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Flashcards in Sensory receptors and identifying sensory lesions Deck (22):
1

Stimulus transduction

-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

2

Rapidly adapting (phasic) receptors

-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

3

Slowly adapting (tonic) receptors

-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

4

Sensory coding

-Converting the sensory stimulus into a recognizable sensation
-Consists of 4 attributes: modality (what it is), location (where it is), intensity, and duration

5

Sensory modality and duration

-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)

6

Stimulus intensity

-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

7

Stimulus location and acuity 1

-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

8

Stimulus location and acuity 2

-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

9

Lateral inhibition

-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

10

Lesions of peripheral nerves

-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

11

Lesions of the SC

-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

12

Lesions in the brainstem

-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

13

Lesions in the thalamus

-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

14

Lesions of the cerebral cortex

-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)

15

Distal symmetrical polyneuropathy

-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

16

Hemicord lesion: brown-sequard syndrome

-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

Central cord syndrom (syringomyelia)

-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

Posterior cord syndrome

-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

Anterior cord syndrome

-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

Brainstem lesions: medial medullary lesion

-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

Brainstem lesions: lateral medullary lesion

-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

Lesions in thalamus and sensory cortex

-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

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