Ch 9 + 11: The Body Senses & Movement

Body Sense: Somatosensory Systems

→ sent to somatosensory cortex (post central gyrus)

1. Proprioception = movement, action & location (awareness of body)

2. Skin senses = conditions a body surface (touch)

3. Vestibular system = body position & movement (balance & position)

4. Interoceptive system = states of internal organs

1. Procrioception

= informs us abt position & movement of our limbs & body

• maintaining posture + moving limbs (ex. used to sit & stand)

• grasping & locating objects (ex. grabbing water bottle w/o looking)

→ how we know our body position w our eyes closed

if damaged:

• floppy ragdoll movements

• rely on vision for movement (ex. cant move w eyes closed)

2. Skin Senses

= touch, temp, texture & pain

• distinct with their own receptors & pathways to brain via spinal cord

• we have more skin receptors (higher density) on areas of skin used to detect more

Types of Receptors

1. Free nerve endings = detect temp & pain

→ at the ends of neuronal dendrites

2. Encapsulated receptors = detect touch & texture

→ enclosed in a membrane

---

Types of Encapsulated receptors: 4 (work in pairs)

1. meissner’s corpuscles = brief burst of impulses

2. merkels disks = sustained response

→ detect texture + fine detail

→ located near surface of skin

3. pacinian corpuscles = fire once @ beginning

4. Ruffini endings = continues firing

→ detect skin stretching (pressure) + perception of grasped objects shape

→ located deeper in skin

Types of Free nerve endings:

1. Temperature receptors = detect temp

• TRPs (family of protein ion channels) : each open @ diff temp

2. Pain receptors: 3 distinct pain types

   1. thermal = TRPs for extreme temps

   2. chemical = TRPS for extreme spicy pain (why u perceive spice as hot & mint as cool)

   3. mechanical = detects painful impact/pressure on skin

3. Vestibular Sense

= to maintain balance + gives info abt head position & movement

• located in ear

mech

• liquid in canals bends hair cells → activates neurons

  • ONLY bend in one direction, THUS only detect one-way movement → why u get dizzy

  • shift in liquid can make signals in both directions

• inside saccule: hair cells feel movement of otoliths

  • if an otolith enter canals → get vertigo

• cochlear & vestibular nerve → combine to form cranial nerve

note: the trickle & saccule are useful when standing still

ex. can detect direction of movement while sitting on a train

note: alcohol thins liquid in canals → faster bending

Somatosensory cortex & posterior parietal cortex

dermatome = segment of the body served by a SIGNLE spinal nerve

process

1. body senss info enters spinal cord (via spinal nerves) or brain (via cranial nerves)

2. info crosses over the midline in medulla → thalamus

—> now L body controlled by R brain

3. thalamus send info to somatosensory cortex (projection area for body sense neurons, located in parietal lobe)

Somatosensory cortex: Somatotopic map

Somatotopic map = represents the body in the somatosensory cortex

• adjacent body parts are represented in adjacent parts of the cortex

Somatosensory cortex: Primary Somatosensory cortex

= 4 areas that play a role in processing sensory info from body

• each area has a somatotopic map

process

1. info → thalamus → 2 subareas ( info from app side of body & from same smaller side)

2. those subareas extract some info → pass to the 2 areas

3. those process into → pass to secondary somatosensory cortex

path: primary → 2 sub areas (extract) → 2 sub areas (process) → secondary

Somatosensory cortex: Secondary Somatosensory cortex

= integrates info from BOTH sides of the body (NO separation by sides)

process

1. neurons here are responsive to stimuli with an acquired meaning (ex. touching something)

2. sends connections to hippocampus (in temporal lobe)

hippocampus: uses info to determine what the sense is

ex. what is the identity of what ur touching

Posterior Parietal Cortex

= association area that joins the body senses + vision + audition

→ integrates body with world - by determine body’s orientation in space

→ subareas repsond to diff senses (not just perceptual)

• neurons fire before & after movement → send info to prefrontal cortex

Body Integrity Identity Disorder (apotemnophilia)

= NO brain damage or disorder, but are convinced their limb isn’t theirs

• when limb is touched → NO response in superior parietal area

HOWEVER

• skin conductance response to that limbs stimulation is 2x → suggests intense emotion abt that limb

ex. when nervous, the disordered hand sweats 2x more than the normal hand

Out-of-Body Experience

= hallucinates seeing their body from another location

• may be caused by something affecting the parietal-temporal junction (electrical stim., TBI, epilepsy)

→ seems to be improper firing @this junction

note: more common in uni students - possibly bc of stress

Detecting Pain

1. begins when free nerve endings are stimulated

• goes thru a diff. pathway thru the spinal cord than other skin senses

  • pain enters spinal cord → cross to other side of the body ] other skin senses cross at the medulla

THUS, we can feel pain but not pressure (touch) is a leg if an injury prevents crossing of touch

2. Inflammatory soup = signalling molecules released when in pain (histamine, proteins, lipids, neurotransmitters, cytokines)

• triggers healing & longterm pain (ex. swelling, redness, pain)

→ glutamate (excitatory neurotransmitter) is released in spinal cord for mild pain, THEN substance P for intense pain

Substance P = hormone that increases pain sensitivity → now have lower pain threshold

2 Pain Pathways

Fast: registers localized pain → sends to somatosensory cortex via A-delta fibres (myelinated)

→ to help locate injury

Slow: sends longer-lasting, aching or burning pain to thalamus via C-fibres

→ a reminder of pain

Treating Pain

• opioids : block inflammatory soup

• Nsaids : prevents creation of further pain ( lowers inflammatory soup)

• anesthetics

• acetaminophen : decrease pain signal, but DOESNT lower inflammatory soup

internal mech of pain relief

endorphins : act as neurotransmitters & hormones → act @ opiate receptors

→ ONLY work with highly specific conditions:

1. inescapable pain

2. during high arousal events (exercise, sex, mom saving baby)

---

naloxone = opioid antagonist → blocks pain relief from opioids & endorphins

Descending Pain Inhibition Circuit: Gate Control Theory

Gate control theory = pressure signals sent to the brain trigger an inhibitory message that’s sent to the spinal cord → closes a neural pain gate

• can still sense pain, but DONT perceive it

• explains how endorphins work by inhibiting substance P (pain)

gate: Periaqueductal gray (PAG) = brain stem structure with endorphin synapses + where opioids act + where the inhibitory message is sent

→ endorphins are released here → inhibits release of substance P → closed pain gate

notes:

• women have less receptors @ PAG → less pain relief from opioids

• there are multiple neural origins for activating the endorphin circuit

• PAG has cannabinoid receptors → weed has pain relief

Extremes of Pain

Congenital analgesia = insensitivity to pain, BUT can still feel some pain

• linked to mutations in genes & elevated endorphin levels in spinal fluid (constantly blocking pain)

• a group of disorders

possible reasons: no pain receptors, no inflammatory soup, no pain pathway

---

Chronic pain = pain lasting after healing

• strongly correlated with depression

• associated with certain genes

• mild pain Is just as likely to become chronic as severe pain !!

ex. chronic back pain:

• the strength of connectivity b/w nucleus accumbens & frontal cortex predicts this

• ppl reward driven : more likely to develop chronic back pain after a surgery

→ NS changes functionally & structurally DURING chronic pain:

• more sensitive pain pathways, easier APs bc of new connections b/w peripheral neurons in spinal cord, lower # of neurons releasing endorphins

→ brain changes occur DUE to chronic pain:

• more responsive brain stem pathways

• higher slow pain (prefrontal cortex, anterior cingulate cortex & insula activation)

• more of the somatosensory cortex is devoted to pain

• longer pain = more grey matter lost

---

Phantom pain = pain in a missing limb

→ due to random firing of cortical areas still devoted to that limb

→ may be due to foreign neruons intruding on the somatosensory area of that limb - another body part trying to use those neurons

• anaesthetics DONT work - bc theres no signal or inflammatory soup to lower

• usually decreases over time

Movement: Muscles

skeletal muscle = move body + CAN fatigue if overused (striated muscle)

• used in voluntary movement

muscle tissue = many cells (muscle fibres)

Muscle cells : controlled by motor neurons that synapse w a muscle cell at the neuromuscular junction

→ use ACh (excites mysoin) to cause contraction

• a single motor neuron can control multiple muscle cells

  • the fewer muscle fibres a motor neurons controls → more precise movements

ex. fingers = small ratio (1 neuron : 1 muscle cell)

ex. bicep = large ratio (1 neuron : 100 muscle cells)

muscle fibres contain: mysoin (actiavted by ACh) + actin filaments

Movement: Antagonistic Muscles

= muscle pairs that produce opposing movements at a joint

result: smooth movements, precision in stopping & minimal tremor → less fatigue

ex. biceps decrease arm angle & triceps increase arm angle

→ controlled by spinal reflexes

Spinal Reflexes = ONLY use the spinal cord for movement (no brain)

triggered by:

→ muscle spindles = stretch receptors in muscles

→ Golgi tendon organs = tension receptors in muscles

-trigger spinal reflexes → inhibit over-contraction of muscles → allowing dynamic adjustment to increased external load

Movement: Central Pattern Generators

CPGs = neuronal networks that produce rhythmic pattern of motor activity until told to stop

• brain ISNT involved

• in the spinal cord/muscles

ex. walking, swimming, flying, breathing

ex. those with spinal injuries can still perform elicited stepping movements

Brain & Movement

using : hierarchical orgnaization of the forebrain, brain stem & spinal cord

via: motor cortex

components of motor cortex

1. primary motor cortex (precentral gyrus)

2. 2 major secondary motor areas

3. supplementary motor area

4. premotor cortex

→ spinal cord doesn’t start VOLUNTARY movement until told by brain

→ movement is still influenced by rest of brain, not just the motor cortex

Brain & Movement: 1. Prefrontal Cortex

roles:

• plans actions & considers their consequences

• receives info from ventral visual stream abt object identity

• does integration of sensory info with body info (from posterior parietal cortex)

  • holds this info in memory while selecting an appropriate movement

“I want to bake a cake”

Brain & Movement: 2. Secondary Motor Areas - Premotor cortex

• programs movement

by: combining info from prefrontal cortex & posterior partial cortex

→ plans exact steps

→ most active right BEFORE a movement

→ has diff. specialized cells

“this is the receipt to use”

Brain & Movement: 3. Secondary Motor Areas - Supplementary motor area

• assembles séquences of movements

Brain & Movement: 4. Primary motor cortex

• organization & execution of VOLUNTARY movements

by: assembling complex movement sequences from input of secondary motor areas, somatosensory cortex & posterior parietal area

→ most active DURING the movement

→ cells aren’t for specific movements, just for specific parts of the body

ex. use same finger cells to do diff movements

send to:

1. basal ganglia

2. cerebellum

Brain & Movement: 5. Basal Ganglia

• use info from primary & secondary motor areas & the somatosensory cortex to integrate + smooth movements

role: fine tunes movements

includes: caudate nucleus, putamen, globus pallidus, substantia nigra

Brain & Movement: 6. Cerebellum

• compares body’s movements to what was planned → adjusts & sends corrections back to primary motor cortex

uses motor cortex info: to determine order & timing of muscular contractions

uses vestibular system info: to maintain posture & balance, refine movements, & control eye movements

Brain & Movement: Summary

Disorders of Movement: Parkinson’s Disease

= motor tremors, rigidity, loss of balance & coordination, difficulty moving & initiating movements

causes:

• deterioration of substantia nigra (basal ganglia)

• lewy bodies may contribute to cognitive deficits (cause scarring → CANT make new neurons)

• genetic & environmental factors (TBIs, toxins)

normal fxn of substantia nigra = sends dopamine to basal ganglia to control stop/start movements

→ lose this signal wit Parkinsons

note:

• can reduce risk by 50% by smoking nioctine

• can reduce risk by 80% by drinking coffee - possibly bc it blocks adenosine receptors

Disorders of Movement: Parkinson’s Disease - Treatments

note: cant just inject dopamine bc it CANT cross the blood brain barrier

• levodopa = to make dopamine, bc the substantia cant make enough

  • doesn’t work in severe cases bc theres not enough cells to use it

• stem cells : has side effects of tics (too much dopamine) + only lasts ~3yrs + develop tumours at injection sites

• lesions to subthalmaic nucleus & globus pallidus (areas controlled by substantia) : stops shaking, BUT difficult to lesson these areas bc they’re defined by fxn not structure

• deep brain stimulation (DBS) = inside brain electrode stimulation

  • invasive, but EFFECTIVE

  • increased risk of weight gain by making food more pleasurable

Disorders of Movement: Huntingtons Disease

= degenerative disorder of motor system, involving cell loss in the striatum & cortex

• death within 15-30 yrs of onset

• takes years to notice & starts w small involuntary movements

result:

• cognitive & emotional deficits : impaired judgment, depression, personality changes

• motor symptoms - due to degeneration of GABA (inhibitory) releasing neurons in striatum

  • involves basal ganglia & cortex

cause: Huntingtin gene - DOMINANT

• have extra bases in gene & the longer the gene the MORE severe w a shorter lifespan

onset: ~40-50yrs old

• this is why it doesn’t prevent passing on the gene to offspring

Disorders of Movement: Huntingtons Disease - Treatments

combinations of:

• antidepressants

• antipsychotics : to lower excess movements & emotional components

• tetrabenazine : to reduce excess dopamine/excitation

note: a new injection silences the gene for 9months in rats & 8weeks in monkeys

Disorders of Movement: Myasthenia graves (MG)

= muscular weakness due to low #’s or sensitivity of AChR → NEED more ACh

• autoimmune disease

• can be so extreme a respirator is needed, bc it affects ALL muscles → diaphragm cant move

• continued loss of AChR as it progresses

Treatments:

• drugs that inhibits acetylcholinesterase (breaks ACh) → prolong ACh in synapse

• Thymetcomy = remove thymus → removes producer of the antibodies destroying AChR

  • full symptoms elimination 8m-1yr for 80% of ppl

  • remaining 20% see some symptoms improve

Disorders of Movement: Multiple Sclerosis (MS)

= motor disorder caused by demyelination & neuron loss in CNS

early sign: impaired synchronous activities (ex. hands moving at diff times bc of signal lag)

leads to: pain, incontinence, double vision, …

causes:

• possibly bc of immune system over-activation (specific T-cells are linked)

• genetic & environmental influences ] need gene & environ to activate

  • certain diseases activate MS

Treatments:

• NO drug can reverse damage done before treatment

• chemotherapy or stem cells can help - 45% don’t progress in symptoms for 4-5yrs