neuron to prevent muscle tearing
Extrafusal fibers Innervated by alpha motor neurons Large fibers that generate force In parallel with muscle spindle Intrafusal fibers Innervated by gamma motor neurons Small fibers inside muscle spindle Do not generate force directly
Local Anesthetic First ® small myelinated and unmyelinated fibers Pain, temperature, gamma motor neurons Then ® large myelinated fibers Touch, pressure, alpha motor neurons
Ischemia First ® large myelinated fibers Then ® small myelinated and unmyelinated fibers Muscle spindle
COMPONENTS 1. Dynamic nuclear bag: velocity of stretch 2. Static nuclear bag: static stretch 3. Nuclear chain fiber: static stretch
INNERVATION Afferent Ia (primary ending) ® all three components II (secondary ending) ® only the two static components Efferent Dynamic gamma motor neuron ® Dynamic nuclear bag Static gamma motor neuron ® Static nuclear bag Nuclear chain fiber
Why do AP’s from Ia afferent decrease after stretch is initiated? *viscoelasticity creep allows bag fibers to creep back into their original shape
Gamma Loop
Prevents unloading Coactivation: alpha contracts the muscle while gamma contracts spindle
Preactivation Because there are separate gamma and alpha systems, muscles can be preactivated
Set sensitivity (gain) of spindle to stretch Activation of gamma increases sensitivity if spindle
SPINAL REFLEXES II
Inhibitory Interneurons
1. Ia Inhibitory interneurons Reciprocal inhibition Inhibits the antagonist muscle \ higher centers do not have to send separate commands to opposing muscles
2. Renshaw cells Recurrent inhibition Excited by collaterals from the alpha motor neuron Inhibits the same motor neuron that excited it (negative feedback loop)
3. Ib inhibitory interneurons Autogenic inhibition Inhibits the homonymous muscle GTO is activates the Ib afferent that synapses on the Ib inhibitory interneuron Synapses on the Ia afferent to hyperpolarize the synapse
4. Presynaptic inhibitory interneuron Modulates the Ia afferent synapse presynaptically Input comes from descending pathways to the presynaptic inhibitory interneuron
Flexor reflex Flexor activated and extensor inhibited Skin receptors Group A fibers (light touch and vibration)
Flexor and Crossed Extension Reflex Activates flexor and inhibits extensor in response to nociceptive stimuli Activates extensor of opposite limb to prevent fall Group III and C fibers (pain and temperature)
Clasped Knife Reflex Autogenic inhibition resistance to movement in muscle followed by a sudden relaxation Substrate is GTO Stretching of homonymous results from firing from the GTO and muscle spindle \ involves Ia’s and Ib’s
Reflex tests Babinski reflex ® (UMN) toes abduct and dorsiflexion of big toe Bing sign ® (UMN) reflex flexion of foot into pin Neonatal mass reflex ® neck drops ® extension and adduction of limbs Neonatal tonic neck reflex ® extension of limb in direction neck is turned
Re-emergence of reflexes after spinal shock Babinski sign Withdrawel reflex Crossed extension reflex Flexor reflex Hyperreflexia and clonus Stretch reflex Autonomics
CRANIAL NERVES
Trigeminal (V)
Nuclei Spinal Nucleus of V – pain and temperature from the face
Chief Sensory Nucleus – (lateral) discriminative touch from the face
Motor nucleus – (medial) innervates muscles of mastication: temporalis, masseter, pterygoids
Mesencephalic Nucleus – proprioception of jaw
Lesions PICA – Wallenburg or lateral medulla syndrome Ipsilateral loss of pain and temperature to the face (spinal trigeminal) Contralateral ¯ of pain and temperature to body (spinothalamic) Contralateral spastic paralysis of motor (corticospinal tract) Descending central Sympathetic loss Horner’s syndrome –ipsilateral ptosis, miosis, anhydrosis
Tic Douloureux – peripheral neuropathy also called trigeminal neuralgia that causes intense pain in the face
Facial Nerve VII
Nuclei Solitary nucleus (rostral part) - relay for taste in anterior 2/3 of tongue
Facial nucleus – supplies muscles of facial expression and the stapedius
Superior salivatory nucleus – supplies lacrimal gland and some salivary glands
Lesions Above facial nucleus - UPM - Contralateral lower facial spastic paralysis
Below facial nucleus - LMN - Ipsilateral upper and lower facial flaccid paralysis - Ipsilateral stapedius paralysis - Ipsilateral corneal relex gone
Corneal reflex Afferent limb = V Efferent = VII
Basilar Artery Contralateral hemiparesis: arm and leg on contralateral body Hyperreflexia Increased tone in muscles Babinski sign Affects abducens nerve: paralysis of lateral gaze on ipsilateral side
Nucleus ambiguus In reticular formation of medulla Contributes to IX, X, XI (9, 10, 11)
Glossopharyngeal IX
Supplies - general sensation and taste to posterior 1/3 of tongue - upper part of pharynx - middle ear - chemoreceptors in carotid body - baroreceptors in carotid sinus
Taste uses anterior part of solitary nucleus Chemo and baroreceptors use the caudal part of the solitary nucleus
Lesions LMN – ipsilateral paralysis of larynx and pharynx mm. (hoarse voice)
Vagus
Nuclei Solitary nucleus – chemoreceptors and baroreceptors
Nucleus ambiguus – ipsilateral pharynx
Dorsal motor nucleus – autonomic to smooth muscle, cardiac muscle, and glands in thorax and abdomen
Lesions UMN – few symptoms LMN – ipsilateral paralysis of pharynx and larynx
Spinal Accessory Lower part of nucleus ambiguus supplies some of the muscles of the soft plate and the intrinsic muscles of the larynx. Lesions will lose control of the vocal cords
Spinal component comes from the cervical part of the cord and supplies the muscles that allow you to turn your head. (sternocleidomastoid, upper trapezius)
Hypoglossal
UMN - spastic paralysis of contralateral tongue (deviates away from lesion) LMN – Flaccid paralysis of ipsilateral tongue (deviates toward lesion)
Vertebral artery Medulla at level of hypoglossal nucleus Damage the hypoglossal at nucleus (LMN \ tongue deviates toward lesion) Contralateral loss of proprioception (medial lemiscus)
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