Neuro Exam Ii Lundy-Ekman

Front 1

1. How are the eyes voluntarily moved to follow an examiner's finger to the right and then look up?
Include both muscle and cranial nerve activity in the answer.

Back 1

Contraction of the lateral rectus (LR) muscle, innervated by the abducens nerve, moves the right eye toward the right. Next, contraction of the SR muscle, innervated by the oculomotor nerve, moves the right eye upward. Contraction of the MR muscle, innervated by the oculomotor nerve, moves the left eye toward the right. Contraction of the IO muscle, innervated by the oculomotor nerve, moves the left eye upward.

Front 2

2. Which cranial nerve provides efferents for the pupillary reflex?

Back 2

The oculomotor nerve provide the efferents for the pupillary reflex

Front 3

3. Which cranial nerve provides efferents to the tongue muscles?

Back 3

The hypoglossal nerve provides efferents to the tongue muscle

Front 4

4. Which cranial nerve provides afferents for the gag reflex?

Back 4

The glossopharyngeal nerve provides afferents for gag reflex

Front 5

5. which cranial nerve provides control of the muscles of facial expression?

Back 5

The facial nerve provides control of the muscles of facial expression

Front 6

6. Which cranial nerve provides somatosensation from the face?

Back 6

The trigeminal nerve provides somatosensation for the face

Front 7

7. Diagram the accommodative reflex.

Back 7

see fig 13.7 p. 349

Front 8

8. What is the function of the organ of Corti?

Back 8

The organ of Corti converts mechanical displacement information into neural signals for the perception of sound

Front 9

9. Why is there a difference b/t an authentic smile and a false smile?

Back 9

Different brain areas produce authentic an inauthentic smiles. The limbic system is the source of authentic smiles, and voluntary signals from the cerebral cortex produce inauthentic smiles

Front 10

10. Which cranial nerves are required for swallowing?

Back 10

Cranial nerves V, VII, IX, X, and XII are all involved in swallowing

Front 11

11. Lesions of what structures could cause double vision?

Back 11

Double vision can result from lesions of cranial nerves III, IV or VI or their nuclei, or from lesions of the medial longitudinal fasciculus

Front 12

1. List the vertical tracts that are modified by the brain stem

Back 12

The dorsal column/medial lemiscus, spinocerebellar, some parasympathetic, corticobulbar, corticopontine, and corticoreticular tracts are modified by the brainstem

Front 13

2. What are the functions of the reticular formation?

Back 13

The reticular formation integrates sensory and cortical information, regulates somatic motor activity, autonomic function, and consciousness, and modulates nociceptive/pain information

Front 14

3. List the major reticular nuclei and the slow-acting neurotransmitters produced by these nuclei

Back 14

The major reticular nuclei and the neuromodulators they produce are
the ventral tegmental area: dopamine;
pedunculopontine nucleus: acetylcholine;
raphe nuclei: serotonin;
locus ceruleu and medial reticular area: norepinephrine

Front 15

4. Which neurotransmitter produced in the brainstem is important in the cerebral processes of motivation and decision making?

Back 15

Dopamine from the ventral tegmental area is involved in activating cerebral areas essential for motivation and decision making

Front 16

5. How does the pedunculoponteine nucleus affect movement?

Back 16

The pedunculopontine nucleus affects movement by its connection w/ the globus pallidus, subthalamic nucleus, and reticular formation areas that are the source of the reticulospinal tracts

Front 17

6. Which medullary nuclei are part of a system that inhibits the transmission of pain information?

Back 17

The raphe nuclei in the medulla are part of the descending pain control system. Other structures that are part of the descending pain control system are the locus ceruleus and the periaqueductsl gray, located in the pons and midbrain, respectively

Front 18

7. What is the role of the ascending fibers from the locus ceruleus?

Back 18

Ascending fibers from the locus ceruleus directs attention

Front 19

8. list the cranial nerve nucleus responsible for the function and the part of the brainstem where the nucleus is located (lower medulla, upper medulla, junction of the medulla and pons, pons, junction of the pons and midbrain, midbrain):
-Control of voluntary muscles in the pharynx and larynx

Back 19

Nucleus:
Ambiguus

Brainstem Location:
Upper medulla

Front 20

8. list the cranial nerve nucleus responsible for the function and the part of the brainstem where the nucleus is located (lower medulla, upper medulla, junction of the medulla and pons, pons, junction of the pons and midbrain, midbrain):
-Integration and transmission of pain information from the face

Back 20

Nucleus:
Spinal nucleus of the trigeminal nerve

Brainstem Location:
Lower medulla

Front 21

8. list the cranial nerve nucleus responsible for the function and the part of the brainstem where the nucleus is located (lower medulla, upper medulla, junction of the medulla and pons, pons, junction of the pons and midbrain, midbrain):
-Processing of information about sounds

Back 21

Nucleus:
Cochlear

Brainstem Location:
Junction of medulla and pons

Front 22

8. list the cranial nerve nucleus responsible for the function and the part of the brainstem where the nucleus is located (lower medulla, upper medulla, junction of the medulla and pons, pons, junction of the pons and midbrain, midbrain):
-Control of tongue muscle

Back 22

Nucleus:
Hypoglossal

Brainstem Location:
Upper medulla

Front 23

8. list the cranial nerve nucleus responsible for the function and the part of the brainstem where the nucleus is located (lower medulla, upper medulla, junction of the medulla and pons, pons, junction of the pons and midbrain, midbrain):
-Perception of timing

Back 23

Nucleus:
Inferior olivary nucleus

Brainstem Location:
Upper medulla

Front 24

8. list the cranial nerve nucleus responsible for the function and the part of the brainstem where the nucleus is located (lower medulla, upper medulla, junction of the medulla and pons, pons, junction of the pons and midbrain, midbrain):
-Control of muscles of mastication

Back 24

Nucleus:
Trigeminal motor nucleus

Brainstem Location:
Pons

Front 25

8. list the cranial nerve nucleus responsible for the function and the part of the brainstem where the nucleus is located (lower medulla, upper medulla, junction of the medulla and pons, pons, junction of the pons and midbrain, midbrain):
-Contraction of the pupillary sphincter and change in curvature of the lens to focus on near objects

Back 25

Nucleus:
Parasympathetic oculomotor

Brainstem Location:
Midbrain

Front 26

9. Which nuclei in the midbrain are part of the basal ganglia circuit?

Back 26

The substantia nigra pedunculopontine nucleus in the midbrain are part of the basal ganglia circuit

Front 27

10. What are the functions of the cerebellum?

Back 27

The function of the cerebellum include coordination of movements, motor planning, and cognitive functions, including rapid shifts of attention

Front 28

11. Why do brainstem lesions about the inferior medulla cause contralateral loss of discriminative touch information from the body?

Back 28

Brainstem lesions above the inferior medulla cause contralateral loss of discriminative touch information from the body b/c the second-order neuron in the dorsal column/medial lemiscus pathway crosses the midline in the inferior medulla

Front 29

12. What midbrain region coordinates somatic and autonomic reactions to pain, threats, and emotions?

Back 29

The periaqueductal gray coordinates somatic and autonomic reactions to pain, threats, and emotions

Front 30

13. What tracts convey motor signals from the cerebral cortex to cranial nerve motor nuclei?

Back 30

Corticobulbar tracts convey motor signals from the cerebral cortex to cranial nerve motor nuclei

Front 31

14. How can a complete lesion of the facial nerve be differentiated from a lesion affecting the corticobulbar tracts that convey information from the cerebral cortex to the facial nerve nucleus?

Back 31

A complete facial nerve lesion produces paralysis of the ipsilateral muscles of facial expression, and the person cannot close the ipsilateral eye. Eye closure is intact w/ a corticobulbar lesion b/c cortical control of muscles in the upper face is bilateral

Front 32

15. Would a person w/ a complete facial nerve lesion on the left side be able to smile involuntarily on the left side of the face? why/why not?

Back 32

A person w/ complete left facial nerve lesion would not be able to smile on the left side of the face b/c there is no neural connection b/t the brainstem and the muscle of the facial expression on the left side.

Front 33

16. Disorders of consciousness can occur w/ damage to what brainstem structures?

Back 33

In the brainstem, damage to the reticular formation or the ascending reticular activating system can cause disorders of consciousness

Front 34

17. A person who has a complete loss of consciousness combined w/ normal vital functions is in what state of altered consciousness?

Back 34

A person w/ complete loss of consciousness and normal vital functions is in a vegetative state.

Front 35

18. Why are space-occupying lesions in the brainstem region, such as benign tumors, so disruptive of brainstem function?

Back 35

b/c the brainstem is tightly confined w/i the bone and dura, space-occupying lesions compress the brainstem and thus interfere w/ its function

Front 36

What are the 4 D's

Back 36

1. Dysphagia - swallowing (can get H2O in lungs)
2. Dysarthria - speaking
3. Diplopia
4. Dysmetria - control distance of movement (body/eye)

Front 37

1. Describe how rotational acceleration of the head stimulates the endings of the vestibular nerve. Describe the mechanism for converting head position relative to gravity into neural signals

Back 37

Inertia of fluid in the semicircular canals causes bending of hairs int he crista during rotational acceleration of the head. Bending of the hairs stimulates or inhibits the hair cells, eliciting excitation of inhibition of vestibular nerve endings, depending on the direction of bend. Head position relative to gravity is signaled by bending of hairs in the macula when the weight of otoconia displaces the gelatinous mass. The bending of the hairs stimulates or inhibits the hair cells, which in turn facilitate or inhibit vestibular nerve endings.

Front 38

2. What does "each pair of semicircular canals produces reciprocal signals" mean?

Back 38

"Each pair of semicircular canals produces reciprocal signals" means that increased frequency of signals from one canal occurs simultaneously w/ decreased signals from its partner.

Front 39

3. Name the tracts that use information from the vestibular nuclei to control posture.

Back 39

The tracts that use vestibular information to control posture include the medial coritcospinal, reticulospinal, tectospinal, and vestibulospinal.

Front 40

4. What tracts convey signals that coordinate eye and head movement?

Back 40

Signals conveyed by the medial longitudinal fasiculus coordinate eye and head movements.

Front 41

5. What is the difference b/t physiological and pathological nystagmus?

Back 41

Nystagmus is involuntary back-and-forth movement of the eyes. Physiological nystagmus is a normal response of an intact nervous system to moving visual objects, head rotation, caloric stimulation of the semicircular canals, or extreme positions of the eyes. Pathological nystagmus is abnormal oscillating eye movements that are caused by a nervous system disorder

Front 42

6. Explain how information from the left visual fields reaches the right visual cortex.

Back 42

Information from the left visual field reaches the right visual cortex via the following pathways: Light from the left visual field strikes the right half of each retina. From the left eye, signals travel in the left optic nerve, cross the midline in the optic chiasm, travel in the optic tract to the right lateral geniculate body, and from the geniculate body to the right optic cortex. Visual information from the right eye travels in the right optic nerve, stays ipsilateral in the optic chiasm, and then follows the same route as visual information from the nasal half of the left eye.

Front 43

7. If a person can see but cannot recognize an object in the left visual field, where is the lesion?

Back 43

The ability to see yet not recognize an object in the left visual field would result from a lesion in the right perceptual stream for visual information. Information in this stream flows from visual areas of the cortex to recognition areas in the temporal lobe.

Front 44

8. Name the source of information used to direct eye movements.

Back 44

Eye movements are directed by information from the vestibular, visual, proprioceptive, limbic, and voluntary eye movement systems.

Front 45

9. What are the objectives of eye movements?

Back 45

The objectives of the eye movements are to stabilize gaze and to direct gaze toward visual targets

Front 46

10. How is the visual world stabilized when the head moves during walking?

Back 46

The vistibulo-ocular reflex stabilizes the visual world when the head moves during walking.

Front 47

11. What is optokinetic reflex?

Back 47

The optokinetic reflex is an involuntary eye movement reaction elicited by moving visual stimuli. The eyes reflexively follow large objects in the visual field.

Front 48

12. Why is there a difference in visual clarity b/t looking at a stationary object while rapidly moving the head and looking at a rapidly moving object w/ the head stationary?

Back 48

When the head is moving rapidly and the visual object is stationary, the vestibulo-ocular reflex compensates for the head movements using feed-forward, producing a clear, stable visual image. When the object is moving rapidly and the head is stationary, the loss of the target and the new position of the target must be recognized, and movements generated to move the eyes to the new position. However, if the object is moving rapidly, the position of the object changes before the eye movements are completed. Thus, when this feedback process is used, the object cannot be seen clearly.

Front 49

13. Normally, what happens to the perception of visual details when the head is quickly turned?

Back 49

Normally, detailed visual information is suppressed when the head is turned rapidly.

Front 50

14. What symptom is most common in peripheral vestibular disorders?

Back 50

Vertigo is the most common symptom in peripheral vestibular disorders.

Front 51

15. If a person has hearing loss, tinnitus, vertigo, and nystagmus, where is the lesion?

Back 51

A lesion tha tproduces hearing loss, tinnitus, vertigo, and nystagmus is most likely to be located in the inner ear.

Front 52

16. What is BPPV?

Back 52

BPPV is benign paroxysmal positional vertigo, a syndrome of a brief (less than 2 min) sensation of whirling movements evoked by a rapid change in head position.

Front 53

17. The abrupt onset of dysequilibrium, spontaneous nystagmus, nausea, and severe vertigo, persisting up to 3 days, indicates what disorder?

Back 53

The abrupt onset of dysequilibrium, spontaneous nystagmus, nausea, and severe vertigo characterizes vestibular neuritis.

Front 54

18. What is oscillopsia?

Back 54

Oscillopsia is a visual sensation of movement of nonmoving objects. The objects appear to jump or bounce.

Front 55

19. How can peripheral vestibular disorders be distinguished from central vestibular disorders?

Back 55

Peripheral vestibular disorders always produce nystagmus, which is near vertical; may be associated w/ hearing loss or tinnitus, but never w/ signs of a brainstem region lesion; are associated w/ severe nausea and vomiting; and do not produce oscillopsia unless there are bilateral peripheral lesions. In contrast, central vestibular disorders may produce nystagmus, which may be vertical; are not associated w/ hearing loss or tinnitus are accompanied by brainstem region signs; cause only mild nausea and vomiting; and oscilopsia is often present

Front 56

20. Describe the ocular tilt reaction

Back 56

The ocular tilt rxn is a triad of signs produced by a unilateral lesion of the otoliths or of the vestibular nuclei. The signs include lateral head tilt, rotation of the eyes toward the downward side of the head, and skew deviation of the eyes w/ one eye looking upward while the other eye looks downward

Front 57

21. What is the location of a lesion that produces a left homonymous hemianopsia?

Back 57

A left homonymous hemianopia is produced by a complete lesion of the visual pathway anywhere posterior to the optic chiasm on the right side: in thge optic tract, lateral geniculate, optic radiations, or primary visual cortex. Any of these lesions produce a loss of information from the contralateral visual field

Front 58

22. What is the difference b/t a phoria and a tropia?

Back 58

Phoria is a tendency for one eye to deviate from looking straight ahead when binocular vision is unavailable. When a person is attempting to look straight ahead at a target w/ both eyes, the deviation of one eye from forward gaze is a tropia

Front 59

23. How are cerebellar, vestibular, and sensory ataxia differentiated?

Back 59

Cerebellar ataxia is unaffected by whether the person is standing, siting, or laying down, and in standing, vision does not improve balance. Vestibular ataxia is gravity dependent; when a person is lying down, coordination is normal. Cerebellar and vestibular ataxia both may be associated w/ vertigo and nystagmus. Sensory ataxia is characterized by decreased or lost proprioceptive and vibratory senses and ankle reflex. No vertigo or nystagmus occurs w/ sensory ataxia

Front 60

1. What neural connections would be lost w/ lesions of each of the thalamic relay nuclei?

Back 60

Damage to the ventral anterior nucleus would interrupt fibers from the globus pallidus to the premotor areas; damage to the ventral lateral nucleus would interrupt circuits from the dentate nucleus to primary motor cotrex and premotor areas; damage to the ventral posterolateral nucleus would prevent relay of somatic information from the body to the somatosensory cortex; damage to the ventral posteromedial nucleus would stop somatic sensation from the face from reaching the somatosensory cortex; and lesions of the medial and lateral geniculate would interrupt axons transmitting auditory and visual information to the cerebral cortex

Front 61

2. Why is compression of or damage to the hypothalamus potentially life-threatening?

Back 61

The hypothalamic regulation of body temperature, metabolic rate, and blood pressure are essential for survival

Front 62

3. What signs would follow destruction of the genu region of the internal capsule?

Back 62

A lesion of the genu of the internal capsule would cause contralateral loss of corticobulbar control, resulting in inability to voluntarily control the cranial nerves that receive cortical input: oculomotor, trochlear, trigeminal, abducens, facial, glossopharyngeal, accessory, and hypoglossal. Thus the person would be unable to voluntarily control the muscles that move the eyes, chew, form facial expressions, swallow, produce speech, elevate the shoulders, and turn the head. Cortical control of reticular activity would be decreased b/c corticoreticular fibers travel through the genu and then project bilaterally to the reticular formation

Front 63

4. What are the five functional categories of the cerebral cortex?

Back 63

The functional categories of the cerebral cortex are primary sensory, sensory association, association, motor planning, and primary motor

Front 64

5. Draw a flowchart of the cortical area activated to comply w/ the request, "please pass the salt."

Back 64

Primary auditory cortex --> Auditory association cortex --> Parieto-temporal association areas --> Visual cortex --> Cortical eye fields --> Visual cortex --> Premotor area --> Sensorimotor cortex --> Spinal cord

Front 65

6. How is the stress response produced?

Back 65

The stress response is produced by activity of the voluntary, autonomic, and neuroendocrine system

Front 66

7. What are the effects of excessive, prolonged cortisol secretion?

Back 66

Excessive, prolonged cortisol secretion may contribute to the development of stress-related diseases, including colitis, adult-onset diabetes, cardiovascular disorders, and emotional and cognitive disorders

Front 67

8. What is the role of the hippocampus in memory?

Back 67

The hippocampus consolidates declarative short-term memory into long-term memory, although the hippocampus does not store the long-term memories

Front 68

9. Which structures are important for learning and storing procedural memories?

Back 68

Motor and parietal cortex and striatum are involved in learning procedural memories. Supplementary motor area and the putamen/globus pallidus are involved in storing procedural memories

Front 69

10. How do we use visual information in the ventral stream?

Back 69

Visual information in the ventral stream is used to identify objects and people.

Front 70

11. Bob is reading intently when he hears someone call his name. He looks up and begins a conversation w/ a friend. What brain area contribute to Bob's ability to maintain his attention while reading, then disengage from reading and shift his attention to his friend?

Back 70

The right frontal and parietal lobes contribute to the maintenance of attention, the right parietal lobe disengages attention, and the midbrain shifts attention to a new focus.

Front 71

1. What is the most likely location of a lesion in a person w/ loss of conscious somatosensation and voluntary movement on the left side of the body and face and loss of conscious vision from the left visual field?

Back 71

the most probable location of the lesion is the right posterior limb of the internal capsule

Front 72

2. Define each of the following terms and identify the area of cortex most commonly damaged w/ each sign: astereognosis

Back 72

inability to recognize an object by touch and manipulation; lesion is in the somatosensory association area

Front 73

2. Define each of the following terms and identify the area of cortex most commonly damaged w/ each sign: visual agnosia

Back 73

inability to recognize objects by vision, despite intact vision; lesion is in the visual association area

Front 74

2. Define each of the following terms and identify the area of cortex most commonly damaged w/ each sign: apraxia

Back 74

inability to perform voluntary movement in spite of preserved sensation, muscular power, and coordination; lesion is in the premotor area

Front 75

2. Define each of the following terms and identify the area of cortex most commonly damaged w/ each sign: spastic dysarthria

Back 75

speech disorder is due to upper motor neuron damage. The damage can cause paralysis, spasticity, and/or uncoordinated activity of the speech muscles; lesion is in the primary motor and primary somatosensory cortex

Front 76

3. A person unable to understand nonverbal communication an exhibiting signs of left neglect probably has a lesion where?

Back 76

The lesion is in the area analogous to Wernicke's area in the right hemisphere

Front 77

4. Is Broca's aphasia an upper motor neuron disorder?

Back 77

Broca's aphasia is not an upper motor neuron disorder. Broca's area provides grammatical function words and planning of speech movements. Information from Broca's area projects to the adjacent sensorimotor cortex, which is the source of most upper motor neurons that control cranial nerves involved in producing speech

Front 78

5. What is the difference b/t dysarrthria and aphasia?

Back 78

Dysarthria interferes w/ the motor production of sounds. Thus dysarthria can be a lower or upper motor neuron disorder. The lower motor neuron form of dysarthria produces flaccidity of the muscles of speech, causing soft, imprecise speech. The upper motor neurons form of dysarthria is characterized by harsh, awkward speech. Unlike dysarthria, a disorder of speech, aphasia interferes w/ understanding language

Front 79

6. A 64-yow has right hemiparesis, hemisensory loss, Broca's aphasia, and intact vision. Where is the most likely site for the lesion?

Back 79

The left inferior frontal cortex and adjacent parietal cortex are the most probable sites of the lesion.

Front 80

7. When working w/ a person who has global aphasia, what type of communication is most effective?

Back 80

Nonverbal communication, using gestures and demonstration, is most effective in conveying information to people who cannot understand language.

Front 81

8. JZ is 2 wks post stroke. Although she has been in the same hospital room for 10 days, she cannot find the bathroomo or the hallway. What is the name for this problem?

Back 81

JZ has spacial neglect