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70 Cards in this Set
- Front
- Back
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With mild cerebellar ataxia, an intention tremor characteristically appears near the
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beginning and end of each such movement, and the patient may overshoot the target.
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With mild cerebellar ataxia, an intention tremor characteristically appears near the
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beginning and end of each such movement, and the patient may overshoot the target.
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With mild cerebellar ataxia, an intention tremor characteristically appears near the
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beginning and end of each such movement, and the patient may overshoot the target.
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In patients with sensory ataxia, joint position sense is always
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always impaired in the legs and may be defective in the arms as well. Testing is accomplished by asking the patient to detect passive movement of the joints
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In patients with sensory ataxia, joint position sense is always
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always impaired in the legs and may be defective in the arms as well. Testing is accomplished by asking the patient to detect passive movement of the joints
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In patients with sensory ataxia, joint position sense is always
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always impaired in the legs and may be defective in the arms as well. Testing is accomplished by asking the patient to detect passive movement of the joints
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Tendon reflexes are typically what in in cerebellar disorders
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Tendon reflexes are typically hypoactive, with a pendular quality
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Tendon reflexes are typically what in in cerebellar disorders
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Tendon reflexes are typically hypoactive, with a pendular quality
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Tendon reflexes are typically what in in cerebellar disorders
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Tendon reflexes are typically hypoactive, with a pendular quality
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Tendon reflexes are typically what in in cerebellar disorders
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Tendon reflexes are typically hypoactive, with a pendular quality
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Positional nystagmus always accompanies vertigo in the benign disorder and is typically
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unidirectional, rotatory, and delayed in onset by several seconds after assumption of the precipitating head position. If the position is maintained, nystagmus
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Positional nystagmus always accompanies vertigo in the benign disorder and is typically
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unidirectional, rotatory, and delayed in onset by several seconds after assumption of the precipitating head position. If the position is maintained, nystagmus
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Positional nystagmus always accompanies vertigo in the benign disorder and is typically
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unidirectional, rotatory, and delayed in onset by several seconds after assumption of the precipitating head position. If the position is maintained, nystagmus
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MENIERE DISEASE
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Treatment is with diuretics, such as hydrochlorothiazide and triamterene
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MENIERE DISEASE
Tx |
Treatment is with diuretics, such as hydrochlorothiazide and triamterene
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MENIERE DISEASE
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Treatment is with diuretics, such as hydrochlorothiazide and triamterene
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Otosclerosis is caused by
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immobility of the stapes, the ear ossicle that transmits vibration of the tympanic membrane to the inner ear. Its most distinctive feature is conductive hearing loss,
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Otosclerosis is caused by
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immobility of the stapes, the ear ossicle that transmits vibration of the tympanic membrane to the inner ear. Its most distinctive feature is conductive hearing loss,
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Otosclerosis is caused by
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immobility of the stapes, the ear ossicle that transmits vibration of the tympanic membrane to the inner ear. Its most distinctive feature is conductive hearing loss,
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Otosclerosis is caused by
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immobility of the stapes, the ear ossicle that transmits vibration of the tympanic membrane to the inner ear. Its most distinctive feature is conductive hearing loss,
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This antineoplastic drug causes ototoxicity in approximately 50% of patients
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CIS-Platinum
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This antineoplastic drug causes ototoxicity in approximately 50% of patients
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CIS-Platinum
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This antineoplastic drug causes ototoxicity in approximately 50% of patients
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CIS-Platinum
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Metabolic disorders associated with acoustic neuropathy include
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hypothyroidism, diabetes, and Paget disease.
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Metabolic disorders associated with acoustic neuropathy include
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hypothyroidism, diabetes, and Paget disease.
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Metabolic disorders associated with acoustic neuropathy include
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hypothyroidism, diabetes, and Paget disease.
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Wernicke Encephalopathy
The major sites of pathologic involvement are |
medial thalamic nuclei, mammillary bodies, periaqueductal and periventricular brainstem nuclei (especially those of the oculomotor, abducens, and acoustic nerves), and superior cerebellar vermis. Cerebellar and vestibular involvement both contribute to the ataxia.
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Wernicke Encephalopathy
The major sites of pathologic involvement are |
medial thalamic nuclei, mammillary bodies, periaqueductal and periventricular brainstem nuclei (especially those of the oculomotor, abducens, and acoustic nerves), and superior cerebellar vermis. Cerebellar and vestibular involvement both contribute to the ataxia.
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Wernicke Encephalopathy
The major sites of pathologic involvement are |
medial thalamic nuclei, mammillary bodies, periaqueductal and periventricular brainstem nuclei (especially those of the oculomotor, abducens, and acoustic nerves), and superior cerebellar vermis. Cerebellar and vestibular involvement both contribute to the ataxia.
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Wernicke Encephalopathy
The major sites of pathologic involvement are |
medial thalamic nuclei, mammillary bodies, periaqueductal and periventricular brainstem nuclei (especially those of the oculomotor, abducens, and acoustic nerves), and superior cerebellar vermis. Cerebellar and vestibular involvement both contribute to the ataxia.
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ateral medullary infarction produces Wallenberg syndrome (Loading
Figure 3-10) and is most often caused by proximal vertebral artery occlusion. Clinical manifestations vary, depending on the extent of infarction. They typically consist of |
They typically consist of vertigo, nausea, vomiting, dysphagia, hoarseness, and nystagmus in addition to ipsilateral Horner syndrome, limb ataxia, and impairment of all sensory modalities over the face. There is also impairment of pinprick and temperature appreciation in the contralateral limbs.
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ateral medullary infarction produces Wallenberg syndrome (Loading
Figure 3-10) and is most often caused by proximal vertebral artery occlusion. Clinical manifestations vary, depending on the extent of infarction. They typically consist of |
They typically consist of vertigo, nausea, vomiting, dysphagia, hoarseness, and nystagmus in addition to ipsilateral Horner syndrome, limb ataxia, and impairment of all sensory modalities over the face. There is also impairment of pinprick and temperature appreciation in the contralateral limbs.
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ateral medullary infarction produces Wallenberg syndrome (Loading
Figure 3-10) and is most often caused by proximal vertebral artery occlusion. Clinical manifestations vary, depending on the extent of infarction. They typically consist of |
They typically consist of vertigo, nausea, vomiting, dysphagia, hoarseness, and nystagmus in addition to ipsilateral Horner syndrome, limb ataxia, and impairment of all sensory modalities over the face. There is also impairment of pinprick and temperature appreciation in the contralateral limbs.
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ateral medullary infarction produces Wallenberg syndrome (Loading
Figure 3-10) and is most often caused by proximal vertebral artery occlusion. Clinical manifestations vary, depending on the extent of infarction. They typically consist of |
They typically consist of vertigo, nausea, vomiting, dysphagia, hoarseness, and nystagmus in addition to ipsilateral Horner syndrome, limb ataxia, and impairment of all sensory modalities over the face. There is also impairment of pinprick and temperature appreciation in the contralateral limbs.
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ateral medullary infarction produces Wallenberg syndrome (Loading
Figure 3-10) and is most often caused by proximal vertebral artery occlusion. Clinical manifestations vary, depending on the extent of infarction. They typically consist of |
They typically consist of vertigo, nausea, vomiting, dysphagia, hoarseness, and nystagmus in addition to ipsilateral Horner syndrome, limb ataxia, and impairment of all sensory modalities over the face. There is also impairment of pinprick and temperature appreciation in the contralateral limbs.
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Paramedian midbrain infarction caused by occlusion of the paramedian penetrating branches of the basilar artery affects the third nerve root fibers and red nucleus (Loading
Figure 3-12). The resulting clinical picture |
The resulting clinical picture (Benedikt syndrome) consists of ipsilateral medial rectus palsy with a fixed dilated pupil and contralateral limb ataxia (typically affecting only the arm). Cerebellar signs result from involvement of the red nucleus, which receives a crossed projection from the cerebellum in the ascending limb of the superior cerebellar peduncle
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Paramedian midbrain infarction caused by occlusion of the paramedian penetrating branches of the basilar artery affects the third nerve root fibers and red nucleus (Loading
Figure 3-12). The resulting clinical picture |
The resulting clinical picture (Benedikt syndrome) consists of ipsilateral medial rectus palsy with a fixed dilated pupil and contralateral limb ataxia (typically affecting only the arm). Cerebellar signs result from involvement of the red nucleus, which receives a crossed projection from the cerebellum in the ascending limb of the superior cerebellar peduncle
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Paramedian midbrain infarction caused by occlusion of the paramedian penetrating branches of the basilar artery affects the third nerve root fibers and red nucleus (Loading
Figure 3-12). The resulting clinical picture |
The resulting clinical picture (Benedikt syndrome) consists of ipsilateral medial rectus palsy with a fixed dilated pupil and contralateral limb ataxia (typically affecting only the arm). Cerebellar signs result from involvement of the red nucleus, which receives a crossed projection from the cerebellum in the ascending limb of the superior cerebellar peduncle
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Paramedian midbrain infarction caused by occlusion of the paramedian penetrating branches of the basilar artery affects the third nerve root fibers and red nucleus (Loading
Figure 3-12). The resulting clinical picture |
The resulting clinical picture (Benedikt syndrome) consists of ipsilateral medial rectus palsy with a fixed dilated pupil and contralateral limb ataxia (typically affecting only the arm). Cerebellar signs result from involvement of the red nucleus, which receives a crossed projection from the cerebellum in the ascending limb of the superior cerebellar peduncle
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Paramedian midbrain infarction caused by occlusion of the paramedian penetrating branches of the basilar artery affects the third nerve root fibers and red nucleus (Loading
Figure 3-12). The resulting clinical picture |
The resulting clinical picture (Benedikt syndrome) consists of ipsilateral medial rectus palsy with a fixed dilated pupil and contralateral limb ataxia (typically affecting only the arm). Cerebellar signs result from involvement of the red nucleus, which receives a crossed projection from the cerebellum in the ascending limb of the superior cerebellar peduncle
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The classic clinical picture of hypertensive cerebellar hemorrhage consists of
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the sudden onset of headache, which may be accompanied by nausea, vomiting, and vertigo, followed by gait ataxia and impaired consciousness, usually evolving over a period of hours. At the time of presentation, patients can be fully alert, confused, or comatose. In alert patients, nausea and vomiting are often prominent. The blood pressure is typically elevated, and nuchal rigidity may be present. The pupils are often small and sluggishly reactive. Ipsilateral gaze palsy (with gaze preference away from the side of hemorrhage) and ipsilateral peripheral facial palsy are common
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The classic clinical picture of hypertensive cerebellar hemorrhage consists of
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the sudden onset of headache, which may be accompanied by nausea, vomiting, and vertigo, followed by gait ataxia and impaired consciousness, usually evolving over a period of hours. At the time of presentation, patients can be fully alert, confused, or comatose. In alert patients, nausea and vomiting are often prominent. The blood pressure is typically elevated, and nuchal rigidity may be present. The pupils are often small and sluggishly reactive. Ipsilateral gaze palsy (with gaze preference away from the side of hemorrhage) and ipsilateral peripheral facial palsy are common
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The classic clinical picture of hypertensive cerebellar hemorrhage consists of
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the sudden onset of headache, which may be accompanied by nausea, vomiting, and vertigo, followed by gait ataxia and impaired consciousness, usually evolving over a period of hours. At the time of presentation, patients can be fully alert, confused, or comatose. In alert patients, nausea and vomiting are often prominent. The blood pressure is typically elevated, and nuchal rigidity may be present. The pupils are often small and sluggishly reactive. Ipsilateral gaze palsy (with gaze preference away from the side of hemorrhage) and ipsilateral peripheral facial palsy are common
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but lumbar puncture should be avoided if cerebellar hemorrhage is suspected, because
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it may lead to a herniation syndrome.
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but lumbar puncture should be avoided if cerebellar hemorrhage is suspected, because
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it may lead to a herniation syndrome.
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but lumbar puncture should be avoided if cerebellar hemorrhage is suspected, because
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it may lead to a herniation syndrome.
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a syndrome characterized by severe gait ataxia that usually resolves completely within months. It generally follows an acute viral infection or inoculation. A full discussion of cerebellar ataxia in childhood is beyond the scope of this chapter.
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Acute cerebellar ataxia of childhood
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a syndrome characterized by severe gait ataxia that usually resolves completely within months. It generally follows an acute viral infection or inoculation. A full discussion of cerebellar ataxia in childhood is beyond the scope of this chapter.
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Acute cerebellar ataxia of childhood
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a syndrome characterized by severe gait ataxia that usually resolves completely within months. It generally follows an acute viral infection or inoculation. A full discussion of cerebellar ataxia in childhood is beyond the scope of this chapter.
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Acute cerebellar ataxia of childhood
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Fisher Variant of Guillain-Barre Syndrome
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Cerebellar ataxia, external ophthalmoplegia, and areflexia constitute this variant of Guillain-Barre syndrome. Symptoms develop over a few days. Ataxia primarily affects the gait and trunk, with lesser involvement of the individual limbs; dysarthria is uncommon. CSF protein may be elevated. Respiratory insufficiency occurs rarely, and the usual course is of gradual and often complete recovery over weeks to months.
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Fisher Variant of Guillain-Barre Syndrome
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Cerebellar ataxia, external ophthalmoplegia, and areflexia constitute this variant of Guillain-Barre syndrome. Symptoms develop over a few days. Ataxia primarily affects the gait and trunk, with lesser involvement of the individual limbs; dysarthria is uncommon. CSF protein may be elevated. Respiratory insufficiency occurs rarely, and the usual course is of gradual and often complete recovery over weeks to months.
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Fisher Variant of Guillain-Barre Syndrome
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Cerebellar ataxia, external ophthalmoplegia, and areflexia constitute this variant of Guillain-Barre syndrome. Symptoms develop over a few days. Ataxia primarily affects the gait and trunk, with lesser involvement of the individual limbs; dysarthria is uncommon. CSF protein may be elevated. Respiratory insufficiency occurs rarely, and the usual course is of gradual and often complete recovery over weeks to months.
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Chronic therapy with phenytoin, often with drug levels in the toxic range, may cause
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cerebellar degeneration that affects the cerebellar hemispheres and inferior and posterior vermis most severely, while the superior vermis is relatively spared. Clinical features include nystagmus, dysarthria, and ataxia affecting the limbs, trunk, and gait. Polyneuropathy may be present. Symptoms are typically irreversible, but tend to stabilize when the drug is discontinued.
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Chronic therapy with phenytoin, often with drug levels in the toxic range, may cause
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cerebellar degeneration that affects the cerebellar hemispheres and inferior and posterior vermis most severely, while the superior vermis is relatively spared. Clinical features include nystagmus, dysarthria, and ataxia affecting the limbs, trunk, and gait. Polyneuropathy may be present. Symptoms are typically irreversible, but tend to stabilize when the drug is discontinued.
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Chronic therapy with phenytoin, often with drug levels in the toxic range, may cause
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cerebellar degeneration that affects the cerebellar hemispheres and inferior and posterior vermis most severely, while the superior vermis is relatively spared. Clinical features include nystagmus, dysarthria, and ataxia affecting the limbs, trunk, and gait. Polyneuropathy may be present. Symptoms are typically irreversible, but tend to stabilize when the drug is discontinued.
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The pathogenetic mechanism in many cases appears to involve antibodies to tumor cell antigens that cross-react with cerebellar Purkinje cells. Cerebellar symptoms may appear before or after the diagnosis of systemic cancer and typically develop over month
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Paraneoplastic Cerebellar Degeneration
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The pathogenetic mechanism in many cases appears to involve antibodies to tumor cell antigens that cross-react with cerebellar Purkinje cells. Cerebellar symptoms may appear before or after the diagnosis of systemic cancer and typically develop over month
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Paraneoplastic Cerebellar Degeneration
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The pathogenetic mechanism in many cases appears to involve antibodies to tumor cell antigens that cross-react with cerebellar Purkinje cells. Cerebellar symptoms may appear before or after the diagnosis of systemic cancer and typically develop over month
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Paraneoplastic Cerebellar Degeneration
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Friedreich Ataxia is due to
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an expanded GAA trinucleotide repeat in a noncoding region of the frataxin gene on chromosome 9
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Friedreich Ataxia is due to
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an expanded GAA trinucleotide repeat in a noncoding region of the frataxin gene on chromosome 9
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Friedreich Ataxia is due to
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an expanded GAA trinucleotide repeat in a noncoding region of the frataxin gene on chromosome 9
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Friedreich Ataxia is due to
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an expanded GAA trinucleotide repeat in a noncoding region of the frataxin gene on chromosome 9
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The vascular lesions, which rarely bleed, spare the central nervous system. Immunologic impairment (decreased circulating IgA and IgE) usually becomes evident later in childhood and is manifested by recurrent sinopulmonary infections in more than 80% of patients.
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Ataxia-telangiectasia (also known as Louis-Bar syndrome)
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The vascular lesions, which rarely bleed, spare the central nervous system. Immunologic impairment (decreased circulating IgA and IgE) usually becomes evident later in childhood and is manifested by recurrent sinopulmonary infections in more than 80% of patients.
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Ataxia-telangiectasia (also known as Louis-Bar syndrome)
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The vascular lesions, which rarely bleed, spare the central nervous system. Immunologic impairment (decreased circulating IgA and IgE) usually becomes evident later in childhood and is manifested by recurrent sinopulmonary infections in more than 80% of patients.
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Ataxia-telangiectasia (also known as Louis-Bar syndrome)
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Type II Arnold-Chiari malformation is associated with
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meningomyelocele (protrusion of the spinal cord, nerve roots, and meninges through a fusion defect in the vertebral column) and has its onset in childhood
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Type II Arnold-Chiari malformation is associated with
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meningomyelocele (protrusion of the spinal cord, nerve roots, and meninges through a fusion defect in the vertebral column) and has its onset in childhood
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Type II Arnold-Chiari malformation is associated with
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meningomyelocele (protrusion of the spinal cord, nerve roots, and meninges through a fusion defect in the vertebral column) and has its onset in childhood
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Type II Arnold-Chiari malformation is associated with
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meningomyelocele (protrusion of the spinal cord, nerve roots, and meninges through a fusion defect in the vertebral column) and has its onset in childhood
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Type II Arnold-Chiari malformation is associated with
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meningomyelocele (protrusion of the spinal cord, nerve roots, and meninges through a fusion defect in the vertebral column) and has its onset in childhood
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