somatosensory system

Question 1

3 interacting systems somatosensory system

Answer 1

• Exteroceptive: stimuli on skin (outside body)
• Propioceptive: input from muscles joints and organs (body position)
• Interoceptive: conditions within
  the body (within body)

Question 2

exteroreceptive system

Answer 2

• mechenical (touch)
• thermal
• nociceptive (pain)

Question 3

types of receptors

Answer 3

• Free nerve endings (pain and temperature)
• Pacinian corpuscles (deep fast-adapting touch receptors. movement of skin, dont react to constant pressure. biggest)
• Merkel disks receptors (slow-adapting, huidindeuking (skin identation))
• Ruffini corpuscles (slow-adapting stretching of the skin)

Question 4

stereognosis

Answer 4

identify objects with touch. using slow and fast adapting receptors

Question 5

Two Major Somatosensory Pathways

Answer 5

Dorsal-column medial-lemniscus system:
* Carries information about touch and proprioception
* Receptors enter spinal cord and ascend ipsilateral dorsal columns to the dorsal column nuclei
* Dorsal column−nuclei decussate and ascend medial lemniscus
* Travels to ventral posterior nucleus
* Axons of the ventral posterior nucleus ascend to the
somatosensory cortex

Anterolateral system:
* Mediates pain and temperature
* Axons synapse as soon as they enter the cord
* Second-order axons decussate and travel up three paths
- Spinothalamic tract:
* Projects to ventral posterior nucleus of thalamus
* Lesions lead to loss of somatosensation and sharp
pain perception
- Spinoreticular tract:
* Projects to reticular formation and then to
parafascicular and intralaminar nuclei of thalamus
* Lesions reduce perception of chronic pain
- Spinotectal tract:
* Projects to mesencephalic tectum

Question 6

2 streams of analysis from S1

Answer 6

• Dorsal: Projects to posterior parietal cortex, participates in multisensory integration and direction of attention
• Ventral: projects to SII and participates in the perception of objects’ shapes

Question 7

S1 schade causes:

Answer 7

• reduced ability to detect light touch (contralateral)
• reduced ability to identify objects with touch (astereognosis) (contralateral)
• werd contralateraal wanneer ook de S2 was aangetast

Question 8

two major types of somatosensory agnosia:

Answer 8

• stereognosia—the inability to recognize objects by touch. Cases of pure astereognosia—those that occur in the absence of simple sensory deficits—are rare
• asomatognosia—the failure to recognize parts of one’s own body. Asomatognosia is usually unilateral, affecting only the left side of the body, and it is usually associated with extensive damage to the right temporal and posterior parietal lobe.
  asomatognosia is often accompanied by anosognosia (the failure of neuropsycho- logical patients to recognize their own symptoms.)
  Asomatognosia is commonly a component of contralateral neglect (the tendency not to respond to stimuli that are contralateral to a right-hemisphere injury)

Question 9

3 paradoxes of pain

Answer 9

• PAIN IS ADAPTIVE (congenital insensitivity to pain, geen pijn kunnen voelen, caused by: a gene that influences the synthesis of sodium ion channels)
• PAIN HAS NO CLEAR CORTICAL REPRESENTATION (veel verchillende delen geactiveerd tijdens pijn maar bij het verwijderen van die hersengebieden kan er nog steeds pijn ervaren worden dus geen specifiek gebied, ACC is wel het meest gelinkt aan pijn –> thermal grid illusion)
• PAIN IS MODULATED BY COGNITION AND EMOTION (pain control circuits: 1: periaqueductal gray (PAG) has analgesic (pain-blocking) effects. 2: PAG and other areas of the brain contain specialized receptors for opioid analgesic drugs such as morphine. 3: the isolation of several endogenous (internally produced) opioid analgesics, the endorphins)

Question 10

neuropathic pain

Answer 10

severe chronic pain in the abscence of recognizable pain stimulus
3 promising lines of research into the neural mechanisms of neuropathic pain
1. aberrant microglial activity in neuropathic pain, including the induction of neuroplastic changes that lead to the persistence of pain long after the injury has healed.
2. involvement of epigenetic mechanisms
3. the aforementioned neuroplastic and epigenetic changes are most prominent in the anterior cingulate cortex and prefrontal cortex (structures that are both involved in descending analgesia pathways)