Skip to main content

Amantadine for Executive Dysfunction Syndrome in Patients With Dementia -- Drayton et al. 45 (3): 205 -- Psychosomatics

Amantadine for Executive Dysfunction Syndrome in Patients With Dementia -- Drayton et al. 45 (3): 205 -- Psychosomatics

INTRODUCTION

TOP
ABSTRACT
INTRODUCTION
METHOD
RESULTS
DISCUSSION
REFERENCES



Executive dysfunction syndrome, also known as "frontal lobe syndrome," is commonly seen in patients with brain diseases from many causes.1 Executive dysfunction syndrome has been associated with damage to "frontal-subcortical" brain circuits believed to be the anatomical basis of executive control function.2 A variety of neuropsychiatric symptoms indicative of executive dysfunction have been associated with damage to these circuits, including cognitive disturbance, personality change, mood symptoms, and a series of challenging behaviors. Among patients with degenerative dementia, especially advanced dementia, symptoms of executive dysfunction syndrome are common and present a challenging clinical dilemma. While executive dysfunction syndrome occurs with some frequency in patients with Alzheimer's disease,3,4 it is one of the cardinal clinical manifestations of frontotemporal degeneration. Frontotemporal degeneration is a group of disorders with a common histopathology5,6 that involves the degeneration of the frontal and anterior temporal lobes.5,6 This disease has been referred to in the literature by various names, including non-Alzheimer's dementia, semantic dementia, or Pick's disease.5,6 The prevalence of frontotemporal degeneration among all cases of dementia has been estimated to range between 3% and 22%. Frontotemporal degeneration usually presents during the fifth to seventh decades of life and has a strong familial link.5,6 The symptoms of executive dysfunction syndrome usually precede cognitive decline in patients with frontotemporal degeneration.6 Behavioral disinhibition, decreased judgment, and poor insight are common. Executive functioning is usually selectively impaired during the early stages of frontotemporal degeneration. However, in an older person with dementia, it is very difficult to distinguish executive dysfunction syndrome due to Alzheimer's disease from that due to frontotemporal degeneration on clinical grounds, other than by careful history taking.7

The treatment of executive dysfunction syndrome, especially in the context of frontotemporal degeneration, has been very challenging and mostly unsuccessful.1 Reports have suggested that selective serotonin reuptake inhibitors, bromocriptine, carbamazepine, lithium, and other agents may have efficacy in treating executive dysfunction syndrome. However, there is a dearth of controlled trials in this area, and there have been only a few case series reported. In general, treatments have focused on manipulation of the dopamine, serotonin, or cholinergic neurotransmitter systems that are thought to be modulators of the frontal-subcortical loops involved in the pathogenesis of executive dysfunction syndrome.1

We report here the results from an open, uncontrolled chart review study of our experience using the antiviral drug amantadine to treat executive dysfunction syndrome in patients with dementia. Several years ago, clinicians on our team began to use amantadine empirically, outside its labeled use, for the treatment of these symptoms without a formal protocol. This was based on a report that amantadine helped executive dysfunction syndrome in patients with traumatic brain injury8 and by a case series suggesting that dopamine "augmentation" with bromocriptine reduces problem behaviors related to executive dysfunction syndrome.9 The precise mechanism of amantadine's brain action is unknown. It appears to have dopamine-modulating activity in the peripheral and CNS by augmenting the release and inhibiting the cellular reuptake of dopamine.10 Amantadine is also a N-methyl-D-aspartic acid receptor antagonist, which may indirectly enhance dopaminergic transmission and confer neuroprotective effects, similar to its analogue, memantine.11 Moreover, amantadine is known to alter the function of nicotinic acetylcholine receptors in muscle and has a weak antagonist effect on mammalian hippocampal nicotinic acetylcholine receptors. This may signify protective effects in neurodegenerative disorders or in cholinergic toxicity.12

Interesting. Bromocriptine also heals insulin resistance, in addition to apparently helping executive dysfunction

Comments

Popular posts from this blog

Insulin Resistance- cause of ADD, diabetes, narcolepsy, etc etc

Insulin Resistance Insulin Resistance Have you been diagnosed with clinical depression? Heart disease? Type II, or adult, diabetes? Narcolepsy? Are you, or do you think you might be, an alcoholic? Do you gain weight around your middle in spite of faithfully dieting? Are you unable to lose weight? Does your child have ADHD? If you have any one of these symptoms, I wrote this article for you. Believe it or not, the same thing can cause all of the above symptoms. I am not a medical professional. I am not a nutritionist. The conclusions I have drawn from my own experience and observations are not rocket science. A diagnosis of clinical depression is as ordinary as the common cold today. Prescriptions for Prozac, Zoloft, Wellbutrin, etc., are written every day. Genuine clinical depression is a very serious condition caused by serotonin levels in the brain. I am not certain, however, that every diagnosis of depression is the real thing. My guess is that about 10 percent of the people taking

Could Narcolepsy be caused by gluten? :: Kitchen Table Hypothesis

Kitchen Table Hypothesis from www.zombieinstitute.net - Heidi's new site It's commonly known that a severe allergy to peanuts can cause death within minutes. What if there were an allergy that were delayed for hours and caused people to fall asleep instead? That is what I believe is happening in people with Narcolepsy. Celiac disease is an allergy to gliadin, a specific gluten protein found in grains such as wheat, barley and rye. In celiac disease the IgA antigliadin antibody is produced after ingestion of gluten. It attacks the gluten, but also mistakenly binds to and creates an immune reaction in the cells of the small intestine causing severe damage. There is another form of gluten intolerance, Dermatitis Herpetiformis, in which the IgA antigliadin bind to proteins in the skin, causing blisters, itching and pain. This can occur without any signs of intestinal damage. Non-celiac gluten sensitivity is a similar autoimmune reaction to gliadin, however it usually involves the

Blue-blocking Glasses To Improve Sleep And ADHD Symptoms Developed

Blue-blocking Glasses To Improve Sleep And ADHD Symptoms Developed Scientists at John Carroll University, working in its Lighting Innovations Institute, have developed an affordable accessory that appears to reduce the symptoms of ADHD. Their discovery also has also been shown to improve sleep patterns among people who have difficulty falling asleep. The John Carroll researchers have created glasses designed to block blue light, therefore altering a person's circadian rhythm, which leads to improvement in ADHD symptoms and sleep disorders. […] How the Glasses Work The individual puts on the glasses a couple of hours ahead of bedtime, advancing the circadian rhythm. The special glasses block the blue rays that cause a delay in the start of the flow of melatonin, the sleep hormone. Normally, melatonin flow doesn't begin until after the individual goes into darkness. Studies indicate that promoting the earlier release of melatonin results in a marked decline of ADHD symptoms. Bett