Exam 2 Flashcards
Pain
an unpleasant sensory and emotional experience associated with actual or potential tissue damage
Nociception
reception of signals in the CNS evoked by activation of specialized sensory receptors that provide information about tissue damage
Aside from the thalamus cerebral cortex, fibers from the lateral spinothalamic tract also travel where?
amygdala, hypothalamus, periaqueductal gray, superior colliculus, and reticular formation
Acute Pain
an essential biological signal of the potential for or the extent of injury; lasts or is expected to last a short time.
Chronic Pain
arbitrarily defined as pain persisting > 1 month beyond the resolution of an acute tissue injury or pain persisting or recurring for > 3 months
*Chronic pain has no adaptive biological role
What are the components of nociception?
transduction (detection of tissue damage by specialized receptors) > transmission (nociceptive information travels from the site of damage along the peripheral nerve) > nociceptive information travels up the spinal cord > modulation (of this information by multiple sites in the brain)
Chemical Nociception
algogenic (pain producing) chemicals are released in the region of nerve endings capable of detecting noxious stimuli; occurs in the PRESCENCE of actual tissue damage
Mechanical Nociception
pain arising from stretching of collagen fibers and thus squeezing nerve endings between them; occurs in the ABSENCE of actual tissue damage, but when tissue is excessively strained
Mechanical nociception is enhanced by:
algogenic chemical sensitization and pre-stressing collagen fibers
A-delta fibers vs. C-fibers
A-delta: lightly myelinated; responsible for initial pain (sharp/prickling or stinging type of pain)
C: unmyelinated; responsible for long-lasting pain (dull aching type of pain)
Lamina I receives:
C-fibers and A-delta fibers; 2nd order neurons project to thalamus
Lamina II receives:
C-fibers and A-delta fibers; synapse on interneurons and dendrites from neurons in Lamina V
Lamina V receives:
A-delta fibers only; 2nd order neurons project to brainstem and thalamus
Ectopic Foci
myelin damaged; increased production of mechanosensitive and chemosensitive ion channels in demyelinated area; results in abnormal sensitivity to mechanical and chemical stimuli
Ephaptic Transmission
crosstalk between nerves (in demyelinated areas); action potential from one neuron may indue an action potential in another neuron
Central Sensitization
excessive responsiveness to peripheral input causing alteration in central function; cellular changes may include: increased spontaneous activity, increased responsiveness to afferent inputs, prolonged after-discharge in response to repeated stimulation, and expansion of receptive field
Size Principle
slow-twitch muscle fibers are recruited first because they require a smaller threshold, these fibers generate less tension and require less energy expenditure; fast fatigue-resistant fibers are recruited next, followed by fast-fatigable fibers
Muscle Spindles
primary endings are velocity sensitive; secondary endings are not velocity sensitive, more important for holding something steady in space
Golgi Tendon Organ
located at the musculotendinous junction; sensitive to changes in tension and involved with proprioception and adjusting muscle tension
What do all normal movements require?
1) the convergence of information from the peripheral sensors in the spinal cord
2) spinal connections
3) descending pathways onto the cell body and dendrite of the motor neurons, as well as descending control of the interneurons
Phasic Stretch Reflex
(DTR, myotatic reflex); Ia afferents and alpha-motor neurons are involved; monosynaptic reflex that DOES NOT involve interneurons
Tonic Stretch Reflex
slow, sustained stretch applied to the central muscle spindle facilitates contraction of the muscle; Ia & II afferents and gamma-motor neurons are involed
Reciprocal Inhibition
activation of Ia afferents; contraction of homonymous and synergistic muscle groups, and inhibition of antagonistic muscle groups due to activation of Ia inhibitory interneurons; used extensively during voluntary movements
Golgi Tendon Organ Reflex
autogenic inhibition; Ib afferents excite antagonistic motor neurons and Ib interneurons inhibit homonymous and synergistic motor neurons; also referred to as reverse myotatic reflex
Flexor Withdrawal Reflexes
requires the integration of multiple spinal levels and multiple muscle groups; activates flexor muscles
Cross Extension and Flexor Withdrawal Reflexes
requires the integration of multiple spinal levels and multiple muscle groups bilaterally, activates flexors on ipsilateral side and extensors on contralateral side
Upper Motor Neurons that control reflexes
- corticospinal tract: lateral and anterior
- reticulospinal tract: interacts with spinal interneurons
- vestibulospinal tract: excitatory to extensor muscles and inhibitory to flexors
- tectospinal tract: involved with reflexes and head movement
Amyotrophic Lateral Sclerosis (ALS)
a disease that destroys only somatic motor neurons and can involve UMN and brainstem, as well as spinal cord LMNs; results in both UMN and LMN sings; astrocytes fail to remove glutamate resulting in excitoxicity
Myasthenia Gravis
an autoimmune disorder that destroys Ach nicotinic receptors on muscle cells, affecting the NMJ activity and causing decreased reflexes
Muscular Dystrophy
myopathy; muscle fibers degenerate resulting in motor units with fewer muscle fibers than normal and a decreased ability to produce force during contraction; decreased reflexes
Guillian-Barre Syndrome
polyneuropathy; an autoimmune disorder that results in acute inflammation and demyelination of peripheral sensory and motor fibers (autonomics fibers can also be affected); patient will get progressively worse for 2-3 weeks and then gradually improve; decreased reflexes
Spasticity
velocity dependent increase in tone in response to passive stretch
Hyperreflexia
muscle spinal input leading to overactivity in disinhibited and excessively excitable LMNs, resulting in muscle contraction (ie spinal cord)
Brainstem UMN overactivity
due to excessive reticulospinal and vestibulospinal tract signals to LMNs
Cerebral Palsy
damage to the CST during development from a decrease in synaptic competition during critical period and persistence of inappropriate connections; abnormal co-contractions and simultaneous activation of agonist and antagonist
Stroke-Related Spasticity
RST overactivity; decrease in inhibition of RST and increase signaling to spinal LMNs resulting in excessive muscle contraction; exaggerated interlimb neural coupling and can lead to concurrent activation of muscles in the UE and LE
Spinal Cord
disinhibition of the LMN below the spinal lesion and increased excitability (hyperreflexia); velocity dependent increase in tonic stretch reflex; brisk deep tendon reflex, exaggerated cutaneous reflexes, involuntary flexor and extensor spasms, and clonus
What are the components of the motor system?
cerebral cortex, brainstem, spinal cord, basal ganglia, and cerebellum
What can be affected by movement disorders?
- voluntary muscle force/contraction
- muscle strength
- muscle tone
- muscle size (atrophy)
- reflexes
- movement efficacy
- speed
- postural control
Muscle Tone
resistance to stretch of a resting muscle
What are the two major types of hypertonia?
rigidity and spasticity
Rigidity
resists stretch independent of velocity
Spasticity
increased resistance to stretch as velocity increases
What are the two types of hypotonia?
general hypotonia and flaccidity
General Hypotonia
abnormally low muscle resistance with passive stretch
Flaccidity
complete loss of muscle tone
Dyskinesias
abnormal movement usually due to basal ganglia damage
What are the two types of hypokinetic?
akinesia and bradykinesia
Akinesia
inability to initiate movement
Bradykinesia
slowed movement
What are the three types of hyperkinetic?
chorea, dystonia, and ballismus
Chorea
involuntary, jerky, rapid movements
Dystonia
abnormal postures or twisted repetitive movements caused by sustained muscle contractions
Ballismus
large amplitude rotary and flinging movements of a large amplitude
Truncal Ataxia vs. Appendicular Ataxia
truncal = wide-based unsteady gait appendicular = uncoordinated movement of extremities
Dysarthria
poor speech control
Dysdiadochokinesia
loss of control in rapid alternating movement
Dysmetria
under or overestimation of distance during movements toward a target
Action Tremor
shaking of the limb during voluntary movement
Fasciculations
twitches of muscles visible through the skin via spontaneous firing of alpha motor neurons; may or may not be pathological
Fibrillations
spontaneous contraction of single muscle fibers from axonal remnants firing spontaneously; ALWAYS pathological
Fractionation
moving muscles independently of each other in an extremity
Paresis
partial loss of voluntary contraction/force
Paralysis
complete loss of voluntary contraction/force
Signs of LMN Disorders
- atrophy
- flaccid paralysis or paresis
- involuntary muscle contractions: fasciculations or fibrillations
- hypotonia
- hyporeflexia
Signs of UMN Disorders
- paresis or paralysis
- spasticity
- loss of fractionated movement
- hypertonia
- hyperreflexia
MCA Stroke
most common site for cerebrovascular accident; involves damage to the corticospinal, corticoreticular, and corticonuclear tracts; treatment includes drug therapy to reduce spasticity and PT/OT to retrain movement
Motor Impairments Associated with MCA Stroke
- spastic paresis of UE
- spasticity
- Babinski’s sign
- Muscle atrophy
- Contracture
- Loss of fractionation of movement
- Decreased movement speed and efficiency
- Impaired postural control
Spinal Cord Injury
UMN disorder; can be complete or incomplete; associated with spinal reflexes present below the lesion, contractures form, and spasticity is present
Signs of ALS
- paresis
- spasticity
- abnormal reflexes: Babinski and clonus
- Hyper or hyporeflexia
- Progressive muscle wasting
- Fasciculations
- Fibrillations
Basal Ganglia Disorders can be either ___________ or ____________
hypokinetic; hyperkinetic
Basal Ganglia Disorders - Hypokinetic
increased inhibitory output of basal ganglia; akinetic/rigig Parkinson’s disease, tremor-dominant Parkinson’s disease, Parkinson-plus syndromes, Parkinsonism
Basal Ganglia Disorders - Hyperkinetic
decreased inhibitory output of basal ganglia; Huntington’s disease, dystonia, Tourette’s disorder, dyskinetic cerebral palsy
Dystonia
hyperkinetic disorder and can be either focal or general; characterized by involuntary muscle contractions causing sustained abnormal postures, twisting, or repetitive movements; may increase during stress and activity and is not present during sleep; may also have tremors
Focal Dystonia
not usually progressive; lack of somatotopic representation specificity in the somatosensory areas of the cortex and thalamus; treatment includes decreasing spasms with modalities, strengthen and teach better movement patterns, and give tools for compensation; stretching is ineffective
General Dystonia
usually progressive; involuntary twisting postures of limbs and trunk; many times begins as plantarflexion and inversion of foot during gait; treatment includes druge to modulate GABA, Ach, and DA, as well as surgical destruction of motor thalamus
Symptoms of Cerebellar Disorders
depend on location of lesion and include ataxic gait, dysarthria, dysdiadochokinesia, dysmetria, and action tremor
Algogenic Substances
- histamine, potassium ions, serotonin, bradykinins
- pro-inflammatory cytokines that are produced by WBCs
- increased expression of NGF and BDNF in inflammatory pain states (increase activity of dorsal horn neurons)
Which two chemicals act as neuromodulators in the chemical nociception pathway?
prostaglandins and substance P
Nociceptors are classified according to:
response characteristics (touch, temp, pressure) and type of nerve fiber from which they are derived
