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20 Cards in this Set

  • Front
  • Back
lesion of the amygdala (bilateral) produces
kluver-Bucy syndrome

hyperorality, hypersexuality, disinhibited behavior
frontal lobe lesion produces
disinhibition and deficits in concentratoin, orientation and judgement

may have reemergent primitive reflexes
Right parietal lobe lesion
spatial neglect (agnosia of the contralateral (left) side of the world)
reticular activating system (midbrain) lesion produces
reduced levels of arousal and wakefulness -- can cause coma
lesion of the mamillary bodies bilaterally porduces
wernicke-korsakoff syndrome

wernicke: confusion, opthalmoplegia, ataxia

korsakoff = memory loss, confabulation, personality changes
basal ganglia lesions
tremor at rest, chorea, or athetosis

resting tremor = pill rolling tremor seen in parkinsons

chorea = sudden jerky purposeless movements - dancing in a sense - seen in huntingotons

athetosis = slow writing movements of the fingers (snakelike) -- also seen in huntingtons
cerebellum hemisphere lesions
intention tremor (characteristic of damage to the cerebellum = zigzag motion when point toward a target)

limb ataxia - dysmetria

dysdiadichokinesias (can't to finger to nose or heel to shin)

speech may be disarthric or scanning


hemispheres are laterally located and thus affect lateral limbs
cerebellar vermis lesions
Imbalance: Romberg + (with eyes open & closed) --ddx from DCML/dorsal column lesion where Romberg + (but nl with eyes open) -- can't do tandem giat

Truncal Ataxia = can't sit unsupported

Eyes: nystagmus, ocular dysmetria, poor pursuit
subthalamic nucleus lesion
contralateral hemiballismus (this is actually part of the basal ganglia)

this is sudden wild flailing of 1 arm +/- 1 leg

commonly seen in lacunar stroke in a patient with a hx of htn, dm, hx smoking
hippocampus leions
anterograde amnesia = inability to make new memories
PPRF lesion
eyes look toward hemiplegia

(lesion is going to be in the pons which and grabs the CST -- so hemiplegia is contralateral to the lesion here)
frontal eye fields lesion

blood supply?
eyes look toward the lesion

located in the frontal lobe (premotor cortex)

MCA
tremor that worsens when holding posuter is a _____

tx?
essential/postural tremor

AD

pts like to use ETOH to self medicate , we like to use BBs
thalamus funciton

blood supply of ventral thalamus? function?

blood supply of LGN and MGN and fucntion?
major relaty for ascending sensory information that ultimately reaches the cortex

ventral thalamus = posterior communicatingl artery from the ICA
VPL = body sensation (all 5)
VPM= facial sensation (CN 5)
Venttral anterior and ventral lateral necule = motor

LGN (visual - projects via optic radiations to the occipital cortex) and the MGN (auditory)
-- both = Posterior cerebral via the basilar
-LG Anterior choroidal via the ICA
what composes the limbic system?

funciton?
cingulate gyrus
hippocampus
fornix
mamillary bodies
amygdala
olfactory bulb

feeding, fleeing, fighting, feeling and fucking (5 f's)
hypothalamus function?

blood supply?
TAN HATs
Thirst/water balance
Adenophypophysis control (ant pituitary)
Hunger
Autonomic regulation
Temperature regulation
Sexual urges

posterior communicating artery (via ICA)
what are the 8 nuclei of the hypothalamus and give there funciton

affect of Leptin here?
1. supraoptic nucleus = makes ADH

2. Paraventricular nucleus = makes oxytocin (induces labor)

3. lateral area = hunger center; leptin inhibits this; destruction>>anorexia, FTT
"leptin helps you LOSE wt by inhibiting the Lateral area"

4. ventromedial area = satiety center; stimulated by leptin (b/c you want to stay satisfied to lose wt); destruction makes you hyperphagic (craniopharyngioma)

5. anterior hypothalamis = coooling, parasymp (A/C) - destroy this and you become hot all the time

6. posterior hypothalamus = heating/sympathetic -- loose this and you become cold all the time

7. septal nucleus = sexual urges

8. suprachiasmatic nucleus = circadian rhythm
Basal ganglia funciton?

what makes up the basal ganglia?

blood supply?

what is the input to the basal ganglia?

what dz results in basal ganglia atrophy?
fine adjustments to motor movement / postural adjustments by providing inhibitory feedback to the motor cortex

substantia nigra pars compacta, which releases dopamine (decreased funciton in parkinsons)

basal atrophy is huntingtons

caudate
putamen
globus pallidus

MCA
(globus pallidus = MCA and anterior choroidal antery)
direct pathway of the basal ganglia has what receptors? function? ultimate result when dopamine is released by the SNc?

indirect pathway?

parkinsons disease ?
Direct = D1
function is to relieve inhibition of the thalamus and allow intended movement

indirect = D2
function is to inhibit thalamus in order stop unintended movement

with parkinsons: SNc is degenerated so no D1 or D2 stimulation
lack of D1 stimulation means difficulty to intiitate intended movements>>akinesia and cogwheel rigidity

lack of D2 stimulation means inability to prevent UNintended movements >>resting/pill rolling tremor
thalamus locatoin
surrounds 3rd ventricle
paired
between cortex and midbrain