Chapter 11 Flashcards
Proprioception
Sense movement, action, location
Skin senses (what do they sense)
Body surface conditions
Vestibular system
Body position, movement
Interoceptive system
Sense state of internal organs
Skin sense uses
Touch, warmth, cold, pain, texture
Free nerve endings
End of neuronal dendrites (warmth, cold, pain)
Encapsulated receptors
Complex structures enclosed in memb. (Touch)
Messiner’s corpuscle (encapsulated)
Breif Burst of impulses (close to surface, pressure and detail)
Merkel’s disks (encapsulated)
Sustained response (close to surface, pressure and detail)
Pacinian corpuscles (encapsulated)
Deeper skin layer, stretch of skin, shape, grasping
Ruffini ending (encapsulated)
Deeper skin layer, stretch of skin, shape, grasping
temperature receptors (free nerve endings)
members of the transient receptor potential family of protein ion channels
pain receptors (free never endings)
3 distinct types (thermal, chemical, mechanical)
vestibular sense uses
maintain balance, head and movement info (mostly controlled by parts of the ear)
semi circular canals
fluid moves within canals to tell you where you are in relation to gravity,
saccule and utricle
semicirclar canals come off them, hair cell at bottom of utricle (bends to detect movement), both have hair cells with geltaus material on them
balance info pathway
same nerve as hearing, they travel together, info goes to somatosensory cortex and other balance involved areas (cerebellum)
dermatome
areas of skin on your body that rely on specific nerve connections on your spine
body sense info pathway
enters the spinal cord (via spinal nerves) or brain (via cranial nerves), crosses , mid-line in the medulla, head to thalamus
somatosensory cortex
projection area for body sense neurons
somatosensory cortex location
parietal lobes, behind the primary motor cortex and central sulcus
primary somatosensory cortex
fours parts, processes sensory info from body
somatotopic map
representation of the body in the somatosensory cortex with adjacent body parts represented in adjacent parts of the cortex (weird Brian human thing)
somatosensory cortex pathway
some info is extracted and then passed from thalamus to 2 subareas, process info (good, bad?) then pass to the secondary somatosensory cortex (put together and integrated)
secondary somatosensory cortex
integrates info from both sides of the body (send info to hippocampus to either identify what it is or make new memories of it
posterior parietal cortex
association area brings together the body senses (vision, and audition)
body integrity identity disorder
condition where people are convinced a limb is not there’s
out-of-body experience
individual hallucinates seeing their Boyd form another relocation
detecting pain
beings when free nerve endings are stimulated (intense pressure, mechanical chemical)
inflammatory soup
made up of many molecules that cause different inflammatory responses in response to pain
fast pain pathway
registers localized pain, relays to the cortex in a fraction of a second
pain pathway
immediately crosses over (NOT at the medulla)
slow pain pathway
conveys less localized pain, longer-lasting (aching or burning)
Glutamate
glutamate (mild pain) and sub. P (intense pain) released in spinal cord and enhance sensitivity
Substance P
increases pain sensitivity
opiates
act on opiate receptor, intense pain, very addictive
acetaminophen
Tylenol, good, not strong
COX-2 inhibitor
decreases inflammation
Anti-inflammatory drug (NSAID)
decreases swelling + inflammatory response, decrease sub. P production
endorphins
neurochemicals that function as a neurotransmitters and hormones (only in extreme conditions) (acts on opiate receptors)
Gate control theory
pressure signals arrive in brain, triggers inhibitory message then goes back down the spinal cord, thus closing neural gate in pain pathway
Periquaductal Gray (PAG)
Brian stem structure surrounding the cerebral ventricles, it has a large number of endorphin synapses
descending pain inhibition circuit
gate control theory, pariquaductal Gray, and endorphins release inhibits sub. P close pain gate in spinal cord
congential analgesia
insensitivity to pain
chronic pain
pain that lasts after healing occurs
nervous system change in chronic pain
pain pathway becomes more sensitive, inhibitory mechanism depressed
Brian change in chronic pain
- brain stem pathways more responsive
- Gray matter lost
Phantom Pain
pain experienced in a missing limb (cortical areas still devoted to missing body parts, possibly due to foregin neurons intruding on somatosensory area for severed body parts)
skeletal muscles
move body and limbs, can fatigue if overused (any muscle attached to bone)
smooth muscle
produce rhythmic contractions in there internal organs (food digesting, constricting blood vessels , voiding the bladder
Cardiac muscles
non-fatiguing muscles in heart
muscle tissue
made individual cells
muscle cells
controlled by motor neurons (neurons that chem out of spinal cord) that synapse with a muscle cells at the neuromuscular junction
Myosin (Muscle fiber)
motor protein, play role in muscle contraction
Acting Filaments (muscle fiber)
linear polymers of globular acting (G) subunits
antagonistic muscles
produce opposite movements at a joint
- bicep decrease arm angle, triceps increase arm angle (smooth movement, precious stopping, minimal tremor)
muscle spindles
stretch receptors in the muscle (are we over extending?)
golgi tendon organs
tension receptors near the muscles (help adjust change in tension of muscle
Central Patterns generators (CPGs)
neronal network that produces a rhythmic pattern of motor activity ( you initiate walking, but once done you stop thinking about it) (found in spinal cord) (chicken no head = keeps walking)
Motor cortex parts
Primary motor cortex, supplementary motor area, premotor cortex (in frontal lobe)
prefrontal cortex
plans action with regard to consequences, integrates sensory info with body info
premotor cortex (secondary motor area)
beings programming movement
supplementary motor area (secondary motor area)
assembles sequence of movements (good for piano playing)
primary motor cortex
execution of voluntary movements
Basal Ganglia
integrate and smooth movements (helps us not walk wonky, helps learn how to ride bike)
Cerebellum
uses info from motor cortex to determine the order and timing of muscle contraction, uses info from vestibular system to maintain posture and balance, refine movement, control eye movement that compensate head movement, returns proceed info to primary motor cortex
Parkinsons disease symptoms
motor tremors, rigidity, loss off balance, and coordination, and difficulty moving, (initiating movements)
parkinson’s cause
substantia nigra deterioration, lewy bodies accumulate
parkinson’s what is it
loss in dopamine being sent it cortex
parkinson’s treatments
Levodopa (L-dopa), stem cells, lesions
Huntington’s diseases what is it
degenerative disorder of the motor system involving cell loss
Huntington’s diseases symptoms
cognitive and emotional deficits, motor symptoms
Huntington cause
mutated gene
Huntington’s treatments
antidepressants (dopamine reduction)
myasthenia gravis (MG) what is it
muscular weakness caused by reduced sensitivity of acetylcholine receptors
Myasthenia gravis (MG) treatment
drugs inhibit action of acetylcholinesterase (enzyme that breaks down acetylcholine), thymectomy
Multiple scelrosis (MS)
motor disorder, caused by demyelination and neuron loss in CNS
multiple scelrosis treatments (MS)
some drugs help symptoms, none reverse
