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445 Cards in this Set
- Front
- Back
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what type of sensory info is processed in the occipital lobe?
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visual
when you have a stroke in this lobe you will have trouble seeing |
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what type of sensory info is processed in the temporal lobe?
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auditory and memory
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what type of sensory info is processed in the frontal lobes?
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cognitive
motor |
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what is the relay station for all the sensory info to to get to the cortex>
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thalamus
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role of thalamus?
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relay station for all the sensory info to get to the cortex
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what is the site of action on the neuron?
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dendritic spine: site of action of all incoming input synapses
*increase surface area on neuron |
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neuronal morphologies vary depending on what/
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where they are in the nervous system (different neurons in different parts of the brain)
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what are sensory neurons? where found?
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afferent neurons
found in dorsal horn |
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what are motor neurons? where found?
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efferent neurons
found in ventral horn |
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what are interneurons?
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make up 95% of neurons. integrate sensory w/ motor and vice versa
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what are the types of motor neurons?
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lower motor neurons: spinal cord and brain stem
upper motor neurons: motor cortex neurons |
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what do lower moter neurons synapse on? what are considered lower?
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brain stem and spinal cord motor neurons synapse on muscle
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what are upper motor neurons? what do they synapse on?
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motor cortex neurons
syanpase on spinal cord |
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which neurons are the conduit for info to enter CNS?
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sensory-afferent
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which neurons are the output from our CNS?
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motor-efferent
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what makes up white matter?
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glial cells w/ myelin (axon tracts)
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what makes up gray matter?
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neuronal cell bodies
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fxn of axons?
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the portion of the nerve cell specialized for signal conduction to the next site of synaptic interaction
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how are glial cells diff than neurons/
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The major distinction is that glia do not participate directly in synaptic interactions and electrical signaling, although their supportive functions help define synaptic contacts and maintain the signaling abilities of neurons.
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is the ventral or dorsal root pseudounipolar?
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dorsal root: 1 process off cell body that splits and 1 goes to periphery
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what type of receptor does Ach bind to?
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nicotinic
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what are the 2 kinds of interneurons?
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projection and local
projection: from spinal cord to the brain local: w/n given tissue |
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what is the NMJ?
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the synapse or junction of the axon terminal of a motoneuron with the motor end plate, the highly-excitable region of muscle fiber plasma membrane responsible for initiation of action potentials across the muscle's surface, ultimately causing the muscle to contract.
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what NT is released at NMJ? what R's bind NT?
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Ach binds cholinergic R's which can be nicotinic or muscarinic
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action of alpha bungarotoxin from snake?
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binds irreversible to AchR present in NMJ causing paralysis
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when is an AP fired?
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when amt of EPSP greater than IPSP (net depolarization)
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what do neurons do?
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process info from thousands of inputs: EPSP and IPSP and when EPSP is greter than IPSP you get AP
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what do glial cells do?
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are non-neuronal cells that provide support and nutrition, maintain homeostasis, form myelin, and participate in signal transmission in the nervous system
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what are the types of glial cells in CNS?
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astrocytes
oligodendrocytes microglial cells |
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action of astrocytes?
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maintain homeostasis: keep NT levels steady, maintain K levels
make GF to keep neurons happy |
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fxn of microglial cells?
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Microglia are specialized macrophages capable of phagocytosis that protect neurons of the central nervous system.
*immune like cells secrete cytokines when activated |
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fxn of oligodendrocytes?
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make myelin in CNS
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fxn of schwann cells?
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Similar in function to oligodendrocytes, Schwann cells provide myelination to axons in the peripheral nervous system (PNS). They also have phagocytotic activity and clear cellular debris that allows for regrowth of PNS neurons.
*there are myelinating and non-myelinating forms |
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what are the glial cells in PNS?
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schwann cells
satellite cells |
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fxn of satellite cells?
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located next to cell bodies of peripheral sensory neurons (Satellite cells are small cells that line the exterior surface of PNS neurons and help regulate the external chemical environment.)
nutritive support ensheath cell bodies |
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components of CNS?
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brain and spinal cord
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components of PNS?
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cranial nerves
spinal nerves *DRG somatic motor division visceral/autonomic motor division |
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what are axons in the CNS gathered into? in the PNS, axons are gathered into ?
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tracts in CNS
nerves in PNS |
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in the PNS, nerve cells are located in? In CNS?
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ganglia in PNS
nuclei and cortex in CNS |
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what do rostral/caudal, ant/pos, sup/inf, dorsal/ventral mean?
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anterior and posterior indicate front and back; rostral and caudal, toward the head and tail; dorsal and ventral, top and bottom; and medial and lateral, the midline or to the side.
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what is diff about the coordinates in teh body vs/ brain?
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For the entire body these anatomical terms refer to the long axis, which is straight. The long axis of the central nervous system, however, has a bend in it. In human and other bipeds, a compensatory tilting of the rostral/caudal axis for the brain is necessary to properly compare body axes to brain axes
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explain dorsal/ventral axis for brain
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The dorsal direction is toward the back for the brainstem and spinal cord, but toward the top of the head for the forebrain. The opposite direction is ventral. The rostral direction is toward the top of the head for the brainstem and spinal cord, but toward the face for the forebrain. The opposite direction is caudal
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what are the 7 basic parts of the CNS?
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the spinal cord, the medulla, the pons, the cerebellum, the midbrain, the diencephalon, and the cerebral hemispheres
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what makes up the brainstem?
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medulla, pons, midbrain
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what makes up the forebrain?
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diencephalon, cerebral hemispheres
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The white matter of the spinal cord is subdivided into what/
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dorsal (or posterior), lateral, and ventral (or anterior) columns, each of which contains axon tracts related to specific functions.
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what is this describing? : Major ascending tracts in the spinal cord that carry mechanosensory information from the first-order sensory neurons in dorsal root ganglia to the dorsal column nuclei; also called the posterior funiculi.
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dorsal column
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fxn of dorsal columsn?
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carry ascending sensory information from somatic mechanoreceptors
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fxn of lateral columns?
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include axons that travel from the cerebral cortex to contact spinal motor neurons. These pathways are also referred to as the cortico-spinal tracts
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fxn of ventral columns?
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carry both ascending information about pain and temperature, and descending motor information
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what component of spinal cord is this describing?: regions of spinal cord white matter that convey motor information from the brain to the spinal cord.
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lateral columns
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CN I: motor/sensory? fxn?
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olfactory nerve
sensory sense of smell |
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CN II: motor/sensory? fxn?
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optic nerve
sensory vision |
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CN III: motor/sensory? fxn?
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occulomotor nerve
motor eye movements, mm of eyelid, papillary constriction and accomodation |
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CN IV: motor/sensory? fxn?
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trochlear nerve
motor eye mmts: supplies superior oblique |
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CN V: motor/sensory? fxn?
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trigeminal nerve
both somatic sensation from the face, mouth, cornea mm of mastication |
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CN VI: motor/sensory? fxn?
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abducens
motor eye movements: supplies lateral rectus |
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CN VII: motor/sensory? fxn?
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facial nerve
both facial expression mm taste from ant tongue lacrimal and salivary glands |
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CN VIII: motor/sensory? fxn?
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vestibulocochlear
sensory hearing and balance |
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CN IX: motor/sensory? fxn?
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glossopharyngeal
both sensation from pharynx taste from post tongue carotid baroR's |
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CN X: motor/sensory? fxn?
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vagus
both autonomic fxns of gut sensation from pharynx mm of focal cords swallowing |
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CN XI: motor/sensory? fxn?
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accessory nerve
motor shoulder and neck mm: sternocleidomastoid and trapezius |
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CN XII: motor/sensory? fxn?
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hypoglossal nerve
motor mvmts of tongue |
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what are the divisions w/n the dorsal column?
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Fasiculus gracilis (most medial)
Fasiculus cuneatus |
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where is faciculus cuneatus (level of spinal cord)? gracilis?
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cuneatus: sensory above T6 (upper body)
gracilis: sensory below T6 (lower body) |
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Facial colliculi has fiber bundles from what CN?
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CN VII
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what are the peduncle seen dorsally on brainstem?
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what is left of slices of cerebellum containing fiber bundles of axons that connect cerebellum to cortex and brainstem
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which colliculus in on the floor of the 4th ventricle?
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facial colliculus
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which CN is located b/n the olive and medullary pyramid?
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CN XII
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what is the only CN that arises dorsally?
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CN IV
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which CN is located off the ventral surface of midbrain and looks like antennae?
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CN III
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where are the mammilary bodies located?
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ventral surface of diencephalon
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what happens if uncus is lesioned?
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it can be pushed across and down on midbrain with symptoms of dilated pupils b/c knocked out CN III
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action of CNIII in terms of dilation or contriction
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constricts pupils therefore if uncus knocks out III, patient will have dilated pupils
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if you take a cross section through the optic tract, what will you see?
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see nerves for both eyes
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ventral to midbrain colliculi is what?
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cerebral aqueduct
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the superior colliculi is for what type of input? inferior?
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superior: visual input
inferior: auditory input |
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fxn of paracentral lobule?
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map for feet seen on medial view of brain
knockout blood vssl to medial surface will have problems with feet |
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what is the name of the fissure that divides the dorsal halves of spinal cord?
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dorsal median septum
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what is the name of the fissure that divides the ventral halves of spinal cord?
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ventral medial fissure
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the dorsal column carries sensory info to where?
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brain
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what does the internal region of the neural tube become?
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ventricles
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what ventricle is formed by the wall of the thalamus?
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3rd ventricle
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what does the Sylvian fissure divide?
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frontal from temporal and parietal from temporal
this is the lateral sulcus |
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rolando sulcus?
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central sulcus that divides the frontal lobe from parietal lobe
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which lobe is Wernicke's area located in?
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temporal lobe for speech
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the sign of weakness should make you think what?
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primary motor cortex located in precentral gyrus
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the Calcarine sulcus is associated with what lobe?
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occipital lobe: visual cortex
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divisions of inf frontal gyrus?
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pars opercularis (most caudal)
pars triangularis pars orbitalis (most rostral) |
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Broca's area is located on what side of brain and in what general area?
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Left side of brain
in area of inf. frontal gyrus specifically pars opercularis and triangularis |
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sitting inside the superior temporal gyrus is what?
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Wernicke's area (auditory cortex)
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where is the primary motor cortex?
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precentral gyrus *upper motor neurons
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where is teh somatosensory cortex located?
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postcentral gyrus
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spatial think _____
language think ______ |
spatial think R parietal
language thinkk L frontal |
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neural crest cells will delaminate epithilial to mesenchymal transition to form what?
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peripheral nervous systm: chain of DRG, symp ganglia, parasym ganglia, adrenal medulla, enteric nervous system, peripheral glia
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what are the 3 initial bulges of the neural tube?
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Prosencephalon
Mesencephalon Rhombencephalon (PMR) |
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In the morphogenesis of neural tube, where is teh cephalic flexure? cervical flexure?
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cephalic flexure is b/n mesencephalon and rhombencephalon
cervical flexure is after rhombencephalon and before spinal cord |
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3/4 of neural tube is what? what is the space called inside this structure?
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spinal cord
central canal |
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as the neural tube matures, what happens to the Prosencephalon?
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walls evaginate to form "C" shaped lateral ventricles and it divides into Telencephalon and Diencephalon
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Telencephalon will eventually form what structures during morphogenesis?
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cerebral hemis
basal ganglia |
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Diencephalon will eventually form what structure during morphogenesis?
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thalamus
hypothalamus retina |
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why is the retina considered part of CNS?
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arises from diencephalon
even though it is CN II it is CNS therefore you will find oligodendrocytes |
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During morphogenesis, mesencephalon forms what? what ventricle?
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forms midbrain
cerebral aquaduct is the associated ventricle |
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during morphogenesis, what does the rhombencephalon become? what are the divisions? what ventricle?
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Metencephalon: pons
Myelencephalon : medulla 4th diamond shaped ventricle |
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during morphogenesis, what happens as the cerebellum emerges?
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it exerts force down making straight neural tube bulge out laterally thefore giving 4th ventricle characteristic diamond shape. Forcing down creates Pontine flexure
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what is the pontine flexure?
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indentation of neural tube due to emergence of cerebellum
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what are the last 2 regions of neural tube to fuse? what happens if they don't?
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anterior neuropore: Anencephaly
Posterior neuropore: spina bifida |
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what does the sulcus limitans?
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divides the spinal cord into the dorsal/sensory ALAR plate and the ventral/motor BASAL plate
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dorsal side of spinal cord is located in what plate? ventral?
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dorsal: alar plate
ventral: basal plate divided by sulcus limitans |
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in the region of the 4th ventricle, the pontine flexure causes the walls of the 4th ventricle to spread apart, what happens to the dorsal/ventral arrangement of sensory and motor areas?
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before: dorsal-superior ventral-inferior
after pontine flexure: dorsal(sensory)-lateral ventral(motor)-medial |
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what happens to the brain durign puberty?
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patterns of neural circitry change even into adulthood neural plasticity will continue
*dont have mature brain until 20yrsw |
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where are neurons born? how many cell layers exist at this point? at their final destination, how many cell layers do we have?
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born in ventricular zone and have 1 cell layer
when at final destination, have 6 cell layers with the oldest neurons in layer 6 *different fxns in each layer |
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how to neurons migrate from ventricular zone to final destination?
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via radial glial cells to form the 6 cortical areas
radial glial cell is like a scaffold *anything that disrupts radial glial cells disrupts neuronal migration |
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when does neural migration into cortex peak? when do they complete migration?
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11 and 15th week of gestation
complete at 24th week |
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how does Fetal Alcohol syndrome affect neuronal migration?
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alcohol interferes with migration. lack normal layering in cortex and cerebellum. dont have all 6 layers therefore MR
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Microcephaly is due to what?
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small head:brain does not achieve full size b/c disorder of neuronal proliferation. there are 6 genes involved in the fxn of proliferation
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Lissencephaly is due to what?
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"smooth brain"-gyri absent or reduced. cortex thickened and has 4 layers instead of 6. Developmental disorders
*due to disorder of neuronal migration with involvement of 2 genes that code for proteins that regulate microtubules |
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after 10 sec of ischemia what hapens? after 20 sec?
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10 sec: lose consceiousnes
20 sec: electrical activity stops |
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all the blood supply to the brain comes off arteries that branch off of the ???
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internal cartoid (anterior blood supply )and the vertbral arteries (posterior blood supply)
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the vertebral arteries join together along the brainstem to form what?
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basilar artery
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PICA arises off of? what does it stand for?
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arises off vertebral arteries
stands for Pos infererior cerebellar artery |
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AICA arises of of ? what does it stand for?
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arises off basilar artery
stands for Ant inferior cerbellar artery |
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waht connects the anterior and posterior circulation of brain?
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posterior communicationg arteries connect basilar artery and internal carotid artery
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what are the 2 kinds of problems that an aneurysm can cause?
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1. as it enlarges, it can compress neighboring brain tissue
2. it can rupture and cause a subarachnoid hemorrhage |
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ACA supplies most of what surface of the hemisphere?
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medial surface of the hemisphere: courses around the genu of the corpus callosum. terminates at the jxn b/n parietal and occipital
**supplies paracentral lobule |
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what happens if you get a stroke in L ACA?
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lose R leg and foot b/c ACA supplies paracentral lobule
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what does the PCA supply?
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posterior regions of the brain including the occipital lobe where the visual cortex is; also supplies the inferior and medial temporal lobe
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pt. with visual field deficits think what?
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PCA
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what happens in your knock out lower moter neuron compared to upper motor neurons?
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lower: mm have no command
upper: dont synapse on mm so knocking them out will have no VOLUNTARY mvmt but will still have reflexes: Hyperreflexia b/c normally upper neurons suppress them somewhat |
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lateral brain is supplied by what?
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MCA
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medial brain is supplied by what?
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ACA from up to border of parietal and occipital
PCA occipital |
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MCA enters what?
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sylvian fissure then exits supplying face and arm sensiorimotor cortex and many areas of association cortex
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what do you have in both the somatosensory and motor cortex?
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Homonculus: map of body
most medial: legs, feet trunk laterl: hand, face |
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branching off MCA are what arteries?
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deep territory:lenticulostriate arteries that penetrate deep to supply the basal ganglia and internal capsule
MCA inferior division MCA superior division |
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what 2 arteries branch off ICA?
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MCA and ACA
off MCA-lenticulostriate arteries, MCA infer division, MCA superior division |
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what supplies the internal capsule?
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lenticulostriate arteries
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if an infarct where to occur at the most proximal region of MCA what would this be called?
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infart at Middle cerebral artery stem = MCA stem infart
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what are the deficits of an infarct in Left MCA superior division?
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nonfluent or Broca's aphasia (brocas located in left hemi)
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what is Broca's aphasia?
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trouble articulating words
due to infarct in Left MCA superior division |
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if you have an infarct in Right MCA stem, what are the deficits?
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"classic" contralateral neglect: don't have awarness of left side of visual world but can see fine (profound left hemineglect)
won't have language problems b/c Brocas(left brain) is fine characteristic of knocking out right parietal lobe |
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what do strokes in ACA produce?
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contralateral weakness and loss of sensation in the lower extremity b/c of paracentral lobule
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who do strokes in PCA produce?
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it supplies visual cortex, so major deficit would be loss of one visual cortex. since each visual cortex processes visual info from the contralateral side, a stroke in L PCA would result in loss of visual info from teh R side of each eye's field: R contralateral homonymous hemianopia (half inability to see)
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what is a watershed?
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region b/n either ACA and MCA or MCA and PCA
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what happens to MCA/ACA watershed with a drop in blood pressure?
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they get very low blood supply at the end termini. the region most affected with decreased BP is the area b/n the 2 vssls since that region depends on diffusion of blood from each of the 2 vssls.
"Man in barrel": head and legs will be supplied, but trunk(wateshed area) will lose motor and sensory |
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PICA supplies?
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medulla and cerebellum
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AICA supplies?
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pons and cerebellum
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SCA supplies?
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midbrain and cerebellum
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Anterior spinal artery supplies?
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part of medulla (midline)
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what are the 2 arteries that supply the spinal cord?
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anterior (single) and posterior (paired) spinal arteries
*ant. supplies ventral midline of medulla |
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if you knockout anterior spinal artery, what happens?
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lose lower motor neurons in that area
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if you knockout posterior spinal artery, what happens?
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get lose of sensation b/c knockeout dorsal column
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venous drainage occurs via a system of veins that flow into a few major sinuses including what?
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sup. sagittal sinus
cavernous sinus great vein of Galen exiting brain at Internal Jugular Vein |
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what is a stroke?
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sudden death of brain cells due to lack of O2 when the blood flow to brain is impaired by blockage or rupture of an artery t othe brain
AKA: cerebrovascular accident or CVA |
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strokes are due to what 2 cuases? mostly which ?
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intracerebral or subarachnoid hemorrhage (20%) or ischemic infarction (80%)
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what is an infarction?
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"plug up or cram"
tissue death due to lack of O2 |
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ischemic stroke?
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when loss of blood supply to the brain is long enough to cuse neuronal death
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"worst headache of my life" describes what?
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stroke typically caused by emboli
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what are lacunar infarcts? what are they associated with?
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small vessel infarcts that involve small penetrating vssls deep into brain including brainstem
typically associated with chronic hypertension |
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what are the 5 major signs of stroke?
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1. sudden numbness or weakness of face, arm or leg especially on one side of body
2. sudden confusion, trouble speaking or understanding. drooling 3. sudden trouble seeing in one or both eyes 4. sudden trouble walking, dizziness, loss of balance 5. sudden severe headache |
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if stroke is due to thrombus what can you treat with? and how soon after?
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within first 3 hrs
treat with tissue plasminogen activator (TPA) to help dissolve the clot but you risk incrased hemorrhage |
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what artery gives off R opthalmic artery?
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right internal carotid artery
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where is the stenosis: transient blindness in R eye followed by stuttering loss of strength on L side with numbness
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stroke in R ICA blocking R opthalmic A and ACA and MCA on right side which affect contralateral side
stroke in ant circulation often preceded by transient monocular blindness or "amarosis fugax" (lampshade over one eye) IPSIlateral to the carotid artery involved |
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if a man has sudden onset of R sided weakness and numbness and a global aphasia, where is the lesion?
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broca's area which is located on Left side explaining aphasia and R weakness
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where is the stroke: pts with untreated hypertension presents with sudden onset of R face, arm and leg weakness?
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hypertension = lacunar infarct
therefore "lacunar" stroke through internal capsule on Left side of brain |
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why use CAT scan?
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can see bones
more sensitive to blood (stroke) readily available in ERs |
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why use MRI?
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DWI (diffusion weighted imaging) best for acute ischemic strokes: looking at water flow-see different signal in region of infarct
*higher resoluation than CTs |
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what type of cell death is associated with infarct? what about the area surrounding infarct?
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infarct: necrosis
penumbra: apoptosis |
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difference b/n necrosis and apoptosis?
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necrosis: rapid and passive
swelling of neurons until burst and leak contents TOXIC, occurs at HIGH levels of excitotoxicity, irreversible APOPTOSIS: prolonged, programmed (excess Ca turns on genes), less toxic, occurs at LOW levels of excitotoxicity **potentially reversible with drugs that block NMDA |
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wht is the major excitatory neurotransmitter in the brain?
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glutamate
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what happens to glutamate in response to brain injury/trauma and ischemia?
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the ability to maintain cellular homeostasis is compromsised and excess glutumate (which is normally cleared quickly) builds up extraceullarly therefore cells tend to be depol enabling the activation of NMDA receptors
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what is the NMDA R? why is it unique?
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glutamate R involved in ischemic conditions
both ligand gated and voltage gated |
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What are EATT transporters? what happens to these in necrosis?
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transporters expressed by glial cells that uptake excess glutamate
In necrosis, they won't sop up excess glutamate therefore develop penumbra |
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explain how the NMDA R works?
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Mg normally blocks the pore, but when the cell becomes depolarized the Mg is displacedd and Ca enters the cell through channel further depol. This is normally good, but when too much glutamate is present, too many NMDA Rs are activated then too much Ca enters triggering chain of intracellular cascades**uncopules the e- transport chain killing the neuron
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how can cells in the penumbra be rescued? what is the potential problem?
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by administering NMDA receptor antagonist
end up turning off processes that need to occur normally |
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what type of lesion should you think of: R hand weakness following cariac arrest?
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hand=lateral
weakness = primary motor cortex therefore think problem with MCA in precentral gyrus on LEFT side |
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hypodensity (black) on CT indicates what?
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cells dying
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why is atrial fib a risk factor for stroke?
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atrial fib leads to clotting!!
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how does a hypertensive hemorrhage present?
|
comes on actuley
bleeding is usually self limiting and rarely occurs at same site siezure and headache common blood freq enters ventricles predisposing pt to hydrocephalus from obstruction prognosis better than stroke when tissue is infarcted |
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which type of hemorrhage is referred to as "worst headache of my life"?
|
subarachnoid hemorrhage (SAH): blood pooling in subarachnoid space
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clinical presentation of subarachnoid hemorrhage?
|
worst headache of life
when pt awakens is confused with nuchal rigidity from the blood irritating the meninges |
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|
common sites of SAH?
|
berry aneurysms occur at bifurcations of vssls (90-95% in circle of willis) most commonly in ant communicating artery, poster communicating artery, MCA bifurcation, and bifurcation of ICA into MCA and ACA
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how is the brain protected from trauma?
|
kept buoyant by CSF
protected by 3 layers of meninges: dura mater, arachnoid matter, pia mater |
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what is located in the subarachnoid space?
|
bridging veins
cerebral artery that penetrate into gray matter arachnoid trabeculae |
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what does the dura include?
|
falx cerebri (divids teh hemispheres) and tentorium cerebelli which is like a hard tent-shaped sheet that covers the top surface of cerebellumw
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where does a epidural hematoma occur?
|
blood pools above dural space (b'n dura and skull)
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in which meninge layer does CSF percolate?
|
arachnoid mater
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purpose of arachnoid villus/granulation?
|
villi that extends from subarachnoid space into dura
allows CSF from subarachnoid to drain through and into venous system |
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where is the subdural space?
|
site of subdural hematoma b/n dura and arachnoid
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which artery supplies the dura? rupture of this causes what?
|
middle meningeal artery off external carotid that runs within epidural space and hence if ruptures can cause epidural hematoma
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how can the 2 common hematomas be distinguished on a scan?
|
epidural: lens-shaped biconvex that is more restricted to flow b/c dura tightly attached to skull
subdural: crescent shape b/c venous blood dissects very easily b/n dura and arachnoid |
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|
cuase of subdural hematoma?
|
rupture of bridging vv that occurs slowly as opposed to epidural hematoma that is very fast (medial emergency)
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what is the tentorial incisura (tentorial notch)?
|
opening where brain stem is
location of midbrain hematoma can squish CN III |
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a hematoma in the tentorial notch can cause what?
|
squish CN III b/c notch is the location of midbrain
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what is the diff b/n strokes in brainstem and w/n brain?
|
when in brainstem see CN problems
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what are the 3 serious neurological symptoms caused by space occupying lesion?
|
1. can compress adjacent tissue
2. increse intracranial P 3. displace neural tissue so the neural structure is shifted from one compartment to another-herniation |
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what are the cerebral peduncles?
|
mickey's ears: collection of corticospinal axons in midbrain
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what is teh uncus?
|
medial temporal lobe
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what is an uncal herniation? triad of Sx?
|
when uncus herniates through tentorial notch causing triad of Sx due to herniation of midbrain: "blown" pupil (fixed dilated b/c damage III), hemiplegia (paralysis of one side of body), and coma (due to damage of reticuloformation in midbrain)
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where is the site or reticular formation that is critical for consciousness?
|
pons
an uncal herniation pushes down on midbrain which then pushes on area of pons where reticular formation is located thus could lead to coma |
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in terms of neural tube, which components comprise which ventricles?
|
telencephalon: lateral vent
diencephalon: 3rd mesencephalon: cerebral aquaduct rhombencephalon: 4th |
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|
what are the components of the lateral ventricles?
|
frontal (ant) horn
body atrium occipital (post) horn temporal (inf) horn |
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|
how do the lateral ventricles connect with the 3rd ventricle?
|
via the interventricular foramen of Monroe
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how does the 3rd ventricle conect with the 4th ventricle?
|
cerebral aquaduct (aquaduct of Sylvius)
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roof of 4th ventricle is what structure? walls of 3rd?
|
cerebellum-roof of 4th
thal and hypthal-walls of 3rd |
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why are there little openeings on the 4th ventricle and what are they called?
|
exit pts for CSF
2 lateral: Lateral Foramina of Luschka midline: Foramen of Magendie |
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|
what is the choroid plexus? where is it?
|
produce CSF w/n each ventricle
fusion of bld vssls with ependymal cells that line the ventricles |
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|
what are ependymal cells?
|
specialized cells that line the ventricles called CHOROID EPITHELIAL cells that produce and secrete CSF
they have TJ b/n them to regulate what enters ventricles |
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|
describe the ionic composition of CSF
|
high Mg and Cl higher than plasma
K lower than plasma |
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|
how is the composition of CSF diagnostic of disease?
|
when bacterial: decrese glucose increase protein
when viral: normal glucose and protein |
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after percolating over the cerebral hemispheres w/n the subarachnoid space and then exiting the arachnoid vili, where does CSF finally drain?
|
into the superior sagitall sinus
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where is the final place that CSF pools after percolating through subarachnoid and around cerebral hemispheres?
|
lumbar cistern (site of lumbar puncture/spinal tap)
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where is the majority of the CSF?
|
in subarachnoid space
smaller amts in ventricles |
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|
how does Hydrocephalus occur?
|
CSF is secreted through arachnoid villi into dural sinuses. if the arachnoid villi become calcified, you stop draining CSF and instead CSF builds up in ventricles
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|
what is hydrocephalus confused with?
|
mistaken for parkinson's syndrome
therefore must do scan before diagnosing |
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|
what are the 3 causes for development of Hydrocephalus?
|
1. excess production of CSF (tumor-Papilloma)
2. obstruction of flow of CSF such that it builds up at certain locations 3 failure to drain CSF properly via the arachnoid granulations |
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|
what is the most common cause of hydrocephalus?
|
obstruction of CSF flow
tumors can block ventricular system or congital reasons: exit foramina dont form properly |
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|
what is a communicating hydrocephalus?
|
ventricles can communicate freely with each other, but CSF flow is obstructed in teh subarachnoid space or not absorbed sufficiently by the arachnoid granulations
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what is a non-communicating hydrocephalus?
|
something is obstructing flow of CSF b/n the ventricles (problem b/n ventricles or b/n ventricles and subarachnoid space)
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what is Dandy-Walker syndrome?
|
exit foramina do not develop properly. CSF could not escape into the subarachnoid space causing a non-communicating hydrocephalus and the enlargement of the ventricles
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|
what is the BBB?
|
due to formation of special TJ b/n endothelial cells JUST in the capillaries of the brain (not present b/n endothelial cells in blood vssls elsewhere in body)
TJ prevent free flow of substances into the brain to minimize infxn and protect the brain |
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|
do astrocytes form the BBB?
|
NOO! they are involved in the formation of TJ by secreting chemical to induce endothelial cells to form TJ therefore if you take away astrocytes, lose signal--no TJs formed
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what forms the TJ of BBB?
|
endothelial cells after receiving signals from astrocytes
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what happens when ependymal cells invaginate?
|
they are now called choroid epithelial cells that form TJs
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|
besides the BBB, what other barrier exits in relation to CSF?
|
b/n choroid plexus and CSF
specialized choroid epthelial cells make TJs b/n themselves to prevnt the free uncontrolled flow of substances from the choroid plexus to the CSF, but the CSF can freely penetrate the ependymal cell layer of the ventricles |
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|
what are the 2 barriers in the brain to protect and prevent infxn?
|
1. BBB w/ TJ b/n capillary endothelial cells
2. TJ b/n choroid epithelial cells |
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|
how do you deliver drugs across BBB?
|
there are certain regions where the BBB is interrupted- called Circumventricular organs
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|
where are circumventricular organs located?
|
where neurohormones are being produced and need to be secreted: Area postrema, Neurohypophysis, Pineal body
|
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|
what is the Area postrema?
|
circumventricular organ located on caudal wall of 4th ventricle in medulla that detects toxins that cause vomiting and hence it is also called the Chemotactic trigger zone
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|
how else can you cause BBB to become leaky?
|
pulse something very osmotic (mannose-sugar) will cause cells to shrivel up and then you can administer chemo
Stressful situations will also make it leaky |
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|
neurons that respond directly to sensory stimuli are called what?
|
receptors
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|
what happens to the nomenclature when you have a Pacinian corpuscle in which the sensory aff neuron's terminal resides?
|
instead to the neuron, the pacinian corpuscle will be the receptor and the sensory neuron that terminates in it will be the sensory afferent
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|
what happens after a receptor detects a signal?
|
the receptor must then transduce that stimulus into an electrical signal. the elecrical potential induced is a local potential which then travels retrograde back up the axon and if great enough will fire an AP and travel towards CNS to relay the mssg
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|
at the site of the stimulus, the electrical potential induced is called what?
|
receptor potential or local potential or generator potential
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|
what is a local potential? what is it not?
|
it is NOT an AP! it is a graded, electronic event
not all or none b/n no v-gated channels |
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|
why is DRG axon pseudopolar?
|
1 branch to spinal cord to synapse on interneuron in dorsal horn
1 peripheral branch that terminates at peripheral target |
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|
what are the attributes of a sensory stimulus that the CNS nees to discern?
|
modality: vision, hearing, touch ,taste (type of sensory)
intensity duration location |
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|
all sensory info with exception to what? is relayed through the thalamus?
|
olfactory system
thalamus is the relay b/n the periphery and the cortex |
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|
each DRG give rise to?
|
spinal nerve
|
|
|
what are the 4 distinct somatic modalities?
|
touch: prssure
proprioception: knowing where limbs are in space pain: elicited by tissue damaging stimuli thermal: cool and warm |
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|
what are teh 3 types of somatosensory receptors?
|
mechanoR's: respond to physcial deformation including proprioceptors
thermoR's: respond to temp and its changes NociR's: respond to stimuli that can damage tissue |
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|
Why is the skin not a unifrom sensory surface?
|
there are different sensory nerve endings throughout the skin: if you place cold probe over area of skin in which there are no thermoR's you will not activate cold R's but instead feel pressure
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|
what do limb proprioceptors tell the brain?
|
sense of position and movement of the limbs
NOT pain, NOT pressure |
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|
what are the submodalities of limb proprioception?
|
stationary position and sense of limb movment
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|
muscle spindles relay info about what? what are they innervated by?
|
muscle length (stretch)
innervated by Ia afferents |
|
|
describe density of mm spindles w/n mm that control coarse mvmts?
|
very few spindles whereas mm that control fine movments such as extraocular mm and hand and neck intrinsic mm contain many mm spindles
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|
golgi tendon organs relay info about what? innervated by?
|
muscle tension
innervated by 1b afferents |
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|
what R's have free nerve endings?
|
thermoR's and nociR's
|
|
|
what type of axons innervate free nerve endings?
|
C and Adelta
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|
|
all mechanoR's are innervated by what axons?
|
Abeta
this includes Meissner's corpsucles, Pacinian corpuscles, Merkel's disks, Ruffini's corpuscles |
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|
MM spindles are innervated by what sensory axons?
|
Ia and II
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|
which of the R's have myelin?
|
muscle spindle
golgi tendon organs Meisnner corpuscles Merkels Pacinian Noci and Thermo for sharp pain and some touch |
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|
which of the Rs aren't myelinated?
|
nociR's and thermoR's for slow pain, heat and itch
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|
|
Adelta innervate what R's?
|
nociRs and thermoR's for sharp pain, cold and some touch
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|
|
C fibers innervate what R's ?
|
nociR's and thermoR's for slow pain, heat, and itch
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|
which of the R's is the faster conductor? slowest?
|
fastest: muscle spindle primary endings (proprioRs)
slowest: nociRs and thermoRs for slow pain, heat, itch |
|
|
which of the Rs have the largest diameter? smallest?
|
largest: proprioRs (m spindle primary endings)
smallest: nociR's and thermoRs for slow pain, heat, itch |
|
|
how does mechanical deformation transduce a change in membrane potential?
|
by leading to opening of Na channels with induces depolarization of the cell. this depolarization is called a Receptor potential
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|
the amplitude of the generator potential is proportional to what?
|
intensity of the stimulus
|
|
|
what happens after mechanical deformation when a generator potential is initiated?
|
if large enough, it triggers AP at the point where myelin sheath begins
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|
|
which portion of the peripheral branch of sensory neuron is sensitive to to stimulus energy?
|
only the terminal portion that involves the different R's
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|
|
each sensory neuron in the DRG can be distingished based on what?
|
morphology of its peripheral terminal
sensitivity to a stimulus energy diamter of its axon and cell body presence (or absence) of a myelin sheath |
|
|
small myelinated afferents=
smaller myelinated afferents= |
small: Abeta (mechnoRs)
smaller: Adelta (sharp pain, cold) unmyelinated = C (slow pain, heat, itch) |
|
|
what are the most numerous type of afferent?
|
unmyelinated c fibers
|
|
|
letter classification of II? III? IV?
|
II= Abeta
III=Adelta IV=C |
|
|
where are muscle spindles located?
|
w/n extrafusal fibers of mm
|
|
|
which Rs are rapid adaptors?
|
meisners and pacinian
|
|
|
what does it mean if a R is rapidly adapting?
|
they only know rate of onset of stimulus only (not the change over time) the longer you deflect a hair, it ends up habituating and you no longer feel it (no longer generate AP)
|
|
|
what does it mean if a R is slowly adapting?
|
acct for info of onset, rate of change and know when chronically mm are being stretched
|
|
|
how do nociR's detect stimuli?
|
they respond to chemicals released from damaged cells: bradykinin, histamine and K
all 3 excite nociRs and cause pain when injected into skin |
|
|
how are nociR's activated following tissue damage?
|
increase K, prostaglandin, serotonin, and bradykinin which bind to the free nerve endings of the NociR. Their binding causes Noci to release substance P which increases cap permeability and contributes to inflammation. Substance P also causes mast cell degranulation to release histamine which also activates NociR
|
|
|
what type of stimulus do you need to activate NociRs?
|
tissue damage
|
|
|
why is your face more sensitive than your back?
|
innervation density is different
more dense in face=smaller receptive field less dense in back=larger receptive field hard to tell exact location of stimulus all you know is that the neuron is active. in face, more info of location of stimulus |
|
|
where afferent density is high, have _____ receptive fields?
|
small
|
|
|
wht is the 2 point discrimination threshold?
|
distance to travel before 2 pts are considered distinct
|
|
|
a receptive field + spinal nerve innervating it =
|
dermatome
|
|
|
knowing dermatome which help what?
|
determine the level of the lesion
|
|
|
where does the primary order mechanosensory afferent fiber (Ia or Abeta) synapse?
|
in cuneate nucleus in medulla
|
|
|
where does the primary order pain and temp afferent fiber (Adelta or C) synapse
|
"pain can't wait" it synapses right away in dorsal horn of spinal cord on projection interneuron
|
|
|
after the 1st order Adelta or C afferent fibers synapse in spinal cord what happens next?
|
they send second order axon to other side of spinal cord "ventrolateral" colliculus and from there it travels to thalamus
|
|
|
after the 1st order Ia or Abeta afferent fibers synapse in medulla, what happens next?
|
they send second order axon to other side of medulla (medial lemniscus) and from there it travels to thalamus
|
|
|
all _____ neurons cross?
|
2nd order neurons
except: spinocerebellar tract (propriception) |
|
|
if you have a lesion b/n spinal cord and medulla what happens to touch and pain?
|
contralateral loss pain/temp
ipsilateral loss touch/pressure |
|
|
what does somatotopy mean?
|
receptors in adjacent portions of the peripheral receptive field project to nn in adjacent portions in the CNS
|
|
|
How do the central axons of Adelta and C fibers enter the dorsal horn?
|
via Lissaur's tract laterally and synapse in L I and II
|
|
|
where do pain and temp neurons synapse?
|
only in dorsal horn as compard to proprioception which has brr to dorsal horn, Clarks nucleus, and to motor neurons in ventral horn
|
|
|
Lamina I-VI correspond to ?
|
dorsal horn
|
|
|
lamina I and II are import areas for what?
|
pain and temp processing
|
|
|
Laminae II is also known as?
|
substantia gelatinosa
|
|
|
what type of info does the substantia gelatinosa receive?
|
afferent info from nonmyelinated and finely myelinatated fibers (Adelta and C)
|
|
|
b/n the substantia gelatinosa and surface of the cord is what?
|
Lissauers tract which contains myelinated and unmyelinated fibers (Adelta and C)
|
|
|
Lamina III-VI contain what nucleus?
|
nuclues proprius which integrates sensory input and info that descends from the brain
|
|
|
Which lamina is roughly equivalent to intermediate zone?
|
lamina VII
|
|
|
which Lamina contains Clark's nucleus? which levels of spinal cord?
|
Lamina VII which is present in the thoracic and upper lumbar segments only (T1-L2) and relays info about limb position and movement to cerebellum
|
|
|
which lamina contains intermediolateral nucleus or cell column in T1-L3?
|
lamina VII
|
|
|
what does the intermediolateral nucleus contain?
|
autonomic pre-ganglionic neurons
|
|
|
which lamina comprise the ventral horn?
|
Lamina VIII and IX
|
|
|
which lamina contain motor nuclei for skeletal mm ex: diaphragm?
|
lamina IX; both alpha and gamma motor neurons
|
|
|
lesions in lamina IX lead to what?
|
flaccid paralysis
|
|
|
motor neurons in the medial portion of the ventral horn in segments C3-C5 comprise what nucleus?
|
phrenic nucleus and innervate the diaphragm
|
|
|
destruction of motor neurons at level C3-C5 causes what problem?
|
pt will be incapable of breathing bc lose innervation of diaphragm
|
|
|
which lamina surround central canal?
|
lamina X and receives afferent input similar to that of lamina I and II
|
|
|
peripheral nn join together to form ?
|
spinal nerves
peripheral nerve = 2-4 spinal nn |
|
|
area of skin innnervated to by a dorsal root is called a?
|
dermatome
|
|
|
what changes occur in vertebrae as we progress from cervial to sacral?
|
dorsal columns become narrower b/c above T6 have both FC an FG, but below T6 only have FG
lateral faniculus decreases bulging of ventral horn in high motor areas such as C8 (cervical enlargment) and L5 (lumbar enlargment) |
|
|
posterior/dorsal column pathway relays what modalities?
|
touch, pressure, proprioception (Abeta and Ia)
|
|
|
where is the first synapse of dorsal column pathway?
|
w/n caudal medulla in either nucleus cuneatus or gracilis on 2 order neurons
|
|
|
what happens after 1st order nuerons synpase on 2nd order neurons in caudal medulla?
|
the 2nd orders decussate and are called internal arcuate fibers and as they travel upward they are then called medial lemniscus
|
|
|
the axons in the medial lemniscus are conveying info from what side of the body?
|
contralateral side of body
|
|
|
axons in the medial lemniscus ascend and synapse on what?
|
3rd order neurons in VPL of the thalamus
|
|
|
where are the 1st order neuron cell bodies in posterior column pathway?
|
in DRG
|
|
|
where are the 2nd order neuron cell bodies in post column pathway?
|
nucleus gracilis or cuneatus
|
|
|
what type of modality does the spinothalamic/ALS patheway carry?
|
pain and temp to brain
|
|
|
what is the spefic tract of ALS pathway that specifically stops in the VPL nucleus of the thalamus?
|
spinothalamic tract
|
|
|
where do sensory pain and temp fibers (Adelta and C fibers synapse) ?
|
in lamina I and II of spinal cord
|
|
|
what happens after 1st order Adelta or C neurons synpase on on 2nd order neurons in Lamina I or II?
|
2nd order neurons decussate across anterior commisure to anterolateral system
|
|
|
2nd order neurons of ALS pathway are called what?
|
as they ascend through the contralateral ALS pathway they are called spinothalamic tract as they synapse in VPL
|
|
|
fibers in spinoreticular tract synapse on what?
|
medullary-pontine reticular formation located in pons which in turn projects to the intralaminar thalamic nuclei
|
|
|
fibers in spinomesencephalic tract project to where?
|
periaquaductal gray area in midbrain to modulate pain
|
|
|
what do the spinothalamic, spinoreticular and spinomesencephalic tracts help you to do?
|
spinothalamic: location of pain and stimulus
spinoreticular: alertness/conscioussnes of pain/ emotion spinomesencephalic: modulate/decrease pain |
|
|
what hapens in Brown Sequard Syndrome?
|
lesion in spinal cord
below the lesion: ipsilateral weakness from corticospinal tract ipsilateral loss of pressure/touch/proprio from dorsal columns contralateral loss of pain and temp at area of stab wound: complete loss of sensation |
|
|
what is happening in posterior/dorsal spinocerebellar tract?
|
1a afferents,proprio, from legs enter spinal cord synapse in clarks nucleus
2nd order neurons project their axons along the ipsilateral margin of the spinal cord forming the dorsal spinocerebellar tract they ascend theorugh the inf cerebellar peduncle and synpase in cerebllum as mossy fibers |
|
|
what is the exception to the rule that all 2nd order neurons decussate?
|
2nd order neurosn of spinocerebellar tract do not cross: they stay and ascen ipsilateral all the way to terminate on cerebellum
|
|
|
the trigeminal ganglion is the equivalent of the ____ for the face
|
dorsal root ganglion
it conveys most of the sensory info from the face, conjunctiva, oral cavity and dura mater as well as motor innervation of the muscle of mastication |
|
|
where do touch and pressure afferents for the face synapse after entering pons?
|
they synapse in main sensory trigeminal nucleus (principal sensory)
|
|
|
what happens after 1st order touch and pressure afferents for the face synapse in the main sensory trigeminal nuclues?
|
teh cross the midline forming the decussating pathway, the trigeminal lemniscus which projects to the VPM of the thalamus
|
|
|
what level is the prinicpal sensory nuclues located?
|
pons
|
|
|
at what level is the spinal trigeminal nucleus located?
|
extends from pons to C2
|
|
|
where do the 1st order pain and temp afferents for the face synapse ? what are they called?
|
Spinotrigeminal Tract
from trigeminal ganglion, then enter the pons and travel downward synpasing anywhere on the spinal trigeminal nucleus located b/n pons and C2 |
|
|
what are the 2nd order neurons called of the pain and temp trigeminal pathway? where does it synapse?
|
trigeminothalamic tract that decussate from spinal trigeminal nucleus and synapses in VPM of thalamus
|
|
|
what is unique about proprioception sensory afferents in the face?
|
the primary sensory afferents have their cell bodies in the CNS w/n the Mesencephalic trigeminal nucleus (TMN) w/n midbrain
*not in trigeminal ganglion |
|
|
explain the proprioception pathway in the face
|
primary afferents are located in the CNS w/n TMN (midbrain). the peripheral sensory axons extend out through the trigeminal ganglion where they are synapsed on jaw mm spindle. The central sensory afferents synapse on trigeminal moter nucleus located in the pons. the sensory neurons synapse on motor neurons which direclty leave through the trigeminal ganglion to synpase on the same muscle spindle and elicit a motor reflex
|
|
|
for the Tx of intractable facial pain, one can cut what?
|
the axons of the primary pain afferents by cutting the descending spinal trigeminal tract w/o affecting other facial sensations
|
|
|
principal spinal nuclues mediates what type of info?
|
tactile info
|
|
|
spinal trigeminal nuclues is mainly involved in waht type of info?
|
pain and temp
|
|
|
proprioceptiove responses in the face are mediated by waht?
|
trigeminal mesencephalic nucleus that has a column of primary sensory neurons that develop from the neural crest (the only neuronal neural crest derivatives in the CNS)
|
|
|
what is the trigeminal reflex?
|
consists of a contrxn of the mm of mastication in response to pressure on the mandibular teeth and depression of lower jaw
|
|
|
what is nociception?
|
the detection of noxious insults
physiological stimulus of pain |
|
|
what types of chemicals/products are released in response to tissue injury?
|
ATP
Prostaglandin Histamine 5-HT H Bradykinin |
|
|
what activates nociR's? what does this cause?
|
the binding of chemicals such as ATP, bradykinin, H, seretonin, histamine
these activate an AP if large enough that spreads retrograde to DRG cell body. In response the NociR will release Substance P |
|
|
action of substance P?
|
released by activated NociR that stimulates vascular perm and dilation as well as activates mast cells to release histamine. Histamine in turn binds to the NociR endings to further activate
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what is the most impt pain synapse?
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b/n central pain afferents and 2nd order neurons in Lamina I or II of dorsal horn b/c when dorsal horn is activated it sends signal to CNS telling of pain
*much plasticity at synapse, anything that shuts down transmission at synapse will decrease relay to CNS |
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What is the ATP receptor located on NociR free nerve endings?
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P2X which stimulates whole pain response
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what are the 3 categories of pain?
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normal (physiological)pain
inflammatory pain neuropathic pain |
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what is happening in inflammatory pain?
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activity in nociR neurons amplifies and extends the inflammatory process, called neurogenic inflammation
ex: TGF beta upreg Substance P |
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what type of pain is caused by injury processes in nerves and by local inflammation in nerves?
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neuropathic pain
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does activation of a nociR always produce pain?
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NOOO
the CNS component of the nociR/pain system makes editorial changes in what sensations a particular stimulus will evoke |
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what are the 3 situations in which an intense stimulus evokes a sensation of pain?
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only if 1: it is sufficiently intense
2. there has been a prior period of stimulation 3. if an inflammatory process is present |
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what is happening in diabetic peripheral neuropathy?
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diabetes affects blood flow and causes degeneration of small pain and temp afferents which elicits sensation of pain
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what is the normal state of pain?
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when normal skin is mechanically stimulated, there is a high threshold for pain: low intensity stimuli produce non-painful sensations such as touch, pressure
with higher intensities of stimulation (above the pain threshold), there is an increase in the mag of the sensation of pain |
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what is allodynia?
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formerly non-painful stimuli now perceived as pain: the threshold of pain has not been decreased, but the mag of pain sensation (y axis) is increased
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what is hyperalgesia?
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stimuli that are ordinarily painful are now perceived as being more painful due to sensitization of nociceptive endings
increased reactivity to a given stimulus (stimulus of same intensity elicits increased perception of pain) |
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describe what is happening in terms of pain threshold graphs for inflammation
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following inflammation there is a sensitization of nociR's and all stimuli are felt as painful
have allodynia and hyperalgesia pain curve is shifted upwards |
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what happens to the nociR endings following inflammation?
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they are sensitized: incresd reactivity to a given stimulus and causes a lowering of the threshold of the nociR
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what are the 3 different types of nociR's?
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mechanical nociRs: + by sharp objects
thermal nociRs: + by heat or cold (heat is above 45C)polymodal nociRs: mechanical, heat, chemical: dull or burning pain |
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if the temp is below 45 C, what type of sensory R's are activated?
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thermoR's
thermal nociR's are only activated when above 45C |
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the majority of nociR's are what type?
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polymodal: respond to mechanical, heat, and chemical mediated by C fibers tehrefore dull pain, heat and itch
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what are some Rs expressed on nociRs?
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TRPVs
P2X for ATP Trk (NGF R) prostaglandin R |
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TRP channels (TRPV1 and V2) are expressed by what type of fibers? what do they respond to?
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respond to pain from heat and Capsaicin from chili peppers
located on Adelta and C fibers |
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what happens if you block TRP channels?
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decrease sensation of pain
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how does hyperalgesia arise?
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increase gene expression
increase expression of P2X R decrease threshold of nocR leading to sensitization at either central or peripheral synapse |
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how does allodynia arise?
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normally there are no R's on dorsal horn projection neuron (2nd order neuron that relays info) for mechanosensory stimuli. But in the cause of inflammation, Abeta axons located in the area of the pain can branch and also synapse on DH projection neuron at which pt they can activate the DH projection neuron: now the brain can't tell the difference b/n pain and mechano and simply brushing a hair in the area of inflammation will cause pain
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what is referred pain?
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from nociRs in deep visceral structures but is felt at sites on the body surface
ex: MI felt as pain in left arm |
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why does referred pain occur?
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convergence of visceral cutaneous nociRs onto the same dorsal horn projection neuron: a single dorsal horn prjoectin neuron receives both inputs, higher centrs cannot distinguish the source of the input and incorrctly attribute the pain to the skin
*cutaneious input normally predominates |
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what is the pathway for pain modulation?
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Spinothalamic tract of the ALS pathway has a synpase off of in that goes to the periaquaductal gray of midbrain and is called spinomesencephalic tract.
these axons travel through Raphe nucleus as serotonineric neurons to synpase on DH interneuron in spinal cord. Here they release seretonin. the interneuron then releases Enkephalin on the DH projection neuron inhibiting signals as well as directly on the C/Adelta fiber also |
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what tract is responsible for the descending control of pain perception?
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spinomesencephalic tract
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in the descending control of pain, what do the interneurons release w/n the spinal cord and on waht?
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release enkaphalins as NT that inhibit both the incoming nocicpetive axons (C or Adelta) and the spinothalamic neurons on which they syanpse
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in the gate theory of pain, transmission of ascending pain info is blocked by what?
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concurrent stimulation of Abeta mechanoR's
ex: rub portion of skin that you receive painful stimulus on |
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why do you rub your skin that you received painful stimulus on?
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by rubbing you are activating mechnoR that then shut down the transmission of pain info
the mchnoR SHUT the GATE so pain transmission is blocked |
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explain the gate theory of pain circuitry?
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C fiber and Abeta fiber both synpase on the same inhibitory interneuron that then synpses on the DH projection neuron
the C fiber inhibits the interneuron while the Abeta fiber ativaties the inhibitory interneuron. the activation of the inhibitory internuruon overrides and the interneuron is inhibited. pain transmission is now blocked |
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if you tap on the patella and dont get a kick reflex what could be wrong?
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problem w/ sensory OR motor
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is sensory input to the CNS off/on or always on?
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CNS requires constant sensory input to ensure the generation of the correct pattern of muscle activity
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at bare minimum, what type of cells are required for a standard spinal reflex?
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sensory neuron and LMN
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what is a monosynaptic reflex?
classic example? |
if a synpase consists of just one sensory neuron and one motor neuron
Stretch or myotactic, deep tendon reflex |
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explain what happens starting when the knee is hit with a reflexhammer?
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the extensor mm is stretched therefore the mm spindle stretches stimulating Ia that innervte intrafusal fibers. this generate an AP that travels to the dorsal column . it can now synapses directly on the alpha motor neuron which will then contract to act on stretch. the afferent also synapses on other interneurons that will inhibit other alpha motor neurons that inervate the antagonistic mm
stimulated mm will contract, and antag mm will relax "recipricol innervation" |
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what happen when there is a lesion in a PNS axon? What is this called?
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Wallerian Degeneration: distal to the lesion, nerves degenerate. myelin sheath surrounding the distal axon segment breaks down and is phagocytosed by infiltrating macrophages. MT and NF fill the axon, the axon swells, and the distal axon falls off
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what do macrophages release upon infiltration during Wallerian degeneration? fxn of this cytokine?
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IL-1
mitogen for immature Schwann cells and stimulates increase in NGF |
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what happens to Schwann cells after lesion during Wallerian degeneration?
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they persist, dedifferentiate and undergo extensive proliferative process
*they basically become immature Schwann cells again and stay w/n endoneurial tubes or Bands of Bungner which are encased by a layer of basal lamina |
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what are the Bands of Bungner?
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the endoneurial tubes that the Schwann cells remain w/n during Wallerian degeneration
they are encasd by layer of basal lamina that is ECM matrix rich providing a critical substrate supporting the regrowth of peripheral axons |
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what happens proximal to the lesion?
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neuronal cell bodies swell
undergo chromatolysis rER breaks apart and relocates in the periphery of the swollen cell body protein and mRNA syn upregulated |
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is it better to lesion near the cell body or further?
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if sever nerve cell body worse for recovery
increase distance from cell body=increase chance of recovery |
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what is transneuronal damage?
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if presynaptic nerve dies, post will probably die b/c dieing cell releases glutamate which can lead to hyperexcitivity and death
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why is an infarct particluarly bad in CNS?
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CNS axons don't regrow and
pre synaptic nerve is dependet on GF from post if post die, pre could also die |
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what is the key component of successful peripheral nerve regeneration?
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the presence of healthy, live Schwann cells
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Besides having Schwann cells, what is critical for the successful nerve regeneration to occur? fxn?
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the invasion and activation of macrophage
1. phagocytose and remove myelin and axonal debris (critical for cleaning up the wound site) 2.when activated secrete GF and cytokines 3. promote Schwann cell prolif 4. release cytokines (IL-1) which then cause schwann cells to upregulated GF, NGF |
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What are the 3 impt factors of the PNS that promote nerve growth regeneration?
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schwann cells
macrophage invasion and activation several cell surface adhesion molecules and ECM glycoprotein that are upregulated following injury (fibronectin and Integrin R: NCAM and LI) |
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what is present on the basal lamina that is impt for nerve cell regrowth?
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Intergrin R NCAM
Laminin Fibronectin *perfect substrates for re-growth |
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why do central axons typically fail to regenerate following injury?
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less ECM: very little laminin and fibronectin
No infiltration of macrophages No Schwann cells (they have oligodendrocytes instead) |
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why did the experiment show when an optic nerve was grafted with a piece of sciateic nerve (PNS)? what does this show?
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retinal ganglion axons would regrow down sciatic but they stopped when they hit CNS
*CNS neurons can regrow, but are inhibited by CNS |
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when you place CNS and PNS nerves on Schann cells what happens? on oligodendrocytes?
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on Schwann: both grow
on Oligo: neither grow |
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what is IN-1?
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antibody that if added to culture medium of CNS axons, will allow CNS axons to be extended on oligodendrocyte membrane
IN-1 is blocking the inhibitor protien, NOGO |
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what is Nogo?
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inhibitory prtein that inhibits CNS nerve regrowth
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do we want to increase or decresae Nogo
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decrease Nogo to increase regrowth
*we want to develop proteins that compete for NogoR to block Nogo |
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to promote regeneration of CNS, what do we want to block?
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Rho and Nogo
increase Rho = inhibit growth |
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what is the glial scar?
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major barrier to regrowth in the CNS: after injury astrocyts prolif and increase their expression of chondroitin sulfate proteoglycans (CSPG) which are extrememly inhibitory to axon growth and increase Rho levels
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what is chondroitin sulfate proteoglycans?
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product produced after CNS injury when astrocytes start to proliferate
it is a potent inhibitor of axon growth and increases levels of Rho |
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injections of what enzyme will facillitate the regrowtn of CNS axons?
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chondroitinase ABC which cleaves the GAG side chains of the chondroting sulfate proteoglycan made by reactive astrocytes
*digests the glial scar |
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fxn of olfactory ensheathing cell?
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promote regrowth by forming a bridge to help neurons grow across the injury site
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what promotes CNS regrowth?
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Chondroitinase ABC
Nogo Ab Nogo peptide Olfactory ensheathing cells Bone marrow stromal cells |
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waht are the 3 cell types that promote nerve regroth?
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schwann cells
olfactory ensheathing cells bone marrow stromal cells |
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why give Nogo antibody?
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binds to neuronal growth inhibitor Nogo blocking its activity
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explain the deep tendon reflex
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sensory signal originates from afferent innervation of mm spindle in reponse to strtech. Ia then synapses directly on the MN which contracts to adjust the stretch. Ia also synapses on inhibitory interneuron that will inhibit other alpha MN that innervate the antagonistic mm
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does the stretch reflex require the nervous system?
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yes, cutting the dorsal root abolishes this stretch relfex
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what is the fxn of the muscle spindle?
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to inform the nervous system of the length and the rate of change in lenght of the extrafusal mm fibers
**need sensory and motor input for proprioception |
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which LMN innervate the extrafusal muscle fibers?
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the alpha motor neurons
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which LMN innervate the muscle spindles or intrafusal muscle fibers?
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gamma motor nuerons
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what is the fxn of the gamma LMN?
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regulate the length of the intrafusal fibers spindles
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what are the 2 types of LMN?
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alpha(larger): synapse on extrafusal mm fibers releasing Ach @ NMJ
gamma(smaller): synapse on msucle spindle which has intrafusal fibers |
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which LMN is constantly active?
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gamma: synapses on poles of mm spindle therefor always maintains tension keeping intrafusal fibers "taut" to stimulate stretch gated channels on Ia afferents
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where is the muscle spindle?
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embedded w/n extrafusal fibers
consists of intrafusal fibers that are attaached at the poles to extrafusal fibers so that whenver the mm is stretched the spindle is also stretched |
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difference b/n GTO and mm spindle?
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The gto lies in series with the muscle, between its fibers and tendon, and is sensitive to changes in muscle tension. The muscle spindle lies in parallel with the muscle and is sensitive to changes in muscle length.
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what are the 2 kinds of sensory input for muscle spindles?
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There are two types of sensory afferents, Type Ia (primary) and Type II (secondary).
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what do Ia sensory afferents provide info about?
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Type Ia sensory neurons respond to the rate of change in muscle length as well as the change in length itself.
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purpose of gamma MN?
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The purpose of the gamma motor neuron is therefore to contract the spindle when the muscle contracts, keeping it taut and able to fire in response to muscle length changes.
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the ends of the intrafusal fibers can contract due to activation by what neurons?
|
gamma MN
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which part of the intrafusal fibers is non-contractile ? why?
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center: wrapped by Ia afferents
when the mm is stretched, the spindle is streteched and that opens stretch activated channels in the termini of the sensory affernts |
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whch of the 2 kinds of sensory iput into the mm spindles is the primary ending? secondary?
|
primary: Ia
secondary: II |
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which sensory ending is especially sensitive to the ONSET of muscle stretch, but discharges at a SLOWER rate as the stretch is maintian?
|
primary Ia
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which sensory ending is less sensitive to the ONSET of stretch, but does NOT habituate to the stretch stimulus as quickly?
|
secondary II
their activity is maintained throughout the mm stretch |
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what is the difference bn Ia and II sensory affernts in terms of information relayed?
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Ia: dynamic info about mm length and rate of change in stretch
II: static info about mm length |
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which fibers are known as "bag" fibers? chain fibers?
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bag=Ia "bag of change"
chain=II |
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which fibers will you recruit for more info on change of lenght of mm? length of muscle?
|
for change of lenght: stimulate dinamtic Ia
for lenght of mm: stimulate static II |
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what are the two types of gamma motor neurons?
|
Dynamic Gamma Motor neurons – regulate the sensitivity of Nuclear Bag Spindles
Static Gamma Motor neurons – regulate the sensitivity of Nuclear Chain Spindles |
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Ia affernts are activated by? Ib afferents are activated by?
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Ia: muscle stretch
Ib: muscle contraction (change in tension) |
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what happens when muscle stretch is completed? in regards to sensory fibers?
|
you would think that they would fall silent, but instead the gamma motor neurons maintain the excitability of the intrafusal fibers by inducing contrxn of the spindle termini therby stretching the central region of the intrafusal fibers which is wrapped with sensory affernts: Ia afferents remain "poised" for action
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why do we have muscle tone?
|
b/c gamma motor neurons that innervate intrafusal fibers are alsoway under some degree of stretch
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what is unique about the intrafusal fibers?
|
The sensory spindle fibers entwined around the intrafusal fibres are tonically active i.e. fire action potentials when the muscle is at its resting length (they do so b/c gamma motor neurons discharge spontaneosly all the time)
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how are muscle spindles arranged to muscle fibers? how are GTO arranged?
|
muscle spindles are in parallel with muscle fibers
GTO are in series with muscle fibers |
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|
Bar bell is lifted by contracting the biceps muscle.
If weight is too great for biceps to lift, the biceps relaxes and the bar bells are dropped. How? |
The Golgi tendon organs detect the excessive force in the muscle and discharge action potentials.
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whre are GTO's located? what do they respond to?
|
at the jxn of tendons and muscle
respond to tension innervated by Ib afferents |
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why don't GTO's respond to stretch?
|
b/c when a muscle is streteched it directly affects muscle spindle rather than tendons
but when a muscle is contracted, force is being imposed directly on the tendon which compresses the GTO |
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what affernt inhibits the continual contxn of muscle?
|
Ib afferent
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|
what is the autogenic inhibition or inverse myotactic reflex?
|
when the force is too great,GTO activate inhibitory interneurons in the spinal cord that then will inihibt the same muscle that is contracting
*inhibition of homonomous muscle |
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|
waht does the Ib affernt release durin the inverse myotactic reflex onto the inhibitory internuron?
|
releases GABA or glycine which opens channels on post synaptic cell causing hyperpolarizoation by opening K channels stopping the contrxn
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|
what reflex allows us to quickly withdraw from a painful stimulus? how is it activated
|
flexion reflex
activated when a nociR responds to a painful stimulus leading to withdrawal of the limb from the source of pain by exciting the ipsilateral flexor mm and inhibitng the ipsilateral extensor muscle |
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|
in the flexion reflex, what is happening to the ipsilateral side of the painful stimulus and the contralateral side when you step on glass?
|
ipsilateral flexors are excited and ipsilateral extensors are inhibited
contralateral flexors are inhibited while the extensores are activated to maintain your balance |
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|
in the flexion reflex, what is the stimulation of the contralateral limb called?
|
cross extension reflex: activate extensors
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|
the flexion reflex is induced by what type of stimulation?
|
cutaneous stimulation, NOT muscle stimulation
ex: step on tack |
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|
what is released from inhibitory interneurons when they are activated?
|
glycine or GABA
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|
knee jerk reflex involves waht sensory receptor?
flexion reflex involves what sensory receptor? inverse myotactic reflex? |
knee jerk: muscle spindle
flexion reflex: cutaneous sensory receptors** inverse myotactic:GTO |
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|
what is spinal shock?
|
Immediately following spinal cord injury there is a period where you have no movement, no sensation, and no reflexes below the level of the lesion. It can last for hours to weeks and then may get better
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|
what happens after spinal shock?
|
It is then followed by heightened spinal reflexes. The limbs become “spastic” and stiff and the deep tendon reflexes become increased (For instance, testing the deep tendon reflex in the knee normally causes the lower leg to move, but in a patient with increased reflexes, tapping the knee may cause the whole leg to move)
**hyperreflexia and increase in muscle tone and abnormal reflexes: Babinski sign |
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|
what is the Babinski sign?
|
The extensor (Babinski’s positive sign) response can indicate upper motor neuron damage to the spinal cord in the thoracic or lumbar region, or brain disease constituting damage to the pyramidal system.
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|
why do you see a + Babinski sign in infants?
|
This happens because the corticospinal pathways (that run from the brain down the spinal cord) are not fully myelinated at this age, so the reflex is not inhibited by the cerebral cortex. The extensor response disappears and gives way to the flexor response around 12-18 months of age.
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what is the normal babinski sign? pathological?
|
Flexor: the toes curve inward and the foot everts; this is the response seen in healthy adults.
Extensor: the hallux (large toe) extends upward, and the other toes fan out; Babinski's sign. |
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|
why is the babinski sign seen after spinal cord injury?
|
b/c supraspinal centers play a key role in modulating spinal relexes
damage spinal cord, lose descending corticospinal tract that would normally inhibit the alpha motor neurons causing the toes to extend. now the toes fan out instead of plantar flexion |
