Exam2 Review Deck Flashcards
What is the path of dorsal column medial lemniscus from sensory resceptors to cortex?
- AB, 1, and 2 fibers enter more medially to spinal cord
- a few fibers stay around for local processing, most fibers go to f. cuneatus (above T6, lateral) and f. gracilis (below T6, medial) and travel up to synapse in gracilis/cuneatus nuclei in medulla
- in medulla decussate and ascend contralaterally in medial lemniscus to VPL of thalamus
- from thalamus go to sensory cortex (S1) cortical layer 4
what is path of spinothalamic tract from sensory receptors to cortex
- Ad, C, 3, 4 fibers enter more laterally to spinal cord
- travel in lissauers tract 2-5 segments up or down
- synapse in ipsilateral gray matter
- decussate via anterior white commissure
- ascend in contralateral spinothalamic tract to VPL
- from thalamus to sensory cortex cortical layer 1
what is path of trigeminal somatosensory tracts from sensory receptors to cortex?
proprioception and vibration path:
- AB and group 1/2 enter brainstem in pons
- synapse in ipsilateral principal trigeminal nucleus
- cross to join contralateral DC-ML tract
- synapse in VPM in thalamus
- fibers project to S1/S2 layer 4
pain and temp path:
- Ad and C fibers enter brainstem in pons
- travel into medulla via ipsilateral spinal tract of V
- synapse in spinal nucleus of CN V
- cross and join contralateral ascending spinothalamic tract
- synapse in VPM in thalamus
- fibers projects to S1/S2 layer 1
What is the somatotopic organization of sensory systems in the brainstem?
medulla: no face there, legs = anterior
pons: face = medial, legs = lateral
midbrain:
arms are medial to legs with two exceptions: posterior columns and S1 cortex
- pain temp systems = no organization
what is the somatotopic organization of sensory systems in the thalamus?
thalamus: face/arms medial, legs lateral
- pain temp systems = no organization
* arms are medial to legs with two exceptions: posterior columns and S1 cortex
what is the somatotopic organization of sensory systems in the cortex?
cortex: legs medial, face lateral
- pain temp systems = no organization
* arms are medial to legs with two exceptions: posterior columns and S1 cortex
What are the characteristics of AB fibers?
sense touch/pressure cutaneously
thick myelinated, fast conducting [but not as fast at group 1, about equal to group 2]
What are characteristics of AD fibers?
sense pain/temp cutaneously
thin myelinated slow conducting
What are characteristics of C fibers?
sense pain/temp cutaneously
not myelinated slow conducting
What are characteristics of Group 1 [a and b] fibers?
1a = primary to muscle spindle 1b = to golgi tendon organ
sense touch/pressure in muscle
thick myelinated, fasted conduction, biggest fibers
what are characteristics of group 2 fibers?
secondary fiber to muscle spindle
sense touch/pressure in muscle
thick myelinated, fast conduction
what are characteristics of group 3 and 4 fibers?
- sense pain and temp in muscle
3: thin myelinated slow conduction
4: not myelinated, slow conduction
What are the 4 areas of S1 and their input info?
1, 3b = cutaneous info [Ab]
2, 3a = proprioception [group 1a, 1b, 2]
What is the function of S2?
process info during bimanual manipulation
- has representation from both sides of body [via internal capsule fro contralateral body and vai corpus callosum from contralateral S1 or ipsilateral body]
What are the principal input layers of S1 for different sensory modalities?
layer 4 = DC-ML
layer 1 = spinothalamic
thalamic VA nucleus: inputs, outputs, function
input –> output:
cerebellum/basal ganglia –> frontal cortex
function: motor
thalamic VL nucleus: inputs, outputs, function
input –> output:
cerebella/basal ganglia –> M1/PM/SMC
function: motor
thalamic VPL nucleus: inputs, outputs, function
input –> output:
medial lemniscus DC-ML –> S1/S2
spinothalamic –> S1/S2
function: somatosensory pain/temp/proprioception from body
thalamic VPM nucleus: inputs, outputs, function
input --> output: spinal nucleus of V --> S1/S2 principal nucleus of V --> S1/S2 spinothalamic --> S1/S2 solitary nucleus --> gustatory cortex spinothalamic --> gustatory cortex
function: somatosensory pain/temp/proprioception from face AND taste
thalamic MGN nucleus: inputs, outputs, function
input –> output:
superior olive and inferior colliculus of tectum –> auditory cortex [heschl’s]
function: hearing
thalamic LGN nucleus: inputs, outputs, function
input –> output:
retina–> visual cortex [calcarine]
function: vision
What do free nerve endings sense?
pain and temperature
what do meissner corpuscles sense?
light touch
what do pacinian corpsucles sense?
vibration, pressure
what do merkel discs sense?
sustained pressure, position sense
If you have loss of pain and temp on right side starting at T5 coming from contralateral spinothalamic injury, where would the level of injury be?
- fibers descend and take 2-3 spinal segments to reach opposite side so lesion is likely 2-3 segments above this [T2-T3]
Importance/function of cortico-thalamic input?
- modulates output of thalamic relay neurons via feedback and feedforward inhibition
Role of thalamus in controlling states of consciousness [tonic vs burst, transition between]?
tonic firing in awake/alert states –> dorsal thalamic relay neurons fire in response to depolarization, allows flow of info to cortex
burst firing in drowsy/deep sleep –> thalamic relay neurons fire in oscillatory manner = blocks flow of info to cortex
to enter tonic state: ACh, histamine, NE depolarize membrane
to enter burst state: 5HT hyperpolarizes membrane
What is effect of thalamic lesion that damages VPL/VPM [thalamic syndrome]?
- contralateral hemianesthesia
- excruciating central pain
What causes a tremor state?
- rhythmic bursts in VA/VLa due to abnormalities in GP-thalamus circuits
What happens if lesion of anterior or MD nuclei in thalamus?
- amnesia –> disrupts amygdala/hippocampus circuitry
What causes absence seizures? what are they?
- due to abnormal sustained TRN GABAergic neuron activity
- characterized by sudden arrest of movement, blank stare, fluttering eyelid, loss of ability to interact
What is path for affective component of pain perception?
- begins in lamina I/V in spinal cord or spinal nucleus of V
- travels via spinothalamic/trigeminothalamic tracts
- go to: midbrain periaqueductal gray [PAG], rostral ventral medulla, amygdala, hypothalamus, VM/MD of thalamus –> insula
What is process by which descending modulatory systems inhibit pain transmission?
PAG in midbrain and RVM [rostral ventral medulla]
- -> locus ceruleus [NE], raphe nuclei [5HT]
- -> release NE/5HT onto local inhibitory interneuron in spine
- -> they release enkephalin [endogenous opioid] onto synapses in lamina 1, V
What is nociceptive pain?
- physiologic [normal] stimulus-dependent pain
first pain by Ad, second pain by C
spinothalamic nerves get info from Ad/C and Ab, Ab activate inhibitory interneurons = dampen throughput of pain info
referred: group 3/4 terminate on spinothalamic neurons that are also getting Ad/C fibers –> pain perceived to be coming from cutaneous receptive field
What is inflammatory pain?
- pain hypersensitivity due to peripheral inflammation
- -> have sponatneous and stimulus dependent pain
- -> protective –> adis in healing
mech: neurochemical mediators secreted by immune cells cause pain fibers to discharge aberrantly –> amplification peripherally and centrally
What is dysfunctional pain?
- same components as inflammatory pain but without evidence of inflammation
- not protective [does not support healing/repair]
What is neuropathic pain?
- pain felt in absence of stimulus = maladaptive, chronic, debilitating
mech:
- any lesion or disease that causes trauma at nerve terminals/axons can cause irritation of nerves
What is central sensitization?
- synaptic signaling strength of pain paths exaggerated; pain hypersensitivity to normal inputs
mech:
- increased membrane excitability in peripheral axons via upregulation Na channels
- increased synaptic efficacy via upregulation glutamate receptors
- decreased inhibition in local interneuron networks
What is action of enkephalin in top down pain inhibition?
- released by local inhibitory interneurons in spine onto synapses in lamina 1/5
- presynaptically: decreases NT release from pain/temp Ad and C fibers
- post-synaptically: causes hyperpolarization of ascending spinothalamic neurons
What is the function of the ciliary body?
- makes aqueous humor
- contains ciliary muscles that change shape of lens
What is the function of the choroid?
- contains connective tissue, blood vessels
provides nutrients
What is a cataract? mech?
- clouding/yellowing of lens –> decrease vision
- develops slowly with age
treat: artificial lens replacement
What is glaucoma? mech?
- excess aqueous humor [due to overproduction or under-drain] –> causes increased IOP [pressure] –> optic nerve injury, optic disc atrophy with cupping –> progressive decreased vision [starting with peripheral]
treat: beta blockers, surgery
what is presbyopia? mech?
- loss of ability to change lens shape [focus near vs far]
- due to normal aging, lens less elastic
what is retinitis pigmentosa? mech?
- progressive retina degeneration
signs: night/low vision blindness, tunnel vision
slow process –> takes decades
what is macular degeneration? two types?
- degeneration of macula [central retina], fovea –> distortion [straight lines look wavy], central loss of vision [scotoma], blurry vision
dry: deposition of drusen = yellow stuff under macula, gradual loss of vision
wet: abnormal blood vessel growth, more rapid loss of vision. treat = VEGF, angiogenesis inhibitors
what is diabetic retinopathy? stages?
- retinal damage due to chronic hyperglycemia
findings: microaneurysms, hard exudates, intraretinal hemmorrhage, cotton wool spots
early = non-proliferative = asymptomatic
pre-proliferative: damaged capillaries leak blood –> macular edema
proliferative: chronic hypoxia –> new blood vessel formation on retina
What is function of cones?
Cones = central vision, color,high spatial resolution, low light sensitivity
- use parvocellular path, slower
What is function of rods?
rods = peripheral vision, light detection, poor spatial detail, more light sensitive, single photon
- use magnocellular path, faster
What is path of light from periphery through retina to optic nerve?
- light crosses entire retina –> rods/cones –> bipolar –> ganglion –> optic nerve
What are the 3 chambers of the eye? what do they each contain?
- anterior and posterior chambers in front of lens [separated by iris]
- vitreous body [between back of lens and retina, contains jelly-like substance
What is optic neuritis? presumed pathogenesis?
- inflammatory optic neuropathy
due to demyelination - -> have unilateral loss of visual acuity, pain on eye movement
- -> high risk of developing MS
What should you think: pt says straight lines appear crooked?
dry ARMD [macular degeneration]
What is contained in “nuclear” layers in retina? what about “plexiform” layers?
nuclear = contains cell bodies plexiform = contains synapse
What layer of retina has ganglion cell axons?
nerve fiber layer
What is contained in outer plexiform layer vs inner plexiform layer?
outer = synapse between photoreceptors, bipolar cells, horizontal cells
inner = synapse between bipolar, amacrine, ganglion cells
What is the order of cells from out to in in the retina?
photoreceptors –>horizontal cells –> bipolar cells –> amacrine cells –> ganglion cells
horizontal = horizontal connections in area where photoreceptors and bipolar cells synapse amacrine = horizontal connections in area where bipolar and ganglion cells synapse
What is function of interneurons in retina?
- release NT but dont generate AP
include: horizontal, amacrine, bipolar - ganglion: only cells that generate APs
What info does left optic tract carry retrochiasmally?
right visual field for both eyes
What info is carried in parietal vs temporal [meyer’s] projections?
parietal = contralateral inferior quadrant in both eyes meyers = contralateral superior quadrant in both eyes
What happens if left optic nerve lesion?
- left anopia = no vision through left eye
What happens if optic chiasm lesion?
- temporal hemianopia = no vision in temporal half [lateral] of visual field on both sides
what happens if left optic tract lesion?
- right homonymous hemianopia = loss of vision in right half of visual field for both eyes
what happens if right temporal optic radiation lesion?
temporal = meyers = pie in the sky
left homonymous superior quadrantopia = loss of vision in left upper quadrant in both eyes
what happens if left parietal optic radiation lesion?
right homonymous inferior quadrantopia = loss of vision in right lower quadrant in both eyes
What happens if left visual cortex lesion due to PCA infarct?
right homonymous hemianopia with macular sparing = loss of vision in right half of visual field for both eyes but central area spared due to collateral MCA circulation
What is the physiologic blind spot
- region where optic nerve exits retina
- no photoreceptors
- on nasal half of visual field
What are the layers of the LGN and their inputs? which are magno vs parvo? which are ipsi vs contra?
layers:
1,2 = magnocellular [rods, light]
3, 4, 5, 6 = parvocellular [cones, color]
1, 4, 6 = contralateral
2, 3, 5 = ipsilateral
What is mech for dilation vs constriction of pupil?
dilate: dilator pupillae, sympathetic
constrict: sphincter pupillae, PNS via edinger westphal
What is the pupillary light reflex [ex. shine light into right eye]?
- afferents from right CN 2 –> synapse in right pretectal nucleus in midbrain –> activates bilateral edinger-westphal nuclei
- pupils contract bilaterally via CN3
What is the pupillary near reflex? triad?
triad all controlled by CN3 and edinger westphal
- accomodation: change lens shape, ciliary muscle
- convergence: eye adduction, medial rectus
- pupillary constriction, pupillary sphincter
What happens in cranial nerve 3 palsy? cause?
cause: aneurysm of posterior communicating artery [Pcom]
signs
- mydriasis [dilation]
- ptosis
- can’t react to light or near
- down and out gaze
What is tonic pupil?
- dissociation of light-near reflexes due to lesion of ciliary ganglion
signs: - mydriasis [dilation]
- absent pupillary light reflex [efferent defect]
- preserved pupillary near reflex
What is argyll-robertson pupil?
- bilateral
- due to tertiary syphilis, diabetes
- pupils accomodate [constrict in near reflex] but don’t react [constrict in light reflex]
What is horner’s syndrome?
- sympathetic disorder –> associated with lesion of spinal cord above T1
triad: PAM is horny - ptosis [drooping eyelid]
- anhidrosis [absence of sweating]
- miosis [constriction]
what is afferent papillary defect/marcus gunn pupil?
- due to optic nerve damage or retinal injury
- affected eye does not constrict as much compared to unaffected eye when you shine light into it
- test with swinging flashlight
What is saccade?
rapid eye movement
What is optokinetic nystagmus?
combination of saccade + smooth pursuits to allow eyes to follow moving object
what is vergence?
disconjugate eye movements –> allow eyes to focus on near [convergence] or far [divergence]
What is abnormality associated wtih PCom aneurysm?
CN 3 palsy
What is path of CN 3?
CN 3 nuclei + edinger westphla in midbrain at level of superior colliculi
- exit ventral –> pass between PCA/SCA –> cavernous sinus –> superior orbital fissure
What is path of CN 4?
CN 4 nuclei in midbrain at level of inferior colliculi –> exit dorsally, cross –> cavernous sinus –> superior orbital fissure
What is path of CN 6?
CN 6 nuclei in pons at facial genu/colliculis –> exits ventrally –> passes under gruber’s ligament –> cavernous sinus –> superior orbital fissure
What happens in CN 4 palsy? cause?
- eye up, diplopia, head tilt toward side of lesion
cause: head trauma, congenital deffect
what happens in CN 6 palsy? cause?
- ipsilateral eye in [adducted], horizontal diplopia, affected eye can’t abduct
cause: high ICP
What is function of MLF? location?
facilitates conjugate horizontal gaze movements between CN 6/CN3
- located along cerebral aqueduct, 4th ventricle
Which lateral rectus and which medial rectus are innervated by the left PPRF?
left PPRF –> left lateral rectus, right medial rectus
What is the path of innervation upstream to the PPRF?
Frontal eye field –> internal capsule –> decussates at midbrain-pontine junction –> PPRF
Which direction conjugate gaze does right frontal eye field [FEF] control?
right frontal eye field –> left PPRF –> look left [left lateral rectus, right medial rectus]
What happens if lesion in left abducens nucleus or PPRF?
- impaired conjugate gaze in both eyes to side of lesion
- -> try to look left = nothing happens
- -> try to look right = normal conjugate gaze
What happens if lesion in right MLF?
INO!
when look righ: fine
when look left: left eye goes and has nystagmus, right eye stays [impaired abduction]
preserved convergence b/c different path
INO due to left MLF lesion can be seen when gaze toward which side?
when try to gaze right
What disease should you think if you see INO in younger vs older pt?
INO in younger = usually bilateral = MS
INO in older = usually unilateral = stroke
What is the function of the PPRF?
- supranuclear control of eye movements –> PPRF is in the pons, receives signals from frontal eye fields and directs conjugate eye movement via MLF
PPRF initiates conjugate movement
What is the vestibulo-ocular reflex?
- eyes move in opposite direction of head rotation to maintain focus on target
What is one and a half syndrome[ex on right side]?
unilateral lesion of right PPRF and MLF [ie dorsal caudal pons stroke]
- ipsilateral horizontal gaze palsy
- ipsilateral INO
look right –> nothing happens [both eyes stay b/c right PPRF lesion]
look right: right eye goes, left eye nothing
What is cause of nerve 3 palsy?
aneurysm of posterior communicating artery [Pcom]
uncal herniation
What happens in frontal eye field lesion?
- gaze preference = ipsilateral gaze deviation to look at the lesion
What is path of action VOR if head turns to left?
- endolymph in left horizontal semicircular canal shifts forward and activates nerve VIII
- projects to ipsilateral vestibular nucleus
- projects to contralateral CN 6 nucleus and via MLF excite right LR and left MR to turn eyes to the right
- other projections from vestibular nuc project to ipsilateral CN 6 to inhibit left LR
What is caloric testing?
way to measure VOR using warm/cold water to generate currents in endolymph of horizontal canals, causes horizontal nystagmus
COWS
cold = opposite –> quick phase of nystagmus toward ear opposite water injected ear
warm = same side –> quick phase of nystagmus toward same side as water injected ear
Different roles of inner vs outer hair cells?
inner hair cells = 1 row, 95% of auditory fibers, dransduce sound to auditory nerve via pressure waves transmitted through perilymph that cause movement of basilar membrane
outer hair cell = 3 row, support for inner cells, amplify movement of basilar membrane, make otoacoustic emissions [low freq hearing loss = outer hair cells]
Parts and function of external ear?
outer = pinna + external auditory meatus
pinna - vertical localization of sound
external auditory meatus - magnify sound
Parts and function of middle ear?
middle = ossicles, tensor tympani, stapedius, eustachian tube
ossicles = malleus, incus, stapes
tensor tympani - attached to malleus, trigeminal = tenses tympanic membrane so you can hear high frequency
stapedius - associated with stapedius, dampens loud noise
Parts and function of inner ear?
inner = cochlea, canals, vestibule
vestibule - contains utricle + saccule
cochlea - converts sound pressure to nerve pulse
semicircular canals - detect rotational movement
Auditory path from ear into CNS?
pinna –> external auditory meatus –> tympanic membrane –> oval widnow –> scala vestibuli –> basilar membrane of scala media –> inner hair cell –> auditory nerve
If ipsilateral hearing loss what does this mean about location of lesion?
- means it much be in cochlear nucleus or auditory nerve or ear itself
- from cochlear nuclei, auditory system goes to superior olives and becomes bilateral
What is place code?
- cells that respond to highest sound frequences are more posterior
What is tonotopy?
- ## sound pitch [frequency] is represented topographically in auditory system
What is the process of sound localization?
- inter-aural intensity differences
- inter-aural timing differences
sound localization in horizontal plane depends on bilateral input to superior olive
in vertical plane = depends on sound reflection at pinna
Why important to screen infants for hearing loss?
- critical point in development of hearing and speech wihtin first 6 months
What is function of vestibular system?
- head motions and head position in space
- angular rotation [canals] and linear acceleration [otoliths]
What is anatomy of the labyrinth?
- semicircular canals = bony canals in orthoganol planes [horizontal, anterior, posterior], filled with perilymph, have swelling at one end = ampulla from which sensory epithelium hangs
- otoliths = filled with endolymph, surrounded by perilymph
- utricle = horizontal, saccule = verticle
What symptoms associated with central vestibular damage vs peripheral?
central: severe imbalance/ataxia, persistent, nystagmus not inhibited by fixation of eyes, changes direction with gaze
peripheral: ataxia, gait veers toward lesion, N/V, hearing loss, fullness in ear, acute, often position dependent, delayed nystagmus away from side of lesion
What is the path from inner ear to vestibular cortex?
- canal/otolith primary afferents get info from hair cells –> form CN VIII cochlear portion
- terminate in vestibular nuclei in medulla/caudal pons
- cross at midline –> VP of thalamus –> vestibular cortex
What is the function of vestibulo-thalamo-cortical path?
conscious perception of balance
What is the function of lateral and medial vestibulo-spinal tracts?
lateral = balance and postural control in spinal cord medial = maintains stability of head and neck as body moves
what is the function of vestibulo-autonomic projects?
control BP, HR, respiration, etc in response to posture
–> this can go wrong in elderly = orthostatic hypotension
How do you distinguish conductive vs sensorineural hearing loss?
conductive = air bone gap, air
- air conduction decreased, bone conduction normal
sensory neural
- AC = BC = both depressed
- usually bilateral
what are common causes of conductive hearing loss?
due to outer or middle ear
- ear wax
- fluid
- eustachian tube swelling
- tympanic membrane perforation
- otosclerosis [genetic fixation of stapes]
what are common causes of sensorineural hearing loss?
due to middle or inner ear
- aging [high freq lost]
- genetic [middle freq lost]
- noise [high freq lost]
- acoustic neuroma [ low speech discrimination]
- meniere’s disease [bilateral]
What is utility of tuning fork tests [weber, rinne]?
weber = lateralizes toward conductive hearing loss, away from sensorineural hearing loss
rinner = normally AC > BC; in conductive B > AC
What is utility of tympanometry?
test movement of ear drum by presenting tone
what is utility of audiogram?
way to diagnose hearing loss
- establish pure tone threshold for air and bone
- test speech reception threshold for each ear
- provide speech discrimination score
How do you distinguish vertigo from imbalance/disequilibrium/lightheadedness?
vertigo = false sense of motion imbalance = sensory disturbance disequilibrium = feels off balance, drunk lightheaded = feels faint
What is anatomy of cochlea?
- bony cavity, coils on itself
- 3 compartments:
scala vestibuli = in
scala media = membrane middle endolymph
scala tympani = out
What is acute unilateral vestibular loss?
due to virus in inner ear, acoustin neuroma, injury to inner ear
- gait ataxia toward lesion
- romberg
- sudden onset vertigo, N/V, nystagmus
What is meniere’s?
due to distension of membranes of inner ear [too much endolymph]
- episodic, spontaneous vertigo
- lasts hours
- accompanied by N/V
- unilateral hearing loss, fullness, tinnitis
What is BPPV?
- otolith/otoconia dislodged and float in endoluymph, go to posterior canal
- abrupt positional vertigo
- 5-10 sec latency of nystagmus
- dix hallpike
What is bilateral vestibular loss?
- age related, head trauma, aminoglycosides
- absent caloric response in both ear, ataxia, oscillopsia [perception of oscillating vision]
what happens in lead poisoning?
children: acute encephalopathy, IQ impairment
adult: ab pain, writ drop
burtons lines = discoloration of upper gums
What happens in mercury poisoning?
= mad hatter –> irritability, shyness, red cheeks, tremor
- encephalopathy, peripheral neuropathy, seizures
What happens in arsenic poisoning?
- encephalopathy, N/V, renal failure, garlic breath
what happens in thallium poisoning = rat poison?
vomiting, diarrhea, paresthesias late hair loss
What happens in manganese poisoning?
bradykinesia [looks like parkinsons], hyperreflexia, confusion
What is marasmus?
balanced starvation
- see in < 1 yo
mental changes, growth retardation
what is kwashiorkor?
not enough protein
- see in 1-3 yo
- muscle wasting, big belly
What happens in vit A toxicity?
- ICP [pseudotumor cerebri], alopecia, teratogen
What are the neuro effects of thiamine deficiency?
- painful peripheral neuropathy
what are neuro effects of pyridoxine [B6] deficiency?
- peripheral neuropathy, microcytic anemia, convulsions
– seizures in infants < 180 mo
what are neuro effects of folic acid [B9] deficiency?
- neural tube defects
what are neuro effects of cobalamine [B12] deficiency?
- subacute combined degeneration [posterolateral column disease]
- -> parastehsias [pins/needles], loss of vibration/position sense
- spastic + ataxic weakness progressive
- babinski
- optic atrophy
What is wernicke’s encephalopathy?
- due to thiamine deficiency, alcoholism
- untreated leads to korskoffs
- lesion of thalamic nuclei
- ataxia, opthalmoplegia, gaze palsies, confusion
what is korsakoff’s psychosis?
- due to thiamine deficiency, alcoholism
- severe memory deficit, confabulation, dementia
What makes olfactory system unique compared to other sensory systems?
- cell bodies of primary afferents directly in olfactory epithelium
- continuous turnover
- no thalamic relay
- ipsilateral
Path of olfactory from periphery to cortex?
- cilia of olfactory receptor cells
- ipsilateral to folfactory bulb
- olfactory tract
- olfactory cortex
Path of gustatory from periphery to cortex?
- taste cells synapse to primary afferents from branches of CN VII [anterior 2/3], IX [posterior 1/3], X [back of tongue]
- project to nucleus of solitary tract
- to thalamus [VPM] via central tegmental tract
- to primary gustatory cortex via internal capsule
== exclusively ipsilateral
Causes of olfactory dysfunction?
- URI, sinus infection
- head trauma
Causes of gustatory dysfunction?
- ipsilateral loss of taste from anterior 2/3 tongue = lesion of CN VII root
- viral infection
- head trauma
Difference alpha and gamma motoneurons [organization, fibers they innervate, function]
alpha = innervate extrafusal, force generating gamma = intrafusal, control and adjust sensitivity of muscle spindle
What is a motor unit?
- one motor neuron and all the fibers it innervates
What is function/innervation of muscle spindle?
- record muscle length and rate of length change
What is function/innervation of golgi tendon organs?
record tension generated at myotendinous junction during contraction
What are the components of deep tendon reflex?
- group 1a/2 sensory afferent sense muscle stretch
- synapse on alpha motor neurons of same muscle that gave rise to afferents as well as synergistic
- also info goes to inhibitory group 1a interneurons that inhibit motor neuron of antagonistic muscles
- aMN causes stretched muscle to shorten/contract
What is pyramidal vs extrapyramidal motor system?
extrapyramidal = cerebllum, basal ganglia
what is the path of corticospinal tract from M1 to muscle?
- descends
- crosses at medulla in great pyramidal decussation
- descends contralaterally
role = fine motor control of distal muscles
What is role of descending motor paths in static posture?
- lateral VST and medial [pontine] RST –> tonic excitation of anti-gravity extensors
- purkinje cells [cerebellum] –> inhibi lateral VST
- cerberal cortex –> stimulate lateral [medullary] RST –> inhibits extensor MNs
Whats spasticity vs rigidity?
spasticity = UMN damage --> hyperactive myotatic reflex, hypertonia of anti-gravity rigidiy = damage to basal ganglia, hypoactive myotatic reflexes, hypertonia in extensors and flexors, cog wheel
Functional impairment of each of different motor cortical areas?
M1 = motor execution. lesion = loss of fine motor control
PM [premotor] = sensory guided movement, severe impairment in performing sensory guided motor tasks
SMA/M2 = internally generated movement, impaired self-initiated tasks, impairment in tasks taht require bimanual coordination
Presentation of UMN vs LMN lesion?
UMN = spastic, hyperreflexia, + babinksi LMN = flaccid, hyporeflexia, atrophy, hypotonia, distribution in particular area, fasciculations
ALS: presentation, course, management, differential
combined anterior horn + pyramidal tract
- spasticity, clumsiness, hyperactive reflex, + babinksi
- weakness, wasting, fasciculations
- need to show disease above foramen magnum otherwise could be cervical spondylosis
How do you differentiate disorder of motor cortex vs brainstem vs anterior horn vs peripheral motor neuropathy vs neuromuscular junction vs muscle
motor cortex: UMN = spastic
internal capsule = contralateral motor + sensory
brainstem = crossed signs
spinal cord anterior horn = LMN –> ipsilateral weakness/atrophy/fasciculations
peripheral neuropathy = distal weakness
NMJ = fluctuating weakness, fatigable muscles, limb weakness
muscle = proximal weakness,
What is effect of corticobulbar vs LMN lesion for facial nerve?
s
What is effect of corticobulbar vs LMN for hypoglossal nerve?
s
What is presentation of brown-sequard?
below lesion:
- ipsilateral loss of proprioception,UMN deficits [spastic]
- contralateral loss of pain/temp
at level
- ipsilateral LMN deficits
- ipsilateral loss of all sensation
What is presentation of syringomyelia?
- bilateral loss of pain/temp sensation in the area
- seen with chiari 1
what is presentation of conus medullaris lesion?
suddne onset, bilateral L1, L2
- symmetric weakness and saddle anesthesia
- LMN bladder/bowel develops early
what is presentation of cauda equina lesion?
- gradual onset, asymmetric, L4, L5, S1 nerve roots
- asymmetric flaccid paralysis/hypotonia, saddle amnesia, radicular/sharp pane
LMN bladder/bowlel develops late
What is presentation of complete spinal cord transection?
- bilateral loss of sensation below lesion + para/quadriplegia
What is presentation of posterolateral column disease?
- demyelination of dorsal columns, corticospinal tracts
- paresthesia in hands and feet, + romberg, impaired proprioception
What is presentation of anterior spinal cord syndrome?
- happens in upper thoracic chord
- bilateral loss of motor control, loss of pain/temp sensation, preserved mechanosensation
What is presentation of disc prolapse?
s
What is presenation of spondylolisthesis?
s
What is presentation of tabes dorsalis?
- due to tertiary symphilis
- degerneation of dorsal columns –> progressive impaired sensation/proprioception and sensory ataxia
no deep tendon reflex, + Romberg
What is presentation of spinal tumor?
- pain, numbeness, UMN spasticity/bowel + bladder
What is presentation of epidural abscess?
- back pain, radiculopathy
What is spinal shock?
immediate areflexia [LMN sign] and motor paralysis below level of shock, reflex gradually returns, reveals true UMN lesion
Why do lesions in brainstem cause more symptoms than in cerebrum?
lots of fiber tracts running in small apce
What are “crossed signs”
face effects on opposite side from body effects
What is wallenberg syndrome?
- lateral medulla, affects CN V, CN 9, 10, 11 in nucleus ambiguus
- loss of pain in ipsi face, contra body
- hoarse voice, dysphagia, decreased gag
- nystagmus, N/V, vertigo, gait ataxia,
- horners
What are defining features of a brainstem syndrome?
crossed signs –> ipsilateral symptoms of face from cranial nerves, contralateral symptoms on body
Medial lesion vs lateral lesion which affects motor vs sensory?
ventromedial lesion = affects motor, corticospinal
dorsolateral = affects sensory, spinothalamic
What is rubrospinal tract?
- contributes to movement of upper limb
- from red nucleus, immediately cross and descend lateral funiculus
What is tectospinal tract?
coordination of head movements
- originate superior colliculus
- crosses near origin and descends to cervical levels only
What is function of corticoreticulospinal tract?
maintenance of posture during complex movement
What is inverse myotatic reflex?
- Group 1b afferents sense tenson on GTO
- inhibit homonymous aMNs and synergists to terminate contraction
- excite antagonits
