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215 Cards in this Set
- Front
- Back
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What is the end result of the Motor Control Systems?
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trying to get the attention of LMN and tell them what to do
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What are the 2 Motor Control Systems?
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Extrapyramidal= involuntary skeletal mm activity
Pyramidal= initiated, voluntary skeletal mm activity |
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DEF Supplemental Motor Area
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part of pyramidal system in frontal lobe
Anterior to primary motor cortex Superior to premotor cortex An association area |
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FXN Supplemental Motor Area
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Finessed movement:
1. initiation of movement 2. orientation of eyes and head 3. sequential and bi-manual movement |
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Where does the Supplemental Motor area go?
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1. interacts with precentral gyrus
2. Sends UMN to cranial nerves to control motor nuclei 3. to ventral horns of SC where UMN synapse with LMN |
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LOCATION pre-motor area
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part of pyramidal system
located in frontal lobe anterior to precentral gyrus |
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FXN pre-motor area
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1. an association area
controls trunk, pelvic, and pectoral girdle mm, changes posture 2. anticipatory postural control and adjustment 3. interacts w/ pre-central gyrus to send UMN to CN nuclei and ventral horns |
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Broca's Area
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part of pyramidal system; frontal lobe
Anterior to pre-central gyrus An association area to instigate speech |
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What are the 2 types of corticofugal tracts?
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Corticospinal and corticobulbar
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Are corticofugal tracts sensory or motor?
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motor
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FXN corticospinal tract
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pyramidal system
voluntary skeletal mm activity from the extremities and trunk |
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Can the corticospinal tract ever experience a complete lesion?
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NO- d/t 90/10 decussation pattern
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FXN corticobulbar tract
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pyramidal system
voluntary skeletal mm activity of the head and neck, mm of facial expression, extrinsic eye mm, tongue, mastication, neck, pharynx, larynx, and scalp |
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Where are the cell bodies of the corticobulbar tract located?
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in the PreCentral gyrus of the frontal lobe
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What 2 cranial nerves that have a UNILATERAL decussation pattern?
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CN VII and XII (therefore stroke will affect these nn)
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What are the only cranial nerves which do NOT have motor input?
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CN I, II, VIII
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What are the 2 major functions of the oculomotor nerve?
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1. innervates extrinsic eye mm
2. innervates iris and ciliary body |
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What does the oculomotor nuclear complex contain?
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cell bodies of LMN in tegmentum of the midbrain
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Is the innervation of the iris and ciliary body involved with the pyramidal or extrapyramidal system?
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Extrapyramidal- not voluntary
controlled by HYPOTHALAMUS (not UMN) |
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FXN Trochlear N
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rec's bilateral input from UMN in corticobulbar tracts
innervates sup oblique extrinsic eye mm |
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where is the trochlear motor nucleus and what does it contain?
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tegmentum of midbrain
contains cell bodies of LMN |
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What does the Trigeminal nerve innervate?
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mm of mastication
(med and lat pterygoid, masseter, temporalis) |
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Where is the motor nucleus of V and what does it contain
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tegmentum of the pons
contains cell bodies of LMN |
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What does the Abducens nerve innervate?
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lateral rectus (abduct the eye)
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Where is the abducens motor nucleus and what does it contain?
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tegmentum of the pons
contains cell bodies of LMN |
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What are the 2 motor functions of the facial nerve?
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1. innervates the mm of facial expression
2. innervates the submandibular, sublingual, and lacrimal glands (parasympathetic) |
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What are the 2 motor functions of the glossopharyngeal nerve?
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1. innervates the stylopharyngeus m of the pharynx
2. innervates the parotid gland (parasympathetic) |
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Where is the nucleus ambiguus and what does it contain
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tegmentum of the medulla
contains LMN of IX, X, and XI |
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What are the 2 motor functions of the vagus nerve?
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1. innervation of mm of the larynx, pharynx, and soft palate
2. heart rate, viscera (parasympathetic) |
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What are the 2 portions of the spinal accessory nerve and what do they innervate?
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Cervical- inn SCM and trapezius
Cranial- intrinsic laryngeal mm |
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Where is the hypoglossal motor nucleus and what does it contain?
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in the tegmentum of medulla
contains cell bodies of LMN |
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What does the hypoglossal nerve innervate?
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extrinsic and intrinsic mm of the tongue via genioglossus m
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DEF modulatory descending motor tracts
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pathways that subserve the corticospinal tract in that they refine and finesse activity of LMN receiving input from UMN
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What are the 4 modulatory descending motor tracts?
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1. Rubrospinal
2. Tectospinal 3. Vestibulospinal 4. Reticulospinal |
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FXN Rubrospinal tract
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excite flexor activity and inhibit extensor activity
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FXN Tectospinal tract
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reflex postural movements of head, neck, and UE in response to visual stimulation
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FXN Vestibulospinal tract
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"righting reflexes"
(catching yourself from falling) |
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FXN Reticulospinal tract
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excites extensor activity and inhibits flexor activity
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Which tracts cause the most damage?
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Corticospinal and corticobulbar
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What are the classical signs of UMN damage?
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1. Paresis 2. Paralysis 3. Exaggerated DTR 4. Clonus 5. Spastic Paralysis 6.Hypertonia 7. Contralateral effects
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Paresis
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weakness b/c skeletal mm are receiving less input
UMN damage |
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Paralysis
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loss of movement and fxn; large range of loss b/c of less input.
UMN damage |
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Exaggerated DTR
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deep tendon reflex.
Hyperreflexia (simple reflex arcs are more active) |
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Clonus
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spasms w/ alterations of contractions and relaxation in rapid succession of antagonistic and agonistic mm
(hyperreflexia of spinal reflexes) UMN damage |
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Spastic Paralysis
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involuntary contraction of 1 or more mm w/ loss of function
*hallmark of UMN lesion *when you have an UMN lesion, it doesn't get to LMN to tell when to fire so LMN fires spastically |
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Hypertonia
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increased mm tone
UMN damage |
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Contralateral effects
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prior to decussation and ipsilateral effects after decussation
UMN damage |
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What accounts for spastic paralysis, hypertonia, increased DTR, and clonus?
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1. damage to UMN
2. LMN is still intact with reflex arc 3. Babinski test for UMN lesion |
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def Babinski test
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run an object up the lateral side of the foot
not done on children normal: toes plantar flex positive: toes dorsiflex |
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Cranial nerves involved with LMN paralysis
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CN III, IV, V, VI, VII, IX, X, XI, XII
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Can LMN be alpha or gamma?
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They can be both
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Where are LMN found?
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motor nuclei of CN w/ motor function
ventral horns of SC |
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How do LMN get damaged?
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1. can damage the ventral horn itself
2. can damage a peripheral nerve |
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Paresis
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weakness; not innervating skeletal mm resulting in dramatic weakness; occurs with UMN or LMN damage
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Flaccid paralysis
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total loss of muscle tone with resultant loss of function
*lost the instructions from LMN *still have innerv from LMN but have lost the control |
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Hypotonia
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decreased mm tone
LMN damage |
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Decreased or absent DTR
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LMN damage
wiped out LMN part of reflex arc |
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Atrophy
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reduction in size of skeletal m due to decreased tone
LMN damage |
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Fibrillations/ Fasciculations
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spontaneous activity of skeletal muscle
physiological response, not neurological LMN damage |
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Is LMN damage ipsilateral or contralateral?
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always ipsilateral
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Categories of collective responses of LMN damage
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1. spinal reflex responses
2. Rhythmic patterned movements 3. Spinal cord reflexes |
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Spinal reflex responses
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deep tendon reflexes
noxious stimulation reflexes |
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Rhythmic patterned movements
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a type of response to LMN damage
-predictable involuntary mvmt involved w/specific motor activity -born with some and some learned -become Central Pattern Generators -reciprocal inhibitory neural circuits are the physiological substrates -rhythmic characteristic at the cell level |
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What are CPGs and where are they remembered?
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Central Pattern Generators: used to delineate rhythmic patterns
-develop from rhythmic patterned movements Stored in: basal ganglia spinal cord brainstem cerebellum |
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T or F: Spinal cord reflexes are segmental in nature?
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True. May involve one segment or several adjacent segments
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What are propriospinal loops/circuits?
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involved with spinal cord reflex. Loops located close to midline of SC that communicate between different levels
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How are spinal cord reflexes modulated by supraspinal influences?
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1. Rubrospinal tract- modifying UMN systems. Biased toward flexor activity
2. Reticulospinal tract- ventral horns of spinal cords. Biased toward extensor activity |
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4 fundamental anatomical parts to a spinal cord reflex
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1. RECEPTOR ORGAN on distal end of a sensory organ
2. AFFERENT SENSORY NEURON with receptor at distal end 3. EFFERENT MOTOR NEURON with effector organ at distal end 4. EFFECTOR ORGAN *can be broken at any time by eliminating one |
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What are the 3 types of SC reflexes?
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1. Flexor reflexes
2. DTR/Myotactic/stretch reflex 3. GTO/inverse/tendon reflex |
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Flexor reflexes
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*protective reflexes
activated by A-Delta and C Fibers (ex: stepping on a nail) |
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DEF DTR/myotactic/stretch reflex
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contraction of agonistic and synergistic muscles following the stretching of agonistic muscles
ex: reflex hammer on knee |
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Purpose of DTR/myotactic/stretch reflex
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maintain upright posture and mm tone
-gravity pulls on skeletal mm-causes them to stretch-activates sensory neurons-go back to SC-synapse with LMN-go back out-causes skeletal mm contract -this creates mm tone b/c it is a partial contraction |
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Is DTR a proprioceptive reflex?
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yes- b/c it involves skeletal mm
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How many neurons are in the pathway for DTR?
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2- receptor organ and synapses
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Receptor Organ
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involved w/DTR
muscle spindle (neuromuscular bundle) -3-4 mm long -measure length and rate of change in extrafusal fibers -cells inside mm spindle are called intrafusal (2-12 in each) -noncontractile portion -annulospiral ending -flower spray ending |
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Intrafusal fibers
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-modified extrafusal fibers
-3 types -differentiate b/t static and dynamic change in length & rate of change of length of skeletal mm (extrafusal fibers) -parallel to extrafusal fibers -mechanical stretch receptors (measure stretch) |
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3 types of intrafusal fibers
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1. dynamic nuclear bag (1a) MOST IMPORTANT
2. Static nuclear bag (II) 3. Nuclear Chain fiber (II) |
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Noncontractile portion
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middle of intrafusal fiber that does not contract
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Annulospinal Ending
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distal end that is wrapped around the noncontractile portion (part of 1a fiber)
-registers length or rate of change of length in intrafusal fiber through mechanical energy -1a fiber =1st order sensory neuron -PRIMARY SENSORY ENDINGS in skeletal structure |
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Flower spray ending
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CONTRACTILE. located laterally on either side of annulospinal ending
-SECONDARY ENDINGS in skeletal structure -type II sensory neurons -on ends of noncontractile portion -innervate 2 of 3 intrafusal fibers |
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DTR Synapses
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sensory info coming in to the spinal cord
-type 1a fibers(annulospiral) synapse in spinal cord w/ alpha motor neuron which innervate the same mm or synergistic mm -type ii fibers (flower spray) only synapse w/ alpha motor neuron of the same mm |
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What component of DTR are the Alpha motor neurons?
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the EFFERENT component.
-cell bodies in ventral horns -fxn: innervate extrafusal fibers (skeletal mm). produce mvmt or inc mm tone |
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How are Alpha motor neurons in the DTR inhibited?
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Reciprocal inhibition. Antagonistic mm activity gets inhibited using RENSHAW CELLS. Can synapse w/ renshaw cells (inhibitory neuron), then synapse w/ alpha motor neuron which goes to antagonistic mm and causes it to relax.
ex: biceps flex, triceps relax |
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GTO reflex/inverse reflex/tendon reflex
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autogenic inhibition
-encapsulated mechanoreceptors at the junction b/t mm fibers & tendon=GTO(1b) -proprioceptive reflex -also known as 1b fibers (afferent) -measure tension & rate of change of tension in tendon |
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3 primary factors that determine muscle tone
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1. intrinsic characteristic of extrafusal fibers
2. gravity pulling on skeletal mm and activating stretch reflexes 3. gamma bias |
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How does gravity pulling on skeletal mm fibers determine mm tone?
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main function of deep tendon reflexes
gravity pulling generates stretch & activates 1a fibers (elicits stretch reflex) Causes DTRs to kick out alpha motor neurons & tell stretched mm to contract |
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Gamma Bias
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-due to supraspinal descending pathways influencing what gamma motor neurons (type of LMN) are doing
*supraspinal influences come from cerebellum and RF; indirect; no neurons projecting directly from SC |
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Gamma Motor Neuron
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-smaller than alpha motor neurons
-discharge spontaneously -not excited monosynaptically by 1a(mm spindles) or 1b(GTO) afferent fibers -not involved w/ Renshaw cells |
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Function of gamma motor neurons
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to alter the sensitivity of the mm spindle by altering the length of the intrafusal fibers and the tension they exert
*brain's way of influencing mm tone *no direct affect on extrafusal fibers |
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pathway for gamma motor neurons
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gamma motor neurons activated- intrafusal contractile portion contract causing tension of non-contractile portions- easier to fire 1a fibers b/c that's where annulospiral endings are- DTR set into play- alpha motor neurons contract- increase mm tone
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DEF Hypotonia
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decreased mm tone associated with decreased resistance to passive movements
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causes of hypotonia
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1. removing LMN (alpha & gamma)
cut ventral roots of spinal nn wipe out ventral horns of spinal cord 2. Eliminated the afferent limb reflex arc is wiped out 3. Lesions of the cerebellum- gamma bias Don't know when to fire |
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DEF Hypertonia
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excessive mm tone associated with increased resistance to passive movement
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What are the 2 types of hypertonia?
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Spasticity and Rigidity
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Spasticity
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a type of hypertonia. Hyperreflexia of deep tendon reflexes
-characteristic of UMN damage -increased resistance to passive movement -Clasp Knife Phenomenon- initial inc in resistance followed by sudden disappearance |
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Rigidity
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form of hypertonia. Increase in tone in ALL mm although the strength and reflexes are not affected
-no hyperreflexia -may be "lead pipe"- rigidity is uniform throughout ROM -may be "cog-wheel"- series of jerks during ROM |
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Does the cerebellum project to the ventral spinal horn?
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NO- influences areas indirectly. It does not initiate skeletal mm activity. Therefore, damage never causes paralysis!
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3 functions of the cerebellum
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1. coordinate voluntary skeletal mm activity
2. coordination/equilibrium 3. influence mm tone |
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What info does the cerebellum need to carry out its functions?
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1. position, mm tone, and activity of mm and joints
2. equilibrium state of the body 3. info being sent via the corticobulbar and corticospinal tracts to the skeletal mm |
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How does the cerebellum get info about the mm tone and activity of mm and joints?
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Anteriorly by sup peduncle
Post by inf peduncle. Both via spinocerebellar tracts. unconscious proprioception |
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How does the cerebellum receive info about equilibrium?
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via the vestibulocerebellar tract. Transmits unconscious proprioception. (vestibular nuclei-inf peduncle-pons)
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How does the cerebellum receive info being sent via corticobulbar and corticospinal tracts to skeletal mm?
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Cerebellum has to know what UMN are doing so it can influence activity. Most info comes from the pons. Transmitted to cerebellum via inf & mid cerebellar peduncles
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What are the 3 functional lobes of the cerebellum?
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1. Anterior-mm tone, posture, gait
2. Posterior- fine voluntary movement 3. Flocculonodular- equilibrium **ipsilateral |
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General Ataxia
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Cerebellar problem. abnormality in muscular coordination leading to abnormality of voluntary movement
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Signs of Ataxia
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1. mm contract weak and irregular (ant)
2. intentional/terminal tremor (post) 3. unsteady or drunken gait (ant) 4. feet spaced far apart (ant) 5. Lean or lurch to affected side (ant) 6. Dysmetria (post) 7. Dyssynergia (post) 8. Dysdiadokinesia (post) 9. Dysarthria (post) 10. Hypotonia (ant) 11. Nystagmus (flocc) |
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intentional tremor/terminal tremor
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occurs when approaching a target
symptoms on side of problem (double decussating) tremor may occur with fine movement |
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Dysmetria
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inability to stop a mm movement at a desired moment
(post lobe of cerebellum) |
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Dysdiadokinesia
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inability to perform rapid and alternating movements
post lobe of cerebellum |
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Dysarthria
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slurred or hesitant speech (scanning speech)
post lobe of cerebellum |
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Nystagmus
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ataxia of the eyes; rapid and slow tracking phase
Flocculonodular problem of cerebellum *rule out proprioceptive, vestibular nuclei, or ear problems |
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Extrapyramidal system
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involuntary, instinctive skeletal mm activity
developed before pyramidal system |
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Basal Ganglia
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deep seated nuclei w/in white matter of cerebral hemispheres
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What are the 3 basal ganglia?
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Caudate nucleus, putamen, globus pallidus (latter 2 make up lenticular nucleus)
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What are the parts of the extrapyramidal system?
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3 basal ganglia, red nucleus, substantia nigra, subthalamic nucleus
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Pathways from basal ganglia to spinal cord (LMN)
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1. Reticulospinal tract: BG-RF-ventral horn
biased toward extensor activity 2. corticospinal: BG-precentral gyrus influence UMN in precentral gyrus 3. Nigroreticular: BG-sub nigra-RF-RSTrac 4. Thalamocortical: BG-thalamus-PCG |
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Functions of the basal ganglia
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1. intimately integrated w/pyramidal system
2. assist to inhibit co-contraction of antagonist mm of limb 3. assist in adjusting body position during mvmt 4. works at subconscious level |
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Do basal ganglia use excitatory or inhibitory mechanisms?
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inhibitory
determine direction, speed, force of mvmt involved w/ CPGs |
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Characteristics of Basal Ganglia damage
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Hypokinesia
Hyperkinesia *multiple types of each |
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DEF hypokinesia
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type of BG damage
reduction in the initiation, implementation, & facilitation of execution of movement (slow movement). Movements initiated slowly & stop w/ difficulty |
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What are the 2 types of hypokinesia?
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1. Hypertonia
2. Rigidity |
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DEF hypertonia
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a type of hypokinesia. BG disorder.
Increase in muscle tone w/ resistance to passive movement of a joint throughout ROM. *if all mm involved=rigidity |
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DEF and types of Rigidity
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associated w/ hypokinesia & hypertonia. BG damage. Entire body presents w/ it.
a. cogwheel- increased jerky resistance to PROM b. plasic- "lead pipe". increased resistance to PROM that is constant, continuous & smooth |
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Symptoms associated with Parkinson's disease
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-conscious mvmt may be suppressed
-abnormal postures -no arm swing during gait -Deep tendon reflex usually normal -facial expression may be masked |
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Pathology of Parkinson's disease
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BG disorder.
Degeneration of substantia nigra of midbrain (BG not kept under control) Dopamine depleted basal ganglia (decreased dopamine=decreased inhibition) Disinhibition |
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Involuntary movements associated with Parkinson's disease
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hyperkinesia/hyperkinetic
1. static tremor 2. athetosis 3. chorea 4. ballism 5. alternating tremor |
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Static tremor
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hallmark of BG dysfunction
rhythmic, fine, involuntary tremor when extremity is in a fixed position *Parkinson's |
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Athetosis
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involuntary movement characterized by slow, writhing, worm-like movements of the fingers
*putamen dysfunction of BG. Parkinson's |
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Chorea
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sudden, involuntary, jerky movements along w/ grimacing or twitching of facial mm & faulty vocalization
*Huntington's |
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Huntington's chorea
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autosomal dominant; damage to caudate nucleus
*Parkinson's |
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Ballism
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involuntary movement of an entire limb; begins proximally & proceeds distally like a wave
dramatic movements monoballism, hemiballism |
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What causes ballism?
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subthalamic stroke
*not part of BG, but still part of extrapyramidal system |
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Alternating tremor
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caudate nucleus dysfunction
occurs when not doing intentional activity |
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BG neurotransmitters and neuromodulators
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Excitatory: ACh, Glutamate, Aspartate
Inhibitory: GABA, Dopamine, Glycine |
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Is cranial nerve damage contralateral or ipsilateral?
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ipsilateral
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What happens if the motor and sensory nuclei associated w/ a CN in the brainstem is damaged?
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ipsilateral results. Same results as nn damage
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What happens if the Olfactory (I) nerve is damaged?
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Anosmia- loss of smell.
*does not occur with unilateral lesion damage to one side only causes loss in one nostril b/c of bilateral projection patterm |
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What happens if the Optic (II) nerve is damaged?
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blindness in that eye
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What nuclei are associated with the oculomotor (III) nerve?
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Edinger-westphal nucleus
oculomotor nuclear complex in midbrain |
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LMN paralysis of CN III
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flaccidity of the ipsilateral extrinsic eye mm & levator palpebrae superioris
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Physical signs of Oculomotor N damage
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1. ptosis
2. diploplia 3. abduction of the eye 4. strabismus 5. mydriasis 6. Anisocoria 7. unresponsiveness of pupillary light reflexes |
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Ptosis
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drooping of upper eye lid due to dysfunction of the levator palpebrae superioris
CN III |
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Diploplia
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double vision; occurs when extrinsic eye mm are paralyzed
a. eyes no longer coordinated b. happens with damage to midbrain caused by CN III, IV, XI damage |
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Strabismus
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eyes crossed & not synchronized during mvmt
-extrinsic eye mm not properly innervated -eye mm are damaged -caused by damage to CN III, IV, XI |
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Mydriasis
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dilated pupil; loss of preganglionic parasympathetic fibers in the nn
-lack of parasympathetic input to iris (Edinger-westphal nucleus) |
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Anisocoria
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pupils of unequal size; d/t one iris being innervated & one not b/c of loss of preganglionic parasympathetic fibers of affected nerve
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Direct reflex
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one eye reflexes with light shined into it
-if no reflex, problems w/ CN II(sensory) or III(motor) |
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Consensus reflex
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both eyes reflex w/ light in one of the eyes
-collateral of CN II goes to edinger westphal nuclei of opposite eye then goes to CN III of that eye & causes it to reflex |
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Damage to Trochlear N (IV)
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LMN paralysis: sup oblique extrinsic eye mm
Diploplia: pt may tilt head toward shoulder of side opposite the paralyzed mm |
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Damage to Trigeminal N (V)
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Loss of general sensation: areas innerv by V1-V3
LMN paralysis: mm of mastication on ipsilateral side Loss of direct & consensual corneal reflex |
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Damage to Abducens (VI)
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diploplia: double vision d/t loss of innerv of lateral rectus
Adducted eye |
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Damage to Facial (VII)
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LMN paralysis: Bell's palsy
Loss of tearing Loss of salivation Loss of taste perception on ant 2/3 of tongue (ipsilateral) |
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Bell's palsy
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ipsilateral mm of facial expression (VII)
forehead may be immobile corner of mouth sags facial lines are lost nasolabial folds of face are flat saliva may drip from mouth cannot whistle (buccinator) trouble smiling unable to close or blink involved eye |
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Damage to vestibulocochlear (VIII)
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loss of hearing (cochlear): ipsilateral ear
loss of equilibrium (semicircular canal): ipsilateral ear |
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Damage to Glossopharyngeal (IX)
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loss of general sensation: ipsilateral post 1/3 of tongue
loss of taste: ips post 1/3 ips loss of gag reflex ips loss of palatal and uvular reflex diminished carotid sinus/carotid body reflex dysphagia: difficulty swallowing ips loss of salivation |
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Damage to Vagus (X)
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LMN paralysis: ips soft palate, (twang)
dysphagia: flaccid paralysis of pharyngeal mm LMN paralysis of laryngeal mm (vocal cord). voice reduced to whisper Loss of gag reflex Loss of palatal and uvular reflex Transient tachycardia: increased HR d/t reduced parasympathetic input to heart |
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Damage to Spinal Accessory (XI)
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LMN paralysis: flaccidity of ips SCM. inability to rotate head so that chin points to opposite side of the lesion
LMN paralysis: flaccidity of Trapezius M. downward and outward rotation of scapula |
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Damage to Hypoglossal (XII)
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LMN paralysis: flaccidity of the ips intrinsic & extrinsic tongue mm. Tongue will point to paralyzed side d/t normal side being unopposed
Paralyzed side will atrophy and become wrinkled Dysphagia |
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Is regeneration more successful in the PNS or the CNS?
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PNS
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Regeneration vs Repair
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Regeneration: replace cells w/ identical cells
Repair: replace living cells w/ cells or tissue of a more primitive nature (scar tissue) |
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Where does PNS regeneration occur?
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cranial nerves, spinal nerves, autonomic system
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Which system can regeneration occur in if the cell body is damaged?
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Neither. Regeneration cannot occur
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Wallerian degeneration
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occurs after a lesion in peripheral nerve.
Everything distal to cut degenerates Inflammatory process (autolysis, phagocytosis) Endoneurial tube stays in place up to 30 days Axon starts to form filopodia at the area of lesion and one becomes dominant |
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Rates of regeneration in arm
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upper forearm: 2.5 mm/day
distal forearm: 2 mm/day distal wrist and hand 1 mm/day |
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What determines the success of regeneration?
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-type of injury
-crush or transect -length of time b/t injury & repair the nn -general nutritional status and health |
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Does mitosis occur in the CNS or PNS?
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PNS only
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Why is there no regeneration in the CNS?
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many theories.
some say environment recent research shows oligodendrocytes produce inhibitory chemicals (NOGO factors) which prevent regeneration |
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What constitutes successful regeneration in the CNS?
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-injured neuron must survive
-damaged axon must extend across its cut or damaged process to its original neuronal target -axon needs to be remyelinated & functional synapses need to form -criteria evaluated in 2 ways: descriptively, functionally |
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What is the problem with CNS research?
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other compensatory mechanisms (neuroplasticity) need to be ruled out as the reason for increase in function
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Where is memory stored in the CNS?
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hippocampus and amygdaloid nuclear complex-deep in temporal lobe
*must go through here to be retained *form neural circuits to other parts of the brain |
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Memory trace
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form of conscious memory. Neural circuit that connects a sensory event w/ a learned behavior response; altered in some way to support the learning
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Memory consolidation
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form of conscious memory. Occurs if experience (memory trace) is somewhat permanently retained. Can occur quickly or take long periods of time
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Variables that influence consolidation
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1. Catecholamine (adrenaline) levels
2. Motivation (context learning) 3. Physiological states 4. all physiological states preclude long-term potentiation |
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How is long-term potentiation (LTP) consolidated?
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through strengthening synapses
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Long-term potentiation
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conscious memory. Molecular processing of memory; learn something over and over.
-studies use neurons in the hippocampus -Hebbian processing -increase in glutamate -increase in glutamate receptors -influx in calcium -enzymatic cascades in postsynaptic cells **post-synaptic membrane becomes more sensitive -nitric oxide is formed -presynaptic & postsynaptic work more efficiently |
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Hebbian processing
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occurs during LTP
research in animals shows that following a heavy train of stimulation, the postsynaptic excitatory potential has an increase in amplitude which can last varying periods of time |
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Long-term depression
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Similar to LTP but w/ a reverse effect
you LOSE memory biochemical changes- synapse less effective Anatomical changes- increase in # synapses; increase in activity use it or lose it membrane loses sensitivity & proper synapses are not in place |
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Declarative Memory (conscious, explicit, cognitive)
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remembering facts, events, concepts, locations
-can be easily verbalized -requires attention during recall |
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3 stages of processing declarative memory
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1st stage- immediate (1-2 sec)
plan a response to stimulus 2nd stage- short-term/working/primary (min, days) prefrontal cortex & association areas 3rd stage- long-term/remote short-term has been permanently consolidated and stored in area that 1st rec'd it |
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Physiology of declarative memory
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-1st processed & stored by hippocampus & amygdala
-then send to other parts of brain to make sense out of it -eventually stored in area where it was 1st processed |
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2 subtypes of declarative memory
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Episodic- remembering own experiences as they happened
Semantic- general knowledge. Database required for thinking |
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Nondeclarative memory (unconscious, explicit, procedural, skills & habit)
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person has no previous awareness of memory; cannot describe the learned information except through behavior; cannot remember how, when, or where learning occurred (ex: tying shoes)
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Where is nondeclarative memory retained
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cerebellum, basal ganglia (CPGs), amygdala
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Amnesia
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loss of long term memory
Retrograde- loss of memory prior to trauma Anterograde- loss of memory after trauma. Amygdala & hippocampus are not processing info |
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Neural plasticity in patients with stroke
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if pt survives a stroke, most will have some degree of recovery of: speech, language, motor function, sensory perception
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Does neural plasticity have a unilateral or bilateral effect?
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Bilateral (contralateral side may be affected)
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What stimulates neural plasticity in the CNS?
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-loss of modified afferent input to the CNS
-damage the CNS -Chemical stimulation (nicotine) -environmental or training stimulation |
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What cranial nerves do NOT have motor input?
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I-olfactory
II-optic VIII-vestibulocochlear |
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What 2 cranial nerves have a unilateral projection pattern?
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VII-facial
XII-hypoglossal |
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What is the difference between alpha and gamma motor neurons?
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Alpha motor neurons stimulate the skeletal mm and are under voluntary control.
Gamma motor neurons are involved with reflexes and adjusting tension on mm spindles |
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What nuclei are located in the midbrain?
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Oculomotor
Edinger-Westphal Mesencephalic Trochlear |
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What nuclei are located in the pons?
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Chief Sensory
Motor Nuc of V Mesencephalic Abducens Motor Nuc of VII Vestibular (1/2) Cochlear |
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What nuclei are located in the medulla?
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Spinal Nuc of V
Solitary Salivatory Vestibular (1/2) Ambiguus Dorsal Motor Hypoglossal |
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Where are the cell bodies of the oculomotor nerve?
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M-oculomotor nuc
Para- Edinger-westphal nuc S-Mesencephalic nuc |
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Where are the cell bodies of the trochlear nerve?
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M-Trochlear nuc
S- Mesencephalic nuc |
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Where are the cell bodies of the Trigeminal nerve?
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V1-3, S- Trigeminal ganglia, Spinal nuc of V, Chief Sensory
V3, M- motor nuc of V V3, S-mesencephalic nuc of V (pons) |
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Where are the cell bodies of the abducens nerve?
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M- abducens nuc
S- mesencephalic nuc of V (pons) |
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Where are the cell bodies of the facial nerve?
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M- motor nuc of VII, salivatory nuc
S- solitary nuc, geniculate ganglia |
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Where are the cell bodies of the vestibulocochlear nerve?
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spiral ganglia, cochlear nuclei
vestibular ganglia, vestibular nuclei |
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Where are the cell bodies of the glossopharyngeal nerve?
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S- inf glossopharyngeal ganglia, solitary nuc
M- salivatory nuc, ambiguus nuc |
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Where are the cell bodies of the vagus nerve?
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M- dorsal motor nuc, ambiguus nuc
S- inf vagal ganglia, solitary nuc, spinal nuc of V |
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Where are the cell bodies of the accessory nerve?
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M, cranial portion- ambiguus nuc
M, spinal portion- mesencephalic nuc S- mesencephalic nuc |
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Where are the cell bodies of the hypoglossal nerve?
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M- hypoglossal nuc
S- mesencephalic nuc |
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What does the oculomotor nerve innervate?
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levator palpebrae, extrinsic eye mm
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What does the trochlear nerve innervate?
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sup oblique for sensory and motor
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What does the 1st branch of the trigeminal n innervate?
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V1- opthalmic
upper 1/3 of face for general sensation |
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What does the 2nd branch of the trigeminal n innervate?
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V2- Maxillary
middle 1/2 of face for general sensation |
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What does the 3rd branch of the trigeminal n innervate?
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V3- Mandibular
lower 1/3 of face for general sensation muscles of mastication- motor |
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What does the abducens nerve innervate?
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lateral rectus for motor and sensation
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What does the facial nerve innervate?
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mm of facial expression, ant 2/3 of tongue for taste, glands
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What does the vestibulocochlear nerve innervate?
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organ of corti and vestibular mechanism
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What does the glossopharyngeal nerve innervate?
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post 1/3 of tongue for taste; visceral sensation from ear, pharynx; parotid gland; stylopharyngeus m for swallowing
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What does the vagus nerve innervate?
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smooth mm of viscera, epiglottis for taste, pharynx and larynx, visceral sensation, sensation of external ear
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What does the cranial portion of the accessory nerve innervate?
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pharynx and larynx (along with vagus)
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What does the spinal portion of the accessory nerve innervate?
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SCM and trapezius for mvmt and sensation
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What does the hypoglossal nerve innervate?
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intrinsic and extrinsic mm of tongue for mvmt
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