Neurophysiology Ii

Front 1

contents of the membranous labrynth

Back 1

hair cells (communicates head position), organ of Corti (audition), vestibular apparatus (semicircular canals for angular displacement, utricle & saccule for forward, backward, & verticle movements)

Front 2

Describe the ionic composition of endolymph.

Back 2

similar to intracellular fluid, high K+

Front 3

Describe the mechanism of hair cell depolarization.

Back 3

movement of stereocilia toward kinocilium depolarizes the hair cell (K+ in), while movement away from the kinocilium hyperpolarizes the hair cell.

Front 4

effect & mechanism of vestibular nerve when head turns left.

Back 4

hyperpolarization of the hair cells in the right horizontal canal, and depolarization of hair cells in the left horizontal canal. This will cause a decrease in firing rate in the right vestibular nerve fibers, and an increase in firing rate on the left.

Front 5

lesions of the upper midbrain or above (for example in the cortex or internal capsule) produce what posture?

Back 5

decorticate posture (arm flexion, leg extension)

Front 6

Lesions in the lower midbrain or pons result in what type of posture?

Back 6

decerebrate (all limbs extended)

Front 7

what does a progression in a patient from decorticate posture to decerebrate posture indicate?

Back 7

rostral to caudal deterioration of the brainstem (dangerous for respiratory center)

Front 8

begins in medial vestibular nucleus, terminates at cervical levels, and controls neck movements that position the head.

Back 8

medial vestibulospinal tract

Front 9

Uses vestibular input to hold images stable on retina, during fast head movements

Back 9

VOR

Front 10

Uses visual input to hold images stable on retina during slow head movements

Back 10

optokinetic reflex

Front 11

Bring objects of interest into the fovea

Back 11

saccade

Front 12

Holds moving targets in the fovea

Back 12

smooth pursuit

Front 13

Adjusts eyes so that both can foveate the object at any depth

Back 13

vergence

Front 14

Horizontal saccades are generated where?

Back 14

in the pontine reticular formation

Front 15

vertical saccades are generated where?

Back 15

in the mesencephalic reticular formation.

Front 16

Damage to any of
the structures involved in vestibulo-ocular or optokinetic reflexes, including the cerebellum, and the vestibular apparati, vestibular nuclei or damage to other parts of the brainstem, results in what?

Back 16

pathological nystagmus

Front 17

a lesion of the MLF (often resulting from multiple sclerosis) results in what?

Back 17

Internuclear ophthalmoplegia (weak conjugated adduction on the affected side)

Front 18

caused by the dislodging of an otolith crystal

Back 18

benign positional vertigo (no hearing loss)

Front 19

caused by the overproduction (or insufficient drainage) of endolymph,
which can rupture the membranous labyrinth and cause mixing of endolymph and perilymph.

Back 19

vertigo (Meniére’s Disease: sustained firing of CN VIII, deafness, N/V

Front 20

caused by the overproduction (or insufficient drainage) of endolymph,
which can rupture the membranous labyrinth and cause mixing of endolymph and perilymph.

Back 20

vertigo (Meniére’s Disease: sustained firing of CN VIII, deafness, N/V

Front 21

What does an EEG measure?

Back 21

Real-time electrical potentials that are generated in the cortex and volume
conducted through the meninges, cranium and skin.

Front 22

created by ann EPSP, which draws current from areas farther away, creating a current source.

Back 22

local current sink

Front 23

Adjacent positive and negative regions are called a(n):

Back 23

dipole

Front 24

the change in EEG that occurs in response to a sensory stimulus, such as a flash of light or shock to the skin. This technique is used to assess the function of an ascending sensory system, from the periphery all the way to cortex.

Back 24

evoked potential

Front 25

EEG characteristics of sleep & wakefulness:

Back 25

awake state--high frequency, low amplitude, desynchronized EEG. Slow wave sleep--low frequency, high amplitude, synchronized EEG.

Front 26

sleep stage characterized by slight slowing of the EEG

Back 26

1

Front 27

sleep stage characterized by high-amplitude k complexes and low-amplitude sleep spindles

Back 27

2

Front 28

sleep stages characterized by slow high-amplitude delta waves

Back 28

3 and 4

Front 29

reticular formation structure located in the tegmentum of the caudal midbrain and rostral pons; stimulation there causes wakefulness, and lesions cause sleep.

Back 29

ascending reticular activating system (ARAS)

Front 30

a set of medial forebrain structures that are interposed between the hypothalamus and lateral forebrain (sensorymotor)structures.

Back 30

limbic system

Front 31

Functions in identification of appropriate object for drives

Back 31

amygdala

Front 32

Functions in identification of appropriate context for drive

Back 32

hippocampus

Front 33

paths that connect the amygdala to the hypothalamus

Back 33

stria terminalis, ventral amydalofugal path

Front 34

path that connects the hippocampus to the hypothalamus

Back 34

fornix

Front 35

Functions in assigning affective (emotional) significance to sensory
stimuli, and initiate appropriate emotional responses.

Back 35

amygdala

Front 36

a constellation of behavioral problems
in monkeys, after bilateral damage to the temporal lobes, specifically the amygdala. These include attempting to eat non-food objects, lack of fear of predators, attempting to copulate with animals from a different species.

Back 36

Kluver-Bucy Syndrome

Front 37

allocortical structure that receives processed sensory input from the entorhinal cortex

Back 37

hippocampus

Front 38

Limbic structures in the medial temporal lobe include:

Back 38

hippocampus, entorhinal cortex, amygdala, parahippocampal cortex.

Front 39

lesion producing anterograde amnesia:

Back 39

medial temporal lobe

Front 40

critical structures involved in memory consolidation:

Back 40

the hippocampus,entorhinal cortex, and perirhinal cortex. Amygdala is not involved

Front 41

type of memory affected by ECT

Back 41

memory consolidation (hippocampus; may take as long as two years)

Front 42

areas of the brain that function in recollection of episodic (events) & semantic (facts) memory

Back 42

Hippocampus, nearby cortical areas, diencephalon

Front 43

area of the brain that functions in recollection of skilled memory

Back 43

striatum, motor areas of the cortex, cerebellum

Front 44

area of the brain that functions in emotional associations

Back 44

amygdala

Front 45

area of the brain that functions in conditioned reflexes

Back 45

cerebellum

Front 46

what is the physical basis for memory formation (what is a memory)?

Back 46

new dendritic spine formation

Front 47

hippocampal neurons that fire to mark a particular location (formation of a cognitive map)

Back 47

place cells

Front 48

first cells to die in the brain during hypoxia

Back 48

CA1 in the hippocampus (Sommer's area)

Front 49

subcortical area of the telencephalon that provides a major cholinergic input to the hippocampus

Back 49

septum

Front 50

adjacent structures to the septum that provide cholinergic input to the neocortex

Back 50

nucleus basalis of Meynert, diagonal band of Broca

Front 51

lesion that produces misdirected aggression (site and name of lesion):

Back 51

septum; septal rage

Front 52

Pathways from the septum, hippocampus and amygdala, traveling through the lateral hypothalamus and ending in the midbrain tegmentum

Back 52

medial forebrain bundle

Front 53

location of "reward center" affected during self-stimulation

Back 53

medial forebrain bundle

Front 54

dopaminergic pathway from the ventral tegmental area (VTA) to the nuc. accumbens.

Back 54

mesolimbic pathway

Front 55

pathway affected in drug abuse (reward center):

Back 55

mesolimbic dopamine pathway

Front 56

damage to the mediodorsal nucleus of the thalamus, MD, and the mammillary bodies of the hypothalamus; patient has problems forming new memories and often confabulates

Back 56

Korsakoff's psychosis

Front 57

two main systems affected in Alzheimer's patients:

Back 57

hippocampus (anterograde), basal forebrain (projects to forebrain w/ ACh; retrograde)

Front 58

toxin that produces Alzheimer's disease; directly related to cholesterol levels:

Back 58

Beta amyloid

Front 59

first neurons to degenerate in Alzheimer's patients

Back 59

perirhinal/entorhinal areas

Front 60

method of diagnosis of Alzheimer's

Back 60

amyloid plaques & neurofibrillary tangles

Front 61

method of diagnosis of Alzheimer's

Back 61

amyloid plaques & neurofibrillary tangles