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CNS
brain and spinal cord; processes and integrates information
PNS
all nerves outside CNS; connects CNS to limbs and organs
Neuromotor system
CNS+PNS components that controls coordinated movement
Cell body
contains nucleus
dendrites
receive signals; many per neurons
axon
transmits signals; one per neuron
axon hillock
summation point for voltage signals
sensory (afferent)
unpolar; send into to cns
motor (efferent)
alpha motor neurons (skeletal muscles); gramma motor neurons (intrafusal fibers)
motor unit
alpha motor neuron + all muscles fibers it innervates
motor unit functions
all fibers contract when neurons fires
motor unit principles
all - or-none activation
Central nervous system structures
cerebrum
diencephalon
Cerebellum
brain stem
spinal cord
Cerebrum
voluntary movement
diencephalon
thalamus: relay station; attention, mood
hypothalamus: endocrine control, homeostasis
cerebellum
smooth movement, coordination, posture, motor learning
Brain stem
pons: chewing,balance
medulla: breathing, internal regulation
midbrain: sensory motor integration
Spinal cord
gray matter: cell bodies
dorsal horns: sensory
ventral horns: motor (alpha motor neurons)
stroke (CVA)
sudden neurological deficit due to ischemia or hemorrhage
Types of stroke ( ischemic)
83%
atherothrombotic, embolic, lacunar, cryptogenic
Types of stroke (hemorrhagic)
17%
intracerebral, subarachnoid
Stroke risk factors
atherosclerosis, HTN, cardiac disease, diabetes
stroke pathophysiology
anoxia→infarction→edema→ increase ICP → herniation
stroke syndromes
ACA, MCA, PCA, vertebrobasilar
stroke symptoms
aphasia
sensory/motor deficits
spasticity
abnormal reflexes
stroke diagnosis
dopller
CT
MRI
Angiography
EKG
Recovery stage of stroke
flaccidity
spasticity & synergies
voluntary movement in synergies
isolated joint control
movement out of synergy
near normal control
Warning signs for strokes
sudden weakness
confusion
vision loss
dizziness
headache
Traumatic brain injury
brain insult from external force
Primary Damage of traumatic brain injury
diffuse axonal injury: shearing of axons
focal injury: contusions, hemorrhages
coup-contrecoup: impact + rebound injury
Secondary damage of traumatic brain injury
hypoxic ischemic injury
edema, increase ICP
Concussion
temporary brainstem dysfunction
Changes in traumatic brain injury
physical: motor, speech, seizures
cognitive: memory, attention, aphasia
behavioral: mood swings, impulsivity
Diagnosis for brain injury
CT, MRI, EEG
Recovery stages for brain injury
coma→vegetative→minimally responsive→ confusion→ independence→ competence→ plateau
Degenerative disorder overview
MS, ALS, PD, MG: each affect nervous system differently
Multiple sclerosis (MS)
demyelinating CNS disease; autoimmune
Types of MS
relapsing- remitting (65%-80%)
primary progressive (10-20%)
secondary progressive
progressive relapsing
MS symptoms
paresthesia
ataxia
vertigo
fatigue
spasticity
vision loss
MS diagnosis
MRI
EEG
EMG
Amyotrophic lateral sclerosis (ALS)
degeneration of UMN + LMS
types of ALS
Progressive muscular atrophy (LMN)
primary lateral sclerosis (UMN)
progressive bulbar palsy
ALS symptoms
weakness
fasciculations
spasticity
dysphagia
dysarthria
Parkinson’s disease
Dopamine deficiency in basal ganglia
hypokinetic disorder
Symptoms of Parkinson’s disease
tremor, ridity (lead-pipe/cogwheel), bradykinesia, postural instability, festination gait, speech changes
Myasthenia gravis (MG)
autoimmune attack on ACh receptors
MG symptoms
fatigue
facial droop
chewing/swallowing difficulty
worsens with activity, improves with rest
Types of MG
ocular
mild generalized
sever generalized
crisis
Peripheral nervous system (PNS)
connects CNS to limbs/organs
PNS motor sensory receptors
input
PNS motor units
output
PNS receptors
Exteroceptors: external stimuli
interoceptors: internal stimuli
proprioceptors: body position/ movement
Sensory receptors
Free nerve ending: pain/temp
merkel discs, root hair plexuses: light touch
meissner’s corpuscles: light touch (hairless skin)
ruffini’s, pacinian corpuscles: deep pressure, stretch, vibration
proprioceptors
muscle spindles: stretch
golgi tendon organs: tension
joint kinesthetic receptors: joint position
info sent to cerebellum and spinal reflex arcs
Motor unist
motor neuron + all innervated fibers
all fibers contract together
fine control: fewer fibers per neuron
Cranial and spinal nerves
mnemonic: oily oranges on tower tickle ants funnily and give velvety angry hands
31 spinal nerves: 8C, 12T, 5L, 5S, 1C
dorsal roots: sensory
ventral roots: motor
rami: branches outside foramen
plexuses: cervical, brachial, lumbar, sacral
Brachial plexus (C5-T1): musculocutaneous, median, ulnar, axillary, radial
Peripheral nerve injuryies
cause: trauma, compression, metabolic, inflammation, surgery, aging
common injuries:
radial (most common)
ulnar (30%)'
median (15%)
lumbosacral plexus (3%)
Classification of nerve injuries
Neurapraxia: temporary; full recovery
axonotmesis: axonal damage: regeneration possible
neurotmesis: complete severance; surgical repair needed
specific nerve injuries & deformities
median: ape hand (thumb adduction, hyperextended index)
ulnar: claw hand
radial: wrist drop (extensor weakness)
thoracodorsal: wining of scapula
lateral popliteal: foot drop
Treatment and repair
Screening:
ulnar: tip of little finger
median: tip of index finger
radial: thumb extension
surgical pns
epineural
fascicular
nerve graft
repair failure for pns
inadequate resection
tension
Pain
IASP: sensory/emotional experience linked to tissue damage
subjective; varies by individual
nociception: detection via A-delta
C fibers
Physiology of pain
components:
detection (nociceptors)
activation (stimulus)
transmission (neural pathway)
modulation (inhibition/ amplification)
Pain classification
Acute: < 6 months; injury/inflammation
chronic: > 6 months; may lack clear cause
Pain Type
nociceptive: proportional; protective
inflammatory: tissue damage
neuropathic: CNS/PNS dysfunction; non-protective
psychogenic: psychological origin
mixed: combo (failed back surgery)
Pain pathway
fast pain: A-delta→ spinothalamic→ reticular formation→ thalamus→ hypothalamus→ limbic system
Slow pain: C fibers→ spinothalamic→ reticular formation→ thalamus→ hypothalamus→ limbic system
Pain modulation (inhibition)
gate control theory: large fibers (A-apha, A-beta) inhibit small fibers (A-delta, C)
descending analgesic system: endorphins/enkephalins inhibit pain via presynaptic inhibition
pain and gender
gender role theory: women more likely to report pain
exposure theory: women face more pain risks
vulnerability theory: women more