Neuro Final

I and II

MS

• III,
• VII,
• IX,
• XII

ganglia

• brainstem
• in nuclei

Sensory

Lesion causes inability to smell

Sensory

• Complete
• lesion of optic nerve results in ipsilateral blindness, loss of pupillary light
• reflex. Lesions in other parts of pathway can cause blindness

• Primarily motor, innervate the six extraocular
• muscles that move eye and control reflexive constriction of pupil

ptosis (drooping of eyelid)

• ipsilateral eye to look outward and down because lateral rectus and superior
• oblique muscles are unopposed,

diplopia (double vision) caused by difference in position of eyes

 deficits moving ipsilateral eye medially, downward, upward,

• loss of pupillary reflex and consensual response to light, loss of constriction of pupil when focusing on
• near object.

• ipsilateral
• eye can’t look down and in

• adducted pupil because lateral rectus is
• paralyzed. Can’t abduct their eye and have double vision.

Mixed sensory and motor.

• Three branches
• ophthalmic, maxillary, mandibular. All three convey sensory from face and
• TMJ.  Mandibular has motor axons to
• mastication muscles.

afferent limb of corneal (blink) reflex

Masseter reflex: downward tap to chin monosynaptic stretch reflex closes jaw.

Mixed sensory and motor

• Sensory fibers transmit touch, pain, pressure info from tongue, pharynx, skin near ear
• canal

• Facial
• innervates muscles that close the eyes, move the lips, produce facial
• expression.

efferent limb of corneal reflex

Sensory, two branches

Vestibular branch transmits info about head position and movement.

Cochlear branch transmits info about hearing

Mixed sensory and motor

Sensory fibers convey somatosensory information from soft palate and pharynx which provides afferent limb of gag reflex and swallowing reflexes

Motor component innervates pharyngeal muscle and parotid salivary gland. Gag reflex

Provides afferent and efferent innervations of larynx, pharynx, viscera

• Complete lesion results in difficulty speaking,
• swallowing, poor digestion due to decreased digestive enzymes and decreased
• peristalsis, asymmetric elevation of palate, hoarseness.

Motor to traps and SCM

• UMN lesions cause paresis because cortical innervations is bilateral and muscles
• become hypertonic rather than hypotonic

Motor innervates intrinsic and extrinsics of ipsilateral tongue

• Damage
• causes ipsilateral tongue atrophy, when tongue is out will go ipsilaterally

• Caudate
• Putamen
• Globus Pallidus
• Subthalamic nucleus
• Sustantia nigra

• in cerebrum
• Assumes C shape in development, adjacent to lateral ventricle

in cerebrum

globus pallidus and putamen

caudate and putamen

in cerebrum

inferior to thalamus, lateral to hypothalamus

• in midbrain
• named for color of cells,
• some have melanin appear black

Coordinates movement and postural control

• Damage doesn’t interfere with sensation or
• muscle strength, just coordination and postural control

Vestibulocerebellum

Spinocerebellum

Cerebrocerebellum

Are the lateral hemispheres

Coordinates fine distal limb voluntary movement

•          
• Functions of Cerebrocerebellum and dentate include coordination of voluntary movements,
• planning of movements, and timing.

Lesions have little effect on posture.

Somatosensory info

Coordinates limb movements

Lesions result in gait and stance ataxia

• a lot of info it processes is from vestibular
• apparatus

regulates equilibrium

•             i.     
• Also
• receives info from visual areas of brain. Via connections with vestibular
• nuclei, influences eye movements and postural muscles.

• Lesions result in
• truncal ataxia.

Postural

Ambulatory

Reaching/grasping

Mossy  fibers

climbing fibers

• Convey
• somatosensory, arousal , equilibrium, and cortex motor information to
• cerebellum

• Convey
• information regarding movement errors to cerebellum to Purkinje cells

Consists of diencephalon and cerebral hemispheres

collection of bilaterally located nuclei

regulates activity level of cortical neurons

Y-shaped sheet of white matter divides thalamus into three

-anterior, medial, lateral

• Essential for survival because integrates
• behaviors with visceral functions.

Maintains homeostasis

• has pineal gland an endocrine gland innervated
• by sympathetic fibers, helps regulate circadian rhythm, pituitary, adrenal,
• parathyroid and islet of langerhans secretions

• Superior to substantia nigra, part of basal ganglia circuit so regulates movement,
• facilitates basal ganglia output

• apical dendrite towards cortex, several basal dendrites off soma, one axon. Most serve
• as projection, commissural, association fibers, serve as output cells for
• cortex

• spindle shaped output cells projecting to
• thalamus

stay in cortex, serve as interneuron

• plans movements of mouth during speech and grammatical aspects of language. Area
• analogous in opposite hemisphere plans nonverbal communication like emotional
• gestures and adjusting tone of voice.

stretch receptors in muscles fire whole time muscle is stretched

• adapt to a constant stimulus and stop responding i.e.
• stretch receptors in muscle only respond briefly to quick stretch. In skin
• brief response of pressure receptors after putting on watch then stop.

• sensitive
• to
• light touch and vibration

• sensitive
• to pressure

touch and vibration

stretch of skin

type Ia afferent wrap around central region of each intrafusual fibers

•                            i.     
• phasic is mostly in quick
• stretch like tendon tap, tonic is sustained during constant stretch, rate of
• firing is proportional to stretch of spindle, info about velocity and muscle
• length

type II afferents end on nuclear chain fibers next to primary endings

•                        
• monitors tonic stretch , info about muscle length

clump of nuclei in central region

nuclei in single file

• 1. Transports substances along an axon at varying speeds, slows with aging and disease
•  
• 2.Occurs in two directions

a. Anterograde: moves substances from soma towards axon

b. Retrograde: Moves substances from synapse to soma to get recycled or reused

• 1.allows small number of ions to diffuse at a
• continuous rate, small channels

• in sensory neurons, open in response to
• mechanical forces, temperature changes and chemicals (like inflammatory
• chemicals with the end result of pain), vibration, stretch, pressure

open in response to neurotransmitters binding to the postsynaptic cell membrane, cause local potentials due to flow of charged ions from extracellular to intracellular environments

electrical charge opens them, they open in response to changes in electrical potential across membrane, open and close quickly, important to release neurotransmitters and forming action potentials

• Three types of electrical potentials are needed
• for information transmission

a. Resting membrane potential

b. Local potential

c. Action potential

smaller than action potentials and graded, spread passively and peters out unless summate

occur when peripheral receptors of a sensory neuron are mechanically stimulated. Most are depolarizing and excitatory but some can be hyperpolarizing and inhibitory.

• created in motor neurons and interneurons when stimulated by other neurons. Neurotransmitter reaches the
• postsynaptic membrane and changes the membrane potential. Again the potential
• can be depolarizing or hyperpolarizing.

• when small potential changes
• within milliseconds of each other add together, one axon gets stimulated so
• fast doesn’t have time to go back to resting and gets to -55 and action potential
• occurs

• when receptor or synaptic
• potentials from different areas of the neuron are added together  (from different spaces)

the membrane won’t respond to stimuli because Na+ channels need a certain amount of time after they close to reopen. No matter what won’t open again. When the cell is still depolarizing and right after the channels have closed(during hyperpolarization)

later in the action potential when the membrane is returning to normal and may even be hyperpolarized. The Na+ channels may be able to be activated but need a stronger stimulus to do so.

acute inflammation and demyelination of peripheral sensory and motor fibers (Schwann Cells)

produce antibodies that attack oligodendrocyes (CNS)

at end of axon, releases neurotransmitters

receives specific neurotransmitters at receptors

between presynaptic terminal and postsynaptic terminal

1. Action potential arrives at presynaptic terminal

2. Presynaptic terminal depolarizes which opens voltage-gated calcium channels

3. Ca2+ rushes into terminal and is released intracellularly which causes the synaptic vesicles with neurotransmitter to go to the release site

4. Synaptic vesicles fuse with membrane and release neurotransmitter

5.Neurotransmitter diffuses across the synaptic cleft

6.Neurotransmitter binds to receptor on postsynaptic cell

7.The receptor changes shape and one of two things happen

• a.An ion channel associated with the receptor opens
•                                                   b.Intracellular messengers associated with the receptor are activated

• Cell body(axosomatic)
• Dendrites (axodendritic)- most common
• Axon (axoaxonic)

a local depolarization on the postsynaptic membrane, summation of these can lead to an action potential

is a local hyperpolarization on the postsynaptic membrane, decreases the possibility of an action potential, involves the influx of Cl- into the cell and K+ out of the cell when the postsynaptic ion channels open, which causes a hyperpolarization and can inhibit an action potential.

allows more neurotransmitter to be released by the postsynaptic neuron at the presynaptic terminal. The following events occur:

• a. Presynaptic neuron releases
• neurotransmitter that depolarizes the axon terminal of a second neuron.
• b. Causes a little Ca2+
• influx into the postsynaptic terminal of the second neuron
• c. Duration of the action
• potential is extended in the second neuron
• d. Causes more Ca2+ to
• enter the postsynaptic terminal of the second neuron
• e. Causes more neurotransmitter
• than usual to come to the membrane and be released

• a. Presynaptic neuron releases
• neurotransmitter that hyperpolarizes the axon terminal of a second neuron

• b. Duration of action potential is
• decreased in the second neuron

• e. Less Ca2+ is then
• released and less neurotransmitter is released from the cell

released into extracellular fluid or interstitial fluid and adjust activity of many neurons (modulate the whole environment), act at a distance from synaptic cleft, may eventually bind,  last longer than neurotransmitters but take a little longer to work, act with neurotransmitters, a molecule can act as both a neuromodulator and a neurotransmitter depending on where it is released either at a specific synapse or into extracellular spaces

Ability of neurons to change their function,chemical profile or structure

a decrease in the response to a repeated, benign stimulus.

techniques and exercises to decrease neural response to stimulus

abnormal sensitivity of skin to touch

learning and memory: persistent, long-lasting changes in strength of synapses between neurons and within neural networks

conversion of silent synapses to active synapses

• conversion of active synapse to silent by
• removing AMPA receptors from membrane into cytoplasm

axonal injury in the periphery

growth of a new branch of intact axon or regrowth of damaged axons

types: collateral, regenerative

when a denervated target is reinnervated by branches of intact axons from neighboring neurons

when an axon and its target cell has been damaged

Regulates organs and vasculature

• Regulates circulation, respiration, digestion, metabolism, secretions, body temp,
• reproduction

pressure(aortic baroreceptors, carotid sinuses, lungs)

 stretch (distention of veins, bladder, intestines)

chemical concentrations in blood

• Carotid and aortic
• bodies(respond to oxygen)

• Medulla (respond to hydrogen
• ions and carbon dioxide)
•      
• Hypothalamus(blood glucose
• levels, electrolyte concentration)

• Stomach, taste buds, olfactory
• bulbs

throughout viscera in walls or arteries(stretch and ischemia)

respond to very small changes in temp of circulating blood

In hypothalamus

• Cutaneous respond to external
• temp changes

Info entering brainstem synapses in solitary nucleus-> to visceral control areas in pons(respiration) , medulla(HR, respiration, vasoconstriction, vasodilatation) modulatory areas in hypothalamus, thalamus, limbic system

Thoracolumbar outflow: cell bodies of sympathetic preganglionic neurons are in lateral horn of spinal cord T1-L2

Innervate adrenal medulla

Craniosacral outflow: cell bodies in nuclei of brainstem and sacral spinal cord

Ganglia are separate and located near or in target organs

Parasympathetic info from brainstem travel in cranial nerves to outlying ganglia

use of sensory info to prepare for movement

use of sensory info during or after movement to make corrections to ongoing movement or future movements

Voluntary movement is top down

• Descending UMN tracts send movement info from brain to LMN in spinal cord or to cranial nerve LMNs in brainstem
•  -Also send to interneurons in spinal cord and brainstem

Control circuits adjust activity in descending tract, excitation or inhibition of motor neurons

Sensory info also adjust motor activity in all of CNS

Cell bodies in Ventral Horn, myelinated

• Alpha motor neurons- large
• Gamma- medium

Alpha Gamma Coactivation

Alpha and gamma motor neuron simultaneous activation

-Maintains stretch on central region of muscle spindle when muscle contracts

Slow twitch muscles activated first then larger alpha motor neurons

Slow twitch continue to contribute during faster actions as fast twitch unites are recruited

• groups of cell bodies in spinal cord whose axons project to a single muscle
•      
• i.  in ventral horn

• ii. actions of pools correlate to
• anatomic position ( medial, lateral, anterior, posterior)

innervate axial and proximal muscles

innervate distal muscles

extensors

flexors

single nerve, focal dysfunction

several nerves individually=multifocal which produces random asymmetric presentation of signs, two or more nerves affected commonly in diabetes and vasculitis that cause ischemia to the nerves

many nerves, symmetric involvement of sensory, motor, and autonomic fibers, progresses distal to proximal is the hallmark

Loss of myelin just at site of injury caused by compression or entrapment

Recovery quickly as area just remyelinates quickly

Usually result from crushing of nerve due to dislocation or fracture

•                                             
• Disrupts axon and wallerian degeneration occurs distal to the lesion

• Affects all axon sizes so reflexes, somatosensation, motor function are all greatly
• reduced or absent with muscle atrophy

Recovery is good because myelin and connective tissue remain intact and serve as a guide and support for regenerating axons to their targets. 1mm/day

When nerves are physically divided by excessive stretch or laceration

Axons and connective tissue are completely disconnected, causes immediate loss of sensation and or muscle paralysis of innervated area

• Wallerian degeneration starts distal to lesion 3-5 days post injury
•                                     
• Nerve function may never return to normal due to poor regeneration

Respond to head position relative to gravity and linear acceleration or deceleration

Responds most to forward flexion or extension

Linear acceleration and deceleration

Responds when head is moved from a laterally flexed position