CSD 210 exam 2

GSE cranial nerves

controls skeletal muscles, extraocular muscles, and glossal muscles

GVE cranial nerves

regulates autonomic innervation of smooth muscles, cardiac muscles, and glands

GSA cranial nerves

mediates somatic input (pain, temp, touch) from somatic muscles, skin, ligaments, and joints

GVA cranial nerves

mediates pain and temperature from visceral organs

SVE cranial nerves

controls muscles of face, larynx, pharynx, and neck

SSA cranial nerves

mediates vision, hearing, and equilibrium

SVA cranial nerves

mediates taste from tongue and olfaction from nose

anosmia

smell is partially or fully impaired, results from CN I nerve damage

loss of monocular vision

results from damage to CN II before optic chiasm

damage to CN III oculomotor

• paralysis of external ocular muscles

• lateral strabismus

• ptosis

lateral stabismus

deviation of ipsilateral muscle to lateral side

ptosis

eyelid drooping

damage to CN IV trochlear

paralysis of superior oblique causes difficulty looking down and out; results in a fixed upward medial gaze

damage to CN V trigeminal (sensory)

• ipsilateral deficits of pain and temperature in face, teeth, tongue, and palate

• loss of sneezing and blinking reflexes

damage to CN V trigeminal (motor)

paralysis and atrophy of ipsilateral chewing muscles

damage to CN VI abducens

ipsilateral eye turns in medially

damage to CN VII facial (motor)

• ipsilateral atrophy of facial expression muscles

• can’t close eyelid

• ipsilateral drooling

damage to CN VII facial (LMN damage)

ipsilateral paralysis of face

damage to CN VII facial (UMN damage)

contralateral weakness of lower face i.e. Bells Palsy

damage to CN X vagus

• ipsilateral atrophy and paralysis of palatine muscles

• hypernasal speech

• nasal regurgitation during swallowing

• uvula deviates towards intact side (say “AHH” test)

• dysphagia

• dysphonia

damage to CN XII hypoglossal

• ipsilateral half of tongue paralyzed, flaccid, and wrinkled

• dysarthria and dysphagia

• tongue protrudes towards affected side

cornea

in charge of refraction

iris

adjusts the amount of light entering the eye

pupil

hole where light enters the eye

lens

accommodation of image

retina

contains roda and cones (color), transmits signals to brain

rods and cones

turn photons in an electrical signal (phototransduction)

rods

in peripheral areas of retina, for light vision and movement

cones

in central area of retina, for color vision

photon

light as energy

lateral geniculate body

part of the thalamus that mediates visual information (gets info. from optic tract and projects that info. to occipital lobe)

dorsal stream

motion processing (where), projects to parietal lobe

ventral stream

object recognition (what) projects to temporal lobe

limbic system functions

• controls emotions (fear, pleasure, reward)

• maintains homeostasis

• memory

hippocampus

• learning and memory

• sensory (olfaction)

• spatial memory and navigation

• conflict processing

thalamus

relay center for sensory information

hypothalamus

• hunger, thirst, temperature control

• autonomic/ homeostasis functions

amygdala

• major emotional processing unit

• agression

• involuntary movements

• sexual urges

fornix

a white matter tract that connects limbic system to the brainstem

medical forebrain bundle

connects brainstem to the basal ganglia and cortex

septal area

thin tissue connecting hypothalamus and midbrain

Kluver-Bucy Syndrome

when the anterior parts of both temporal lobes are destroyed and removes the amygdalas → causes fearlessness, extreme curiosity, memory loss, vicious/ unnatural sex drive

displacement of basilar and tectorial membrane

causes a “shearing” force which displaces stereocilia

depolarization of IHCs

influx of potassium ions, causes influx of calcium, causes release of neurotransmitter (AP)

depolarization of OHCs

causes shortening

hyperpolarization of OHCs

causes lengthening

superior olivary complex

important for sound localization (ITDs and ILDs), binaural hearing, and acoustic reflex

afferent information for hearing

carries signals from cochlea to brain, important for speech sound representation

efferent information for hearing

from brain to cochlea, provide feedback from brain to regulate cochlea and auditory sensitivity

information coded by the cochlea

frequency, intensity, timing

dorsal root

part of the spine, afferent (sensory) fibers that transmit impulses to the CNS

dorsal root ganglion

formed by dorsal root fibers before they join the spinal cord, contain sensory nerve cell bodies

dorsal horns

gray matter, secondary sensory, gets information from the DRG

ventral horns

gray matter, motor, activates muscles, glands, and cells

sensory information in the skin

temperature, touch, pain, pressure

sensory information in muscles

angle, length, contraction of muscle fibers

posterior column (medial lemniscus) function

large myelinated fibers for fine discriminative touch, vibration, limb position, etc

spinothalamic tract function

small unmyelinated fibers for pain, temperature, and gross touch

decussation point of posterior column/ medial lemniscus

medulla (midbrain), lesions cause ipsilateral touch deficits

decussation point of STT

spinal cord, lesions cause contralateral pain and temperature deficits

motor unit

a single motor neuron and all the muscle fibers it innervates

components of a motor unit

• motor cell bodies

• efferent fibers (motor neuron axons)

• motor end plate

• innervated muscle fiber

role of ACh in NMJ

when released, triggers an action potential in the muscle

role of calcium in NMJ

ACh release (muscle action potential) releases calcium where sliding filament theory causes a shortening of fibers that results in a muscle contration

innervation ratio

the number of fibers controlled by 1 motor neuron

low innervation ratio

when one neuron controls few fibers → precise control and fine movement

high innervation ratio

when one neuron controls many fibers → powerful and less precise movements

myasthenia gravis

dysfunction of the NMJ → ACh receptor cites don’t work, meaning there is a decreased ability of ACh to act as a neurotransmitter to contract muscles

effects of MG

weakness, reduced contraction efficiency, fatigue, inability to contract muscles repeatedly, ptosis, dysphagia

assessment of MG

tensilon test (fast acting antagonist drug)

reflexes

automated, stereotyped movements in response to sensory information; can be modulated

central pattern generator

neuron network that carries out patterned motor responses i.e., walking, flying, swimming, swallowing

skilled movements

organized around the performance of a purposeful task

lower motor neurons

controls ipsilateral muscles, cranial and spinal nerves, mostly in brainstem or spinal cord, leads to muscles as “final common pathway”

peripheral sensory system

an input into LMNs for reflexes and ongoing modulation

direct activation system

an input into LMNs that activates volitional movement

indirect activation system

an input into LMNs that have “extrapyramidal” influences

LMN damage

flaccid weakness, hyporeflexia, atrophy, fasiculation, fibrillation

flaccid weakness

LMN damage prevents normal activation of muscle fibers

hyporeflexia

diminished reflexes

fasiculation

twitches

fibrillation

muscles contact regularly, can’t be seen through skin

upper motor neurons

form the descending motor pathways from the brain to the spine/ brainstem (CST and CBT pyramidal tracts)

corticospinal tract

• fibers originate from cerebral cortex and descend to spinal cord

• decussation point in pyramids of medulla

• control contralateral muscles

corticobulbar tract

• fibers originate from cerebral cortex and descend to LMN nuclei (cranial nerves)

• decussation point at the brainstem at that level of the CN they innervate

• control head and face muscles through CNs

• bilateral control

damage to UMNs

spastic weakness, increased passive muscle activity/ stretch (muscle tone), hyper-reflexia

direct activation pathway (pyramidal system)

motor pathway responsible for skilled movements, includes the CST and CBT (innervation of UMN into LMN)

innervation of direct activation pathway

• CST → UMN innervates LMN contralaterally

• CBT → UMN innervates LMN bilaterally

damage to the direct activation pathway

causes reduction or loss of skilled movements (rapid, intentional fine motor control)

indirect activation pathway (extrapyramidal system)

motor pathways that influence movement indirectly for background muscle activity, reflexes/ involuntary movement, and coordination

primary motor cortex

direct projections involved in the execution of movements, contains the motor homunculus

premotor cortex

projects to primary motor cortex and brainstem to plan skilled and goal-directed movements

supplemental motor cortex

sequences actions under internal control

pyramidal neurons

in layer V of the motor cortex, controls movement by directly activating LMN

basal ganglia

controls background muscle activity, goal directed movements, movement learning and initiation, and adjusts movements based on the environment

damage to the circuitry of the basal ganglia

contralateral deficits

striatum

major input to the basal ganglia from the motor cortex, includes the caudate and putamen

globus pallidus

contains internal and external segments; internal segment is a major output from the basal ganglia to the thalamus

substantia nigra

• pars compacta → dopamine production

• pars reticulata → major output to the brainstem

common neurotransmitters in the basal ganglia

glutamate and GABA, acetylcholine, dopamine