Neuro Rehab

Lecture 1

Neuroanatomy
Central Nervous System (CNS)
 Cerebral Cortex
o Central sulcus divides the frontal lobe from the parietal lobe. Lateral sulcus divides the frontal
lobe from the temporal lobe.
o Insular cortex: helps regulate homeostatic
function
o Limbic lobe: emotions
o Thalamus, hypothalamus, pituitary gland
o Corpus Callosum- thick band of nerve fibers that
divides the cerebral cortex lobes into left and
right hemispheres. Allows for communication
between hemispheres.
 Cortical lobes (lobes of the cortex)
o Prefrontal lobe/ Prefrontal cortex
 Located at the front of the frontal lobe
 Planning, initiating movement
 Fibers project to supplementary
and premotor areas (go to other
parts of the brain)
 Executive functioning, reason, abstract thought, monitoring behavior, prioritizing,
coordinating motor and sensory info into behavior
 Mental status assessed with Mini-Mental State Exam (MMSE)
1. Level of consciousness
a. Alert- awake and attentive to normal stimulation
b. Lethargic- drowsy, may fall asleep
c. Obtunded- difficult to arouse from somewhat somnolent state, confused when
awake
d. Stupor- semi- coma
e. Comatose
2. Attention
a. Awareness if environment without being distracted by other stimuli
3. Orientation
a. Person, Place, Time (A & O x3)
4. Language
a. Dysphonia – impaired voice (or change in voice quality)
b. Dysarthria – slurred speech
c. Dysphasia – difficulty swallowing
5. Learning and memory
a. Immediate memory, STM, LTM, transfer from STM to LTM
i. Things that influence memory:
1. Emotional state
2. Rehearsal
3. Association
4. Automatic memory
 6. Cortical/ cognitive functions
a. Fun of knowledge
b. Calculation ability
c. Proverb interpretation
Apraxia- in ability to carry out on
request a complex or skilled
movement
 Ideomotor apraxia- pt is
unable to mimic action when
asked but when task arises,
performs it normally
 Ideational apraxia- unable to
perform task in correct sequence.

7. Thought content
8. Mood/ affect
o Frontal lobe
 Primary motor cortex (#4)
 Located in dorsal portion of the frontal lobe
 Controls ability to move on contralateral side
o Lateral precentral gyrus: hip, trunk, UE, hand, face
o Medial precentral gyrus: LE
 Damage to this area affects opposite side of the body
 Somatosensory map controls movement
o Waist, UE, and face, upper body on outside and leg is on inside (to the opposite
side)
 Premotor area (ant/ lat #6)
 Area of motor cortex located in frontal lobe just anterior to the primary motor
cortex – learning of movements (baby doesn’t have this)
 Motor planning of learned movements on contralateral side, as well as learning new
movements
 Supplementary motor (ant/ med #6)
 Located on the midline surface of the hemisphere just anterior to the primary
motor cortex
 Initiation, sequencing movements, retrieval of motor memory on contralateral side
o Parietal lobe
 Primary somatosensory cortex (1, 2, 3)
 Somatotopic representation of primary sensations
o Lateral postcentral gyrus is the location of the primary somatosensory cortex
 Association somatosensory (5, 7)
 Just posterior to the primary somatosensory cortex
 Processing somatic (and visual) stimuli into meaningful information
 Discriminative sensations, i.e. cortical sensations (what happens on his right hand is
being interpreted on the left side of the brain
 Sensorimotor Homunculus
 Somatic representation of the body in the sensorimotor cortex
o Overlies primary motor cortex and primary somatosensory cortex

Motor control – better control

Sensory – more discriminative
touch
 for face and hand than butt or
foot
 o Temporal lobe (below lateral sulcus)
 Superior: primary auditory and association auditory areas
 Primary: hearing sounds
 Association: processing stimuli into information
o Wernicke’s area for language (left side only) (makes sense of words for
language)
 Middle and inferior
 Long term memory and short term memory
o Medial/ superior
o Hippocampus damage can produce anterograde amnesia
 Inability to create new memories, failure of encoding and storage
o Other temporal and prefrontal lobe damage produces retrograde amnesia
 Inability to recall old memories that occurred before the event

o Occipital lobe
 Primary
 Visual stimulus from optic nerve
 Association
 Processing visual stimulus into recognizable
objects

Cerebral circulation
 Left side common carotid artery  feeds ICA and ECA
 Anterior circulation: internal carotid artery
o Feeds the front part of the Circle of Willis
 Middle cerebral artery (dominate on lateral cortex)
 **TRUNK,UE, FACE of CONTRALATERAL
SIDE
 Anterior cerebral artery (dominate on front medial)
 LE of CONTRALATERAL SIDE
 Posterior circulation: vertebral artery (comes off subclavian)
o Dominate on posterior
Subcortical Structures (involved in refining the motions)
 Basal ganglia (5 parts)
o Caudate nucleus and Putamen = striatum
o Globus pallidus, subthalamic nucleus, and substantia nigra
o Initiation or inhibition of movement, control of postural adjustments, muscle tone
o Damage to basal ganglia (lack of dopamine production) causes Parkinson’s disease (to little
movement)
 Cerebellum
o Helps provide smooth, coordinated body movement
o Contributes to balance/ equilibrium
o Plays a vital role in motor learning

Motor Pathways
 CNS components involved in motor function
 Information for movement travels down corticospinal tract after it has been fine-tuned at the basal ganglia
and cerebellum
 Basal ganglia and cerebellum also influence tone of muscles
o Parkinson’s disease —» rigidity
 Not all movement comes from motor cortex ***
o Reflex movement comes from brainstem (midbrain, pons, medulla), i.e. pushing someone

Brainstem
 Midbrain  pons  medulla
 Reticular system (ascending and descending) – activates the cerebral cortex, level of alertness
o Sensory goes up, wakes up the brain
o Descending – motor tracts, tone and gross movements
 Nuclei of extrapyramidal descending motor tracts
o Contains brainstem motor tracts
 “pyramidal tracts” are the corticospinal and corticobulbar tracts *** (UMN)
 “extrapyramidal” are the motor tracts that start in the brain stem, NOT corticospinal or
corticobulbar
 Cranial portion of PNS (CN 3,7,9 and 10)
(PNS also S2,3,4)
 Contains cranial nerves
o Midbrain (eyes)
o Pons (face movement and sensation)
o Medulla (vital functions and spinal accessory and tongue function)
 Damage here is more severe
 Cardiac centers and respiratory centers
 Reticular Activating System
o Sensation from the brainstem going to the cortex
 Ascending general sensory fibers of spinoreticular tracts
  Descending motor projections of reticulospinal tracts
o Activates the cerebral cortex, level of alertness
 i.e. loud sounds, lights, shaking someone

Ventricles of the Brain

 CSF: cushions the brain from sudden movement or impact
 4 ventricles: 2 lateral, 3rd ventricle and 4th ventricle

Internal Capsule (main pipe)

 Tunnel for pathway of corticospinal and corticobulbar tracts, as well as
ascending somatosensory tracts from thalamus to cortex (conscious
sensations)
o Damage to these tracts will cause UMN signs ***
 Corticospinal Tract
o Pyramidal tract, descending (motor)

o Pathway
 Cell bodies are found in the cerebral cortex —»
corona radiata (subcortical white matter) —»
internal capsule (posterior limb) —» ventral pons
—» pyramid of upper medulla (decussates
(crosses) in lower medulla) —» into lateral
funiculus of SC
 Damage in the internal capsule can cause
both sensory and motor deficits OR just
motor deficits (depends on what tracts in
the internal capsule are damaged)
 Cortical Motor Tracts
o Corticospinal Tract
 Splits in the medulla
 Lateral CST (cross over above the
medulla)
o Crosses over, fine movement (90%)
 Above medulla: movement of
contralateral extremities
 Below medulla: movement of
ipsilateral extremities
 Inside = arm and outside = leg
 Anterior CST (5 – 10%) –
o Postural (axial) muscles, gross movement
o Corticobulbar Tract
 Innervate motor CNs
 Lower motor neurons of brainstem that innervate face
 Usually bilateral but more innervation of contralateral motor CN – feeds both sides
except 7 and 12 feed contralateral side

****in CNS THE ONLY PLACE YOU WILL SEE UMN SIGNS IS IN CORTICOBULBAR AND CORTICOSPINAL
TRACTS(Lateral and Anterior) OR primary motor cortex (3 total tracts, 4 possible area of injury) THE REST IS
EXTRAPYRAMIDAL!!!!
  Brainstem motor tracts (Extra pyramidal)
o Rubrospinal, vestibulospinal, reticulospinal
 Descending Motor Pathways
o Dorsolateral system motor control of extremities, fine and more advanced movement
 Lateral Corticospinal (LCST)
 Rubrospinal: flexor tone of upper extremities
 Highest of brainstem tracts

o Ventromedial system motor control of trunk muscles, gross movement

 Vestibulospinal: balance, posture
 Lateral (LVST): facilitates extensor tone of muscles
 Medial (MVST): primarily to cervical region
o Stabilize head, head righting, and eye righting reflexes (VOR)
 Reticulospinal: mass movement patterns
 Medial tract (pons) facilitates extensor tone (posture) – higher part
 Lateral tract (medulla) inhibits extensor tone (movement) – lower part
Ant Corticospinal Tract

When these are damaged: your posture is compromised

o Decorticate posture = in trouble (lesion separating the cortex from midbrain (separating control
between Corticospinal from Rubrospinal) UE’s are flexed (since RST does flexor tone), LE’s are
extended (vestibulospinal and perhaps reticulospinal facilitation of extensor tone)
 Rubrospinal  arms flexed, legs extended
 Damage gets worse as it goes below rubrospinal tract isolated cerebrum so now rubro isn’t
controlling it anymore and vestibulo and reticulo are controlling it and end up with and
extended posture

Peripheral Nervous System (PNS)

Cranial Nerves
ANS
Spinal Nerves (LMN)
Enteric Nervous System

 Cranial nerves
o Midbrain
 Eye movements, pupil constriction (I and II are above midbrain)
 III and IV
o Pons
 Facial sensation, chewing, facial expressions, equilibrium
 CN V-VIII
o VIII is really on the pons-medulla junction
o Medulla
 Swallowing, gagging, respiration, circulation, tongue movements, SCM, and trapezius
 CN IX- XII
o CN I-XII
 Olfactory, optic, oculomotor, trochlear, trigeminal, abducens, facial, vestibulocochlear,
glossopharyngeal, vagus, accessory, hypoglossal
o (LR6SO4)3
   ANS
o Sympathetics (fight or flight)
 T1-T5: cardio-excitatory, dilates lungs and pupils
 T6-T12: constrict splanchnic & LE blood vessels, stimulate kidneys and adrenals
 T12-L3: genitourinary function
 i.e. increase heart rate, lungs dilate, increase muscle tone
o Parasympathetics
 Cranial Nerves
 CN III, VII, IX: constricts pupils, stimulates salivation and lacrimation
 CN X: slows heart, constricts lungs, dilates splanchnic blood vessels, stimulates GI
mobility
 Sacral
 S2, 3, 4: genitourinary function (bowel and bladder)
o Note – normal genitourinary function requires intact SNS T12-L3, PNS S2-S4,
spinal nerve S2-S4

 LMN: “final common pathway”

o Alpha motor neuron: transmit impulse of UMN or Ia afferents to skeletal muscle (extrafusal) for
contraction
 Motor unit: all the muscle fibers one motor nerve innervates
 Motor nerves
o Cranial nerves
o Spinal nerves —» branch into peripheral nerves
o Gamma motor neuron: transmit impulse of descending tracts to muscle spindle (intrafusal)
 Make muscle spindles more sensitive to stretch

Ascending Tracts (Sensory Tracts)

1. Spinothalamic Tract (non- descrimitive)
 Lateral Spinothalamic Tract: pain, temperature
 Anterior Spinothalamic Tract: crude light touch,
o **decussates (crosses) at the level of the spinal segment**

2. Posterior/ Dorsal Column or Medial Lemniscus (discrimitive)

 Dorsal Column: transmit proprioception, vibration, pressure, fine touch
o Decussates at the medulla, becomes medial lemniscus above medulla
3. Spinocerebellar Tract transmits unconscious sensations to the cerebellum – none of them cross, ipsilateral!!!!
 Dorsal Spinocerebellar (L2-T1 or –C8)
o Touch, pressure, kinesthesia, fine coordination, posture of LEs
 Receptors: muscle spindles, GTOs, touch, pressure
 Ventral Spinocerebellar
o Gross coordination and posture of LEs
 Receptors: flexor reflex, GTOs
 Cuneocerebellar (T4-C2 or C8-C2) - FINE MVMT
o Upper body equivalent of dorsal spinocerebellar
o Cervical and UEs, fine coordination and posture of UEs
 Rostral Spinocerebellar Tract - GROSS MVMT
o Upper body equivalent of ventral spinocerebellar

Lesions of movement pathways typically cause impairments that contribute to functional impairments and result in
disability. Lesion sites can be…
 CNS
o Upper CNS: motor cortex, premotor cortex, supplementary motor cortex, sensory cortex,
cerebellum, basal ganglia
o Descending tracts: corticospinal, corticobulbar, rubrospinal, vestibulospinal, reticulospinal
o Ascending tracts: spinothalamic, dorsal column, spinocerebellar
 Damage to motor cortex, corticospinal, and corticobulbar will cause UMN signs
 Damage to everything else will cause LMN signs
 PNS
o Efferents: (ventral spinal n) alpha motor neurons, gamma motor neurons, motor units (n + muscle
fibers it innervates)
o Afferents: (dorsal spinal n) afferent n, sensory receptors, etc
 Damage to alpha motor neuron and motor units will cause LMN signs
 Effector target: muscle fibers

UMN: Red
LMN: Green

Lesions can result in impairments…

 Weakness
 Incoordination
 Balance dysfunction
 Sensory and perceptual dysfunction
o Perceptual dysfunction = problem with awareness, not sensation
 Pain
 Abnormal muscle tone

Anatomic Region Typical Impairment

Primary motor cortex (on opposite side) Weakness or paralysis, UMN signs, synergy
Sensory cortex (on opposite side) Loss of sensation, perception, agnosias,
proprioception, motor control difficulty,
sensory ataxia
Premotor region Apraxia, difficulty planning motor task, disuse
weakness
Supplemental motor region Apraxia, complex motor task and sequencing
difficulty, disuse weakness
Basal ganglia Paucity of movement (hypo), abnormal
 movements (chorea, tremor) (hyper), rigidity,
disuse weakness
Cerebellum Incoordination, balance problems, intention
tremors, motor learning difficulty, disuse
weakness, hypotonia
Corticospinal tract Weakness, UMN signs
Alpha motor neuron Weakness, atrophy, LMN signs
Muscle Weakness, atrophy
Afferent sensory input Impaired sensory awareness, uncoordinated
movement (sensory ataxia), balance problems

Anatomical Lesions and Signs

 UMN – weakness, hypertonicity (spasticity type), increased myotatic reflexes (DTRs, clonus), + Babinski
 LMN – weakness, hypotonicity, hyporeflexia/ areflexia (decreased or no DTRs), weakness/ paralysis,
atrophy, fasciculations

UMN Lesions
 Corticospinal (pyramidal): crosses at lower medulla
o Lesion above medulla = contralateral signs
o Lesion below medulla = ipsilateral signs
 Weakness/ plegia below the lesion (UE and/or LE)
 Increased myotatic stretch reflexes (DTRs)
 Clonus, hypertonicity
 Babinski
 Pronator drift
 Corticobulbar
o Weakness/ plegia of facial muscles, SCM, traps
 LMN (CN VII) = all of face is paralyzed
 Ipsilateral damage
o UMN (corticobulbar or cortex) = can wrinkle forehead but lower face is paralyzed
 Upper CN VII (facial) has bilateral innervation from cortex – contralateral damage
 Both L and R corticobulbar innervate upper part of CN VII
 Only contralateral corticobulbar innervates lower part of CN VII
o Ipsilateral CN XII damage (LMN)
 Nerve damage is on the same side as LMN signs
 If you can still wrinkle your forehead, it is contralateral UMN damage
o Do CN testing to locate brainstem lesion
 Midbrain: III, IV
 Pons, V, VI, VII, VIII
 Medulla: IX, X, XI, XII
 Rubrospinal: midbrain
o Flexor tone UEs
 Vestibulospinal: pons and medulla
o Extensor tone UE and LE
 Reticulospinal: pons and medulla
o Extensor tone UE and LE
 *** See decorticate (flexed arms and extended legs) and decerebrate posture (extended arms and legs)

Extrapyramidal = cerebral cortex, BG, thalamus, cerebellum, brainstem, descending tracts (except primary motor
cortex, corticospinal and corticobulbar tracts)
Cerebral Cortex Lesions
 Primary Sensory area: contralateral impaired…
o Pain, temperature, light touch, vibration, proprioception
 Association area: contralateral impaired cortical sensations…
o 2 pnt discrimination, stereognosis, graphesthesia
 Motor cortex: contralateral…
o Paresis/ plegia of face, arm, leg
o Initially flaccid (hypotonic) followed by UMN signs
 Weakness, hypertonicity, hyperreflexia, Babinski, pronator drift

Extrapyramidal – Basal Ganglia

 Substantia nigra to caudate nucleus/ putamen pathway damage…
o Hypokinesia, bradykinesia, akinesia (difficulty initiating movement), resting tremor, rigidity
(leadpipe or cogwheel)
 Caudate nucleus/ pudamen (striatum) to globus pallidus damage…
o Hyperkinesia, chorea, athetosis (twisting of axial muscles), dystonias
 Subthalamic nuclei…
o Hyperkinesia, rotatory component

Extrapyramidal – Cerebellum
 Cerebellar lesion will cause ipsilateral cerebellar signs
o Dysdiadochokinesia: rapid alternating movements
o Dysmetria: decreased accuracy
o Intention tremor = shaking as approaching target
o Rebound phenomena – cant shut down the muscle
o Ataxia (motor: appendicular or trunkal)
 Loss of smoothness of movement
 Including eye movements, i.e. nystagmus, saccades, smooth pursuit
o Impaired balance
o Decreased muscle tone (hypotonic)
o Dysarthria (speech articulation – scanning speech), weakness (asthenia)

LMN Lesions
 LMN to effector organ
o Hypotonicity
o Areflexia (no DTRs), hyporeflexia (decreased DTRs)
o Weakness, paralysis
o Atrophy
o Fasciculations (acute)

Ascending Tract Lesion

 Spinothalamic – crosses at SC level
o Contralateral loss of pain and temperature below lesion level
 Dorsal Column/ Medial Lemniscus – crosses at medulla
o Lesion above brainstem: contralateral loss
o Lesion below brainstem: ipsilateral loss below lesion level
 Loss of proprioception, vibration, 2 pnt discrimination, astereognosis, sensory ataxia, etc
 + Romberg sign (narrow stance and arms crossed with eyes open and asked to keep balance)

Neuroplasticity
  Certain cortices, especially sensory and visual, have ability to change
o Heightened responsiveness of neighboring cortical areas to compensate for a deficit
o Ability of nervous system to recognize new demands and adapt to them
 Reason why receiving PT is superior to bedrest when recovering from neuropathological
event
 Promote neuroplasticity by increasing sensory and motor neuron firing to encourage
neighboring, undamaged neurons to compensate

Confirm/ Determine PT Dx and POC

 Impaired motor function and sensory integrity associated with nonprogressive disorders of the CNS –
acquired in adulthood
o CVA, TBI, seizures, aneurysm, neoplasm, anoxia, Bell’s palsy
 Impaired motor function and sensory integrity associated with progressive disorders of the CNS
o PD, MS, ALS, Alzheimer’s, AIDS, Huntington’s Disease, alcoholic ataxia
 Impaired peripheral nerve integrity and muscle performance associated with peripheral nerve injury
o Neuropathies: CTS, Erb’s palsy, peripheral vestibular disorders, motor nerve lesions
 Impaired motor function and sensory integrity associated with acute or chronic polyneuropathies
o Guillian Barre, post-polio syndrome, DM, alcoholic, renal, amputation, leprosy, ANS
 Impaired motor function, peripheral nerve integrity, and sensory integrity associated with non-progressive
disorders of the SC
o Traumatic SCI, SC neoplasm, SC compression, HNP

Establish prognosis…
Prognosis – “predicted optimal level of improvement in function and time needed”

Establish POC…
POC – based on pt hx, exam, dx
1. Goals, outcomes
a. Goals decrease impairments (increase strength, balance, coordination, ROM) for the purpose of
improving function (bed mobility, transfers, ambulation, ADL, IADL, etc)
i. STG and LTG
b. Outcomes decrease functional limitations and disabilities (lnd amb apt to curb with s cane, ind
transfers, etc) optimize health status and pt’s satisfaction
i. Pt must be involved in setting goals/ outcomes specific for that pt
2. Interventions: based on identified impairments and functional limitations/ ther ex, muscle re-ed, resistive
ex, balance ex, coordination ex, modalities, transfer training, gait training, HEP
3. Frequency and duration: 3x/ wk x 2 wks, 2x/ wk x 3 wks
4. Discharge criteria
a. Pt able to ambulate 200’ ind with s cane and 4 steps (apt to curb distance), ind in all transfers, risk
of fall minimized
b. Enable pt to return to premorbid occupation
c. Enable pt to return premorbid occupation on a part-time/modified basis

Re-evaluate in progress notes…

 Progress towards goals and outcomes, evaluate intervention effectiveness
 Revise POC if necessary
o Are goals/ outcomes reasonable given progress and dx
o Are interventions appropriate
o Pt’s motivation
 Update DC planning
o Evaluation and modification of home environment
 o Pt, family, caregiver education
o Plans for follow up or referral
o Instruct in HEP

Documentation
 Initial eval note
 Progress notes (SOAP)
 DC note

Conceptual Models of Disability

1. Nagi: task-oriented approach
o Treat disability caused by functional limitation (limited transfers, ambulation, etc) by addressing
impairment (weakness, balance, coordination, ROM, pain, etc) in order to improve task performance
o Pathology —» impairment —» functional limitation —» disability
Pathology:
Impairment:
Functional Limitation:
Disability:

 Denervated iliopsoas —» can’t actively flex hip —» gait abnormalities —» difficulty walking
stairs/ ramps
2. ICIDH (International Classification of Impairment Disabilities, and Handicaps)
o Based on Nagi model
o Not a clear distinction between disability and handicap
o Handicap is based on the environment a person finds him/herself in, not the person alone
o Disease —» impairment —» disability —» handicap
 Stroke —» paralysis —» decreased ADL, mobility, transfers, ambulation —» decreased work
role in current environment
3. ICF (International Classification of Functioning, Disability and Health)
a. System of classification of domains & categories of human functioning.
i. Functioning & disability are outcomes of interactions between intrinsic factors of the
person & environment
ii. Specific for each diagnosis

Standardized Measures of Disability

 Allows for uniform language for measuring rehab outcomes
1. Barthel
o Population: adult, all dxs
o Measures functional limitations and disabilities, NOT impairments
 10 questions: ADL, transfers, amb, stairclimbing, B&B
o Measures function, mobility, and need for assistance
 60-100 = independent
 less than 60 = need assistance, nursing home
2. Rivermead Mobility Index
o Population: pts post-acute or chronic stroke
o Measures functional limitations and disabilities
o Assesses motor performance (transfers, sitting and standing balance, walking, no assessment of
bathroom transfers)
3. Functional Independence Measure (FIM)
o Population: adult rehab, all dxs
o Mandatory inpatient assessment
 o Measures function and disability (ADL, amb, transfers, B&B, cognition, communication)
 Designed to be an improvement in sensitivity over Barthel
4. OASIS
o Measures functional limitations and disabilities of homebound persons
o Mandatory homecare assessment
o More specific than Barthel

Standardized Measure of Impairment

1. Fugl-Meyer Assessment of Sensorimotor Recovery after Stroke
o Population: adults post-CVA
o Measures impairment (motor, sensory, balance) NOT disability
o Includes reflexes, voluntary movement, dexterity, coordination/ speed, sensation, ROM
o Used to determine disease severity, describe motor recovery, and to plan and assess rx

Standardized Measures of Quality of Life (QOL) subjective measures

1. SF-12 (short form- 12)
2. SF-36 (short form- 36)
3. QOL (quality of life scale)
4. HSQ-12 (12-item health status questionnaire)

Sensory and Motor Tracts

*** If the tract begins with “spino” (as in spinocerebellar), the tract is a sensory tract delivering information from
the spinal cord to the cerebellum (in this case). If the tract name ends with “spinal” (as in vestibulospinal), the
tract is a motor tract that delivers information from the vestibular apparatus (in this case) to the SC.

Sensory Tracts (Ascending Tracts)

 Posterior Column tract (Dorsal Column or Medial Lemniscus)
 Spinothalamic tract: transmits pain and temperature sensations to thalamus and then to cerebrum
o Lateral Spinothalamic tract: transmits pain and temperature sensation to the thalamus
o Anterior Spinothalamic tract: transmits pressure and crude touch sensations to the thalamus
 Spinocerebellar tract: transmits proprioception sensations to the cerebellum

Motor Tracts (Descending Tracts)

 Corticospinal tract: conscious control of skeletal muscles, comprised of mostly motor axons that carry
motor information from the cerebral cortex and brainstem to the musculature for voluntary movement
o Corticobulbar tracts: conscious control over eye, jaw, and face muscles
o Lateral corticospinal tracts: conscious control over skeletal muscles
o Anterior corticospinal tracts: conscious control over skeletal muscles
 Subconscious tract: subconscious regulation of balance, muscle tone, eye, hand, and UE position
o Vestibulospinal tracts: send info from inner ear to monitor position of hand, vestibular nuclei
respond by altering muscle tone, neck muscle contraction, and limbs for posture and balance
o Tectospinal tracts: sends info to the head, neck, and upper limbs in response to bright and sudden
movements and loud noises
o Reticulospinal tracts: send info to cause eye movements and activate respiratory muscles
o Rubrospinal tracts: send info to the flexor and extensor muscles