Diagnosis

Diagnosis of Alzheimer’s is difficult and often presumptive based on a number of non-invasive tests and records of progressive symptoms. It has been suggested that it is important to diagnose earlier mild cognitive impairment (or MCI) to adequately plan and implement care and treatment strategies. About one-third of people with MCI due to Alzheimer’s develop dementia within five years. However, few people – about one in five – are at all familiar with the signs for MCI. Further complicating diagnosis is that while 90% of physicians surveyed note the importance of diagnosing MCI due to Alzheimer’s and assessing patients 60 years and older for cognitive impairment, more than half say that they are not comfortable making the diagnosis. Few (one in four) primary care physicians are familiar with current research and even fewer (one in five) are aware of clinical trials that may be available to their patients.

There are many common behavioral and physical symptoms associated with the progression of Alzheimer’s dementia. These may range from personality changes, such as aggression and loss of awareness to progressively needing assistance with personal care, managing incontinence, and walking.

Common clinical tests and procedures to diagnose Alzheimer’s include a number of evaluations. Physical examination and specifically reflexes involves the ability to get up from a chair and walk across the room. Neurological examination checks for senses of sight, hearing, coordination, and balance. Lab tests may include a complete blood count (CBC) that looks at liver function, electrolyte balance, blood glucose levels, and vitamin tests such as folate and vitamin B12 concentration.

Biological evidence of Alzheimer’s can be seen on brain scans or microscopic viewing of brain tissue as an accumulation of neuron-destroying amyloid plaques and tau tangles. The plaques are abnormal, insoluble proteins that accumulate in nerve cells because the nerve cells cannot process and remove them. The neuritic plaques are tangles or clumps of dead nerve cells around a core of the beta-amyloid protein. A CT scan of the head may be used to evaluate brain degeneration, MRIs may be used to identify the presence of a tumor or nerve damage, PETs may be used to identify the amyloid proteins associated with Alzheimer’s, and EEGs may be used to identify abnormal brain wave activity. The plaques and tangles can also be seen in spinal fluid samples, but this method of evaluation is not commonly used in the United States.

 

Vascular Cognitive Impairment

Vascular dementia or Vascular Cognitive Impairment (VCI) is seen when there is an interruption of blood flow and oxygen to the brain because of damaged blood vessels. Thus, this type of dementia may be seen in stroke patients, including those who have a major stroke or multiple minor strokes, and is the second most common form of dementia, possibly accounting for as much as 20% of dementia cases.

Results from blockage of blood flow and oxygen in the brain   Symptoms occur soon after major stroke   Risk reduction and treatment options

It's important to note that not all people who experience a stroke will have vascular dementia. But, when stroke causes a restriction of blood to the brain there exists the risk for impairments, depending on the brain region that is affected.

Typical symptoms may include some short-term memory issues, difficulty in concentrating, getting lost in familiar places, money management problems, and lack of bowel or bladder control. It may also include confusion, disorientation, trouble speaking or understanding speech, poor balance and difficulty walking. Small vessel disease that is associated with multiple smaller strokes may cause widespread changes, such as impaired judgment and planning, impaired social function, and uncontrolled laughing and crying.

Early diagnosis can help to identify and implement behavioral interventions to prevent additional damage and decline. Some research suggests that VCI can shorten the expected life span with an average life expectancy of three years after stroke with dementia. Recommended diagnostic criteria includes neurocognitive testing to evaluate specific thinking skills and brain imaging, usually MRI, to confirm recent stroke or other vascular changes. Strictly speaking, a diagnosis of VCI would rule out other nonvascular factors. However, we need to keep in mind that other forms of dementia may co-exist.

Risk reduction includes typical healthy living advice, such as avoiding smoking and limiting alcohol consumption, healthy diet and weight maintenance, and exercise along with maintaining appropriate blood pressure, blood lipids, and blood sugar levels. Treatment includes controlling risk factors and treating underlying diseases that contribute to vascular damage.

 

Dementia with Lewy bodies (DLB)

Characteristics: both similar and unique to other dementia types Diagnosis: clinical judgement and differentiate Treatment: pharmacologic options

 

Lewy body dementia typically includes dementias associated with Lewy bodies in the brain and with Parkinson’s disease dementia. Lewy bodies can be found in Parkinson’s disease dementia and in Alzheimer’s dementia. In these cases, the protein alpha-synuclein is abnormally processed in the brain, leading to the malfunction of brain cells. Symptoms of dementia with Lewy bodies are both shared with other types of dementia and unique. For our purposes, we will narrow our focus to dementia with Lewy bodies (or DLB). In DLB, there are changes in thinking and reasoning, but there may also be recurrent and well-formed hallucinations, delirium-like fluctuating cognition, episodes of acting out dreams with REM sleep behavior disorder, and spontaneous Parkinsonism that includes low movement, resting tremor, or body rigidity. Memory loss tends to be less prominent in DLB than in Alzheimer’s, and the person with DLB may have trouble interpreting visual information along with malfunctioning autonomic nervous system functions, such as sweating, blood pressure, digestion, and others.

Diagnosis is based on the best clinical judgement of symptoms because the identification of Lewy bodies can only be done during post-mortem examination of the brain. Lewy bodies may exist in Alzheimer’s brain changes, making it hard to differentiate between DLB and Alzheimer’s. More commonly noted in DLB than in Alzheimer’s, symptoms such as movement changes, hallucinations and misidentification of familiar people, sleep disorder, and malfunction of the autonomic nervous system, such as a blood pressure drop, falls, and urinary incontinence is more common in early DLB. While changes in movement may never occur for a person living with DLB, if dementia is present either before, at the same time, or within one year of symptoms of Parkinson’s disease as opposed to developing a year or more after the onset of Parkinson’s disease, it may include Lewy body dementia.

Treatments include pharmacologic options, such as cholinesterase inhibitors that are commonly used in Alzheimer’s to address thinking problems. Antidepressant medications, most commonly selective serotonin reuptake inhibitors (SSRIs), may be used for treatment of the depression that is common with DLB. Antipsychotic medications can cause serious side effects for up to half of DLB patients, such as sudden changes in consciousness, delusions and hallucinations, or worsening of Parkinson’s symptoms. Thus, this option is used only with extreme caution.