What is Dementia?

Jul 29

Dementia is a general term referring to problems with thinking, memory, and social interaction. There are a number of different diseases that may cause dementia. While dementia usually affects older adults, it is not a normal part of aging. Dementia can profoundly impact every aspect of a person’s life.

How Common is Dementia?

Dementia is unfortunately very common. The most common form of dementia is Alzheimer’s disease, responsible for 60% of cases. It effects up to 11% of people over age 65, and up to 47% of people over age 85 (1). As the population ages, Alzheimer’s disease is expected to affect 135 million people by 2050. Alzheimer’s disease currently costs the US healthcare system $236 billion per year, a number that does not account for over 18 billion unpaid hours by those family and friends caring for Alzheimer’s patients (2).

What are the Symptoms of Dementia?

There are many symptoms of dementia, with different causes leading to different presentations. The most common symptoms are cognitive and psychological in nature.

Cognitive symptoms include memory loss, which is usually more obvious to a spouse or close relative. People can have difficulty with word finding, and expressing thoughts can become difficult.

Problem solving and reasoning can be affected, as can attention and focus. It can become difficult to complete tasks. Spatial orientation can become challenging, leading to becoming easily lost and disoriented while driving.

Executive functions such as organization and planning can be affected, as can coordination and motor function. Balance can become challenging, and the risk of falls increases as dementia progresses.

Psychological symptoms can include depression, anxiety and agitation. Personality changes can develop, leading to socially inappropriate behavior, paranoia, and hallucinations. Confusion and disorientation are common as dementia progresses (21).

What Causes Dementia?

Dementias are caused by neurodegeneration. Neurodegeneration involves damage to neurons and their connections, leading to death of cells in the brain. Depending on the areas of the brain involved, dementia can cause a wide array of symptom presentations.

Most dementias appear to have multiple causative factors. They may involve genetics, but diet, lifestyle, exercise, sleep, trauma, and a host of other factors may be involved.

Alzheimer’s disease is the most common form of dementia. Alzheimer’s disease is a protein aggregation disorder, which means that proteins build up between cells. These proteins include beta-amyloid, which clumps together to form plaques, and tau, which forms fibrous strings called tangles. Plaques and tangles build up to the point where neurons are damaged and die off (22).

Vascular dementia involves damage to blood vessels that supply the brain. This can lead to a progressive series of tiny strokes, or damage white matter brain fibers. Vascular dementia causes brain atrophy in the regions supplied by the involved blood vessels. It leads to difficulty with executive function, including things like planning, organization, concentration, and problem solving (23).

Lewy body dementia is another protein aggregation disorder linked to Parkinson’s disease. It involves a protein called alpha-synuclein which clumps together to form Lewy bodies. This can lead to problems with attention and focus, and visual hallucinations. It often involves motor symptoms such as tremors, slow movement, a shuffling gait, and body stiffness (24).

Frontotemporal dementia involves degeneration and death of neurons in the frontal and temporal lobes. This leads to personality changes, difficulty modulating behavior, poor judgment, impaired reasoning. It also leads to difficulty with expressing or understanding language, and problems with memory (25).

Mixed dementia can involve several different causes and symptoms.

What are the Risk Factors for Dementia?

Many risk factors increase the chance of developing dementia. The risk increases with age, particularly over age 65. Not everyone develops dementia as they age, and dementia is not a normal part of getting older. Family history of dementia increases the risk as well, however not all people with a family dementia history will develop symptoms, and many people with no family history will develop dementia.

Lack of exercise increases the risk of developing dementia. Eating a poor diet will also increase the risk of developing symptoms. Heavy alcohol use increases dementia risk. High blood pressure, elevated cholesterol, and obesity also increase the chances of developing dementia. Diabetes and sleep problems are major risk factors for dementia later in life (26).

How is Dementia Diagnosed?

Dementia can be challenging to diagnose early, and often the diagnosis is not made until much later in the disease progression. There is no single test that can diagnose dementia, and often the input of family members is required to form an accurate picture of the condition.

The Alzheimer's Association (3) lists 10 key warning signs of Alzheimer’s disease:

Memory loss
Difficulty performing familiar tasks
Problems with language
Disorientation to time and place
Poor or decreased judgment
Problems with abstract thought
Misplacing things
Changes in mood or behavior
Changes in personality
Loss of initiative

Cognitive and neuropsychological tests can be employed to measure skills such as memory, reasoning, judgment, and orientation in space, place, and time. Other tests can assess language and attention.

A neurological examination can demonstrate problems with sensory and motor systems, coordination, balance, gait, and visual function.

Advanced imaging such as MRI and CT can show signs of vascular damage, and rule out other causes for dementia symptoms such as tumor or hydrocephalus. PET scans can show the presence of protein aggregation and patterns of impaired brain activity (27).

How is Dementia Usually Treated?

The primary therapy for dementia is usually medication management. These may act on neurotransmitters, including acetylcholine to improve memory, or glutamate to slow neurodegeneration. Other medications may be employed to address the psychological agitation, depression, or sleep disturbances (28).

Medications so far have only been shown to slow the progression of most forms of dementia for a short period of time.

Speech and occupational therapy are often employed to help manage cognitive symptoms and create safe environments for people living with dementia.

How is the NeuroRescue Program Different?

We design your NeuroRescue program to evaluate and address as many factors promoting your dementia as possible. We assess your metabolic and immune functions, as well as your environmental and lifestyle factors that may be contributing to your dementia.

There are simple healthy lifestyle modifications that have been specifically proven to help with Alzheimer’s and other neurodegenerative diseases. Exercise has shown to promote better sleep. Sleep is the time our brain really has the ability to “clean” itself or “take out the trash,” through a process called autophagy. Sleep is an issue for many people, but one study by Shih et al found that patients with Alzheimer’s who went on more walks had better sleep. In addition, they found that people who went on walks with their relatives had better sleep than those who walked with non-relatives (4).

Other lifestyle factors that can be changed are adopting a low inflammatory, low glycemic index, and low grain diets. Meal timing can also be of benefit, as intermittent fasting has been shown to enhance DNA health, cell repair and autophagy (5).

Besides lifestyle modifications, another way to improve brain function is through specific and physiological brain testing and treatment. Alzheimer’s disease has been shown to impair eye movements, and in particular fast eye movements called saccades. A prosaccade is when you quickly jump your eyes to a target. An anti-saccade involves jumping your eyes away from a presented target.

Saccades are generated by the frontal lobe, from an area called the fontal eye fields (FEF). Neurodegeneration in the frontal lobe impairs saccade performance, and also impairs the many cognitive functions involving frontal lobe pathways.

Anti-saccades are generated by a frontal area called the dorsolateral prefrontal cortex (DLPFC). An anti-saccade is a high-level executive task. It requires response inhibition to suppress the reflex to look at the presented target, and a cognitive decision to look in the opposite direction. The DLPFC plays a role in many different executive function tasks, including the maintenance of attention and focus. It also functions in networks that regulate emotions, and is underactive in cases of chronic depression.

Research shows that individuals living with Alzheimer’s disease demonstrate significantly worse accuracy with anti-saccade testing compared to normal subjects. Similar findings are seen in people demonstrating mild cognitive impairment. Alzheimer’s patients had slower visual reaction times, and took longer to initiate saccades and anti-saccades during testing (6).

Memory saccades involve a challenge to the working memory system. To test these, a sequence of dots appear and disappear on a screen in random positions while the subject saccades to each target. Once the sequence is complete, the subject must identify the position of a particular target in the sequence. Studies demonstrate that frontotemporal dementia patients demonstrate deficits on anti-saccade and memory saccade tasks, both of which involve higher cognitive demands (7).

When neurodegeneration affects the posterior aspects of the cerebral cortex, problems with eye movements are even more pronounced. Patients with posterior cortical atrophy make significantly shorter saccades especially for distant targets. Time to reach saccadic targets was significantly associated with parietal and occipital cortical degeneration. On fixation stability tasks, patients with typical Alzheimer’s disease showed more frequent square wave jerks, with a frequency that was associated with lower cerebellar grey matter volume. Patients with posterior cortical atrophy showed large saccadic intrusions whose frequency correlated significantly with generalized reductions in cortical thickness. Patients with both posterior cortical atrophy and typical Alzheimer’s disease showed lower gain in smooth pursuit compared to controls (8).

We work very carefully to rehabilitate and optimize saccades, anti-saccades and other associated eye movements. We use specific therapies and precise exercises to improve reaction times and accuracy of these eye movements. Research shows that by exercising these brain regions through eye movements, improvement can be seen in other cognitive and executive function tasks performed by these brain areas. Improvement in saccades and anti-saccades has been shown to improve executive function and attentional control (9).

Saccade rehabilitation is only one of a host of different therapies we employ in the NeuroRescue program.

We may employ targeted electrical therapies, such as transcranial direct current stimulation. tDCS applied above the frontal lobes in dementia patients has been shown to improve global cognition and language function (10). When applied above the temporal lobes, tDCS promoted a significant improvement in working memory tasks (11).

We may use photobiomodulation strategies as well. LED photobiomodulation has been shown to significantly improve cognitive function, as well as improve sleep, decrease anxiety, decrease angry outbursts, and decrease wandering behavior in Alzheimer’s patients (12). It has also been shown to improve executive function, and restore the sense of smell (13). Laser photobiomodulation has been demonstrated to decrease brain inflammation, promote formation of new blood vessels, improve blood flow and oxygenation, promote stem cells to create new neurons, enhance connections between neurons, decrease oxidative stress, and decrease neuronal cell death (14).

We may also employ transcranial magnetic stimulation in your NeuroRescue Program. TMS has been demonstrated to significantly improve performance on standard measures of cognition and executive function (15), as well as effectively treat depression (16).

We may employ hyperbaric oxygen therapy. HBOT has been shown in research to significantly improved the cognitive function assessed by standardized Mini Mental Status Examination and Montreal Cognitive Assessment testing in Alzheimer’s patients, with durable effects seen at 3-month follow-up assessments. Significant improvements in activities of daily living were also seen (17).

We may also engage in vestibular rehabilitation exercises. Fall risks are always a concern with dementia patients. Vestibular function has been assessed in dementia sufferers through vestibular evoked myogenic potential responses and vestibular ocular reflex gain measurement, which were significantly reduced in dementia patients. These findings not only mandate vestibular rehabilitation to mitigate fall risk, but also confirm an association between vestibular dysfunction and cognitive impairment (18).

We may even employ exercises conducted in a virtual reality environment. Studies demonstrate that VR exercises can be effective for enhancing navigation and orientation abilities in patients with spatial memory disorders (19).

We take a close look at metabolic and neurochemical factors in all of our dementia patients. Research has shown that by assessing and addressing metabolism, inflammation, neurotransmitter production, and cofactors for energy producing reactions, cognitive decline can be slowed, stopped, or even reversed in some cases (20).

Every NeuroRescue Program is different, with your therapies chosen based on your diagnostic testing and the realities of your condition. It is impossible to take a cookie-cutter approach to the treatment of a condition as complex as dementia. The therapy plan we develop will be tailored to your unique neurological presentation.

How Does the NeuroRescue Program Work?

We design your unique NeuroRescue Program to be among the most comprehensive diagnostic and therapeutic protocols available today. We create individual NeuroRescue Programs based on a comprehensive analysis of every relevant neurological system and pathway, using gold-standard, cutting edge neurodiagnostic technologies and examination procedures and state-of-the-art therapies.

We begin with your Discovery Day, wherein we perform a comprehensive history of not only your condition, but your life on a timeline. This allows us to dive deeply into your case and see all of the factors that led to where you are now. It helps us uncover hidden problems and associated conditions that may be making it difficult for you to move your recovery forward.

Our examination allows us to identify the areas and pathways of your brain that have been impacted by your dementia. We begin by precisely quantifying the function of your visual, vestibular, and proprioceptive systems through computerized analysis of your eye movements, your inner ear reflexes, and your balance in a host of different sensory conditions.

We employ technologies including Videooculography and Saccadometry to measure several classes of eye movements. We use Video Head Impulse Testing to measure the function of your inner ear, and Computerized Dynamic Posturography to assess your balance in different sensory conditions.

We use NeuroSensoryMotor Integration testing to evaluate hand-eye coordination and cognition, and Virtualis testing to assess dynamic eye tracking and perception of vertical in a virtual reality environment.

We combine all of this with a comprehensive physical and neurological examination of your sensory, motor, autonomic, and cognitive systems. We review any relevant laboratory testing, radiological imaging, and prior neurodiagnostic testing, and integrate that information with our findings.

We use this information to identify which parts of your brain are working properly, which systems are struggling, and the precise point at which your systems fatigue.

We can then design a NeuroRescue Program that is unique and specific to your brain, and yours alone. Your NeuroRescue Program works to rejuvenate and reintegrate the damaged neurons and pathways in your brain. It works to improve energy, endurance, and functional capacity within your fragile systems.

We use our technologies and procedures to not only see what we need to address, but also when it is time to stop and let you rest. We address your impaired neurological function from multiple angles of therapy, and provide metabolic support to improve neurological recovery.

While we cannot bring back neurons that have been lost, your NeuroRescue Program allows us to take the pathways that remain and maximize their efficiency and endurance. And by focusing on the integration of systems, we can do more than just get pathways working better, we can get them working together again. This gives us our best opportunity to help you live a healthy, vibrant, and fulfilling life.

Your Next Best Step:

Living with any form of dementia is challenging. While we cannot offer a cure for dementia, many of the symptoms are manageable, function can often be significantly improved, and quality of life can often be enhanced.

To see if the NeuroRescue Program is right for you, contact one of our patient care coordinators to schedule your Discovery Day.

And remember, it’s never too late to start getting better.