- Shuffle
Toggle OnToggle Off
- Alphabetize
Toggle OnToggle Off
- Front First
Toggle OnToggle Off
- Both Sides
Toggle OnToggle Off
Front
How to study your flashcards.
Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key
Up/Down arrow keys: Flip the card between the front and back.down keyup key
H key: Show hint (3rd side).h key
PLAY BUTTON
PLAY BUTTON
105 Cards in this Set
- Front
- Back
|
denotes rapid alternating movements that are clumsy and irregular in terms of rhythm and amplitude.
|
Dysdiadochokinesia
|
|
denotes rapid alternating movements that are clumsy and irregular in terms of rhythm and amplitude.
|
Dysdiadochokinesia
|
|
denotes rapid alternating movements that are clumsy and irregular in terms of rhythm and amplitude.
|
Dysdiadochokinesia
|
|
denotes rapid alternating movements that are clumsy and irregular in terms of rhythm and amplitude.
|
Dysdiadochokinesia
|
|
is the overshooting of the limb when resistance to a movement or posture is suddenly withdrawn.
|
rebound phenomenon
|
|
is the overshooting of the limb when resistance to a movement or posture is suddenly withdrawn.
|
rebound phenomenon
|
|
is the overshooting of the limb when resistance to a movement or posture is suddenly withdrawn.
|
rebound phenomenon
|
|
is the overshooting of the limb when resistance to a movement or posture is suddenly withdrawn.
|
rebound phenomenon
|
|
Jerk nystagmus, which is commonly seen in patients with a
|
unilateral lesion of the cerebellar hemisphere, is slowest and of greatest amplitude when the eyes are turned to the side of the lesion. Nystagmus is not present in patients with lesions of the anterior cerebellar vermis.
Speech becomes dysarthric and takes on an irregular and explosive quality in patients with lesions that involve the cerebellar hemispheres. Speech is usually unremarkable when only the midline structures are involved. |
|
Jerk nystagmus, which is commonly seen in patients with a
|
unilateral lesion of the cerebellar hemisphere, is slowest and of greatest amplitude when the eyes are turned to the side of the lesion. Nystagmus is not present in patients with lesions of the anterior cerebellar vermis.
Speech becomes dysarthric and takes on an irregular and explosive quality in patients with lesions that involve the cerebellar hemispheres. Speech is usually unremarkable when only the midline structures are involved. |
|
Jerk nystagmus, which is commonly seen in patients with a
|
unilateral lesion of the cerebellar hemisphere, is slowest and of greatest amplitude when the eyes are turned to the side of the lesion. Nystagmus is not present in patients with lesions of the anterior cerebellar vermis.
Speech becomes dysarthric and takes on an irregular and explosive quality in patients with lesions that involve the cerebellar hemispheres. Speech is usually unremarkable when only the midline structures are involved. |
|
With neurogenic disorders, muscle biopsy specimens show atrophied fibers occurring in groups, with adjacent groups of larger, uninvolved fibers. In myopathies, atrophy occurs in a
|
random pattern; nuclei of muscle cells may be centrally situated, in contrast to their normal peripheral location;
|
|
With neurogenic disorders, muscle biopsy specimens show atrophied fibers occurring in groups, with adjacent groups of larger, uninvolved fibers. In myopathies, atrophy occurs in a
|
random pattern; nuclei of muscle cells may be centrally situated, in contrast to their normal peripheral location;
|
|
With neurogenic disorders, muscle biopsy specimens show atrophied fibers occurring in groups, with adjacent groups of larger, uninvolved fibers. In myopathies, atrophy occurs in a
|
random pattern; nuclei of muscle cells may be centrally situated, in contrast to their normal peripheral location;
|
|
With neurogenic disorders, muscle biopsy specimens show atrophied fibers occurring in groups, with adjacent groups of larger, uninvolved fibers. In myopathies, atrophy occurs in a
|
random pattern; nuclei of muscle cells may be centrally situated, in contrast to their normal peripheral location;
|
|
With neurogenic disorders, muscle biopsy specimens show atrophied fibers occurring in groups, with adjacent groups of larger, uninvolved fibers. In myopathies, atrophy occurs in a
|
random pattern; nuclei of muscle cells may be centrally situated, in contrast to their normal peripheral location;
|
|
lesion below T1 affects only the
|
lower limbs on one or both sides.
|
|
lesion below T1 affects only the
|
lower limbs on one or both sides.
|
|
lesion below T1 affects only the
|
lower limbs on one or both sides.
|
|
lesion below T1 affects only the
|
lower limbs on one or both sides.
|
|
lesion below T1 affects only the
|
lower limbs on one or both sides.
|
|
In the acute stage, there is flaccid paralysis with loss of tendon and other reflexes, accompanied by sensory loss and by urinary and fecal retention. This is the stage of
|
spinal shock
|
|
In the acute stage, there is flaccid paralysis with loss of tendon and other reflexes, accompanied by sensory loss and by urinary and fecal retention. This is the stage of
|
spinal shock
|
|
In the acute stage, there is flaccid paralysis with loss of tendon and other reflexes, accompanied by sensory loss and by urinary and fecal retention. This is the stage of
|
spinal shock
|
|
Hyperextension injuries of the neck can lead to focal cord ischemia that causes
|
bibrachial paresis (weakness of both arms) with sparing of the legs and variable sensory signs.
|
|
Hyperextension injuries of the neck can lead to focal cord ischemia that causes
|
bibrachial paresis (weakness of both arms) with sparing of the legs and variable sensory signs.
|
|
Hyperextension injuries of the neck can lead to focal cord ischemia that causes
|
bibrachial paresis (weakness of both arms) with sparing of the legs and variable sensory signs.
|
|
Hyperextension injuries of the neck can lead to focal cord ischemia that causes
|
bibrachial paresis (weakness of both arms) with sparing of the legs and variable sensory signs.
|
|
Hyperextension injuries of the neck can lead to focal cord ischemia that causes
|
bibrachial paresis (weakness of both arms) with sparing of the legs and variable sensory signs.
|
|
The disorder -MS-is characterized pathologically by the development of focal—often perivenular—scattered areas of demyelination followed by a
|
a reactive gliosis; there may be axonal damage as well.
|
|
The disorder -MS-is characterized pathologically by the development of focal—often perivenular—scattered areas of demyelination followed by a
|
a reactive gliosis; there may be axonal damage as well.
|
|
The disorder -MS-is characterized pathologically by the development of focal—often perivenular—scattered areas of demyelination followed by a
|
a reactive gliosis; there may be axonal damage as well.
|
|
The disorder -MS-is characterized pathologically by the development of focal—often perivenular—scattered areas of demyelination followed by a
|
a reactive gliosis; there may be axonal damage as well.
|
|
The disorder -MS-is characterized pathologically by the development of focal—often perivenular—scattered areas of demyelination followed by a
|
a reactive gliosis; there may be axonal damage as well.
|
|
MS Relapses may be triggered by infection and, in women, are more likely in the
|
3 months or so following childbirth (but are reduced during the pregnancy itself)
|
|
MS Relapses may be triggered by infection and, in women, are more likely in the
|
3 months or so following childbirth (but are reduced during the pregnancy itself)
|
|
MS Relapses may be triggered by infection and, in women, are more likely in the
|
3 months or so following childbirth (but are reduced during the pregnancy itself)
|
|
MS Relapses may be triggered by infection and, in women, are more likely in the
|
3 months or so following childbirth (but are reduced during the pregnancy itself)
|
|
MS Relapses may be triggered by infection and, in women, are more likely in the
|
3 months or so following childbirth (but are reduced during the pregnancy itself)
|
|
xamination in advanced cases of MS commonly reveals
|
optic atrophy, nystagmus, dysarthria, and upper motor neuron, sensory, or cerebellar deficits in some or all of the limbs
|
|
xamination in advanced cases of MS commonly reveals
|
optic atrophy, nystagmus, dysarthria, and upper motor neuron, sensory, or cerebellar deficits in some or all of the limbs
|
|
xamination in advanced cases of MS commonly reveals
|
optic atrophy, nystagmus, dysarthria, and upper motor neuron, sensory, or cerebellar deficits in some or all of the limbs
|
|
xamination in advanced cases of MS commonly reveals
|
optic atrophy, nystagmus, dysarthria, and upper motor neuron, sensory, or cerebellar deficits in some or all of the limbs
|
|
xamination in advanced cases of MS commonly reveals
|
optic atrophy, nystagmus, dysarthria, and upper motor neuron, sensory, or cerebellar deficits in some or all of the limbs
|
|
f clinical evidence of a lesion exists at only one site in the CNS, a diagnosis of multiple sclerosis cannot properly be made unless other regions have been affected subclinically, as detected by the
|
electrocerebral responses evoked by one or more of the following: monocular visual stimulation with a checkerboard pattern (visual evoked potentials); monaural stimulation with repetitive clicks (brainstem auditory evoked potentials); and electrical stimulation of a peripheral nerve (somatosensory evoked potentials).
MRI may also detect subclinical lesions and has become nearly indispensable in confirming the diagnosis (Figure 5-2 A and B5-2), as is detailed in the following section on diagnosis. |
|
f clinical evidence of a lesion exists at only one site in the CNS, a diagnosis of multiple sclerosis cannot properly be made unless other regions have been affected subclinically, as detected by the
|
electrocerebral responses evoked by one or more of the following: monocular visual stimulation with a checkerboard pattern (visual evoked potentials); monaural stimulation with repetitive clicks (brainstem auditory evoked potentials); and electrical stimulation of a peripheral nerve (somatosensory evoked potentials).
MRI may also detect subclinical lesions and has become nearly indispensable in confirming the diagnosis (Figure 5-2 A and B5-2), as is detailed in the following section on diagnosis. |
|
f clinical evidence of a lesion exists at only one site in the CNS, a diagnosis of multiple sclerosis cannot properly be made unless other regions have been affected subclinically, as detected by the
|
electrocerebral responses evoked by one or more of the following: monocular visual stimulation with a checkerboard pattern (visual evoked potentials); monaural stimulation with repetitive clicks (brainstem auditory evoked potentials); and electrical stimulation of a peripheral nerve (somatosensory evoked potentials).
MRI may also detect subclinical lesions and has become nearly indispensable in confirming the diagnosis (Figure 5-2 A and B5-2), as is detailed in the following section on diagnosis. |
|
f clinical evidence of a lesion exists at only one site in the CNS, a diagnosis of multiple sclerosis cannot properly be made unless other regions have been affected subclinically, as detected by the
|
electrocerebral responses evoked by one or more of the following: monocular visual stimulation with a checkerboard pattern (visual evoked potentials); monaural stimulation with repetitive clicks (brainstem auditory evoked potentials); and electrical stimulation of a peripheral nerve (somatosensory evoked potentials).
MRI may also detect subclinical lesions and has become nearly indispensable in confirming the diagnosis (Figure 5-2 A and B5-2), as is detailed in the following section on diagnosis. |
|
f clinical evidence of a lesion exists at only one site in the CNS, a diagnosis of multiple sclerosis cannot properly be made unless other regions have been affected subclinically, as detected by the
|
electrocerebral responses evoked by one or more of the following: monocular visual stimulation with a checkerboard pattern (visual evoked potentials); monaural stimulation with repetitive clicks (brainstem auditory evoked potentials); and electrical stimulation of a peripheral nerve (somatosensory evoked potentials).
MRI may also detect subclinical lesions and has become nearly indispensable in confirming the diagnosis (Figure 5-2 A and B5-2), as is detailed in the following section on diagnosis. |
|
T1-weighted images in MS may reveal what representing areas of permanent axonal damage
|
hypointense "black holes"
|
|
T1-weighted images in MS may reveal what representing areas of permanent axonal damage
|
hypointense "black holes"
|
|
T1-weighted images in MS may reveal what representing areas of permanent axonal damage
|
hypointense "black holes"
|
|
T1-weighted images in MS may reveal what representing areas of permanent axonal damage
|
hypointense "black holes"
|
|
T1-weighted images in MS may reveal what representing areas of permanent axonal damage
|
hypointense "black holes"
|
|
hypointense black holes on what type of MRI represent permanently damaged axons
|
T1
|
|
hypointense black holes on what type of MRI represent permanently damaged axons
|
T1
|
|
hypointense black holes on what type of MRI represent permanently damaged axons
|
T1
|
|
hypointense black holes on what type of MRI represent permanently damaged axons
|
T1
|
|
hypointense black holes on what type of MRI represent permanently damaged axons
|
T1
|
|
Gadolinium-enhanced T1 images may highlight areas of what in MS
|
areas of inflammation with breakdown of the blood-brain barrier.
|
|
Gadolinium-enhanced T1 images may highlight areas of what in MS
|
areas of inflammation with breakdown of the blood-brain barrier.
|
|
Gadolinium-enhanced T1 images may highlight areas of what in MS
|
areas of inflammation with breakdown of the blood-brain barrier.
|
|
-weighed images provide information about disease burden or lesion load (i.e., total number of lesions), which typically appear as areas of high-signal intensity
|
T2-weighed images
|
|
-weighed images provide information about disease burden or lesion load (i.e., total number of lesions), which typically appear as areas of high-signal intensity
|
T2-weighed images
|
|
-weighed images provide information about disease burden or lesion load (i.e., total number of lesions), which typically appear as areas of high-signal intensity
|
T2-weighed images
|
|
-weighed images provide information about disease burden or lesion load (i.e., total number of lesions), which typically appear as areas of high-signal intensity
|
T2-weighed images
|
|
an α-4 integrin antagonist,
|
Natalizumab
|
|
an α-4 integrin antagonist,
|
Natalizumab
|
|
an α-4 integrin antagonist,
|
Natalizumab
|
|
an α-4 integrin antagonist,
|
Natalizumab
|
|
The most common side effects of interferons are
|
flu-like syndrome and (in the case of interferon (β-1b) injection site reactions.
|
|
The most common side effects of interferons are
|
flu-like syndrome and (in the case of interferon (β-1b) injection site reactions.
|
|
The most common side effects of interferons are
|
flu-like syndrome and (in the case of interferon (β-1b) injection site reactions.
|
|
Fatigue is a serious problem for many MS patients and typically responds to
|
responds to amantadine or one of the selective serotonin reuptake inhibitor antidepressants. When associated with excessive daytime sleepiness, fatigue may respond to modafinil; 100 mg taken once daily in the morning may be sufficient but, if not, an additional 100 mg may be taken in the afternoon (before 3 PM). Higher doses are sometimes required.
|
|
Fatigue is a serious problem for many MS patients and typically responds to
|
responds to amantadine or one of the selective serotonin reuptake inhibitor antidepressants. When associated with excessive daytime sleepiness, fatigue may respond to modafinil; 100 mg taken once daily in the morning may be sufficient but, if not, an additional 100 mg may be taken in the afternoon (before 3 PM). Higher doses are sometimes required.
|
|
Fatigue is a serious problem for many MS patients and typically responds to
|
responds to amantadine or one of the selective serotonin reuptake inhibitor antidepressants. When associated with excessive daytime sleepiness, fatigue may respond to modafinil; 100 mg taken once daily in the morning may be sufficient but, if not, an additional 100 mg may be taken in the afternoon (before 3 PM). Higher doses are sometimes required.
|
|
Fatigue is a serious problem for many MS patients and typically responds to
|
responds to amantadine or one of the selective serotonin reuptake inhibitor antidepressants. When associated with excessive daytime sleepiness, fatigue may respond to modafinil; 100 mg taken once daily in the morning may be sufficient but, if not, an additional 100 mg may be taken in the afternoon (before 3 PM). Higher doses are sometimes required.
|
|
Fatigue is a serious problem for many MS patients and typically responds to
|
responds to amantadine or one of the selective serotonin reuptake inhibitor antidepressants. When associated with excessive daytime sleepiness, fatigue may respond to modafinil; 100 mg taken once daily in the morning may be sufficient but, if not, an additional 100 mg may be taken in the afternoon (before 3 PM). Higher doses are sometimes required.
|
|
This relapsing disorder (formerly known as Devic's disease and once considered a variant of multiple sclerosis) is associated with a specific antibody marker, NMO-IgG, that targets the
|
water channel aquaporin-4. - Neuromyelitis Optica
|
|
This relapsing disorder (formerly known as Devic's disease and once considered a variant of multiple sclerosis) is associated with a specific antibody marker, NMO-IgG, that targets the
|
water channel aquaporin-4. - Neuromyelitis Optica
|
|
This relapsing disorder (formerly known as Devic's disease and once considered a variant of multiple sclerosis) is associated with a specific antibody marker, NMO-IgG, that targets the
|
water channel aquaporin-4. - Neuromyelitis Optica
|
|
This relapsing disorder (formerly known as Devic's disease and once considered a variant of multiple sclerosis) is associated with a specific antibody marker, NMO-IgG, that targets the
|
water channel aquaporin-4. - Neuromyelitis Optica
|
|
The fully established disorder is characterized by optic neuritis and acute myelitis associated with MRI changes that extend over at least three segments of the spinal cord.
|
Neuromyelitis Optica
This relapsing disorder (formerly known as Devic's disease and once considered a variant of multiple sclerosis) is associated with a specific antibody marker, NMO-IgG, that targets the water channel aquaporin-4. |
|
The fully established disorder is characterized by optic neuritis and acute myelitis associated with MRI changes that extend over at least three segments of the spinal cord.
|
Neuromyelitis Optica
This relapsing disorder (formerly known as Devic's disease and once considered a variant of multiple sclerosis) is associated with a specific antibody marker, NMO-IgG, that targets the water channel aquaporin-4. |
|
The fully established disorder is characterized by optic neuritis and acute myelitis associated with MRI changes that extend over at least three segments of the spinal cord.
|
Neuromyelitis Optica
This relapsing disorder (formerly known as Devic's disease and once considered a variant of multiple sclerosis) is associated with a specific antibody marker, NMO-IgG, that targets the water channel aquaporin-4. |
|
The fully established disorder is characterized by optic neuritis and acute myelitis associated with MRI changes that extend over at least three segments of the spinal cord.
|
Neuromyelitis Optica
This relapsing disorder (formerly known as Devic's disease and once considered a variant of multiple sclerosis) is associated with a specific antibody marker, NMO-IgG, that targets the water channel aquaporin-4. |
|
In contrast to multiple sclerosis, the MRI does not show widespread white matter involvement in typical cases, although such changes do not exclude the diagnosis. Treatment is with long-term immunosuppressive therapy. Rituximab may also help in reducing the relapse rate and is undergoing further clinical trials.
|
Neuromyelitis Optica
|
|
In contrast to multiple sclerosis, the MRI does not show widespread white matter involvement in typical cases, although such changes do not exclude the diagnosis. Treatment is with long-term immunosuppressive therapy. Rituximab may also help in reducing the relapse rate and is undergoing further clinical trials.
|
Neuromyelitis Optica
|
|
In contrast to multiple sclerosis, the MRI does not show widespread white matter involvement in typical cases, although such changes do not exclude the diagnosis. Treatment is with long-term immunosuppressive therapy. Rituximab may also help in reducing the relapse rate and is undergoing further clinical trials.
|
Neuromyelitis Optica
|
|
In contrast to multiple sclerosis, the MRI does not show widespread white matter involvement in typical cases, although such changes do not exclude the diagnosis. Treatment is with long-term immunosuppressive therapy. Rituximab may also help in reducing the relapse rate and is undergoing further clinical trials.
|
Neuromyelitis Optica
|
|
In contrast to multiple sclerosis, the MRI does not show widespread white matter involvement in typical cases, although such changes do not exclude the diagnosis. Treatment is with long-term immunosuppressive therapy. Rituximab may also help in reducing the relapse rate and is undergoing further clinical trials.
|
Neuromyelitis Optica
|
|
Acute Disseminated Encephalomyelitis
|
This occurs as a single episode of neurologic symptoms and signs that develop over a few days in association with a viral infection, especially measles or chickenpox. The neurologic deficit resolves, at least in part, over the succeeding few weeks. Pathologically, perivascular areas of demyelination are scattered throughout the brain and spinal cord, with an associated inflammatory reaction.
|
|
Acute Disseminated Encephalomyelitis
|
This occurs as a single episode of neurologic symptoms and signs that develop over a few days in association with a viral infection, especially measles or chickenpox. The neurologic deficit resolves, at least in part, over the succeeding few weeks. Pathologically, perivascular areas of demyelination are scattered throughout the brain and spinal cord, with an associated inflammatory reaction.
|
|
This occurs as a single episode of neurologic symptoms and signs that develop over a few days in association with a viral infection, especially measles or chickenpox. The neurologic deficit resolves, at least in part, over the succeeding few weeks. Pathologically, perivascular areas of demyelination are scattered throughout the brain and spinal cord, with an associated inflammatory reaction.
|
Acute Disseminated Encephalomyelitis
|
|
This occurs as a single episode of neurologic symptoms and signs that develop over a few days in association with a viral infection, especially measles or chickenpox. The neurologic deficit resolves, at least in part, over the succeeding few weeks. Pathologically, perivascular areas of demyelination are scattered throughout the brain and spinal cord, with an associated inflammatory reaction.
|
Acute Disseminated Encephalomyelitis
|
|
Acute Disseminated Encephalomyelitis - initial Sx are ?
|
he initial symptoms often consist of headache, fever, and confusion; seizures may also occur, and examination reveals signs of meningeal irritation. Flaccid weakness and sensory disturbance of the legs, extensor plantar responses, and urinary retention are common manifestations of cord involvement. Other neurologic signs may indicate involvement of the optic nerves, cerebral hemispheres, brainstem, or cerebellum.
Examination of the CSF may show an increased mononuclear cell count, with normal protein and glucose concentrations |
|
Acute Disseminated Encephalomyelitis - initial Sx are ?
|
he initial symptoms often consist of headache, fever, and confusion; seizures may also occur, and examination reveals signs of meningeal irritation. Flaccid weakness and sensory disturbance of the legs, extensor plantar responses, and urinary retention are common manifestations of cord involvement. Other neurologic signs may indicate involvement of the optic nerves, cerebral hemispheres, brainstem, or cerebellum.
Examination of the CSF may show an increased mononuclear cell count, with normal protein and glucose concentrations |
|
Acute Disseminated Encephalomyelitis - initial Sx are ?
|
he initial symptoms often consist of headache, fever, and confusion; seizures may also occur, and examination reveals signs of meningeal irritation. Flaccid weakness and sensory disturbance of the legs, extensor plantar responses, and urinary retention are common manifestations of cord involvement. Other neurologic signs may indicate involvement of the optic nerves, cerebral hemispheres, brainstem, or cerebellum.
Examination of the CSF may show an increased mononuclear cell count, with normal protein and glucose concentrations |
|
Acute Disseminated Encephalomyelitis - initial Sx are ?
|
he initial symptoms often consist of headache, fever, and confusion; seizures may also occur, and examination reveals signs of meningeal irritation. Flaccid weakness and sensory disturbance of the legs, extensor plantar responses, and urinary retention are common manifestations of cord involvement. Other neurologic signs may indicate involvement of the optic nerves, cerebral hemispheres, brainstem, or cerebellum.
Examination of the CSF may show an increased mononuclear cell count, with normal protein and glucose concentrations |
|
Acute Disseminated Encephalomyelitis - initial Sx are ?
|
he initial symptoms often consist of headache, fever, and confusion; seizures may also occur, and examination reveals signs of meningeal irritation. Flaccid weakness and sensory disturbance of the legs, extensor plantar responses, and urinary retention are common manifestations of cord involvement. Other neurologic signs may indicate involvement of the optic nerves, cerebral hemispheres, brainstem, or cerebellum.
Examination of the CSF may show an increased mononuclear cell count, with normal protein and glucose concentrations |
|
Spinal epidural abscess is a neurologic emergency that requires prompt diagnosis and treatment the study of choice is
|
MRI with gadolinium enhancement is the imaging study of choice and should be sufficient to determine the extent of the abscess.
|
|
Spinal epidural abscess is a neurologic emergency that requires prompt diagnosis and treatment the study of choice is
|
MRI with gadolinium enhancement is the imaging study of choice and should be sufficient to determine the extent of the abscess.
|
|
Spinal epidural abscess is a neurologic emergency that requires prompt diagnosis and treatment the study of choice is
|
MRI with gadolinium enhancement is the imaging study of choice and should be sufficient to determine the extent of the abscess.
|
|
Spinal epidural abscess is a neurologic emergency that requires prompt diagnosis and treatment the study of choice is
|
MRI with gadolinium enhancement is the imaging study of choice and should be sufficient to determine the extent of the abscess.
|
|
Spinal epidural abscess is a neurologic emergency that requires prompt diagnosis and treatment the study of choice is
|
MRI with gadolinium enhancement is the imaging study of choice and should be sufficient to determine the extent of the abscess.
|
