Neuro 2

Start Studying!

Terms

undefined, object

copy deck

Place Theory: brain knows which frequencies are being heard based on which neurons are firing
volley theory: one to one; each stimulus frequency results in an AP (up to 3kHz)
prestin: membrane protein in the OHCs. The basal end of the cochlea has more of this motor protein, generates more force, and has increase BM stiffness
olivocochlear input: terminates directly on the hair cell, or on the afferent fibers of the IHC, and leads to a decrease in auditory sensitivity. Allows us to focus our attn on particular sounds.
endolymphatic potential: +80mV (more postive) than the perilymph. This is also called the endocochlear potential.Inside of hair cell is -45 so this translates to a 125mV potential difference and high driving force for K to enter the cell and cause depolarization quickly
otoacoustical emmissions: echo the sound that arrives at the inner ear and are made by the cochlear OHCs. used to asses congenital deafness.
hyperacusis: usually damage to CN 7: abnormal sensitivity to sounds. Seen with Bell's Palsy
periodic condensation vs rarefaction: increase pressure vs decreased pressure: in regards to the air molecules produced by vibrating tunes of a tuning fork
BAER: brainstem auditory evoked response: measures the response in brain waves that are stimulated to evaluate the central auditory pathways of the brainstem
PICA infarct: ipsilateral hearing loss
first place the auditory pathway from both ears interacts: superior olive
Heschl's gyri: primary auditory cortex: finger like gyri that lie in the lateral sulcus (transverse sulcus)
pontine vascular lesion or MS: difficulty localizing sound
interaural time differences: medial superior olive
difficulty detecting interaural phase and intensity cues: lesions of the pons that involve the trapezoid body and superior olive
lesions of pontine tegmentum (SO, trapezoid body, other auditory circuits): auditory hallucinations
Brodmann's 41 and part of 42: transverse temporal gyrus and superior temporal gyrus
unilateral hearing loss can be from:: EAM middle ear cochlea 8th nerve cochlear nuclei
conduction deafness: external/middle ear: occlusion (wax), TM rupture, otosclerosis (most common), otitis media. Can give a hearing aid to boost sound and compensate for reduced efficiency of conduction
sensorineural deafness: disease of cochlea, cochlear nerve, or central auditory connections
causes of sensorineural deafness: ototoxic drugs: aspirine, quinine, aminoglycosides shearing of cilia from loud noise infections, Meniere's, Tumor or infart
ototoxicity via aspirin: possilby a change in membrane permeablity and blood supply, causd from the imbalance of prostaglandins and leukotrienes.
ototoxicity of aminoglycosides: interference with production of ATP in mitochondria of the hair cells. EX: kanamycin, gent, tobra, neo, strepto
ototoxicity via infections/disease: syphillis, rubella, meningitis, head trauma, meniere's, cerebellopontine angle tumors
Meniere's disease: rupture of endolymphatic chamber due to excessive pressure. causes cochlear and vestibular problems. Tx with diuretics and anti-Htn. Symptoms: nausea, vomiting, vertigo, tinnitus, progressive deafness
presbycusis: age related: usually 4000-8000Hz
Tinnitus: conductive: low frequencies sensorineural: high freq tinnitus
cerebellopontine angle tumor: unilateral hearing loss, tinnitus, unsteadiness. will often involve CN 7 (facial pain and sensory loss) and CN V (decreased corneal reflex)
Weber Test: SND- heard in good ear (bc both bone and air are bad) CD: heard in affected ear bc bone conduction is louder than air and overrides the good ear
Rinne Test: SND: AC>BC (normal), but heard better in good ear. CD: BC>AC
static functions: antigravity actions
dynamic functions: maintenance of stable visual field as the head moves.
Static Reflexes (2): VCR: vestibulocollic VSR: Vestibulospinal **maintain posture
VCR: -a static reflex 1. Tonic Labyrinth reflex 2. Labyrithne righting reflex 3. ocular torsion reflex
Tonic labyrinthe reflex: -a VCR -continuous (against gravity)
Labyrinthe righting reflex: -muscles fo neck and axial muscles of trunk -keeps head up and keeps posture of body
VSR: -static reflex -on limbs (legs) -helps to keep your stance with changes in body position
Cervicocollic Cerivicospinal reflex: compliment the vestibular reflexes -uses proproceptive signals to contract neck and back/limb muscles
Dynamic Reflex (1): Vestibulo-ocular reflex (VOR)
VOR: -dynamic reflex (eyes) -eye movements are compensatory to head/body movements so can keep focus
release of NT from a vestibular hair cell is dependent on what ion?: calcium!
utriclepedal: stereocilia of ampula in semicircular duct moves TOWARD the utricle: depolarizaiton
utriclefugal: stereocilia of hair cell in the ampulla of semicircular duct moves AWAY from the utricel= hyperpolarization
Olfactory Transduction: G-protein coupled and second messenger mediated
Adequate Stimulus for olfactory: the one odorant molecule that makes the sensory neuron's receptor maximally responsive
Olfactory tract projections: olfactory tubercle entorhinal cortex amygdala piriform cortex
piriform cortex projections: thalamus hypothalamus amygdala frontal cortex
lesion in pathway from thalamus to oribtofrontal cortex: unable to discriminate odors
Pathways to amygdala and hypothalamus: emotional, motivational, and visceral effects of odors (visceral motor reponses can be salivation, gagging, etc.
Specific anosmia: unable to detect one or more specific odorants due to genetic defect in receptor
General anosmia: unable to detect ALL odors ex: cribiform plate fracture infection meningitis, tumors, pshycosis, seizures, drugs, chemicals
Tongue/taste innervations: primary afferents of: 7: ant tongue and palate 9: post tongue 10: epiglottis and esophagus
Gustatory Transduction: Ionic AND second-mesenger mediated (olfaction was only 2nd messenger): get depolarization and chemical transmission
Gustatory Pathways: CN 7,9, and 10 all go to the Nucleus of Solitary Tract, then to VPM, hypothal, or amygdal. VPM goes to insula and then to amygdala.
A: A
Superior Colliculus involvement in Vision: Optic Tract to LGN normally, or sidetrack to superior colliculs where pretectum is located. can cross the posterior commisure or go anterior to PAG and synapse in Edinger-Westphal nucleus to go to ciliary ganglion to operate sphincter muscles: purpose of coordination/modification of optic reflexes (synapses on both R and L sides)
Suprachiasmatic nucleus involvement in vision: SCN is located in the anterior part of the hypothal, immed superior to the optic chiasm. Optic Tract can synapse here rather than Edinger-Westphal n. or the normal LGN. The SCN synapses with the paraventricular n, goes down the SC, sends a symp up to the pineal gland to regulate circadian rhythms.
purpose of GSH in eye: located in lens to maintain proteins in a reduced state (keep the SH from aggregating) -also in retina to form glutathione peroxidase to break down hydrogen peroxide radicals
aldose reductase: converts Glucose to Sorbitol in the sorbitol pathway in the lens, also conversion of Gal to Dulcitol.
glucose cataracts: cloudiness of the lens: can be caused by diabetes: glucose converted to sorbitol which gets stuck in the lens and causes pressure to build up. Then the lens swells: cataract.
galactose cataracts: same principle as glucose/sorbitol, except converte to dulcitol, which isn't metabolized at all. Thus the pathway of cataract formation is FAST.
Cataract formation (3 things): 1. changes in permeablitiy of membranes of lens 2. changes in physical state of proteins (oxidation of SH groups) 3. changes in the enzymatic properties of lens.
glutamine synthetase: 5x in retina than anywhere else (in Muller cells) Purpose: to fix nitrogen and get rid of glutamate
dark current: on in the dark: current that is created by the Na/K pump which uses an active Na/K ATPase to pump Na out and K in, thus creating a current.
glutathione peroxidase: in retina for breaking down hydrogen peroxide from superoxide radicals (radicals formed form the UFA double bonds: in the presence of light, 02 with break the bonds and form radicals)
Selenium: in GSHPx to maintain reduced state with no radicals
without Vit E and Se...: Won't have GSHPx and will get free radicals that destroy the retina
Lens characteristics: 1. low h20 2. high protein 3. grows throughout life (onion). 4. NO blood supply 5. anaerobic metabolism 6. Vit C important in regeneration fo GSH
Retina Metabolism: 1. high 02 and glucose consumption 2. high requirement for protein and phospholipid synthesis
Retinal Phototransduction: light converts Rhodopsin from cis to trans, which activates the G-protein Transducin, which activates PDE, which cleaves cGMP, which now won't open the Na channels, blocking them to stay closed and turning off the current.
molecules that play rolein oxidation protection in the retina:: 1. superoxide dismutase 2. GSH 3. Vit C 4. Vit E 5. Selenium 6. Taurine 7. poss Chromium
dyschromatopsia: inability to distinguish colors (color blindness)
scotoma: small visual field defect
anopsia: larger visual field defects
agnosia: inability to recognize/name objects. Can see it but can't identify it
emmetropia: normal vision
myopia: nearsightedness (in front)
hyperopia: farsightedness (behind)
Astigmatism: multiple focal points bc cornea is not perfectly spherical
macular degeneration: loss of central acuity, still have peripheral vision for ambulatory vision
Retinitis Pigmentosa: loss of night vision bc of loss of peripheral vision
papilledema: swelling of optic disk due to intracranial pressure
glaucoma: loss of rim neuro-retinal tissue (ganglion cell axons)
Optic neuritis: MS!!
acquired color vision deficit: ie. r/g or b/y -can be a sign of macular disease or optic nerve disease (MS)
Ventral pathway of vision (temporal lobe): object recognition
Dorsal pathways of vision (parietal lobe): spatial and movement processing (the Where; visual neglect and motion detection problmes)
If lesion in temporal lobe causing visual defect, what other symptoms could you see?: Superior quandrantopsia with hallucinations and agnosias
If lesion in parietal lobe with visual defect, what associated symptoms might you see?: motor or sensory deficits R-L confusion spatial disorientation visual neglect (inferior quandrantopsia
bitemporal heminopsia: problem with optic chiasm: pituitary tumor
internal opthalmoplegia: iris and ciliary body muscles
external opthalmoplegia: extraocular muscles
Anisocoria: Efferent pathway problem! Can be damage to Iris from Sx, Glaucoma, Trauma Pharmacologic or toxic 3rd nerve palsy, Meniere's disease
dorsal midbrain syndrome: affects elevation of eyes: pretectal area of midbrain. ie. pineal tumor
contralateral sensory neglect syndrom: completely deny that one side of the body is there, so won't shave it, dress it, etc.
Clark's nucleus: involved in Dorsal Spinocerebellar Tract for Unconscious proprioception. primary afferents synapse there to send second order neurons to the cerebellum
the afferents that synapse in the chief sensory nucleus and rostral spinal nucleus of CN V have cell bodies that reside where?: in the trigeminal ganglion, otherwise known as teh semilunar or Gasserian ganglion
Afferents taht synapse int he motor nucleus of CN V reside where?: in the mesencephalic nucleus of CN V
What creates the reflex control of chewing?: unconcious proprioception is detected by fibers whose cell body sits in the mesencephalic nucleus. it then synapses in the motor nucleus of CN V and that nucleus sounds out efferents
neurons with soma in trigem ganglion that are carrying fine touch, vibration, and proprioception synapse where?: in the chief sensory nucleus, or they descend a short ways to the rostral 2/3 of the spinal nucleus of CN V
At what location has all of the trigeminal lemniscus (ventral trigeminothalamic tract) crossed to the contralateral side?: above the mid-pons (where it runs with the ML). All the actually crossing occurs below the mid-pons
Where does the Trigeminal Lemniscus (ventral trigeminothalamic tract) terminate?: in the VPM
Where does the Trigeminal System have descending control?: 1. chief sensory nucleus 2. spinal nucleus 3. VPM
anterior choroidal artery :: Branch of MCA: post limb of internal capsule: affects ALS, DC/ML, and Trigem sensory (everything from VPL and VPM)
Thalamogeniculate and thalamoperforator arteries supply:: branches of PCA that supply the posterior side of the thalamus: VPM and VPL
DC/ML symptoms with lesions: 1. directional sensibility 2. 2-point discrimination 3. texture discrim. 4. vibration sense 5. limb position 6. ataxia 7. graphesthesia 8. astereoagnosis
DC/ML primary afferents synapse....: usually don't!, but if they do, its in III-IV laminae of dorsal horn (otherwise called nucleus proprius)
ALS primary afferents synapse...: lamina I,II, and V (II is substantia gelatinosum), otherwise distributed in Lissauer's tract up or down a few before synapsing)
lateral cervical nucleus: fromt he SCT: spinocervical tract that runs with the DC/ML system (runs in ML)
Points of descending control for DC/ML system:: thalamus dorsal column nucleu (gracilis and cuneatus 3. spinal cord's dorsal horn (where the primary afferents synapse)
substantia gelatinosum with inhibition: contains enkephalinergic neurons that can be stimulated by descending neurons carrying serotonin or noriepinephrine to be inhibitory to pain afferents.
ALS system is served by what kinds of nerves?: Adelta and C
TRP channels: Transiet Receptor Potential Channels: polymodal nociceptors: respond to things like Capsaicin and elicit burning pain (one kind of family of receptors found within the ALS system)
ALS composed of which three tracts?: STT SRT SMT
Lesion of the STT on one side of spinal cord causes:: hypalgesia and therm-anesthesia several segments below the level of the lesion on the contralateral side (bc takes ~3 segments for the secondary (or tertiary) afferent to cross the ventral white commisure)
The STT synapses where? and then synapse in the cortex where?: VPL and primary somatosensory cortex (3,1,2)
Neospinothalamic systme: -STT Adelta fibers -localization and quantitiation -First pain (fast) -when we do hot/cold, pinprick, pinch, etc testing, we are testing this part of the ALS--and use it as a marker for the integrity of the entire ALS
collateral projection of the ALS: collaterals come off the STT to the reticular formation, PAG, and intralaminar thalamus, which create SRT and SMT parts of the ALS
SRT: made by either: 1. collateral fibers from the STT 2. direct secondary or tertiary fibers -both end in the RETICULAR FORMATION
SMT: -fibers end in PAG fibers from: 1. STT collaterals 2. direct seondary or tertiary afferents
Paleospinothalamic system: 1. C fibers from STT 2. SRT 3. SMT -SECOND pain: slow, persistant, annoying -subjective, affective, and motivational aspects of pain
SRT: paleospinothalamic system's component: alerting and arousal -intralaminar thalamic nuclei -hypothalamus -limbic areas
Ventral Trigeminal System: counterpart to ALS -uses slow receptors also: Adelta and C -uses CN V's descending tract and the caudal spinal nucleus (ventral spinal nucleus was used in Trigem Lemniscal System--counterpart to DC/ML
nucleus caudalis: most caudal portion of the CN V spinal nucleus; serves the Ventral Trigem System
VTT: ventral trigeminal thalamic tract: fibers cross midline in medulla, so they have formed the VTT below the level of the mid-pons. Run with the STT of the ALS (which makes sense since its the counterpart)
lesion of VTT at mid-pons will produce an ipsi or contra lesion?: contra: the VTT is substantially formed and compact at the caudal pons. Below the caudal pons (in the medulla) the VTT fibers are still crossing the midline and would then be ipsilateral
a tooth ache would be mediated by...: the non-somatotopic Ventral Trigem System terminations: ie. rather than the normal postcentral gyrus (analgous to the neospinothalamic)this terminates in the limbic system and hypothal via the intralaminar nuclei (thus analagous to the paleospinothalamic) and mediates the SECOND pain: slow and annoying= tooth ache!
The levels of control for Descending Pain inhibition that originates from the PAG and runs in the STT and VTT:: SC dorsal horns (STT) CN V Spinal Nucleus (caudal) (VTT) VPL and VPM
Syringomyelia: fluid filled cavity in the SC that can occur with tumors, congenital defects, or post-truama
Congenital Analgia: peripheral neuropathy -can involve motor, sensory, and autonomic -absence of Ad and C fibers: can't feel pain! -mutation in TRK A gene -can be accompanied by anhydrosis, hyperthermia, and postural hypotension
PAG receives input from:: SMT (also STT, SRT) hypothalamus and limbic
PAG activates what?: 1. Raphe magnus (serotonin) 2. Locus Coerulueus (noriepinephrine) 3. medullary reticular formation 4. parabrachial nucleus -also can involve opiate and non-opiates: morphine and endocannabinoids)
primary vs secondary hyperalgesia: primary: enhanced pain at the site of injury secondary: surrounding the site of injury due to chemical mediators (inflammatory pain)
Pathologic pain: everything except superficial initial pain, so: 1. visceral 2. Deep (muscle cramp, headache) 3. superficial Delayed (slow and persistant)
Allodynia: SEVERE sensitization: to the point where stimulit that is normaly non-painful (non-noxious), becomes very painful= INFLAMMATORY PAIN
Neuropathic Pain: a disease state: caused by an altered receptor, damaged nerve or CNS path, or facilitated CNS transmission -can be persisting or chronic
why can capsaicin ointment be used as a topical analgesic?: receptor desensitization
Thalamic Syndrome/Dejerine-Roussy Syndrome: From inadequate supply from the PCA: thalamus is sensory relay, so you get decreased sensation, but increase pain sensation in face, arms, and legs.
Therepeutic drugs fro neuropathic pain that is poorly controlled by opioids (morphine): Gabapentin Pregabalin tricyclic antidepressants
Complex Regional Pain Syndrom (CRPS): -neuropathic pain with two subtypes, both involve hyperactivity of the sympathetic nervous system (NE) 1. CRPS I: can occur with NO identifying injury 2. CRPS II: had an identifiable nerve injury
Gate control Theory: large diameter fibers can be used to inhibit activity on small diameter pain transmission neurons
primary site of CSF absorption: arachnoid villi -CSF moves across the sinuses via bulk flow

Start Studying!

Deck Info

Number of cards 142

Created By mjfish18