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103 Cards in this Set
- Front
- Back
Concentration Gradient:
always more Na+, K+, Cl- ions in or outside the cell? |
more Na out of cell
more K inside cell more Cl out of cell |
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voltage (V) (membrane potential)
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separation of charge across a membrane
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current
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flux or flow of and ion
-ampheres (I) |
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Hyperpolarization
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when Voltage in cell becomes more negative
happens when cell membrane becomes more permeable to K+ |
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Concentration Gradient is maintained by:
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Na/K pump (uses ATP)
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Depolarization
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When voltage in the cell becomes more positive
happens when cell membrane becomes more permeable to Na+ |
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Goldman-Hodgkin-Katz Eqn:
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60mV log *
[Pna[na]o+Pk[k]o+Pcl[cl]i] ----------------------- [Pna[na]i+pk[k]i+Pcl[cl]o] takes into account concentration of ions and permeability of membrane to ions |
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voltage gated ion channels
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are ion specific, throughout length of axon
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K leaky gated ion channel
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k leaks out of cell, according to concentration gradient
are open at rest only |
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2 Na+ voltage gated ion channels
and 1 K+ voltage gated ion channel |
Na+ activation gate (m3)
Na+ inactivation gate (h) = plug K+ activation gate (n4) |
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scorpion and snake venom
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prevents Na+ inactivation gate (h) from closing.
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Bee sting
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blocks K+ activation
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Action potential:
REST Vm at rest= -70mv |
m3 is closed
h is open n4 is closed K+ leaky gates are open so K+ exits the cell and cell is close to Vk (hyperpolarized) |
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Action Potential:
UPSTROKE depolarization to threshold |
m3 open
h open n4 closed so now Na goes in cell and it becomes more + (depolarized) |
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The highest (most depolarized) the cell can get =
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Vna
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Action Potential:
DOWNSTROKE Hyperpolarization |
m3 open
h close n4 open K leaves cell and cell hyperpolarizes (becomes more negative) |
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Action Potential
ABSOLUTE REFRACTORY PERIOD from undershoot to Vrest |
m3 close
h close n4 close no AP possible because all are closed can go as low as Vk But leaky K+ gate open so goes back to Vrest |
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scorpion venom
and snake |
keeps h open
so upstroke plateau seizures |
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TTX from pufferfish
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permanently blocks Na+ channels
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Frontal Lobe function
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personality
motor LTM |
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Parietal Lobe
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somatosensory
pain temp taste pressure touch vibration |
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occipital
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vision
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temporal
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hearing
STM |
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insular
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olfaction
limbic |
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Longitudinal Fissure
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separates L and R hemispheres
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Central Sulcus
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separates Frontal and Parietal
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Pre-Central Gyrus
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Primary Motor Cortex
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Post-Central Gyrus
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Primary Somatosensory Cortex
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Lateral Sulcus
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separates temporal from frontal and parietal lobe
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superior temporal gyrus (STG)
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primary auditory cortex
ie transverse gyrus of Heschl |
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Uncus/ Piriform cortex
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primary olfactory cortex
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gray matter v.s. white matter
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gray = collection of cell bodies
white = collection of axons |
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Subcortical Structures on caudal aspect
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optic nerve, chiasm, tract
pituitary gland mamillary bodies (limbic system) oculomotor nv cerebral peduncles/ crus cerebri |
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pons
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big flat area on Ventral side
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Medulla Oblongata
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precursor to spinal cord
pyramids inferior olives (next to pyramids) |
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thalamus
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on Dorsal side
filters all sensory info |
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Dorsal Aspect
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*pineal gland/body
*sup colliculi (secondary vision- coordinates head and eye movement) *inferior colliculi (secondary hearing) *trochlear nv |
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Main Blood Supply
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2 vertebrals
and 2 internal carotid arteries |
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Blood Supply from Vertebrals
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1 anterior spinal aa
2 dorsal spinal aa 2 PICA (post cerebellar aa) to Basillar |
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Blood Supply from Basilar
(at beginning of PONS) |
2 AICA (ant inf cerebellar aa)
2 CN III 2 PCA (post cerebral aa) * 2 post comm aa come of PCA |
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Internal Carotid aa
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become MCAs (middle cerebral aa) which follow the lat sulcus and supply the lat aspects of the brain.
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Circle of Willis:
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1 ant communicating aa
2 ACA (ant cerebral aa) 2 internal carotid aa -opthalmic aa comes off 2 Post Comm aa 2 PCA (Post cerebral aa) -off Basilar aa |
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Which lobes do the cerebral arteries supply/:
ACA MCA PCA |
ACA- medial aspects of all lobes but occipital
MCA- lateral aspects of all lobes except occipital PCA- occipital *MCA and ACA anastamose |
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Opthalmic artery
- comes off - supplies |
comes of internal carotid artery (MCA)
supplies the eye ball |
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Radicular arteries:
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1 ant spinal a and
2 post spinal aa anastamose |
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action potential is faster if
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axon has larger diameter
and axon is myelinated |
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Multiple Sclerosis
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autoimmune d/s: attack your oligo's in CNS (not schwann in PNS), so slows conduction of APs, and since ions leak out of axon there isn't enough voltage change to activate m3 channels once gets there.
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CNS neurons can't regenerate
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astrocytes inc in # (proliferation)
astrocytes in in size (hypertrophy astrocy secrete more growth factor BUT there is permanent astroglial scarring so cell dies! |
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PNS neurons can regenerate if cell body still intact
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schwan cells proliferate, hypertrophy, secrete more growth factor too.
but they also create collagen and remylinate the axon and the macrophages eat debri |
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ACh (acetylcholine)
- chemical pathway |
mitochondria make Acetyl CoA
acetyl co-a + choline ---acetylcholine transferase---> ACh ---acetylcholinesterase---> choline + acetate |
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ACh
- limiting factor - nucleus in brain -important for |
- choline
- Basal Optic Nucleus of Meynert -important for LTM and NMJ -also leads to NE which is important for STM |
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Myesthenia Gravis
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ACh receptors don't work
so give meds to block acetylcholinesterase so ACh doesn't get broken down and Post synaptic receptors that do work have more time to get ACh. *in a healthy person the med's would cause spasms |
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Fast and slow receptors for ACh
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fast = nicotinic (fires EPSPs)
slow = muscarinic (agonist) *shrooms are permanent muscarinic |
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Altzeimer's
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lack ACh production so give them choline. the choline binds to Acetyl Co-A to make ACh
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Dopamine
- is an "Amine" b/c is derived from an Amino Acid |
tyrosine---tryrosine hydroxylase--> L-Dopa --> DA --> NE --> epinephrine (adrenaline)
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Parkinson's
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give L-Dopa b/c DA doesn't travel through BBB
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Dopamine
-location -important for |
released by Pars Compacta of the Substantia Nigra
- Parkinsons - addiction (cocaine increases DA) |
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Serotonin
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tryptophan--5 hydroxy tryptophan (5HT)-->histadine-->histamine
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Glutamate and Asparate
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excitatory NTs
-too much glutamate causes adult seizures |
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GABA
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an inhibitory NT in adults
but excitatory in babys -causes seizure in baby's -prevents unwanted motor in adults |
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How does GABA prevent unwanted motor in adults?
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it is released by the Striatum (caudate and putamen) and travels to pars reticulata of the substantia nigra
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Supstance P
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is a peptide PT occuring in the substantia nigra that is used for SLOW PAIN
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Nucleus Basalis of Meynert
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In the forebrain (frontal lobe)
- for long term memory - releases ACh - altzeimer's |
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Pars Compacta of Substantia Nigra
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in midbrain (where colliculi are)
- releases DA - parkinson's - addiction |
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Locus Coerulus
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found in M.O. and Pons
- NE - important for STM |
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Raphe nucleus
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found in M.O. and Pons
- 5HT (which leads to serotonin) - consciousness - sleep d/o - depression |
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Telencephalon
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5 lobes
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Diencephalon
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Thalamus and Hypothalamus
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Mesencephalon
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Midbrain: pineal gland, crus cerebri, mamillary bodies, colliculi, optic nv/chiasm/tract
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Hind Brain/ Brainstem
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Pons, M.O.
* cerebellum is here but separate anatomically/functionally |
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3 layers of Meninges
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Dura matter
Arachnoid matter Pia matter |
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Denticulate Ligaments
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anchor the pia matter to the spinal cord (throughout the length of the S.C.)
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Filum Terminale
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pure pia matter
prevents |
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Rexed Lamina I
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marginal nucleus
for fast pain |
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R.L. II
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substantia gelatinosa
for slow pain |
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R.L. III
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nucleus proprius
for fast pain |
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R.L. IV
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nucleus dorsalis
for slow pain |
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R.L. V, VI
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interneurons
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R.L. VII
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clarke's nuc
coopersharington nuc centrobasal nuc intermediate lateral horn (IML) |
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R.L. VIII, IX
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motor nuclei
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R.L. X
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central gray nuclei
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Dorsal Horn
Intermediate Horn Ant Horn |
R.L. I-IV
R.L. V-VII R.L. VIII-IX |
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Epicritic
-dorsal column |
sensory system for fine touch:
Nucleus Gracilis and Nucleus Cuneatus Travel in the Medial Lemniscus to the VPL of the Thalamus |
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Protopathic
- ALS (anterolateral column) |
sensory system for pain and temp:
Spinothalamic and Spinoreticular RL interneurons decussates at AWC to thalamus (VPL or nonspecific) |
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DCST (descending corticospinal tract)
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LSCT (80%)
VSCT (20%) LCST decussates at pyramids VCST decussates at AWC |
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AWC
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spinoreticular
DCST |
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DCRST
descending corticoReticularSpinal Tract |
post limb IC
decussates to R.F. reticulospinal tract to Ant to Ant column RL 8 and 9 to NMJ |
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mm spindle fibers
and GTO fibers |
Ia and II
Ib contain alpha, beta and gamma motor neuron signals |
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Signs of LMN lesion
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hyporeflexia
mm atrophe hypotonia flacidity eg polio (ALS is both LMN and UMN) |
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Signs of UMN lesion
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hyperreflexia
mm bulk preserved hypertonia (stiff) spasticity eg. stroke, multiple sclerosis, parkinsons |
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fibrillation
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UMN problem
single m fiber can't see |
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fasciculation
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UMN problem
motor unit can see twitching |
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clonus
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UMN problem
muscle firing on own because unwanted motor is not being dampened by CNS |
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chorea
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UMN problem
whole body moving like snake eg. huntington's (autosomal dominant) |
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Left Hemisphere
secondary ctx problem affected by L MCA |
Aphasia: Brocca's or Wernicke's
(both = global aphasia) Alexia- reading Agraphia- writing Dyscalcula- math |
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L and R Hemisphere
secondary ctx problem |
Amnesia - MCA or ACA
Apraxia- ACA- Corpus Collosum- problem following directions Agnosia: tactile - ACA auditory- MCA |
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Amnesia
- anterograde - retrograde |
anterograde- hippocampus- cant remember new memory
retrograde- frontal lobe- cant remember old memory |
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3 Retinal layers
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1) Photoreceptor- secrete NT
2) Bipolar cell - secrete NT 3) Retinal Ganglion layer - sends AP down CN 2 |
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Fovea (visual macula)
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cones only, sharpest vision
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Photobleaching
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in dark: depolarized b/c cGMP props Na channel open
light: rhodopsin --photon--> opsin and trans retinal energy released activates cGMP phosphodiesterase wich removes cGMP from Na channel, so becomes HYPERPOLARIZED and releases NT |
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opsin vs retinal
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opsin = genetic
retinal = from diet (retinol from carrots easily converted to retinal) |
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cuneus ctx
calcarine fissure lingual ctx |
inf visual field
sup visual field |
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Fibers in Lissaure's Zone
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A delta
C Ia/II Ib |