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119 Cards in this Set

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where do lower motor neurons synapse? what types of neurons do they involve?
synapse directly with mm tissue.

they are IPSILATERAL to the mm they innervate.

involve gamma and alpha motor neurons.
what are alpha motor neurons? where are they found?
they are neurons found in the spinal cord which synapse and cause contraction of skeletal mm.

mm fibers innervated by a-MNs are mixed in the mm itself. Ach is the transmitter.
how many mm fibers will one a-MN innervate? how is the size of the motor unit related to quality of motion?
ll: 1/2000
ul: 1/200
eye: 1/20

the more motor units = more fine control.
where in the spinal cord are motor neurons found?
ventral horn, lamina IX.

lamina IX is greatest in cervical region (bp), lumbar and sacral. (smallest in thoracic)
identify innervation levels for dx of spinal injury for the following mm:

iliopsoas
quads
hams
TA(DF)
EHL
Gastroc (PF)
iliopsoas: L2,3
quads: L3,4
hams: L4,5
TA(DF): L4
EHL: L5
Gastroc (PF): S1
what are muscle spindles? what innervates them?
they are small groups of mm surrounded by special sensory fibers. gamma MN innervate them. they are smaller than alphas and report proprioception to the brain.
when would a muscle spindle synapse on an alpha motor neuron or interneuron?
a stretch reflex
what is a lower motor neuron injury?
damage to a-MN or it's brainstem equivalent.
causes immediate denervation and paralysis of mm fibers supplied by nerve.

IPSILATERAL FLACCID PARALYSIS
what is considered an upper motor neuron?
all nerve cell bodies and their axons in the cortex or brainstem which synapse with LMNs (ie a-MNs).
where does the corticospinal tract originate? what does it supply?
starts in PRECENTRAL GYRUS, travels with corona radiata, internal capsule to midbrain.

supplies deep back, upper and lower limb musculature.
what structure does the corticospinal tract create in the medulla (name arterial supply)? where does it decussate? does the entire tract decussate here?
it forms the pyramids, supplied by the ASA.

85% decussates in the closed medulla. LCST

15% decussates at level of innervation. ACST
what is the hierarchy of motor function with regards to the frontal lobe?
pre-frontal gyrus dictates the actions of pre-motor area #6.

#6 dictates the actions of the precentral gyrus.

** basal ganglia and cerebellum are also involved with motor fxn**
what types of cells are involved in the corticospinal tract?
pyramidal cells
what are the cortical fibers from the precentral gyrus called when they reach the midbrain? what is the arterial supply to this area?
the basis pedunculus.

bbr off the PCA and sometimes the posterior communicating artery.
what is the arterial supply to the internal capsule? what is the somatotopy of the internal capsule?
lateral striate aa (off MCA)

arm is lowest and most medial. legs are highest and most lateral (same pattern after decussation)
describe the path of the corticospinal tract and it's arterial supply as it changes.
1.internal capsule (lateral striate - MCA)

2.basis pedunculus (PCA & sometimes post.comm.artery)

3.basilar pons (basilar artery)

4.pyramids of open medulla (ASA)

5.closed medulla (85% decussate).
LCST:PSA
ACST:ASA
post-decussation, what is the pyramidal tract now called? what is it's path and arterial supply?
lateral corticospinal tract.
continues down lateral funiculus of SPINAL CORD ipsilateral to mm innervated.

leave tract to penetrate ventral horn, terminate on a-MNs. PSA supplies the lcst.
what is the path of the acst? what is it's somatotopy?
it is pyramidal fibers which do NOT decussate, but continue straight into the anterior funiculus of the spinal cord.

contralateral to mm innervated in SPINAL CORD.

decussates AT LEVEL, crosses via anterior white commisure.

somatotopy: UE is posterior/dorsal. LE is anterior/ventral.
how does the corticospinal tract control most motor neurons? what type of movement are they most critical for? why?
they control most motor movements thru interneurons (small amt directly contact a-MNs).

critical in fine motor b/c most deep back/postural mm have alternate pathways for activation.
what are the extra-pyramidal pathways? how do they work?
reticulospinal
vestibulospinal
rubrospinal

they influence spinal motor neurons but cells originate outside motor cortex.
not dependent on precentral gyrus.
what are the inputs to the reticulospinal pathway? where is it's nucleus? what is it's path?
input: sensory, area 6, fastigial nucleus(balance)

nucleus: central nucleus of reticular formatin (midline of lower/middle pons. and medulla)

path: bilateral (in cord). elicit delayed movement in limbs. mostly proximal and post-axial nn and mm, few flexor mm (fine movement).
which alternate pathway affects primarily extensor and deep back mm (postural control)? what is it's path?
vestibulospinal.

axons arise ipsilaterally to affected mm and synapse on interneurons in spinal cord.
what is the input for the rubrospinal tract? what levels in humans are mostly affected?
input is from cortex and cerebellum. red nucleus gives rise to some motor fibers which decussate at ventral tegmental decussation.

in humans this only reaches the cervical and upper thoracics.
what alternate path arises from the superior colliculus? what types of movement does it deal with?
the tectospinal tract.
it ends in the cervical region, may also affect CN XI. deals mostly with neck motion associated with eye movements.
where does a UMN injury occur? what are the characteristics of the syndrome?
damage to any UM neuron OR IT'S AXON.

injury will cause shock with initial flaccid paralysis.

initial recovery characterized by the following syndrome:

babinski (+)
spasticity
paresis
why can fxn return to the ipsilateral motor paresis in brown-sequard syndrome?
acst is intact on contralateral side and won't decussate until it reaches side of lesion. over time this tract can develop, returning fxn to 90% of patients.
why is spasticity characteristic of an UMN injury? paresis?
spasticity: LMN, a-MN and g-MNs are still intact. so are reflexes. (no inhibitory signals get thru)

paresis: this type of weakness can occur with stroke b/c the extra-pyramidal pathways are intact.
what is the difference btwn the arterial supply of the PSA and the ASA?
PSA: UNILATERAL LL area

ASA: BILATERAL UL area
what is lost if the ASA is occluded?
the ASA supplies the midline medulla (pyramids). an occlusion results in loss of the medial lemniscus and medial motor portion of corticospinal tract (UE).
what occlusion would cause loss of LE motor fxn?
occlusion of the vertebral aa which supplies the lateral pyramid.
what does an infarct of the ACA cause?
it affects sense and motor function of the lower extremity up to the waist.
what major sulcus does the MCA run in? what does it supply?
it runs in the central sulcus (rolandic).

supplies motor and sensory from waist/trunk up to UE/face.
what artery supplies the lentiform nucleus and the internal capsule?
lateral striate aa (small) off the MCA. **prone to hemorrhage**
describe LMNs of the cranial nerves.
they fxn like a-MNs of the spinal cord.
not as large, but multipolar and controlled by UMNs.
where would you find the nucleus to CN III? name the defining structures and any additional nuclei.
oculomotor nucleus is at the level of the superior colliculus and the cerebral aqueduct.

edinger-westphal nucleus: pre para to ciliary mm

red nucleus: III and E-W fibers pass thru
which LMN CN decussates? where is it located and what does it innervate?
trochlear n (IV)
it's located in low midbrain (inferior colliculus) and it innervates the superior oblique mm.
what CN is under the 4th ventricle? what tegmental structure interconnects the CN involved with sight?
Abducens (VI), lateral rectus mm.

MLF interconnects III, IV and VI to give fine control of the eyes.
what structure indicates the presence of the motor nucleus of the trigeminal nerve?
the superior cerebellar peduncle (found in the upper pons).
describe the path of the facial nerve. what level is it found at? what other nuclei/fiber types are present here?
the facial nucleus is found just rostral to the pontomedullary junction. the fibers course dorsally around the ABDUCENS nerve (VI).

parasympathetic fibers from the superior salivatory and lacrimal nuclei are also present.
where is CN IX found? what other fibers course with it?
open medulla:

The sensory information in IX goes to the solitary nucleus, a nucleus it shares with VII and X.

All motor information, essentially the innervation of the stylopharyngeus muscle, comes from the nucleus ambiguus, also shared with X.
what two cranial nerves are present in the open medulla? what is notable about their nuclei and fibers?
CN IX and X (gloss. and vagus)

nucleus ambiguous gives motor fibers to BOTH nerves. pre-para motor to X as well.
what can cause the deviation of the uvula to the right?
a LMN injury of the vagus N (X) on the LEFT side.

lesion could be to the nucleus ambiguous in the brainstem (open medulla) or thru the jugular foramen as the X leaves the brainstem.
where is the nucleus for XII found? how does it course?
hypoglossal nucleus is in closed medulla, dorsally. it courses ventrally, medial and inferior to the olivary nucleus.
where does CN XI come from? what mm are controlled?
the spinal accessory nerve (XI) comes from C1-C5. the fibers ascend and exit through the jugular foramen to innervate the SCM (ipsilateral) and trap (contralateral).
how are UMN of the cranial nerves similar to corticospinal fibers? how are they different?
both mostly come from the precentral gyrus.

CN UMNs have bilateral axons, but most of these axons will be contralateral.
where are the corticobulbar fibers found in the somatotopy of the internal capsule?
corticobulbar fibers are found in the genu of the internal capsule.
what is the path of the corticobulbar fibers after passing thru the internal capsule?
after passing thru the genu of the internal capsule, the corticobulbar fibers pass thru the basis pedunculus, just medial to the corticospinal axons.
what type of result can you expect from a one-sided UMN lesion of the trigeminal nerve motor nucleus?
a one-sided UMN of V will often not have much affect b/c the innervation is bilateral.

LMN lesion, however, will result in paralysis of the mm of mastication on the AFFECTED side.
how does the unique innervation path of CN VII effect the clinical picture presented post-UMN lesion and LMN lesion?
UMN = bilateral innervation due to supplementary area (BA6).

LMN = contralateral innervation by CN VII only.

UMN lesion (above nucleus)= loss of motor to contralateral LOWER face only.

LMN lesion = lose upper and lower face innervation. can't blink, keep drool in mouth.
an UMN lesion of CN XI will cause what type of motor damage?
SCM: ipsilateral deficit

trapezoid: contralateral deficit
what is unusual about they hypoglossal nerve? (w.regards to it's UMN path)
CN XII (hypoglossal) is mostly bilateral. BUT, rarely it does CL innervation.

an UMN lesion in these (CL) individuals can cause tongue deviation toward the opposite (good) side or CONTRALATERAL to the lesion.
what is the clinical picture of a LMN injury? an UMN injury?
LMN: ipsilateral flaccid paralysis (VI is exception, but nuclei so close, hard to lose one without the other).

UMN:
cl input - cl paresis.
bilateral input - weakness of mm, but no lack of fxn.
what are some side effects to loss of the oculomotor nerve?
VI and IV still work, eye remains inferior and lateral.

ptosis: levator palpebrae superioris m inactive

dilation, lack of accomodation and consequent double vision: no parasymp.
a patient presents with extortion of one eye, weakness of downward gaze (when looking medially) and consequent double vision. what is the problem?
LMN injury to the trochlear nerve (VI). (contralaterally)
what are the consequences of LMN damage to CN VI?
LMN injury to the abducent nerve results in adduction of affected eye and diplopia.
what are some possible sites of UMN injuries to the eye?
1.superior colliculus
2.pontine lesions in lateral gaze center.
3.frontal eye fields
4.optic cortex (fixation, accomodation, fusion of images).
5.MLF (btwn VI nucleus and III nucleus)
how does a LMN lesion to the trigeminal nerve manifest? an UMN lesion?
LMN: ipsilateral loss of mm of mastication (temporalis, masseter and pterygoids).

UMN: one-sided lesions cause only a minor effect due to bilateral innervation.
what is the result of a LMN lesion of the facial nerve? and UMN lesion?
LMN: complete paralysis of mm of facial expression, upper and lower parts. parasymp and taste loss vary with location of lesion.

UMN: unilateral lesion results if loss of motor control of lower 1/2 of face only (orbicularis oris, buccinator, levator labii mm).
frontalis and orbicularis oculi are retained.
LMN lesion of which CN is particularly tough to spot? what additional symptoms makes it more identifiable?
IX damage is tough to spot b/c it only innervates the stylopharyngeus. additional damage to X results in hoarseness (loss of ipsilateral motor nn to larynx). uvula deviates to unaffected side (levator veli palatini m.)

vagus UMN unilateral lesion results in little observable effect.
what will a vascular accident in the upper pons cause?
LMN injury to V and an UMN injury to everything below (VII, IX and XI). CN III and IV are still intact.

**lower VII is injured, can't blink, etc...
an injury to the MLF causes loss of what eye mm?
lateral rectus m. (abducens N, VI)
what is the precursor for glycerophospholipids? what is usually the fatty acid in it's structure?
phosphatidic acid = precursor

arachidonic acid = fatty acid
how many pathways are available to add a head group to the glycerophospholipid precursor? what is required?
there are 2 paths in which a head group can be added to phosphatidic acid. both require cytodine nucleotides.
what is the head group for lecithin?
choline (phosphatidylcholine)
what are the functions of lecithin? how do deficiencies manifest?
lecithin is necessary for alveolar surfactant and in dermal structure.

RDS of infant and TPN can result in blue lips/fingers (infant) and scaly red skin (TPN).
where is phospholipase A2 located? what does it do?
it's found mostly in pancreatic secretions and it acts on phosphatidylinositol to rls arachadonic acid. (cleaves fatty acid at 2nd position). it's inhibited by glucocorticoids (cortisol).
where is phospholipase C found? what is it's action?
it's found in liver lysosomes and the alpha-toxin of clostridia and other bacilli.

it's membrane bound and activated by PIP2 system (produces 2nd messengers). **describe the 8 step pathway**
what is the actin of Lithium with respect to phosphatidylinositol?
PI is involved in signal transduction. Lithium prevents the recycling of IP3 which slows neurotransmission.
what structures are clinically considered
'basal ganglia'?
1.corpus striatum (caudate nucleus and lentiform nucleus)
2.subthalamic nuclei
3.substantia nigra
which parts of the 'old basal ganglia' are not involved in motor fxn ?
amygdala (limbic)
claustrum (unknown)
how is the lentiform nucleus divided? the substantia nigra?
lentiform:
medially: globus pallidus (gpl & gpm)
laterally: putamen

substantia nigra:
medial: pars compacta (SNpc)
lateral: pars reticula (SNpr)
what is historically phylogenetically known as the neostriatum? paleostriatum? archistriatum? what is another name for neo + paleo?
neo: caudate and putamen
paleo: globus pallidus
arch: amygdala

neo + paleo = striatal motor system
why is the globus pallidus paler than the putamen? which part is bigger?
more myelinated fibers in gp.

putamen is lateral and broad, while gp is the medial, narrow, pale apex.
how is the caudate distributed?
head: ant horn of lat. ventricle
body & tail: lateral floor of lat. ventricle

terminates in TEMPORAL lobe, near amygdala.
how are the caudate and lentiform linked?

what connects the caudate with the putamen? where?
caudate and lentiform are connected via bridges across the anterior limb of the internal capsule.

the caudate and putamen are linked via the nucleus accumbens around the inferior side of the anterior limb of the internal capsule.
what are the boundaries of the lentiform nucleus?
the apex points to the genu of internal capsule.

medial: internal capsule
laterally: external capsule
separated from caudate: anterior limb of internal capsule (rostrally)

*ant limb of IC also separates it from the THALAMUS* (caudally)
how is the caudate nucleus united with the putamen (and nucleus accumbens)?
at cellular tissue level, the caudate is connected to the putamen via:
1.gray matter bridge inferior to the IC (=ventral striatum)
2.multiple cellular bridges through the IC
where is the gpm located? what fibers does the gp principally contain?
the gpm is nestled against the genu of the IC. the gp consists of large, multipolar neurons which are principal EFFERENT neurons of the corpus striatum.
what are the inputs to the caudate-putamen?
1.CORTICOSTRIATE from cerebral cortex
+ to spiny neurons

2.NIGROSTRIATAL from substantia nigra
from pars compacta = dopaminergic
name 4 cortical loops and the types of info they relay.
1.prefrontal cognitive: learn & plan motor programs

2.limbic: coordinate mm with emotional states (smile)

3.oculomotor: coordinate eye movements

4.motor: organize motor sequences and scale mm contractions.
what are the caudate putamen outputs?
output is inhibitory to:

1.to GPL and GPM via striopallidal fibers
2.to SNpf via strionigral fibers
what is the function of the GPM and SNpr?
they project inhibitory fibers to the ventrolateral nucleus of the thalamus.

they are the output nuclei of all the other basal nuclei to the thalamus.
what are the two pallidothalamic tracts from GPM? where do they go?
ansa lenticularis (around PLIC)

lenticular fasiculus (penetrates thru PLIC)

both combine in the thalamic fasiculus beneath the thalamus.
what constitutes the direct pathway? how does it work?
CP to GPM and SNpr to thalamus = direct

after deciding to move:
1.cortex excites spiny neurons in CP
2.CP inhibits GPM and SNpr
3.thalamus is disinhibited
4.thalamus excites frontal lobe motor cortex.

NORMAL, COORDINATED MOVEMENT
describe the indirect pathway. what is the ultimate result?
1. CP projects to GPL (inhibitory)
2. GPL to STN (inhibitory)
3. STN to GPM and SNpr (excitatory)
4. excitation to thalamus, causing inhibition!
5. inhibited thalamus = no cortical stimulation

NORMAL INHIBITION OF MOVEMENT
why is substantia nigra dark? in what patients is this darkness notably absent?
pars compacta synthesizes dopamine, a byproduct of which is melanin.

parkinsons patients do not have this darkeness.
how do dopaminergic neurons act on the direct pathway? indirect?
direct:
excite direct pathway via D1 (promotes movement)

inhibit indirect pathway via D2 (promotes movement)
what is hypokinesia? what causes it?
hypokinesia is understimulation of direct pathway and overstimulation of indirect pathway.

this occurs via loss of dopaminergic neurons of pars compacta.

parkinsons: bradykinesia, akinesia, rigidity and tremor.
what is huntington's disease?
characterized by loss of spiny neurons in CP and anterior horn ventricular enlargement.

choreic movement.
what does lesion to the subthalamic nucleus cause?
hemiballismus (large amplitude flinging) and athetosis.
where is the zona inserta found?
it's an extension of midbrain reticular system between thalamic fasiculus and lenticular fasiculus.
what is the arterial supply to the caudate and lentiform nuclei?
penetrating bbr of the MCA called lateral striate arteries.
how is taenia solium contracted?
this pork tapeworm can be contracted via eating undercooked pig mm with cystercerci. it will hatch an adult worm which breaks off organ segments, proglottids. these segments produces eggs and are expelled in the feces.
when is one considered to have cysticercosis?
eggs from another human infected with the adult worm of taenia solium. the eggs ingested form oncospheres in the mm, get into the bloodstream and can affect CNS, eyes, etc...
what is foster-kennedy syndrome? how can it be tested for?
foster-kennedy is usually the result of a mass lesion (meningioma) in the olfactory groove. this compression of the olfactory nerve results in ipsilateral anosmia and optic atrophy, contralateral papilledema.

have pt close one nostril and try to id scent via other nostril.
describe the visual pathway.
visual impulses are transmitted from the retina to LGB to BA 17.

nasal retinal field 'sees' temporal area.

temporal retinal field 'sees' the nasal field of vision.

upper retinal quadrants rcv image from lower visual pathways and vice versa.
what is wilbrand's knee?
an anatomical feature which affects a lesion to the optic nerve and optic chiasm on one side.
the lesion will effect the ipsilateral temporal and nasal retinal fibers and a portion of the CONTRALATERAL inferonasal retinal fibers.

RESULT: varying ipsilateral blindness (via ipsi optic nerve) and CL upper temporal scotoma (secondary to inferonasal retinal fibers rcving input from CL superior temporal FOV)
what causes a bitemporal hemianopsia? a binasal hemianopsia?
bitemporal: midsagittal lesion of the chiasm (eg pituitary neoplasm) interdicts the decussating nasal hemiretinal fibers.

hemianopsia: damage to temporal hemiretinal fibers bilaterally (calcified internal carotids resulting in ischemia)
what does damage to the optic tract cause?
contralateral homonymous hemianopsia and degeneration of ipsilateral LGB.
what is the inferior geniculocalacrine tract also known as? what does a lesion to it cause?
meyer's loop.

it extends from LGB to the calacrine sulcus and lingual gyrus.

meyer's loop rcvs input from the inferior retinal quadrants representing superior visual fields.

LESION: contralateral upper homonymous quadrantanopia
what comprises the pupillary light reflex pathway? how are the pupils constricted (nerve type, nucleus)?
afferent: CNII
efferent: CNIII

pre-para fibers from Edinger Westphal nucleus run with III and exit the midbrain.
they synapse with post-para fibers of the ciliary ganglion, innervate the sphincter mm of the iris, causing pupillary constriction.
what comprises the pupillary dilation pathway?
sympathetics:
hypothalamic neurons project thru brain stem to ciliospinal center of budge (T1-T2).

pre-symp fibers run with symp trunk to superior cervical ganglion over apex of lung.

the fibers re-enter skull via the carotid canal. innervate radial dilator and levator palpebrae superioris.
what are the symptoms of horner's syndrome? what can cause it?
eyelid ptosis
pupil constriction
facial anhidrosis

this is caused by constriction of the sympathetic nerve fibers entering the skull. compression is often caused as the fibers traverse the apex of the lung via pancoast tumors (lung cancer).
what is the convergence accomodation reaction?
this rxn is essential for visual fixation and acuity at close range.

it is initiated by conscious visual fixation on near object.

converge: medial recti mm
accomodation: ciliary mm
pupillary constriction: increased depth of field vision and depth of focus. mediated by rostral EWN.
what is aniscoria? when is it seen?
aniscoria is unequal pupils (can be normal)
horners, oculomotor palsies, adie's syndrome, holmes- adie's syndrome.
what is adie's syndrome? holmes-adie's?
adie's syndrome is found predominantly in young females. characterized by tonically dilated pupil secondary to damage to the ciliary ganglion or short ciliary nn.

holmes-adies = adies + decreased tendon reflexes.
how is the MLF related to vision?
the subcortical center for vertical conjugate gaze involves the MLF which projects to III and IV nuclei.
what is MLF syndrome?
caused by damage to one or more MLF btwn VI and III nuclei is midbrain and pons.

characterized by medial rectus palsy on the side of the lesion (failure to ADDUCT) + effort monocular horizontal nystagmus of contralateral ABducting globe.

**MS**
what is one and a half syndrome of fisher?
VI or PPRF lesion associated with an ipsilateral MLF lesion. localizes to midbrain and pons on one side.

ONE: pontine conjugate gaze palsy to one side (inability to ABduct the eye on lesion side secondary to sixth nerve palsy).

HALF: medial rectus palsy (can't ADDUCT on lesion side secondary to MLF lesion interrupting III afferents). causes FROZEN GLOBE on lesion side + effort nystagmus of opposite eye as pt attempt to ABduct it.
what is transtentorial herniation?
a tumor causes increased supratentorial pressure and forces the parahippocampal uncus thru the tentorial notch, compressing CN III.

1.IL hemiparesis
2.fixed, dilated pupil, ptosis and down & out eye.
3.CL homonymous hemianopia (PCA compression)

aneurysms of the carotid, p. communicating, PCA or SCA can compress CN III in the cavernous sinus or interpeduncular cistern.
what is Bielchowsky sign?
due to a lesion of IV, pt complains of 'vertical diplopia' (images appear on top of e/o) and tilts head OPPOSITE to lesion to compensate for lack of INTORSION.

superior oblique mm is affected.
what is trigeminal neuralgia?
an inflammation of trigeminal nerve (V2 or V3 usually) causing stabbing facial pain; usually the result of trauma, vascular, neoplastic or demyelinative disease.

(more common in women, idiopathic post 50 yrs. symptomatic 30-35 yrs)
what is herpes zoster opthalmicus? which nerve is affected?
this is a viral infection affecting V1 which with corneal ulceration can cause blindness.
what is raeder's paratrigeminal syndrome?
it's secondary to a lesion of the trigeminal ganglion and sympathetic fibers in the parasellar region. characterized by miosis, ptosis (Horner's), facial pain and trigeminal palsy.
what causes numb chin syndrome? what is it associated with?
it's generally due to metastases of the inferior alveolar nerve (mental foramen region), which is a terminal branch of V3. it's often associated with lymphomas, leukemias, metastatic breast, lung, prostate, pharyngeal cancer and myeloma.
what characterizes argyll-roberston pupil?
*prostitutes pupil*

absence of mitotic rxn to direct and consensual stimulation with light, but preservation of miotic rxn to NEAR stimulus (accomodation-convergence).

assoc with syphilis, diabetes, lupus (collagen vascular dzs).

pupil is small, irregularly shaped and poorly reactive to light (at best).
what disorder does the swinging flashlight test indicate?
marcus-gunn pupil:

'afferent pupillary defect' characterized by lesion of the afferent limb of pupillary light reflex.

dark room: light in 'good' eye causes dilation of both. light swung over to bad eye causes it's dilation.

**no light getting thru optic nerve**
only consensual response is intact!
(MS)
what is saccades? what area of the brain is it related to?

what does damage to this area cause?
saccades = fast eye movements

BA 8 is the cortical center for saccades.

irritate lesion (seizure): contralateral conjugate deviation of the eyes

destructive lesion (stroke): ipsilateral conjugate deviation of the eyes
what part of the brainstem acts complimentarily with the frontal eye fields triggering saccades?
the superior colliculus.