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Cognitive Impairment Treatment CSF diversion through a ventriculoperitoneal shunt is the definitive treatment. Gait disturbance is the clinical symptom most amenable to ventricular shunting. The longer cognitive impairment has been present and the more pronounced the memory problem, the less certain is the response to shunting. If response to high-volume CSF removal is uncertain, referral to a neurosurgeon for a lumbar drain can be pursued. In the absence of a clear response to either high-volume CSF removal or lumbar drainage, a permanent ventricular shunt should not be pursued, and another diagnosis should be considered. e Normal pressure hydrocephalus is characterized by the triad of gait changes, urinary incontinence, and cogni- tive impairment. e Normal pressure hydrocephalus cannot be diagnosed without evidence of ventriculomegaly (enlarged cere- FIGURE 21. Axial 12-weighted MRI of the brain showing diffuse subcortical bral ventricles) on a brain MRI or CT scan of the head; white matter hyperdensities (arrows) in the bilateral hemispheres. These findings cerebrospinal fluid diversion through a ventriculoperi- are consistent with a severe microangiopathy seen in advanced vascular cognitive toneal shunt is the definitive treatment. impairment. acetylcholinesterase inhibitors in vascular cognitive impair- Vascular Cognitive Impairment ment, and treatment with this class of medications is generally Vascular cognitive impairment encompasses a category of recommended. Trials with memantine additionally indicated disorders in which the causal link between cerebrovascular a modest cognitive benefit. Regular moderate intensity exer- disease and cognitive impairment is strong. In older popula- tions, vascular cognitive impairment is likely second only to cise has more benefit for cognitive slowing than pharmaco-

acetylcholinesterase inhibitors in vascular cognitive impair- Vascular Cognitive Impairment ment, and treatment with this class of medications is generally Vascular cognitive impairment encompasses a category of recommended. Trials with memantine additionally indicated disorders in which the causal link between cerebrovascular a modest cognitive benefit. Regular moderate intensity exer- disease and cognitive impairment is strong. In older popula- tions, vascular cognitive impairment is likely second only to cise has more benefit for cognitive slowing than pharmaco- Alzheimer disease as the most common primary cause of logical therapy. Aggressive treatment of vascular risk factors, especially hypertension, may be most beneficial in preventing dementia (but not of neurodegenerative dementia; see earlier progression. discussion of dementia with Lewy bodies). This disorder may occur concurrently with Alzheimer disease in older patients. The likelihood of vascular cognitive impairment increases e Two major signs of vascular cognitive impairment are with age and is associated with systemic vascular risk factors early gait impairment and personality or mood changes. and a history of stroke (either clinically diagnosed or based on neuroimaging evidence). Several features distinguish vascular Rapidly Progressive Dementia cognitive impairment from Alzheimer disease (see Table 29). Because of the many possibly treatable causes of rapidly pro- Two major signs of vascular cognitive impairment are early gressive dementia, a systematic approach is required and can gait impairment and personality or mood changes. identify the underlying cause in most patients. The differential

Alzheimer disease as the most common primary cause of logical therapy. Aggressive treatment of vascular risk factors, especially hypertension, may be most beneficial in preventing dementia (but not of neurodegenerative dementia; see earlier progression. discussion of dementia with Lewy bodies). This disorder may occur concurrently with Alzheimer disease in older patients. The likelihood of vascular cognitive impairment increases e Two major signs of vascular cognitive impairment are with age and is associated with systemic vascular risk factors early gait impairment and personality or mood changes. and a history of stroke (either clinically diagnosed or based on neuroimaging evidence). Several features distinguish vascular Rapidly Progressive Dementia cognitive impairment from Alzheimer disease (see Table 29). Because of the many possibly treatable causes of rapidly pro- Two major signs of vascular cognitive impairment are early gressive dementia, a systematic approach is required and can gait impairment and personality or mood changes. identify the underlying cause in most patients. The differential Evaluation diagnosis includes Creutzfeldt-Jakob disease (CJD), paraneo- Evaluation of vascular cognitive impairment relies on identifi- plastic syndromes (see Neuro-oncology), autoimmune/ cation of vascular risk factors and, particularly, previous inflammatory encephalopathy (lupus encephalopathy, Sjogren stroke. A cognitive pattern of disproportionate cognitive slow- syndrome, Hashimoto encephalopathy, multiple sclerosis), ing compared with memory impairment is often noted. granulomatous disease (central nervous system sarcoidosis,

cation of vascular risk factors and, particularly, previous inflammatory encephalopathy (lupus encephalopathy, Sjogren stroke. A cognitive pattern of disproportionate cognitive slow- syndrome, Hashimoto encephalopathy, multiple sclerosis), ing compared with memory impairment is often noted. granulomatous disease (central nervous system sarcoidosis, As with NPH, brain imaging is a critical component sup- Behcet syndrome, neurosyphilis), vasculitis (primary or sec- porting the diagnosis. In vascular cognitive impairment, MRIs ondary), some infections (HIV, herpes simplex virus, Borrelia typically display a pattern of diffuse and confluent changes in burgdorferi-caused disease), and toxicities (from alcohol or the white matter of the brain (Figure 21), cerebral microhem- drug abuse, exposure to heavy metals). orrhages, and/or cortical infarcts beyond the mild periven- Prions cause rare but relentlessly progressive and rapidly tricular hyperintensities commonly seen in older patients. fatal neurodegenerative diseases characterized by dementia and ataxia, and thus prion disease should be part of the dif- Treatment ferential diagnosis in a patient of any age with these symp- Medications useful in treating Alzheimer disease are toms. The cause of disease is an abnormally folded prion not approved for use in vascular cognitive impairment. protein, which occurs by a spontaneous mutation (85%), is However, some evidence suggests a modest benefit of the acquired by exposure to a transmissible protein, or is an 49