Chapter 4. Disturbances Of Vision Part 2

Front 1

bnormal protrusion of the eye from the orbit (exophthalmos or proptosis) is best detected by standing behind the seated patients and looking down at their eyes. The causes include hyperthyroidism, orbital tumor or pseudotumor, and

Back 1

carotid artery-cavernous sinus fistula. A bruit may be audible on auscultation over the proptotic eye in patients with carotid artery-cavernous sinus fistula or other vascular anomalies.

Front 2

bnormal protrusion of the eye from the orbit (exophthalmos or proptosis) is best detected by standing behind the seated patients and looking down at their eyes. The causes include hyperthyroidism, orbital tumor or pseudotumor, and

Back 2

carotid artery-cavernous sinus fistula. A bruit may be audible on auscultation over the proptotic eye in patients with carotid artery-cavernous sinus fistula or other vascular anomalies.

Front 3

bnormal protrusion of the eye from the orbit (exophthalmos or proptosis) is best detected by standing behind the seated patients and looking down at their eyes. The causes include hyperthyroidism, orbital tumor or pseudotumor, and

Back 3

carotid artery-cavernous sinus fistula. A bruit may be audible on auscultation over the proptotic eye in patients with carotid artery-cavernous sinus fistula or other vascular anomalies.

Front 4

bnormal protrusion of the eye from the orbit (exophthalmos or proptosis) is best detected by standing behind the seated patients and looking down at their eyes. The causes include hyperthyroidism, orbital tumor or pseudotumor, and

Back 4

carotid artery-cavernous sinus fistula. A bruit may be audible on auscultation over the proptotic eye in patients with carotid artery-cavernous sinus fistula or other vascular anomalies.

Front 5

On visual field testing, there is usually a central scotoma

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Optic Neuritis

Front 6

On visual field testing, there is usually a central scotoma

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Optic Neuritis

Front 7

On visual field testing, there is usually a central scotoma

Back 7

Optic Neuritis

Front 8

On visual field testing, there is usually a central scotoma

Back 8

Optic Neuritis

Front 9

Idiopathic infarction of the anterior portion of the optic nerve is termed anterior ischemic optic neuropathy. It occurs after the age of 50. Such visual loss is sudden in onset, usually painless, always monocular, and without premonitory ocular symptoms. Visual loss is usually maximal at onset and frequently subtotal, producing a field defect that is typically

Back 9

altitudinal

Front 10

Idiopathic infarction of the anterior portion of the optic nerve is termed anterior ischemic optic neuropathy. It occurs after the age of 50. Such visual loss is sudden in onset, usually painless, always monocular, and without premonitory ocular symptoms. Visual loss is usually maximal at onset and frequently subtotal, producing a field defect that is typically

Back 10

altitudinal

Front 11

Idiopathic infarction of the anterior portion of the optic nerve is termed anterior ischemic optic neuropathy. It occurs after the age of 50. Such visual loss is sudden in onset, usually painless, always monocular, and without premonitory ocular symptoms. Visual loss is usually maximal at onset and frequently subtotal, producing a field defect that is typically

Back 11

altitudinal

Front 12

Idiopathic infarction of the anterior portion of the optic nerve is termed anterior ischemic optic neuropathy. It occurs after the age of 50. Such visual loss is sudden in onset, usually painless, always monocular, and without premonitory ocular symptoms. Visual loss is usually maximal at onset and frequently subtotal, producing a field defect that is typically

Back 12

altitudinal

Front 13

Associated nonspecific symptoms of raised intracranial pressure include headache, nausea, vomiting, and diplopia from

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abducens nerve palsy

Front 14

Associated nonspecific symptoms of raised intracranial pressure include headache, nausea, vomiting, and diplopia from

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abducens nerve palsy

Front 15

Associated nonspecific symptoms of raised intracranial pressure include headache, nausea, vomiting, and diplopia from

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abducens nerve palsy

Front 16

ith the exception of --------- , chiasmal visual loss is gradual in onset and the resulting impairment in depth perception or in the lateral visual fields may not be noted for some time

Back 16

pituitary apoplexy

Front 17

ith the exception of --------- , chiasmal visual loss is gradual in onset and the resulting impairment in depth perception or in the lateral visual fields may not be noted for some time

Back 17

pituitary apoplexy

Front 18

ith the exception of --------- , chiasmal visual loss is gradual in onset and the resulting impairment in depth perception or in the lateral visual fields may not be noted for some time

Back 18

pituitary apoplexy

Front 19

ith the exception of --------- , chiasmal visual loss is gradual in onset and the resulting impairment in depth perception or in the lateral visual fields may not be noted for some time

Back 19

pituitary apoplexy

Front 20

Headache, endocrine abnormalities, and occasionally blurred or double vision may occur in patients with an enlarged sella turcica (shown on radiographic examination) but in whom neither tumor nor increased intracranial pressure is found. This is what

Back 20

empty sella syndrome

Front 21

Headache, endocrine abnormalities, and occasionally blurred or double vision may occur in patients with an enlarged sella turcica (shown on radiographic examination) but in whom neither tumor nor increased intracranial pressure is found. This is what

Back 21

empty sella syndrome

Front 22

Headache, endocrine abnormalities, and occasionally blurred or double vision may occur in patients with an enlarged sella turcica (shown on radiographic examination) but in whom neither tumor nor increased intracranial pressure is found. This is what

Back 22

empty sella syndrome

Front 23

Headache, endocrine abnormalities, and occasionally blurred or double vision may occur in patients with an enlarged sella turcica (shown on radiographic examination) but in whom neither tumor nor increased intracranial pressure is found. This is what

Back 23

empty sella syndrome

Front 24

With lesions in the temporal lobe, where tumors are the most common cause, the field deficit is denser superiorly than inferiorly, resulting in a

Back 24

superior quadrantanopia ("pie in the sky" deficit;

Front 25

With lesions in the temporal lobe, where tumors are the most common cause, the field deficit is denser superiorly than inferiorly, resulting in a

Back 25

superior quadrantanopia ("pie in the sky" deficit;

Front 26

With lesions in the temporal lobe, where tumors are the most common cause, the field deficit is denser superiorly than inferiorly, resulting in a

Back 26

superior quadrantanopia ("pie in the sky" deficit;

Front 27

With lesions in the temporal lobe, where tumors are the most common cause, the field deficit is denser superiorly than inferiorly, resulting in a

Back 27

superior quadrantanopia ("pie in the sky" deficit;

Front 28

Lesions affecting the optic radiations in the parietal lobe may be due to tumor or vascular disease and are usually associated with contralateral

Back 28

weakness and sensory loss. A gaze preference is common in the acute phase, with the eyes conjugately deviated to the side of the parietal lesion. The visual field abnormality is either complete homonymous hemianopia or inferior quadrantanopia (see Figure 4-7). The optokinetic response to a visual stimulus moved toward the side of the lesion is impaired, which is not the case with pure temporal or occipital lobe lesions.

Front 29

Lesions affecting the optic radiations in the parietal lobe may be due to tumor or vascular disease and are usually associated with contralateral

Back 29

weakness and sensory loss. A gaze preference is common in the acute phase, with the eyes conjugately deviated to the side of the parietal lesion. The visual field abnormality is either complete homonymous hemianopia or inferior quadrantanopia (see Figure 4-7). The optokinetic response to a visual stimulus moved toward the side of the lesion is impaired, which is not the case with pure temporal or occipital lobe lesions.

Front 30

Lesions affecting the optic radiations in the parietal lobe may be due to tumor or vascular disease and are usually associated with contralateral

Back 30

weakness and sensory loss. A gaze preference is common in the acute phase, with the eyes conjugately deviated to the side of the parietal lesion. The visual field abnormality is either complete homonymous hemianopia or inferior quadrantanopia (see Figure 4-7). The optokinetic response to a visual stimulus moved toward the side of the lesion is impaired, which is not the case with pure temporal or occipital lobe lesions.

Front 31

Lesions affecting the optic radiations in the parietal lobe may be due to tumor or vascular disease and are usually associated with contralateral

Back 31

weakness and sensory loss. A gaze preference is common in the acute phase, with the eyes conjugately deviated to the side of the parietal lesion. The visual field abnormality is either complete homonymous hemianopia or inferior quadrantanopia (see Figure 4-7). The optokinetic response to a visual stimulus moved toward the side of the lesion is impaired, which is not the case with pure temporal or occipital lobe lesions.

Front 32

Bilateral occipital lobe involvement produces cortical blindness. Pupillary reactions are normal, and bilateral macular sparing may preserve central (tunnel) vision. With more extensive lesions, denial of blindness may occur

Back 32

(Anton syndrome

Front 33

Bilateral occipital lobe involvement produces cortical blindness. Pupillary reactions are normal, and bilateral macular sparing may preserve central (tunnel) vision. With more extensive lesions, denial of blindness may occur

Back 33

(Anton syndrome

Front 34

Bilateral occipital lobe involvement produces cortical blindness. Pupillary reactions are normal, and bilateral macular sparing may preserve central (tunnel) vision. With more extensive lesions, denial of blindness may occur

Back 34

(Anton syndrome

Front 35

Bilateral occipital lobe involvement produces cortical blindness. Pupillary reactions are normal, and bilateral macular sparing may preserve central (tunnel) vision. With more extensive lesions, denial of blindness may occur

Back 35

(Anton syndrome

Front 36

Bilateral occipital lobe involvement produces cortical blindness. Pupillary reactions are normal, and bilateral macular sparing may preserve central (tunnel) vision. With more extensive lesions, denial of blindness may occur

Back 36

(Anton syndrome

Front 37

Acutely, hemispheric lesions produce tonic deviation of both eyes toward

Back 37

the side of the lesion and away from the side of the hemiparesis (Figure 4-19 A)

Front 38

Acutely, hemispheric lesions produce tonic deviation of both eyes toward

Back 38

the side of the lesion and away from the side of the hemiparesis (Figure 4-19 A)

Front 39

Acutely, hemispheric lesions produce tonic deviation of both eyes toward

Back 39

the side of the lesion and away from the side of the hemiparesis (Figure 4-19 A)

Front 40

Acutely, hemispheric lesions produce tonic deviation of both eyes toward

Back 40

the side of the lesion and away from the side of the hemiparesis (Figure 4-19 A)

Front 41

Acutely, hemispheric lesions produce tonic deviation of both eyes toward

Back 41

the side of the lesion and away from the side of the hemiparesis (Figure 4-19 A)

Front 42

Lesions of the ---------- affect the center responsible for voluntary upward gaze and may therefore produce upgaze paralysis

Back 42

dorsal midbrain

Front 43

Lesions of the ---------- affect the center responsible for voluntary upward gaze and may therefore produce upgaze paralysis

Back 43

dorsal midbrain

Front 44

Lesions of the ---------- affect the center responsible for voluntary upward gaze and may therefore produce upgaze paralysis

Back 44

dorsal midbrain

Front 45

Lesions of the ---------- affect the center responsible for voluntary upward gaze and may therefore produce upgaze paralysis

Back 45

dorsal midbrain

Front 46

cause eye deviation toward, rather than away from, the side of the hemiparesis (Figure 4-19 C) because the corticobulbar pathways that regulate gaze have decussated but the descending motor pathways have not yet crossed

Back 46

Brainstem lesions at the level of the pontine gaze centers produce disorders of conjugate horizontal gaze. Gaze palsies from pontine involvement (unlike those from hemispheric lesions) cause eye deviation toward, rather than away from, the side of the hemiparesis (Figure 4-19 C) because the corticobulbar pathways that regulate gaze have decussated but the descending motor pathways have not yet crossed

Front 47

cause eye deviation toward, rather than away from, the side of the hemiparesis (Figure 4-19 C) because the corticobulbar pathways that regulate gaze have decussated but the descending motor pathways have not yet crossed

Back 47

Brainstem lesions at the level of the pontine gaze centers produce disorders of conjugate horizontal gaze. Gaze palsies from pontine involvement (unlike those from hemispheric lesions) cause eye deviation toward, rather than away from, the side of the hemiparesis (Figure 4-19 C) because the corticobulbar pathways that regulate gaze have decussated but the descending motor pathways have not yet crossed

Front 48

cause eye deviation toward, rather than away from, the side of the hemiparesis (Figure 4-19 C) because the corticobulbar pathways that regulate gaze have decussated but the descending motor pathways have not yet crossed

Back 48

Brainstem lesions at the level of the pontine gaze centers produce disorders of conjugate horizontal gaze. Gaze palsies from pontine involvement (unlike those from hemispheric lesions) cause eye deviation toward, rather than away from, the side of the hemiparesis (Figure 4-19 C) because the corticobulbar pathways that regulate gaze have decussated but the descending motor pathways have not yet crossed

Front 49

cause eye deviation toward, rather than away from, the side of the hemiparesis (Figure 4-19 C) because the corticobulbar pathways that regulate gaze have decussated but the descending motor pathways have not yet crossed

Back 49

Brainstem lesions at the level of the pontine gaze centers produce disorders of conjugate horizontal gaze. Gaze palsies from pontine involvement (unlike those from hemispheric lesions) cause eye deviation toward, rather than away from, the side of the hemiparesis (Figure 4-19 C) because the corticobulbar pathways that regulate gaze have decussated but the descending motor pathways have not yet crossed

Front 50

cause eye deviation toward, rather than away from, the side of the hemiparesis (Figure 4-19 C) because the corticobulbar pathways that regulate gaze have decussated but the descending motor pathways have not yet crossed

Back 50

Brainstem lesions at the level of the pontine gaze centers produce disorders of conjugate horizontal gaze. Gaze palsies from pontine involvement (unlike those from hemispheric lesions) cause eye deviation toward, rather than away from, the side of the hemiparesis (Figure 4-19 C) because the corticobulbar pathways that regulate gaze have decussated but the descending motor pathways have not yet crossed

Front 51

Unlike cavernous sinus lesions, orbital lesions that affect the oculomotor nerve are often associated with

Back 51

optic nerve involvement and exophthalmos

Front 52

Unlike cavernous sinus lesions, orbital lesions that affect the oculomotor nerve are often associated with

Back 52

optic nerve involvement and exophthalmos

Front 53

Unlike cavernous sinus lesions, orbital lesions that affect the oculomotor nerve are often associated with

Back 53

optic nerve involvement and exophthalmos

Front 54

Unlike cavernous sinus lesions, orbital lesions that affect the oculomotor nerve are often associated with

Back 54

optic nerve involvement and exophthalmos

Front 55

Unlike cavernous sinus lesions, orbital lesions that affect the oculomotor nerve are often associated with

Back 55

optic nerve involvement and exophthalmos

Front 56

the most common cause of an isolated trochlear nerve palsy

Back 56

trauma

Front 57

the most common cause of an isolated trochlear nerve palsy

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trauma

Front 58

the most common cause of an isolated trochlear nerve palsy

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trauma

Front 59

Patients with abducens nerve lesions complain of

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horizontal diplopia due to weakness of the lateral rectus muscle

Front 60

Patients with abducens nerve lesions complain of

Back 60

horizontal diplopia due to weakness of the lateral rectus muscle

Front 61

Patients with abducens nerve lesions complain of

Back 61

horizontal diplopia due to weakness of the lateral rectus muscle

Front 62

Patients with abducens nerve lesions complain of

Back 62

horizontal diplopia due to weakness of the lateral rectus muscle

Front 63

Patients with abducens nerve lesions complain of

Back 63

horizontal diplopia due to weakness of the lateral rectus muscle

Front 64

what type of tumor can cause Horizontasl diplopia (Abducens nerve palsy)?

Back 64

nasopharyngeal carcinoma

Front 65

what type of tumor can cause Horizontasl diplopia (Abducens nerve palsy)?

Back 65

nasopharyngeal carcinoma

Front 66

what type of tumor can cause Horizontasl diplopia (Abducens nerve palsy)?

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nasopharyngeal carcinoma

Front 67

what type of tumor can cause Horizontasl diplopia (Abducens nerve palsy)?

Back 67

nasopharyngeal carcinoma

Front 68

e presence of a concurrent Horner's syndrome with abducenas palsy indicates localization in the

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cavernous sinus

Front 69

e presence of a concurrent Horner's syndrome with abducenas palsy indicates localization in the

Back 69

cavernous sinus

Front 70

e presence of a concurrent Horner's syndrome with abducenas palsy indicates localization in the

Back 70

cavernous sinus

Front 71

e presence of a concurrent Horner's syndrome with abducenas palsy indicates localization in the

Back 71

cavernous sinus

Front 72

In known diabetics, painful ophthalmoplegia with exophthalmos and metabolic acidosis requires urgent attention to determine the possibility of

Back 72

fungal infection in the paranasal sinus, orbit, or cavernous sinus by mucormycosis

Front 73

In known diabetics, painful ophthalmoplegia with exophthalmos and metabolic acidosis requires urgent attention to determine the possibility of

Back 73

fungal infection in the paranasal sinus, orbit, or cavernous sinus by mucormycosis

Front 74

In known diabetics, painful ophthalmoplegia with exophthalmos and metabolic acidosis requires urgent attention to determine the possibility of

Back 74

fungal infection in the paranasal sinus, orbit, or cavernous sinus by mucormycosis

Front 75

In known diabetics, painful ophthalmoplegia with exophthalmos and metabolic acidosis requires urgent attention to determine the possibility of

Back 75

fungal infection in the paranasal sinus, orbit, or cavernous sinus by mucormycosis

Front 76

Ocular myopathies are painless syndromes that spare pupillary function and are usually bilateral. The most common is the myopathy of

Back 76

hyperthyroidism, a common cause of double vision beginning in midlife or later

Front 77

Ocular myopathies are painless syndromes that spare pupillary function and are usually bilateral. The most common is the myopathy of

Back 77

hyperthyroidism, a common cause of double vision beginning in midlife or later

Front 78

Ocular myopathies are painless syndromes that spare pupillary function and are usually bilateral. The most common is the myopathy of

Back 78

hyperthyroidism, a common cause of double vision beginning in midlife or later

Front 79

Ocular myopathies are painless syndromes that spare pupillary function and are usually bilateral. The most common is the myopathy of

Back 79

hyperthyroidism, a common cause of double vision beginning in midlife or later

Front 80

progressive external ophthalmoplegias are a group of syndromes characterized by

Back 80

slowly progressive, symmetric impairment of ocular movement that cannot be overcome by caloric stimulation. Pupillary function is spared, and there is no pain; ptosis may be prominent. This clinical picture can be produced by ocular or oculopharyngeal muscular dystrophy.

Front 81

progressive external ophthalmoplegias are a group of syndromes characterized by

Back 81

slowly progressive, symmetric impairment of ocular movement that cannot be overcome by caloric stimulation. Pupillary function is spared, and there is no pain; ptosis may be prominent. This clinical picture can be produced by ocular or oculopharyngeal muscular dystrophy.

Front 82

progressive external ophthalmoplegias are a group of syndromes characterized by

Back 82

slowly progressive, symmetric impairment of ocular movement that cannot be overcome by caloric stimulation. Pupillary function is spared, and there is no pain; ptosis may be prominent. This clinical picture can be produced by ocular or oculopharyngeal muscular dystrophy.

Front 83

progressive external ophthalmoplegias are a group of syndromes characterized by

Back 83

slowly progressive, symmetric impairment of ocular movement that cannot be overcome by caloric stimulation. Pupillary function is spared, and there is no pain; ptosis may be prominent. This clinical picture can be produced by ocular or oculopharyngeal muscular dystrophy.