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neurolocalization yields a
differential list
functional divisions of the brain
cerebrum
diencephalon (thalamus, hypothalamus)
brainstem (midbrain, pons, medulla)
cerebellum
vestibular system
UMN (upper motor neuron)
located entirely within CNS
descend from brain to every segment of spinal cord
imitate voluntary movement
both excitatory and inhibitory influence on LMN to maintain muscle tone and reflex arcs
LMN (lower motor neuron)
located in CNS and PNS
involved with reflex arc (sensory and motor)
carry out motor function
the upper motor neuron system originates in
pyramidal system (motor cortex) → corticospinal tracts
extrapyramidal system (basal nuclei) → rubrospinal tracts
the pyramidal system and extrapyramidal system stimulate or inhibit the neurons that
directly innervate the muscles
responsibilities of UMN system
initiate/influence voluntary movement
regulation of posture → maintain muscle tone to oppose gravity, keep reflex arcs in check
gait in UMN system
mainly from basal nuclei and brainstem
red nucleus of the midbrain is thought to play the biggest role in gait

what are 22a, 24, 25, and 26 representing?
basal nuclei

what are the 2 red circles representing?
red nucleus of midbrain

what is the top arrow pointing at?
motor cortex

what is the bottom arrow pointing at?
basal nuclei and red nucleus
frontal lobe of cerebrum
motor areas
piriform lobe/cortex of cerebrum
smell → olfactory bulbs
parietal lobe of cerebrum
somatosensory
temporal lobe of cerebrum
hearing and vestibular input
occipital lobe of cerebrum
vision
somatosensory cortex
important for both brain and spinal diseases
conscious perception of touch, pain, pressure, temperature
conscious perception of proprioception
forebrain signs of lesions in the cerebrum
alterations in behavior or mental status
walking in circles/pacing
seizures (most common)
central blindness (contralateral) → intact PLR
decrease in facial sensation (contralateral)
postural reaction deficits (contralateral)
no gait deficits
circling, head pressing, compulsive pacing
decrease in facial sensation and postural reaction deficits are involved with
somatosensory cortex in parietal lobe
gait deficits for cerebrum lesions
usually none!
fine control/discrimination lost (steps of ladder)
± mild ataxia (usually not noticed)
circling signs with lesions in the cerebrum
usually towards side of lesion
can also be seen with brainstem/vestibular disease
diencephalon
chief sensory integrating center of nervous system
plethora of relay nuclei
5 major divisions
what are the 5 major divisions of the diencephalon?
thalamus
metathalamus → geniculate nuclei, LGN involved with vision, MGN involved with hearing and balance
epithalamus
hypothalamus
subthalamus
what is the most rostral position of the diencephalon?
ARAS
the reticular formation runs through
the entire brainstem into thalamus
ascending reticular activating system (ARAS)
carries afferents going to thalamic nuclei
awakens and prepares the cerebral cortex
switchboard → accepts what is needed for consciousness and rejects what is irrelevant
influenced by sleep centers in pons and medulla
hypothalamus (in diencephalon)
functions as higher center for regulation of visceral motor activity → home office of ANS, functions with voluntary control
influenced by olfaction and limbic systems
many important nuclei → superoptic and paraventricular
what hormone is highly associated with superoptic nuclei?
ADH
what hormone is highly associated with paraventricular nuclei?
oxytocin
clinical signs of diencephalon issues
signs of dysfunction often similar to cerebral
they may circle to either side
visual impairment
possibly endocrine dysfunction
behavioral problems
temperature regulation
non-specific pain
midbrain
ARAS → maintains consciousness, alerts the cerebral cortex
red nucleus → axons cross immediately and descend as rubrospinal tract
what is the major motor component of the midbrain?
red nucleus
nerves associated with midbrain
oculomotor (III) nuclei → motor (GSE) to extraocular muscles, parasympathetic (GVE) to constrict pupil
trochlear (IV) nuclei
tectotegmentospinal tract → sympathetic innervation to the eye (dilate), possibly hypothalamus
clinical signs of midbrain lesions
typically cause severe gait abnormalities → UMN paresis and ataxia
abnormal mentation → disruption of ARAS, stupor or coma
decerebrate rigidity → massive release of UMN inhibition
structures of the pons
more of the ARAS
motor nucleus of trigeminal (CN V) nerve
sensory nuclei of trigeminal (CN V)
pontine micturition center (PMC)
clinical signs of pons lesions
marked mentation change
gait disturbance
dysfunction of CN V
possibly dysuria
medulla contains
nuclei of CN VI through XII → vestibular nuclei
reticular formation of medulla
ARAS
respiratory centers
autonomic control of HR and BP
sleep centers
medullary reticulospinal tract (UMN tract)
nucleus ambiguus → larynx, pharynx, and esophagus
medial longitudinal fasciculus (MLF)
connects CN III, IV, and VI + vestibular nuclei to coordinate conjugate eye movements and head/eye position
clinical signs of medulla lesions
alterations in consciousness
autonomic dysfunction → abnormal HR, BP
respiratory problems (the UMN for respirations) → cheyne-stokes respirations
UMN paresis
cerebellum is anatomically made up of
cerebellar cortex (arbor vitae)
medulla
nuclei
the cerebellum is functionally made up of
cerebrocerebellum → cerebellar hemispheres and dentate nucleus
spinocerebellum → vermis, fastigial, and interposital nuclei
vestibulocerebellum → flocculonodular lobe and fastigial nucleus
cerebellum does not initiate
movement
cerebellum regulates
rate, range, and force of movements
clinical signs of cerebellum lesions
intention tremor
truncal sway
cerebellar ataxia and hypermetria
disequilibrium
ipsilateral menace deficits
cerebellum lesions subject to congenital diseases
hypoplasia
abiotrophy
spinal cord motor section
UMN tracts descend in white matter to synapse on the LMN in the gray matter
UMN that facilitate to flexors =
walking → corticospinal, rubrospinal, medullary reticulospinal
UMN that facilitate to extensors =
standing → vestibulospinal, pontine reticulospinal
spinal cord sensory section
ascending fibers for proprioception and pain are located mainly dorsally and laterally
lesions on the sensory spinal cord are usually affecting
both the ascending GP and the descending UMN for a combination of proprioceptive ataxia and paresis
interference with the UMN influence over the LMN results in
release of muscle inhibition

what is this showing?
ascending tracts

what is this showing?
descending tracts
what are the clinically important spinal cord LMNs?
limbs, bladder, sphincters
C6-T2 and L4-S3 segments
damage to the spinal cord LMN will cause
paresis or plegia
depressed or absent spinal reflexes
decreased muscle tone
pertinent anatomy of C1-C5
descending UMN tracts to all 4 limbs
ascending GP and nociception from all 4 limbs
origins of the phrenic nerve (C5-C7)
descending sympathetic fibers to the eye
lesions at C1-C5
gait affected in all 4 limbs
UMN signs to all 4 limbs → increased extensor tone, normal to hyperactive spinal reflexes
delayed postural reactions in all 4
UMN bladder
rarely respiratory difficulty
rarely Horner’s syndrome
pertinent anatomy of C6-T2 (brachial plexus)
descending UMN tracts to all 4 limbs
ascending GP and nociception from all 4 limbs
LMNs to the front limb
pre-ganglionic sympathetic fibers
LMN of phrenic nerve
lateral thoracic nerve
lesions at C6-T2
gait affected in all 4 limbs
delayed postural reactions in all 4
LMN signs to forelimbs → decreased muscle tone and reflexes in forelimbs
UMN to hindlimbs → normal to hyperactive reflexes in rear
UMN bladder
pertinent anatomy of T3-L3
descending UMN to rear limbs only
ascending GP and nociception from rear limbs
hypogastric nerve = L1-L4
border cells
border cells
located in dorsolateral border of the ventral gray column in lumbar segments
provide tonic inhibitory influence on muscle of the forelimbs → schiff-sherrington phenomenon (posture)

what is this showing?
schiff-sherrington phenomenon
lesions at T3-L3
gait affected in hind limbs only
normal postural reactions and reflexes in forelimbs
UMN to hindlimbs → normal to hyperactive reflexes in hindlimbs, possible crossed extensor reflex
delayed postural reactions in hindlimbs
UMN bladder/sphincter
possible schiff-sherrington
pertinent anatomy of L4-S3 (lumbosacral plexus)
UMN to the rear limbs only
GP and nociception from rear limbs only
LMN to the rear limb
L4-L6 = femoral nerve
L6-S1 = sciatic nerve
S1-S3 = pudendal nerve
S1-S3 = pelvic nerve
lesions at L4-S3
gait affected in hindlimbs only
normal postural reactions and reflexes in forelimbs
LMN signs to hindlimbs → decreased spinal reflexes in hindlimbs, decreased muscle tone in hindlimbs, tail, and anal sphincter
delayed postural reactions in hindlimbs
LMN bladder/sphincter
S1-S3 (pelvic plexus, pudendal nerve)
forelimbs normal
gait may be normal
posture could be normal or only slightly plantigrade in hindlimbs
LMN anal sphincter
LMN bladder
caudal nerves (Cd1-5)
LMN tail
bladder should be normal
anal tone should be normal