Neuro Wk 1-4

Front 1

outside layer of cells of the neural tube?

Back 1

meninges

Front 2

Purpose of the meninges

Back 2

ionically isolated the nerves inside; water-tight

Front 3

Dorsal and ventral rami

Back 3

mixed functions

Front 4

characteristics of nerve cell

Back 4

*Large nucleus,* large nucleolus, dendrites cytoplasmic extensions, axon

Front 5

afferent neurons

Back 5

carries information to the CNS, derived from the neural crest

Front 6

efferent neurons

Back 6

carries information away from the CNS, derived from the basal lamina

Front 7

association neurons (interneurons)

Back 7

connect neurons and no part them exists outside of the meninges, derived from the alar lamina

Front 8

alar lamina

Back 8

form the dorsal side of the neural tube; form the association neurons

Front 9

basal lamina

Back 9

form the vental side of the neural tube; form the efferent neurons

Front 10

gray matter

Back 10

cell bodies and dendrites, not myelinated; called the cortex when on the surface, and called nuclei when buried deep within the brain

Front 11

white matter

Back 11

myelinated axons of the cells that make up the gray matter

Front 12

cerebellar cortex

Back 12

3 layers vs 6 layers in the cerebrum

Front 13

what is this stained for?

Back 13

this is stained for the myelin..the purple here is fibers not cell bodies. in the middle is the cell bodies.

Front 14

when does neural tube fold over and begin to close?

Back 14

end of 3rd wk day 21

Front 15

brain growth in the last trimester

Back 15

No new cells; dendrites and axons just grow. At the end of 2nd tri, you have already finished cell division but now cell maturation begins. Then there is programmed cell death after the end of the 2nd trimester that continues through the 3rd trimester and throughout life (we being losing brain cells before we are even born!)

Front 16

brain development and size

Back 16

at birth 25% of adult brain
at 1yr 75% of adult brain

Front 17

effector organs of voluntary nervous pathways?

Back 17

skeletal muscle

Front 18

effector organs of involuntary nervous pathways?

Back 18

smooth, cardiac, and myoepithelial cells

Front 19

List the major types of neuroglial cells

Back 19

1) oligodendrocytes
2) astrocytes
3) microglia
4) ependymal cells

Front 20

astrocytes

Back 20

Astrocytes are star-shaped glial cells. They are important in supporting the endothelial cells that make up the blood brain barrier. They are also important in providing nutrients to the nervous tissue, exchange of metabolites between the neurons and blood vessels, repair mechanisms of the brain and spinal cord after injury, maintaining extracellular ion balance

Front 21

structure of myelin

Back 21

bascally, the axon becomes enclosed/enveloped in the cytoplasm of the Schwann cells (or oligodendrocyte). The cytoplasmic membrane of the Schwann cell/oligodendrocyte apposes itself, this area being called the mesaxon. The mesaxon then rotates numerous times around the axon to form the myelin sheath.

Front 22

microglia

Back 22

"Considered to be the CNS representatives of the macrophage-monocyte defense system”
 Microglia are a type of glial cells that are the resident macrophages of the brain and spinal cord (CNS). They have defense and immunological functions. They are derived from mesenchymal cells that invade the CNS in late fetal development. Have elongated nuclei and relatively little cytoplasm which forms fine, highly branched processes

Front 23

protoplasmic astrocyte

Back 23

have short, thick highly branched processes. Typically found in gray matter

Front 24

fibrous astrocyte

Back 24

long, thin, less branched processes. Typically found in white matter

Front 25

reactive gliosis

Back 25

aka glial scar formation; main component of these scars is astrocytes, followed by microglia. Function of these scars is the re-establish the physical and chemical integrity of the CNS after injury

Front 26

fascicular oligodendrocytes

Back 26

found in myelinated tracts (white matter)

Front 27

perineuronal oligodendrocytes

Back 27

found on neural cell body surface (gray matter)

Front 28

excitotoxicity

Back 28

the pathological process by which nerve cells are damaged and killed by excessive stimulation by neurotranmitters, eg glutamate

Front 29

rough ER is present where--dendrites or axons?

Back 29

dendrites only

Front 30

neural crest cells differentiate from where?

Back 30

cells located along the lateral border of the neural plate

Front 31

peripheral process

Back 31

in bilpolar and pseudounipolar neurons, carry information from the synaptic end back to the neural cell body, acting physiologically like a dendrite except its myelinated

Front 32

central process

Back 32

in bilpolar and pseudounipolar neurons, carry away from the neural cell body, acting physiologically like a axon

Front 33

astrocyte role in glutamate regulation

Back 33

astrocyte can reuptake glutamate from the synaptic cleft, convert it, and recycle it as glutamine back into the presynaptic neuron. prevent excitotoxicity

Hint 33

Front 34

astrocyte role in glucose regulation

Back 34

glucose is picked up by astrocyte when released by endothelial cells, GLUT 1 transport. foot processes of astrocytes almost completely ensheath the endothelil cells. then pass from the astrocytes to the neuron

Hint 34

Front 35

Difference between oligodendrocytes and Schwann cells

Back 35

One oligodendrocyte can ensheath MANY axons whereas Schwann cells it is one to one...one schwann cell can only ensheath one axon

Front 36

Types of astrocytes?

Back 36

fibrous (W) and protoplasmic ( G)

Front 37

Types of oligodendrocytes?

Back 37

fascicular (W) and perineuronal (G)

Front 38

Nissl substance

Back 38

basically it is rough ER and ribosomes, site of protein synthesis. present only in dendrites not axons!

Front 39

orthograde transport

Back 39

transport away from the neuronal body to the terminal bouton. Kinesin mediated. Can be either slow or rapid, Rapid transport carries neurotransmitters, membrane proteins, AAs

Front 40

Retrograde transport

Back 40

transport to the neuronal cell body from the terminal bouton. Rapid. Dynein mediated. Carries toxins, viruses, tropic factors (which give cell info on the status of things in the synapatic area)

Front 41

axon hillock

Back 41

the junction bw cell body and the axon..typically a part of the cell that is not ensheathed in myelin…naked membrane. More susceptible to changes in ion concentration. This is the spot of the lowest threshold for the action potential to take off

Front 42

Astrocytes and K+ buffer

Back 42

neurons release K+ into extracellular space. Astrocytes “vaccum up” the potassium. Astrocytes also have intercellular junctions call gap junctions that allows for the free flow of ions between adjacent astrocyts

Hint 42

Front 43

Dura mater

Back 43

Outermost meningeal membrane. Consists of 2 layers in the cranium area (periosteal and meningeal). and only the meningeal layer in the spinal cord. 4 main reflections from the meningeal layer create septa that compartmentalize the brain

Hint 43

Front 44

tentorium

Back 44

formed by reflections of the meningeal layer of the dura mater. forms a tent like structure which lies directly above the cerebellum. Immediately abovie it is the occipital lobes and part of the temporal lobes. The midbrain can be seen through the tentorial notch

Hint 44

Front 45

middle meningeal artery course

Back 45

branch of the external carotid, enters the skill through the foramen spinosum and runs in the epidural space between the dura and the skull...most likely source of epidural hematoma after trauma. supplies the dura

Hint 45

Front 46

middle cerebral artery

Back 46

branch of the internal carotid artery, supplies the brain

Front 47

subdural space

Back 47

potential space between the meningeal layer of the dura and the arachnoid layer. Bridging veins traverse this space and drain the cerebral hemispheres, pass through this space to reach the dural venous sinuses

Front 48

dural venous sinuses

Back 48

large venous channels that lie between the two dural layers. They drain blood mainly via the sigmoid sinuses to reach the IJV.

Hint 48

Front 49

locations of the superior and inferior sagittal sinuses

Back 49

Front 50

pterion

Back 50

junction of the greater wing of the sphenoid, squamous temporal, frontal, and parietal bones; overlies the course of the anterior division of the middle meningeal artery

Hint 50

Front 51

lambda

Back 51

junction on the cranium, meeting of the lamboid and sagittal sutures

Hint 51

Front 52

bregma

Back 52

junction on the cranium, meeting of the sagittal and coronal sutures

Hint 52

Front 53

asterion

Back 53

junction on the cranium, meeting of the parietomastoid, occipitomastoid, and lamboid sutures; star shaped

Hint 53

Front 54

most prominent point of the external occipital protuberance?

Back 54

inion

Hint 54

Front 55

dura mater

Back 55

dense CT dervied from mesoderm. 2 layers held together by collagen fibrils and fibroblasts. periosteal layer is glued to the skull via "sharpies fibers". The meningeal layer "peels off" the periosteal layer to form septa that compartmentalize the cranium and are where sinuses are contained

Hint 55

Front 56

dural sinuses

Back 56

endothelial lined, intracranial, valveless veins that are found between the layers of the dura. valveless because gravity assisted flow...only need to go one way, down

Hint 56

Front 57

the most vulnerable part of skull to trauma?

Back 57

the pterion. It is very thin and bony fragment can lacerate the vein, arteries, or both--> epidural hemorrhage

Hint 57

Front 58

collagen fibrils in the meningeal layers?

Back 58

plentiful in the periosteal and meningeal layer. little to no collagen in the subdural area/dural-arachnoid border. So this area is what is susceptible to shearing forces and can cause subdural hematomas

Hint 58

Front 59

tentorium cerebelli

Back 59

tent that supports the cerebrum above, and forms a tent over the cerebellum below. tentorial notch is where the midbrain can be seen through

Hint 59

Front 60

falx cerebelli

Back 60

septa between the cerebellum

Hint 60

Front 61

falx cerebri

Back 61

septa between the two lobes of the cerebrum

Hint 61

Front 62

supratentorial

Back 62

above the tentorium...cerebrum is here

Front 63

diaphragma selli

Back 63

piece of dura that covers the sella turcica.

Front 64

tentorial notch contains

Back 64

brainstem, blood vessels passing up from the infratentorial compartment, one cranial nerve.

Front 65

uncal herniation

Back 65

tentorial notch is the only opening from the supratentorial compartment. so if increase in pressure, can have uncal hernation where a part of the temporal lobe can squeeze through

Front 66

cause of headache?

Back 66

the meninges/the blood vessels of the meninges

Front 67

arachnoid mater

Back 67

“cellophane” layer over the surface of the sulci and fissures. the subarachnoid space is the area below, CSF lives here. also comprised from collagen fibers and fibroblasts. derived from the neural crest portion of the ectoderm

Hint 67

Front 68

pia

Back 68

"spray paint" that gets into all fissures and sulci. Derived from neural crest ectoderm and made up of 2 layers. A superficial layer that is fibroblasts and collagen (epipia) and a deep layer that touch glial foot processes, (intima pia) make of reticular and elastic fibers. The intima pia never any part of the neuron itself. no tight junctions in the pia so free movement between the glial foot proceses, intima pia, and epipia and can get into subarachnoid space.

Hint 68

Front 69

subarachnoid space

Back 69

just below the arachnoid layer where the arachnoid trabeculae are. contains cerebral arteries and veins, CSF also lives here

Hint 69

Front 70

cisterns

Back 70

subarachnoid spaces within the cranium

Front 71

superficial layer of the arachnoid mater

Back 71

waterproof because bound by tight junctions. maintains the ionic environment of the brain

Front 72

glia limitans

Back 72

consists of the glial foot processes, intima pia, and epipia

Hint 72

Front 73

leptomeninges

Back 73

consists of the arachnoid and pia. when pts have meningiomas these layers are what gives rise to the tumor cells

Front 74

Virchow–Robin spaces

Back 74

perivascular, fluid-filled canals that surround perforating arteries and veins in the parenchyma of the brain. One of the most basic roles of the VRS is the regulation of CNS fluid movement and drainag

Front 75

cavernous sinus

Back 75

on either side of the pituitary fossa...first "station off the train" when the pitituary factors are released. carotid artery also lies within there as well as several cranial nerves..can be clinically impt. some veins from the surface of the face drain into there as well (receieves blood from extracranial drainage!)

Hint 75

Front 76

epidural hemorrhage..when will bleeding stop?

Back 76

dura separated from the skull, blood can accumulate from fx that damaged meningeal vessel. typically middle meningeal artery...this bleeding stops when systolic P = intracranial P. bleeding can happen RAPIDLY. one of the features is biconvex shape and actually depresses the brain

Front 77

subdural hemorrhage

Back 77

hemorrhage occurs above the arachnoid, dissect the dural border cell layers where they are no collagen fibers. blood here comes from rupture of the cerebral veins that are welded to and drain into the sinus. veins are stretched in acceleration deceleration accidents, shearing and rupturing them. these progress more SLOWLY because they are venous bleeders. convex on the outside but concave on the inside...bleed slowly and push CSF away rather than brain

Front 78

bleeding from aneurysms leak where?

Back 78

subarachnoid space

Front 79

"worst headache of my life"...blood likely where??

Back 79

subarachnoid space. blood in the leptomeningeal layers irritate the sensory fibers there

Front 80

blood in the CSF found on spinal tap...where from?

Back 80

subarachnoid space

Front 81

ependymal cells

Back 81

what is left over after all cells migrate away from the CNS..they line the ventricles are are epithelial-like

Front 82

choroid plexus

Back 82

produces 85% of CSF. lined the floor of the lateral ventricles and the roofs of the 3rd and 4th ventricles

Hint 82

Front 83

choroid epithelial cells

Back 83

where the ependymal cells peel off the the ventricle wall onto the villi. they have tight junctions. in the areas of the choroid epithelium, things can freely leak out of fenestrated capillary cells. but the tight junction disallow intercellular movement.

Front 84

production of CSF

Back 84

Energy requiring process to pump CSF out of the choroid epithelial cells,
endocytose and exocytose ions. water flows freely. ions is what makes CSF similar to blood plasma in terms of composition but diff in terms of concentration. pump mechanisms on the interstital and basal side

Hint 84

Front 85

CSF composition

Back 85

similar to blood just different concentrations. something notable is protein concentration which is very very low in CSF

Front 86

CSF production and changes in ICP?

Back 86

does not change (alway 0.35-0.37 ml/min) . the production of CSF depends on ATP and will do it irrespective od intracranial pressure---this is how you get hydrocephaly. its is NOT a pressure phenomenon but rather a metabolic on

Front 87

CSF leaks from the ventricles into the infra or supratentorial compartment?

Back 87

infratentorial compartment

Front 88

CSF total volume

Back 88

100-150ml.

range because CSF is the buffer for maintaining correct pressures to maintain blood flow

Front 89

lumbar cistern CSF volume

Back 89

25-30ml

Front 90

Arachnoid granulations

Back 90

projections of arachnoid that pierce meningeal layer of dura and stick into the sinus. one way value when pressure of CSF > that in venous system, movement of CSF into the venous sinuses. in the supratentorial compartment

Hint 90

Front 91

how do you get CSF from infratentorial compartment where CSF goes after production in the ventricle to supratentorial compartment where the arachnoid granulations are?

Back 91

through the tentorial notch. Supratentorial P must be < infra so CSF will percolate up. and then sinus pressure must be<supra so that CSF flows one way

Front 92

meningitis and CSF movement

Back 92

inflammation and scarring of the meninges. the rate at which CSF is removed from the cisternal compartment is decreased. can cause hydrocephalus

Front 93

Functions of CSF

Back 93

buoyancy, intracranial volume adjustment, micronutrient supply system, source of osmolytes within the brain. buffering reservoir, supply and distribution of peptides and growth factor

Front 94

endometrium

Back 94

innermost CT layer covering peripheral nerves. External to the schwann cell BL. Consists of type III collagen fibers and occasional fibroblasts bw individual nerve fibers

Hint 94

Front 95

Perineurium

Back 95

2nd level of CT covering of peripheral nerves. coveres each fascicle of axons. composed of several concentric layers of flattened atypical fibroblasts which have a BL and many pinocytotic vessels. Perineural cells are connected to each other by tight junctions

Hint 95

Front 96

epineurium

Back 96

outermost CT layer of peripheral nerves. entire peripheral nerve convered by it. dense and consists of Type I collage and typical fibroblasts

Hint 96

Front 97

Peripheral nerves CT layers

Back 97

endoneurium, perineurium, epineurium

Hint 97

Front 98

Important dates in development and closure of neural tube

Back 98

day 18- neural plate begins to thicken at its lateral margins

day 21- closure of the tube begin, in the middle portion

day 26- closure of the anterior neuropore

day 18- closure of the posterior neuropore

Front 99

Cerebral perfusion pressure

Back 99

=MAP-ICP

this is why increased ICP can be very dangerous and cause ishchemia

Front 100

Monro-Kelli Doctrine

Back 100

within a closed spaced with more than one substance, one can increase only at the expense of another substance. idea of ICP increase in brain

Front 101

Derivatives of Neural Crest Cells

Back 101

1) melanocytes
2) some bones of the neurocranium
3) Odentocytes
4) C-cells of the thyroid
5) Conotruncal cushions and aortopulmonary septa
6) Adrenal medulla
7) Schwann cells

Front 102

Describe the process of neuromuscular transmission on the presynaptic end

Back 102

action potential comes down the motor nerve to the motor nerve ending. Depolarization there triggers the opening of depolarization dependent Ca2+ channels, allowing influx of Ca2+. Influx of Ca2+ activates special proteins on the vesicle and the nerve ending membrane (synaptobrevin and syntaxin respectively). The vesicle fuses with the membrane, exocytosing the ACh contained within the vesicle

Front 103

Describe the process of neuromuscular transmission on the postsynaptic end

Back 103

Once ACh has been released into the synaptic cleft, it can bind to special receptors on the motor end plate of the muscle called nicotinic cholinergic receptors. When ACh (or nicotine) bind, these receptors become permeable to cations, namely Na+ moving in and K+ out. Since the RMP is already near K+ equil., the mass movement is Na+ in. These causes a local depolarization, which can bring that area to the end plate potential. This can then bring adjacent area to its threshold potential and action potential can ensue. The ACh left in the cleft is degraded by acetylcholinersterase, which allows for choline to be recycled and acetate reabsorbed into ecf. Vesicles reproduced with help of clathrins

Front 104

clathrins

Back 104

help to 'recycle' the vesicle after it has been exocytosed (ie help reform it from the membrane)

Front 105

Myesthenia Graves

Back 105

Autoimmune disease in which antibodies are made against the nicotinic cholinergic receptors on the motor end plate. These pts have persistent muscle weakness and treatment with acetylcholinesterase inhibitor fixes the issue

Front 106

Eaton-Lambert myesthenic syndrome

Back 106

Autoimmune disease in which antibodies are made against the Ca2+ channels on the nerve ending that allow for Ca2+ influx and movement of vesicle to membrane. These pts will start off fatigued when trying to do an activity but will 'gain strength' with several action potentials

Front 107

Toxins at the NMJ

Back 107

1) Hemicholinium- blocks choline transporters that recycle choline
2) Vasamicole- blocks the NT channels on the vesicles cant concentrate ACh in vesicle
3) Botulinium toxin- destroy synaptobrevin and syntaxin so cant fuse vesicle with membrane

Front 108

Drugs (Rx) at NMJ

Back 108

1) Tubucurarine- block the nicotinic cholingergic receptors on motor end plate and paralyzes pt
2) Succinylcholine- binds to the nicotinic cholinergic receptors on motor end plates and overstimulates them...prolonged depolarization takes RMP near threshold for long time and Na+ channels get stuck in the inactive state-- paralyze pt

Front 109

hemicholinium

Back 109

toxin that binds the choline receptors on the nerve ending that usually reuptake and recycle choline. result is decreased ACh synthesis and release, less EPP produced on motor end plate and muscle weakness

Front 110

Vasamicole

Back 110

binds to the NT channels on the vesicle. ACh cannot become concentrated within the vesicle

Front 111

Botulinium toxin

Back 111

destroys the synaptobrevin and syntaxin proteins that are essential in the ACh-containing vesicle to fuse with the membrane. No ACh release= "floppy muscles"

Front 112

Tubocarinine

Back 112

drug used to paralyze pt during procedure. binds to the nicotinic cholinergic receptors in the motor end plate and prevent their stimulation. very short lived, can be fatal though if too much given

Front 113

Succinylcholine

Back 113

binds to the nicotinic cholinergic receptors on the motor end plate and overstimulates them. Result is that you depolarize the membrane for too long, raising its RMP close to the TP for prolonged time. Accomodation then causes voltage gated Na+ to become stuck in inactive state and cannot stimulate any action potentials

Front 114

premotor cortex does what?

Back 114

PLANS motor activity, specifically "advanced movements"; ie finer movements like the limbs. neurons from here can stimulate neurons in the primary motor cortex to go down and ultimately carry out desired action

Front 115

supplementary motor cortex

Back 115

primitive movement planning, usually bilaterally. stimulates neurons in the primary motor cortex to ultimately carry out action.

Front 116

primary motor cortex

Back 116

stimulated by neurons in the planning centers, neurons from here can stimulate lower motor neurons to carry out the desired action. cannot carry out movements on their own, must be told what to do

Front 117

areas of the premotor cortex and function

Back 117

superior frontal gyrus--> contains neurons that planned SKILLED movement
middle frontal gyrus--> contains neurons that plan neck movement and frontal eye field (eye movment)
inferior frontal gyrus--> Broca's area - language

Front 118

Efferent cell types

Back 118

1) General Somatic
2) Special Somatic
3) General Visceral

Front 119

Afferent fiber types

Back 119

Type Ia and Ib (rapid)
Type II and Abeta (slow)
Type Adelta (slower)
Type C (slowest, unmyelinated)

Front 120

3 types of cells of the nervous system based on embryology

Back 120

alar lamina--> association
basal lamina --> efferent
neural crest --> afferent

Front 121

Basal lamina derived cells

Back 121

GVE (most dorsal, innervate smooth muscle, cardiac, and glands; always 2 cells connected in series)
GSE (most ventral, innervate skeletal muscle derived from somites)
SVE (intermediate, innervate skeletal muscle derived from branchial arches, only found in brainstem)

Hint 121

Front 122

Neural crest derived cells in the NS

Back 122

somatic afferent- transmit info into spinal cord from receptors in tissues that are embryology derived from ectoderm and somatic mesoderm visceral afferent- transmit info into spinal cord from receptors in tissues that are embryology derived from endoderm and splanchnic mesoderm

Hint 122

Front 123

Alar derived cells

Back 123

Somatic association, visceral association. These receive from the somatic and visceral afferent respectively

Hint 123

Front 124

monosynaptic vs multisynaptic

Back 124

monosynaptic is faster. the delay occurs at the synapse. Majority of behavior is mediated by multisynaptic organizations

Hint 124

Front 125

clonus

Back 125

suggest failure to inhibit antagonistic muscles that are activated with reflex

Front 126

axonal branching

Back 126

a single neuron can influence many neurons or can influence a single neurons multiple times. axons more often than not actually have branches....Therefore there is more effect on the postsynaptic cell that usually depicted.

Hint 126

Front 127

dendritic spread

Back 127

The areas where nerves talk to other nerves can be far away from cell body, not just how the diagram shows. in these pics, it shows axo-somatic synapses, but in real life there are DENDRITES present as well where synapses can also occur.

Hint 127

Front 128

convergence and divergence

Back 128

II. 99.9% are this type. Cell 1A gives rise to axonal branches that influence B2, B1, and B3. this is called DIVERGENCE (A cell divereges its effect to more than one target cell, doing it by means of collateral branches

Cell B1 recieves synaptic input from A1, A3, and A2. This is called CONVERGENCE (any cell can be spoken to by multiple cell. may be excitatory or inhibitory, and maybe from several synaptic endings)

in this pic, it is disynaptic and so the convergence/divergence happens twice. Gives a ton of permutations and combinations

Front 129

Intersegmental divergence and convergence

Back 129

Particularly important C5-T1 and L2-S2. Ex is biceps muscle--need to recruit both C5 and C6 since these form musculocutaneous branch

Hint 129

Front 130

ventral ramus

Back 130

mixed fibers, highway to the hypomeric derived structures. bigger than the dorsal primary ramus. gives rise to cutaneous and muscular branches

Front 131

cutaneous branches- pure or mixed?

Back 131

have both afferent and efferent (GVE)

Front 132

muscular branches-- pure or mixed?

Back 132

have both afferent and efferent

Front 133

dorsal ramus

Back 133

highway to the epimeric derived structures. mixed fibers. give rise to muscular and cutaneous branches

Front 134

"blood-nerve barrier"

Back 134

formed by the water tight perinerium. The perineurium is water tight (tight junctions) and helps to maintain the ionic environment. It sequesters groups of axons (each fasicle)

Front 135

endoneurium

Back 135

within fascicles; gives substance to surroudning areas and give support to the capillaries

Front 136

epineurium

Back 136

varies in thickness and acts as protective layer around the nerve and b/w fasicles

Front 137

vasa nervorium

Back 137

vessels of the neuron

Front 138

Remak bundles

Back 138

one schwaan cell with several axons or peripheral processes invaginated in it. UNMYELINATED. rate of transmission is about 0.5-2m/sec. majority are these

Front 139

shoulder abduction

Back 139

axillary nerve
*C5, C6

Front 140

elbow flexion

Back 140

muscultcutaneous nerve
*C6, C5

Front 141

elbow extension

Back 141

radial nerve
C7*, C6

Front 142

wrist extension

Back 142

radial nerve
*C6, C7

Front 143

wrist flexion

Back 143

median nerve
*C7, C8

Front 144

finger extension

Back 144

radial nerve
*C7, C8

Front 145

finger flexion

Back 145

median/ulnar
C8, T1

Front 146

Finger abduction

Back 146

ulnar nerve
*T1

Front 147

knee extension

Back 147

femoral nerve
L2,L3,L4

Front 148

hip flexion

Back 148

L1,L2,L3

Front 149

hip adduction

Back 149

obturator nerve
L2,L3,L4

Front 150

ankle dorsiflexion

Back 150

anterior tibial
*L4, L5

Front 151

hip abduction

Back 151

Superior gluteal nerve
*L5, L4, S1

Front 152

Toe extension

Back 152

anterior tibial nerve
*L5, L4

Front 153

Ankle plantar flexion

Back 153

Posterior tibial nerve
*S1, L5, S2

Front 154

hip extension

Back 154

inferior gluteal nerve
*S1, L5, S2

Front 155

Major classes neurotransmitters of the CNS?

Back 155

-esters (ACh)
-monoamines (NE, DA, Serotonin)
-amino acids (GABA)

Front 156

Mechanisms of Drug Actions on the CNS (review of types)

Back 156

Direct agonist action at receptor
Indirect agonist action (indirect agonists increase action of exogenous neurotransmitter, usually by decreasing degradation)
Direct antagonist action (competitive inhibition at receptor)
Indirect antagonist action by decreasing availability of neurotransmitter

Front 157

Neurotransmitters- 5 action

Back 157

Synthesis, storage, release, reception, inactivation

Front 158

Adrenergic Neurotransmission

Back 158

NE, DA (degradation pathway via MAO and COMT)

Front 159

Cholinergic Neurotransmission

Back 159

ACh (degradation via AChE)

Front 160

"Other" Neurotransmitter

Back 160

GABA -- inhibitory NT
Glutamate -- stimulatory NT

Front 161

7 major NTs

Back 161

ACh, NE, DA, serotonin (5-HT), GABA, Glutamate, enkephalins (role in analgesia)

Front 162

Receptor types for NTs

Back 162

ionotropic (voltage gated, ligand-gated), metabotrophic

Front 163

GABA receptor subtypes

Back 163

GABA(A) and GABA(B) receptor subtypes. GABA(A) is ionotropic and more important clinically. GABA(B) is metabotropic.
activation of GABA receptor = CNS inhibition.

Front 164

GABA

Back 164

Action: Activation of GABA receptor = CNS inhibition.
Ion channel used: Cl-
Drug analogues: uses include tranquilizers, anticonvulsants, sleep aids.
Drugs include benzodiaepines, barbitutes, general anethetics, nonbarbituate sleep aids (have a different binding site on the receptor than GABA itself)

Hint 164

Front 165

Alcohol and GABA receptor

Back 165

alcohol has binding site on GABA receptor so can have depressant effects

Front 166

picrotoxin

Back 166

poison that can bind to the chloride channel of the GABA(A) receptor. acts as an antagonist and causes convulsions

Front 167

Glutamate (as a NT)

Back 167

Action: Glutamate is an excitatory NT. Receptor type: Ionotropic receptor
Multiple sites on it, different sites for different amines to bind-- includes glutamate, glycine, hallucinogens (PCP).
Ion channel used: Na+,Ca2+
Inactivation by glial cells (astrocytes)

Front 168

Overstimulation of the Glutamate receptor

Back 168

seizures and brain damage can result. STROKE. in case of stroke outpouring of glutamate causes scarring of hte brain and damage

Front 169

Ketamine

Back 169

Glutamate receptor antagonist. called as "dissociative anathestic". Gives the pt amnesia. Date rape drug is

Front 170

Natural opioids

Back 170

Enkephalins, endorphins --> act on opioid receptors to relieve mild to moderate pain.
Not ion channels,
Mu, kappa receptors: full and partial agonist
Adverse effects: resp. and cardio depressants*, tolerance, addicting (heroin is ex of opiod drug), emetics, antitussants (these two are impt for pts after surgery and risk of aspiration pneumonia with opioid use)

Front 171

Nalaoxone

Back 171

full competitive antagonist of mu and kappa opioid receptors. may be used for overdose treatment.

Front 172

Partial opioid agonist uses

Back 172

to ween pt off opioid addictions. ex

Front 173

How opioids stop pain

Back 173

They block the release of NT from the presynaptic neuron. Primary way is blocking glutamate receptors. Morphine blocks the Na,Ca2+ channels on the glutamate receptor. Decreased release of Ca2+ decreases release of NT filled vesicles

Front 174

Dopamine

Back 174

The "pleasure" neurotransmitter. Agonists are emetics and antagonists are antiemetics and antipsychotics.

Front 175

Cocaine

Back 175

reduces reuptake of DA and NE. more stimulus of postsynaptic site

Front 176

Amphetamines

Back 176

harder to ween amphetamine addicts off it than cocaine addicts bc it depletes the storage of MAs in vesicles

Front 177

Parkinsons treatment

Back 177

In Parkinsons, there is a loss of dopaminergic nerurons. Try to get DA levels up. Must give a precursor though. challenge in keeping it from being degraded

Front 178

Dopamine Antagonists

Back 178

use as antipschyotic agents
SE: Parkinson like sxs with extended use

Front 179

MOA of Depression

Back 179

not enough MA NTs. Thought to be caused by changes in NT or serotonin signaling.
Txt: MAOIs (keep DA and NE around in syanptic cleft longer...lots of SE though); inhibit reuptake of serotonin via SSRI or tricyclics (less specific than SSRI bc prevent reuptake of both serotonin and NE). these differ from cocaine in that cocaine prevents reuptake more of NE and also are short acting. must be weened off these med very carefully

Front 180

ACh and Alzheimers

Back 180

ACh has role in cognition. In cognitive disorders such as alzheimers there is decr. Ach so give ACh agonist to slow progession

Front 181

ACh and Parkinsons

Back 181

ACh antagonists used as adjuncts in Parkinson's treatment

Front 182

Anterolateral system functions

Back 182

Function: Activate responses to tissue-damaging stimuli. Initiates systems for PROTECTION and REPAIR

Front 183

Stimuli for the anterolateral system to act

Back 183

These stimuli are:
1) thermal
2) pain (nociception)
3) crude touch

Front 184

initiation of the anterolateral system

Back 184

exposure of nerve ending to a nociceptive stimuli- disrupts cell cytosol, changes the "ionic mileu" and intiates action potential.

Front 185

deciding whether stimuli is irritating vs pain happens where?

Back 185

takes place in the frontal lobe

Front 186

Effects of activating the anterolateral system

Back 186

1) stimulis perception and localization (in the primary somatosensory cortex)
2) significance evaluation (happens in the frontal lobe)
2) skeletal muscle responses (so we know there must be collateral DIVERGENT branches)
4) autonomic responses (sweating, incr HR in response to nociceptive stimulus)
5) Endocrine and hormonal response (collateral branches to hypothalmus)
6) experiential storage (learning) - via collateral branches to the limbic system

Front 187

important of collateral branching in the anterolateral system

Back 187

import in carrying out protection and repair. The perception of pain is only 1/6 of the picture. Need DIVERGENT, collateral branches in order to actually carry out the things that provide protection and repair in response to tissue-damaging stimuli

Front 188

Component operations of the ascending system (4)

Back 188

1) transduction (via receptors that are transducers themselves. )
2) transmission
3) perception
4) localization

Front 189

Receptors of the anterolateral system

Back 189

Act as transducers

Classification--> low and high threshold. slow and rapidly adapting

High threshold means needs more stimuli to elicit response.

Slowly adapting receptors tell you about the presence or absence of a stimulus.

Fast adapting tells you about CHANGE in the stimuli

Front 190

2 families of receptors

Back 190

capsulation and free

Front 191

free nerve fibers transmit at what velocity

Back 191

0.5-2m/sec

Front 192

eponyms for sensory receptors

Back 192

Ruffini – low threshold, slowly adapting
Merkel – low threshold, slowly adapting
Meissner – low threshold, rapidly adapting
Pacinian – low threshold, very rapidly adapting
Free nerve endings – high threshold, slowly adapting

Front 193

Both A(delta) and C fibers respond to what kind of stimuli?

Back 193

nociceptive

when cell gets damaged and environment is flooded with the cell's cytosol. change in the ionic environment cause action potential

Front 194

Where are the cell bodies of the Adelta and C fibers? Where are their central proceses? Peripheral?

Back 194

cell bodies in the dorsal root ganglia. central processes in the dorsal rootlets. Peripheral fibers can be anywhere

Front 195

Upon entering the dorsal horn, where do the C fibers and Adelta fibers terminate?

Back 195

terminate in the spinal gray matter on association cells

Front 196

Lissauer's tract

Back 196

when A delta and C fibers come into the dorsal horn, then trifurcate and create a "tract" . one branch stays at that level, one branch goes up, and one goes down (as many as 3 vertebrae in 3 direction). This is protective--if one area of the spinal cord is damaged, have a "back-up system".

Front 197

Rexed's Lamina

Back 197

When A delta/ C fibers enter the dorsal horn, one branch forms synaptic endings end in a very specific part of the gray matter (different Rexed Lamina). These afferents will always be in laminas I,II, and V. Important to note that the axon will synapse either on association or interneurons and CROSS the midline in an ascending, diagonal direction. Takes about 2 segments to cross

Front 198

medially in the anterolateral column corresponds to which body parts?

Back 198

cervical-thoracic areas (upper limbs)

Front 199

laterally in the anterolateral column corresponds to which body parts?

Back 199

lumbar-sacral (lower limb)

Front 200

Cell bodies of the anterolateral tract cells are found where?

Back 200

all spinal gray matter except lamina II and IX

Front 201

Synapses of the afferent nerves occur in which lamina?

Back 201

Lamina I, II, V

Front 202

"fates" of an anterolateral tract after crossing midline

Back 202

There are several because of DIVERGENCE (collateral branches)
a few important ones are....
1) spinoreticular tract- will activate cells in the reticular formation ( of brain stem) involved in initiating repairative process
spinothalamic tract (terminate in VPL, project up to primary somatocortex so perceptive responses)
3) spinohypothalmic patheway (branch to hypothalmus)
4) spinotectal pathway (fibers to the superior caliculus)

Hint 202

Front 203

internal capsule

Back 203

projections from VPL and DM cross through. The anterior limb receives projections from the CM and the posterior limb receives projections from the VPL

Front 204

receptors of the leminscal system

Back 204

low threshold, rapidly adapting. these are encapsultated receptors (which lower the threshold)

Front 205

2 "main players" cutaneous receptors

Back 205

Pacincian and Meissner's.

Front 206

tuning form actives which receptor?

Back 206

tuning fork activates the pacinian corpusle

Front 207

Muscle spindle

Back 207

"length detector" (detector of length of skeletal muscles, lets the cortex know what position the joints are in);
help regulate muscle tone and reflex responsivity. These are Type Ia or Abeta fibers.

Front 208

Golgi tendon organ

Back 208

"tension detector" (measures tension applies to the musculoskeletal apparatus.)
help regulate muscle tone and reflex responsivity. These are type Ib fibers.

Front 209

where would you find the muscle spindles and golgi tendon organs looking at this pic

Back 209

spinal nerve, dorsal and vental primary ramus, MUSCULAR branch (not cutaneous)

Front 210

where do the Abeta fibers enter the spinal cord?

Back 210

the dorsal funiculus (dorsal column)

Front 211

Fibers from upper limbs "add on" where?

Back 211

upper limb fibers pile on laterally. These lateral fibers form the fasiculus cuneatus (from T6 above)

Front 212

What makes up fasiculi?

Back 212

tracts

Front 213

What makes up funiculi?

Back 213

fasiculi

Front 214

Where do the fasiculis gracilis and fasiculis cuneatus terminate?

Back 214

in their nuclei in the caudal medulla oblongata

Front 215

Somatotrophy of the anteriolateral vs dorsal-lemniscal tracts

Back 215

Front 216

lesion that damages medial part of VPL- where would the symptoms be localized?

Back 216

upper, contralateral. the medial part of the VPL receives input from the nucleus cuneatus

Front 217

lesion in brain receiving info from lateral VPL

Back 217

symptoms in lower limb, contralateral

Front 218

agnosia

Back 218

loss of ability to recognize objects, persons, sounds, shapes, or smells while the specific sense is not defective nor is there any significant memory loss

Front 219

tactile agnosia

Back 219

inability to recognize an object based on touch alone

Front 220

128HZ tuning fork

Back 220

should be used on a bony prominence. "impales" the pacinian receptors against the periosteum

Front 221

Back 221

gray matter is big and dorsal-lemniscal column is relatively small. this makes us likely to believe is from the sacral spine. The ventral horns are bigger as you move down particular plexuses.

The white on the dorsal horns is substancia gelatinosa

if this is L5 fibers in the dorsal column will contain fibers from L5 and below.

Front 222

Back 222

gray matter is small --> so we are at nonlimb level. we known we are between T2 and L1 because we see the intermediolateral nucleu which is the home of preganglionic ic sympathetic nerve cell bodies.

relatively large dorsal column

Front 223

where do you find the intermediolateral nuclei?

Back 223

T1 and L2 ( home of preganglionic ic sympathetic nerve cell bodies. )

Front 224

Back 224

limb segement because of gray matter (pretty large ventral horn and dorsal horn). Also see large dorsal columns, and can see divisions between the fasiculis gracilis and cuneatus.

Front 225

Lesion in L fasiculis cuneatus at the level of C3. Which will you encounter on PE?
a) vibratory deficit in ipsilateral upper limb
b) vibratory deficit in contralateral upper limb
c) pinprick deficit in ipsilateral lower limb
d) pinprick deficit in ipsilateral upper limb

Back 225

vibratory deficit in ipsilateral upper limb

Front 226

Back 226

we are about at C1

Front 227

Back 227

we are in the medulla, The stuff in the middle is the pyramidal (motor) decussation. This is the landmark for being in the caudal part of the caudal medulla. You see a nuclear mass that looks like they are sitting atop the fasciulis gracilis and fasiculis cuneatus--> these are their respective nucleus

Front 228

the nuclei gracilis and nuclei cuneatus are present in which part of the medulla

Back 228

caudal part of the caudal medulla

Front 229

crossing of the fibers from the nuclei gracilias and cuneatus occurs how

Back 229

fibers from both cross upwards and diagonally. The gracilis ends up at the "back of the bus" and then cuneatus crosses to from the front

Front 230

what marks level of the rostal medulla ?

Back 230

inferior olivary nuclues. the L side of the section is lower than the right because smaller inferior olivary nucleu

Front 231

where do the collateral branches of the anterolateral tracts "peel off"?

Back 231

medulla, pons, and midbrain. so by the time you get up to the thalmus, not much of the anterolateral left. that is why the major contribution to the spinothalmic tract is the medial lemniscus

Front 232

Back 232

rostral medulla. c an see the medial leminiscus in the middle sections. can see part of 4th ventricle

Front 233

Back 233

this is at hte level of the pons. can see the lemincus lateral edges kicking out. if you have a lesion in the medial part of these lemnicus areas, then you will have deficit in LIGHT TOUCH, UPPER limb, contralateral side

Front 234

where are we in this section?

Back 234

ponto-mesencephalic junction (see the cerebral aqueduct). Can see fibers of the spinal lemnicus on the lateral sides of the medial lemnicus

Front 235

Back 235

now see medial and spinal lemnicus overlapped. also can see infereior caliculus. lesion there would affect both vibritaory and pinprick, contralateral, both limbs

Front 236

Back 236

now medial and spinal lemnicus is totally intermingled. most are from the dorsal pathway. can see the superior caliculus

Front 237

where are the VPL in this pic

Back 237

Front 238

Which nerve provides sensory innervation to the small area between the 1st and 2nd toes?

Back 238

The deep branch of the common peroneal (fibular) nerve

Front 239

Which nerve is commonly compressed by the inguinal ligament?

Back 239

Lateral femoral cutaneous nerve

Front 240

Trendelenburg gait..likely issue with which nerve?

Back 240

superior gluteal nerve

Front 241

Weakened hip extension; pt has difficulty rising from sitting position or climbing stairs...injury to which nerve?

Back 241

inferior gluteal

Front 242

Sensory loss on medial thigh..damage to which nerve?

Back 242

obturator

Front 243

Sensory loss on dorsum of foot except 1st web space..which nerve is damaged?

Back 243

superficial peritoneal

Front 244

polyol pathway

Back 244

excess of glucose--> conversion to sorbitol via aldose reductase. This leads to osmotic stress via accumulation of sorbitol and
Oxidative stress via depletion of NADPH. NADPH is required by the enzyme glutathione reductase in a reaction that regenerates reduced glutathione (GSH). Recall that GSH is one of the important antioxidant mechanisms in the cell and any reduction in GSH increases cellular susceptibility to oxidative stress

Hint 244

Front 245

3 main courses of diabetic neuropathy

Back 245

1) distal symmetric sensory or sensorimotor neuropathy (Lower extremities. Both motor but particularly sensory function; (“glove and stocking” polyneuropathy); ulcers)
2) Autonomic neuropathy (Disturbances in bowel/bladder function; BP regulation and sometimes sexual impotence)
3) Focal or multifocal asymmetric neuropathy (May manifest as sudden footdrop, wristdrop, or isolated cranial nerve palsies)

Front 246

extrafusal muscle

Back 246

large muscle fibers comprised of fibers that contain actin and myosin and is striated muscle, outside the spindle. Innervated by alpha motor neurons. Impt in posture and the purposeful perturbation of posture

Front 247

Intrafusal muscle

Back 247

Specialized encapsuled muscle located within the extrafusal muscle. also contains actin and myosin filaments on the periphery of the muscle spindle, and are innervated by gamma motor neurons.

Front 248

alpha motor neurons

Back 248

innervate extrafusal muscle, transmits impulses at 70-120m/sec

Front 249

gamma motor neurons

Back 249

innervate intrafusal striated muscle, transmits impulses at 15-30m/sec

Front 250

final common pathway

Back 250

system of the lower motor neuron connected to the skeletal muscle that it innervates. Lower motor neuron diseases always result in depressed activity

Front 251

segmental input

Back 251

afferent input, affects behavior of LMNs

Front 252

neural crest derived cells release NTs that are excitatory or inhibitory?

Back 252

excitatory. any inhibition is a result of the INTERNEURONS

Front 253

Efferent cells are excitatory or inhibitory?

Back 253

excitatory. any inhibition is a result of interneurons

Front 254

upper motor neurons

Back 254

cells in the cerebral cortex that communicate with lower motor neurons

Front 255

suprasegmental input

Back 255

arise from the brainstem and forebrain and influence the LMNs, May act through the basal nuclei/cerebellum, or directly

Front 256

alpha/gamma coactivation or coinactivation

Back 256

Same input"talk" to the alpha and gamma, just differ in which types of neurons have more of a say in the action (the relative influence of converging input differs). So when input comes in, it excites both/inhibits both

Front 257

The sources of motor inhibition is always which type of neuron?

Back 257

interneurons, specifically Renshaw cells which are told what to do by a collateral branch of the efferent cell. This is called a recurrent colateral which happens close to the cell body. Interneurons they may also have excitatory function.

Front 258

Renshaw cells

Back 258

inhibitiroy interneurons that recieve input from collateral branchs of efferent cells. What makes them special is that they are activated by recurrent collateral branches of EFFERENT cells as opposed to higher descending input. One Renshaw cell can inhibit several different LMNs. Renshaw mediated inhibition is a disynaptic mediated response

Front 259

Rexed lamina

Back 259

Front 260

Synaptic endings of C fibers terminate in which Rexed lamina

Back 260

I and II

Front 261

Synaptic endings of A delta fibers terminate in which Rexed lamina

Back 261

I, II, an V

Front 262

cell bodies in the medial part of the ventral horn innervate

Back 262

axial movement

Hint 262

Front 263

cell bodies in the lateral parts of the ventral horn innervate...

Back 263

distal movement of the upper and lower limbs

Hint 263

Front 264

Cells in the intermediate part of the lateral horn innervate...

Back 264

Movements of the proximal limbs

Hint 264

Front 265

when looking at a portion of the spinal cord where there is not innervation of the limbs, why is the ventral horn small?

Back 265

because the areas laterally that are concerned with limbs is absent.

Front 266

"Map" of lamina 9 cells

Back 266

Front 267

motor unit

Back 267

LMN its axons, and all of the muscle cells it innervates. it innervates >1muscle cells because of collateral branches

Front 268

2 important principes of efferents

Back 268

1) all make and release ACh
2) all are excitatory

Front 269

types of motor units

Back 269

small--> tend to be in fine control muscles (tongue, hand muscles, etc). have smaller cell bodies, fewer collateral branches, slower conduction velocity, and more spindle input (muscle spindles have the most 'say'), lower threshold to excitation. fatigue slowly (red fibers), tonically active (antigravity muscles), greater response to disuse

big--> tend to be in larger in, less fine movement muscles (glutes, quads, etc).

Front 270

if you want to lift something heavy, the first motor units you will recruit are ?

Back 270

small motor units recruited first. Henamen size principle

Front 271

disuse atrophy

Back 271

shrinking of a size of a muscle cell when that muscle is not being used. muscle tone is RETAINED

Front 272

dennervation atrophy

Back 272

shrinking of the size of the muscle cell because the influence of ACh or the neural input to the muscle is taken away . muscle tone is LOST

Front 273

muscle spindle

Back 273

"Length detector"
Muscle spindles are sensitive to muscle length. An increase in the length of the equatorial region of the muscle spindle results in an increase in the firing rate along the muscle spindle afferent axon (type1a and type II fibers).

Front 274

GTO

Back 274

"Tension detector", embedded in the musculotendinous junction. Receptor that transduces changes in muscle tension. Compression of the axons between collagen fibers is what stimulates golgi organ, will send impulse via Type 1b fiber. The type 1b fiber will cause inhibition of the agonist muscle when there is tension on that muscle. This is a disynaptic circuit

Front 275

nuclear bag fiber

Back 275

nuclei in the middle, and actin/myosin located on either end of the spindle cell. attached in parallel to the extrafusal muscle. So when extrafusal cell elongates, the nuclear bag fiber also elongates

Front 276

nuclear chain fiber

Back 276

nuclei organized in bead like fashion and the actin/myosin located on either end of the spindle cell. Attached in parallel to nuclear bag fibers.

Front 277

Muscle spindle-->Primary nerve endings on the afferent side

Back 277

lie in the equatorial region of the bag and chain fibers. These fibers are 1a type, stimulated by stretch of the equatorial region and send info back to CNS more rapidly when depolarized

Hint 277

Front 278

Muscle spindle--> Secondary nerve endings on the afferent side

Back 278

lie in the periequitorial regions of the nuclear bag/chain, These fibers are Type II and also respond to elongaton of the equatorial region. when depolarized send info back to CNS a little more slowly than Type 1a of the equatorial region when depolarized

Hint 278

Front 279

gamma motor neurons on the efferent side innervate which region(s) of the muscle spindle?

Back 279

the polar regions

Front 280

strongest influence on LMNs in inducing alpha motor neuron activity?

Back 280

1a. Very potent so they are automatic responses. Total convergence and divergence is characteristic of connections between 1a fibers and alpha motor neurons (talks to all of the LMNs innervating a particular muscle and does it monosynaptically). Clinical 'pearl'- you can elicit these reflexes even in pts who are unconscious because its such a potent and automatic effect.

Front 281

how is clonus inhibited during the activation of a muscle spindle?

Back 281

inhibiton of the antagonist muscle via interneurons

Front 282

2 ways to activate muscle spindle

Back 282

1) increase muscle length 2) increase gamma motor neuron activity (this would cause the polar regions alone to contract, and the equatorial region will stretch if the spindle overall doesnt change length

Front 283

Muscle enlongation effects on primary and secondary ending?

Back 283

Secondary endings response to muscle length at any instance in time, only responding to the change in length. The primary ending, during the change, will fire faster than it does at the resting length. the primary ending also responds to RATE of change of length.

Front 284

spasticity

Back 284

velocity dependent change in resistance to passive elongation of muscle

Front 285

Two ways to activate GTO

Back 285

Golgi tendon organs are sensitive to muscle tension. An increase in the tension in a muscle (extrafusal) results in an increase in the firing rate along the golgi tendon organ afferent axon (type1b fiber). Two ways to activate is to elongate the muscle or contract the muscle

Front 286

5 physiological principles regarding muscle spindles and GTOs

Back 286

1) muscle spindles respond to increases in muscle length, increasing firing rate of type 1a and type II fibers (afferent axon)
2) primary and secondary endings response differ. primary response to changes in RATE whereas secondary responds simply to change
3) increase in firing rate along afferent axon results in excitation of alpha motor neurons innervating extrafusal fibers of agonist muscle
4) GTOs response to muscle tension, and increases firing rate in type 1b fibers (afferent axon)
5) increasing firing rate of 1b fibers results in inhibition of the alpha motor neurons innervating extrafusal fibers of the antagonist muscle

Front 287

muscle spindle and GTOs general purpose

Back 287

maintenance of muscle tone and muscle. NOT movement really, more of a maintenance of "idle speed" of muscles

Front 288

Example of a placing reaction

Back 288

putting baby on floor, the plantar reflex (toes point down with non non-nocieptive stimuli)

Front 289

Withdrawal reflex and placing reflex

Back 289

Both are multisegmetal reflexes. Withdrawal is activated by nociceptive stimuli whereas placing reaction is activated by non-nociceptive. Both systems are "hard-wired in the same way" the other difference is which way it is activated depending on whether the stimulus is nociceptive or not.

Hint 289

Front 290

hanging reflex

Back 290

you elicit reflex, response occurs, and it takes a while to be extinguished. This is a neurologial abnormality and can be dur to a spinal cord issue

Front 291

crossed adductor reflex

Back 291

- "spread". The crossed response affects the hips adductors. For ex, stimulating quad on right elicits adductors on L side. This is because postaxial muscles on the R and preaxial muscles on the L are innervated by anterior division nerves ie the obturator.

Front 292

What is latency and what could an increase in latency be due to?

Back 292

The time it takes from time you tap to time you see the reflex. An increase in latency could suggest a demyelinating diseases

Front 293

The only place you can have a lesion that results in increased tone and increase in the dynamic component of the stretch reflex?

Back 293

Upper motor neuron

Front 294

afferent nerve injuries and efferent nerve injuries cause?

Back 294

decreased muscle tone, decrease in reflexes

Front 295

evaling the static component of the tonic stretch reflex

Back 295

this thing or also pronator drift test

Front 296

Back 296

Front 297

evaling dynamic component of the tonic stretch reflex

Back 297

moving pt around while they are relaxed. Any resistance to passive motion (spasticity) may indicate upper motor neuron disease

Front 298

pronator drift

Back 298

ask pt to hold hands, supine up in front of them. Side contralateral of the affected side will being to pronate (have lost supinator function) . this is a way to eval the static component of the tonic stretch reflex

Front 299

is this a segmental, multisegmental, or suprasegmental reflex?

Back 299

segmental

Front 300

do automatic or "less automatic" responses have a greater dependence higher center ?

Back 300

"less automatic" responses are more dependent on higher centers. Automatic responses are even intact in unconscious pts

Front 301

Theoretically: Decrease presynaptic inhibition to 1a fiber input?

Back 301

would let 1a release more excitatory NT, excite alpha motor neuron --> hypertonia. No evidence for this though so it is not what causes spasticity

Front 302

Tracts for the extensor system (antigravity muscles)

Back 302

Vestibulospinal is the main one, assisted by the pontinereticospinal tract

Front 303

Tracts for the flexor system

Back 303

Rubrospinal tract and medually reticulospinal tract

Front 304

Sympathetic outflow

Back 304

thoracolumbar outflow (T1-L2), primarily comes from descending sympathetic fibers from the hypothalmus (preganglionic).

some fibers from T1 and T2 come up and go up to the head/neck. if these are interrupted, you develop Horner syndrome (lose sympathetic innervation...loss sweating to half of face, pupils constrict, upper eyelid droops- ptosis)

Front 305

Parasympathetic outflow

Back 305

craniosacral outflow (from the 3rd, 7th, 9th, 10th cranial nerves then also from the sacrum S2, S3, S4), primarily comes from descending parasympathetic fibers from the hypothalmus

Front 306

Theoretically: Decrease excitation to Renshaw cells?

Back 306

You would let excitiatory influences on alpha motor neurons, increased alpha motor activity --> hypertonia. no evidence for this being possible though so it is not what causes spasticity

Front 307

Theoretically: Taking away gamma neurons inhibition?

Back 307

Gamma firing goes up, polar regions contract, equatorial regions stretch, firing of 1a neurons goes up, alpha motor neurons activity goes up --> hypertonia . but there is not any evidence on selective inhibition of gamma (without alpha, because of coactivation), so it is not what causes spasticity

Front 308

Reflex responses will always be most brisk where?

Back 308

in the lower limbs, particularly the antigravity muscles (gastrocs and achilles especially). The upper limbs have been more modified not for anti-gravity purposes and are now "freed up" for more voluntary responses

Front 309

Explain each piece in this picture ?

Back 309

1) Normal resting state
2) Stretch the bicep…If gamma did nothing increase length of spindle equatorial region without changing polar regions, which would activate more 1A fibers-->increase alpha firing rate-->hypertonia
3) …But the gammas will compensate but reducing their firing rate so they can maintain a fixed 1a firing rate
4) If gammas stay the same when elbow is flexed, equatorial region drops down, firing on 1a goes down, number of alpha nurones excited will also go down-->hypotonia
5) …but the “slack” is taken up by actin/myosin but increased firing of gamma

Front 310

passive stretching of the muscle in evaluating muscle tone

Back 310

↑ muscle length ( ↑1a ) offset by ↑ muscle tension ( ↑Ib) → no change in motor unit activity

Front 311

superior and inferior colliculi

Back 311

Bumps on the dorsal surface of the midbrain. Form the tectum, the roof of the cerebral aqueduct. Together called the tectal nuclei.

The superior colliculi is primarily influence based on input from the retina. The tectospinal tract is thus important in visual fixation as well as head and neck movement. Other sources of influence is cerebral cortex

Front 312

reticular formation

Back 312

collection of mixed white and gray matter in the brainstem

Front 313

Decreased excitation to alpha motor neurons?

Back 313

Decreased excitation to alpha motor neurons--> decreased motor unit activity --> decreased tension detected by Golgi tendon organ--> decreased impulse transmission in type Ib fibers-->decreased inhibition (disinhibition) of alpha motor neurons --> increased (relatively unopposed) response to muscle stretch (1a ) input. This is actually how spasticity occurs

Front 314

Babinski sign

Back 314

Extension of the big toe and fanning the lateral sign in response to plantar reflex (when plantar aspect of the foot is stimulated by non-nonciceptive stimuli). Sign of an upper motor neuron injury** most common pathologic sign of UMN injury.

Front 315

Evolution and the reticular formation

Back 315

The reticular formation is more primitive and is often found in lower species alone. These RT projection are typically bilateral.

Front 316

brainstem UMNs show a predominantly crossed/uncrossed effect?

Back 316

crossed

Front 317

red nuclei

Back 317

Found in the midbrain, and consists of two parts. Caudal part has larger cells bodies with longer, crossing axons, influencing both alpha and gammas, forming rubrospinal tract and ending in the the dorsal part of the lateral funiculus. They primarily influence the distal limb FLEXORS. The rostral part of the red nuclei has smaller cell bodies which give rise to smaller axons. Receive input from the cerebral cortex, cerebellum, and the basal nuclei.

Red nuclei also have collaterals that will influence cranial nerves

Front 318

brainstem UMNs tend to influence which more- gammas or alphas?

Back 318

gammas- muscle tone moreso rather than actual motor function

Front 319

Input to the red nuclei

Back 319

cerebellum- coordination of TIMING of the movements.
basal ganglia- picks which LMN you need to EPSP and IPSP
cerebral cortex- red nuclei serves as a " rest stop" on its way down to the spinal cord

Front 320

tectospinal pathway

Back 320

go to alpha and gamma neurons in the spinal cord but go to the ventral (medial) motor system--> AXIAL movement, specifically the neck muscles, and mostly the extensors (since axial muscles are usually extensors)

Front 321

input from above the brainstem nuclei will affect which side?

Back 321

clinical sxs manifested on the OTHER SIDE. this is impt because strokes tend to be in the cerebrum. Sxs are then ultimately manifested on the contralateral side

Front 322

Which brainstem UMNs end up in the lateral motor system? Medial (ventral)?

Back 322

Rubrospinal--> lateral = distal flexors

Reticulospinal, vestibulospinal, and tectospinal--> medial (ventral system) = axial muscles

Front 323

Vestibulospinal tract

Back 323

located in the ventral motor system, innervation of axial muscles. extends from vestibular nuclei to the spinal cord

Front 324

Radial nerve actions

Back 324

Extension at all arm, wrist, and proximal finger joints below the shoulder; forearm supination; thumb abduction in plane of palm

Front 325

ulnar nerve actions

Back 325

Ulnar: Finger adduction and abduction other than thumb; thumb adduction; flexion of digits 4 and 5; wrist flexion and adduction

Front 326

Musculocutaneous nerve actions

Back 326

Flexion of arm at elbow, supination of forearm

Front 327

Axillary nerve actions

Back 327

Abduction of arm at shoulder beyond first 15°

Front 328

Brainstem nuclei- spinal tracts: The phylogenetically “oldest” of the rubro, reticulo, and tectospinal pathways is...?

Back 328

reticulospinal tract (75% gamma, 25% alpha); this tract is involved in "less automatic" movement

Front 329

After the reticulospinal tract, what evolutionary developed next?

Back 329

tectospinal (70% gamma, 30% alpha). this tract is involved in eye movement and neck movement to increase field of vision

Front 330

The "last" tract to come in of the brainstem UMNs is which?

Back 330

rubrospinal (65% gamma, 35% alpha).

Front 331

Evolution of brainstem UMN vs cortical and their function

Back 331

as we have evolved, there has been a shift from regulation of muscle tone to cells that allow for perutbation of posture (reflexive control via gamma to voluntary control via alpha). the geographically lower UMNs in the brainstem have been around forever and will thus be used for large gross anti-gravity type functions. The discrete finer movements is coordinated by the corticospinal UMNs which are more recent and advanced in development

Front 332

what is the name of the medial continuation of the precentral gyrus?

Back 332

anterior paracentral gyrus

Front 333

Brodman numbers

Back 333

Areas 3, 1 & 2 - Primary Somatosensory Cortex and posterior paracentral area
Area 4 - Primary Motor Cortex
Area 5 and 7 - Somatosensory Association Cortex
Area 6 - Premotor cortex and Supplementary Motor Cortex
Area 7 - Somatosensory Association Cortex

Front 334

cortical UMNs: most rostral decussating fibers come from?

Back 334

upper limb. also recall that 85% ish cross, 15% stay ipsilateral. of the lateral tract, upper limb ends up medial, lower limb lateral

Front 335

if you knock out the corticospinal tract somewhere below the cerebral cortex (once the fiber have condensed together) as in a stroke, where in the body would sxs be most profound?

Back 335

upper limb. this is because 55% of fibers of the corticospinal tract go to the upper limbs (C5-T1) . you would affect everything but most severe in upper limb because of this

Front 336

Betz cells

Back 336

3-4% of the UMNs in the primary motor cortex. Those that go to the distal musculature of the limb tend to be more direct (cortical UMN to alpha, without interneuron involvement)

Front 337

cortical spinal cells are influenced by?

Back 337

convergent input (excit & inib) from:
1) cortical cells elsewhere (eg auditory, olfactory cortex)
2) cerebellum (tell the motor cortex WHEN to fire. there will be corticopontine, pontocerebellar, then cerebellothalamic, thalamicortico signaling to coordinate)
3) basal ganglia (decided in frontal lobe to pick something up, corticostriato, striatopalido, palidothalamic, thalamicortico signaling. tells body WHICH muscles need to be engaged; write programs to inhibit antagonistic muscles in carrying out actions)

Front 338

cortical UMNs talk more to which alpha or gamma? how to assess cortical UMN function vs subcortical UMN function?

Back 338

both, but moreso on the alpha. assessing integrity of this system= give pt task to do. as opposed to testing gamma function, YOU do something to assess automatic function rather than their voluntary function. gamma= measure tone, doctor initiated activity alpha= measure strength/power, pt intiated activity

Front 339

Back 339

1 internal capsule
2 Cereb peduncdle
3 Longitudinal pontine bundles

Same coriticospinal tract travelling through just changes names. Note that these fibers are MIXED with there so you cant actually make a pure corticospinal injury. The only place where there is only corticospinal fibers is the medullary pyramid. Knocked out in monkey? No detected effects in the lower limb! Meant that the descending influences from the brainstem must be sufficient for proper lower limb function. The only deficit was flexion of the distal upper limb. This is b/c corticospinal tract mainly goes to excitation of flexors of the upper extremity (and inhibition of the extensors)

Front 340

Back 340

1- VPL
2 VPN

Front 341

Back 341

1- superior colliculi (tectispinal tract projects from here)
2- aqueduct of sylvuis
3- Red nucleus
4- cerebral peduncle (corticospinal tract in there)

Front 342

cluster of fibers in the middle?

Back 342

deccusation of the superior cerebellar peduncle, which occurs at occurs at the level of the interferior colliculi (the bumps at top are inferior colliculi)

ventral tegmental decussation= region where the axons from the red nucleus cross. end up laterally (rubro goes into lateral funiculis)
dorsal tegmental decussation=region where the axons from the superior colliculus cross. end up in the middle (tecto end up in the anterior funiculis)

Front 343

Back 343

this is called the MLF (medial longitudinal fasciculus ). It is important in interconnecting the eye nuclei so we get conjugate eye movements. this is the first myelinated pathway in the human (before birth!) . immediately below the MLF = tectospinal fibers (ie axons from the superior collicul. they stay there forever)

Front 344

The white fibers shown ?

Back 344

are the pontine nucleus “breaks up” the formerly compact axons of the cerebral peduncle (corticospinal axons) into longitudinal pontine bundles

Front 345

Back 345

we are at the caudal pons but now will less pontine nuclei, we see the longitundinal pontine bundles (corticospinal tract) have compacted. the same is about to change as you pass into medulla

1- longitudinal pontine bundles compact
2- 4th ventricle
3- inferior cerebellar peduncle (sign of caudal pons)

Front 346

majority of the coriticospinal axons are found where in the descending tract

Back 346

middle 1/3

Front 347

Back 347

1- medial lemnical
2- tectospinal
3- MLF
4- rubrospinal tract
5- olive
6- medullary pyramid

also see 4th ventricle open at top

Front 348

where?

Back 348

this is the pyramidal decussation. Below the olives so in caudal half of medulla. In the midline fibers occupying space= decusssation.

if lesion here, bilateral sxs. if lesion at upper end of decussatoin, upper ex sxs will be affected bc upper cross first

Front 349

lesion is midline?

Back 349

vibratory sensory deficits affecting the medial leminscus system

Front 350

Erb's palsy

Back 350

Paralysis of the arm caused by injury to the upper group of the arm's main nerves, specifically C5–C6 nerves. Results in prominent weakness of the deltoid, biceps, infraspinatous, and wrist extensors. The arm assumes a characteristic “waiter’s tip” pose, held at the side, internally rotated, and with the wrist flexed. Finger and hand movements are relatively spared.
Common causes include traction on an infant’s shoulder during a difficult delivery as well as motorcycle accident

Front 351

Klumpke's Palsy

Back 351

Caused by damage to the lower trunk of the brachial plexus. See weakness and sensory loss in C8-T1 innervated areas. Symptoms include claw hand, paralysis of intrinsic hand muscles, and ulnar nerve distribution numbness (ulnar part of hand and forearm)

Common causes include upward traction produced by grabbing a branch during a fall from a tree, thoracic outlet syndrome, and Pancoast’s syndrome, and birth trauma.

Front 352

Claw hand

Back 352

Chronic ulnar nerve injury causes weakness of the lumbricals for digits 4 and 5 when the patient is asked to extend the fingers. numbness over the ulnar side fingers

Front 353

Thoracic outlet syndrome

Back 353

In thoracic outlet syndrome, the lower brachial plexus is compressed as it passes between the clavicle and the first rib

Front 354

Motor: Foot dorsiflexion, toe extension
Sensory: Webspace between 1st and 2nd toes

Back 354

Deep peroneal nerve

Front 355

Motor: Foot plantar flexion and inversion, toe flexion
Sensory: lateral foot

Back 355

posterior tibial nerve

Front 356

Explain the differences between an epidural, subdural, and subarachnoid hematoma.

Back 356

Ppidural hemorrhage is arterial in origin. Blood from torn branches of a middle meningeal artery collects between the external periosteal layer of the dura and the calvaria.

A dural border hematoma is classically called a subdural hematoma. However, this term is a misnomer because there is no naturally occurring space at the dura–arachnoid junction. Hematomas at this junction are usually caused by extravasated blood that splits open the dural border cell layer. The blood does not collect within a preexisting space, but rather creates a space at the dura–arachnoid junction. Dural border hemorrhage usually follows a blow to the head that jerks the brain inside the cranium and injures it. The precipitating trauma may be trivial or forgotten. Dural border hemorrhage is typically venous in origin and commonly results from tearing a superior cerebral vein as it enters the superior sagittal sinus. Sxs include LOC then lucid period then drowniness

Subarachnoid hemorrhage is an extravasation of blood, usually arterial, into the subarachnoid space (Fig. B7.19C). Most subarachnoid hemorrhages result from rupture of a saccular aneurysm (sac-like dilation on the side of an artery), such as an aneurysm of the internal carotid artery. Sxs are severe headache, neck stiffness, LOC

Front 357

The artery of Adamkiewicz is an especially large spinal medullary artery supplementing the arterial blood supply to the spinal cord. Which of the following represents the most consistent location of this vessel?

Back 357

At T12–L1 on the left

Front 358

A 41-year-old man is brought to the emergency department after an accident at a construction site. The examination reveals a weakness (hemiplegia) and a loss of vibratory sensation and discriminative touch all on the left lower extremity, and a loss of pain and thermal sensations on the right lower extremity. CT shows a fracture of the vertebral column adjacent to the T8 level of the spinal cord.

Damage to which of the following fiber bundles or tracts would most likely explain the loss of vibratory sensation in this man?

(A) Anterolateral system on the right
(B) Cuneate fasciculus on the left
(C) Cuneate fasciculus on the right
(D) Gracile fasciculus on the left
(E) Gracile fasciculus on the right

Back 358

D

Front 359

An 88-year-old man is brought to the emergency department by his daughter. She indicates that he complained of weakness of his “arm” and “leg” (upper and lower extremities) on the right side and of “seeing two of everything” (double vision—diplopia). CT shows an infarcted area in the medial area of the pons at the pons-medulla junction. The infarcted area is consistent with the vascular territory served by paramedian branches of the basilar artery.

Weakness of the extremities on the right can be explained by damage to which of the following structures?

(A) Corticospinal fibers on the left
(B) Corticospinal fibers on the right
(C) Middle cerebellar peduncle on the left
(D) Rubrospinal fibers on the left
(E) Rubrospinal fibers on the right

Back 359

A

Front 360

A 47-year-old man is transported to the emergency department from the site of an automobile collision. The examination reveals a paralysis of both lower extremities. Which of the following most specifically identifies this clinical picture?

(A) Alternating hemiplegia
(B) Hemiplegia
(C) Monoplegia
(D) Quadriplegia
(E) Paraplegia

Back 360

E

Front 361

Label parts of this image

Back 361

Front 362

Back 362

? = terminal bouton, filled with vesicles (the circles)

Front 363

Back 363

1= epineurium
2= vasoneurium
3= perineuium
4= fasicles

Front 364

label the sinuses

Back 364

Front 365

Pt presents with weakness in both hi[ adduction and knee extension. Which nerve or nerve roots are likely affected?

Back 365

L2-L4

Front 366

Pt presents with inability to dorsiflex the ankle and loss of sensation between the 1st and 2nd toe webspace. Which nerve or nerve roots are likely affected?

Back 366

Deep peroneal nerve (aka anterior tibial). L4, L5

Front 367

Pt presents with numbness over the medial aspect of the upper thigh. Which motor function is also likely impaired?

Back 367

Hip adduction (obturator nerve injury)

Front 368

Pt presents with sensory loss over the dorsum of the foot except for the webspace between the first and second toes. Which nerve or nerve roots is likely affected?

Back 368

Superficial peroneal (L5, S1, S2)

Front 369

Label the cranial nerves

Back 369

Front 370

Which two nuclei form the striadum?

Back 370

putamen and caudate nucleus

Front 371

What forms the "gaps" in this picture?

Back 371

The fibers from the internal capsule

Front 372

amygdaloid nucleus is located in which lobe?

Back 372

Temporal

Front 373

corpus striatum consists of?

Back 373

globus pallidus, putamen, and caudate nucleus

Front 374

lenticular nucleus consists of?

Back 374

globus pallidus + putamen

Front 375

striatum consists of?

Back 375

putamen + caudate nucleus

Front 376

Back 376

1= caudate nucleus
2= putamen

Front 377

Back 377

1= putaman
2= caudate nucleus
3= globus pallidus
4= GPi
5= GPe
6= optic chiasm
7=internal capsule

note that globus pallidus is darker, has more mylelination

note also that globus pallidus is divided into TWO segments (external and interna). GP(e) GP (i), separated by internal medullary lamina. the external medullary lamina separates that globus pallidus from the putamen

Front 378

in this picture, 1=thalmus. What is the white matter just adjacent to it?

Back 378

if you see thalmus in a coronal section, the white matter adjacent to it must be the POSTERIOR limb of the internal capsule

Front 379

Back 379

1= thalmus
2= temporal horn of the lateral ventricle
3= sylvian fissure
4= mammilary body
5= third ventricle
6= lateral ventricle (body)
7=caudate nucleus
8= putamen
9= GPe
10= GPi

Front 380

Label the lamina in this picture

Back 380

1= internal medullary lamina of the thalmus (separates the medial and lateral nuclear groups)
2= internal medullary lamina of the globus pallidus
3= external medually lamina

Front 381

The internal medually lamina of the thalmus divides the thalmus into?

Back 381

medial and lateral nuclear groups
medial nuclear group is called DM. The lateral group is subdivided into a ventral and dorsal group. The ventral groups are VA, VM, VPL, VPM,

Front 382

ventral striatum

Back 382

looks histologically the same as the striatum and are chemically/structurally the same but lie below the anterior commisure

Front 383

ventral pallidum

Back 383

looks histologically the same as the globus pallidus and are chemically/structurally the same but lie below the anterior commisure. Contains the basal nuclei of Meynert, which are a cholinergic cluster of cells- these are some of the first cells to die in the alzheimers disease

Front 384

Basal nuclei of Meynert,

Back 384

cholinergic cluster of cells found in the ventral pallidum. These are some of the first cells to die in the alzheimers disease

Front 385

Claustrum

Back 385

separate the external capsule from the extreme capsule

Front 386

Back 386

1= cerebral peduncle
2= red nucleus
3= substancia nigra

Front 387

More dorsal part of the substancia nigra?

Back 387

More dorsal part of the substancia nigra is more densely packed so called substancia nigra compacts. Cells here make DA. When these cells die, pt develops parkinsons .

Globus pallidus internal segment is continuous with the substancia nigra

Hint 387

Front 388

Back 388

L is pt wtith parkinsons. Less darkly stained substancia nigra

Front 389

DM projects to where?
VA projects up to where?

Back 389

DM projects to prefrontal cortices
VA projects up to the posterior part of frontal/anterior part of parietal lobe

Front 390

3 "pathways" out of the globus pallidus?

Back 390

1) fascicularis lenticularis (H2 field of forel)
2) ansa lenticularis
3) subthalamic fasiculis (H1 field of forel)

these all meet up, along with the fibers from the opposite side, immediately in front of the red nucleus (prerubral field of forel aka H0 field of forel)

Front 391

output of the striatum to the GP is influenced by what?

Back 391

the substancia nigra's influence. Will dial up the things needs for movement and dial down the antagonists. SN uses Dopamine to do this

Front 392

striatum efferents use which neurotransmitter?

Back 392

GABA

Front 393

GPe and GPi use which neurotransmitter?

Back 393

GABA (inhibitory)

Front 394

Subthalamic nucleus uses which neurotransmitter?

Back 394

Glutamate (excitatory)

Front 395

frontal eye field is located where?

Back 395

brodman area 8, just anterior to the prefrontal sulcus

projections from here to the striatum will specifically go to the caudate nucleus (closer than putamen)

Front 396

"simple circuits"

Back 396

occulomotor and motor circuits
(more voluntary movements impaired if damaged)

Front 397

"complex circuits"

Back 397

dorsolateral, orbitofrontal, anterior cingulate (problem solving, behavior, emotional, motivation psychiatric presentation if damaged)

Front 398

Dorsolateral loop function

Back 398

execulive function--> damage here would lead to poor problem solving, impaired shift setting

Front 399

Orbitofrontal loop function

Back 399

emotion--> damage here would lead to irritability, bevhavioral disinhibition, and emotional liability

Front 400

Anterior cingulate loop

Back 400

Motivation --> damage here would lead to apathy, abulia, akinetic mutism

Front 401

hemibalismus

Back 401

if you kill subthalamic nucleus cells, you take away the inhibiton from the thalamus. Over excitiation of the corticospinal cells and uncontrolled muscle contralaterally on one side.

Front 402

Huntington's disease

Back 402

Hyperkinetic motor abnormality. Cells of the striatum are killed and you have too much excitation. Result is choriatic movements (pt implements inappropriate motor programs+

Front 403

Parkinsonism

Back 403

Characterized by akinesia, pill-rolling tremors, postural instability, and rigidity.

Caused if you knock out substancia nigra. You take away excitation to the direct pathway (which normally excites corticospinal neurons) and take away inhibition to the indirect pathway (which again normally would allow for movement). Result is decreased cortical activity and disregulated behavorial, which is worst in the distal upper limb flexors. Also issues with full hip flextion and knee flexion so gait problems. Too much inhibtion of intended muscle groups.

Front 404

hyomemia

Back 404

lessened movements of the face

Front 405

persistant glabellar reflex

Back 405

tap on glabella several times and pt cannot stop from blinking each time. It is a sign of parkinsonism; it is a "release behavior" (response occurs and you cant shut it off, lack of ability to inhibit a persistent response)

Front 406

abnormal finger and nose and abnormal heel to shin...what is dysfunctioning?

Back 406

the cerebellum (TIMING of movements on the millisecond level)

Front 407

primary fissure of the cerebellum separates which two lobes

Back 407

anterior lobe from posterior lobe.

Hint 407

Front 408

The posterolateral fissure of the cerebellum separates which two lobes ?

Back 408

Posterior lobe from the flocculonodular lobe

Hint 408

Front 409

first lobe of the cerebellum to evolve?

Back 409

flocculonodular lobe

Front 410

label

Back 410

Front 411

where is the superior cerebellar peduncle?

Back 411

6

Front 412

Where is the middle cerebellar peduncle

Back 412

9

Front 413

Where is the inferior cerebellar peduncle

Back 413

7

Front 414

name the layers

Back 414

molecular layer, most superficially (few cells in it). Granular layer most internally (LOTS of cells in it). Purkinje cells separating the two.

Front 415

Types of cells in the molecular layer of the cerebullum

Back 415

stellate cells tend to be more superficially and the basket cells are more near the border (closer to the purkinje layer)

Front 416

Types of cells in the granular layer of the cerebellum

Back 416

golgi cells and granule cells

Front 417

5 cell types of the cerebellar cortex?

Back 417

Stellate cells, basket cells, purkinje cells, golgi cells, and granule cells

Front 418

climbing fibers of the cerebellum

Back 418

EXCITATORY.
can excite 2-12 purkinje cells. will also give a collateral branch to the deep nucleus

Front 419

deep nuclei in the hemispheric region of the cerebellum?

Back 419

dentate nucleus

Front 420

deep nucleus in the vermal region of the cerebellum?

Back 420

fastigial nuclues

Front 421

Deep nucleus in the paravermal region of the cerebellum?

Back 421

globose nucleus, and emboliform nucleus

Front 422

Parallel fibers

Back 422

EXCITATORY. excites purkinje fibers at their distal dendritic fields. also will excite stellate and basket cells, which are both inhibitory.

Front 423

Two excitatory and two inhibitory cells that provide input to the purkinje cells?

Back 423

Excitatory--> Climbing fibers and parallel fibers

Inhibitory --> stellate and basket cells

Front 424

What is the NT synthesized and utilized by the Purkinje cells?

Back 424

GABA (inhibitory). Provides careful regulation of the deep nucleus (which recieved input from the purkinjes) . This is important because the deep nucleus are the main fibers coming out of the cerebellum, going to the midbrain and spinal cord

Front 425

mossy fibers

Back 425

all of the afferent input to the cerebullum except for those fibers coming from the inferior olivary nucleus (which are called climbing fibers)

Front 426

Archaecerebellum

Back 426

This is made up of the flocculonodular lobe (the most primitive of the 3 lobes). The major input into this lobe is VESTIBULAR, so it also called the vestibulocerebellum. When the head moves in space, receptors are activated, info comes in thru the vestibulocochlear nerve (CNVIII), and goes to the vestibulocerebellum

Front 427

Vestibular system dysfunction?

Back 427

Damage to this system would present as nystagmus and blurry vision.

The vestibular system normally influences the extraoccular muscles so that they move in correspondence to the head. It allows you to maintain visual fixation on an object while the head is moving in space.

Front 428

juxtarestiform body

Back 428

part of the inferior cerebellar peduncle, next to the restiform part of it. this the "highway" in and out of the cerebellum

Front 429

Vestibulospinal tract innervates what?

Back 429

extensors

Front 430

Decerebrate rigidity

Back 430

overactive vestibulospinal system causing persistent extension of the limbs

Front 431

The vestibular is activated when?

Back 431

AFTER movement has occurred. It is activated by head movement.

Front 432

Role of muscle spindles in cerebellum function

Back 432

Muscle spindles monitor instantaneous length of every muscle in the body which the cerebellum translates as "where is that muscle in space".

Information from the LIMBS:
1a fibers come into the spinal cord from muscle spindle, synapse on nucleus dorsalis (between T1 and L2) if from lower limb, or lateral cuneate nucleus (in the medulla) if from the upper limb. They then send information up to the cerebellum via the dorsal spinocerebellar or cuneocerebellar tracts (go thru the inferior cerebellar peduncle).

Information from the AXIAL muscles: the information goes to the spinal border cells. Then goes through the ventral spinocerebellar tract and enters the cerebellum by way of the superior cerebellum peduncle.

All three enter as mossy fibers (which recall send branches to deep nucleus and then up to the cortex where they activate parallel fibers) The axial muscle fibers go to the globosus nucleus and up the vermal cortices. Limb muscles fibers go to the emboliform nucleus and up to the paravermal cortices.

Front 433

Paleocerebellum is activated when?

Back 433

Activated after the onset of movement. The stimulus is elongation of the muscle spindle.

Front 434

Clark's column

Back 434

eponym for the nucleus dorsalis, from which the dorsal spinocerebellar tract projects up to the inferior peduncle of the erebellum

Front 435

recording electrodes in each of the deep nuclei... what would happen??

Back 435

If put in the fastigial nuclei, would start recording activity AFTER head movement. If in globulbosa nuclei, would respond after muscle spindle elongation. If put in dentate nucleus will fire BEFORE onset of any movement

Front 436

Neocerebellum is activated when?

Back 436

BEFORE movement

Front 437

testing the neocerebellum

Back 437

must be PATIENT INDUCED in order to test the integrity of it. Others you would test by doctor induced movements.

Front 438

the climbing fibers enter the cerebellum through which peduncle?

Back 438

The inferior cerebellar peduncle

Front 439

Climbing fibers

Back 439

enter the cerebellum from the contralateral inferior olivary nucleus

Front 440

Ataxia

Back 440

motor incoordination

Front 441

Dysmetria

Back 441

refers to a lack of coordination of movement typified by the undershoot or overshoot of intended position with the hand, arm, leg, or eye. It is a type of ataxia

Front 442

lesion in the cerebral hemispheres and peduncles affect which side

Back 442

ipsilateral

Front 443

Back 443

1- caudate
2- putamen
3- nucleus accumbens
4- septum palucidum (cells just underneath are the septal nuclei)
5- anterior limb of internal capsule
6- claustrum

Front 444

Back 444

1= red nucleus
2= substantia nigra
3= caudate (body)

Front 445

Back 445

1- anterior commisure
2- optic chiasm
4-ventral siriatum
5- ventral pallidium
6- caudate

Front 446

Back 446

1- Ansa lenticularis
2- choroid plexus
3- hypothalamus

Front 447

GPi-synaptic endings of projections from here go where?

Back 447

thalamus-- specifically CM, DM, and VA

Front 448

Clarke's column

Back 448

Group of interneurons found in the medial part of Lamina VII, also known as the intermediate zone, of the spinal cord. It is located from the T1 to L2levels and is an important structure for proprioception. If you destroy this, ipsilateral sxs

Front 449

at which level do the dorsalspinocerebellar tracts "peel off" and merge with cuneocerebellar axons?

Back 449

the lateral cuneate nucleus

Front 450

axial muscle spindles enter the cerebellum through?

Back 450

superior cerebellar peduncle

Front 451

fibers from the globose and emboliform nuclei send their axons where?

Back 451

red nucleus, contralateral side

Front 452

middle cerebellar peduncle are formed by

Back 452

pontocerebellar fibers from the CONTRALATERAL side

Front 453

most of the fibers in the middle are what?

Back 453

dentato thalamic and cerebellorubral

Front 454

anosmia

Back 454

Olfactory loss

most are related to nose issues rather than neuro issues

2nd most common cause of acute anosmia (after head trauma), shearing off of olfactory filla (bundles of axons) can impair or destroy sense of small

Front 455

olfactory epithelial cells

Back 455

BIPOLAR cells. with a central process (axon) that passes through the cribiform plate in bundles (as fllla) and synapses with cells of the olfactory bulb.

Front 456

Bowman cells of the olfactory epithelium?

Back 456

glands in the nasal cavity whose secretions help makes incoming odors soluble

Front 457

subtentacular cells of the olfactory epithelium?

Back 457

the supporting cells of the olfactory epithelium

Front 458

basal cells of the olfactory epithelium?

Back 458

basal cells are stem cells capable of division and differentiation into either supporting or olfactory cells. The constant divisions of the basal cells leads to the olfactory epithelium being replaced every 2–4 weeks.

Front 459

periglomerular and granule cells

Back 459

important for rapid extinguishing of smells so that a new one can be detected. These are inhibitory celle

Front 460

Lateral olfactory gyrus

Back 460

layer of cells wrapping around the lateral olfactory stria before reaching the base of the frontal lobe

Front 461

fibers of the medial olfactory stria head where?

Back 461

go to the septal nuclei. Will end up in the hypothalamus.

some cross the midline and terminate in the olfactory bulb of the opposite site. These is inhibitory (in addition to the granules in the ipsilateral bulb which also inhibit)

Front 462

olfactory system is unique compared to other sensory systems how?

Back 462

no thalamic relay! very primitive system

Front 463

Lateral olfactory stria goes through the temporal lobe to activate what?

Back 463

amygdaloid nucleus (emotion)
hippocampus (first "leg" in memory making)

Front 464

Medial olfactory area will end up where?

Back 464

hypothalmus.

Front 465

fovea

Back 465

area within the macula lutea that has the highest degree of visual acuity in this area, largest concentration of cones in this area. it is lateral to the optic disc.

over 50% of the axons from the optic nerve serve the macula (including the fovea)

Front 466

optic disc

Back 466

point where retinal vessels and veins gain access to the cells of the retina. It is the physiological blindspot. it is always towards the nasal side

Front 467

retinal arteries vs veins- distinguishing with ophthalmoscope?

Back 467

the arteries have a "silver wire" appearance from where the light reflects off of them. Veins are slightly larger and may pulsate

Front 468

papillomacular bundle

Back 468

forms an arching pathway

Front 469

first place the axons of the optic nerve acquire a myelin sheath?

Back 469

after passing through the cribiform plate

Front 470

changes in the eye with increase in intracranial pressure?

Back 470

pushes up on cribiform plate and the physiologic cup will become less depressed. Recall this is because CSF is found in the arachnoid space which expands all the way to the back of the eyeball and so increased pressure will cause bulging

Hint 470

fluid has been artificially added in this image

Front 471

segments of the optic nerve

Back 471

intraocular segment (0.7-1.0 mm)
intraorbital segment (25-30 mm) -- this part is about 8mm longer than it needs to be, this is important so that eye can move around without "tension on the cord"
intracanalicular segment (6-10 mm)
intracranial segment (10-25 mm)

Front 472

optic chiasm lies where normally?

Back 472

right above the sella turcica.

in some pts there are clinically releveant abnormalities (prefixed and postfixed chiasms). if there is a pituitary tumos...it will affect different dysfunctions in these people with anatomical differences. For prefixed chiasms, will have central deficits whereas postfixed pts wouldnt.

Front 473

percentages of fibers of hte optic tract crossing?

Back 473

53% cross, 47% do not cross

Front 474

optic radiaiton

Back 474

after lateral geniculate nucleus....

fibers from inferior retina pass through the temporal lobe, forming Meyer's loop and then to the lingual gyrus
fibers from superior retina pass through the parietal lobe and then to the cuneate gyrus

Front 475

ranges of visual field for each eye

Back 475

60, 70, 80, 90 degrees (up, nasal, down, temporal)

Front 476

temporal visual crescents (monocular fields) are only seen by which eye? ipsilateral or contralateral?

Back 476

ipsilateral

Front 477

Wilbrand's knee

Back 477

fibers from the lower nasal quadrant hook onto the fibers on the contralateral side before returning back to the chiasm