Vascular Dementia

Progressive Vascular Dementia

Vascular dementia is a progressive loss of cognitive skills over time, secondary to a blockage or rupture of a blood vessel in the brain. This term used to be called “multi-infarct dementia”, and other classification systems refer to it as an “arteriosclerotic dementia.” The primary form is atherosclerosis, in which the plaques of fatty deposits form in the innermost layer of the cerebral artery. It is almost exclusively a problem of the older adult. Very young children are prone to arteriovenous malformations, which are congenital defects of the cerebral vascular system. Most of these AVM’s are located in the brain stem, and do not result in the sort of symptoms observed in the older adult.

The primary deficit of multiple strokes is an impairment of memory. The impairment may be the ability to recall old information or learn new information. It is rare that someone forgets old information, yet learns new information at an average level. The most common scenario is a decreased ability to retain new information, with increasing impairment of long-term personal information that declines with every subsequent stroke. The specific deficit regarding loss of old personal information is called “episodic memory”, and it may be affected in isolation of other memory impairments. A specific deficit of this type of memory is exceedingly rare, such that an impairment of new learning is much more common.

Vascular dementia is not limited to memory impairment alone. The diagnostic criteria stipulates that a patient must have a memory impairment, as well as one other cognitive deficit, in order to be appropriately diagnosed with “Vascular Dementia”. The most common cognitive impairment from stroke is difficulty with motor control; not just unilateral paralysis, but an impaired ability to carry out motor routines, despite a functional motor system. Many stroke victims have difficultly recognizing and utilizing objects, despite having an intact sensory system. Lastly, many stroke suffers have difficulty switching between mental tasks, making plans, and organizing the steps necessary to accomplish a plan.

Patients with a vascular dementia are impaired in work and/or social functioning. If one performs well at work and socially, despite having multiple strokes, the diagnosis of “Vascular Dementia” would not be appropriate. Usually, there are hard neurological signs of the multiple strokes; e.g., unilateral paralysis, gait disturbance (difficulty walking), unilateral weakness and lesions that appear on brain images. It is also common to suffer with a delirium in the acute phase, which is an altered mental state where a person is incapable of focusing their attention. Immediate attention is often impaired after a stroke, but tends to resolve over several months.

Psychological problems are common after suffering one or more strokes. It is not common to have delusions of persecution or grandiosity after a stroke. Some forms of progressive dementia affecting the right prefrontal-temporal area exhibit delusions as an early symptom of the disease. Neglect of the right or left visual space should not be mistaken for a delusion. It is frequently the case that the patient suffered with a Delusional Disorder prior to the onset of the stroke. The most common psychological symptom of “Vascular Dementia” is depression. The depression may arise from difficulty with psychological adjustment to their declined condition, or a general psychomotor retardation without any awareness as to their own psychological condition. This takes the form of a significantly reduced reaction time, both simple and complex. The person appears chronically fatigued, laconic, and wanting to be left alone. This type of depression is often deemed to be “organic” in nature.

The neuropsychological treatment of “Vascular Dementia” is to first determine the exact nature of the deficits through testing. If the patient is experiencing psychological symptoms of depression or delusions, the clinician must determine if the patient is aware of their abnormal state. For example, psychotherapy is appropriate for an adjustment problem in a self-aware person, but inappropriate for a severely depressed person with no awareness of their symptoms. Neuropsychologists use the patient’s remaining cognitive strengths to compensate for their deficits.

Is My Dementia Clean or Dirty?

Is it possible to find someone with a “clean” dementia? While this sounds like a misnomer, it is intended to describe people who suffer with a specific dementing pathology, and no other complications are known to exist. It is a form of progressive cognitive deterioration that corresponds perfectly with its diagnostic category. Only symptoms of this particular dementia are present, uncontaminated by other forms of physical or mental illness. Hypothetically, such a “clean” dementia should readily conform to existing treatment protocols. When a patient consults a neuropsychologist, they expect some sort of diagnosis with treatment recommendations, and not “well, it might be this, or it might be that.” Families often vacillate between different factors to explain the changes in behavior and cognition, such that they expect definitive answers from a professional. It is not unusual for the patient to become agitated when the doctor invariably, stereotypically, calls for more tests before they can arrive at a definitive diagnosis. Why can’t we just do our job?

Here is where I frustrate my audience by reporting that diagnoses are rarely simple and clear cut, and that it’s typically a disservice to the patient to arrive at a quick and dirty diagnosis. For example, a new patient came into the office yesterday with an old severe closed head injury. This person exhibited classic signs of a severe traumatic brain injury. Their personality and mental functioning were permanently altered in a way that is very consistent with the pathology of TBI that I was taught in school. The easiest route is to dazzle the family with my knowledge of traumatic brain injury, make some behavioral and medication recommendations, and then sit back until they return in two weeks. During the course of the interview with the family and patient, it became apparent that the patient endured a cerebral vascular accident immediately subsequent to the closed head injury. Unfortunately, this is not an uncommon occurrence after severe closed head injury, though rare in mild to moderate injuries without a period of coma. There are aspects of the patient’s balance and overall ambulation that would be uncommon in a “clean” closed head injury. While the patient is walking in a functional manner, they often trip and fall into objects. Weakness in one of their arms makes it difficult to perform tasks that require two hands. Functional impairment from the stroke is as or more important than the impairment secondary to the closed head injury. Formulating recommendations based on one or the other diagnosis would be unsafe and unwise. Only by thinking in terms of the patient’s holistic or overall functioning would I be able to make their life safer and more stimulating. Stated another way, diagnoses are typically less important than the obvious difficulties the patient confronts in their environment every day.

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The common sense approach to treatment of damage to the central nervous system is driven by symptoms and their expression in the patient’s unique environment. A diagnosis helps alleviate the anxiety of family members and the insurance industry, but in isolation, does little to assist the patient. Medications prescribed for their main effect rather than by their side-effect may help in one area and cause problems in another, rendering little to no net gain for the patient. Clinicians that need to find neat categories and rapid solutions will please the family shopping for confidence more that the family looking for real gains. Lastly, even the best of treatment protocols needs adjustment. People change over time, and the cognitively impaired are no exception. Any intervention that has positive results for a year or more should be considered a success-even if there is a subsequent decline. Consider periodic adjustments to behavioral and medication protocols to be necessary and expected.

To answer the initial question, it is rare, indeed, to find a “clean” dementia. Even if the initial stages of the dementia are uncomplicated and according to protocol, the illness rarely remains so orderly for its entire course. Patients and family members often gain confidence from hurried and decisive experts; tending to view their curt behavior as a sign of social importance. A clinician who is unsure and vacillating about treatment options exudes less confidence to others, but may ultimately be the most concerned and helpful.

Drugs to Improve Memory

It was a bit shocking. The wife remarked on the comments of her husband’s neurologist. He was rumored to malign memory enhancing drugs used in the treatment of Alzheimer’s Disease. He was of the opinion that this class of drugs benefited the drug companies more than the victims of a senile dementia. The wife was understandably confused by the disparity between the opinion of the neurologist and the claims of the drug companies. The shock was the public admission of what many physicians voice in private.

Over the last ten years, most patients I’ve evaluated with a change in mental status, due to any cause, have already been prescribed memory enhancing medications. The drug companies caution that these drugs should be limited to the victims of a senile dementia of the Alzheimer’s type. It is very common to observe these drugs used in the treatment of stroke and head injuries. Is this a good thing?

Unfortunately, this clinician has never witnessed a significant increase of verbal memory performance as a consequence of these medications. This experience applies both to the preferred use of these drugs in the treatment of Alzheimer’s, as well as off-label use of memory enhancing medications. It is not intended as a blanket condemnation, rather it reflects the lack of statistically significant benefit displayed on well-normed tests of verbal memory. There may be many people who have a significant increase of verbal memory with the use of these drugs, but none of these responders have been evaluated by this clinician. Memory enhancing drugs that boost the neurotransmitter acetylcholine may display increased agitation, weight loss, and even chronic nausea with vomiting. These reactions are fortunately not universal. This clinician has witnessed the resolution of these symptoms many times after a reduction or discontinuation of the medication. Personal experience of medication that affects glutamate levels in the brain is that they are neither very harmful or helpful in the treatment of moderate to severe Alzheimer’s Disease.

Given the modest benefits advanced by the drug companies, and the lack of personal observation as to their effectiveness, it may not come as a shock that I rarely recommend memory enhancers. Family members are often convinced of their benefit based upon commercial advertising. I have never witnessed a family member request memory enhancers based upon their personal experience, or the experience of a close friend. This is not to say that memory enhancers never have beneficial effects, just not in this clinician’s limited experience. Much of the public and even some physicians are highly influenced by these drug advertisements.

The latter stages of Alzheimer’s Disease are often fraught with weight loss and agitation. Victims of a senile dementia become too inattentive to sit through a whole meal, requiring frequent prompts and even hand feeding to keep up their body weight. By the middle stages of Alzheimer’s, the loss of other cognitive functions largely negates a mild increase in verbal memory. These mid-stage patients would still have trouble with planning, praxis, attention, judgment, flexibility, etceteras. Even a significant increase in verbal memory would not return these victims to an independent lifestyle. Memory enhancing drugs that commonly produce symptoms of weight loss and agitation should be used with obvious caution.

This clinician’s advice is to proceed with, you guessed it, caution. Consider having a neuropsychologist perform pre and post testing to measure any significant increase in verbal memory as a consequence of these medications. If there is not a significant increase in verbal memory after a six week trial, consider requesting the attending physician to reduce and eventually discontinue the medication. If an acetylcholine boosting medication is utilized, and the patient develops weight loss and agitation, work with the physician to determine if the symptoms are secondary to the memory medication. Senile dementia of the Alzheimer’s type is a horrid disease that can cripple an entire family. Pills without a clear benefit should be considered as a risk to the patient over time; possibly creating undesired symptoms and interacting with other medications in an unpredictable fashion. I strongly suggest to formulate conclusions based upon observation-not advertising.