Cognitive impairment can arise from virtually any poorly controlled chronic disease of the brain or the body’s organs, including hypertension, high cholesterol, heart disease, stroke, peripheral vascular disease, hypothyroidism, diabetes, chronic obstructive lung disease, kidney disease, infections, severe pain syndromes, obesity, sleep apnea, depression, anxiety, bipolar disorder, obsessive compulsive disorder, attention deficit disorder, multiple sclerosis, epilepsy, and alcohol, sedative, opiate or other chemical dependency. Single or repeated head injuries can impair cognition. Certain medications that get into the brain can impair cognition, such as tranquilizers, anticonvulsants, antipsychotics, older antidepressants, pain medications, and older bladder incontinence medications. Most of these conditions are treatable, particularly when memory cognitive disorders are detected early through annual monitoring of cognition after age 50 years old.
The degenerative brain disorders account for less than 50% of all people with memory cognitive disorders in primary care medical settings. These include Alzheimer’s Disease (AD), Parkinson’s Disease, Lewy Body Disease, Frontal Temporal Lobe Disease, and prion disease.
Recent studies show that although Alzheimer’s disease is not curable, it can be effectively treated to largely preserve independence and eliminate institutionalization in most individuals. In 2008, Atri Ali and colleagues at the Massachusetts General Hospital Memory Disorders Unit reported in the journal, AD and Associated Disorders, one of the most well analyzed longitudinal studies of Alzheimer’s disease. Patients treated for up to four years with the combination of Namenda and a cholinesterase inhibitor (Aricept, Exelon or Razadyne) delayed the functional rates of decline during the MCI stage by 33%, and during the dementia stage by 50-60%. This means that over the 14-year course of the MCI and dementia stages of AD, early detection, accurate diagnosis and combined therapy with Namenda and a cholinesterase inhibitor can delay the functional decline in AD patients by an average of 5-6 years. Since AD individuals spend an average of 4 years in institutions, the proper current approach can largely eliminate institutionalization.