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The diagnosis of AD is divided into three categories: possible, probable, and definite AD. A diagnosis of definite AD requires post-mortem confirmation of AD pathology, including the presence of extracellular beta amyloid plaques and intraneuronal neurofibrillary tangles in the cerebral cortex. Probable AD dementia is diagnosed clinically when the patient meets core clinical criteria for dementia and has a typical clinical course for AD. A typical clinical course is defined as an insidious onset, with the initial and most prominent cognitive deficits being either amnestic or non-amnestic, e.g., language, visuospatial, or executive function deficits, and a history of progressively worsening cognition over time. A diagnosis of possible AD dementia is made when the patient meets the core clinical criteria for AD dementia but has an atypical course or an etiologically mixed presentation. 

Mild cognitive impairment (MCI) may be diagnosed when there is a change in cognition, but not sufficient impairment for the diagnosis of dementia. Features of MCI are evidence of impairment in one or more cognitive domains, and preservation of independence in functional abilities. In some patients MCI may be a predementia phase of AD. Patients with MCI may undergo ancillary testing (e.g., neuroimaging, laboratory studies, and neuropsychological assessment) to rule out vascular, traumatic, and medical causes of cognitive decline and to evaluate genetic factors. Because clinical diagnosis can be difficult, particularly early in the course of disease, there has been considerable interest in developing biomarkers for AD. One biomarker that is being evaluated is amyloid plaque density in the brain detected in vivo by PET. 

PET images biochemical and physiological functions by measuring concentrations of positron-emitting chemicals in the body region of interest. Radiopharmaceuticals used for beta amyloid imaging may be generated in a cyclotron or nuclear generator and introduced into the body by intravenous injection. A number of 11C and 18F-labeled PET radiopharmaceuticals have been investigated for imaging brain beta amyloid. However, due to the short half-life (20 minutes), 11C radiotracers are not convenient for commercialization. Several 18F beta amyloid radiotracers are currently in phase II and III clinical trials. To date, only florbetapir (18F-AV-45) has received approval for clinical use by the U.S. Food and Drug Administration (FDA).

In 2012, the FDA approved florbetapir (Amyvid™, Avid Radiopharmaceuticals, a subsidiary of Eli Lilly) as a radioactive dye for visualization of amyloid plaque in the brain. The FDA document prepared for the advisory committee meeting indicated that while florbetapir may detect pathology, there could be no claim of disease detection, since beta amyloid aggregates can be found in cognitively normal elderly individuals as well as patients with AD. 

Amyvid™ is indicated “for PET [positron emission tomography] imaging of the brain to estimate beta-amyloid neuritic plaque density in adult patients with cognitive impairment who are being evaluated for Alzheimer’s disease and other causes of cognitive decline.”

Related medical policies are –

• Biochemical Markers of Alzheimer’s Disease 
• Miscellaneous Applications of Positron Emission Tomography (PET) 

The coverage guidelines outlined in the Medical Policy Manual should not be used in lieu of the Member's specific benefit plan language.

Non-Covered Codes

This is not an all-inclusive list of non-covered procedure codes.

All codes billed for this procedure are considered investigational and not eligible for coverage. 

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