Week 3 Learning Issues Part 2 Flashcards
motor neurons
axons form ventral root; somatic efferents and visceral efferents
somatic efferents
LMNs in VH
visceral efferens
preganglionic cell bodies in intermediate grey
interneurons
involved in local processing in spinal corx, short axons, can be inhibitory or excitatory and are important for information processing and modulating activity
projecting neurons
technically these are interneurons but they go long distances; these receive input from primary afferents or spinal cord interneurons and send axons up the spinal cord to brain via what matter
dorsal horn
sensory processing; interneurons and projecting neurons
ventral horn
motor processing; LMN
intermediate grey
- sympathetic preganglinic neurons
- parasympathetic preganglionic neurons
sympathetic preganglionic neurons
in LH of thoracolumbar spinal cord segments
parasympathetic preganglionic neurons
found in sacral spinal cord intermediate grey; no LH
spinal cord grey matter can be divided into
horizontal laminae based on cytoarchitectural and connectional differences numbered D to V; spinal cord grey matter can also be divided into nuclei base don fx
fxs of nuclei of spinal cord grey matter
nociceptive afferents, nociceptive input, proprioception from hindlimbs; motor neuron pools (associated with specific muscles in VH), intermediolateral cell column (sympathetic preganglionic neurons)
white matter of spinal cord divided by
dorsolateral and ventrolateral sulci; divided into dorsal funiculus, lateral funiculus, and ventral funiculus
dorsal funiculus
contains ascending axons (sensory pathway carrying info to brain)
lateral funiculus
contains descending and ascending axons (motor and sensory)
ventral funiculus
contains predominantly descending axons (motor pathway carrying information to LMNs in spinal cord)
ascending and descending pathways
ascending: spinal cord -> brainstem -> cerebral cortex
descending: cerebral cortex -> brainstem -> spinal cord
ventral commissure
ventral to central canal, major site of decussation (crossing) of axons
propriospinal tract
axons from interneurons traveling btwn spinal cord segments to coordinate motor activity between segments (ex cutaneous trunci and withdrawal reflex)
primary afferent neurons
pseudounipolarl; central axonal process enters spinal cord via dorsal root and divides into multiple collateral branches which synapse on neurons in DH of spinal cord segment or adjacent pathways for further processing in brain
branches of primary afferent neuron central axonal process that mediate reflexes
synapse on interneurons in DH or LMNs in VH
categlories of afferent neurons
- Low threshold mechanoreceptors
- Nociceptors and thermoceptors
- Proprioceptors
- Visceral afferents
Low threshold mechanoreceptors respond to
touch, pressure, vibration
low threshold mechanoreceptors fiber types
Abeta fibers: large diameter, myselinated, fast conducting axons
How does CNS use mechanoreceptor information
- Locally in spinal cord (mediates reflexes and modulates activity in spinal cord)
- Travels to brain for conscious perception and motor fx (may take path that synapses in DH the takes different axon or may run thorugh white matter without synapsing and go straight to brain)
Nociceptors and Thermoceptors Receptor types
free nerve endings that respond to thermal, chemical, or intense mechanical stimulation
Nociceptors and thermoceptors fiber types
AS fibers (S is actually a greek letter see notes) and C fibers
AS fibers
(S actually greek symbol see notes); small diameter, lightly myelinated; mediate fast pain (first pain)= sharp and well localized; go to spinal cord then project to neuron and brain
C fibers
small diameter, unmyelinated; slow pain (second pain); throbbing/ burning ect; well localized; occurs after delay can persist for long time after injury
How does CNS use nociceptive information
- Locally in spinal cord (mediate reflexes, modulate activity in other spinal cord neurons)
- Travels to brain for conscious perception and emotional and autonomic responses to pain (increased HR ect)
** nociceptive information is carried bilaterally in spinal cord and by more than one pathway. Only severe spinal cord lesions will block all pathways the mediate conscious awareness of pain**
Proprioceptors receptors
muscle spindles, golgi tendon organs, joint receptors
proprioceptor fiber types
A alpha fibers
large diameter, heavily myelinated, fast conducting, can be further subdivided based on conduction speed
How does CNS use proprioceptive information
- Locally in spinal cord
- Travel in DCML pathway to be used by cerebrum for conscious awareness of position/ coordinate cortically controlled motor fx
- travel in spinocerebellar pathways in lateral funiculus; to be used by cerebellum to regulate motor fx; cerebellar processing done w/o conscious awareness
afferent axon categlorizatoin
based on diameter; larger axon diameter conduct action potentials more rapidly and tend to be more heavily myelinated; diameter and degree of myelination of an axon can affect its susceptibility to damage and locally acting drugs
visceral afferents
includes chemoreceptors, thermoreceptors, mechanoreceptors; may get to CNS via autonomic pathways back to spinal cord or travling in vagus, glossopharyngeal or other CNs to brainstem
Primary afferents may synapse on interneurons in spinal cord to control reflexes or projecting neurons to carry information to the brain
LMN
usually used in terms of SEs; alpha-motor neurons and gama-motor neurons; motor pathways must contact both types of these for motor system to fx properly
alpha-motor neurons
innervate skeletal muscle fibers
gama-motor neurons
innervate intrafusal muscle fibers within muscle spindles (keep muscle spindle length in register with muscle length)
*muscle spiindles= sensory receptors that realy info about muscle length and tension to CNS
motor end plate
each muscle fiber (cell) contacted by one branch of an alpha motor neuron at motor endplate where axon divides forming up to 50 terminal buttons
terminal boutons
contact muscle cell membrane
neuromuscular junciton
where terminal boutons contact cell membrane (action potential crosses this)
single LMN typically innervates
multiple muscle fibers within a single muscle (a given muscle fiber will be innervated by only one LMN but one LMB will innervate multiple muscle fibers)
Motor unit
LMN and all the muscle fibers it innervates
smaller motor units
generally responisble for delicate less forceful movements; contain smaller motor neurons with smaller diameter axons with less myelin (slower conduciton)
larger motor units
usually repsonsible for rapid forceful mvoements; contain larger motor neurons with larger diameter axons with more myelin (faster conduction)
motor neuron pool
group of LMNs that innervate a given muscle; cell bodies of neurons within MNP grouped into longitudinal cluster (nucleus) within VH of spinal cord
LMNs controlled by
local reflex pathways and descending pathways from the brain
upper motor neurons
neurons in the brain that synapse on LMNs and control their activity
final common pathway in somatic motor system
LMNs; without them contraction of muscle does not occur
LMNs get input from
many different places
interneurons can be
inhibitory or excitatory
visceral effernts
autonomic nervous system (ANS) utilizes 2 or more efferent neurons to relay commands from CNS to effector organs (smooth and cardiac muscles, glands)
cell body VE preganglionic neuron
located in the CNS either in the spinal cord or brainstem; in spinal cord in int grey; symp preganglionic neurons located in thoracolumbar spinal segments in lateral horn; parasympathetic preganglinic neurons in sacral spinal cord segments in int grey but no LHl parasympathetic preganglionc neurons also in located in brainstem nuclei
preganglionic neurons in ANS
multipolar neurons that fx like somatic motor neurons; receive input from primary afferents, locate interneurons and descending projections from the brain; may be involved in simple reflexes or more complex processes controlled by higher centers in brainstem and hypothalamus
postganglionic cell bodies ANS
located in peripheral NS in peripheral ganglia
myotactic or stretch reflex reflex center excitatory
spindle afferents synapse on alpha motor neurons that innervate same muscle and synergistic muscle; synapse is excitatory -> muscle contraction to -> original muscle length or desired position of limb
* this is monosynaptic*
myotactic or stretch reflex center inhibitory
spindle afferents synapse on inhibitory interneurons that inhibit LMNs to antagonistic muscles to facilitate the return to normal position (antagonistic muscles relax making the movement easier)
clinical test of myotactic reflex
tap on tendon of muscle or muscle itself so it stretches and stimulates muscle fibers (ex. patellar)
what happens if you have a lesion cr to level of LMN cell bodies interrupting only the descending input to reflex center
if axons of descending UMNs eliminated then the reflex will not be eliminated or dimisined by may -> hyper-reflexia bc loss of descending inhibition
myotactic reflex
provides a feedback system that monitors and maintains desired muscle length
withdrawal reflex
aka flexor reflex; mediates withdrawal of limb from noxious stimuli; reflex center is polysynaptic
withdrawal reflex reflex center
involves multiple segments of spinal cord b/c mult. muscles at mutt joints; afferent or interneuron axons may have to travel a few segments cr or cd in spinal cord; pinch skin at autonomous zone, ipsilateral limb flexes at all joints, in standing animal extensor tone will increase in contralateral limb for weight bearing bc of crossed extensor response
withdrawal reflex effectors stimulated limb
stimulate limb -> ipsilateral flexors at all its excited (contracting) while all extensors are inhibited (and therefore relax) -> joints flex and limbs withdraw from painful stimuli
withdrawal reflex contralateral limb
crossed extensor reflex; contraction of extensors in contralateral limb os it can support additional weight when one limb is flexed and lifted off the ground if animal Is standing; should not see this in standing animal; if you see this in recumbent animal most likely an interruption of descending pathways and UMN damage
interneuron circuits mediating flexion/ crossed extensor reflex
also receive input from local circuits at level of spinal cord as well as descengin pathways that influence these circuits; normally spinal cord can’t mediate gait without input of UMNs in brainstem
- afferents such as cutaneous mechanoreceptors can stimulate the reflex (ie some animals will move foot if you touch paw)
reflex loop
does not go directly to brain is locally in spinal cord
cutaneous trunk reflex
segmental afferent neurons are stimulated when skin of trunk is pinched in thoracic and lumbar regions; afferents synapse in spinal cord on interneurons which ascending within spinal cord white matter to C8/ T1 spinal cord segments and synapse on LMNs that control cutaneous trunici muscle; these axons travel in lateral thoracic nerve and -> contraction of cutaneous muscles and -> a visible twitching of the skin
perineal reflex loop
elicited by stimulating anus with mild noxious stimuli; should see contraction of anal sphincter and flexion of tail. Spinal cord segments S1-S3 provide afferent ascending pathway to perineal region and motor control of this region is controlled by pudendal nerve which is D1-S3
maintenance of muscle mass
requires intact LMNs and local spinal cord circuits; if UMNs damaged then will see disuse atrophy but will see severe generation atrophy if LMNs damaged
muscle tone and reflexes
maintinated by local spinal cord circuits connecting afferent and efferent neurons; influenced by UMNs but do not require UMN input to be present
postural rxns
require afferent neurons, ascending sensory pathways to cerebral Cortex, descending motor pathways and LMNs in the spinal cord
locomotion
intact LMNs and afferent feedback from sensory nerves, pathways between the spinal cord and brainstem and critical for normal locomotion, cerebellar cortex and cerebellum refine the movement; look for paresis and ataxia when assessing locomotion
paresis/ paralysis
weakness/ lack of voluntary movement; typically interpreted in context of locomotion and weight bearing
flacid paresis/ paralysis
LMN damage
spastic paresis/ paralysis
UMN damage
ataxia
uncoordinated movement bc loss of proprioceptive information input or processing
voluntary movements
impossible to reliably asses in vet med; asses cortical fx by observing cortically controlled movements like postural rxns and animal’s ability to navigate obstacles or uneven terrain
conscious awareness of stimuli
observe cortically controlled responses to stimuli (ex crying); ascending sensory pathway transverses the spinal cord, brainstem, and cerebrum; must be intact for animal to demonstrate conscious awareness; cortically controlled responses include vocalization, and targeted movements to eliminate stimulus
division of spinal cord into 4 regions for localizing lesion
C1-C5: segments cr to cervical enlargement
C6-T2: cervical enlargement; associated with brachial plexus; sensory and motor to thoracic limb; motor to cutaneous trunk muscle (C8/T1); motor to phrenic nerve (C5,C6,C7)
T3-L3: between cervical and lumbar enlargements
L4-S3: lumbosacral plexsus
L4-S3
lumbosacral plexus; can be divided into L4-S1 (lumbar enlargement) and S1-S3 (sacral spinal cord segments)
L4-S1 lesion
may damage LMNs to the muscles of pelvic limbs, the circuitry associated with pelvic limb reflexes and the origin of the ascending sensory pathways from pelvic limb
Lower motor neuron deficits L4-S1 muscle tone
decreased to absent in pelvic limbs (chronic lesion may -> dramatic muscle atrophy)
Lower motor neuron deficits L4-S1 reflexes
decreased (hyporeflexia) or absent in pelvic limbs
Lower motor neuron deficits L4-S1 postural reactions
decreased or absent in pelvic limb
Lower motor neuron deficits L4-S1 locomotion/ voluntary movement
paresis or flaccid paralysis
sensory deficits deficits L4-S1
reduced or absent pain perception to pelvic limbs; incoming sensory info and origin of ascending pathway may be interrupted so loss of proprioceptive input form limb may -> ataxia
lesion affecting S1-S3
may damage LMNs and VE neurons that supply bladder, external uretheral sphincter and anal sphincter, and origin of ascending pathway from perineum
Motor deficits lesion s1-s3
- muscle ton in detrusor, external uretheral and anal sphincters: decreased to absent (inability to empty bladder effectively and completely, atonic bladder, urine dribbling)
- perineal reflex: decreased to absent (pudendal nerve)
- voluntary control of micturition and defication: decreased to absent
- may cause weak withdrawal reflex, mild ataxia, paresis of pelvic limb bc S1 controls sciatic nerve
sensory deficits lesions s1-s3
reduced or absent pain perception when noxious stimuli applied to perineum
lesions T3-L3
damage ascending sensory pathways form lumbar enlargement and sacral spinal cord to brain and descending motor pathways from brain to lumbar enlargement and sacral spinal cord. These pathways = essential for postural rxns, locomotion, conscious perception of stimuli and micturition
Upper motor neuron defiicits T3-L3
damage to UMNs descending from brain to lumbar enlargement (pelvic limb( and sacral spinal cord (lower urinary tract fx)
muscle tone UMN deficitis T3-L3
normal or increased (hypertonia) in pelvic limbs since reflex circuitry that controls tone is intact but dissociated form brain regulation which is mostly inhibitory
reflexes UMN deficitis T3-L3
normal or increased (hyperreflexia) +/- crossed extensor response bc loss of UMN inhibition
postural rxns UMN deficitis T3-L3
slow or absent in pelvic limb
locomotion UMN deficitis T3-L3
paresis or spastic paralysis of pelvic limb
urinary tract UMN deficitis T3-L3
increased tone in urinary sphincters -> inability to empty bladder; can also -> abolished conscious control of urination bc interruption of ascending and descending pathways associated with urinary fx (requires severe/ bilateral lesion)
sensory decificts T3-L3
lesions between cervical and lumbar enlargements may interrupt ascending pathways traveling to brain
- may have reduced to absent pain perception when noxious stimulus applied to pelvic limbs, perineum, rump, or cd trunk (won’t turn to look at stimulus)
- interruptions of proprioceptive pathways from pelvic limb to brainstem, cerebellum, and cerebrum
interuptions proprioceptive pathways form pelvic limb to brainstem, cerebellum, and cerebrum
can -> ataxia, uncoordinated gate, in pelvic limbs
how to more accurately localize lesions in thoracic and cr lumbar regions
cutaneous trunci reflex
Lesions damaging c6-t2
can produce LMN signs in thoracic limb, UMN signs in pelvic limb and loss sensory pathways to brain from thoracic and pelvic limbs
LMN signs in thoracic limbs
include loss muscle tone (+/- atrophy), decreased or absent reflexes, slow or absent postural rxns and paresis or flaccid paralysis of locomotion
sensory pathway damage to thoracic limb
reduced or absent pain perception in thoracic limb and ataxia in thoracic limb if damage to sensory pathways that originate in these segments
lesion affecting LMNs in segments in C8/T1
cutaneous trunci reflex can be absent with lesions affecting cutaneous trunci LNs in segments C8/T1
lesion affecting LMNs c5-C7
respiration may be compromised by lesions affecting LMNs of segments c5-c7 bc phrenic nerve
UMN signs pelvic limb
reduced or absent pain perception and ataxia bc interruption of same descending and ascending pathways that produced these signs with lesions in T3-L3 range
UMN urinary tract with damage to C6-T2
present similar to lesion in T3-L3 lesion (ie increased tone in urinary sphincters -> inability to empty bladder; can also -> abolished conscious control of urination bc interruption of ascending and descending pathways associated with urinary fx (requires severe/ bilateral lesion)
lesions affecting T1 and T2
can -> Horner’s syndromes bc symp trunk is T1-L4
lesions c1-c5
lesions here are cr to cervical enlargement and don’t interfere with LMNs or local reflex circuits for limbs; deficits caused by interruption of ascending and descending pathways involved in postural rxn, locomotion, conscious perception, respiration, and micturition
pelvic limb and urinary tract deficits C1-C5 lesions
same as T3-L3 lesions but cutaneous trunci reflex won’t help further localize lesions in this region bc not cutaneous trunci in this part of the neck
thoracic limb signs C1-C5 lesion
may include hyper-reflexia, hypertonia, slow or absent postural reactions, spastic paresis, ataxia and decreased pain perception when noxious stimuli applied to thoracic limb
severe lesions in c1-c5
interrupt descending pathways that control respiration and can -> death
voluntary movement evaluation animals
generally we evaluate locomotion/ gate and postural rxns to asses UMNs in animals bc can’t ask them to move something; postural rxns require forebrain (cerebral cortex) processing, basic locomotion coordinated by brainstem does not asses forebrain fx unless the animal is presented with locomotion challenges
paresis
weakness in context of voluntary motor fx and or locomiton
paralysis
complete loss of voluntary motor fx and or locomotion
flaccid paralysis
lacking muscle tone and reflexes as observed with LMN damage
spastic paralysis
muscle tone and reflexes persist as observed with UMN damage
LMN damage -> paralysis
presents more dramatically as difficulty during weight bearing phase of gait. Will bear weight on affected limb for shorter duration of time
UMN damage -> paresis
presentes more dramatically as delayed protraction of limb as if muscles (LMNS) not getting signals to imitate stride
mono paresis/ plegia
1 limb affected
paraparesis/plegia
pelvic limbs are affected
quadraparesis/plegia (tetra paresis/plegia)
all 4 limbs affected
ataxia
lack of coordination that occurs when processing proprioceptive info is disrupted w/o norma proprioceptive information receipt and processing CNS can’t coordinate or adjust movements appropriately. Spinal cord lesions interrupt ascending proprioceptive patwhays to brainstemand cerebellar circuits that are critical for gate
3 types ataxia
- Interruption of proprioceptive pathways to brain -> lesion blocking ascending path from spinal cord to brain -> general proprioceptive ataxia unocridanted gate due to interruption of proprioceptive pathway to brain can be in spinal cord or brainstem usually (lesion)
- Cerebellar dys fxn
- Vestibular dys fx
