eMedicine Specialties > Neurology > Behavioral Neurology and Dementia

Alzheimer Disease in Individuals With Down Syndrome: Differential Diagnoses & Workup

Author: Norberto Alvarez, MD, Assistant Professor, Department of Neurology, Harvard Medical School; Consulting Staff, Department of Neurology, Boston Children's Hospital
Contributor Information and Disclosures

Updated: Jan 10, 2008

Differential Diagnoses

Also note that, in general, the same differential diagnoses that apply to individuals without DS apply to those with DS.
Parkinson-Plus Syndromes
Alzheimer Disease
Pelizaeus-Merzbacher Disease
Cortical Basal Ganglionic Degeneration
Pick Disease
Dementia in Motor Neuron Disease
Subdural Hematoma
EEG in Dementia and Encephalopathy
Thyroid Disease
Frontal and Temporal Lobe Dementia
Vitamin B-12 Associated Neurological Diseases
Frontal Lobe Syndromes
Wegener Granulomatosis
HIV-1 Associated Cerebrovascular Complications
Wilson Disease
HIV-1 Associated CNS Complications (Overview)
Normal Pressure Hydrocephalus

Other Problems to Be Considered

Depression
Other psychiatric disorders
Computed tomography in neurovascular diseases
Dementia in Parkinson disease
Dementia in progressive supranuclear palsy
Multi-infarct dementia

Workup

Laboratory Studies

  • The workup is no different than that recommended for patients with dementia who do not have Down syndrome (DS). Excluding treatable forms of dementia is important.
    • Liver function tests
    • Renal function tests
    • Electrolytes
    • Blood glucose
    • CBC
    • Folic acid
    • Vitamin B-12
    • Possibly tests for syphilis and HIV (Among patients without DS, these tests are not recommended as part of routine evaluation but only when clinically indicated.)
    • Thyroid stimulating hormone (TSH) and thyroxine (T-4) levels (likely to be abnormal due to high incidence of immune-dependent hypothyroidism in patients with DS)
  • Although the APOE epsilon 4 allele is associated with increased risk of AD, its use as a diagnostic tool in patients without DS is generally not recommended. At present, there is no role for this testing in patients with DS.
  • Lumbar puncture is indicated in evaluation of dementia without DS when conditions that could be diagnosed by examination of the cerebrospinal fluid (such as fungal meningitis) are reasonable diagnostic possibilities. Most of the time such conditions are so unlikely that lumbar puncture is rarely performed as part of routine medical care in the evaluation of dementia. These same criteria should be used when considering lumbar puncture in patients with dementia and DS.

Imaging Studies

  • Imaging studies are useful to exclude other causes of dementia, including subdural collections, tumors, and multiple infarcts. Once the diagnosis is established, repeat imaging is indicated when the course of progression is not consistent with AD (such as very rapid deterioration).
  • Brain CT scan
    • CT scan studies comparing young individuals with DS (19-34 y) and a comparable group of healthy individuals without mental retardation found no significant differences between the 2 groups in white or gray matter volumes or ventricular volumes.
    • Quantitative studies with CT scan and MRI demonstrated that young adults with DS have no ventricular dilatation, no atrophy, and no consistent malformation that could explain the mental retardation. However, small brain size was reported consistently. This is probably an expression of small stature and a small cranial vault.
    • Bilateral symmetric basal ganglia calcification is a frequent finding in people with DS (see Media files 1-3); in fact, it exceeds the prevalence in the general population. However, the relationship with the clinical presentation of AD in DS is unclear.
    • The results were different when people with DS and cognitive deficiencies were compared with individuals without cognitive deficiencies. In individuals with DS and cognitive deficiencies, cerebral atrophy and ventricular enlargement that suggested brain atrophy were reported consistently (see Media files 4-6).
    • In advanced cases, atrophy was generalized. However, regional differences can exist with greater involvement of the temporal horns. The relationship between enlargement of the temporal horns of the lateral ventricles and dementia in elderly DS patients has been a consistent feature.
  • Brain MRI
    • MRI studies have shown several developmental findings in persons with DS—reduction in the whole brain volume (including cerebellum) and gray and white matter of the brain, decrease in the volume of the hippocampus, focal reductions in the volume of the frontal and occipital lobes, and relative preservation of the temporal lobe but decreased volume of the planum temporale and the superior temporal gyrus.
    • MRI studies might show a decrease in the volume structures of the temporal lobe (hippocampus and adjacent medial temporal lobe) in patients with DS without dementia. A significant atrophy of the corpus callosum, an indication of neocortical atrophy, more obvious in the splenium, was also demonstrated in persons with DS before the development of AD.
    • MRI findings in symptomatic individuals are similar to those of CT scan and reveal progressive atrophy of the brain with enlargement of the ventricular system.
    • Volumetric analysis of selective areas of the brain is a research tool not available from routine MR studies.
    • Results of studies suggest that CT scan and MRI can differentiate nondemented and demented older individuals with DS.
  • Brain positron emission tomography (PET)
    • Schapiro et al found that PET did not demonstrate any difference between healthy people with DS and individuals without mental retardation.1
    • Studies with xenon-133 inhalation technique, which evaluates the cortical cerebral blood flow, showed no abnormalities in young, healthy people with DS.
    • Significant differences were observed in individuals with DS and dementia; the greatest reduction occurred in the parietal-temporal association neocortex.
    • PET is not considered a routine test for AD in individuals with DS.

Other Tests

  • Generally, the methods used for testing the non-DS population (eg, Mini Mental Status Examination) are unreliable. Additionally, many people with DS cannot be evaluated by standard neuropsychologic tests.
    • Several tests have been designed that are more appropriate. Generally, these tests emphasize a change in function as measured by a decline in activities of daily living (ADL) such as eating, dressing, and bathing.
    • A simple tool developed at Wrentham Developmental Center is included in this chapter (see Alzheimer Functional Assessment Tool). The information can be obtained by interviewing relatives or caregivers. This tool, based on ADL, is appropriate for the follow-up care of individuals with DS and Alzheimer disease (AD). A decline in functions documented through this tool can also be used as a diagnostic test; however, this tool was not intended to be used as a diagnostic test.
    • The Dementia Scale for Down Syndrome (DSDS) can be a useful screening tool. In individuals in the middle or latter stage of the disease, the DSDS showed a high correlation between the diagnosis of AD and the findings. The correlation was not as good in the early stage of the disease.
    • The Dementia Questionnaire for Mentally Retarded Persons is a diagnostic screening test that can be completed by caregivers. Is as effective as the DSDS.
  • Electroencephalogram
    • Patients with DS have a high baseline prevalence of seizures and the prevalence increases further as patients develop AD. It is prudent to obtain an EEG in the baseline evaluation of a patient with DS and dementia.
  • Dementia screening tests marketed to consumers are of questionable usefulness in patients with DS and of no value in patients with DS.

Procedures

  • During the course of the disease, patients may need placement of gastrostomy or jejunostomy tubes for enteral feeding.

More on Alzheimer Disease in Individuals With Down Syndrome

Overview: Alzheimer Disease in Individuals With Down Syndrome
Differential Diagnoses & Workup: Alzheimer Disease in Individuals With Down Syndrome
Treatment & Medication: Alzheimer Disease in Individuals With Down Syndrome
Follow-up: Alzheimer Disease in Individuals With Down Syndrome
Multimedia: Alzheimer Disease in Individuals With Down Syndrome
References
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Further Reading

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Keywords

Alzheimer's disease, Alzheimer's, AD, dementia, Alzheimer dementia, presenile dementia, dementia presenilis, primary neuronal degeneration, primary senile dementia, trisomy 21, trisomy 21 syndrome, Down's syndrome, DS, mental retardation

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Contributor Information and Disclosures

Author

Norberto Alvarez, MD, Assistant Professor, Department of Neurology, Harvard Medical School; Consulting Staff, Department of Neurology, Boston Children's Hospital
Norberto Alvarez, MD is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society, and Child Neurology Society
Disclosure: Nothing to disclose.

Medical Editor

Robert A Hauser, MD, Professor, Departments of Neurology, Pharmacology, and Experimental Therapeutics, Director, Parkinson's Disease and Movement Disorders Center, University of South Florida and Tampa General Healthcare
Robert A Hauser, MD is a member of the following medical societies: American Academy of Neurology and Movement Disorders Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Richard J Caselli, MD, Professor, Department of Neurology, Mayo Medical School, Rochester, MN; Chair, Department of Neurology, Mayo Clinic of Scottsdale
Richard J Caselli, MD is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, American Medical Association, American Neurological Association, and Sigma Xi
Disclosure: Nothing to disclose.

CME Editor

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital
Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association
Disclosure: Nothing to disclose.

Chief Editor

Howard A Crystal, MD, Professor, Departments of Neurology and Pathology, State University of New York Downstate; Consulting Staff, Department of Neurology, University Hospital and Kings County Hospital Center
Howard A Crystal, MD is a member of the following medical societies: American Academy of Neurology and American Neurological Association
Disclosure: Pfizer Honoraria Speaking and teaching; Myriad Honoraria Consulting

 
 
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