Week 41-Traumatic Brain/Spinal Injury (Muscle)
Normal Motor Control
Direct Motor Path (Pyramidal)
-Voluntary movement cortex to
skeletal muscles.
-Lateral Corti: distal limb
-Anterior Corti: proximal limb/trunk
-Corticobulb: head muscles
Indirect Motor Path (Non-Pyramidal)
-Automatic movement; brain stem to
skeletal muscle.
-Tectosp: head/eye response
-Vestibulosp: balance/posture
-Reticulosp: posture/orientation
-Rubrosp: precise movement distal
limb
Decussation Points
-Lateral corticospinal=pyramids
-Anterior corticospinal=spinal levels
-Corticobulbar (not all)=brainstem
-Rubrospinal=tegmentum
-Tectospinal=under superior colliculus
Autonomic Nervous System Overview
-Centres in brainstem and hypothalamus.
Structure
!Sympathetic Division (S like “senter=center”
aka short preganglionic)
-Short preganglionic neuron, long
postganglionic neuron.
!Parasympathetic Division (P=Peripherals
aka long preganglionic)
-Long preganglionic neuron, short
postganglionic neuron.
Neurotransmitters & Receptors
-⍺1 and β1=excitation
-⍺2 and β2=inhibition
-NE stimulates ⍺ better than β; Epi. is strong
stimulating both.
-NE activity ends when taken up by axon that
released it or inactivated by COMT/MAO.
Function
-SNS catabolic system enabling the body to deal
with stress; PaNS homeostatic or anabolic
system promoting quiet and orderly bodily
processes.
Stretch Reflex
Function
—maintain balance
and posture
Motor Control
—allows reflex signal
to return to muscle
with shortest possible
time delay; stretch isn’t
interpreted consciously
before contraction.
Pathway
-When a muscle is suddenly stretched, muscle spindles are
excited initiating the reflex arc.
-Reflex arc→contraction of stretched skeletal muscle fibres.
-Monosynaptic (2 neurons, 1 synapse) and polysynaptic (3
neurons, 2 synapses) stimulated simultaneously.
Muscle Tone -Monosynaptic:
-Slight muscle toughness due to weak involuntary contractions of •Originates in stretched muscle spindle→dorsal root
motor units. spinal cord→synapse with anterior motor
-When a motor neuron is cut the muscle becomes flaccid. neuron→motor neurons extend effector→same muscle
-Muscle tone sustained via small groups of motor units are contracts relieving stretch.
alternatively activated/inactivated in a constantly shifting pattern. -Polysynaptic (antagonist muscles):
-Tone keeps skeletal muscle firm but doesn’t result in movement. •Collateral muscle spindles synapse with inhibitory
interneurons in spinal cord→synapses with motor
Changes in Tone neuron→antagonistic muscle relaxes (reciprocal
Hypertonia—reduction in muscle stretch due to increased muscle innervation/inhibition)
tension.
-Causes: UMN lesions (no LMN inhibition=↑ excitability of muscle Structure
fibres). 1) Sensory receptor—intrafusal muscle fibre stretching
-Leads to 2 states: stimulates muscle spindle (receptor)
spasticity (prolonged muscle contractions) & rigidity (muscle 2) Sensory neuron—muscle spindle generates impulse
stiffness/decreased flexibility). conducted via Ia afferent neuron to dorsal root and
-Rigidity has 2 types: leadpipe (muscle stiffness maintained spinal cord.
through entire range of movement) and cogwheel (combination of 3) Integrating center—sensory neuron synapses with
rigidity with tremors producing spastic movements). motor neuron in anterior gray horn.
Hypotonia—state of reduced muscle tone and tension resulting in 4) Motor neuron—strong excitations cause impulse to
lessened ability to generate force from muscle contractions. initiate in motor neuron propagating along axon from
-Strokes can cause lesions of motor cortex removing continual spinal cord through peripheral nerves to stimulated
tonic stimulation of spinal motor neurons; LMN lesions also a cause. muscle.
HYPERtonia=UMN lesions, PD, CP. 5) Effector—impulse causes ACh release at the MNJ
HYPOtonia=LMN lesion, stroke, Huntington’s. causing action potential thus contraction in stretched
muscle.
 Week 41-Traumatic Brain/Spinal Injury (Sensation)
Sensation Pathways Pain
-Relays information from the somatic sensory receptors -An unpleasant sensory and emotional experiences
to cortex and cerebellum associated with actual or potential tissue damage.
-3 pathways with 3 neurons. Nociception—the ability of the body to sense potential
1) Dorsal Column Medial Limniscus harm from stimulation of nociceptors which respond to
(cuneate=upper, gracile=lower) tissue damage caused by chemical, mechanical, or
-Sensation: touch, pressure, vibration, propriocep. thermal stimulation.
-Areas: Limbs, trunk, neck, posterior head.
-Decussation: medulla oblongata Types of pain
-1st-order: sensory receptor→spinal cord→medulla. Somatic—pain from the skin and deeper tissues;
-2nd-order: medulla→medial limniscus→thalamus. well localized.
-3rd-order: thalamus→primary somatosensory area Visceral—pain from internal organs; usually not well localized.
2) Anterior and 3) Lateral Spinothalamic Pathway Neuropathic—pain from primary lesion/disease in
-Anterior Sensation: light touch. somatosensory NS; typically from nerve damage.
-Lateral Sensation: crude touch, pain, temperature. Psychogenic—pain disorder attributed to psychological
-Areas: limbs, trunk, neck, posterior head. factors causing pain.
-Decussation: spinal cord Nociceptive—pain from tissue damage
-1st-order: sensory receptors→posterior gray horn described as sharp, aching, or throbbing.
-2nd-order: posterior gray horn→thalamus
Gate Theory
-3rd-order: thalamus→primary somatosensory area.
-Non-painful stimuli closes “gates” to painful input
4) Trigeminothalamic Pathway
-A fibre stimulation via peripheral receptors depress
-Sensation: touch, pain, temperature.
pain signal transmission.
-Areas: face -Contralateral,
inverted, and -3 factors involved in opening and closing this ‘gate’
-Decussation: pons or medulla disproportional
(more sensory 1) amount of activity in pain fibres Fibre Type
-1st-order: sensory receptors→pons (CN V)/medulla given to areas of
2) amount of activity in other peripheral fibres Fast: perception within .1 sec., Impulses along
-2nd-order: pons/medulla→thalamus precision and
tactility). 3) messages descend from the brain medium diameter myelinated A fibres, described
-3rd-order: thalamus→primary somatosensory area.
Opioids as acute, sharp, prickling, not felt in deeper
Referred Pain
-Any substance producing morphine-like effects that can be blocked by tissue.
Pain felt in parts of the body remote from stimulated tissue.
ant agonists (ie naloxone) Slow: perception after 1 sec. gradually
-Pain from internal organs can refer to dermatome served
Classes increasing, impulses conducted along slams
by same spinal nerve.
-3 receptor classes (GPCR linked to G-inhibitory protein) unmyelinated C fibres, described as chronic,
Mechanism
i) μ receptor—most analgesic effects & some unwanted effects. burning, aching, throbbing, in skin and deep
-Visceral pain fibre branches synapse in spinal cord on
ii) δ receptor—analgesia; can also be pro-convulsant. tissue.
same second-order neurons receiving pain signals from
iii) κ receptor—analgesic contributor; sedation, dysphoria, hallucination. Neurophysiology
skin.
MOA -Stimulus carried along axon→dorsal horn of
-Stimulation of these visceral pain fibres are conducted
-Opiates bind to opioid receptor in CNS→ascending pain path inhibited spinal cord (synapse).
through some of same neurons responsible for conducting
-All receptors open K+ channels (cause hyperpolarization) & inhibit -Dorsal horn neurons decussate in anterior white
signals from the skin
Ca2+ channels opening (inhibits neuron transmission). commissure.
-Shared nature of the neurons causes feeling that
Indications—moderate to severe pain relief. -Anterior white commissure→ascend in
sensations originated in the skin itself.
Side Effects—CNS effects, sedation, resp. depression, N/V, anterolateral tract→thalamus
-Pain from somatic afferents occur more often than visceral
constipation, urinary retention. -Synapse in thalamus→thalamic neuron travels
pain, causing the brain to assume that the sensation is
Contraindications—Hypersensitivity, respiratory depression, asthma, to somatosensory cortex
somatic pain felt by the dermatome.
paralytic ileus.
 Week 41-Traumatic Brain/Spinal Injury (Other Stuff)
Concussion vs Confusion Post Traumatic Stress Disorder
Concussion Intense psychological distress marked by horrifying memories, recurring fears, &
-Trauma'c brain injury altering mental status that may involve LOC. feelings of helplessness that develop after a psychologically traumatic event.
-Result of forceful mo'on of the head/impact causing brief change in mental Symptoms—flashbacks, avoidance of trauma associated stimuli, memory
status or LOC less than 30 min. disturbances, withdrawn, increased aggression irritability, insomnia, startle
-Effects usually temporary; include headaches, difficult with concentra'on, response.
Diagnosing Criteria—Exposure to traumatic event meeting criteria with
memory, balance, and coordina'on. symptoms from each 4 clusters.
1) Intrusion (flashbacks, insomnia, emotional blunting)
Confusion 2) Avoidance (discussing event)
-Symptom of not thinking clearly, disorientated, difficult focusing/making 3) Negative cognitive/mood alterations (detachment, lack of interest)
decisions; lack of orienta'on x 3. 4) Alterations in arousal/reactivity (irritability)
-Indicates problem with coherent thinking.
-Hallmark of symptoms of concussion.
Effect Neurotransmitter Receptor

Detrusor Contraction ACh M3

Detrusor Relaxation NE Beta Adrenergic

Internal Sphincter Contraction NE Alpha 1 Adrenergic

External Sphincter Contraction ACh Nicotinic

Neurological Control of Bladder Function

Nerves & Receptors
-3 nerves to consider: pelvic, pudendal, hypogastric.
i) Pelvic nerve
-Parasympathe'c
-ACh
-M3 receptor on detrusor
-S'mula'on=detrusor contrac'on (voiding)
Empty Bladder
ii) Pudendal nerve -Detrusor minimally stretched→slow impulses via pelvic
Full Bladder
-Soma'c -Large amount of urine stretches bladder→increased
nerve to sacral spinal cord. impulses to sacral region
-ACh -Sacral nerve→thoracolumbar region→hypogastric -Sacral nerve to pontine micturition center stimulation
-Nico'nic receptors on external sphincter nerve stimulated a) Hypogastric inhibition
-S'mula'on=external sphincter contrac'on (holding in) a) Hypogastric stimulation i) relaxation of internal sphincter
i) internal sphincter contraction
iii) Hypogastric nerve ii) no relaxation of detrusor
ii) detour relaxation
-Sympathe'c (post-ganglionic) b) Higher brain/pons signals thoracolumbar/sacral level
b) Pelvic stimulation→detrusor contraction
-NA c) Pudendal inhibition→external sphincter relaxation
i) Hypogastric simulated as above
-Stimulation beta 3 receptor=detrusor relaxation ii) Pelvic inhibited (detrusor relaxation)
-Stimulation alpha 1 receptor=internal sphincter contraction iii) Pudendal stimulated (external sphincter
contraction)