Sensory receptors and identifying sensory lesions Flashcards

1
Q

Stimulus transduction

A
  • The process of a sensory receptor converting a sensory stimulus into an electrical signal
  • A sensory receptor is specialized to respond to a type of stimulus, by having a lower threshold for APs to that stimulus (stimulus specificity)
  • But other stimuli can still activate it if the stimulus is strong enough
  • An increase in a magnitude of a receptor potential (stronger stimulus), causes an increase in frequency of action potentials
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Rapidly adapting (phasic) receptors

A
  • Respond very rapidly at the onset of a stimulus (high frequency), then the frequency decreases over time and the axons my stop responding completely
  • In part from rapidly decaying generator potential and part due to accommodation in the nerve
  • Are important for indicating when there is a change in the stimulus intensity and designating onset/offset
  • Ex: pressure receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Slowly adapting (tonic) receptors

A
  • These maintain their response to a stimulus overtime (tonic info) due to slowly decaying generator potential
  • Useful for monitoring important aspects that should always be watched (O2 tension, proprioception, cold/hot and pain)
  • Ex: proprioceptors, pain and temp receptors, O2 tension receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Sensory coding

A
  • Converting the sensory stimulus into a recognizable sensation
  • Consists of 4 attributes: modality (what it is), location (where it is), intensity, and duration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Sensory modality and duration

A
  • Sensory modality is based on the particular type of receptor conveying the signal
  • This distinguishes a touch signal from a pain signal
  • Since each peripheral nerve contains many modalities for that area, a peripheral nerve lesion will result in the loss of all modalities to that dermatome
  • However in a SC lesion (where the various modalities run in 2 separate pathways and somatotopic locations), it is possible to lose only some of the sensory modalities to a particular lesion (either touch/vibration/prop or pain/temp)
  • For stimulus duration the most important feature is adaptation (whether the neuron is slow or rapid adapting)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Stimulus intensity

A
  • Conveyed by the frequency of APs sent to the CNS
  • The stronger the stimulus, the higher the frequency
  • As a stimulus increases in intensity it tends to spread over a larger area, by activating sensory units in adjacent areas
  • This is called recruiting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Stimulus location and acuity 1

A
  • The degree of acuity (resolution) of a sense is related to the size of the receptive fields of those neurons
  • The larger the receptive field, the lower the acuity (and vice versa)
  • This is because small receptive fields means more neurons to cover a given area, thus the CNS gets more information about sensory modalities
  • Small receptive fields allow for better 2 pt discrimination
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Stimulus location and acuity 2

A
  • On top of this, most receptive fields overlap w/ those from another neuron to give a more precise location
  • More neurons means more overlapping and more specificity
  • Thus the brain increases resolution and location by decreasing the size of receptor fields and increasing the overlapping of receptor fields
  • Location is largely dependent on somatotopic organization
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Lateral inhibition

A
  • Ability of an excited neuron to reduce the activity of its neighbors and thereby sharpen the spatial profile of excitation
  • Receptors at the edge of a receptive field are inhibited relative to the receptors in the center of the receptive field
  • Lateral inhibition serves to enhance the boundaries of a particular stimulus, enabling accurate and precise localization of a stimulus
  • Esp important for touch and vision
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Lesions of peripheral nerves

A
  • Most peripheral nerves are SS, SM, sym/post, therefore lesions to peripheral nerves usually involved both motor and sensory deficits
  • These are targeted to a dermatome where the nerve would’ve innervated, and the corresponding muscles
  • Can be unilateral or bilateral deficits based on the cause of damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Lesions of the SC

A
  • DCML and STT are separated in the SC, so the sensory modalities can be lost separately or together (based on site of lesion)
  • Damage to one or both results in loss of sensory info at and below the level of damage
  • Damage to DCML results in loss of sensory info to ipsilateral side (crosses at lower medulla)
  • Damage to STT results in loss of sensory info to contralateral side, and 1-2 segments below lesion (once it crosses after entering)
  • Does not affect sensory to face
  • If pt has functioning touch but no pain/temp, damage must be to SC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Lesions in the brainstem

A
  • Sensory loss from face is characteristic of lesion in pons or midbrain (CN V)
  • Brainstem contains long ascending tracts and cranial nerve nuclei, so lesions typically involved sensory and motor loss to body and face
  • STT and descending tract of V lie close to each other in medulla, so damage there may cause loss of both (loss of only pain/temp to body and face, contralateral to lesion for body but ipsilateral for face since V has not decussated)
  • DCML and STT have already decussated (DMCL in medullar-SC junction), so damage to brainstem results in contralateral sensory loss to body
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Lesions in the thalamus

A
  • Loss of sensation of all modalities to the contralateral side of body and face
  • If body has contralateral sensory loss, but face has ipsilateral sensory loss, then it must be before thalamus
  • Lesions involving both thalamus and internal capsule (carries motor pathways) leads to loss of sensory and motor on contralateral side of body and face
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Lesions of the cerebral cortex

A
  • Vascular lesions of the primary sensory cortex will result in the contralateral loss of sensory info to body and/or face depending on site of vascular injury (ACA: lower limbs, MCA: upper limbs and face)
  • Lesions of parietal lobe will result in contralateral deficits in higher order sensory processing (asterognosis and agraphesthesia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Distal symmetrical polyneuropathy

A
  • Bilateral sensory loss distributed to most distal areas (hands and feet), vibration may be earliest to be affected
  • Accompanied by weakness, flaccidity (LMN symptoms)
  • Common causes: metabolic diseases (diabetes, deficiencies in malnutrition), acute inflammation causing demyelination (guillan-barre), toxins/drugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Hemicord lesion: brown-sequard syndrome

A
  • One half (either left or right side) of SC is destroyed
  • Leads to loss of vibration, touch, proprioception to ipsilateral side of lesion (DCML)
  • Loss of pain and temp to contralateral side of lesion (STT)
  • UMN symptoms ipsilateral to side of lesion (UMNs already decussated and are on the side of innervation)
  • Causes: penetrating injury, lateral compression from tumor
17
Q

Central cord syndrom (syringomyelia)

A
  • Damage to white commissure, for a few segments, in middle of spinal cord (where STT and ACST decussate)
  • Leads to segmental loss of pain and temp bilaterally at the levels of the lesion
  • Doesnt damage ACST (bilaterally innervates), motor symptoms only if large enough to damage anterior horn
  • Common causes: congenital, or trauma/tumor
18
Q

Posterior cord syndrome

A
  • Damage to dorsal side of the SC (affecting dorsal horns and DC). Dorsal blood supply: posterior spinal arteries
  • Loss of vibration and position sense at and below level of lesion (DCML)
  • Pain and temp are normal (STT on anteriolateral part of SC)
  • Motor symptoms only affected if lesion is large enough to affect CST
  • Common causes: compression from tumor, B12 deficiency, tertiary syphilis, MS
19
Q

Anterior cord syndrome

A
  • Damage to ventral side of SC (affects CST, STT, anterior horns). Ventral blood supply: anterior spinal artery
  • Loss of pain and temp from STT at and below level of lesion
  • UMN symptoms due to damage to ant horns and CST
  • Causes: trauma, MS, ASA infarct
20
Q

Brainstem lesions: medial medullary lesion

A
  • Paramedian branches of vertebral arteries (or ASA) supply medial sides of medulla
  • Affects the medullary pyramids (descending UMNs), ML, and CN XII
  • For unilateral lesion, you get contralateral loss or decrease in vibration, touch, and proprioception (ML)
  • Also get contralateral loss or weakness in muscles to body (loss of UMNs before decussation)
  • Ipsilateral tongue weakness from damage to CN XII (LMN, since UMN for XII synapsed then decussated in upper medulla)
  • Causes: infarct of paramedic branches of ASA or VA
21
Q

Brainstem lesions: lateral medullary lesion

A
  • Affects the spinal tract of V, STT, CNs IX and X, and ANS (sympathetics)
  • Ipsilateral loss of pain and temp to face due to loss of spinal tract of V
  • Contralateral loss of pain and temp to body (STT)
  • Unilateral and ipsilateral horner’s syndrome (loss of sympathetics to ipsilateral eye)
  • Hoarseness, difficulty swallowing, loss of gag reflex due to loss of CN IX and X (LMN)
22
Q

Lesions in thalamus and sensory cortex

A
  • Results in contralateral sensory deficits of all modalities to parts of body and/or face dependent on size of injury
  • Hemineglect if damage to left parietal lobe
  • Contralateral astereognosis and agraphesthesia from lesions in parietal lobe