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477 Cards in this Set
- Front
- Back
- 3rd side (hint)
outside layer of cells of the neural tube?
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meninges
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Purpose of the meninges
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ionically isolated the nerves inside; water-tight
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Dorsal and ventral rami
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mixed functions
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characteristics of nerve cell
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*Large nucleus,* large nucleolus, dendrites cytoplasmic extensions, axon
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afferent neurons
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carries information to the CNS, derived from the neural crest
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efferent neurons
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carries information away from the CNS, derived from the basal lamina
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association neurons (interneurons)
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connect neurons and no part them exists outside of the meninges, derived from the alar lamina
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alar lamina
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form the dorsal side of the neural tube; form the association neurons
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basal lamina
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form the vental side of the neural tube; form the efferent neurons
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gray matter
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cell bodies and dendrites, not myelinated; called the cortex when on the surface, and called nuclei when buried deep within the brain
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white matter
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myelinated axons of the cells that make up the gray matter
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cerebellar cortex
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3 layers vs 6 layers in the cerebrum
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what is this stained for?
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this is stained for the myelin..the purple here is fibers not cell bodies. in the middle is the cell bodies.
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when does neural tube fold over and begin to close?
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end of 3rd wk day 21
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brain growth in the last trimester
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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!)
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brain development and size
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at birth 25% of adult brain
at 1yr 75% of adult brain |
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effector organs of voluntary nervous pathways?
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skeletal muscle
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effector organs of involuntary nervous pathways?
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smooth, cardiac, and myoepithelial cells
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List the major types of neuroglial cells
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1) oligodendrocytes
2) astrocytes 3) microglia 4) ependymal cells |
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astrocytes
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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
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structure of myelin
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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.
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microglia
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"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 |
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protoplasmic astrocyte
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have short, thick highly branched processes. Typically found in gray matter
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fibrous astrocyte
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long, thin, less branched processes. Typically found in white matter
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reactive gliosis
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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
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fascicular oligodendrocytes
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found in myelinated tracts (white matter)
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perineuronal oligodendrocytes
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found on neural cell body surface (gray matter)
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excitotoxicity
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the pathological process by which nerve cells are damaged and killed by excessive stimulation by neurotranmitters, eg glutamate
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rough ER is present where--dendrites or axons?
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dendrites only
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neural crest cells differentiate from where?
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cells located along the lateral border of the neural plate
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peripheral process
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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
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central process
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in bilpolar and pseudounipolar neurons, carry away from the neural cell body, acting physiologically like a axon
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astrocyte role in glutamate regulation
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astrocyte can reuptake glutamate from the synaptic cleft, convert it, and recycle it as glutamine back into the presynaptic neuron. prevent excitotoxicity
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astrocyte role in glucose regulation
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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
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Difference between oligodendrocytes and Schwann cells
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One oligodendrocyte can ensheath MANY axons whereas Schwann cells it is one to one...one schwann cell can only ensheath one axon
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Types of astrocytes?
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fibrous (W) and protoplasmic ( G)
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Types of oligodendrocytes?
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fascicular (W) and perineuronal (G)
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Nissl substance
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basically it is rough ER and ribosomes, site of protein synthesis. present only in dendrites not axons!
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orthograde transport
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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
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Retrograde transport
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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)
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axon hillock
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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
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Astrocytes and K+ buffer
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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
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Dura mater
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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
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tentorium
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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
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middle meningeal artery course
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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
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middle cerebral artery
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branch of the internal carotid artery, supplies the brain
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subdural space
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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
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dural venous sinuses
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large venous channels that lie between the two dural layers. They drain blood mainly via the sigmoid sinuses to reach the IJV.
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locations of the superior and inferior sagittal sinuses
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pterion
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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
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lambda
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junction on the cranium, meeting of the lamboid and sagittal sutures
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bregma
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junction on the cranium, meeting of the sagittal and coronal sutures
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asterion
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junction on the cranium, meeting of the parietomastoid, occipitomastoid, and lamboid sutures; star shaped
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most prominent point of the external occipital protuberance?
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inion
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dura mater
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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
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dural sinuses
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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
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the most vulnerable part of skull to trauma?
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the pterion. It is very thin and bony fragment can lacerate the vein, arteries, or both--> epidural hemorrhage
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collagen fibrils in the meningeal layers?
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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
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tentorium cerebelli
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tent that supports the cerebrum above, and forms a tent over the cerebellum below. tentorial notch is where the midbrain can be seen through
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falx cerebelli
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septa between the cerebellum
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falx cerebri
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septa between the two lobes of the cerebrum
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supratentorial
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above the tentorium...cerebrum is here
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diaphragma selli
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piece of dura that covers the sella turcica.
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tentorial notch contains
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brainstem, blood vessels passing up from the infratentorial compartment, one cranial nerve.
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uncal herniation
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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
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cause of headache?
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the meninges/the blood vessels of the meninges
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arachnoid mater
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“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
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pia
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"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.
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subarachnoid space
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just below the arachnoid layer where the arachnoid trabeculae are. contains cerebral arteries and veins, CSF also lives here
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cisterns
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subarachnoid spaces within the cranium
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superficial layer of the arachnoid mater
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waterproof because bound by tight junctions. maintains the ionic environment of the brain
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glia limitans
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consists of the glial foot processes, intima pia, and epipia
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leptomeninges
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consists of the arachnoid and pia. when pts have meningiomas these layers are what gives rise to the tumor cells
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Virchow–Robin spaces
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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
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cavernous sinus
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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!)
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epidural hemorrhage..when will bleeding stop?
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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
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subdural hemorrhage
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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
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bleeding from aneurysms leak where?
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subarachnoid space
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"worst headache of my life"...blood likely where??
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subarachnoid space. blood in the leptomeningeal layers irritate the sensory fibers there
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blood in the CSF found on spinal tap...where from?
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subarachnoid space
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ependymal cells
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what is left over after all cells migrate away from the CNS..they line the ventricles are are epithelial-like
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choroid plexus
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produces 85% of CSF. lined the floor of the lateral ventricles and the roofs of the 3rd and 4th ventricles
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choroid epithelial cells
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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.
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production of CSF
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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 |
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CSF composition
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similar to blood just different concentrations. something notable is protein concentration which is very very low in CSF
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CSF production and changes in ICP?
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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
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CSF leaks from the ventricles into the infra or supratentorial compartment?
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infratentorial compartment
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CSF total volume
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100-150ml.
range because CSF is the buffer for maintaining correct pressures to maintain blood flow |
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lumbar cistern CSF volume
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25-30ml
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Arachnoid granulations
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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
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how do you get CSF from infratentorial compartment where CSF goes after production in the ventricle to supratentorial compartment where the arachnoid granulations are?
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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
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meningitis and CSF movement
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inflammation and scarring of the meninges. the rate at which CSF is removed from the cisternal compartment is decreased. can cause hydrocephalus
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Functions of CSF
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buoyancy, intracranial volume adjustment, micronutrient supply system, source of osmolytes within the brain. buffering reservoir, supply and distribution of peptides and growth factor
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endometrium
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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
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Perineurium
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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
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epineurium
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outermost CT layer of peripheral nerves. entire peripheral nerve convered by it. dense and consists of Type I collage and typical fibroblasts
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Peripheral nerves CT layers
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endoneurium, perineurium, epineurium
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Important dates in development and closure of neural tube
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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 |
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Cerebral perfusion pressure
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=MAP-ICP
this is why increased ICP can be very dangerous and cause ishchemia |
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Monro-Kelli Doctrine
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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
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Derivatives of Neural Crest Cells
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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 |
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Describe the process of neuromuscular transmission on the presynaptic end
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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
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Describe the process of neuromuscular transmission on the postsynaptic end
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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
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clathrins
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help to 'recycle' the vesicle after it has been exocytosed (ie help reform it from the membrane)
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Myesthenia Graves
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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
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Eaton-Lambert myesthenic syndrome
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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
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Toxins at the NMJ
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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 |
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Drugs (Rx) at NMJ
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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 |
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hemicholinium
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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
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Vasamicole
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binds to the NT channels on the vesicle. ACh cannot become concentrated within the vesicle
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Botulinium toxin
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destroys the synaptobrevin and syntaxin proteins that are essential in the ACh-containing vesicle to fuse with the membrane. No ACh release= "floppy muscles"
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Tubocarinine
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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
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Succinylcholine
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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
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premotor cortex does what?
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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
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supplementary motor cortex
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primitive movement planning, usually bilaterally. stimulates neurons in the primary motor cortex to ultimately carry out action.
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primary motor cortex
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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
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areas of the premotor cortex and function
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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 |
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Efferent cell types
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1) General Somatic
2) Special Somatic 3) General Visceral |
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Afferent fiber types
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Type Ia and Ib (rapid)
Type II and Abeta (slow) Type Adelta (slower) Type C (slowest, unmyelinated) |
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3 types of cells of the nervous system based on embryology
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alar lamina--> association
basal lamina --> efferent neural crest --> afferent |
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Basal lamina derived cells
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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) |
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Neural crest derived cells in the NS
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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
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Alar derived cells
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Somatic association, visceral association. These receive from the somatic and visceral afferent respectively
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monosynaptic vs multisynaptic
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monosynaptic is faster. the delay occurs at the synapse. Majority of behavior is mediated by multisynaptic organizations
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clonus
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suggest failure to inhibit antagonistic muscles that are activated with reflex
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axonal branching
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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.
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dendritic spread
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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.
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convergence and divergence
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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 |
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Intersegmental divergence and convergence
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Particularly important C5-T1 and L2-S2. Ex is biceps muscle--need to recruit both C5 and C6 since these form musculocutaneous branch
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ventral ramus
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mixed fibers, highway to the hypomeric derived structures. bigger than the dorsal primary ramus. gives rise to cutaneous and muscular branches
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cutaneous branches- pure or mixed?
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have both afferent and efferent (GVE)
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muscular branches-- pure or mixed?
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have both afferent and efferent
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dorsal ramus
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highway to the epimeric derived structures. mixed fibers. give rise to muscular and cutaneous branches
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"blood-nerve barrier"
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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)
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endoneurium
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within fascicles; gives substance to surroudning areas and give support to the capillaries
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epineurium
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varies in thickness and acts as protective layer around the nerve and b/w fasicles
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vasa nervorium
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vessels of the neuron
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Remak bundles
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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
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shoulder abduction
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axillary nerve
*C5, C6 |
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elbow flexion
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muscultcutaneous nerve
*C6, C5 |
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elbow extension
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radial nerve
C7*, C6 |
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wrist extension
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radial nerve
*C6, C7 |
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wrist flexion
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median nerve
*C7, C8 |
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finger extension
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radial nerve
*C7, C8 |
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finger flexion
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median/ulnar
C8, T1 |
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Finger abduction
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ulnar nerve
*T1 |
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knee extension
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femoral nerve
L2,L3,L4 |
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hip flexion
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L1,L2,L3
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hip adduction
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obturator nerve
L2,L3,L4 |
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ankle dorsiflexion
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anterior tibial
*L4, L5 |
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hip abduction
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Superior gluteal nerve
*L5, L4, S1 |
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Toe extension
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anterior tibial nerve
*L5, L4 |
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Ankle plantar flexion
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Posterior tibial nerve
*S1, L5, S2 |
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hip extension
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inferior gluteal nerve
*S1, L5, S2 |
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Major classes neurotransmitters of the CNS?
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-esters (ACh)
-monoamines (NE, DA, Serotonin) -amino acids (GABA) |
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Mechanisms of Drug Actions on the CNS (review of types)
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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 |
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Neurotransmitters- 5 action
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Synthesis, storage, release, reception, inactivation
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Adrenergic Neurotransmission
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NE, DA (degradation pathway via MAO and COMT)
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Cholinergic Neurotransmission
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ACh (degradation via AChE)
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"Other" Neurotransmitter
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GABA -- inhibitory NT
Glutamate -- stimulatory NT |
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7 major NTs
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ACh, NE, DA, serotonin (5-HT), GABA, Glutamate, enkephalins (role in analgesia)
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Receptor types for NTs
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ionotropic (voltage gated, ligand-gated), metabotrophic
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GABA receptor subtypes
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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. |
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GABA
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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) |
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Alcohol and GABA receptor
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alcohol has binding site on GABA receptor so can have depressant effects
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picrotoxin
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poison that can bind to the chloride channel of the GABA(A) receptor. acts as an antagonist and causes convulsions
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Glutamate (as a NT)
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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) |
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Overstimulation of the Glutamate receptor
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seizures and brain damage can result. STROKE. in case of stroke outpouring of glutamate causes scarring of hte brain and damage
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Ketamine
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Glutamate receptor antagonist. called as "dissociative anathestic". Gives the pt amnesia. Date rape drug is
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Natural opioids
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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) |
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Nalaoxone
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full competitive antagonist of mu and kappa opioid receptors. may be used for overdose treatment.
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Partial opioid agonist uses
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to ween pt off opioid addictions. ex
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How opioids stop pain
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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
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Dopamine
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The "pleasure" neurotransmitter. Agonists are emetics and antagonists are antiemetics and antipsychotics.
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Cocaine
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reduces reuptake of DA and NE. more stimulus of postsynaptic site
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Amphetamines
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harder to ween amphetamine addicts off it than cocaine addicts bc it depletes the storage of MAs in vesicles
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Parkinsons treatment
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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
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Dopamine Antagonists
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use as antipschyotic agents
SE: Parkinson like sxs with extended use |
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MOA of Depression
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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 |
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ACh and Alzheimers
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ACh has role in cognition. In cognitive disorders such as alzheimers there is decr. Ach so give ACh agonist to slow progession
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ACh and Parkinsons
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ACh antagonists used as adjuncts in Parkinson's treatment
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Anterolateral system functions
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Function: Activate responses to tissue-damaging stimuli. Initiates systems for PROTECTION and REPAIR
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Stimuli for the anterolateral system to act
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These stimuli are:
1) thermal 2) pain (nociception) 3) crude touch |
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initiation of the anterolateral system
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exposure of nerve ending to a nociceptive stimuli- disrupts cell cytosol, changes the "ionic mileu" and intiates action potential.
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deciding whether stimuli is irritating vs pain happens where?
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takes place in the frontal lobe
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Effects of activating the anterolateral system
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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 |
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important of collateral branching in the anterolateral system
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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
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Component operations of the ascending system (4)
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1) transduction (via receptors that are transducers themselves. )
2) transmission 3) perception 4) localization |
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Receptors of the anterolateral system
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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 |
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2 families of receptors
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capsulation and free
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free nerve fibers transmit at what velocity
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0.5-2m/sec
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eponyms for sensory receptors
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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 |
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Both A(delta) and C fibers respond to what kind of stimuli?
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nociceptive
when cell gets damaged and environment is flooded with the cell's cytosol. change in the ionic environment cause action potential |
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Where are the cell bodies of the Adelta and C fibers? Where are their central proceses? Peripheral?
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cell bodies in the dorsal root ganglia. central processes in the dorsal rootlets. Peripheral fibers can be anywhere
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Upon entering the dorsal horn, where do the C fibers and Adelta fibers terminate?
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terminate in the spinal gray matter on association cells
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Lissauer's tract
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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".
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Rexed's Lamina
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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
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medially in the anterolateral column corresponds to which body parts?
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cervical-thoracic areas (upper limbs)
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laterally in the anterolateral column corresponds to which body parts?
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lumbar-sacral (lower limb)
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Cell bodies of the anterolateral tract cells are found where?
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all spinal gray matter except lamina II and IX
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Synapses of the afferent nerves occur in which lamina?
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Lamina I, II, V
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"fates" of an anterolateral tract after crossing midline
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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) |
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internal capsule
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projections from VPL and DM cross through. The anterior limb receives projections from the CM and the posterior limb receives projections from the VPL
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receptors of the leminscal system
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low threshold, rapidly adapting. these are encapsultated receptors (which lower the threshold)
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2 "main players" cutaneous receptors
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Pacincian and Meissner's.
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tuning form actives which receptor?
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tuning fork activates the pacinian corpusle
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Muscle spindle
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"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. |
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Golgi tendon organ
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"tension detector" (measures tension applies to the musculoskeletal apparatus.)
help regulate muscle tone and reflex responsivity. These are type Ib fibers. |
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where would you find the muscle spindles and golgi tendon organs looking at this pic
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spinal nerve, dorsal and vental primary ramus, MUSCULAR branch (not cutaneous)
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where do the Abeta fibers enter the spinal cord?
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the dorsal funiculus (dorsal column)
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Fibers from upper limbs "add on" where?
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upper limb fibers pile on laterally. These lateral fibers form the fasiculus cuneatus (from T6 above)
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What makes up fasiculi?
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tracts
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What makes up funiculi?
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fasiculi
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Where do the fasiculis gracilis and fasiculis cuneatus terminate?
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in their nuclei in the caudal medulla oblongata
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Somatotrophy of the anteriolateral vs dorsal-lemniscal tracts
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lesion that damages medial part of VPL- where would the symptoms be localized?
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upper, contralateral. the medial part of the VPL receives input from the nucleus cuneatus
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lesion in brain receiving info from lateral VPL
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symptoms in lower limb, contralateral
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agnosia
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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
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tactile agnosia
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inability to recognize an object based on touch alone
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128HZ tuning fork
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should be used on a bony prominence. "impales" the pacinian receptors against the periosteum
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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. |
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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 |
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where do you find the intermediolateral nuclei?
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T1 and L2 ( home of preganglionic ic sympathetic nerve cell bodies. )
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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.
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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 |
vibratory deficit in ipsilateral upper limb
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we are about at C1
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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
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the nuclei gracilis and nuclei cuneatus are present in which part of the medulla
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caudal part of the caudal medulla
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crossing of the fibers from the nuclei gracilias and cuneatus occurs how
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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
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what marks level of the rostal medulla ?
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inferior olivary nuclues. the L side of the section is lower than the right because smaller inferior olivary nucleu
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where do the collateral branches of the anterolateral tracts "peel off"?
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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
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rostral medulla. c an see the medial leminiscus in the middle sections. can see part of 4th ventricle
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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
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where are we in this section?
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ponto-mesencephalic junction (see the cerebral aqueduct). Can see fibers of the spinal lemnicus on the lateral sides of the medial lemnicus
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now see medial and spinal lemnicus overlapped. also can see infereior caliculus. lesion there would affect both vibritaory and pinprick, contralateral, both limbs
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now medial and spinal lemnicus is totally intermingled. most are from the dorsal pathway. can see the superior caliculus
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where are the VPL in this pic
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Which nerve provides sensory innervation to the small area between the 1st and 2nd toes?
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The deep branch of the common peroneal (fibular) nerve
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Which nerve is commonly compressed by the inguinal ligament?
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Lateral femoral cutaneous nerve
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Trendelenburg gait..likely issue with which nerve?
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superior gluteal nerve
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Weakened hip extension; pt has difficulty rising from sitting position or climbing stairs...injury to which nerve?
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inferior gluteal
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Sensory loss on medial thigh..damage to which nerve?
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obturator
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Sensory loss on dorsum of foot except 1st web space..which nerve is damaged?
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superficial peritoneal
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polyol pathway
|
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 |
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3 main courses of diabetic neuropathy
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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) |
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extrafusal muscle
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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
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Intrafusal muscle
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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.
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alpha motor neurons
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innervate extrafusal muscle, transmits impulses at 70-120m/sec
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gamma motor neurons
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innervate intrafusal striated muscle, transmits impulses at 15-30m/sec
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final common pathway
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system of the lower motor neuron connected to the skeletal muscle that it innervates. Lower motor neuron diseases always result in depressed activity
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segmental input
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afferent input, affects behavior of LMNs
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neural crest derived cells release NTs that are excitatory or inhibitory?
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excitatory. any inhibition is a result of the INTERNEURONS
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Efferent cells are excitatory or inhibitory?
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excitatory. any inhibition is a result of interneurons
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upper motor neurons
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cells in the cerebral cortex that communicate with lower motor neurons
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suprasegmental input
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arise from the brainstem and forebrain and influence the LMNs, May act through the basal nuclei/cerebellum, or directly
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alpha/gamma coactivation or coinactivation
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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
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The sources of motor inhibition is always which type of neuron?
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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.
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Renshaw cells
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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
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Rexed lamina
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Synaptic endings of C fibers terminate in which Rexed lamina
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I and II
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Synaptic endings of A delta fibers terminate in which Rexed lamina
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I, II, an V
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cell bodies in the medial part of the ventral horn innervate
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axial movement
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cell bodies in the lateral parts of the ventral horn innervate...
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distal movement of the upper and lower limbs
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Cells in the intermediate part of the lateral horn innervate...
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Movements of the proximal limbs
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when looking at a portion of the spinal cord where there is not innervation of the limbs, why is the ventral horn small?
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because the areas laterally that are concerned with limbs is absent.
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|
"Map" of lamina 9 cells
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motor unit
|
LMN its axons, and all of the muscle cells it innervates. it innervates >1muscle cells because of collateral branches
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2 important principes of efferents
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1) all make and release ACh
2) all are excitatory |
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types of motor units
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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). |
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if you want to lift something heavy, the first motor units you will recruit are ?
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small motor units recruited first. Henamen size principle
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disuse atrophy
|
shrinking of a size of a muscle cell when that muscle is not being used. muscle tone is RETAINED
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dennervation atrophy
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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
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muscle spindle
|
"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). |
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GTO
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"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
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nuclear bag fiber
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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
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nuclear chain fiber
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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.
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Muscle spindle-->Primary nerve endings on the afferent side
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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
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Muscle spindle--> Secondary nerve endings on the afferent side
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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
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gamma motor neurons on the efferent side innervate which region(s) of the muscle spindle?
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the polar regions
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strongest influence on LMNs in inducing alpha motor neuron activity?
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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.
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how is clonus inhibited during the activation of a muscle spindle?
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inhibiton of the antagonist muscle via interneurons
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2 ways to activate muscle spindle
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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
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Muscle enlongation effects on primary and secondary ending?
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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.
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spasticity
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velocity dependent change in resistance to passive elongation of muscle
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Two ways to activate GTO
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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
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5 physiological principles regarding muscle spindles and GTOs
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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 |
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muscle spindle and GTOs general purpose
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maintenance of muscle tone and muscle. NOT movement really, more of a maintenance of "idle speed" of muscles
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Example of a placing reaction
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putting baby on floor, the plantar reflex (toes point down with non non-nocieptive stimuli)
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Withdrawal reflex and placing reflex
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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.
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hanging reflex
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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
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crossed adductor reflex
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- "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.
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What is latency and what could an increase in latency be due to?
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The time it takes from time you tap to time you see the reflex. An increase in latency could suggest a demyelinating diseases
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The only place you can have a lesion that results in increased tone and increase in the dynamic component of the stretch reflex?
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Upper motor neuron
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afferent nerve injuries and efferent nerve injuries cause?
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decreased muscle tone, decrease in reflexes
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evaling the static component of the tonic stretch reflex
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this thing or also pronator drift test
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evaling dynamic component of the tonic stretch reflex
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moving pt around while they are relaxed. Any resistance to passive motion (spasticity) may indicate upper motor neuron disease
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pronator drift
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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
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is this a segmental, multisegmental, or suprasegmental reflex?
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segmental
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do automatic or "less automatic" responses have a greater dependence higher center ?
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"less automatic" responses are more dependent on higher centers. Automatic responses are even intact in unconscious pts
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Theoretically: Decrease presynaptic inhibition to 1a fiber input?
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would let 1a release more excitatory NT, excite alpha motor neuron --> hypertonia. No evidence for this though so it is not what causes spasticity
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Tracts for the extensor system (antigravity muscles)
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Vestibulospinal is the main one, assisted by the pontinereticospinal tract
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Tracts for the flexor system
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Rubrospinal tract and medually reticulospinal tract
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Sympathetic outflow
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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) |
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Parasympathetic outflow
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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
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Theoretically: Decrease excitation to Renshaw cells?
|
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
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Theoretically: Taking away gamma neurons inhibition?
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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
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Reflex responses will always be most brisk where?
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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
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Explain each piece in this picture ?
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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 |
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passive stretching of the muscle in evaluating muscle tone
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↑ muscle length ( ↑1a ) offset by ↑ muscle tension ( ↑Ib) → no change in motor unit activity
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superior and inferior colliculi
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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 |
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reticular formation
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collection of mixed white and gray matter in the brainstem
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Decreased excitation to alpha motor neurons?
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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
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Babinski sign
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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.
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Evolution and the reticular formation
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The reticular formation is more primitive and is often found in lower species alone. These RT projection are typically bilateral.
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brainstem UMNs show a predominantly crossed/uncrossed effect?
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crossed
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red nuclei
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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 |
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brainstem UMNs tend to influence which more- gammas or alphas?
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gammas- muscle tone moreso rather than actual motor function
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Input to the red nuclei
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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 |
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tectospinal pathway
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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)
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input from above the brainstem nuclei will affect which side?
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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
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Which brainstem UMNs end up in the lateral motor system? Medial (ventral)?
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Rubrospinal--> lateral = distal flexors
Reticulospinal, vestibulospinal, and tectospinal--> medial (ventral system) = axial muscles |
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Vestibulospinal tract
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located in the ventral motor system, innervation of axial muscles. extends from vestibular nuclei to the spinal cord
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Radial nerve actions
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Extension at all arm, wrist, and proximal finger joints below the shoulder; forearm supination; thumb abduction in plane of palm
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ulnar nerve actions
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Ulnar: Finger adduction and abduction other than thumb; thumb adduction; flexion of digits 4 and 5; wrist flexion and adduction
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Musculocutaneous nerve actions
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Flexion of arm at elbow, supination of forearm
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Axillary nerve actions
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Abduction of arm at shoulder beyond first 15°
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Brainstem nuclei- spinal tracts: The phylogenetically “oldest” of the rubro, reticulo, and tectospinal pathways is...?
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reticulospinal tract (75% gamma, 25% alpha); this tract is involved in "less automatic" movement
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After the reticulospinal tract, what evolutionary developed next?
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tectospinal (70% gamma, 30% alpha). this tract is involved in eye movement and neck movement to increase field of vision
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The "last" tract to come in of the brainstem UMNs is which?
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rubrospinal (65% gamma, 35% alpha).
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Evolution of brainstem UMN vs cortical and their function
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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
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what is the name of the medial continuation of the precentral gyrus?
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anterior paracentral gyrus
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Brodman numbers
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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 |
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cortical UMNs: most rostral decussating fibers come from?
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upper limb. also recall that 85% ish cross, 15% stay ipsilateral. of the lateral tract, upper limb ends up medial, lower limb lateral
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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?
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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
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Betz cells
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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)
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cortical spinal cells are influenced by?
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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) |
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cortical UMNs talk more to which alpha or gamma? how to assess cortical UMN function vs subcortical UMN function?
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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
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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) |
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1- VPL
2 VPN |
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1- superior colliculi (tectispinal tract projects from here)
2- aqueduct of sylvuis 3- Red nucleus 4- cerebral peduncle (corticospinal tract in there) |
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cluster of fibers in the middle?
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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) |
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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)
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The white fibers shown ?
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are the pontine nucleus “breaks up” the formerly compact axons of the cerebral peduncle (corticospinal axons) into longitudinal pontine bundles
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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) |
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majority of the coriticospinal axons are found where in the descending tract
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middle 1/3
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1- medial lemnical
2- tectospinal 3- MLF 4- rubrospinal tract 5- olive 6- medullary pyramid also see 4th ventricle open at top |
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where?
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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 |
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lesion is midline?
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vibratory sensory deficits affecting the medial leminscus system
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Erb's palsy
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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 |
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Klumpke's Palsy
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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. |
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Claw hand
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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
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Thoracic outlet syndrome
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In thoracic outlet syndrome, the lower brachial plexus is compressed as it passes between the clavicle and the first rib
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Motor: Foot dorsiflexion, toe extension
Sensory: Webspace between 1st and 2nd toes |
Deep peroneal nerve
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Motor: Foot plantar flexion and inversion, toe flexion
Sensory: lateral foot |
posterior tibial nerve
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Explain the differences between an epidural, subdural, and subarachnoid hematoma.
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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 |
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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?
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At T12–L1 on the left
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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 |
D
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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 |
A
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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 |
E
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Label parts of this image
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? = terminal bouton, filled with vesicles (the circles)
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1= epineurium
2= vasoneurium 3= perineuium 4= fasicles |
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label the sinuses
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Pt presents with weakness in both hi[ adduction and knee extension. Which nerve or nerve roots are likely affected?
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L2-L4
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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?
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Deep peroneal nerve (aka anterior tibial). L4, L5
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Pt presents with numbness over the medial aspect of the upper thigh. Which motor function is also likely impaired?
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Hip adduction (obturator nerve injury)
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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?
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Superficial peroneal (L5, S1, S2)
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Label the cranial nerves
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Which two nuclei form the striadum?
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putamen and caudate nucleus
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What forms the "gaps" in this picture?
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The fibers from the internal capsule
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amygdaloid nucleus is located in which lobe?
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Temporal
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corpus striatum consists of?
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globus pallidus, putamen, and caudate nucleus
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lenticular nucleus consists of?
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globus pallidus + putamen
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striatum consists of?
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putamen + caudate nucleus
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1= caudate nucleus
2= putamen |
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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 |
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in this picture, 1=thalmus. What is the white matter just adjacent to it?
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if you see thalmus in a coronal section, the white matter adjacent to it must be the POSTERIOR limb of the internal capsule
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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 |
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Label the lamina in this picture
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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 |
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The internal medually lamina of the thalmus divides the thalmus into?
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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, |
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ventral striatum
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looks histologically the same as the striatum and are chemically/structurally the same but lie below the anterior commisure
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ventral pallidum
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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
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Basal nuclei of Meynert,
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cholinergic cluster of cells found in the ventral pallidum. These are some of the first cells to die in the alzheimers disease
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Claustrum
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separate the external capsule from the extreme capsule
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1= cerebral peduncle
2= red nucleus 3= substancia nigra |
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More dorsal part of the substancia nigra?
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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 |
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L is pt wtith parkinsons. Less darkly stained substancia nigra
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DM projects to where?
VA projects up to where? |
DM projects to prefrontal cortices
VA projects up to the posterior part of frontal/anterior part of parietal lobe |
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3 "pathways" out of the globus pallidus?
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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) |
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output of the striatum to the GP is influenced by what?
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the substancia nigra's influence. Will dial up the things needs for movement and dial down the antagonists. SN uses Dopamine to do this
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striatum efferents use which neurotransmitter?
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GABA
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GPe and GPi use which neurotransmitter?
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GABA (inhibitory)
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Subthalamic nucleus uses which neurotransmitter?
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Glutamate (excitatory)
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frontal eye field is located where?
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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) |
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"simple circuits"
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occulomotor and motor circuits
(more voluntary movements impaired if damaged) |
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"complex circuits"
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dorsolateral, orbitofrontal, anterior cingulate (problem solving, behavior, emotional, motivation psychiatric presentation if damaged)
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Dorsolateral loop function
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execulive function--> damage here would lead to poor problem solving, impaired shift setting
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Orbitofrontal loop function
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emotion--> damage here would lead to irritability, bevhavioral disinhibition, and emotional liability
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Anterior cingulate loop
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Motivation --> damage here would lead to apathy, abulia, akinetic mutism
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hemibalismus
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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.
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Huntington's disease
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Hyperkinetic motor abnormality. Cells of the striatum are killed and you have too much excitation. Result is choriatic movements (pt implements inappropriate motor programs+
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Parkinsonism
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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. |
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hyomemia
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lessened movements of the face
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persistant glabellar reflex
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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)
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abnormal finger and nose and abnormal heel to shin...what is dysfunctioning?
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the cerebellum (TIMING of movements on the millisecond level)
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primary fissure of the cerebellum separates which two lobes
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anterior lobe from posterior lobe.
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The posterolateral fissure of the cerebellum separates which two lobes ?
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Posterior lobe from the flocculonodular lobe
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first lobe of the cerebellum to evolve?
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flocculonodular lobe
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label
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where is the superior cerebellar peduncle?
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6
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Where is the middle cerebellar peduncle
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9
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Where is the inferior cerebellar peduncle
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7
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name the layers
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molecular layer, most superficially (few cells in it). Granular layer most internally (LOTS of cells in it). Purkinje cells separating the two.
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Types of cells in the molecular layer of the cerebullum
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stellate cells tend to be more superficially and the basket cells are more near the border (closer to the purkinje layer)
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Types of cells in the granular layer of the cerebellum
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golgi cells and granule cells
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5 cell types of the cerebellar cortex?
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Stellate cells, basket cells, purkinje cells, golgi cells, and granule cells
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climbing fibers of the cerebellum
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EXCITATORY.
can excite 2-12 purkinje cells. will also give a collateral branch to the deep nucleus |
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deep nuclei in the hemispheric region of the cerebellum?
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dentate nucleus
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deep nucleus in the vermal region of the cerebellum?
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fastigial nuclues
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Deep nucleus in the paravermal region of the cerebellum?
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globose nucleus, and emboliform nucleus
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Parallel fibers
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EXCITATORY. excites purkinje fibers at their distal dendritic fields. also will excite stellate and basket cells, which are both inhibitory.
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Two excitatory and two inhibitory cells that provide input to the purkinje cells?
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Excitatory--> Climbing fibers and parallel fibers
Inhibitory --> stellate and basket cells |
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What is the NT synthesized and utilized by the Purkinje cells?
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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
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mossy fibers
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all of the afferent input to the cerebullum except for those fibers coming from the inferior olivary nucleus (which are called climbing fibers)
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Archaecerebellum
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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
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Vestibular system dysfunction?
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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. |
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juxtarestiform body
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part of the inferior cerebellar peduncle, next to the restiform part of it. this the "highway" in and out of the cerebellum
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Vestibulospinal tract innervates what?
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extensors
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Decerebrate rigidity
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overactive vestibulospinal system causing persistent extension of the limbs
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The vestibular is activated when?
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AFTER movement has occurred. It is activated by head movement.
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Role of muscle spindles in cerebellum function
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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. |
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Paleocerebellum is activated when?
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Activated after the onset of movement. The stimulus is elongation of the muscle spindle.
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Clark's column
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eponym for the nucleus dorsalis, from which the dorsal spinocerebellar tract projects up to the inferior peduncle of the erebellum
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recording electrodes in each of the deep nuclei... what would happen??
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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
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Neocerebellum is activated when?
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BEFORE movement
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testing the neocerebellum
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must be PATIENT INDUCED in order to test the integrity of it. Others you would test by doctor induced movements.
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the climbing fibers enter the cerebellum through which peduncle?
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The inferior cerebellar peduncle
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Climbing fibers
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enter the cerebellum from the contralateral inferior olivary nucleus
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Ataxia
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motor incoordination
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Dysmetria
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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
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lesion in the cerebral hemispheres and peduncles affect which side
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ipsilateral
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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 |
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1= red nucleus
2= substantia nigra 3= caudate (body) |
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1- anterior commisure
2- optic chiasm 4-ventral siriatum 5- ventral pallidium 6- caudate |
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1- Ansa lenticularis
2- choroid plexus 3- hypothalamus |
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GPi-synaptic endings of projections from here go where?
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thalamus-- specifically CM, DM, and VA
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Clarke's column
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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
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at which level do the dorsalspinocerebellar tracts "peel off" and merge with cuneocerebellar axons?
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the lateral cuneate nucleus
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axial muscle spindles enter the cerebellum through?
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superior cerebellar peduncle
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fibers from the globose and emboliform nuclei send their axons where?
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red nucleus, contralateral side
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middle cerebellar peduncle are formed by
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pontocerebellar fibers from the CONTRALATERAL side
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most of the fibers in the middle are what?
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dentato thalamic and cerebellorubral
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anosmia
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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 |
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olfactory epithelial cells
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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.
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Bowman cells of the olfactory epithelium?
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glands in the nasal cavity whose secretions help makes incoming odors soluble
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subtentacular cells of the olfactory epithelium?
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the supporting cells of the olfactory epithelium
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basal cells of the olfactory epithelium?
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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.
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periglomerular and granule cells
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important for rapid extinguishing of smells so that a new one can be detected. These are inhibitory celle
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Lateral olfactory gyrus
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layer of cells wrapping around the lateral olfactory stria before reaching the base of the frontal lobe
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fibers of the medial olfactory stria head where?
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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) |
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olfactory system is unique compared to other sensory systems how?
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no thalamic relay! very primitive system
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Lateral olfactory stria goes through the temporal lobe to activate what?
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amygdaloid nucleus (emotion)
hippocampus (first "leg" in memory making) |
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Medial olfactory area will end up where?
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hypothalmus.
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fovea
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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) |
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optic disc
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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
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retinal arteries vs veins- distinguishing with ophthalmoscope?
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the arteries have a "silver wire" appearance from where the light reflects off of them. Veins are slightly larger and may pulsate
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papillomacular bundle
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forms an arching pathway
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first place the axons of the optic nerve acquire a myelin sheath?
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after passing through the cribiform plate
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changes in the eye with increase in intracranial pressure?
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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
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fluid has been artificially added in this image
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segments of the optic nerve
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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) |
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optic chiasm lies where normally?
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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. |
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percentages of fibers of hte optic tract crossing?
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53% cross, 47% do not cross
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optic radiaiton
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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 |
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ranges of visual field for each eye
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60, 70, 80, 90 degrees (up, nasal, down, temporal)
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temporal visual crescents (monocular fields) are only seen by which eye? ipsilateral or contralateral?
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ipsilateral
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Wilbrand's knee
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fibers from the lower nasal quadrant hook onto the fibers on the contralateral side before returning back to the chiasm
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