Neuro: Lecture 3 - Sensory Flashcards
Sensory system parts
Receptors, peripheral nerves, spinal cord, thalamus, cerebral cortex
Where is cerebral (somatosensory) cortex located?
Postcentral gyrus of parietal lobe
First order neurons
Brings info from sensory receptors to spinal cord or brainstem
-AKA primary afferent neurons, peripheral somatosensory axons
-Enter spinal cord through dorsal roots
Second order neurons
Conveys info between spinal cord or brainstem to thalamus
Third order neurons
Convey info from thalamus to cerebral cortex
Types of cutaneous information
Touch (tactile/mechanoreception), pain (nociception), temperature (thermoreception)
Discriminative/light touch
-Where am I being touched?
-What kind of touch?
Proprioception
-Sensory info from MSK system
-where body is in space, without vision
-Static and kinesthetic sense
What is proprioception based on?
-Stretch of muscles and skin
-Tension on tendons
-Positions of joints
-Deep vibration
Stimulus
-When applied to receptors, triggers graded membrane potential in receptor
-Change in environment that activates receptors
-Determines types of receptors activated and pattern of signal transmission
Receptors
-Converts stimulus energy into action potential (if stimulus is large enough)
-Respond to a specific type of stimuli
Conduction
Impulse over sensory pathways to CNS
Translation
-CNS receives impulse, integrates info and may prepare response
-Giving meaning to signal
-Receptor level, circuit level, perceptual level
Components of sensory system
Stimulus, receptor, conduction, translation
3 types of stimulus
Mechanical, chemical, thermal
If receptor potential exceeds threshold of trigger zone (-55 mV)
-Action potential is generated
-Receptor converts stimulus energy into action potential
Mechanoreceptors
Respond to mechanical deformation of receptor by touch, pressure, stretch or vibration
Chemoreceptors
-Respond to exogenous chemicals or substances released by cells, including damaged cells following injury or infection
-Includes taste and smell
Thermoreceptors
Respond to temperature
Proprioceptors
Found in muscles, tendons, ligaments (position and kinesthetic sense)
Photoreceptors
Vision
How do nociceptors work?
Each type of receptor has a subset of nociceptors that are sensitive to stimuli that either damage or have the potential to damage tissues
Mechanoreceptors are _____ to physical distortion
Highly sensitive (have a low threshold)
Meissner’s corpuscles function
-LIGHT TOUCH (superficial in skin)
-VIBRATION
-Texture
LVT
Merkel disc function
-Light touch
-Texture
-PRESSURE (bottom of epidermis)
LTP
Pacinian corpuscle function
-Deep Pressure (deep in skin)
-Touch
-VIBRATION (deep in skin)
DVTo
Ruffini endings function
-STRETCH (middle of skin)
-Deformation within joints (horizontal shape)
-Heat
Free nerve endings function
-Course touch (pleasant touch/pressure, tickle, itch)
-Pain
-Temperature
Receptors with small receptive fields
Meissner and merkel (MM)
light touch
Receptors with large receptive fields
Pacinian and Ruffini (larger size)
Receptors with fast adaptation speed
Meissner and Pacinian (both corpuscles)
Receptors with slow adaptation speed
Merkel, Ruffini
General receptors
-Widely distributed
-Broad range of stimuli
-Multiple types of input
-Simple structure (free nerve endings, simple encapsulated structures)
-Important for basic sensory functions (somatic, visceral)
Specialized receptors
-Located in specific areas of the body to detect specific stimuli
-Allow us to perform precise sensory functions (Smell, taste, vision, hearing, balance, equilibrium)
Exteroreceptors
-React to stimuli from external environment (light, sound, temp, vibration, pressure, chemicals)
-Superficial
Interoreceptors
-React to stimuli from within the body (BP, pH, O2 concentration, internal temp)
-Deep
-Important for maintaining homeostasis
Tonic receptors
-Respond continuously as long as stimulus is present
-Slow adapting
-Detect object pressure and form (static)
-Ex: holding gin and tonic, don’t want to drop it
Phasic receptors
-Adapt to continuous stimulus and then stop responding, even when stimulus is still present
-Alert body to change in stimulus (motion, vibration, rate of change)
-Fast adapting
-Ex: putting on wedding ring or watch
Peripheral sensory axon diameters from largest to smallest
-Ia, Ib, II, III, IV
-Abeta, adelta, C
Abeta axons
-Largest and fastest
-Conduct touch, pressure, vibration sensations via cutaneous receptors
C axons
-Smallest and unmyelinated, slowest
-Mediate temperature, throbbing, pain, itch
-Transmit dull achy pain slowly
Sensory neuron receptive field
-Area of skin innervated by one afferent neuron
-Where it can transduce pressure or vibration into action potential
When moving from distal to proximal, receptive fields get
Larger and less dense
Which area has highest 2 point discrimination?
Fingers
-Higher density of mechanoreceptors
-Lots of Merkel discs (small receptive fields)
4 attributes of conduction
Modality, intensity, location, duration (MILD)
Modality
-Type of stimulus
-Diverse sensations
-Receptors are specialized for different types of stimulus
Location
-Receptor’s receptive field and precise area
-Tracts/pathways between receptors and CNS
Intensity
-Importance of stimulus
-Amplitude
-# of receptors activated
-Frequency of potentials and activation
Duration
-Tonic/phasic
-Time course of receptor potential, # of receptors activated
Receptor levels processing
-Graded membrane potential in receptors
-Strong receptor potential with depolarization initiates AP’s and causes NT release
Circuit level processing: convergence and divergence
-Convergence: synapses can focus AP’s from several sensory neurons onto narrowed area of CNS
-Divergence: synapses can spread AP’s to several areas of CNS
Peripheral nerve
-Connects motor or sensory end organs with CNS
-Nerve that branches out for spinal cord and carries signals to different parts of the body
Dermatome
-Specific area of skin innervated by a single spinal nerve
Where is mixing of dorsal spinal roots seen?
Limbs, not trunk
Testing for sensory deficits: nerve conduction velocity testing (NCV/NCS)
Electrical stimulation to PERIPHERAL nerve, comparing results to normal
-Latency: time from stim to distal recording site
-Amplitude: number of axons conducting
-Velocity: indication of myelination
Testing for sensory deficits: somatosensory evoked potentials (SSEP)
-Test PERIPHERAL and CENTRAL pathways
-Stimulation at distal site recording more proximally and cerebral cortex
Order of sensory loss in peripheral nerve lesions
-Conscious proprioception and light touch: DCML
-Cold: Spinothalamic
-Fast sharp, stinging pain: spinothalamic
-Heat: spinothalamic
-Slow aching pain: slow medial nociception
Sensation returns in reverse order
Causes of sensory ataxia
-njury to peripheral sensory nerves, dorsal roots/columns, medial lemnisci
Sensory vs. cerebellar ataxia
-Cerebellar: similar performance with eyes open or closed, proprioception and kinesthesia is intact
-Sensory: Marked worsening in symptoms with eyes closed
Herpes zoster
-Caused by varicella zoster virus
-Dermatomal distribution
-Unilateral
Nociceptive pain
Acute or chronic tissue injury stimulates nociceptor activation to cause pain perception
Non-nociceptive pain
-Malfunction of neural pain regulating processes causes pain without tissue injury present
-Includes neuropathic pain, central sensitivity syndromes, and pain syndromes
Edema and endogenous chemicals can sensitize
Free nerve endings in periphery
Mechanisms of pain inhibition
-Descending analgesic pathways
-Endogenous opioid system
-Cingulate gyrus and insula of brain (register pain)
-Spinothalamic tract (pain and temp in body)
-Trigeminal tract (pain and temp in face/head)
Endogenous opioids
-AKA endorphins
-enkephalins
-dynorphins
-beta-endorphins
-Opiate receptors bind both endogenous AND exogenous opioids
Brain areas that provide intrinsic antinociception from a neuronal descending system
-Rostal ventromedial medulla (raphe nuclei in reticular formation, raphespinal tract)
-Periaqueductal gray in midbrain
-Locus coeruleus in pons (ceruleospinal tract)
The spinal cord has inhibitory neurons that respond to
Enkephalin and dynorphin
Which fibers transmit pain info?
Adelta and C
Pain control at segmental level: gate control theory
-Activation of non-nociceptive neurons closes a gate for the transmission of nociceptive signals
-Ex: rubbing a bruise stimulates Abeta fibers and inhibits the pain signal coming from C fibers
Both adelta and C fibers synapse within
-substantia gelatinosa of dorsal horn
-2nd order neurons decussate and ascend
Main NT of pain afferents
Glutamate
Antinociception: Periphery (level 1)
Analgesics decrease synthesis of prostaglandins that sensitize nociceptors
Antinociception: Dorsal horn (level 2)
-Release of enkephalin or dynorphin by inhibitory neurons, or exogenous analgesics
-Could use modalities like heat and TENS
Antinociception: Brainstem (level 3)
-Neuronal descending system (PAG, rostra ventromedial medulla, locus coeruleus)
-Can be naturally occurring or stimulated by narcotics
Antinociception: Hormonal system (level 4)
-Periventricular gray (PVG) in hypothalamus, pituitary, adrenal medulla
-Can be naturally occurring or stimulated with direct electrical stimulation of PVG or TENS
Antinociception: Cerebral cortex and amygdala
-Involves prefrontal lobe, insular lobe, cingulate cortex
-Spinolimbic, spinomesencephalic, spinoreticular tracts
-Amygdala: emotional aspects of pain
-Placebo and distraction strategies can be effective here
Referred pain
-Felt at site different from injured or diseased organ or body part
-Occurs due to convergence of nociceptive and somatic info onto secondary neuron
-Brain misinterprets source of nociceptive info
Primary chronic pain
-Pain syndrome is disease, no evidence of tissue damage or injury
-Fibromyalgia
-Complex regional pain syndrome (CRPS)
-Chronic nonspecific low back pain (NSLBP)
-Migraines
Secondary chronic pain
Symptom of another condition such as arthritis, cancer, traumatic injury
Secondary chronic pain causes
-Continued stimulation of nociceptors from tissue injury
-Damage to somatosensory system (neuropathic chronic pain)
Neuropathic chronic pain
-Pain that arises as a direct result of a lesion or disease that affects the somatosensory system
-Symptoms: burning, painful cold, electric shocks, tingling, pins and needles, etc
-Nociceptors NOT stimulated
Nociceptive chronic pain
-Arises from continued stimulation of nociceptors
-Result of tissue damage or potential damage
-Usually well localized
-Ex: tendonitis, osteoarthritis pain, cancer and myofascial pain
Main neurophysiologic mechanism underlying chronic pain
-Central sensitization
-Excessive excitability of central neurons of nociceptive system
-Affects multiple parts of CNS (dorsal horn, brainstem, thalamus, cerebral cortex)
-Ex: premier league players
What mediates central sensitization?
Changes in cellular structure and function of neurons within nociceptive system, seen in both acute and chronic pain states
Cellular changes with central sensitization
-Excessive spontaneous activity
-Excessive responsiveness to afferent stimuli that shouldn’t be painful
-Lengthened discharge period following stoppage of stimuli
-Receptive fields of central neurons are larger than normal
-All changes caused by glutamate and neuropeptides
When central sensitization and peripheral inputs cause neuropathic pain, treatment must be directed
-To both areas
-Peripheral tissue and pain processing/inhibition
Dysesthesias (definiton and types)
-Unpliant abnormal sensations
-Allodynia
-Hyperalgesia
-Spontaneous pain
-Temporal summation
(TASH)
Allodynia
-Pain caused by something that wouldn’t normally be painful
-Ex: putting on shirt when sunburned
-Could be caused by inncouous stimuli being processed by areas responsible for physical and emotional components of pain or activation of microglia
Hyperalgesia
Increased pain in response to nociceptive stimulus
Primary hyperalgesia
-Stimuli that are normally mildy painful in injured tissue are causing excessive sensitivity
-Ex: stubbing toe twice in one day
Secondary hyperalgesia
-Pain spreads to uninjured areas close to injury site
-Can be pronounced in people with chronic pain
Spontaneous pain
-Pain unrelated to external stimulus
-Likely do to ectopic firing of nociceptive axons (in abnormal place) or neuroplastic changes within central nociceptive system
Temporal summation
-Perception of increased pain in response to repeated stimulus or continued presence of stimulus
-Ex: person with chronic pain experiences rapid increase in pain from one rep to the next while performing the same therapeutic exercise
-“Wind up” occurs at cellular level due to heightened output of 2nd order neurons
Paresthesia
-Abnormal sensation that is painless with no nociceptor stimulation
-Tingling sensation when foot falls asleep
Fibromyalgia signs and symptoms
-Tenderness and stiffness of muscles and neighboring tissues
-Achy pain
Fibromyalgia causes
-Abnormal pain processing causes perception of pain without painful external stimuli
-Small fiber neuropathy contributes
-Less gray matter density/activity in pain inhibition areas (medial frontal cortex, mid/posterior cingulate cortex, insular cortex, rostral cingulate cortex)
Headache red flags
-Signs of excessive pressure (upon wakening, caused by coughing or sneezing, worse when lying down)
-Serious intracranial disease (progressive worsening, neck stiffness, rash and fever, cancer or HIV history)
-Possible hemorrhage (post brain impairment, abrupt onset)
Complex regional pain syndrome (CRPS)
-Syndrome of pain, vascular changes, atrophy not related to peripheral or spinal nerve distribution
-Primary syndrome: involvement of multiple areas of nervous system
CPRS causes and symtoms
-Triggered by abnormal response to injury (crush injury, surgery, sprain)
-Can occur spontaneously, time between trauma and onset is highly variable
-Regional distribution that is worse unilaterally and distally (stocking or glove distribution)
CPRS early phase
-Warm phase
-Classic signs of inflammation
-During this phase individuals often don’t move affected limb, leads to fibrosis
CPRS later phase
-Cold phase
-3-6 months
-Skin becomes dry and cold, joints stiffen and swell (osteoporosis and arthritis)
-Autonomic deficits: hypohidrosis or hyperhidrosis
-Motor signs: partial loss of muscle control, tremor, spams
CPRS pathology (not super important but main facts)
-Raised levels of neurochemicals that produce peripheral neurogenic inflammation
-Dysfunction of sympathetic regulation of circulation and sweating
-Central sensitization with structural and functional changes of thalamus, somatosensory cortex, cingulate cortex, hippocampus, amygdala
Nonspecific low back pain
-90% of people seeking primary care have no definitive specific tissue injury
-Likely due to central sensitization
-Muscle guarding, disuse, abnormal movements
Mechanisms that cause neuropathic pain
-Central sensitization
-Ectopic foci
-Ephaptic transmission
-Structural reorganization
Ectopic foci
-Locations that are outside nociceptor or soma that trigger action potential
-Leads to demyelinated regions of axon being able to generate and not just conduct AP
Ephaptic transmission
-Cross talk
-Demyelination allows AP in one neuron to cause AP in another neuron, both send signals to the brain
-Likely to cause allodynia
Structural reorganization
-Long lasting central sensitization facilitates rewiring of CNS
-New synapses between Abeta and 2nd order neurons replaces C fibers (Abeta is big and fast transmission)
Neuropathic pain: Small fiber neuropathy
-Partial differentiation and central sensitization seen in people with post-herpetic neuralgia, diabetic neuropathy, Guillain-Barre syndrome)
Neuropathic pain: central pain
-Caused by CNS lesion, localized to area of the body deafferented by lesion
-Burning, shooting, aching, freezing, tingling pain
-SCI
-Stroke
-MS
Phantom limb sensations
-Sensations related to posture, length, volume, movement
-Touch, temperature, pressure, itchiness
Phantom limb pain
-Smaller percent of people with phantom limb sensations have pain
-Due to absence of sensory inputs causing neurons in central nociceptive pathways to be overly active
-Not the same as residual limb pain
