Mental Reserves keep brain agile

There is evidence of cognitive reserves in use all around us, we all know somebody whose sharp brain and intelligence at old age surprises us, some of us might even know someone facing health issues within their brain and have witnessed the brain's ability to cope with extreme, sometimes hopeless situations and amazingly start a recovering process.

Medical Science combined with people's strong will and spirit and sufficient financial resources can achieve amazing results that lead to overcome and prevent terrible conditions like Alzheimer’s and other illnesses that affect cognitive functions including old age which is a natural process. Information is a vital issue to achieve this goal.

Published December 11, 2007

The brain, like every other part of the body, changes with age, and those changes can impede clear thinking and memory. Yet many older people seem to remain sharp as a tack well into their 80s and beyond. Although their pace may have slowed, they continue to work, travel, attend plays and concerts, play cards and board games, study foreign languages, design buildings, work with computers, write books, do puzzles, knit or perform other mentally challenging tasks that can befuddle people much younger.

But when these sharp old folks die, autopsy studies often reveal extensive brain abnormalities like those in patients with Alzheimer’s. Dr. Nikolaos Scarmeas and Yaakov Stern at Columbia University Medical Center recall that in 1988, a study of “cognitively normal elderly women” showed that they had “advanced Alzheimer’s disease pathology in their brains at death.” Later studies indicated that up to two-thirds of people with autopsy findings of Alzheimer’s disease were cognitively intact when they died.

“Something must account for the disjunction between the degree of brain damage and its outcome,” the Columbia scientists deduced. And that something, they and others suggest, is “cognitive reserve.”

Cognitive reserve, in this theory, refers to the brain’s ability to develop and maintain extra neurons and connections between them via axons and dendrites. Later in life, these connections may help compensate for the rise in dementia-related brain pathology that accompanies normal aging.

Source: nytimes.com

Cognitive reserve is greater in people who complete higher levels of education. The more intellectual challenges to the brain early in life, the more neurons and connections the brain is likely to develop and perhaps maintain into later years. Several studies of normal aging have found that higher levels of educational attainment were associated with slower cognitive and functional decline.But brain stimulation does not have to stop with the diploma. Better-educated people may go on to choose more intellectually demanding occupations and pursue brain-stimulating hobbies, resulting in a form of lifelong learning.

Source: nytimes.com

Long-term studies in other countries, including Sweden and China, have also found that continued social interactions helped protect against dementia.

Source: nytimes.com

As Sandra Aamodt, editor of Nature Neuroscience, and Sam Wang, a neuroscientist at Princeton University, recently stated on The New York Times’s Op-Ed page, physical exercise “improves what scientists call ‘executive function,’ the set of abilities that allows you to select behavior that’s appropriate to the situation, inhibit inappropriate behavior and focus on the job at hand in spite of distractions. Executive function includes basic functions like processing speed, response speed and working memory, the type used to remember a house number while walking from the car to a party.”

Although executive function typically declines with advancing years, “elderly people who have been athletic all their lives have much better executive function than sedentary people of the same age,” Dr. Aamodt and Dr. Wang reported.

Source: nytimes.com

The concept of a Cognitive Reserve has been around since 1989, when a post mortem analysis of 137 people with Alzheimer's Disease showed that some patients exhibited fewer clinical symptoms than their actual pathology suggested. These patients also showed higher brain weights and greater number of neurons when compared to age-matched controls. The investigators hypothesized that the patients had a larger "reserve" of neurons and abilities that enable them to offset the losses caused by Alzheimer's. Since then, the concept of Cognitive Reserve has been defined as the ability of an individual to tolerate progressive brain pathology without demonstrating clinical cognitive symptoms.

Source: sharpbrains.com

Dr. Yaakov Stern is the Division Leader of the Cognitive Neuroscience Division of the Sergievsky Center, and Professor of Clinical Neuropsychology, at the College of Physicians and Surgeons of Columbia University, New York.
He is one of the leading proponents of the Cognitive reserve theory, which aims to explain why some individuals with full Alzheimer's pathology (accumulation of plaques and tangles in their brains) can keep normal lives until they die, while others -with the same amount of plaques and tangles- display the severe symptoms we associate with Alzheimer’s Disease. He has published dozens of peer-reviewed scientific papers on the subject.

Source: sharpbrains.com

Cerebral reserve, a notional quality that gives individuals differing levels of mental resilience, is a proposal that has all the ingredients needed to stoke a controversy - intelligence, genes, social status, education and health. Behind it all is a set of widely accepted scientific results that suggest that people with high intelligence and superior education cope better with the progress of Alzheimer’s disease and other forms of dementia and recover more rapidly from stroke, head injuries, depression and even intoxication than the average. And while mental faculties always decline with age, there are marked differences in the rate at which the years dull the mind. Cerebral reserve was dreamt up to explain such anomalies.
The brain’s plasticity makes a strong case for measuring reserve. Cognition can be modified, even in the adult years, and neurons can be rearranged, by physical and mental exercises, be it crossword puzzles, juggling, or taking night classes. If the dwindling reserve is spotted early, it opens a biological window in which to boost cognition and slow the rate of decline.

Source: novartisfound.org.uk

Lifelong bilingualism can help delay the onset of Alzheimer's disease

Lifelong bilingualism can help delay the onset of Alzheimer's disease and other dementia in the elderly by an average of four years, according to a small study by Canadian researchers.

Patients who spoke more than one language reported memory loss or other dementia symptoms on average four years later than people who spoke only one language.

Researchers with the Rotman Research Institute at the Baycrest Research Centre for Aging and the Brain in Toronto carried out the study and published their findings in the February 2007 issue of Neuropsychologia.

"If you have two languages in your brain, you need a way to keep them straight, otherwise you might say the wrong thing," she said.

"It's one of the things that often goes wrong with people suffering from dementia. They can no longer control their speech."

The frontal lobes, which control planning and other high-level functions, are also used in language. Research has found exercising that part of the brain can help build up a "cognitive reserve," which can stave off dementia.

The study follows earlier work in which Bialystok and colleagues showed bilingualism enhances attention and cognitive control in both children and older adults.

Scientists have increasingly studied activities that help build cognitive reserve in later years. Studies have found evidence that physical activity, social engagement and mental activities such as reading and doing crossword puzzles can also help stave off dementia.

http://www.blogger.com/post-create.g?blogID=6109167951728382621

Learning Slows Physical Progression Of Alzheimer's Disease

Learning appears to slow the development of two brain lesions that are the hallmarks of Alzheimer's disease, scientists at UC Irvine have discovered. The finding suggests that the elderly, by keeping their minds active, can help delay the onset of this degenerative disease.

This study with genetically modified mice is the first to show that short but repeated learning sessions can slow a process known for causing the protein beta amyloid to clump in the brain and form plaques, which disrupt communication between cells and lead to symptoms of Alzheimer's disease. Learning also was found to slow the buildup of hyperphosphorylated-tau, a protein in the brain that can lead to the development of tangles, the other signature lesion of the disease. Scientists say these findings have large implications for the understanding and treatment of Alzheimer's disease, as it is already known that highly educated individuals are less likely to develop the disease than people with less education.

http://www.sciencedaily.com/releases/2007/01/070123182024.htm

cortical atrophy

Effects of White Matter Lesions and Lacunes on Cortical Function

Why do frontal lobe symptoms predominate in vascular dementia with lacunes?
Nobuyoshi Ishii, Yasuo Nishihara and Tsukasa Imamura

Department of Pathology (Neuropathology) (Dr. Ishii), University of Occupational and Environmental Health, Yahatanishiku, Kitakyushushi; and the Departments of Pathology and Neuropsychiatry (Drs. Nishihara and Imamura), Kurate Kyoritsu Hospital, Miyatacho, Kurategun, Fukuokaken, Japan.

We studied 30 necropsy cases of vascular dementia with a lacunar state. Manifestations included dementia, lack of volition, emotional lability, small-stepped gait, dysarthria, urinary incontinence, grasp reflex, pyramidal signs, paraplegia in flexion, and akinetic mutism. Pathologically, there was diffuse incomplete softening of white matter in all cases. Both lacunes and diffuse softening were found predominantly in the frontal lobes. The prominent clinical features were therefore frontal lobe symptoms, with good correlation between the symptoms and the distribution of pathologic lesions.

Corticobasal degeneration, or cortical-basal ganglionic degeneration

It is a slowly progressive neurodegenerative disease characterized by a peculiar combination of extrapyramidal and cortical symptoms, including rigidity of the trunk and extremities, dystonias, apraxias, cortical sensory losses, the alien limb phenomenon, and myoclonus. Histopathologic features include atrophy of the frontoparietal cortex; neuronal losses and gliosis in the cortex, basal ganglia, and substantia nigra; and the presence of swollen, achromatic neurons. Asymmetric clinical presentation and asymmetric involvement at gross and microscopic pathologic examination have been emphasized. This pattern of atrophy has been demonstrated by means of neuroimaging studies. Radionuclide studies, which provide information about cortical dysfunction, are reported to be useful in the diagnosis of corticobasal degeneration. Computed tomography and magnetic resonance (MR) imaging, which demonstrate structural changes, also have a role in evaluating clinical-pathologic correlation and in the diagnosis. Results of several studies of single cases or case series have demonstrated high-grade cerebral atrophy in corticobasal degeneration, which may be bilateral or asymmetric and involve the frontoparietal region contralateral to the side that was first affected and that is most severely affected (1–7). However, to our knowledge, there are no neuroimaging studies systematically and quantitatively documenting the cortical atrophy in corticobasal degeneration. The in vivo pattern of cortical involvement and the role of neuroimaging in the assessment remain to be determined, as cortical or neuropsychologic symptoms are central and distinctive features in this disorder.
Pathology examination results indicate that cortical atrophy in corticobasal degeneration is located mainly in the frontal, parietal, and central regions (1–4). The greatest histologic changes, including neuronal loss with disruption of the normal cortical layering, fibrillary gliosis, and status spongiosus, are found in the parietal and posterior frontal cortex, especially in the precentral and postcentral gyri (4,22). Although results of previous MR imaging studies (5–7) showed asymmetric parietal and frontal cortical atrophy and asymmetric dilatation of the lateral ventricles, results of these studies could not be used to specify the exact location of cortical atrophy. Using MR imaging and computer technology, we documented the extent and the precise anatomic location of the cortical atrophy in corticobasal degeneration in vivo. The results of our atrophy rating in the present study showed that the atrophy was accentuated in the parasagittal and paracentral regions in patients with corticobasal degeneration despite widespread cortical involvement. We also demonstrated quantitatively the asymmetric hemispheric involvement in patients with corticobasal degeneration. The most important disease to differentiate from corticobasal degeneration is Alzheimer disease, since Alzheimer disease is the most common cause of cognitive impairment in the elderly. Our study results clearly demonstrated that parasagittal frontoparietal and paracentral cortical atrophy in corticobasal degeneration, which has often been emphasized in pathology studies (4,23,24), was an MR imaging sign that could be used to discriminate corticobasal degeneration from Alzheimer disease. Although asymmetry of atrophy in corticobasal degeneration was stressed in the previous studies (1–7) and was also demonstrated in the present volumetric study, we did not note a significant difference between the two groups.
In a previous study (8) of frontotemporal dementia in which we used the same technique, we found that cortical atrophy in frontotemporal dementia is widespread over the affected hemisphere and is accentuated in the frontal and anterior temporal lobes. Asymmetry of atrophy is also a distinctive feature of frontotemporal dementia. Therefore, the distribution of atrophy in frontotemporal dementia is very similar to that in corticobasal degeneration, although the focus of the atrophy in frontotemporal dementia is different from that in corticobasal degeneration. Severe focal gyral atrophy with a knife-blade appearance, which is characteristic of Pick disease (26), was observed in patients with corticobasal degeneration. Although atrophy with a knife-blade appearance appears in the frontal and temporal lobes in Pick disease, it may appear in the parietal lobe in corticobasal degeneration.

Therapy in a Middle-Aged Adult With Cortical Atrophy and depression

Case Report
Journal of ECT. 21(2):122-124, June 2005.
Amison, Terako MD; Foster, Adriana MD

Abstract:
A 48-year-old male with treated hypothyroidism presented with a long-standing history of depression that had been refractory to treatment. A computed tomography scan of the brain revealed atrophy in the frontal regions. This finding is significant because the patient has no known history of traumatic brain injury, inhalant or alcohol abuse, or prolonged exposure to gasoline. On the basis of the results of the brain imaging in conjunction with the patient's clinical presentation and neuropsychological testing, frontotemporal dementia was considered in the diagnosis and was thought to explain his chronic symptoms of apathy, anhedonia, and suicidal ideation. Electroconvulsive therapy was implemented, with resolution of the patient's depressed mood and neurovegetative symptoms of depression as well as improvement in his Mini Mental Status Examination scores.[/q]

The brain has a role in blood pressure regulation

It is not clear whether the cerebral changes that occur with aging contribute to the decline in blood pressure in the very elderly. We examined a population-based sample of 484 85-year-old persons (344 nondemented and 140 demented, 61 with Alzheimer's disease, 65 with vascular dementia, and 14 with other types of dementia) with a neuropsychiatric examination and blood pressure measurements. Dementia was diagnosed according to the criteria proposed in the Diagnostic and Statistical Manual of Mental Disorders, edition 3, revised. Brain atrophy was measured by CT of the brain. In the nondemented group, frontal (r=-0.18, P=0.037) and parietal (r=-0.23, P=0.008) cortical atrophy and bifrontal ratio (r=-0.20, P=0.013) were associated with lower systolic blood pressure, and frontal (r=-0.23, P=0.010) and parietal (r=-0.24, P=0.008) cortical atrophy and bifrontal ratio (r=-0.23, P=0.006) with lower diastolic blood pressure. Systolic blood pressure was lower in subjects with Alzheimer's disease and vascular dementia, and diastolic blood pressure was lower in those with vascular dementia compared with the nondemented. Systolic (r=-0.27, P<0.0001)>r=-0.10, P=0.020) blood pressure was negatively correlated to dementia severity. In the demented subjects, frontal cortical atrophy was correlated to lower diastolic blood pressure (r=-0.21, P=0.043). Our findings suggest that age-related changes in brain structure may contribute to the decrease in blood pressure in the very elderly and that low blood pressure in dementia disorders is mainly a secondary phenomenon.

Sean Paul song gave her seizures.

Tired of living in fear, she sought out Dr. Ashesh Mehta, a neurosurgeon and director of epilepsy surgery at the medical center.


Mehta said at first he was skeptical of Gayle's claims.


"It's extremely rare," Mehta said of "musicogenic" epilepsy. "There are only 50 to 100 cases ever reported of this disorder."


But he was convinced after Gayle gave herself a seizure by listening to Paul's song.


On Oct. 3, doctors removed a 3-inch portion of her right front temporal lobe, the same area that processes music.



The operation worked. Gayle said she has returned to singing in her church choir and attending York College, where she is studying to become a teacher. She said she waited a month after her surgery before she worked up the courage to listen to "Temperature."


"I think his music is awesome," she said. "Now I can see why everyone liked this song."

Source: nydailynews.com

Certain songs really got to Stacey Gayle - and she had surgery to make them stop.

For four years, Gayle, 25, who has epilepsy had unpredictable epileptic seizures despite taking a regimen of medications. Then in 2006, she figured out that music, and specifically Sean Paul's chart topper "Temperature," could set off the attacks.

"I don't know why Sean Paul was giving me seizures," she said Thursday at Long Island Jewish Medical Center in New H yde Park, where she underwent the operation. "But as soon as the beat came on, it just triggered a seizure. I'd go somewhere and I'd be like, 'Don't play that song!'"

Source: nydailynews.com

January 18, 2008 -- It took "miracle" brain surgery, but now a Queens woman can listen to rapper Sean Paul without getting sick.

It had nothing to do with musical taste - Stacey Gayle, 24, happens to love the musician, especially his hit song "Temperature." It's just that the dancehall tune would trigger grand mal seizures in the Rosedale woman.

Gayle is one of five people in the world who suffer from a bizarre and nightmarish condition called musicogenic epilepsy, said her doctors at Long Island Jewish Hospital.

Yesterday Gayle explained that around her 21st birthday, she was at a barbecue when "Temperature" began playing.

Instantly, she experienced the peculiar "aura" sensation epileptics feel just before a seizure, she said.

"As soon as the beat comes on, I don't know what it is, it just triggers my seizure," Gayle said.

"It's like a weird sensation you get, like a tingling in your head. I smelled something funny, a weird smell."

When she woke up in the hospital after that seizure, she recalled that the Sean Paul song had triggered a prior seizure.

Source: nypost.com

Music-Triggered Seizures Prompt Unusual Treatment

Dog Becomes Guardian Angel For Boy With Epilepsy

Groups offer 'lifeline' when children have epilepsy

I have noticed a little hint of aggressiveness that wasn't in my own life before the treatment, it has only been a few months and I feel miserable about it, I hate aggressiveness! I have a peaceful essence and it is being affected. The following article confirms my suspicions about the treatment.

Gill and her husband, Kevin, watched helplessly as medication made their intelligent daughter become aggressive and angry, while seizures kept her from recognizing her ABCs or walking across a room without help.

Valentine's Day Connected to Epilepsy

Valentine's Day Connected to Epilepsy