Chapter 1. Disorders Of Cognitive Function - Part 4

Front 1

Taboparesis is characterized by

Back 1

In taboparesis, the coexistence of tabes dorsalis (see Chapter 6) with general paresis, signs and symptoms include Argyll Robertson pupils (see Chapter 4), lancinating pains, areflexia, posterior column sensory deficits with sensory ataxia and Romberg sign, incontinence, impotence, Charcot (hypertrophic) joints, and genu recurvatum (hyperextended knees). Optic atrophy may also be present.

Front 2

Taboparesis is characterized by

Back 2

In taboparesis, the coexistence of tabes dorsalis (see Chapter 6) with general paresis, signs and symptoms include Argyll Robertson pupils (see Chapter 4), lancinating pains, areflexia, posterior column sensory deficits with sensory ataxia and Romberg sign, incontinence, impotence, Charcot (hypertrophic) joints, and genu recurvatum (hyperextended knees). Optic atrophy may also be present.

Front 3

Taboparesis is characterized by

Back 3

In taboparesis, the coexistence of tabes dorsalis (see Chapter 6) with general paresis, signs and symptoms include Argyll Robertson pupils (see Chapter 4), lancinating pains, areflexia, posterior column sensory deficits with sensory ataxia and Romberg sign, incontinence, impotence, Charcot (hypertrophic) joints, and genu recurvatum (hyperextended knees). Optic atrophy may also be present.

Front 4

Taboparesis is characterized by

Back 4

In taboparesis, the coexistence of tabes dorsalis (see Chapter 6) with general paresis, signs and symptoms include Argyll Robertson pupils (see Chapter 4), lancinating pains, areflexia, posterior column sensory deficits with sensory ataxia and Romberg sign, incontinence, impotence, Charcot (hypertrophic) joints, and genu recurvatum (hyperextended knees). Optic atrophy may also be present.

Front 5

Herxheimer reaction

Back 5

Neurosyphilis is treated with a 10-day course of aqueous penicillin G, 2-4 ´ 106 units intravenously every 4 hours. Tetracycline or erythromycin can be used for patients allergic to penicillin. Fever and leukocytosis may occur shortly after therapy is started (Herxheimer reaction) but are transient

Front 6

Progressive Multifocal Leukoencephalopathy pathos:

Back 6

The virus infects oligodendrocytes, leading to diffuse and patchy demyelination that primarily affects white matter of the cerebral hemispheres but also involves the brainstem and cerebellum

Front 7

Progressive Multifocal Leukoencephalopathy pathos:

Back 7

The virus infects oligodendrocytes, leading to diffuse and patchy demyelination that primarily affects white matter of the cerebral hemispheres but also involves the brainstem and cerebellum

Front 8

Progressive Multifocal Leukoencephalopathy pathos:

Back 8

The virus infects oligodendrocytes, leading to diffuse and patchy demyelination that primarily affects white matter of the cerebral hemispheres but also involves the brainstem and cerebellum

Front 9

Progressive Multifocal Leukoencephalopathy pathos:

Back 9

The virus infects oligodendrocytes, leading to diffuse and patchy demyelination that primarily affects white matter of the cerebral hemispheres but also involves the brainstem and cerebellum

Front 10

PML CT will show

Back 10

scan or MRI shows multifocal white matter abnormalities

Front 11

PML CT will show

Back 11

T scan or MRI shows multifocal white matter abnormalities

Front 12

PML CT will show

Back 12

T scan or MRI shows multifocal white matter abnormalities

Front 13

PML CT will show

Back 13

T scan or MRI shows multifocal white matter abnormalities

Front 14

Marchiafava Bignami syndrome is characterized by

Back 14

ecrosis of the corpus callosum and subcortical white matter and occurs most often in malnourished alcoholics

Front 15

ecrosis of the corpus callosum and subcortical white matter and occurs most often in malnourished alcoholics

Back 15

Marchiafava Bignami syndrome is characterized by

Front 16

Marchiafava Bignami syndrome is characterized by

Back 16

ecrosis of the corpus callosum and subcortical white matter and occurs most often in malnourished alcoholics

Front 17

ecrosis of the corpus callosum and subcortical white matter and occurs most often in malnourished alcoholics

Back 17

Marchiafava Bignami syndrome is characterized by

Front 18

The EEG shows paroxysmal high-voltage slowing with intermixed spikes and slow waves; these abnormalities can be reversed by diazepam. Aluminum in the dialysate is a major etiologic suspect,

Back 18

Dialysis Dementia

This rare disorder typically occurs in patients receiving chronic hemodialysis. Clinical features include dysarthria, myoclonus, and seizures. These are initially intermittent, but later become permanent, and dementia supervenes. The EEG shows paroxysmal high-voltage slowing with intermixed spikes and slow waves; these abnormalities can be reversed by diazepam. Aluminum in the dialysate is a major etiologic suspect, and removing trace metals from the dialysate has decreased the syndrome's incidence. Mean survival is 6 months

Front 19

The EEG shows paroxysmal high-voltage slowing with intermixed spikes and slow waves; these abnormalities can be reversed by diazepam. Aluminum in the dialysate is a major etiologic suspect,

Back 19

Dialysis Dementia

This rare disorder typically occurs in patients receiving chronic hemodialysis. Clinical features include dysarthria, myoclonus, and seizures. These are initially intermittent, but later become permanent, and dementia supervenes. The EEG shows paroxysmal high-voltage slowing with intermixed spikes and slow waves; these abnormalities can be reversed by diazepam. Aluminum in the dialysate is a major etiologic suspect, and removing trace metals from the dialysate has decreased the syndrome's incidence. Mean survival is 6 months

Front 20

The EEG shows paroxysmal high-voltage slowing with intermixed spikes and slow waves; these abnormalities can be reversed by diazepam. Aluminum in the dialysate is a major etiologic suspect,

Back 20

Dialysis Dementia

This rare disorder typically occurs in patients receiving chronic hemodialysis. Clinical features include dysarthria, myoclonus, and seizures. These are initially intermittent, but later become permanent, and dementia supervenes. The EEG shows paroxysmal high-voltage slowing with intermixed spikes and slow waves; these abnormalities can be reversed by diazepam. Aluminum in the dialysate is a major etiologic suspect, and removing trace metals from the dialysate has decreased the syndrome's incidence. Mean survival is 6 months

Front 21

The EEG shows paroxysmal high-voltage slowing with intermixed spikes and slow waves; these abnormalities can be reversed by diazepam. Aluminum in the dialysate is a major etiologic suspect,

Back 21

Dialysis Dementia

This rare disorder typically occurs in patients receiving chronic hemodialysis. Clinical features include dysarthria, myoclonus, and seizures. These are initially intermittent, but later become permanent, and dementia supervenes. The EEG shows paroxysmal high-voltage slowing with intermixed spikes and slow waves; these abnormalities can be reversed by diazepam. Aluminum in the dialysate is a major etiologic suspect, and removing trace metals from the dialysate has decreased the syndrome's incidence. Mean survival is 6 months

Front 22

dementia pugilistica is what

Back 22

Cognitive impairment is nonprogressive and the cause is usually obvious. Delayed, progressive posttraumatic dementia in boxers (dementia pugilistica) is characterized by cheerful or labile affect, mental slowness, memory deficit, and irritability. Associated neurologic abnormalities include tremor, rigidity, bradykinesia, dysarthria, cerebellar ataxia, pyramidal signs, and seizures. Neuroradiologic investigations may show cortical atrophy and cavum septi pellucidi.

Front 23

dementia pugilistica is what

Back 23

Cognitive impairment is nonprogressive and the cause is usually obvious. Delayed, progressive posttraumatic dementia in boxers (dementia pugilistica) is characterized by cheerful or labile affect, mental slowness, memory deficit, and irritability. Associated neurologic abnormalities include tremor, rigidity, bradykinesia, dysarthria, cerebellar ataxia, pyramidal signs, and seizures. Neuroradiologic investigations may show cortical atrophy and cavum septi pellucidi.

Front 24

dementia pugilistica is what

Back 24

Cognitive impairment is nonprogressive and the cause is usually obvious. Delayed, progressive posttraumatic dementia in boxers (dementia pugilistica) is characterized by cheerful or labile affect, mental slowness, memory deficit, and irritability. Associated neurologic abnormalities include tremor, rigidity, bradykinesia, dysarthria, cerebellar ataxia, pyramidal signs, and seizures. Neuroradiologic investigations may show cortical atrophy and cavum septi pellucidi.

Front 25

dementia pugilistica is what

Back 25

Cognitive impairment is nonprogressive and the cause is usually obvious. Delayed, progressive posttraumatic dementia in boxers (dementia pugilistica) is characterized by cheerful or labile affect, mental slowness, memory deficit, and irritability. Associated neurologic abnormalities include tremor, rigidity, bradykinesia, dysarthria, cerebellar ataxia, pyramidal signs, and seizures. Neuroradiologic investigations may show cortical atrophy and cavum septi pellucidi.

Front 26

cardiac arrest or carbon monoxide poisoning, can produce amnestic syndromes because of

Back 26

Because of the selective vulnerability of pyramidal neurons in the Sommer sector (h1 sector of Scholz) of the hippocampus,

Front 27

cardiac arrest or carbon monoxide poisoning, can produce amnestic syndromes because of

Back 27

Because of the selective vulnerability of pyramidal neurons in the Sommer sector (h1 sector of Scholz) of the hippocampus,

Front 28

cardiac arrest or carbon monoxide poisoning, can produce amnestic syndromes because of

Back 28

Because of the selective vulnerability of pyramidal neurons in the Sommer sector (h1 sector of Scholz) of the hippocampus,

Front 29

cardiac arrest or carbon monoxide poisoning, can produce amnestic syndromes because of

Back 29

Because of the selective vulnerability of pyramidal neurons in the Sommer sector (h1 sector of Scholz) of the hippocampus,

Front 30

cardiac arrest or carbon monoxide poisoning, can produce amnestic syndromes because of

Back 30

Because of the selective vulnerability of pyramidal neurons in the Sommer sector (h1 sector of Scholz) of the hippocampus,

Front 31

The posterior cerebral artery supplies the

Back 31

medial temporal lobe, thalamus, posterior internal capsule, and occipital cortex (Loading
Figure 1-22). Ischemia or infarction in this territory, typically when bilateral, may produce a transient or permanent amnestic syndrome. Emboli in the vertebrobasilar system (see Chapter 9) are frequent causes of such disorders.

Front 32

The posterior cerebral artery supplies the

Back 32

medial temporal lobe, thalamus, posterior internal capsule, and occipital cortex (Loading
Figure 1-22). Ischemia or infarction in this territory, typically when bilateral, may produce a transient or permanent amnestic syndrome. Emboli in the vertebrobasilar system (see Chapter 9) are frequent causes of such disorders.

Front 33

The posterior cerebral artery supplies the

Back 33

medial temporal lobe, thalamus, posterior internal capsule, and occipital cortex (Loading
Figure 1-22). Ischemia or infarction in this territory, typically when bilateral, may produce a transient or permanent amnestic syndrome. Emboli in the vertebrobasilar system (see Chapter 9) are frequent causes of such disorders.

Front 34

The posterior cerebral artery supplies the

Back 34

medial temporal lobe, thalamus, posterior internal capsule, and occipital cortex (Loading
Figure 1-22). Ischemia or infarction in this territory, typically when bilateral, may produce a transient or permanent amnestic syndrome. Emboli in the vertebrobasilar system (see Chapter 9) are frequent causes of such disorders.

Front 35

The posterior cerebral artery supplies the

Back 35

medial temporal lobe, thalamus, posterior internal capsule, and occipital cortex (Loading
Figure 1-22). Ischemia or infarction in this territory, typically when bilateral, may produce a transient or permanent amnestic syndrome. Emboli in the vertebrobasilar system (see Chapter 9) are frequent causes of such disorders.

Front 36

Wernicke encephalopathy is caused by thiamine deficiency and classically produces an

Back 36

acute confusional state, ataxia, and ophthalmoplegia.

Front 37

Wernicke encephalopathy is caused by thiamine deficiency and classically produces an

Back 37

acute confusional state, ataxia, and ophthalmoplegia.

Front 38

Wernicke encephalopathy is caused by thiamine deficiency and classically produces an

Back 38

acute confusional state, ataxia, and ophthalmoplegia.

Front 39

Wernicke encephalopathy is caused by thiamine deficiency and classically produces an

Back 39

acute confusional state, ataxia, and ophthalmoplegia.

Front 40

Wernicke encephalopathy is caused by thiamine deficiency and classically produces an

Back 40

acute confusional state, ataxia, and ophthalmoplegia.

Front 41

The memory disorder may be related to bilateral degeneration of the dorsomedial thalamic nuclei.

Back 41

ALCOHOLIC KORSAKOFF AMNESTIC SYNDROME

Front 42

The memory disorder may be related to bilateral degeneration of the dorsomedial thalamic nuclei.

Back 42

ALCOHOLIC KORSAKOFF AMNESTIC SYNDROME

Front 43

The memory disorder may be related to bilateral degeneration of the dorsomedial thalamic nuclei.

Back 43

ALCOHOLIC KORSAKOFF AMNESTIC SYNDROME

Front 44

An inflammatory and degenerative disorder of gray matter regions of the CNS can occur as a remote effect of systemic cancer

Back 44

PARANEOPLASTIC LIMBIC ENCEPHALITIS

Front 45

An inflammatory and degenerative disorder of gray matter regions of the CNS can occur as a remote effect of systemic cancer

Back 45

PARANEOPLASTIC LIMBIC ENCEPHALITIS

Front 46

An inflammatory and degenerative disorder of gray matter regions of the CNS can occur as a remote effect of systemic cancer

Back 46

PARANEOPLASTIC LIMBIC ENCEPHALITIS

Front 47

An inflammatory and degenerative disorder of gray matter regions of the CNS can occur as a remote effect of systemic cancer

Back 47

PARANEOPLASTIC LIMBIC ENCEPHALITIS

Front 48

An inflammatory and degenerative disorder of gray matter regions of the CNS can occur as a remote effect of systemic cancer

Back 48

PARANEOPLASTIC LIMBIC ENCEPHALITIS

Front 49

Paraneoplastic limbic encephalitis is most often associated with

Back 49

small-cell cancer of the lung, and symptoms typically precede diagnosis of the underlying cancer

Front 50

Paraneoplastic limbic encephalitis is most often associated with

Back 50

small-cell cancer of the lung, and symptoms typically precede diagnosis of the underlying cancer

Front 51

Paraneoplastic limbic encephalitis is most often associated with

Back 51

small-cell cancer of the lung, and symptoms typically precede diagnosis of the underlying cancer

Front 52

Paraneoplastic limbic encephalitis is most often associated with

Back 52

small-cell cancer of the lung, and symptoms typically precede diagnosis of the underlying cancer

Front 53

Paraneoplastic limbic encephalitis is most often associated with

Back 53

small-cell cancer of the lung, and symptoms typically precede diagnosis of the underlying cancer

Front 54

Anti-Hu antibodies are most common

Back 54

PARANEOPLASTIC LIMBIC ENCEPHALITIS

Front 55

Anti-Hu antibodies are most common

Back 55

PARANEOPLASTIC LIMBIC ENCEPHALITIS

Front 56

Anti-Hu antibodies are most common

Back 56

PARANEOPLASTIC LIMBIC ENCEPHALITIS

Front 57

Anti-Hu antibodies are most common

Back 57

PARANEOPLASTIC LIMBIC ENCEPHALITIS