06-05-2009, 10:14 AM
Yes D is the correct answer
Key Point
Vascular dementia is suggested by a history of vascular risk factors, abrupt onset with subsequent improvement, periventricular white matter ischemia on imaging, and focal neurologic findings.
This patient probably has vascular dementia, because of the history of vascular risk factors, abrupt onset with subsequent improvement, suggestion of periventricular white matter ischemia on imaging, and a focal neurologic sign (Babinski sign). Follow-up imaging may demonstrate a recent infarct not yet evident on the earlier scan that can be temporally associated with the episode of cognitive decline.
Many patients with coronary artery disease have carotid artery stenosis, but carotid artery evaluation will not support a diagnosis of vascular dementia.
Analysis of cerebrospinal fluid for 14-3-3 antigen is appropriate only for evaluation of subacute dementia with normal brain imaging studies, that is, to support a diagnosis of Creutzfeldt“Jakob disease. In this case, in which cerebrovascular disease is the most likely explanation, the neuronal damage due to a recent cerebral infarct might give a falsely elevated 14-3-3 test. Also, this patient has had a partial remission, which is not characteristic of Creutzfeldt“Jakob disease.
Electroencephalography can be useful to support a diagnosis of metabolic encephalopathy. However, in this patient, the focal neurologic sign (Babinski sign) indicates a structural disorder. Complex partial seizures might be invoked to explain encephalopathy followed by focal neurologic signs, but postictal signs usually do not persist longer than a few hours. Ultimately, imaging is the more direct way to evaluate a focal structural disorder.
Presenilin 1 gene testing is used only for the evaluation of familial primary dementia, or presenile dementia.
Key Point
Vascular dementia is suggested by a history of vascular risk factors, abrupt onset with subsequent improvement, periventricular white matter ischemia on imaging, and focal neurologic findings.
This patient probably has vascular dementia, because of the history of vascular risk factors, abrupt onset with subsequent improvement, suggestion of periventricular white matter ischemia on imaging, and a focal neurologic sign (Babinski sign). Follow-up imaging may demonstrate a recent infarct not yet evident on the earlier scan that can be temporally associated with the episode of cognitive decline.
Many patients with coronary artery disease have carotid artery stenosis, but carotid artery evaluation will not support a diagnosis of vascular dementia.
Analysis of cerebrospinal fluid for 14-3-3 antigen is appropriate only for evaluation of subacute dementia with normal brain imaging studies, that is, to support a diagnosis of Creutzfeldt“Jakob disease. In this case, in which cerebrovascular disease is the most likely explanation, the neuronal damage due to a recent cerebral infarct might give a falsely elevated 14-3-3 test. Also, this patient has had a partial remission, which is not characteristic of Creutzfeldt“Jakob disease.
Electroencephalography can be useful to support a diagnosis of metabolic encephalopathy. However, in this patient, the focal neurologic sign (Babinski sign) indicates a structural disorder. Complex partial seizures might be invoked to explain encephalopathy followed by focal neurologic signs, but postictal signs usually do not persist longer than a few hours. Ultimately, imaging is the more direct way to evaluate a focal structural disorder.
Presenilin 1 gene testing is used only for the evaluation of familial primary dementia, or presenile dementia.