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70 Cards in this Set
- Front
- Back
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MRI T1-weighted is useful for what, not good for what?
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MRI T1- weighted is good for anatomy, not good for pathology
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What is SPGR?
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Spoiled Gradient Recalled. Tradename for MRI
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What is FLAIR MRI? What is it good for. What is it not good for? What is a unique characteristic of FLAIR?
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FLAIR MRI = FLuid Attenuated Inversion Recovery. It is good for pathology but not anatomy. The special feature of FLAIR is that it can have a threshold so only voxels of the image with intensities above the threshold are displayed.
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T/F The fMRI directly measures neuronal action
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False- indirectly measures metabolic activity. The point is that neuronal activity increases blood flow, removing deoxygenated hemoglobin. Oxygenated hemoglobin is left, and that doesnt interfere with water's ability to produce a signal.
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What is DTI? What is it used for?
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Diffusion tensor imaging. Its used to track white matter because the fibers are parallel so the signal travels fast.
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What is smooth pursuit?
What area of the brain controls it? What else needs to occur in order for smooth pursuit to occur? |
Smooth pursuit is used to track a moving an object (Follow my finger).
The ipsilateral POT controls smooth pursuit. The VOR must be supressed in order for smooth pursuit to occur. |
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What are saccadic pursuits? Where can the lesion be localized to?
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Saccadic pursuits are also called Jerky pursuits. The lesion can be localized to the ipsilateral POT.
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What are saccades? What controls this?
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Voluntary or Reflex rapid eye movements to bring an object into focus. These are controlled by the contralateral frontal eye field.
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What is the pathway of saccades (to look right)?
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Left frontal eye field (precentral/middle frontal lobe) -> R PPRF -> CN VI nucleus -> abduct right eye
also from R CN VI -> L MLF -> CN III -> Adduct left eye Overall the saccade is right (opposite of the LEFT frontal eye field). |
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What is the pathway of saccades (to look left)?
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Right front eye field (precentral/middle frontal lobe) -> Left PPRF -> Left CN VI nucleus -> abduct Left eye
Also from L CN VI nucleus -> R MLF -> R CN III -> Adduct R eye Overall net movement left (opposite of RIGHT frontal eye field) |
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Which way does the eye deviate in a hyperactive frontal eye front lesion (seizure)?
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The eye will deviate to the contralateral side.
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Which way does the eye deviate in a hypoactive frontal eye front lesion (infarct)
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The eye will deviate to the ipsilateral side.
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How does a wrong way lesion work?
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A wrong way lesion is localized to the pons. Suppose the lesion is in the left pons. You will have weakness in the right body, you will also have eyes deviating right.
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How does a right way lesion work?
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A right way lesion is a cortical (frontal eye field lesion). Suppose you have a lesion in the left cortex. The body will be weak on the right side. The eyes will deviate left though.
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What is INO caused by?
Sx? |
MLF lesion caused by ALS, MS, or pontine infarct.
Contralateral nystagmus, impaired adduction of ipsilateral side. Can adduct during convergence. |
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If you have impaired adduction in only 1 eye and intact convergence, what kind of lesion?
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Ipsilateral MLF
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If you have impared horizontal gaze in one direction; vor intact
What if the VOR is knocked out? |
ipsilateral pprf if the VOR is intact. Ipsilateral CN VI nuclei if it is knocked out.
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What is 11/2 syndrome?
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Ipsilateral MLF leads to ipsilateral loss of adduction.
Ipsilateral CN VI nucleus/PPRF leads to ipsilateral loss of abduction and Contralateral loss of adduction |
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What is the function of vergence? Through what pathway does this occur?
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Vergence helps you maintain fixation as objects move towards or away from you. Convergence is mediated by the MEDIAL RECTUS. Divergence is mediated by the LATERAL RECTUS. These mediations go through the PRECTECTAL pathway.
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What is optokinetics?
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Stabilizes image of visual scene when sustained head rotations are occuring
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What is fixation?
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Maintaining fixation on an object - staring.
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What is the relationship between the UMN and LMN?
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The LMN is always on and stimulating muscles to contract. The UMN is inhibitory to the LMN to prevent constant firing.
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What is the UMN pattern of weakness?
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Flexed upper extremities.
Extended lower extremities (except at the knee to compensate on the affected side), Babinski sign. |
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Where is the deficit with diabetic peripheral neuropathy?
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They dont have the deep tendon reflex= areflexia.. This is lost in the sensory neuron.
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Where are the various locations for LMN lesions?
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Anterior Horn,
Spinal root, Brachial Plexus, Peripheral Nerve, NMJ, Muscle |
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Anterior horn cell injuries involve what conditions? What characterizes them?
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ALS, polio.
Flaccidity and atrophy. |
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Spinal root lesions are also called. What do they lead to?
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Radiculopathy(disc herniation)- leads to weakness, atrophy, ain.
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Brachial plexus lesions are often caused by?
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Pancoast tumor - tumor that compresses brachial plexus
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What is an example of a peripheral nerve lesion?
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Carpal tunnel.
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What are the 3 NMJ associated conditions?
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1. MG- fatigue worse throughout day, autoantibodies to ACh R
2) Lambert Eaton - antibody to Ca++ at presynapse 3) Botox- inhibits docking via v and t snare. |
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Muscle lower motor neuron lesions include?
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DMD and myositis
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How long does hyperreflexia and hypertonia take to develop following a UMN lesion?
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Takes up to 6 weeks to occur. Can be hyporeflexive and flaccid initially after an UMN lesion.
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What body part is affected in ACA infarct for UMN lesion?
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A LEG
The LEG >> Arm Sensory and motor deficits May have altered mental status. |
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What is characteristic of an MCA infarct in an UMN lesion?
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MCA is the fam
Face and arms more affected than leg. -Extinction present (cant perceive 2 different stimuli if presented at the same time but can if presented independently) Dysarthria, aphasia. |
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What characteristics does an ACA/MCA watershed infarct have in an UMN lesion
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These arteries pass over the homunculus - ARM weakness...with trunk being affected. Man in a barrel
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What characteristics does the PCA infact have in an UMN lesion
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Optic radiations affected.
Leads to hemianopsia Visual agnosia CN III palsy |
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MCA/PCA watershed infarct characteristics?
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Face weakness
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What characteristics does the vertebrobasilar infarct have
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4 DS
Dysphagia Dysarthria Diplopia Disconjugate gaze Vertigo Nystagmus If Right face affected, left limb affected. |
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What characteristics does Lacunar artery infarct have
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purely sensory or purely motor loss
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What is the pathway of CN I
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olfactory bulb-> tract -> entorhinal cortex
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What are the injuries associated with CN I
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1. Trauma - sheering of cribriform plate
2) Meningioma tumor 3) Seizures start in entorhinal cortex - aura with odor uncinate fit- seizure manifest as false sense of smell. |
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What kind of fibers can mediate CN I
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Cortical fibers
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What muscles does the CNIII innervate?
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CN III inervates all eye muscles except LR6 SO4
It also innervates the levator palpebrae and the sphincter papillae. |
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What are the characteristics associated with a CN III lesion?
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ptosis,
down and out (diagonal diplopia), blown pupil |
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The p comm artery is important in what cranial nerve pathology?
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CN III. P Com aneurysm can cause problems...
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What is a pupillary sparing CN III palsy?
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No blown pupil because pcom not involved- ischemia of vaso nervorum supplying CN III fascicle.
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CN IV pathology involves?
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Superior oblique - Vertical diplopia.
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CN VI pathology involves?
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Lateral Rectus - Horizontal diplopia
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What is the difference in sensory innervation between V1, V2, and V3?
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V1 - forehead and nose,
V2 - cheeks V3 - jaw |
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What are the muscles of mastication?
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medial pterygoid
masseter temporalis CLOSE JAW and lateral pterygoid open (say La requires you to open mouth; mmm is closed mouth) |
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What is the CN 5 pathology?
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Trigeminal neuralgia/tic doulareux- something jammed up against CN V
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What are the functions of CN 7?
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Salivation/lacrimation
Sound dampening Muscles of facial expression Taste - ant 2/3rd |
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Dysfunction of CN 7 is called? What does it involve?
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Bell's palsy.
1) No smiling 2) No crinkling forehead 3) Flat nasolabial fold 4) Hyperacusis 5) Widened Palpebral fissure 6) Incomplete Ptosis |
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Dysfunction of CN IX is called?
What artery involved. |
Glosopharyngeal neuralgia.
INTERNAL CAROTID |
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Dysfunction of CN IX/X is called? What artery is involved?
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Glosopharyngeal nerualgia with bradycardia--> asystole.
PICA |
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CN XI dysfunction?
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Cant turn head when hand is on contralateral cheek. Cant raise arm above horizontal position.
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CN XII dysfunctions.
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If UMN - deviation contralaterally
If LMN - deviation ipsilaterally |
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Dysfunction of CN IX is called?
What artery involved. |
Glosopharyngeal neuralgia.
INTERNAL CAROTID |
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What's in the cavernous sinus?
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3, 4, V1, V2, 6.
Internal carotid-> central retinal |
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Dysfunction of CN IX/X is called? What artery is involved?
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Glosopharyngeal nerualgia with bradycardia--> asystole.
PICA |
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CN XI dysfunction?
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Cant turn head when hand is on contralateral cheek. Cant raise arm above horizontal position.
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CN XII dysfunctions.
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If UMN - deviation contralaterally
If LMN - deviation ipsilaterally |
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What's in the cavernous sinus?
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3, 4, V1, V2, 6.
Internal carotid-> central retinal |
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Cavernous sinus thrombosis has what issues, causes, etc?
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Mastoiditis,sinusitis = cause blood clot...
Chemosis = bloodshot sclera Proptosis = foreward eyes Blindness = if central retinal artery compressed. You get all deficits of CN 3, 4, v1, v2, and 6. |
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Ptosis is associated with which nerves?
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CN 3 - full
CN 7 - partial SNS - partial but has horners syndrome also. |
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Pupillary dilation is associated with which nervous system not working
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PNS not working.
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Pupillary constriction is associated with which NS not working
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SNS not working
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Midbrain has which CN associated with it?
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1-4
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Pons has which CN associated with it?
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Upper 5
Lower 7,8 |
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Medulla has which CN associated with it?
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9-12
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