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UTSW Neuro Block 3
UT Southwestern School of Medicine 2010 Neuroanatomy (Block 3 Neuroscience)
| Question | Answer |
|---|---|
| How does the eye accommodate to focusing on distant vs. nearby objects? | Distant: flat lens, relaxed ciliary body. Nearby: round lens, contracted ciliary body |
| What is the difference between fovea and foveola? | Macula Lutea surrounds Fovea (area of high density cones). Foveola = subregion of Fovea w/no blood vessels & thinned neural tissue. |
| What is the purpose of the macula lutea? | Xanthophyll pigments attached to neuronal/glial processes absorb short wavelengths (e.g. UV) to protect the cells. |
| What is normal, short-sighted, and far-sighted vision called? | 1) Emmetropia, 2) Myopia (eye too long/cornea too curved;lens can't get flat enough to diverge entering light), 3) Hyperopia (eye too short/cornea too flat) |
| How many rods and cones are in the human retina? | 90 million rods, 5 million cones -> 95 million total (vs. only 1 million ganglion cells) |
| What is the lifespan of visual transduction disks in RODS? | 10% shed daily (lifespan 10-12 days). 1000 membranous organelles synthesized in soma, move to outer segment, several pinched off & endocytosed by pigment epithelium, broken down & recycled. |
| Where are visual transduction molecules located in rods vs. cones? | RODS: intracellular plates, CONES: modified plasma membrane |
| What is retinal detachment? | Separation of retina from pigment epithelium |
| How are rods different from cones? | 95% of receptors, longer cell, discs = organelles in cytoplasm, more sensitive (night vision), slower to inactivate (lower temporal resolution), signaling saturates, rhodopsin, larger cells (lower spatial acuity) |
| How are cones different from rods? | 5% of receptors, shorter w/conical outer segment, modified plasma membrane, low intensity sensitivity, high spatial & temporal resolution, high [] in fovea, don't saturate |
| How does light intensity affect receptor response? | HYPERPOLARIZATION. Higher Intensity-> greater magnitude & longer duration depolarization |
| Which primary sensory cells (auditory/olfactory/gustatory/visual) fire an AP? | ONLY olfactory. (+ primary gustatory cells are not neurons) |
| Describe phototransduction: | 1) opsin senses light & 11-cis-retinal converts to all-trans, 2) transducin G-protein exchanges GDP for GTP 3) G-alpha activates PDE (alpha/beta subunit dissociates from inhibitory gamma)-> breaks down cGMP-> closes cation Ch-> hyperpolarization |
| How is 1 photon converted to a change in membrane potential in RODs vs. CONES? | ROD: 1 photon/1 mV. (1 photon-> 1 rhodopsin-> 800 transducins-> 800 PDEs activated-> each inactivates 6 cGMP-> 200 Ch's close-> 1 mV change in membrane potential.) CONE: 100 photons/1 mV. |
| How is 11-cis-retinal recycled? | -> all-trans retinAl-> all-trans retinOl-> binding protein carries it to pigment epithelium, reconverted to 11-cis-RetinAl-> same binding protein carries it back to photoreceptor. |
| What is Retinitis Pigementosa? | loss of function mutation in PDE of photoreceptors-> massive Na influx & apoptosis of RODS |
| What are the light sensitivities for blue, green, & red opsins? | blue 437, green 533, red 564 nm. (all use the same 11-cis retinaldehyde). |
| How is orange visual input signaled? | In local region of cones: RED>Green>blue opsin activation |
| What makes 2 colors appear the same? | Same intensity pattern of blue/green/red cone stimulation viewed |
| What is the intensity sensitivity of rods & cones? | 1) SCOTOPIC: pitch black-> starlight (rods), 2) MESOPIC (rods & cones): starlight-> low indoor light, 3) PHOTOPIC (cones) indoor lighting-> brightest sunlight. |
| What happens if someone loses all cones vs. losing all rods? | Cones loss-> legally blind. Rods loss-> night blindness. |
| What is the difference in connections of rods vs. cones on bipolar cells? | ROD: 15-30/bipolar cell (easy activation/low res). CONE: 1/bipolar cell (harder activation/high res). |
| When are photoreceptors most sensitive to changes of intensity? | @ dark-adapted states. Sensitivity decreases @ high baseline illuminations. |
| What is the mechanism for decreased sensitivity of photoreceptors in bright light? | light-> low Ca-> 1) cation Ch increases sensitivity to cGMP, 2) more cGMP is made, 3) more rhodopsin kinase activity-> P'ates & inactivates light-activated rhodopsin |
| How is vision transmitted in the brain? | 1) LGN (CONTRA=layers 1,4,6), 2) SUP retina-> SUP optic radiation temporal-> MED occipital 3) INF retina-> INF optic radiation (Meyer's) parietal, 4) SUP retina -> upper lip & INF-> lower lip Calcarine Cx |
| What do magno vs. parvocellular divisions of the visual system mediate? | M: Movement, Location, Contrast. P: Color, Form, Detail, "Familiar". M-> dorsal pathway, P-> Ventral pathway, but many interconnections + output to the pulvinar nucleus of thalamus. |
| What are synonyms for primary visual Cx? | 1) Calcarine Cx, 2) Striate Cx, 3) Brodmann Area 17 |
| Where is binocular vision first assessed? | In the space between vertically-oriented ocular dominance columns in calcarine Cx (DEPTH PERCEPTION) |
| Where does primary visual Cx send outputs? | 1) Association Cx, 2) Superior Colliculus, 3) Pulvinar, 4) LGN, 5) Pons, 6) Claustrum |
| What results from lesion of an optic nerve? | monocular loss of vision |
| What results from lesion of the optic chiasm? | Bitemporal Hemianopsia: loss of nasal retina information = lateral visual field |
| What results from lesion of the LGN? | Loss of either right vision (left LGN) OR left vision (right LGN) |
| What results from lesion of Myer's Loop? | (Temporal lesion) loss of superior left vision (right lobe) or superior right vision (left lobe) |
| What results from lesion of the superior optic radiation? | (Parietal lesion) loss of inferior left vision (right lobe) or inferior right vision (left lobe) |
| What results from lesion of primary visual Cx? | variable visual losses w/sparing of macular (foveal) vision |
| What visual pathway involves the Superior Colliculus? | IPSI temporal/CONTRA nasal from optic tract or directly from discrete retinal ganglion cells. Via Brachium of the Superior Colliculus. Integration w/primary visual/auditory/somatosensory info. |
| What visual pathway involves the Pretectal Neurons? | Retinotectal pathway. Retinum-> brachium of Superior Colliculus-> pretectal neurons-> posterior commissure & ventral fibers-> BILATERAL Edinger-Westphals-> pupillary constriction of BOTH pupils |
| What visual pathway involves the Hypothalamus? | Subset of Ganglion Cells (no rods/cones)-> light information-> SCN-> PVN, etc.-> lateral column sympathetics-> superior cervical ganglion-> pineal gland: melatonin |
| How many different odors can humans sense and what is the mechanism? | 10k different odors. 1000 odorant receptor genes (~4% of genome), of which 400 true genes, + splice variants. |
| What is the vapor sensitivity of human olfaction? | 1 part in 10^12 |
| What is the structure of the olfactory system? | olfactory epithelium in dorsal posterior nasal cavity-> cribiform plate in frontal bone-> mitral & tufted cells in glomeruli (1000 axons per)-> lateral olfactory tract-> Amygdala, & Pyriform Cx-> Thal, Hypothal, Hippocamp |
| How does the human olfactory system compare to phylogenetically older species? | fewer olfactory neurons, less dense olfactory epithelium, smaller relative size of primary olfactory Cx |
| What cells synthesize mucus in the nasal passages & what does it contain? | Bowman's glands. Mucus contains odorant binding protein that may present odorants to olfactory R's |
| Which variables modify olfaction in humans? | 1) age (acuity declines), 2) male vs. female, 3) healthy people can have <100% recognition & anosmics can perceive some %, 4) TBI -> CN1 axonal shearing & olfaction loss |
| Describe olfactory R's | 7 TM GPCR, one type per neuron, low affinity binding site for odorant, highly variable aa structure but v. conserved |
| How is information from a single odorant receptor type synthesized in the brain? | All neurons w/same receptor type synapse @ the same glomerulus |
| What is the signaling pathway for olfactory signal transduction? | ACTIVATION: 1) GPCR, 2) G.olf beta/gamma, 3) Adenylate Cyclase-> cAMP, 4) cAMP-Gated Cation Ch, 5) Ca-Gated Cl Ch-> further depolarization! (-) FEEDBACK: 6) Ca-Calmodulin-> reduced Cl Ch sensitivity to cAMP, 7) Ca-> out via Na/Ca exchanger |
| What event causes molecular signaling of olfaction & what is the timescale? | UNBINDING of odorant from receptor activates GPCR, lasts seconds |
| What is the specificity of olfaction? | 1) Odorants stimulate ~1/4 of neurons expressing correct R, 2) Multiple odorants can activate the same GPCR on a neuron, 3) topographical map in olfactory bulb |
| What is the Functional Hypothesis of Olfaction? | 1) Discrete odorant stimulates many R's w/diff strength, 2) Ensemble of stimulated cells-> unique pattern of mitral cell activation, 3) brain interprets pattern as unique smell |
| How does meningioma of olfactory groove present? | Foster-Kennedy Syndrome. IPSI anosmia & optic atrophy, CONTRA papilledema (swollen optic disc) |
| What is Kallmann Syndrome? | Developmental disorder: anosmia & hypogonatotropism |
| What is the central pathway for taste sensation? | sensory cell (5HT)-> neuron from autonomic ganglion (7, 9, 10)-> Solitary Nucleus-> Amygdala & Hypothal, OR Solitary-> VPM-> Insula & Frontal Cx |
| Where are the different taste sensations localized? | SWEET anterior, SALTY lateral, SOUR lateral, BITTER posterior, UMAMI ?. Can be multiple types of taste receptors on single cells. |
| What determines sensitivity to different tastes? | high sensitivity to potential toxins, lower sensitivity to common tastes |
| Where are the different types of papillae located? | FUNGIFORM (anterior), FOLIATE (posterior), CIRCUMVALLATE (posterior) |
| How are the different taste sensations signaled molecularly? | 1) GPCR: SWEET T1R2/3, BITTER T2R & Gustducin-> PLC-> TRPM5, UMAMI (aa's) T1R1/3-> PLC-> TRPM5. 2) IONOTROPIC: SALT Amiloride-sensitive Na Ch, ACID H-activated TRP_pkd. |
| What are the branches of the CN's that carry taste information? | 7: Chorda Tympani (ant. 2/3 tongue) + Greater Superior Petrosal (Palate). 9: Lingual (post. 1/3 tongue). 10: Superior Laryngeal (Epiglottis, esophagus) |
| What is a dB? | 1 dB SPL=20*log(P/P0). in humans, P0 = 0.0002 dynes/cm^2 = lowest detectable pressure @ common frequency 1000 Hz (normal speech = 0.2, v. loud = 200). SPL = sound pressure level. |
| What is the relationship b/tw sound & pressure? | increase P 10x (20 dB) -> loudness increases 2.5-4x |
| Why is there a dip in the equal loudness curve @ 1000-3000 Hz? | That is the most sensitive range of freq/intensity, so it sounds louder to us |
| What is the relationship b/tw Pitch & Amplitude/Frequency? | Pitch is correlated but not the same as Frequency. Pitch is less correlated w/Amplitude (decreases w/increasing volume). 2x change in pitch = 3x change in frequency. |
| What is the importance of the head & pinna in sound localization? | 1) Cast a shadow-> intensity difference for high freq tones >3KHz w/wavelength< width of head. 2) Resonator b/tw 2-5KHz (increases intensity x 10dB; freq's for human speech) |
| How does the inner ear amplify sound? | 1) Focuses force from large to small diameter (17x amp), 2) Lever action (1.3x amp), 3) transfers wave from low to high impedance medium |
| What are middle ear reflexes to decrease overly loud stimuli | 1) Tensor Tympani dampens malleus-> stiffens tympanic membrane. 2) Stapedius retracts stapes away from oval window |
| What is the structure of the cochlea? | Spiral ganglion perforates Basilar Membrane that separates Scala Vestibuli from Tympani, Hair Cells on Organ of Corti (b/tw Tectorial & Basilar Membrane) jut into Scala Media. |
| What is the difference b/tw inner & outer hair cells? | INNER 1 row: 95% afferent, OUTER 3 rows: efferent (from superior olivary complex) |
| What is the transduction mechanism that stereocilia use? | 1) Tip Links amplify, 2) Endolymph = high K & +80 mV relative to low K Perilymph, 3) MechanoR's on cilia-> K depolarizes-> Ca Ch's @ base of cell-> vesicle release, 4) Ca-Activated K Ch's repolarize cell |
| What is the electrical activity of hair cells? | Basal Firing Rate + Hyperpolarize/Depolarize in response to sound wave (exact correlation @ low frequencies, 1000 AP's/sec). Basilar moves up-> depolarize, down-> hyperpolarize. |
| How is the location of sounds encoded? | 1) phase locking = compare phase of sound wave @ each ear. 2) Tonotopic Encoding = for mid & high freq (basilar membrane vibrates most @ location dpdt on specific freq) |
| What is tonotopic encoding? | = encodes frequency x physical location & properties of basilar membrane -> vibration. Thinnest @ base of cochlea (high freq), thicker & wider @ apex (low freq) |
| What is the sequence of events in auditory signal transduction? | 1) tympanic membrane-> stapes pushes oval window-> 2) compression wave around Helicotrema (hole that connects scala vestibuli to tympani)-> round window, 3) basilar membrane vibrates (traveling wave) (rarefaction-> suction from stapes) |
| What property of the basilar membrane leads to the tonotopic map? | Basilar membrane is thicker & wider from base to apex-> diff frequencies vibrate basilar membrane in different places (near oval & round windows = high freq stim; apex = low freq stim). Tonotopic map maintained all the way up to the Cx. |
| How do cochlear implants work? | bypass hair cells, stimulate afferent nerves directly, capitalizes on tonotopic map |
| How is sound frequency encoded? | 1)Volley Theory (low freq,=1:1 correspondence phase-locking), 2) Tonotopic Map (mid & high freq) |
| How is sound intensity encoded? | 1) recruit more neurons, 2) increase firing of each neuron, 3) HIGH volume-> recruit neurons that don't normally respond to a freq |
| What is conduction deafness? | When damage to a middle ear-> no air transduction of sound |
| What is sensorineural deafness? | damage to CN8 -> no bone conduction audition. |
| What tests can be done for conduction vs. sensorineural hearing? | 1) Rinne's test (bone & air conduction) tuning fork on auditory bulla (normal = air>bone), 2) Weber's test (conduction deafness) tuning fork @ cranial midline (normal = both ears same). |
| What signals conduction deafness in Rinne & Weber tests? | RINNE: bone>air conduction in bad ear. WEBER: sounds louder in bad ear. |
| What results signal sensorineural deafness in Rinne & Weber tests? | RINNE: air>bone conduction in bad ear & both are decreased. WEBER: louder in normal ear. |
| What are characteristics of efferent auditory inputs? | 1) increases acuity (freq), 2) outer hair cells, 3) otoacoustic emissions NOT the same as tinnitus |
| What is the central pathway for auditory information? | 1) cochlear nuclei synapse, 2) superior olive synapse (mid-pons, many fibers decussate here; some don't synapse), 3) lateral lemniscus contra synapse (some fibers don't), 4) IC (ALL synapse), 5) Medial Geniculate, 6) Auditory Cx |
| What happens when a lesion occurs in the CNS post-cochlea? | Many fibers have already decussated & sound was processed -> general hearing deficit, not deafness of one ear. |
| What does the MSO do for sound processing? | Localization x phase shift (<3K Hz) 1) path lengths; phase shifts, 2) inputs = bilateral cochlear nuclei |
| What does the LSO do for sound processing? | Localization x intensity (high freq). Ant/Vent cochlear-> excites IPSI LSO & excites IPSI MNTB-> inhibits CONTRA LSO. Each LSO compares amt. of inhibition & excitation to determine interaural intensity diff. |
| What does the lateral lemniscus do for sound processing? | Monaural from CONTRA cochlea, Onset & Duration. (Some fibers don't synapse here) |
| What does the inferior colliculus do for sound processing? | 1) auditory space map, 2) socially relevant sounds, 3) frequency comparisons, temporal comparisons (msec time scale for i.e. echoes) |
| What does the MGN do for sound processing? | 1) Input from IC, 2) Freq comparisons, 3) echo: msec temporal comparisons (not phase locking) |
| What does primary auditory Cx do for sound processing? | 1) tonotopic map, 2) columnar inputs (EE, EI), 3) 2ndary Cx (inf)-> complex sounds i.e. Wernicke's, 4) speech recognition (post) |
| When is the developmental window for speech perception & use? | 1) before teens = fluency, 2) after 14 = accent & difficulty perceiving subtle sounds in other languages |
| What do the 2 hemispheres contribute to sound/speech? | LEFT dominant, RIGHT emotional tone/inflection, Wernicke's: convey idea (lesion -> word salad) |
| Which peripheral nerve fibers conduct which sensory modalities? | 1) A-beta: large myelinated 50 m/sec, Vibration/Pressure/Stretch/Touch, 2) A-delta: small myelinated 20 m/sec Touch/Cold/Pain, 3) C: **small unmyelinated 2 m/sec Cold/Warm/Thermal Pain |
| Describe the sensory pathway for Body Hair Neurofibers: | A beta & delta, fast-adapting, neurites in Schwann Cell "sandwich". Sense hair movement but NOT direction. |
| Describe the sensory pathway for Pacinian Corpuscles: | A beta, fast-adapting, naked axon in "onion" corpuscle, v. sensitive, Fast Vibrations (<500 Hz; ideal = 128) Dermis/Subcut, ligaments, joints, pleura, peritoneum, nipples, genitalia |
| Describe the sensory pathway for Meissner's Corpuscles: | A beta, fast-adapting, Slow Vibration <40 Hz), Light Touch, changing P, 2-Point Discrim. Several axons/corpuscle. Dermal papillae of fingers, palmar hand, plantar feet (glabrous hairless skin) |
| Describe the sensory pathway for Merkel Discs: | A beta, SLOW adapting, light static P i.e. for holding object, rapid AP burst + sustained response proportionate to skin indentation. Naked axon against tactile cell. Glabrous hairless skin of fingertips, lips, genitalia, hair follicles |
| Describe the sensory pathway for proprioceptors: | muscle, tendon, joint, ligament. compare agonist/antagonist muscle group info. Ia Spindles (stretch)-> + monosynaptic motoneuron to agonist muscle. Ib Golgi Tendon Organ (tension)-> + polysynaptic antagonist muscle & inhibits agonist muscle |
| Describe the sensory pathway for thermoreceptors: | 1) warm-> activates warm & inhibits cool fibers, & vice versa, 2) slow-adapting, 3) sustained AP's, 4) COLD: A-delta & C, WARM: C only. |
| Describe the sensory pathway for nociceptors: | 1) slow-adapting, 2) free nerve ending, 3) mechanical (painful), polymodal (chemical/mechanical/thermal C-fibers), 4) Visceral Pain R's = stretch sensitive, 5) After-discharge beyond stimulus, Sensitize to chronic stim (esp polymodal)! |
| What is the mechanism for chemoreceptor signal transduction? | GPCR-> adenylate cyclase -> cAMP-> Ch's increase conductance-> depolarization |
| What is the mechanism for mechanoreceptor signal transduction? | stretch/tension-> anchored carb chains pull on membrane-> Ch's increase conductance (depolarization) |
| How does intensity & duration alter neuron firing? | 1) stronger stim-> more AP's & higher freq, 2) longer stim-> longer duration AP train |
| What is sensory adaptation? | decreased generator potential over time |
| How is fine touch achieved in fingers & lips? | more encapsulated mechanoreceptors, smaller receptive fields |
| What is the difference between pain & nociception? | Nociception = perception of injury, or event associated with injury, not necessarily w/pain. Pain = emotionally-sensed hurt associated w/actual/potential/perceived damage. |
| What is it called when an inoccuous stimulus produces pain? | Allodynia (light touch/vibration/temperature). = extreme form of hyperalgesia. |
| What is the most common sensory fiber? What is the most common sensory receptor? | C-fibers (10x more than all other sensory nerve fibers combined), Nociceptors |
| What are the 3 types of dermal nociceptors? | 1) Mechanosensitive nociceptors (A-delta), 2) Mechanothermal nociceptors (A-delta), 3) Polymodal Nociceptors (C) |
| What are the nociceptors? | 1) VR-1 (A-delta & C) heat & capsaicin. 2) VR-2 (A-delta) stronger heat. |
| How does tissue damage alter nociception? | 1) Potentiated nociception w/tissue damage (bradykinin, histamine, prostaglandin), 2) fiber endings release substance P & CGRP to increase the inflammatory response |
| What is the local circuitry of Wide Dynamic Range (WDR) neurons? | 1) excited x A-delta, 2) Excited x C (& inhibits inhibitory interneuron), 3) Inhibited x A-beta (& excites inhibitory interneuron) |
| What is Wall's Gating Theory of Pain? | Because A-beta inhibits Wide Dynamic Range neurons in the pain pathway, rubbing a pain can diminish it |
| How is visceral pain transmitted to the brain? | Dorsal columns, Nucleus Gracilis, Ventral Thalamus, Insular Cx (source of "referred" pain/hard-to-localize pain) |
| How is dermal pain transmitted to the brain? | 1) spino/trigeminothalamic tracts, VPL/M, primary somatosensory Cx -> LOCATION of pain. 2) spino/reticulothalamic tracts, dorsal thalamus, supllementary motor/PFCx/Association Cx/Limbic -> NATURE of pain. |
| How is pain modulated centrally? | Cx/Amygdala/Hypothal/Brainstem-> Periaqueductal Gray-> Parabrachial Nucleus/Reticulum/Locus Coeruleus/Raphe Nucleus-> dorsal horn modulation |
| What is the role of endogenous opioids on pain sensation? | CNS activates interneurons containing Enkephalin/Endorphin/Dynorphin -> axo-axonal inhibition of C-fibers on dorsal horn neurons |
| Where is the membranous vestibular labyrinth? What does it contain? | Petrous portion of temporal bone, inside the bony labyrinth. Contains anterior/horizontal/posterior semicircular canals + utricle & saccule otolith organs. |
| What fluids are located where in the vestibular labyrinth? Which fluid stimulates hair cells? | Endolymph (high K low Na) in membranous-> stimulates hair cells. Perilymph (low K high Na) outside membranous, in bony. |
| How do hair cell ion channels open & close in the vestibular system? | Stereocilia TOWARD Kinocilium = OPEN (K-in depolarizes). Kinocilium TOWARD Steriocilia = CLOSED. Baseline activity b/c mid-position = some Chs open. |
| What are the structures supporting the vestibular hair cells? | macule where hair cell bundles are imbedded in gelatin layer topped x otolithic membrane (w/otoconia CaCO3 crystals). Hair cells on either side of striola face opposite directions. |
| What is the orientation of the macula in the utricle vs. the saccule? | Utricle: horizontal. Saccule: vertical. Mirror images on each side of the head. |
| What do the otolith organs sense? | Static position (firing = slightly lower), Dynamic Movements |
| What do the semicircular canals sense? | Rotation, Angular Acceleration |
| How do semicircular canals sense? | Endolymph movement displaces cupula-> signals through hair cells. Ampulla (bulb @ base of semicircular canal) has epithelium, hair cells, crista, cupula (gelatin around hair bundles) |
| Which modalities must be intact to maintain posture? | Vestibulocerebellar (lesion-> swaying posture, even w/good visual input & proprioception). Either good vision/proprioception are permissive for maintaining posture. |
| What is the pathway for the lateral gaze vestibulo-ocular reflex? | Turn LEFT-> left horizontal canal activated/right inhibited. Left Medial Vestibular Nucleus-> + CONTRA Abducens Nucleus, - IPSI Abducens Nucleus, - CONTRA Oculomotor nucleus. |
| How do you test the vestibulo-ocular reflex? | Ask patient to turn head rapidly to one direction & see if eyes maintain gaze. |
| What is the pathway for vertical gaze vestibulo-ocular reflex? | UPWARD head movement-> + posterior canals-> + CONTRA inferior rectus & IPSI superior obliques. DOWN head movement-> + anterior canals-> + CONTRA inferior oblique & IPSI superior rectus. |
| What is Nystagmus? | Slow drift of gaze, then rapid correction. Caused by spinning & suddenly stopping-> eye movement in opposite direction, or error in vestibular afferents. |
| What causes Nystagmus? | Vestibular afferents fire more on one side-> + CONTRA lateral rectus + IPSI medial rectus |
| How is Nystagmus clinically induced? | Caloric Test (cold water in ear canal-> changes thermal fluctuation of endolymph-> decreased vestibular firing in that canal OR hot water in ear-> increased vestibular firing). eyes move to cold side. |
| What happens during right-sided Caloric Test of a normal person? | Cold in right ear->left vestibular fires more-> right CN6 & left CN3 activate-> both eyes drift right. Right eye field signals left Parapontine Reticular Formation-> rapid left correction. Vomiting. |
| What happens during right-sided Caloric Test of someone w/impaired corticobulbar signaling? | Eyes drift right but there is no correction. |
| What happens during right-sided Caloric Test of someone w/lesion in ascending MLF or midbrain? | cold right ear-> CN6 activated on right, but no signal to CN3 = internuclear ophthalmoplegia (INO) (only right eye moves left, i.e. eye that is supposed to move to midline doesn't) |
| What happens during right-sided Caloric Test of someone w/lesion in vestibular nerve/organ/nucleus or pons? | cold right ear-> no FX |
| What is the pressure @ which the tympanic membrane ruptures? | 160 dB (pain @ 140 dB) |
| What is the relationship between sound frequency & wavelength? | Higher Frequency, Lower Wavelength. |
| What is the relationship between physical pressure & loudness? | If pressure increases x 10 (20dB), loudness increases 2.5-4 fold |
| What is the equal loudness curve? | v. low & high frequencies have to be much louder to detect it. |
| What is special about the frequencies that human hearing is attuned to? | 1-5k Hz. Impt't for distinguishing human speech consonants. |
| Where do hair cells & stereocilia reside? | basilar membrane houses soma, tectorial membrane = where stereocilia are attached. 1 row afferent, 3 rows efferent hair cells on basilar membrane. |
| How do hair cells respond to stimulation? | Sinusoidal change in membrane potential (after 2KHz, just general depolarization)-> change in shape & size of cell. may be efferent lateral inhibition or efferent excitation of stimulated hair cells to increase their response to sharpen tone. |
| Which fluids are located where in the cochlea? | Perilymph: Scala Tympani & Vestibuli. Endolymph: Scala Media. |
| What do Types Ia, Ib, II fibers innervate? | Ia: muscle spindles (tendon reflex), Ib: Golgi Tendon, II: vibration/proprioception |
| What do small sensory fibers Type III & IV innervate? | III: temperature & fast pain, IV: slow pain |
| What are some examples of large fiberopathies? | Tabes Dorsalis (syphilis), B12 deficiency, Guillain-Barre. Sensory Ataxia & Areflexia. |
| What are some examples of small fiberopathies? | Diabetes, Amyloidosis, HIV. Loss of pin-prick & heat sensation + neuropathic pain + normal reflex. |
| What proprioceptive event goes on when lifting weights for biceps? | Muscle contracted = spindle activity low, Huge force on tendon -> Golgi Tendon organ inhibits muscle |
| How do you test muscle & tendon proprioception? | Have someone stand still, feet together, with eyes closed. See if they fall over = Romberg Sign. |
| What is the pain called that persists after a peripheral nerve injury? | Causalgia |
| What is abnormally diminished pain perception called? | Abnormally low sensation/pain perception. = reflex sympathetic dystrophy = complex regional pain syndrome (CRPS) |
| Where do nociceptive fibers synapse? | 1) Spinoreticular: reticular formation (arousal/wake-up), somatosensory Cx, 2) Spinomesencephalic: periaqueductal gray-> hypothal, Frontal Lobe & Limbic, 3) Spinothalamic: somatosensory Cx |
| Where do pain fibers synapse in the SC? | Lamina II (Types 3 & 4 pain fibers) |
| Where do spindle & GTO sensations travel in the SC? | anterior horn |
| Which pathway associates emotion with pain sensation? | spinomesencephalic tract. also causes autonomic activation (sweating, goosebumps, etc.) |
| In what situation do Type I & II peripheral sensory fibers synapse in the SC? | for spinal reflex pathways, e.g. GTO & Spindle reflexes. |
| What are characteristics of visceral pain? | Poor Localization, Emotional Context, Referred |
| What causes pain to be "referred"? | Visceral Nociceptors-> synapse @ DRG-> synapse @ SC central gray-> dorsal columns WITH BODY TOUCH FIBERS-> limbic & primary somatosensory Cx (no somatosensory Cx allocated to guts, so referred) |
| What is the Wall Theory? | Gating theory for pain sensation. Wide Dynamic Range neurons project in anterolateral spinothalamic tract. Non-painful stim in painful area inhibits (gates) WDR pain relay. |
| What is odd about C & A-beta synapses on Wide Dynamic Range (WDR) neurons? | C inhibits inhibitory interneuron but stimulates WDR (increased gain). A-beta mechanoR's mostly EXCITE inhibitory interneuron & stimulates WDR-> net inhibition. |
| What are central controls of pain sensation? | Somatosensory Cx-> Amygdala, Hypothal, Periaqueductal Gray -> midbrain nuclei-> Dorsal Horn interneuron activation to inhibit WDR neurons. |
| What is the neurotransmitter used by inhibitory interneurons? | Enkephalins (use opioid R's) |
| What happens when C-fibers are damaged? | A-beta fibers change gating to activate pain in WDR neurons. Allodynia (non-painful stimulus now feels painful) |
| What happens when A pain fibers are damaged? | C-fiber inputs to WDR neurons are never inhibited (x A-beta) -> chronic pain. |
| What are 3 ways for patients to explain pain? | 1) Likert Scale (1-5 w/faces), 2) Visual Analog Scale (mark on 10 cm line how bad is pain), 3) Pain Drawings (free form) |
| What is the goal of eye movements in vestibulo-ocular sensation? | Foveation: putting the image on the fovea (macula) |
| When head & eye movements are aligned, what is that called? | Cancellation of the VOR (vestibulo-ocular reflex) |
| How does cerebellar degenerative disorder present? | Loss of head-eye coordination (VOR or cancellation) -> abnormal saccadic eye movements to catch up between head & eye directions. |
| How many sensory organs determine angular movements of the head? | 6 (3 semicircular canals/ear: horizontal, ant, post) for Angular movements. + 4 (Utricle & Saccule for Linear movements). |
| Which semicircular canal registers head movement down, up, or to the side? | Ant: down (eyes move up), Post: Up (eyes move down), Horizontal: side |
| What are Circular Vection or Corealis Effects? | When visual inputs give the sensation of movement. Linear vection = sensation of moving forward/back, Circular = sensation of rotating. Visually static, but sensation of movement-> nausea/vertigo. |
| Neurophysiology of semicircular canal angular & linear accelerators is based on what? | hyperpolarization when stereocilia move away kinocilium, & depolarization when stereocilia move toward kinocilium + K influx |
| What is the lateral Vestibulo-Ocular Reflex? | endolymph in horizontal canal, stereocilia-> kinocilium, firing, CN8 in internal auditory meatus, MEDIAL vestibular nucleus, Abducens nucleus (6) +CONTRA & -IPSI, Nucleus of 6-> + CONTRA oculomotor nucleus (3) |
| What are the 2 types of neurons in the Abducens nucleus? | 1) CN6 projection neurons, 2) neurons that excite contralateral medial rectus region of Oculomotor nucleus (III) via MLF |
| What info is transmitted in MLF? | Saccades, Smooth pursuit eye movements, vestibulo-ocular reflexes. (few exceptions, but don't need to know) |
| What are the 3 visual yoke-pairs? | 1) lateral & medial rectus, 2) inferior rectus, superior oblique, 3) superior rectus, inferior oblique |
| What structure can override the VOR? vestibulo-ocular reflex | flocculus of the cerebellums |
| How does an abnormality of the saccule present? | feeling of floating above the ground, lightness (vertically-oriented organ) |
| How does an abnormality of the utricle present? | feeling of veering to left/right |
| What is the major structural difference between the semicircular canals & the utricle/saccule | macula with OTOLITHS instead of christae with ? |
| If patient has true horizontal vertigo, what nystagmus is present? | both eyes slowly move toward lesion, then beat back to center. |
| What happens with inflammation of the 8th nerve? | = vestibular neuritis, happens w/basilar meningitis. reduces activity of nerve -> bias of activity on opposite side. |
| How is nystagmus identified? | via FAST beat (even though slow phase is more indicative of a particular disorder) |
| Where does the fast phase of nystagmus come from? | Cerebral Hemispheres. CAN'T HAVE FAST PHASES WITH COMA! |
| Why does the patient vomit who is faking coma and is given a caloric test? | chemosensitive trigger zone in brainstem also, affected by caloric test |
| What does the slow phase of nystagmus indicate? | Moves towards the side of the paretic lesion (brainstem lesion). Due to brainstem defect. |
| What is the result of a lesion in the 6th nerve fascicle? | weakness in lateral rectus. eye moving toward midline fine, eye moving laterally is weak. |
| What is the result of a lesion affecting the abducens nucleus? | affects projection to lateral rectus & interneuron to medial rectus -> neither eye can move in one direction (gaze palsy) |
| What is the result of a lesion affecting the abducens & MLF on one side? | Can't look away from the lesion w/both eyes. Can't look toward lesion side w/contra eye (1 1/2 syndrome) |
| Why is Acoustic Neuroma a misnomer? | 1) Arises in vestibular system, not cochlea, 2) Schwannoma not neuroma. Occurs on 8th nerve, can cause vertigo & dizziness. |
| What is the lateral vestibulo-spinal tract? | Lateral Vestibular Nucleus -> SC -> antigravity & balance system motoneurons (MLF->cervical SC for head & neck movements) |
| What is the vestibulo-thalamic tract? | CN8-> CONTRA thalamus-> CONTRA primary somatosensory Cx (accelerators in ear -> vestibular Cx) = conscious sensation of balance |
| What is the cause of benign positional vertigo? | Utriculus (w/macular membrane & hair cells) loses otolith that migrates into posterior semicircular canal-> endolymph moves in opposite direction-> reverses polarity of signaling |
| What is the signaling pathway when an otolith migrates into the posterior semicircular canal & the head is raised? ???? | 1) abnormal depolarization in affected ear, -> + CN8 -> + right vestibular complex -> + CONTRA nuclei of 3 & 4 -> CN4 crosses back to + IPSI superior oblique, CN3-> CONTRA inferior oblique |
| Which eye muscles are "in-towarder" vs. "ex-towarder"? | superior oblique = depressor & in-towarder (upper pole-> toward nose), inferior rectus = depressor & ex-towarder (upper pole-> away from nose) |
| What is the Dix Hallpike test? | Tests BPPV. Turn head rapidly to right, lower below plane of table, see nystagmus, ask if room spinning, when resolves flip head rapidly to other side (Apley Maneuver). Ask them to get up on all fours. Patient sleeps upright for 3-4 days. |
| How does the Dix Hallpike maneuver work? | resituates stone away from hair cells (deeper in canal, comes back onto macular membrane) (long arm of posterior canal next to utricle) |
| If a lady turns onto right side & notices vertigo for 15 sec, & comes into clinic, do Dix Hallpike & find tortional vertical nystagmus, what is the diagnostic? | BPPV, do Apley Maneuver to reposition particle back onto macular membrane |
| What if you strongly suspect benign positional vertigo & you do the Dix Hallpike & Apley, but vertigo does not go away? | Otolith gets stuck on a component of semicircular canal (e.g. cupula) -> cupulolethiasis. Vibrate mastoid to dislocate. |
| How does one ear control both eyes? | Cross, & Double Cross paths |
| Which eye muscles do intorsion vs. extorsion, & when are the various muscles better/worse @ elevator movements? | uppers = intorsion, lowers = extorion. sup/inf rectuses best @ elevator movements when eye is abducted. sup/inf obliques best when eye is adducted. |
| What does the anterior semicircular canal mediate? | moves eyes up as head moves down |
| How do you achieve eye movement directly up? | inferior oblique-> elevation & extorsion, superior rectus-> elevation & intorsion. both together-> directly up |
| What characterizes a supranuclear lesion? (outside the final pathway) | Head movements-> desired movement of eyes overcomes decrement (or, cover one eye & other works fine) |
| What is a skew deviation? | Eye misalignment not due to weakness: rolling of eyes, tilting of head. Supranuclear vertical misalignment of the 2 eyes that can be overcome w/testing the muscles (muscles themselves are not weak, but brain is tricked) Cover 1 eye, & other works fine. |
| What do the linear acceleration organs give information on? | anti-gravity (upright), alignment of eyes, spatial orientation |
| What is a vestibular "matched defect"? | BOTH 8 nerves lesioned. No vertigo/nystagmus. Imbalance, Impaired dynamic visual acuity, VOR gain, saccades w/rapid head movment. WORLD IS JIGGLING: Oscillopsia (illusion of movement). Can be caused x aminoglycosides (antibiotics) |
| What are some causes of Oscillopsia (illusion of movement)? | 1) Bilateral Vestibular nerve injury (matched defect), 2) eye muscle weakness, 3) Nystagmus |
| What are symptoms of otolith linear accelerator organ disorders? | eye movement linearly, eye tilting/floating, ocular torsion reaction. SIMPLIFIED: movement of the head, elevation of the eye. |
| What is the most common cause of vertigo? What is the most worrisome cause of vertigo? | MOST COMMON: BPPV benign positional paroxysmal vertigo. MOST WORRISOME: Stroke! vertigo due to TIA's |
| What information can duration of vertigo contribute to a diagnosis? | Duration of: 1) SEC's = BPPV, 2) MIN's = VBI/Migraine/Ictal, 3) HOURS = Meuniere's, 4) DAYS = Neuritis/Labyrinthine Infarction (vertigo w/out hearing loss for TIA's, until stroke-> hearing loss) |
| What is the second most common cause of vertigo? | Vestibular Neuritis |
| What is phobic postural vertigo? | Someone has recent vestibular event that resolves on its own over >several weeks, patient's vestibular system adapts & now the adaptation is maladaptive -> subjective balance disturbance, anxiety, fatigue, vertigo in sensory-rich environments |
| If a patient presents with unilateral hearing loss & dizziness, what is a likely cause? | STROKE. Hard to get 1-sided hearing loss, unless cochlea is affected. 2/3 of posterior circulation strokes-> vestibular problems. |
| What is the difference in blood supply to the cochlea & vestibular system? | Cochlea gets multiple redundant blood supplies from AICA (from basilar). Vestibular system = end-organ gets few blood supplies. |
| What's the trouble with using aminoglycosides? | No way to predict who will have ototoxicity -> matched vestibular defect |
| How do you measure VOR gain? | Hamagyi head thruse (high acceleration movements, short, quick) |
| What is Horner's Syndrome? | small pupil, some ptosis (from sympathetic innervation of Muller's muscle), impaired sweating of upper 1/2 of the face, can be caused by mass in apex of lung. |
| What are the most common symptoms of MS? | 1) optic neuritis, 2) myelitis (partial SC syndrome), 3) have to run to the bathroom to urinate (hyperreflexia), 4) chronic fatigue |
| What are symptoms associated w/migraine? | photophobia, nausea, pulsatile headache, nystagmus of all sorts (central type) |
| What is an Arnold-Chiari Malformation? | Tonsillar herniation that is made worse x high P (e.g. cough, valsalva, laugh, sneeze). Nystagmus w/downbeat, hoarseness, postural dysequilibrium. |
| What are the causes of hyperventilation-induced vertigo? | 1) vestibular schwannoma compressing CN8, 2) vascular compression , 3) perilymphatic fistula, 4) MS |
| What are the signs of perilymphatic fistula? | valsalva/pressure on outer ear, loud noises, swallowing, Hennebert's sign (puff of air on trachea), Tulio's sign |
| What are signs of a lesion of CN3? | 1) Down & Out! (only SO & LR remain intact -> eye abducts & looks down w/some intorsion). 2) ptosis. 3) Mydriasis (pupillary dilation), 4) far-sightedness (relaxation of ciliary muscle-> lens flattens-> far-sighted vision) |
| What does the Edinger-Westphal nucleus mediate? | pupillary constriction (circular muscle), + ciliary muscle contraction (round lens-> near-sighted viewing) |
| Which cranial nerve is most susceptible to damage after head injury? | CN4: longest peripheral CN. Exits posterior & innervates ONLY CONTRA SO. |
| Unilateral weakness in CN3 muscles is most likely due to damage of the nerve or of the nucleus? | NERVE. CN3 nuclei are located so close together that it is highly unlikely that only 1 will be affected. |
| Lesions to which Cranial Nerve Nuclei are almost always bilateral? | 3,4,6, & MLF |
| What most likely causes loss of all muscles to one eye? | peripheral nerve lesion b/c CNs 3,4,6 all run along same pathway |
| Which inputs are required for saccadic eye movements? | Brodmann 8 (frontal eye field) + superior colliculus |
| What is the Near Triad? | crossed eyes: 1) eyes converge (MR, CN3), 2) Lens rounds (ciliary muscles, EW-> CN3), 3) Pupil constricts (Pupillary sphincter, EW->CN3 |
| What is the stimulus for the Near Triad? | nearby blurry image-> Visual Cx-> occipito-mesencephalic tract |
| What is the visual system sign of CNS syphilis***? | Argyll-Robertson pupil: small pupil unresponsive to bright light, but responsive to the Near Triad. A-R = "Accommodation Retained" |
| Which nerves provide sensation to the outer ear? | CNs 5, 7, 9, 10 (Pain from X-> Spinal Nucleus of 5) |
| Which nerves provide sensation to the neck & back of the head? | Cervical spinal nerves 3 & 4 |
| What is the pathway for mandibular proprioception? | INPUTS: jaw joints, muscles of mastication, teeth. CELL BODIES: Mesencephalic Nucleus of 5. OUTPUTS: motor nucleus of 5 (reflex of chewing) & eye muscle nuclei. |
| What is the pathway of tactile information from the face? | 1) Chief Sensory Nucleus of 5, 2) Spinal Nucleus of 5 |
| What does the Motor Nucleus of 5 supply? | Mastication Muscles, Tensor Tympani |
| What is the relationship of the Motor to the Mesencephalic Nucleus of 5? | Motor nucleus = more ventral |
| What structure do the root fibers of 5 pass through? | Middle Cerebellar Peduncle |
| What type of nucleus is the nucleus solitarius? | Visceral Afferent (sensation of viscera & pharynx, taste) |
| What type of nucleus is the Salivatory Nucleus? | Visceral Motor (superior salivatory = CN5, inferior salivatory = CN7) |
| What type of nucleus is the Motor Nucleus of 7? | Somatic Motor |
| How is the Motor Nucleus of 7 divided, and what innervates each? | 1) Dorsal section-> CONTRA inputs to Lower Face, 2) Ventral section->BILATERAL inputs to Upper Face. NOTE: CNS lesion-> only CONTRA lower face droopiness. |
| What causes Bell's Palsy? | Lesion of the Motor Nucleus of 7 or its root. Can still chew! Cannot close IPSI eyelid (orbicularis occuli). Hyperacusis (hypersensitive to loud noise) = no IPSI stapedius control. Whole side of face affected. |
| Which glands are innervated by CN7? | Lacrimal (tears), Submandibular, Sublingual (NOTE: Parotid gland innervated x CN9!!!) |
| Which CN conveys taste from the glottis? | CN10 |
| Which CN enters b/tw the inferior olive & inferior cerebellar peduncle? | CN9 |
| What structure houses the nucleus ambiguus? | reticular formation |
| What do CN9 fibers from the nucleus ambiguus do? | 1) BILATERAL stylopharyngeus (raises pharynx), 2) swallowing (w/CN10 & 12) |
| What do CN9 motor fibers from the salivatory nucleus do? | parotid gland |
| What sensory information is carried in CN9, and to which nucleus? | SOLITARIUS: 1) all sensation from pharynx & posterior tongue, afferent gag reflex, 2) BP from BILATERAL carotid sinus (unilateral lesion doesn't affect BP), 3) Taste from posterior 1/3 tongue, 4) Pain from external auditory meatus |
| What happens if the tongue is paralyzed on the right? | Deviates to the RIGHT!!! "Lick the Lesion" caused by CONTRA Cerebral Cx lesion |
| Which nucleus slows the heart & what else does it do? | Mainly Ambiguus (also motor to levator veli palatini, esophagus, larynx, pharynx), also Dorsal Nucleus of the Vagus (increases Peristalsis & parasympathetic digestive secretions). |
| Where do thoracic & abdominal viscera sensations get processed? | Solitarius (via CN10) -> outputs to dorsal motor nucleus of 10 for visceral control |
| What is the reflex loop for swallowing? | Nucleus Ambiguus. CN9 dilates pharynx to permit food entry. CN10 & 11 constrict pharynx to force bolus down. |
| Which nucleus provides major motor innervation of the pharynx & larynx? | Ambiguus |
| Which CN's have which role in swallowing? | 9 dilates pharynx, 10 & 11 activate constrictors to force food downward. |
| Which CN controls voice? | CN10 from nucleus ambiguus to larynx (lesion -> dysarthria = hoarseness) |
| Where is the Accessory Nucleus located? | Cervical SC levels 1-6 (bulbar portion of CN11-> pharynx & larynx) |
| Where do CN11 fibers exit the SC? | mid-laterally b/tw sensory & motor spinal roots |
| What does the spinal portion of CN11 do? | trapezius & sternocleidomastoid innervation. Shrug & Turn head to opposite side |
| Which lesions can alter voice? | Unilateral lesions of Ambiguus |
| Which nucleus mediates swallowing (deglutition)? | Ambiguus (9,10 & Bulbar 11, 12) |
| Which nucleus mediates phonation? | Ambiguus (10 & Bulbar 11) |
| Which nucleus mediates taste? | Rostral Solitarius (7, 9, 10) |
| Which nucleus mediates thoracic/abdominal visceral afferents? | Solitarius (10) |
| Which nucleus mediates parasympathetic motor thoracic/abdominal viscera? | Dorsal Efferent Nucleus of 10 |
| Which nucleus mediates touch sensation from the pharynx? | Solitarius (9 & 10) |
| Where do the root fibers of CN11 arise, and where do they exit the SC? | arise in Ventral Horn, exit SC Mid-Laterally |
| What is a motoneuron pool? | All the motoneurons innervating the same muscle. Soma @ different levels of the SC. |
| What is the spatial organization of motoneurons in the SC? | Flexors Dorsal, Extensors Ventral, Axial Medial, Distal Lateral (Rexed Lamina 9) |
| What is a motor unit? | 1 neuron + all the extrafusal muscle fibers it innervates |
| When do muscle AP's begin to fuse? | ~10 Hz ->-> plateau (tetanus) (smoothing effect in whole muscle recordings = b/c not phase-locked) |
| Which muscle fibers are recruited first? | smallest (SR, slow fibers), then FR (intermediate size) then FF. Each type increases firing rate as you recruit larger soma neurons. |
| What are characteristics of lower motoneuron disorders? | 1) focal atrophy & wasting of affected muscles, 2) fasciculations (due to denervation), 3) weakness, 4) decreased tendon reflexes |
| Where does the bulk of central input and peripheral sensory input go to in the SC? | inhibitory interneurons |
| How do you get a patient to show a stronger reflex? | Ask them to flex another muscle -> gain increased in desired reflex |
| What is a difference in the structural arrangement of GTO's vs.spindles? | Spindles arranged in parallel (detect length), GTO's arranged in series (detect force). large myelinated fibers. discharge faster w/increased signal. |
| What do gamma motoneurons do? | innervate intrafusal muscle fibers -> contraction @ same time as alpha fibers to fine-tune sensitivity of detection (spindles can adapt to being slack) |
| What is alpha-gamma coactivation? | both alpha & gamma neurons activated x descending central inputs |
| What is the Hoffman Reflex? | H-wave stimulated @ lower intensities but longer latencies than the M reflex, due to 1a spindle fiber recruitment to same muscle (agonist) |
| What is the Golgi Tendon Organ pathway? | Ib afferent (prevents muscle damage) -> interneurons-> inhibits agonist muscle & activates antagonist muscle |
| What is the Renshaw Cell? | Glycinergic interneuron that receives input from collateral branch of motorneuron-> 1) inhibits self (temporally limits duration of motor response)= RECURRENT INHIBITION. 2) Inhibits antagonists as well (inhibits 2ndary inhibitory interneuron) |
| What is the cutaneous nociceptor reflex in the leg? | polysynaptic reflex -> flexors activated, extensors inhibited. Opposite occurs on other leg. |
| What is the type 1a spindle reflex? | STRETCH REFLEX. monosynaptic, excitatory to agonist (+) & to inhibitory interneuron to antagonist (-) |
| What do intraspinal rostral-caudal projections do? | coordinate all limbs (travel medially): long-distance, short-distance. bilateral connections. |
| Why are the vestibular nuclei like a displaced deep cerebellar nucleus? | receive DIRECT projections from Purkinje cells |
| Where do spinocerebellar efferents to the red nucleus travel next? | interposed & dentate nuclei of cerebellum -> CONTRA red nucleus -> cross back to IPSI rubrospinal tract (fine motor control, distal hand muscles) |
| How does the cerebellum alter motor patterns? | Decreases strength of motor pathway |
| What are firing patterns like in cells of the cerebellum? | Parallel fibers = vigorous activity due to excitation tunes mossy fiber input. Climbing fiber activity infrequent, only active when system performs poorly (error detector!)-> complex spike in Purkinje cell. |
| Where do climbing fiber inputs come from? | CONTRA inferior olive, carrying info from IPSI body |
| How does motor learning work in the cerebellum? | Purkinje cell = coincidence detector for climbing fibers + parallel fibers. Climbing fibers inhibit parallel-> purkinje synapse. |
| When the monkey's unilateral LR tendon is damaged and the other eye is patched, how is it that the damaged eye is able to jump to target again in a few days? | tendon still damaged (hasn't healed) but central input to the CN6 nucleus increases |
| What happens if you lesion the tendon to the LR of one eye, & lesion the IPSI vermis of the cerebellum? | The eye can never adjust to damage to the tendon, i.e. never fixates on visual target with a single movement, requires step-wise eye movements. |
| What cerebellar lesion is common in MS? | cerebellar peduncle demyelination disorders |
| What happens if there is a midline lesion in the human cerebellum? | Vermal-> abnormal eye movements, balance, Truncal Ataxia. Paravermal-> Appendicular Ataxia, Intention Tremor, Overshoot (dysmetria), impaired rapid alternating movements, hypotonic (loss of rubro- & corticospinal inputs), "scanning cerebellar speech" |
| What happens if there is a lateral lesion in the human cerebellum? | problems with complex motor plans, hand coordination, memory |
| What are the 3 things Dr. Cannon wants us to remember about the cerebellum? | 1) cerebellum-> motor performance coordination, 2) cerebellum adapts/learns & fine-tunes, 3) cerebellum controls IPSI body!!! |
| Why do cerebellar lesions have IPSI effects? | cerebellar Purkinjes-> IPSI dentate-> CONTRA thalamus & red nucleus-> CONTRA Cx-> IPSI corticospinal (decussate @ lower medulla) |
| Where do the 3 distributions of CN5 exit the skull? | V1 Superior Orbital Fissure, V2 Foramen Rotundum, V3 Foramen Ovale |
| What passes through the jugular foramen? | CNs 9, 10, 11 |
| Where are the eye muscles best @ elevator movements? | sup/inf rectus -> 23 degrees abducted. sup/inf obliques 51 degrees adducted. |
| What eye motions do the eye muscles make? | IO: elevator, extorter. SO: depressor, intorter. **all SUPERIOR muscles are in the IN crowd (INtorters!) & vice versa for inferior muscles. |
| What types of neurons are located in the abducens nucleus? | 1) direct projection to LR, 2) interneuron projecting via MLF to contralateral nucleus of 3. |
| What are the 2 muscles innervating the eye lid? | levator palpebrae superioris (CN3), Muller muscle (sympathetic innervation; doesn't do much work). |
| What innervates the ciliary body? | CN3-> + ciliary muscle -> -zonules -> lens becomes round for nearby viewing |
| How do people tilt their head for better vision when a CN4 lesion? | AWAY from the High Eye (unilateral loss of SO) because other eye muscles of eye reflex counter-roll are intact. |
| What does MLF lesion cause? | Adduction Failure (no connection b/tw CN3 & 6 for conjugate deviation of the eyes) |
| What is the signaling pathway for conjugate deviation of the eyes? | Cx (smooth pursuit, conscious saccades), vestibular -> CONTRA PPRF -> IPSI Nucleus of 6-> CONTRA Nucleus of 3 |
| What is found in the midline of the tegmentum of the brainstem? | MLF, PPRF, nucleus of 6 |
| What does a left INO (intranuclear ophthalmoplegia) cause? | = lesion b/tw CN6 & CN3. When right eye looks left, info from the frontal visual field cannot reach the right CN3 MR muscle, so left eye still looks straight. |
| What is the pathway for consensual pupillary constriction? | CN2 carries light information to midbrain (bipasses LGN) -> Edinger-Westphal -> bilateral CN3 reflex (parasymp to ciliary ganglion to pupil meiosis (constriction)) |
| What is the swinging flashlight test used for? | Shows afferent pupillary defect = lesion of retina/demyelination due to i.e. MS. Shine flashlight in 1 eye then other, observe paradaoxical dilation of affected pupil (really both constric, but affected constricts less due to slower signaling). |
| What is Argyll-Robertson pupil? | =light-near dissociation. = small bilateral pupils constrict poorly to light, but well to near stimulus (CNS syphilis) |
| Where are sympathetic neurons located & where do they synapse? | hypothalamus, brainstem, spinal cord. synapse @ interomediolateral column of thoracic SC. |
| What is the sympathetic pathway for pupil dilation (mydriasis)? | sympathetic neuron in CNS-> interomedial column of SC synapse-> superior cervical ganglion synapse-> travel w/internal carotid to cavernous sinus-> pupillary dilater, Muller, sudomoter (sweat) for 1/2 face |
| What causes Horner Syndrome? | =unilaterally impinged sympathetic input to eye. Caused by Pancoast Tumor (in apex of lung) or anything that compresses the sympathetic pathway peripherally. |
| Where does C2 sensation on the head begin? | behind the lambdoidal suture, against V1 region |
| What muscles does the trigeminal nerve innervate? | V3: Masseter, Pterigoids, Tensor Tympani, Tensor Villi Pallatini. |
| What is the blink reflex for sensation on the cornea? | CN-V1-> BILATERAL CN7-> BILATERAL orbicularis occulis-> blink |
| What happens w/unilateral lesion of CN5? | 1) Lost Eyeball sensation (blink reflex), tickling of nasal mucosa (sneeze reflex) + noxious sensation of inhaling ammonia/vinegar. 2) jaw deviates TOWARD side of lesion |
| What is the motor component of the glossopharyngeal nerve? | Stylopharyngeus from nucleus ambiguus (not as important as inputs from 10 & 11 in swallowing) |
| Which CN mediates the gag reflex? | 9 |
| Which CN carries carotid sinus BP information? | 9 -> solitarius (also senses PCO2 & PO2 @ carotid bodies) |
| Which CNs carry sensation to external ear? | 5,7,9,10. (9,10,11 = pain from external auditory meatus) |
| Where does the uvula deviate in case of CN lesion, & which CN mediates palatal elevation? | CN9. Uvula deviates away from lesion (b/c palate still taught on normal side = pulls). Left palate pulls left, right palate pulls right. |
| Which nuclei carry vagal motor information? | Ambiguus = motor to pharynx/larynx. Dorsal motor = thoracic/abdominal viscera |
| Which sensory modalities are carried in the vagus? | pain from external ear, sensation from viscera & pharynx, TASTE from epiglottis |
| What mediates tongue movement & how? | Right CN12-> right tongue-> contraction causes LEFT tongue movement |
| What happens if lesion in brainstem vs. central for hypoglossal nerve? | "Lick the lesion" lower lesion. Cx lesion-> weakness on opposites side-> tongue deviates to the normal side. |
| Where are autonomic neurons located in the brain? | EMOTION & PAIN: Insular Cx, Amydala, Anterior Cingulate gyrus, Medial PFCx (near Limbic areas). AUTONOMIC REGULATION: Hypothalamus & brainstem. |
| What are the fxnl divisions of the autonomic nervous system? | 1) Neurohumoral (hormones for metabolism & blood vol). 2) Intrinsic Enteric (gut). 3) Symp. 4) Parasymp. |
| Where do all sympathetic nerves originate & what is their path? | T1-L3 interomediolateral column-> myelinated fibers exit ant root w/motor fibers-> white ramus-> paravertebral symp chain ganglion (ACh)-> postganglionic fiber->SC or target organ (NE) |
| Which are the displaced sympathetic ganglia? | celiac, superior & inferior mesenteric (PREVERTEBRAL) + adrenal medulla |
| Where does signal amplification/integration occur in the sympathetic NS? | paravertebral ganglia |
| Which nerves innervate the viscera of the thorax & abdomen? | Vagus-> down to lower 1/3 of colon. Sacral Autonomics (interomediolateral column)-> rectum, bladder, reproductive organs |
| Which NTs & receptors are associated with the parasympathetic NS? | ACh, nAChR's @ ganglion, mAChR's in peripheral target organs |
| Which sympathetic fibers do not use NE? | Post-Ganglionics to sweat glands, piloerector muscles, some blood vessels (ACh) |
| Where do central parasymptahteic neurons lie? | Brainstem + Sacral SC |
| Which CN nucleus decreases HR & enacts bronchial constriction? | Nucleus Ambiguus |
| Where are parasymp ganglia located? | from cranial peripheral ganglia & diffuse cell networks in heart/gut/bladder walls |
| What do the celiac & mesenteric ganglia do? | Gut vasoconstriction & inhibit secretion |
| What do sympathetic chain ganglia mediate? | 1) high HR, 2) dilate bronchi, 3) vasoconstrict, 4) vasodilate active muscle, 5) sweat |
| What is the pathway for parasympathetic afferents? | Vagus-> Nodose Ganglion-> nucleus of solitary tract. BP, CO2, gut distension. |
| What effect do parasympathetics have on metabolism (glycogen, fat, basal)? | NONE. Sympathetics-> 2x metabolism, break down fat & glycogen. |
| How is urination controlled? | parasymp-> Relax sphincter & Contract Detrusor-> +Urination |
| Which autonomic system is pro-defecation? | parasymp |
| Which conditions may be signs of autonomic failure? | 1) orthostatic hypertension, 2) Excercise intolerance, 3) Constipation/diarrhea/nausea, 4) Urine retention, 5) Dry mouth/eyes, 6) Heat intolerance, 7) Sex impairment, 8) Fixed pupils |
| What is the cause of a patient presenting w/loss of all sympathetic & sacral parasympathetic fxn? | SC lesion above T2-> early atonic rectum & bladder, bradycardia (vagus wins)-> late autonomic sympathetic dysreflexia (i.e. severe hypertension & sweating) |
| What are the types of integration occurring in autonomic ganglia? | 1) paravertebral chain-> concerted fight-or-flight, 2) prevertebral & intrinsic plexi-> reflex digestion, 3) decreased blood to gut during exercise |
| What do lumbar/sacral parasymp's have primary control over? | Micturition, Defecation, Sexual reflexes |
| What is the pathway for the baroreceptor reflex? | High BP @ carotid body-> CN9-> solitarius-> INHIBITS chronically-active Descending Sympathetics in SC-> lower HR (more effective than increasing parasymp tone) |
| What are the subdivisions of the reticular formation? | 1) descending = motor tone, 2) ascending = arousal (sleep/wake), 3) Rostro-Lateral = HR Pressor + Expiration, 4) Caudal = HR Depressor + Inspiration |
| What happens if you lesion the reticular pressor or depressor regions? | Not a whole lot. HR remains relatively normal. |
| Ventilation is mediated x which spinal nerves? | C3-C5 |
| Why doesn't increase in CNS respiratory drive _necessarily_ increase ventilation? | High rate of shallow breathing not efficient. |
| What types of CNS inputs modulate respiratory drive? | VAGUS: 1) Lung Stretch R's-> pneumotaxic center-> rate & TidalVol, 2) Carotid ChemoR's-> hypervent. 3) PAIN-> hypervent (SC lesion can-> apnea). 4) SNEEZE/COUGH= high rate & TidalVol. 5) Joint/Muscle Sensation-> hypervent during exercise. 6) Cx & Limbic |
| What is Ondine's Curse? | Cervical SC lesion of pain fibers-> hypoventilation that is exacerbated to complete apnea during sleep when arousal tone is removed. |
| What causes Cheyne Stokes respiration? | Bilateral diencephalic lesions-> hyperpnea alternating w/apnea w/smooth transitions |
| What type of lesion leads to polypnea? | (= CNS hypervent = rapid panting) Midbrain/Rostral Pons |
| What are the symptoms of a lesion of the respiratory centers in the lower pontine tegmentum? | Apneustic breathing (long inspiration + prolonged pause @ end) |
| What is the effect of lesions of the respiratory centers in the dorsal tegmentum of the medulla? | Ataxia (irregular unpredictable pauses + shallow breaths) |
| What is the effect of lesions in the medulla respiratory centers? | Ataxic (completely randomized breathing pattern) or complete cessation of breathing |
| What are possible ways to elicit the vomit response? | 1) Excessive CN8, 2) Pharyngeal stim (CN9 & Vagus), 3) blood chemicals @ CTZ (ChemoR trigger zone) |
| Where is the CTZ located? | ChemoR Trigger Zone = right next to nucleus of solitary tract & vomiting control region |
| What is the output of the vomiting control center? | 1) Relaxes gastroesophageal sphinter (vagus), 2) Contracts abdominal muscles, 3) delta Respiration |
| When a patient goes from lying down to standing up, what drop in systolic/diastolic BP is considered to be orthostatic hypotension? | Drop of 30 Systolic or 20 Diastolic (mmHg) |
| When a patient goes from lying down to standing up & the HR doesn't increase, what does this suggest? | BaroReflex FAILED |
| What is the normal response to HR & BP when a patient goes from lying down to standing up? | 1) Either NO sig change OR 2) Small drop in systolic P + small increase in diastolic P + small increase in HR. Blood pools in feet & CO drops, autonomics prevent drop in BP. |
| What is the sign of autonomic failure in a patient who lies down & then moves to standing up? | Drop in BP when stand up & HR doesn't increase enough to accommodate |
| What lesion causes hemiballism? | Unilateral Lesion of Subthalamic Nucleus -> CONTRA flinging. MECH: loss of excitation to Internal Pallidus-> decreased inhibition of thalamus-> increased IPSI Cx -> increased CONTRA motor |
| What is blood supply to the basal ganglia? | Ant + Post circulation |
| What is the direct motor pathway of the basal ganglia? | Thal-> Cx-> D1 putamen-> INT pallidus-> Thal |
| What is the indirect motor pathway of the basal ganglia? | Thal-> Cx-> D2 putamen-> EXT pallidus-> SubThal-> INT pallidus-> Thal |
| What is the basal ganglia effect of Parkinson's? | No D1 excitation/D2 inhibition-> INT putamen released from inhibition-> HYPOkinesia |
| What is the effect of Huntington's on the basal ganglia? | striate k/o. 1) loss of LAT putamen D2-> release from inhibition of EXT capsule pallidus-> inhibits Subthal-> decreased inhibition of Thal-> HYPERkinesia |
| Which tracts are lateral, pseudolateral, & medial? | LAT: cortico, rubro. PSEUDOlat: tecto, medial cortico. MED: vestibulo, MLF, reticulo. |
| What is the path/fxn of the vestibulospinal tract? | 1) LAT vestibular nuc & tract-> IPSI ventromedial SC alpha motoneurons (trunk balance). 2) MED vestibular nuc-> BILATERAL MLF-> BILATERAL cervical SC (head & neck). |
| What is the path & fxn of the reticulospinal tract? | Input from Cx. 1) Spinoreticular Tract + Cx-> PONTINE RETICULUM-> IPSI medial SC tract-> EXCITEs bilateral gamma motoneurons. 2) Cx-> medulla reticulum-> IPSI lateral reticulospinal tract-> INHIBITs ipsi gamma motoneuron |
| What is the path & fxn of the rubrospinal tract? | Input from Cx. Red Nucleus-> CONTRA rubrospinal tract in cervical SC-> excites distal flexors of the upper extremity |
| What is the path & fxn of the tectospinal tract? | Retina-> Sup Colliculus-> CONTRA ventromedial cervical SC-> head & neck position muscles. Pseudo-Lateral tract (medial SC position, lateral physiology) |
| Which corticospinal pathways are topographically organized? | ALL of them (by the time they get down to the pyramid, the face fibers have already exited) |
| What neurons are innervated x the corticospinal tract? | Alpha & Gamma motoneurons. Motor Cx maps movements (activities) + direction (1 neuron: 1 task) |
| What is the definition of decerebrate posturing and when does it occur? | Gamma Rigidity = Midbrain/upper pontine lesion-> Pontine reticulum wins over medullary reticulum-> net excitation of proximal extensors. Elbow & Leg EXTEND, Arm PRONATE, Wrist/Finger FLEX, Plantar FLEX. |
| What effect do gamma motoneurons have on muscle contraction? | contract intrafusal muscle fibers-> activate Ia & II afferents-> causes agonist muscle contraction |
| Why is one of the reticulocerebellar pathways favored over the other in gamma rigidity? | Both Cx and Ascending spinoreticular fibers excite the excitatory PONTINE reticulospinal tract, whereas the inhibitory MEDULLARY tract is only excited by Cx. In the derecerebrate prep Cortical input is removed, so only PONTINE fibers remain excited. |
| Why does severing the dorsal root minimize some of the effects of gamma rigidity? | pontine reticulospinal tract activation -> gamma motoneuron firing-> Ia fibers signal via DRG-> activates alpha motoneurons-> rigidity |
| Why does removing the cerebellar Cx renew some of the effects of gamma rigidity after severing the dorsal root? | Vestibular signaling excites extensor alpha motoneurons. Cerebellar Cx direct Purkinje projections are inhibitory, while Fastigials are excitatory to the Vestibulars. Removing Cx-> Fastigials release alpha motoneuron inhibition. |
| What is the clinical portrait of a brain motor pathway lesion sparing the midbrain & below? | DECORTICATE. Rubrospinal tract intact-> FLEX every joint in arm + EXTEND legs + PLANTARFLEX feet. (Rubrospinal only extends through cervical cord) |
| What is the clinical portrait of upper motoneuron disease? | SPASTICITY: increased muscle tone & stretch reflex (incl. pathological reflex), maintained muscle integrity & strength, decreased fine motor control. |
| What is the clinical portrait of lower motoneuron disease? | Decreased muscle stretch reflex, tone, tissue integrity, strength, fine motor control, but NO PATHOLOGICAL REFLEXES. |
| What is the organization of olfactory receptors & their projections? | Cells of each type = found only in 1 of 4 zones (stripes along turbinates). Axons from each cell all-> single glomerulus-> single mitral cell. Glomeruli topographically arranged x receptor type. |
| where are taste buds located? | lateral surface of each papilla. Rapidly adapting. |
| What are the nuclei of CN7? | Solitarius, Motor, Salivatory |
| Where are frontal eye fields located in the Cx and where do they project? | Superior frontal lobe somatosensory association Cx (Brodmann 8)-> CONTRA Sup Colliculus AND -> CONTRA PPRF |
| What input contributes to Brodmann Area 8 (frontal eye fields)? | Visual Cx and Extrastriate Visual Cx (Brodmann 18 & 19) |
| What are the divisions of the motor nucleus of 7? | Dorsal =lower face, CONTRA input from Cx. Ventral = upper face, BILATERAL input from Cx. Central lesion-> unilateral contra lower face droop. Bell's Palsy = peripheral lesion-> entire 1/2 face droops |
| Which nuclei are associated w/CN9? | Solitarius (taste, sensation, gag reflex of post tongue, BP from carotid sinus), Salivatory (Parotid), Ambiguus (swallow: stylopharyngeus) |
| When does a moroneuron fire repetitively? | @1.5x the synaptic current necessary to recruit it |
| What is the fasciculus proprius? | The tract that functionally connect leg movements with arm swings in the spinal cord |
| What is the Motor Learning Hypothesis of the cerebellum? | =climbing fibers convey existence of motor error (e.g. missing target when pointing)-> delta strength of parallel fiber-> Purkinje synapse (relies on coincident activity of climbing & parallel fibers for same Purkinje) |
| What causes LTD vs. LTP at the parallel fiber-> Purkinje Cell synapse? | LTD: HIGH climbing fiber activity. LTP: LOW CF activity. |
| Where do corticobulbar fibers terminate? | In & near Nuclei of cranial nerves |
| What are the relative contributions of motor, premotor, & supplementary motor areas to movements? | single finger = only primary motor. Complex movements of sequences of fingers = all areas. Mental rehearsal = premotor & supplementary motor. |
| What are the components of the Neurological Exam? | 1) Mental Status, 2) CNs, 3) Motor, 4) Sensory, 5) Deep Tendon Reflex, 6) Coordination, 7) Station/Gait |
| What is the most important component of the neurological exam? | SUBJECTIVE!!! Critical info = go back & ask more. Tailor Neuro exam to subjective HPI (avoids patient/physician fatigue). Physical evidence may be normal for phasic disorders. |
| What are the components of the mental status exam? | 1 Consciousness (Awake/Lethargy/Coma/Stupor NOT sleepy) 2 Cx (memory, 3 objects) 3 Left Cx (slur/no/telegraphic speech, comprehends, word salad). 4 Right Cx (draw/copy, left neglect, count downs). 5 Frontal Lobe (what would you do if...). 6 Psychological |
| What are some psychological components of the mental status exam? | depression, mood/affect, thought content, insight, judgement, fund of knowledge |
| What causes a patient to be comatose? | Both cortices or 1 reticular complex is knocked out |
| what is the clinical difference between delirium & dementia? | Delirium: sensorium (sense of self & location & context) comes & goes, can do math/spell. Dementia: sensorium preserved but can't math/spell/remember (advanced loses sensorium as well). |
| What are typical left hemisphere tasks in the mental status exam? | Broca's, Wernicke's, math, spell, left/right distinction, praxis (multi-step motor commands) |
| What are typical right hemisphere tasks in the mental status exam? | Attention & persistence (e.g. count back from 100, left hemi-neglect, copy interlocking polygons, prosody (giving/understanding emotion in language) |
| What are common reasons that olfaction might be impaired? | anosmia due to pathology in nose, cribiform plate, TBI (axonal shearing), insular Cx, smoking, sinusitis/rhinitis |
| How is visual acuity tested? | Snellen chart 14" from eye, pupil light reflex, fundiscopic exam |
| What are common causes of CN3 & CN6 palsies? | CN3: aneurysm of PC1 of the Circle of Willis. CN6: intracranial pressure (CN6 passes along several bony ridges) |
| How can you visually distinguish someone with a CN4 palsy? | Tilts there head down & toward the eye that is malfunctioning. |
| Disarthria is a sign of a problem in which CN? | (= nasal-sounding speech). CN10 lesion-> soft palate excursion & uvular deviation. CN10 mediates all soft palate muscles except tensor pallati (CNV-3) |
| What does a pathology at the forament magnum affect? | CN11 (motoneurons live in upper cervical SC but axons ascend in foramen magnum & exit @ jugular foramen) |
| What are bulbar vs. spinal functions of CN11? | BULBAR: Ambiguus-> motor phaynx/larynx, Dorsal Motor-> motor to thorax/abdomen. SPINAL: Spinal gray-> motor trapezius & SCMs |
| Which CN pathologies can alter speech? | 7 (lips: say "pa"), 12 (tongue: say "la"), 9 (pharynx: say "ca"), 10 (pharynx: say ga") |
| How can midbrain->pons CN dysfunctions be tested? | Lateral gaze reflex (MLF, CN3 & 6). "oculocephalic doll's eyes test" = eyes remain fixed despite head movement. Cold caloric test (vomit if patient is awake) |
| If the CN exam is not normal and the patient is comatose, what is a likely explanation? | Damage to the reticular activating system |
| What is motor tone and what are the most likely reasons for increased tone? | Tone = resistance to passive movement. Cogwheeling (high tone) caused x UMN (closed knife response) or basal ganglia lesion (limb stays in position after release) |
| What does pronator drift indicate? | Barre Test: eyes closed, forearms out palms up, weak side-> hand drifts out & down (UMN disorder) |
| In a muscle strength exam, what is the rating system? | 0 = no strength. 1 = contraction but no movement. 2 = can move, but not against gravity. 3 = can move against gravity, but not resistance. 4 = can move weakly against resistance. 5 = normal strength. |
| What are the 3 types of tremor, and the location of the pathology? | RESTING: basal ganglia, INTENTION: cerebellum, RUBRAL: coarse, presents both @ rest and w/intention. |
| Where are reflexes tested for deep tendon reflex exams? | Biceps, Triceps, Patella, Achilles tendon; jaw |
| What is the grading scale for testing reflexes? | 0 ABSENT. 1+ DECREASED. 2+ NORMAL. 3+ INCREASED & SPREADING |
| What is the definition of stretch reflex clonus? | to & fro oscillations after stretch. suggests gain is too high, most severe after UMN lesion. |
| What is the Hoffman test? | Same as Babinsky, but with the hand |
| What do you look for in the heel to shin test? | Coordination, extra-pyramidal motor, tremor, dysmetria |
| What are the extra pyramidal motor systems? | cerebellum, basal ganglia |
| Why do patients exhibit a "slapping" gait? | Peripheral Neuropathy: try to increase sensory signals from their feet to brains. |
| Why do patients exhibit a "circumducting" gait? | Stroke: swing a stiff leg with decreased hip, knee & ankle flexion to avoid tripping. |
| Why do patients exhibit an ataxic gate? | Cerebellar dysfunction: unsteady, wide based, variable step size & speed. Alcohol. |
| Why do patients exhibit an Antalgic gait? | Leg/hip/back pain: ginger, slow, foreshortened stepping. |
| What do Auerbach's vs. Meissner's plexi do? | Auerbach;s: intermyenteric-> peristalsis. Meissner's: submucosal-> secretion, blood supply. |
| What are common syndromic problems for sympathetic vs. parasympathetic disorders? | SYMP: orthostatic hypotension, anhydrosis. PARA: decreased pupil dilation, dry mouth & eyes, impotence, bladder problems. |
| Which brain regions does the solitary nucleus project to in the baroreceptor reflex? | 1) Excitatory to Vagus Motor Nucleus (-> inhibits HR & CO), 2) Inhibatroy to HR Pressor in Medulla (-> excites Sympathetic outflow) |
| What are some typical causes of orthostatic hypotension? | Autonomic Disorder, Low Blood Vol, Alcohol/Meds causing Vasodilation |
| what do Carotid ChemoR's respond to? | LOW O2, HIGH CO2, change in pH |
| Where are magnocellular hypothalamic cells located? | SON, PVN, make AVP/OXT. Project to Post Pit. |
| What are parvocellular hypothalamic cells? | PVN (TRH, CRH, Somatostatin), Arc (GHRH, GnRH, DA) project to the median eminence via tuberoinfundibular tract. AVP/OXT/CRH/ENK parvocellulars project to preganglionic parasymp & symp neurons in medulla & SC. |
| Where are projection hypothalamic cells located? | PVN (AVP/OXT as neuromodulator, diff cells than those going to post pit), LHA (MCH/ORX), Arc (POMC/CART). |
| What is the clinical profile of ob/ob mice? | infertile, low TH, high CORT, . same phenotype when k/o MC4R. |
| What does fasting usually do that leptin treatment prevents? | Low TRH, HPG axis inhibition, HPA axis activation (-> catabolic state), low body temp, low activity,low metabolism |
| Where is leptin R expressed? | All over the brain, but enriched in MBH |
| What is the dual center hypothesis? | Medial hypothal-> leptinR, lesion-> obesity. Lateral hypothal-> MCH/ORX, lesion-> starve. |
| Where is orexin made and where does it project to? | Made in LHA exclusively, projects to Cx, Hippocamp, PFCx, SC. ORX or OR1/2 mutation-> Narcolepsy. |
| What structures are located in the medial hypothal? | PVN, Arc, VMH, DMH |
| What structure connects the hypothal w/other brain regions? | Medial Forebrain Bundle (lateral hypothal)-> polysynaptic to brainstem autonomic contral areas |
| What are the 3 zones of the median eminence? | Ependymal (ependymal cells + microvilli & tight jxns, tannycytes + tight jxns), Internal Zone (magnocell axons) , External Zone (portal vessels + terminals for peptides, DA, NE) |
| What is the pathway from the amygdala to the hypothalamus? | stria terminalis |
| What is the column of the fornix? | portion of the fornix that remains in a tight bundle in the hypothal to synapse in the mammillary bodies |
| The cat with a severed forebrain showed sham rage because what structure was severed? | descending forebrain afferents to the hypothal |
| Where are the limbic inputs to the hypothal? | Mostly heavily myelinated to mamillary bodies (not understood) -> mamillotegmental tract & mammillothalamic tract (->Ant Thal) |
| Which brain region mediates sterotyped behaviors? | LHA-> midbrain reticulum-> medial integrative nuclei |
| What are the 2 pathways for visceral sensory info to enter the CNS? | 1) SYMP sensory in DRG-> adds to sensation from same dermatome-> dorsal columns-> Thal & Cx (referred pain), 2) PARA sensory info from CN7, 9, 10 in Solitarius -> Parabrachial Nuc (pons)-> Hypothal, Amyg, Cx |
| What is cortisol's mineralocorticoid effect in the kidney? | Na conservation |
| What is the brain pathway for shivering? | hypothal-> midbrain reticulum |
| What are the main components of the Circle of Papez***? | Mammillary Bodies-> Mammillothalamic Tract-> Ant Thal-> Cingulate Gyrus-> Entorhinal Cx & Subiculum-> Hippocamp (Subiculum)-> Fornix->Mammillary Bodies |
| What are additional structures added to the circuit of Papez? | 1) Orbital/Medial PFCx, 2) Ventral Basal Ganglia (Nucleus Accumbens), 3) Medial Dorsal Thal, 4) Amygdala |
| Which emotions could be elicited merely by stimulating the Hypothal? | rage, fear |
| What causes Wernicke-Korsakoff Syndrome? | Thymine Deficiency: memory prob's but retained vocab. Due to mammillary body degradation (same abnormalities seen in autism). |
| Where is the entorhinal Cx located? | Parahippocampal gyrus |
| What is the source of cholinergic input to the hippocamp? | Medial Septal Nuc & Nuc of Diagonal Band of Broca (gets branch of fornix) |
| What is the Subiculum? | Subregion of the hippocamp = source of fornix & projects reciprocally w/entorhinal |
| Where does the Fornix project? | Mammillary Bodies, Septal Nuclei, Ant & Dorsomedial Thal |
| What is the Basolateral Nuc of the amygdala? | (emotional significance) inputs from temporal/insular/association Cx, outputs to cingulate/temporal/orbitofrontal Cx, Hippocamp, Basal Nucleus of Meynert (cholinergic nuc), Mediodorsal Thal, Central Nuc of Amyg |
| What is the Central Nuc of the Amygdala? | (emotional response) input viscerosensory from brainstem & Basolateral Nuc. Output to Autonomics, Periaqueductal Gray, Hypothal, Reticulum. |
| What is the Corticomedial Nuc of the Amygdala? | Food intake, reproduction, reward. Reciprocal connections w/Olfactory structures. Output stria terminalis to VMH |
| What is Kluver-Bucy Symdrome & what causes it? | remove Ant Med Temporal lobe bilaterally (i.e. amygdala): placid, hyperoral, hypersexual, no fear |
| What are the divisions of the Cingulate? | ANT: initiation, motivation, goal-directed behavior. inputs from Thal. Rostral = autonomic/emotional mediation, cognitive division = skeletomotor responses. POST: viuospatial processing & memory. |
| What do lesions of the cingulate cause? | Abulia (lack of will power), Akinetic Mutism, Low pain response, Impaired social behavior. |
| What does the orbital frontal Cx do? | Judgement of Risk, Learn from Mistakes, Empathy. Connections: Amyg (reciprocal), Mediodorsal thal (recip), through ventral basal ganglia |
| Which metabotropic NTs are important in the Papex Circuit? | 5HT, NE, DA, Epi |
| What characterizes major depression in the Papez Circuit? | Decreased Thal activity, (may happen post-stroke), basal ganglia & frontal Cx also decreased. |
| How do schizophrenia drugs work? | Inhibit temporal lobe DA R's |
| What is the difference between Seizure, Epilepsy, & Epilepsy Syndrome? | Seizure = paryxysmal hypersynchronous discharge from CNS neurons. Epilepsy = >2 unprovoked seizures. Epilepsy Syndrome = speciic underlying cause |
| What % of Americans have epilepsy? | 1% . Risk increases for retarded & cerebral palsy kids, stroke, Alzheimer's, & 1/3 people who had previous unprovoked seizure. |
| What is a partial seizure? | unilateral focal origin (judged by symptoms @ onset). Simple = stay conscious. Complex = amnestic/confused, sometimes in coma. |
| What is a Generalized Seizure? | Bilateral, sudden nonfocal origin. TONIC/CLONIC: stiff/tense. ABSENCE: petit-mal. MYOCLONIC: twitches. ATONIC/ACONIC: ataxic. |
| What is the definition of a seizure spike? | Sharp wave on EEG diagnostic of epilepsy 35-90% of the time. Alpha rhythm ~10 Hz (adult), less in child. |
| What are characteristics of absence seizures? | instant on/off, ~10 sec average, motor movements still possible w/eyes open, but no consciousness/cognition, amnestic. |
| What are Juvenile Myoclonic Seizures? | 10% of all epilepsy cases. idiopathic, usually on awakening, BILATERAL arm jerks |
| What is the most common type of focal epilepsy? | 50% focal epilepsy = temporal |
| What is Lennox Gastaut Syndrome? | Slow EEG spike wave, type of Cryptogenic/Symptoatic epilepsy associated with mental retardation |
| What are some typical causes of infantile epilepsy? | congenital (lissencephaly, Cx dysplasia), birth injury, metabolic (low Ca, not enough B6 for GAD, phenylketonuria) |
| What are the odds of pharm treatments for refractory epilepsy (after 3 drugs fail), and what is the alternative? | 10% odds that another drug will work. other option = surgery (anteromesial temporal lobectomy-> 70-95% success) |
| What % of time is spent in each stage of sleep? | 50% II, 25% REM, 20% III/IV, 5% I |
| What characterizes REM on EEG? | Sawtooth waves |
| What are the major categories of sleep disorders? | Parasomnias (prob's w/arousal/sleep-wake, REM). Dysomnias (in/extrinsic, circadian). Associated (med, neuro, psych disorders) |
| What are some examples of dysomnias? | Narcolepsy, Restless Legs, Disordered Breathing, Essential Insomnia |
| What are some examples of parasomnias? | Sleep walking/paralysis/terrors, REM behavior disorder, confusion on waking |
| What are the risk factors for restless leg syndrome? | (disinhibited descending pontine reticulospinal) 20% pregnant, 20-60% dialysis, Fe deficient, polyneuropathy, 63-92% family history |
| What are the clinical features of narcolepsy? | daytime sleepy (90%), cataplexy (70% = drop w/loud noise or laugh), hallucination (30%), disturbed nocturnal sleep (90%), automatic behavior (50%) |
| How do you treat an orexin deficiency? | amphetamines. diagnosed w/sleep study + 4 daytime naps. enter REM in several minutes in 2 or more naps. normal = enter REM in 90 min. |
| What is Aphasia? | disorder of speech and/or comprehension (not due to hearing loss/weakness of facial muscles |
| What are the characteristic problems of aphasia? | problems with COMPREHENSION, REPETITION, CONFRONTATIONAL NAMING (difficulty depends on frequency), FLUENCY (independent of content), PARAPHASIA (misspoken words) |
| What are the types of paraphasias? | PHONEMIC (1/2 word okay, other half gibberish), VERBAL (substitute wrong word, i.e. semantic = substitute related word), NEOLOGISMS (word-like but not real) |
| What is the left hemisphere more important for? | speech production, but not necessarily language formation/comprehension |
| What does a lesion in Wernicke's Area cause? | Increased Fluency, Decreased Comprehension (most), decreased Repetition & Naming ability |
| What is the cause of dysfunction with Wernicke's aphasia? | SOUNDS NOT MATCHED TO WORD MEANINGS, provides the target sound for motor production of Broca's. Fluent but senseless speech. Reproduction of overlearned speech/singing. |
| What is the Arcuate Fasciculus? | connects Wernicke's to Broca's |
| What characterizes Broca's Aphasia? | NON-FLUENT, slow, halted, agrammatic speech. words left out (impoverished). severly impaired = no words, yes/no/profanity. Repetition impaired. Aware & frustrated. |
| What characterizes Wernicke's aphasia? | FLUENT/sensory/receptive, no memory of the sound of words. Normal phrase length, mispronounced words, wrong words, neologisms, grammatically correct phrases w/no meaning. Unaware of abnormal speech output. Impaired repetition & Comprehension. |
| What is Conduction Aphasia? | Arcuate Fasciculus lesion, fluent speech w/phonemic errors, impaired repetition, intact comprehension (aware of what words should sound like) |
| What is Apraxia? | Can't do something someone tells you, understand but can't do it. CAN mimic action that you see. 50% patients w/left hemisphere damage (<10% in R hemisphere). R-L confusion. |
| What is the anatomical underpinning of apraxia? | L supramarginal gyrus stores praxicons (knowledge of motor commands). L supplementary motor translate praxicons to motor program. Corpus Callosum (ant 2/3) transfers info b/tw L & R. |
| What region is responsible for hemi-spatial neglect? | R INF parietal lobe |
| How is L & R organized in the brain? | R hemisphere both L & R space. L hemisphere ONLY R space. |
| What causes hemispatial motor intentional neglect? | Frontal R hemisphere. Motor activity of right decreases as it approaches midline. NOT PERCEPTION PROBLEM. |
| What is the pattern of brain atrophy before & after 50yo ? | before 50 gray matter shrinks. After 50 white matter shrinks.frontal lobe decreases most< temporal. ventricles dilate & volume of CSF. Substantia nigra, basal forebrain neocortex most susceptible to atrophy. |
| What are the effects of aging on the hippocampus? | Decreased volume, not neuron #. |
| Which abilities remain intact in elderly? | vocab, facts, history/personal history, gist. slower processing. Cuing helps. Wisdom & Perspective. |
| What are age-related changes in fxn? | Harder to problem-solve, decreased strength/posture/gait, special sensory probs, deficit of vibration/tactile in legs, low beta adrenergic sensitivity (low HR & SV, bronchodilation. |
| What are causes of age-related brain decrements? | apoptosis, DNA repair issues, toxic metabolite build-up (e.g. free radicals), mifolded proteins, hypercortisolemia-> smaller hippocamp, head injury-> neurodegen disease. Diabetes & hypternsion-> microvascular disease |
Created by:
rbxbrown