Chapter 11: The Body Senses and Movement Flashcards

1
Q

What are the four somatosensory systems?

A

Proprioception: kinesthesia, senses movement, action and location (what is your body doing and where is it)
Skin senses: senses condition at the bodies surface (touch and temperature)
Vestibular system: senses body position and movement
Interoceptive system: senses states of our internal organs (acts in background)

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2
Q

What sense is proprioception? What happens if you are deficient in this system?

A

Sense that informs us about the position and movement of our body and limbs. Its key to many basic functions such as maintaining posture and moving limbs and grasping/locating objects. If you are deficient in this system then you would be floppy and ragdoll like, you would have to rely heavily on other senses such as visual, and your body would fully collapse in dark environment as you have no visual input

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3
Q

What does the skin sense system detect? What is important about their receptors and pathways and what are they called? What does this system not detect?

A

Detects touch, warmth, and cold, as well as pain, includes tickling and touching. They are distinct with their own receptors and pathways to the brain which may be called a “labeled line”. This system does not detect “wetness”, you can only perceive it not sense it, instead you sense the temp changes

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4
Q

What are the types of receptors in the skin senses system?

A

Free nerve endings: processes at the ends of neuronal dendrites, at the surface of the skin to absorb stimuli, they detect warmth, cold, and pain
Encapsulated nerve endings: more complex structures enclosed in a membrane, detect touch, deeper in the skin than FNE

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5
Q

What are the four types of encapsulated nerve endings?

A

Meissner’s corpuscles
Merkel’s discs
Ruffini endings
Pacinian corpuscles

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6
Q

What are the Meissner’s corpuscles and Merkel’s disks? Where are they mostly located?

A

They are both encapsulated receptors, the MC respond with a brief burst of impulses, MD gives more sustained responses, and they detect texture and fine detail
They are mostly located in the fingers and lips, as well as places that are more sensitive such as hands and feet

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7
Q

What are the Pacinian corpuscles and Ruffini endings? Are they deep in the skin or near the surface?

A

They detect the stretching of skin which contributes to perception of shape of grasped objects. They are deeper in skin layers.

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8
Q

What are the types of free nerve endings?

A

Temperature receptors: members of the transient receptor potential (TRP) family of protein ion channels
Pain receptors: which respond to three different types of pain which are thermal (hot and cold pain, we have not identified the cold receptors), as well as chemical, and finally mechanical (not identified)

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9
Q

True or False. The number of receptors in the skin correlates to number of neurons in the brain.

A

TRUE

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10
Q

What is involved in the vestibular sense? What structures are involved in this system?

A

Helps us maintain balance, provides info about head position and movement.
Semi-circular canals: we have 3 of them that respond to and detect movement in three directions
Saccule: monitor head position in relation to gravity (with the ventricle)
Cupula: have tufts of hair within them that bends in response to movement speed/direction, and only tells us about acceleration of our bodies not the deceleration

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11
Q

What happens when the vestibular system is not working?

A

You get vertigo and sea sickness type feeling due to disruptions in the semi-circular canal

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12
Q

What is a dermatome? What phenomena does this explain?

A

A segment of the body powered by a single spinal nerve, sensory neurons will feed into one nerve, this explains why when you injure your spinal cord you cannot feel anything below it

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13
Q

Where does information coming into the CNS via spinal/cranial nerves cross the midline? Where are they sent to?

A

They cross the midline in the medulla, and they are then sent to the thalamus and then sends it to the somatosensory cortex.

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14
Q

What happens in the somatosensory cortex? What is it?

A

It is the projection areas for the body sense neurons, it is located in the parietal lobes just behind the primary motor cortex and the central sulcus

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15
Q

What is a somatotropic map? Where is it located?

A

Representation of the body in the somatosensory cortex, with adjacent body parts represented in adjacent parts of the cortex

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16
Q

What are the parts of the somatosensory cortex?

A

Primary somatosensory cortex (4 areas), secondary somatosensory cortex

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17
Q

What is the purpose of the primary somatosensory cortex?

A

It contains 4 areas, each containing a somatotropic map, and plays role in processing sensory info from the body. Information is processed from the thalamus into two subareas, some info is extracted, then sent to the other two areas, and then this information is passed to the secondary somatosensory cortex

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18
Q

What is the purpose of secondary somatosensory cortex?

A

Integrates information from both sides of the body, neurons in this area are responsive to stimuli that have acquired meaning (integrates info from other areas and sends info to other areas to gain meaning)
Also sends connections to the temporal lobe which contains the hippocampus which may form somatosensory memories

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19
Q

What happens in the posterior parietal cortex?

A

This is an association area that brings together the body senses, vision and hearing. It integrates the body with the world by determining the bodies orientation in space.

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20
Q

What is body integrity identity disorder (apotemnophilia)? What causes it?

A

Condition where individuals with no apparent brain damage or disorder are convinced that a limb does not belong to them. It appears to happen randomly and we have no been able to pinpoint any brain damage that causes it. When the specific limb is touched there is no response in the superior parietal area

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21
Q

In BIID, skin conductance in response to stimulation is doubled in the limb, what does this suggest?

A

That there is an intense emotion about the limb, therefore we have emotions about the limb BUT no perception

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22
Q

What is an out-of-body experience? What could it be caused by? Why are they hard to study?

A

An illusion where a person hallucinates seeing themselves/ their body from an outsiders POV, from a different location. You are conscious but watching your body from another location.
Causes could be seizures from epilepsy that affect the temporal-parietal junction, intentional electrical stimulation, or TBI. HOWEVER, anyone can experience them.
They are hard to study because they are difficult to ethically induce.

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23
Q

How does pain begin? What is the bodies first response to pain?

A

Pain begins when the free nerve endings in the skin are stimulated by intense pressure/temperature either by tissue damage or various chemicals.
The bodies first response is to release an inflammatory soup of molecules to combat the pain such as cytokines, chemokines, NT, histamine, proteins, lipids. Some of these molecules stimulate the pain receptors, some cause pain symptoms or increase the excitability of neurons.

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24
Q

Why do some molecules in the inflammatory soup increase the excitability of neurons? Why is this adaptive?

A

They increase the excitability of neurons therefore enhancing their sensitivity to stimuli. This means that now, less painful stimuli is required for us to feel pain as the threshold of the neuron is lowered. This prevents us from hurting ourselves further or exacerbating an existing injury.

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25
Q

What are the two pain pathway? What are the fibers that each uses?

A

FAST: uses A-delta fibers, it registers localized pain and relays it to the cortex (somatosensory) in a fraction of a second
SLOW: conveys the less localized, long lasting, aching or burning pain, and uses C fibers (midbrain/thalamus first)

26
Q

Are A-delta or C fibers myelinated, and how does this relate to their pathways?

A

The A-delta fibers are myelinated, therefore it makes sense that they are part of the fast pathway as myelin increases transmission speed.

27
Q

What is the main difference between sensory neurons and pain neurons?

A

Sensory neurons do not cross the midline until the medulla, but pain neurons cross the spinal cord/ hemispheres immediately

28
Q

What type of pain is substance P and glutamate released for?

A

Substance P is released in response to severe pain and glutamate is released in response to mild pain . They are both released in the spinal cord and increase pain sensitivity

29
Q

TRUE OR FALSE: Mechanisms of general anesthetic are poorly understood.

A

TRUE

30
Q

What neurochemical is responsible for our internal mechanism of pain relief? What does it do? WHEN do they work?

A

Endorphins which are endogenous and they act as neurotransmitters and bind to the opioid receptor in the nervous system to relieve pain
They only work in highly specific conditions
- Release more during inescapable pain when you are in a severe situation and the sympathetic NS is active

31
Q

What does naloxone due in relation to pain reduction?

A

Naloxone eliminates the analgesia induced by inescapable shock BUT not the milder escapable induced analgesia. They block the opioid receptor

32
Q

What is the gate control theory? What brain region is involved here and how?

A

This theory says that pressure signals arriving from the brain trigger an inhibitory message that travels back down the spinal cord where it closes a neural gate pathway
The PAG is involved and it surrounds the ventricles with a large number of endorphin synapses.
It is believes that endorphin release inhibits the release of substance p, therefore closing the pain gate in the spinal cord (not sensitive to pain anymore)

33
Q

What is chronic pain? Is it related to severity of the injury? What are its causes and is it genetic?

A

Chronic pain is pain that lasts long after healing occurs, even when no longer injured. It is NOT related to the severity of the injury.
It is due to the strength of the functional connectivity between the NAc and the frontal cortex (specifically for chronic back pain), and the stronger the connection the more risk of producing it, and this suggests an emotion and stress aspect to chronic pain.
There are some genes associated with chronic pain such as SCN9A, COMT, and six variation of a glucocorticoid gene

34
Q

During chronic pain, what happens to the nervous system?

A

It changes functionally and structurally, pain pathways become more sensitive and new connections form between peripheral neurons and the spinal cord, and normal inhibitory mechanisms are depressed. HIGHER SENSITIVITY TO PAIN OVERALL

35
Q

What are some brain changes that occur due to chronic pain?

A

Brain stem pathways become more responsive, more PFC, ACC and insula activation, more parts of the somatosensory cortex are devoted to painful areas, and gray matter is lost proportional to the amount and intensity of the pain

36
Q

What is phantom pain? What are some treatments?

A

Phantom pain is pain experienced in a missing limb due to the presence of cortical areas still devoted to the missing body parts. It also may be due to foreign neurons intruding on the somatosensory cortex area for the missing part or due to unmasking.
Anesthetics do not typically treat phantom pain as cut/severed neurons are not the cause of the pain

37
Q

What are the three types of muscles? Which one do we focus on?

A
  1. Skeletal muscle: muscles that move the body and limbs but can fatigue if overused (voluntary muscles, also called straited due to their appearance) we focus on these
  2. Smooth muscles: muscles that produce rhythmic contractions of the internal organs, such as peristalsis blood vessels and bladder
  3. Cardiac muscles: non-fatiguing muscles of the heart
38
Q

What is muscle made up of? How does fiber number relate to precision of movement?

A

Muscle tissue is made up of individual cells called muscle fibers, and these are controlled by motor neurons what synapse with a muscle cell at the neuromuscular junction where the use acetylcholine.
The fewer fibers a neuron controls, the more precise a movement can be, for example there are 3 fibers per axon in the eye therefore very precise movement

39
Q

What 2 things are a muscle fiber made up of?

A
  1. Myosin: motor proteins best known for their roles in muscle contraction
  2. Actin filaments: linear polymers of globular actin subunits
40
Q

What are the three steps in a muscle contraction?

A

Release of acetylcholine -> depolarize motor neuron -> Ca influx -> contract by the myosin pulling on the actin filaments

41
Q

What are antagonistic muscles? What are the controlled by and why are they important?

A

Muscles that produce opposite movements at a joint, ALL muscles are paired therefore when one contracts the other expands. For example the bicep and the tricep are antagonistic muscles.
They are controlled by spinal reflexes and they allow for opposing contractions rather than one muscle doing all the work, and results in smooth movements, precision in stopping and minimal tremor (because less NRG required therefore less fatigue)

42
Q

What are the two structures involved in our spinal reflexes and what do they do?

A
  1. Muscle spindles: stretch receptors in the muscle, tells us when to stop and prevents us from hurting ourselves
  2. Golgi tendon organs: tension receptors in the muscles, adjust muscle strength and usage depending on what we are doing
    These prevent over contraction of muscles and allow dynamic adjustments to increased external load
43
Q

What is the name of the spinal reflex that allows us to maintain an upright position? How do they test this at the doc?

A

Myosynaptic reflex, the doc taps your knee which activates the stretch receptor (muscle spindle) which sends a signal to the brain via the spinal cord telling it to contract via a motor neuron, therefore we maintain upright position

44
Q

What is a central pattern generator? (CPG)

A

Neuronal networks that produce a rhythmic pattern of motor activity. The brain is only involved when initiating the activity, but once it is started the CPG takes over and the spinal cord/nerves are responsible now

45
Q

What 3 structures comprise the motor cortex?

A

Primary motor cortex, 2 major secondary motor areas( supplementary motor area, and the premotor cortex)

46
Q

What is a major difference between the sensory info pathway and the motor info pathway?

A

In the sensory pathway, information begins in the primary somatosensory cortex and then is sent to the association areas, BUT in the motor pathway the info starts in the association areas and is then sent to the primary motor cortex to organize the info into complex act

47
Q

What is the role of the prefrontal cortex?

A

Plans actions with regard to their consequences, plans movement and words etc. It receives information from the ventral visual stream about object identity and is responsible for integrating sensory info with body information (from PPC). It then holds this info in memory while selecting an appropriate movement and its target.

48
Q

What is the role of the premotor cortex?

A

It is a secondary motor area, and it begins programming a movement by combining information from the PFC and the PPC, and consists of many cell types

49
Q

What is the role of the supplementary motor area? What happens when you damage this area?

A

This assembles the sequence of movements, it is considered a secondary motor area. When this area is damaged, your limbs must move together now, you cannot do two different things with them

50
Q

What is the role of the primary motor cortex?

A

Responsible for the organization and execution of the voluntary movements. Here the cells fire the most during movement and they are not reserved to specific movement (specific to part of body NOT type of movement).
It assembles the information coming from all other areas (premotor, supplementary, PFC and PPC)

51
Q

What is the role of the basal ganglia? Does it produce movement?

A

This is a group of brain regions including the caudate nucleus, substantia nigra, putamen and the globus pallidus, that uses info from the primary and secondary motor areas and the somatosensory cortex to integrate smooth movements. DOES NOT PRODUCE MOVEMENT, it simply smooths it

52
Q

What disease may lead to the death of the basal ganglia?

A

Parkinson’s, cannot learn new movements

53
Q

What is the role of the cerebellum?

A

Uses info from the motor cortex to determine TIMING and ORDER of muscular contraction.
Uses info from the vestibular system to maintain POSTURE and BALANCE, as well as refine movements, control eye movements and compensate for head movements.
It returns processed info to the primary motor cortex so it can learn and do better next time

54
Q

What would you see if your cerebellum was damages?

A

You would need to constantly pause and readjust position and would have jerky movement, would appear drunk when walking because struggle with balance and posture, refined movement

55
Q

What is Parkinson’s disease? What is it caused by?

A

Condition characterized by motor tremors, rigidity, loss of balance and coordination, difficulty moving, especially in initiating movement. It is caused by deterioration of the substantia nigra so there is less DA going to the basal ganglia
Also caused by accumulation of Lewy bodies which are protein aggregates which can cause the cognitive symptoms.
It is environmental and genetic

56
Q

What are 4 potential treatments for parkinson’s?

A
  1. Levodopa: dopamine precursor that can cross the BBB, and used to replenish the bodies dopamine stores, BUT may increase restlessness and cause hallucinations. People also become tolerant quickly
  2. Stem cells: not usually used for long term, people may develop ticks and tumors
  3. Lesions to subthalamic nucleus and globus pallidus: limits tremors but also causes damage to nearby structures
  4. Deep brain stimulation: electrodes that stimulate DA release, also increases pleasurable effects of normal things
57
Q

What is Huntington’s disease? What causes it?

A

Degenerative disorder of the motor system involving cell loss in the striatum and cortex. Has cognitive and emotional effects seem in all patients.
Motor symptoms are due to the degeneration of inhibitory GABA neurons in the striatum.
Caused by a mutated form of the huntingtin gene which leads to accumulation of the huntingtin protein, and this is a DOMINANT gene

58
Q

What are some treatments for Huntington’s disease?

A

We can only treat the symptoms, cannot cure it.
Antidepressants, antipsychotics, as well as tetrabenazine which reduced excess dopamine to reduce movement

59
Q

What is myasthenia gravis (MG)?

A

A disorder of muscle weakness caused by reduced numbers or sensitivity of acetylcholine receptors. This causes less muscles contraction of the diaphragm and may become so severe that people need respirators

60
Q

What are some treatments for MG?

A

Drugs that inhibit the action of acetylcholinesterase to increase ACH in synapse
Thymectomy to remove the thymus, which reduced antibodies attacking ACH and therefore lessens symptoms BUT leads to compromised immune system

61
Q

What is multiple sclerosis?

A

Motor disorder with many varied symptoms, caused by demyelination and neuron loss in the CNS. Neurons eventually die which leads to accumulation of hardened scar tissue (sclerosis) and new neurons cannot grow leading to pain. Symptoms include slower, weaker movements, confusion and double vision, decreased neuronal synchronization as well as vibrating sensations

62
Q

What are possible treatments for MS?

A

Many drugs can treat the symptoms but few modify the problematic immune activity of MS patients, no drug can reverse the damage done