Anatomy 2 Flashcards
what’s in a neuronal circuit? exception?
stimulus –> *sensory neuron –> *spinal cord response/1+ interneuron –> *motor neuron –> effector muscle. stretch reflex (no interneurons –> monosynaptic)
Propriospinal fibers
fibers travel b/t levels of the spinal cord –> link limbs together for a single reflex; Part of white matter immediately adjacent to gray matter, present in all funiculi; Form fasciculi propri
innate vs acquired/conditioned reflexes
connections that form b/t neurons during development & are genetically programmed
o Ex: spinal reflex— occur w/o immediate conscious awareness –> sent to higher centers & conscious sensation may result (e.g., pain)
Most are never consciously sensed
Spinal reflexes can be suppressed by conscious thought arising from higher centers
vs
enhanced by repetition; more complex, learned (somatic) motor patterns
Effective spinal reflexes (in correcting & adjusting muscle movement) –> need very detailed motor output & very accurate sensory input describing fxnal status of ea muscle at ea instant. How?
2 sensory receptors in skel muscle provide subconscious, continuous feedback to the spinal cord –> cerebellum –> cortex: Golgi tendon organs for muscle tension, muscle spindle organs for muscle length. both = proprioceptors (conscious in post column, subconsc in spinocerebellar tracts)
muscle spindles. explain all their fibers
elongated, sac-like structures W/IN skel muscles. 8-12 modified intrafusal fibers in parallel w/ extrafusal fibers. 2 classes of intrafusal: nuclear bag (clustered nuclei, #2-4 per spindle) supplied by type Ia sensory nerve fibers/primary endings & dynamic y-motor neurons, nuclear chain (single-file, #6-8 per spindle) supplied by type II sensory nerve fibers/secondary endings & static y-motor neurons
how do muscle spindles receive SENSORY info about muscle length? why does CNS need to care?
intrafusal fibers in parallel w/ extrafusal –> when extrafusal stretches, intrafusal feels it too. muscle = always feeling some amt of stretch –> type Ia & II give info to CNS abt amt => static response; type Ia give info to CNS abt rate of change of stretch => dynamic response… CNS cares b/c stretching w/o correction can dmg muscle
how do muscle spindles receive MOTOR info about muscle length? –> primary vs secondary response? do alpha and y-motor neurons need to be coactivated & why?
sensory input –> activate alpha motor neurons –> extrafusal fibers ctx to counter stretch & potential injury vs activate y-motor neurons –> reg activity intrafusal fibers to report amt & rate of change. yes or else intrafusal = slack relative to extrafusal –> can’t efficiently report muscle length to CNS
what is myotatic/stretch reflex? what neurons = involved?
what’s reciprocal inhibition?
sudden stretch of muscle –> reflexive ctx of that muscle. single type Ia sensory neuron w/ homonymous alpha motor neuron
seen in patellar reflex: type Ia sensory neurons excite inhibitory interneurons that innervate motor neurons in flexors/hamstrings –> hamstrings relax –> quads ctx
dynamic/phasic vs static/tonic stretch reflex
type Ia sensory fibers oppose sudden changes in muscle length vs BOTH type Ia & II sensory fibers respond to slower/steady stretch –> make small instantaneous corrections –> prevent us from falling while standing and smooth ctx
when is stretch reflex strongest? can it be suppressed?
in gravity-opposing extensors. yes in higher centers b/c strength of reflex = low enough
golgi tendon organs. what happens to GTO w/ inc muscle tension?
encapsulated nerve endings of unmyelinated type Ib afferent fibers entwined in collagen of muscle, equalize contractile forces among groups of muscle fibers. nerve endings = compressed by collagen –> impulses sent in proportion to degree of compression
type Ib sensory fibers of GTO synapse on 2 types of interneurons in ant horn of gray matter:
inhibitory interneurons: inhibit alpha motor neurons of active muscle –> relaxes them to avoid tension overload
excitatory interneurons: activate alpha motor neurons of antagonist muscles –> ctx them to unload active muscle
what is inverse myotatic/stretch reflex? what’s lengthening rxn?
inc muscle tension –> GTO causing relaxation. spinal cord can mediate instant relaxation of entire muscles in extreme tension –> prevents tears or tendon avulsion
what’s flexor reflex? does it always involve flexor muscles? what’s crossed extensor reflex?
involves whole limb (stretch reflex and GTO reflex involve single muscle) –> quicker ctx of flexor muscles to w/draw from noxious stimuli detected by nociceptors to type II & III afferents. no. after flexor reflex –> contralat limb extends to support & push body away from stimulus (LE) and provide bal (UE)
hyperalgesia vs analgesia vs allodynia
inc pain from something that nmlly provokes pain vs no pain from something that nmlly provokes pain vs pain for something that doesn’t provoke pain
what are nociceptors? where are their free nerve endings?
sensory receptors detecting stimuli that elicit tissue dmg, or signals/chemicals from dmged tissue; free/bare nerve endings in skin, muscle, joints/bone, viscera
Aalpha/beta vs Adelta vs C fibers
myelinated, lg, proprioception/light touch vs lightly myelinated, medium, nociception vs unmyelinated, small, innocuous temp/itch/nociception, responds to inflam –> gives pain sensation after a cut
what is pain? acute vs chronic pain. mechanism for chronic pain?
submodality of somatic sensation –> unpleasant sensory & emotional experiences assoc w/ tissue dmg. activation of nociceptors for short time, no sig tissue dmg vs pain lasting mo+ from tissue injury, inflamm, nerve dmg, tumor/lesion, occluded blood vessels –> evoke chemical, fxnal, structural changes (like activating G proteins). noxious peripheral stimuli –> excitatory gluE and asp bind to NMDA receptors –> hyperalgesia, neuropathic pain
pain categories: fast pain/pinprick/sensory pain vs burning/soreness pain vs aching pain
sharp/stinging pain, well localized, on skin, neospinothalamic tract; Adelta vs inflamm secondary to tissue dmg, diffuse & lasts longer, on skin or muscle, paleospinothalamic & archispinothalamic tracts; C fibers vs poorly localized pain form deep structures like joints or viscera, paleospinothalamic & archispinothalamic tracts; C fibers
know how pain = transmitted
noxious stimulus from periphery –> primary afferent neurons (A or C fibers) –> DRG –> dorsal root projection neurons in spinal cord –> higher centers
somatic pain = classified into: superficial/cutaneous/peripheral pain vs deep pain
pain from skin, muscle, peripheral nerves; has initial response then later response vs pain form joint receptors, tendon, fascia; has autonomic response like sweating, nausea, change in bp & HR
visceral nociceptors. where are their free nerve endings?
contain mechanical pressure, temp, chemical and silent nociceptors. free nerve endings = scattered –> any stimulus that excites them cause visceral pain
cause vs s/s of visceral pain
GI lesions/tumors, artery thrombosis, tissue obstruction or stretching vs low grade diffuse pain, low HR and bp, cold sweats, nausea, hunger, thirst, electrolyte imbal, irreg circ/resp systems
referred pain vs phantom pain
pain from same myotome b/c innervated by same nerve, but not where pain actually originated from vs pain receptors = activated post amputation b/c brain can’t understand it
gate control theory
nonpainful input closes painful/noxious input –> prevent pain sensation from traveling to CNS; large sensory fibers w/ cutaneous sensory input activate inhibitory interneurons –> inhibit pain transmission by pain fibers
syringomyelia. s/s?
when fluid-filled cavity/cyst forms w/in spinal cord => syrinx; syrinx can expand over time –> destroy surrounding nerve tissue. pain in neck & shoulders, pain & stiffness in legs, muscle weakness, numbess/dec sensation, scoliosis, chiari malformation
mechanoreceptors: rapidly adapting vs slowly adapting
signal a change in stimulus; Meissner corpuscles (touch), Pacinian corpuscles (pressure, vibration); respond at beginning & end of stimulus vs signal continued presence and intensity of stimulus; Merkel discs (touch), Ruffini corpuscles (steady pressure); respond at beginning of stimulus then dec then stops when stimulus stops
what is a receptor potential?
when sesnsory receptors transduce physical stimulus ot electrical signal –> open/close ion channels
mechanoreceptors produce what type of RP? deformation of ion channels are?
depolarizing RPs. stretch-gated –> dendrite stretches –> ions flow in/out
short duration vs long duration stimuli
make constant RP and AP; proportion to duration vs time dependent decline in RP and AP; more robust NT release
what is receptive field?
area of sensory space = stimulated –> elicits neuronal responses
know DCML
primary neurons at DRG & ascend in dorsal funiculus –> secondary neurons in gracile/cuneate nucleus –> decussate as internal arcuate fibers –> ascend thru med lem –> thal –> postcentral gyrus
2 point discrimination
most densely innervated body regions –> most sensitive –> have smallest 2pt discrim threshold, greatest somatosensory cortical representation
what types of sensations are detected in anterolat system vs post column?
pain, temp vs vibration, joint position/proprioception
midbrain vs pons vs medulla oblongata
from forebrain to pons w/in tentorial notch; has nuclei for CN3, 4; cerebral peduncles, interpeduncular fossa, optic tracts lat around midbrain vs from midbrain to med obl; CN5-8 at pontomedullary jxn; middle cerebellar peduncle-C5-basilar pons, rhomboid fossa vs from pons to spinal cord; CN10-12; pyramids, corticospinal tracts & DCML, inf olivary eminences
brainstem: tectum vs tegmentum vs basis
in dorsal midbrain; 2 sup + 2 inf colliculi => corpora quadrigemina; sup colliculus + lat geniculate body => visuo/motor system via brachium of sup colliculus, inf colliculus + med geniculate body => auditory system via brachium of inf colliculus vs ventral to aqueduct in midbrain & ventral to 4th ventricle in pons; cranial nerves & most reticular formation vs most ventral; corticospinal and corticobulbar tracts
medial medullary/Dejerine syndrome
disrupt ant spinal a –> medulla infarct; dmg corticospinal tract/pyramid –> contralat hemiparesis, medial lemniscus –> contralat loss of position/ vibration/discrim touch, CN12 –> tongue deviation to ipsi/tongue atrophy/fasciculations
lateral medullary/Wallenburg syndrome
disrupt PICA; dmg spinothalamic tract –> contralat loss pain/temp on body, spinal trigeminal tract of V –> ipsi loss pain/temp on face, nucleus ambiguus (motor for CN9&10) –> dysphagia/palate paralysis/ hoarse/dec gag reflex, descending hypothal –> ipsi Horner syndrome, vestibular nuclei –> N/V/nystagmus/vertigo, inf cerebellar peduncle/spinocerebellar fibers –> ipsi ataxia
medial pontine syndrome
disrupt paramedian branches of basilar a –> ipsi 6th nerve palsy; dmg corticospinal tract –> contralat hemiparesis, medial lemniscus –> contralat loss position/vibration/discrim touch, CN6 –> /esotropia
locked in syndrome
occluded basilar a, bil pons lesion –> only movement in eyes & eyelids
medial midbrain/Weber syndrome
disrupt paramedian branches of post cerebral a –> 3rd nerve palsy; dmg corticospinal tract –> contralat hemiparesis UE, corticobulbar tract –> contralat paresis of lower face, CN3 –> ipsi paralysis of ocular adduction/exotropia/mydriasis/ptosis
know which eye muscles are innervated by what and conseq
“LR6, SO4, all others 3”. Lec 13-14, slide 61
what does cerebellum do? know anatomic, phylogenetic, fxnal name of lobes
timing & force of ctx of voluntary muscles for smooth muscle ctx; fold in to folia. Lec 16, slide 4
sup vs middle vs inf cerebellar peduncle
fibers decussate, cerebellum output vs pontocerebellar fibers from pontine nuclei & project to contralat cerebellum, cerebellum input vs lg part of restiform body in med & sm part of juxtrarestiform body in 4th ventricle, spinal cord fibers, cerebellum input
what are cerebellar nuclei?
paired nuclear bodies in white matter near roof of 4th ventricle, influences motor activity
cerebellar nuclei divisions: vermis vs intermediate/paravermal hemisphere vs lat hemisphere vs floccolonodular lobe. globose + emboliform make up what?. know what ea nuclei look like in section
head, trunk, prox limb; fastigial nuclei vs distal appendicular muscle; interposed nuclei vs motor planning in extremities & multi-joint motor programs; dentate nuclei vs bal & vestibulo-ocular reflexes. interposed nuclei. Lec 16, slide 10
lesions to cerebellum or cerebellar peduncle cause what effects? know diagram on Lec 16, slide 16. spinal lvls of Clarke’s column
ipsi effects; ataxia (discoordination of agonist & antag muscles in multi-joint movements) –> unsteady trajectory, over/undershooting target => dysmetria, abnl timing => dysrrhythmia. Lec 16, slide 16. T1-L2
cerebellar cortex: molec layer vs Purkinje cell layer vs granule cell layer
granule cell axons, purkinje dendrites, interneurons vs all cerebellar output in white matter vs excitatory neurons
2 primary axonal inputs to cerebellum: mossy fibers vs climbing fibers
cerebellar cortex –> synapse w/ granule cells –> granule axons bifurcate to parallel fibers –> parallel fibers excitatory synapse w/ Purkinje cells –> Purkinje axons inhibitory synapse w/ cerebellar nuclei vs contralat inf olivary complex excitatory wrap around Purkinje cells –> desensitize Purkinje from parallel fibers (parallel fibers stellate cells & basket cells laterally inhib neighboring Purkinje)
know AICA, PICA, SCA territories
Lec 16, slide 20
cerebellar lesions: ant lobe vs post lobe vs flocculonodular lobe syndrome
from alc, malnutrition; Purkinje cells first affected; lose coordination in LE and progress to UE if not txed vs from CVA, tumor, accidents, degen dz; intention tremor w/ volitional movement vs truncal ataxia (wide stance to bal); common in children w/ tumors in roof of 4th ventricle
basal nuclei/ganglia. dorsal vs ventral divisions?
gray matter masses in cerebral hemispheres influencing motor activity. caudate & putamen ( => striatum –> primary input), globus pallidus (interna –> output); fxnally related to dorsal: substantia nigra, subthal nucleus, pedunculopontine tegmental nucleus vs nucleus accumbens, substantia innominate, basal nucleus of Meynert, olfactory tubercle
4 loops of basal ganglia: motor vs executive vs motivational vs visuomotor loop
influence motor activity vs cog mechanisms to multitask vs having drive, pleasure, want, emotion vs sup colliculus influencing extraocular movement
3 NT and their pathways: gluE vs GABA vs dopamine
excitatory influence on striatum vs inhibitory output from striatum to substantia nigra & globus pallidus interna vs faciliatory effects w/ D1 receptors & depressant effects w/ D2 receptors from substantia nigra to nigrostriatal pathway. can modulate both in/direct but DRIVES DIRECT
direct/globus pallidus medial vs indirect/globus pallidus lateral pathway BG motor circuit
premotor cortex –> striatum –> substantia nigra pars reticulata & GPi –> inhib output nuclei on thal –> cortex –> spinal cord vs premotor cortex –> striatum to GPe –> to subthal nucleus –> excite output nuclei on thal –> cortex –> spinal cord
dyskinesia vs bradykinesia vs akinesia vs hypokinetic vs hyperkinetic vs dystonia vs ballismus vs chorea vs athetosis vs rigidity. know ranking movement d/o by speed
abnl movement from BG d/o vs dec vel & amp in movements vs unable to initiate voluntary movements vs dec movement vs inc movement vs slow, repetitive, sustained, twisting movements vs unctrlled flinging and/or rotaory movements vs rapid, irreg, involuntary, dance-like movements flowing from 1 region to another vs continuous writhing of distal portions of 1+ extremities esp UE vs inc resistance to passive movement. Lec 17, slide 13
Huntington’s chorea vs Sydenham chorea
caudate > putamen in indirect pathway degenerate –> choreiform movements, cog & speech deteriorate –> bedridden; auto dom vs beta hemolytic streptococci –> ab against bacteria attack epitopes of BG => autoimmune dz –> rapid irreg movements of limb, face, trunk
hemiballismus
vasc lesion, infarct, dmg to contralat subthal nucleus –> more ballismus
Parkinson’s
degen melanin in granule-containing dopaminergic cells from substantia nigra pars compacta –> pill roll tremors, shuffling gait, stooped posture, mask-like facial expression, lose “arm swing” during gait
deep brain stimulation
electrodes placed on various nuclear structures esp subthal nucleus –> connect to subq electrical stimulator; replaced ablation procedures
Wilson dz/hepatolenticular degen
auto rec mutation in gene for copper-transporting protein –> copper accumulates in liver, lenticular nucleus, eye –> hyperkinetic d/o, Kayser-Fleischer rings around iris
hypothal has 3 sites of fxnal influence: ant pit vs post pit vs non-pit of hypothal. know which site does HEAL
f/light, stress, sex/reprod, growth, metab vs body fluid bal, maternal behavior vs temp, circadian rhythem, immunity, appetite, autonomic nervous system. Lec 18, slide 8
know Lec 18, slide 11
yep
medial vs ant preoptic nucleus vs suprachiasmatic nucleus
neuronal maturation –> sexual dimorphism, high GnRH make neurons produce lg peptides to target cells in ant pit vs maintain body temp vs direct retinal input, circadian rhythm
paraventricular vs supraoptic nuclei
both of their axons project to post pit that store their NT in terminals; circumventricular organs esp OVLT give systemic feedback to hypothal. secrete oxytocin vs secrete vasopressin
dorso/ventromedial nuclei vs ant nuclei of hypothal; what happens if there is a lesion?
feed, reprod, parenting, thermoreg vs appetite; medial (satiety center) –> obesity, lateral (hunger center) –> anorexia
post hypothal vs mammillary body
respond to temp changes –> sweat/shiver, lesion –> hypothermia; arousal, shift of attn, behavior vs limbic forebrain & midbrain fxnal integration –> emotions
epithal vs thal. thal blood supply
periventricular nuclei, habenular nuclei, stria medullaris, post commissure, pineal gland vs 2 ovoid grey matter masses making lat borders of 3rd ventricle, connected by interthalamic adhesion, have internally medullary lamina, separated in 3 groups: ant, med, lat. ant: thalamoperforating branches of P1; post: thalamogeniculate branches of P2; caudomedial area: medial post choroidal a (P2)
know thal nuclei
Lec 19, slide 14
relay nuclei vs association nuclei vs reticular nuclei
receive specific info and relay it to precise cortical target vs receive input from diverse regions & project to mult cortical regions; dorsomedial nucleus: receive afferents from olf, amygdala –> projects efferents to frontal lobe (dmg –> Wernicke-Korsakoff syndrome); pulvinar: process secondary visual info –> reciprocal projection relationship w/ sup colliculus, visual cortex, frontal & temp cortices (dmg –> visual attn d/o); centromedian: arousal, attn vs receive collateral afferents & to thal
internal capsule: ant limb vs genu vs post limb
b/w head of caudate nucleus & tentiform nucleus. frontopontine fibers: from frontal lobe to pontine nuclei for cerebellar involvement, thal radiations: connect thal to cortex, FEF fibers: from front eye field to CN nuclei vs closest to ant tubercle of thal; corticobulbar fibers: project to motor nuclei of CN vs b/w thal & lentiform nucleus; corticospinal tract: projects to ventral horn, thal radiations
what are the 4 limbic fxns? HOME
homeostasis (autonomic, neuroendocrine), olf, mem, emotion/drive
hippocampus fxns. what are its 3 parts?
mem, learning. dentate gyrus, hippocampus proper, subiculum
Papez circuit. Wernicke’s encephalopathy vs Wernicke-Korsakoff syndrome
transfer short term mem to long term mem; hippo emits signals to reverberate circuit –> store permanently in cerebral cortex for long term mem. hippo –> fornix –> mamillary nuclei/bodies –> mamillothalamic tract –> ant thalamic nucleus –> thalamogeniculate radiation –> cingulate gyrus –> cingulum –> hippo. thiamine defic exac by alc –> atxia, ophthalmoplegia, confusion –> thiamine supplements, stop alc vs advanced Wern’s encephalopathy –> dmg Papez circuit –> ant/retrograde amnesia, confabulation, apathy; dmg dorsomedial thal nuclei
Alzheimer’s
irreversible senile dementia; assoc w/ reduced cholinergic activation, degen neurons in entorhinal cortex & subiculum of hippo
dopaminergic pathways = in midbrain: mesolimbic vs mesocortical vs mesostriatal/nigrostriatal vs tuberoinfundibular pathways
ventral tegmental area –> limbic structures vs VTA –> prefrontal cortex vs substantia nigra pars compacta –> caudate/putamen vs hypothal –> pituitary
nucleus accumbens. what happens if excess dopamine?
primary mesolimbic DA target –> motivation/drive/reward. euphoria related to psychostimulants, schizo
amygdala. know pathway. Kluver-Bucy syndrome
in uncus of med temporal lobe. experience consequences, fear, f/light, anxiety, aggression. Lec 20, slide 32. bil destruction of amygdala –> no fear, hypersexuality, docile, overly attentive to all sensory stimuli
hypothal reg for water bal
dec plasma vol –> renin –> angiotensin II –> hyperosmolality –> hypothal-hypophyseal tract –> circumventricular organs –> paraventricular & preoptic nuclei activated by OVLT –> release vasopressin/ADH –> renal receptors –> H2O & electrolyte reabsorption from urine –> restore nml osmolality
