Posts Tagged ‘parietal cortex’

Attention

March 29, 2020

The focused extreme of the Attention dimension is the result of enhanced activation in brain regions, including the prefrontal cortex and the parietal cortex, that constitute a circuit for selective attention. The prefrontal cortex is critical for maintaining attention, while the parietal cortex acts as the brain’s steering wheel, pointing attention to particular places and thereby focusing attention on a specific target. At the unfocused extreme, the prefrontal cortex is underachieving and attention is stimulus driven: Whatever occurs around you draws your attention. You veer from one stimulus to the next with no internal rudder to guide your attention. Improving focus requires increasing activity in the prefrontal and parietal cortices.

To improve focus he recommends mindfulness meditation. Follow the instructions in the Self-Awareness section for mindful breathing. Once you feel comfortable you can move on to focused-attention meditation, which is also known as one-pointed concentration.

In a quiet room free of distractions, sit (or recline with your eyes open. Find a small object such as a coin, a button on your shirt, or an eyelet on your shoe. It is important that the object of attention be visual, rather than your breath, your body image, or other mental objects.
Focus all your attention upon this one object. Keep your eyes trained on it.
If your attention wanders, calmly try to bring it back to that object.

Do this daily, initially for about ten minutes. If you find that you are able to maintain your focus most of that time, increase your practice about ten minutes per month, until you reach one hour.

If you feel your attention is excessively focused and wish to broaden it in order to take in more of the world, then open-monitoring or open-presence meditation can nudge you toward that end of the Attention dimension. In open-monitoring meditation, your attention is not fixed on any particular object. Instead, you cultivate an awareness itself. He recommends beginning with a focused-attention meditation practice such as breath meditation, which will give you a basic level of attentional stability and make open-monitoring meditation easier. The basics are:

Sit in a quiet room on a comfortable chair, with your back straight but the rest of your body relaxed. Keep you eyes open or closed whichever you find more comfortable. If your eyes are open, gaze downward and keep your eyes somewhat unfocused.
Maintain a clear awareness of and openness to your surroundings. Keep your mind calm and relaxed, not focused on anything specific, yet totally present, clear, vivid, and transparent.
Lightly attend to whatever object happens to rise to the top of your consciousness, but do not latch on to it. You want to observe the thinking process itself, perhaps saying to yourself, Oh, I notice the the first thing I am thinking of as I sit down to meditate is…
Give your full attention to the most salient current object of consciousness focusing on it to the exclusion of everything else but without thinking about it. That is, you are simply aware of it, observing it as disinterestedly as possible, but do not explore it intellectually. Think of an object of attention as if if were an image in a frame in a museum, or in a movie, with no strong relevance to you.
Generate a state of total openness, in which the mind is as vast as the sky, able to welcome and absorb any stray thought, feeling or sensation like a new star that begins shining. When thoughts arise, simply let them pass through your mind without leaving any trace in it. When you perceive noises, images, tastes, or other sensations, let them be as they are, without engaging with them or rejecting them. Tell yourself that they can’t affect the serene equanimity of you mind.
If you notice your mind moving toward another thought or feeling, let it do so, allowing the newcomer to slip into consciousness. Unlike Attention-strengthening forms of meditation, you do not try to shoo away the “intruding” thought, but allow your mind to turn to it. The key difference from the breath-focused meditation described previously is the in open-monitoring meditation were is no single focus to which the attention is redirected if it wanders. Rather, you simply become aware of whatever is in the center of attention at any moment.
Turn to this new object of attention as you did the first.
Do this of five to ten minutes.

In a study done by Prof. Richardson’s group using EEG found that when people practice open-monitoring meditation it modulates their brain waves in a way that makes them more receptive to outside stimuli—that is, they experience phase-locking, a signature of Focused Attention

Much more extensive guidance is provided in The Six Dimensions of Emotional Style
How Its Unique Patterns Affect the Way You Think, Feel and LIve—And How You Can Change Them by Richard J. Davidson, Ph.D. with Sharon Begley.

Alzheimer’s Disease (AD)

September 24, 2019

This post is based on an important book by Scott D. Slotnick titled “Cognitive Neuroscience of Memory.” Remember to consult the website http://www.brainfacts.org/
to see the anatomical information referred to in this post.

As AD progresses from earlier to later stages, atrophy starts in the medial temporal lobe, extends to the parietal lobe, and finally includes the frontal lobe. The long-term memory impairment in early AD patients can be attributed to the disrupted processing in the hippocampus and parietal cortex, to regions that have been associated with this cognitive process. As the disease progresses, other cognitive processes are disrupted such as attention and language, which both depend on the dorsolateral prefrontal cortex.

In early AD patients, as atrophy begins in the parietal cortex and the frontal cortex, there have also been reports of increases in fMRI activity within cortical regions. It is unknown whether these increases in cortical fMRI activity reflect a compensatory mechanism, which is often assumed to be the case, or reflect non-compensatory hyperactivity due to neural disruption.

In addition to brain atrophy, AD patients have abnormal high levels of proteins in different brain regions. In the medial temporal lobe, the accumulation of tau protein leads to neurofibrillary tangles. In cortical regions, such as the parietal cortex in early AD, the accumulation of amyloid-B protein leads to amyloid plaques. The neurofibrillary tangles in the medial temporal lobe and amyloid plaques in cortical regions can be assumed to disrupt neural processing in these regions.

Dr. Slotnick writes, “There is an influential hypothesis that there is a causal relationship between default network activity that leads to deposition of amyloid that results in atrophy and disrupted metabolic activity, which impairs long-term memory in AD patients. The regions in the default network are active when participants are not engaged in a task and include the dorsolateral prefrontal cortex, the medial prefrontal cortex, the inferior prefrontal cortex and the medial parietal cortex. In AD patients, amyloid deposition occurs in the same regions, which suggest the default network activity may lead to amyloid deposition. Dr. Slotnick suggests that perhaps higher level of amyloid deposition, which occurs in late AD patients, is necessary to produce atrophy in the frontal cortex.

Healthy memory readers should recognize the similarity between the default network and Kahneman’s System 1 processing. System 1 processing is the default network that needs to be disrupted to engage in System 2 processing, better known as thinking.

Dr. Slotnick continues, “If high amyloid deposition is a causal factor in developing AD, older adults with low levels of amyloid should be at decreased risk for developing this disease. There is some evidence that cognitive engagement and exercise throughout life may reduce the amyloid level in the brains of healthy older adults as a function of cognitive engagement (System 2 processing), and this was compared to the cortical amyloid levels . Participants rated the frequency which they engaged in cognitively demanding tasks such as reading, writing, going to the library, or playing games at five different ages (6, 12, 18, 40, and their current age). Healthy older adults with greater cognitive engagement throughout their lifetime, as measured by the average cognitive activity at the five ages, had lower levels of amyloid in default network regions. Moreover, the healthy older adults in the lowest one-third of lifetime engagement had amyloid levels that were equivalent to AD patients, and the healthy older adults in the highest one-third of lifetime cognitive engagement had amyloid levels that were equivalent to young adults.

It should also be noted that many have died who upon autopsy had levels of amyloid plaque and neurofibrillary tangles definitive of AD, but who never exhibited any of the behavioral or cognitive symptoms characteristics of the disease. The explanation typically offered for these individuals is that they had built a cognitive reserve as a result of the mental activities they had engaged in during their lifetimes.

There is a wide variety of products sold to prevent AD, such as computer games and pills that increase short-term memory. But it should be clear from the posts on cognitive science that the entire brain is involved. That is why the healthy memory blog strongly recommends growth mindsets with continual learning throughout the lifespan. These make heavy use of System 2 processing. Of course, a healthy lifestyle that includes physical exercise must also be part of the mix.

Memory and Other Cognitive Processes

September 20, 2019

This post is based on an important book by Scott D. Slotnick titled “Cognitive Neuroscience of Memory.” Remember to consult the website http://www.brainfacts.org/
to see the anatomical information referred to in this post.

Memory is involved in all cognitive processes. Neuroscience is a new emerging, field and the research into other cognitive processes is just beginning. Much further research is needed before it is ready for public consumption.

The few definitive facts on this topic appear in the Chapter Summary, which follow:

“*Visual attention increases activity in visual sensory regions and is also associated with activity in dorsolateral prefrontal cortex and parietal cortex control regions.

Visual working memory is associated with the same sensory regions and control regions associated with attention, which likely reflects attention to the contents of working memory.

*Visual long-term memory is associated with the same regions associated with visual attention in addition to the medial temporal lobe, which indicates this cognitive priocess is distinct from attention.

*Imagery and working memory share the same cognitive operations and are associated with the same brain regions (i.e., the sensory cortex, the dorsolateral prefrontal cortex (i.e., Broca’s area) and the left posterior superior temporal cortex (i.e., Wernicke’s area).

*Memory for emotional information is thought to be enhanced through the interaction of the amygdala and the hippocampus.”

Brain Regions Associated with Long-Term Memory

September 11, 2019

This post is based on an important book by Scott D. Slotnick titled “Cognitive Neuroscience of Memory.” Remember to consult the website http://www.brainfacts.org/
to see the anatomical information referred to in this post.

Dr. Slotnick writes, The term episodic memory can refer to many other related forms of memory including context memory, source memory, “remembering,” recollection, and autobiographical memory, which refers to a specific type of episodic memory for detailed personal events. As the names imply context memory and source memory refer to the context in which something occurred and source memory refers to where the event occurred.

Episodic memories are related to activity in both control regions and sensory regions of the brain. Sensory cortical activity reflects the contents of memory. The control regions that mediate episodic memory include the medial temporal lobe, the dorsolateral prefrontal cortex, and the parietal cortex. There are many regions associated with episodic memory but the primary regions are the medial temporal lobe, the dorsolateral prefrontal cortex, and the parietal cortex. The parahippocampal cortex processes the context of previously presented information such as the location or the color.

The hippocampus binds item information and context information to create a detailed episodic memory. Dr. Slotnick provides the following example. “If an individual went on a vacation to Newport Beach in California and later recalled meeting a friend on the beach, that individual’s perirhinal cortex would process item information (the friend), the parahippocampal cortex would process context information (the area of the beach on which they were standing), and the hippocampus would bind this information and context information into unified memory.”

Semantic memory refers to knowledge of facts that are learned through repeated exposure over a long period of time. These facts are processed and organized in semantic memory, which provides the basis for much thought. Subjectively, semantic memory is associated with “knowing.” Semantic memory includes definitions and conceptual knowledge, and this cognitive process is linked to the field of language.

Semantic memory has been associated with the left dorsolateral prefrontal cortex (in a different region associated with episodic memory), the anterior temporal lobes, and sensory cortical regions. The left dorsolateral prefrontal cortex may reflect the processing of selecting a semantic memory that is stored in other cortical memories. For example, naming animals activates more lateral inferior occipital-temporal cortex that has been associated with the perception of living things, while naming tools activates more medial inferior occipital-cortex that has been associated with perception of nonliving things.

In a study of Alzheimer’s patients, the impairment in an object naming task, which depends on intact semantic memory, was more highly correlated with cortical thinning in the left anterior temporal lobe. This finding suggests that the left anterior temporal lobe is necessary for semantic memory.

During long-term memory the hippocampus binds information between different cortical regions. But long-term memory may only depend on the hippocampus for a limited time. In the standard model of memory consolidation, a long-term memory representation changes from being based on hippocampal-cortical interactions to being based on cortical-cortical interaction, which takes a period of somewhere between 1 to 10 years. A person with hippocampal damage due to a temporary lack of oxygen might have impaired long-term memory for approximately 1 year before the time of damage from retrograde amnesia and have intact long-term memories for earlier events. This suggests that the hippocampus is involved in long-term memory retrieval for approximately 1year as more remote long-term memories no longer demand on the hippocampus so they are not disrupted.

The activity in the hippocampus did not drop to zero for older semantic memories but was well above baseline for events that were 30 years old. This indicates that the hippocampus was involved in memory retrieval for this entire period. If the hippocampus was no longer involved, the magnitude of activity in this regions would have dropped to zero for remote memories.

There is a growing body of evidence that the hippocampus is involved in long-term memories throughout the lifetime. As such, the process of consolidation does not appear to result in the complete transfer from hippocampus-cortical memory representation to cortical-cortical memory representations.