Cognitive Rehabilitation Strengthens Brain Connections

There is increased interest in brain and cognitive rehabilitation to treat people with mild thinking and memory problems. Parkinson’s disease, while typically viewed as a neurodegenerative motor disorder, also affects thinking and memory. In a small clinical trial with Parkinson’s disease patients, patients received either occupational therapy or cognitive rehabilitation. Those who had cognitive rehabilitation showed increases in functional connectivity (a measure of time-linked correlations between changes in blood flow in different parts of the brain) between the left inferior temporal lobe and the left and right dorsolateral prefrontal cortex. These are brain areas important for a number of cognitive functions including memory, planning, and mental manipulation of information. Those who did not receive cognitive intervention did not have increases in connectivity.

What does this mean for Parkinson’s disease and for cognitive rehabilitation? It’s difficult to say with this small study. It’s also unknown how long the changes last. Without a restructuring of the brain and continued cognitive rehabilitation it is not likely that the effects will last more than weeks or months after the rehabilitation ends.

To expand on this study (to bring in other research) and put things in simple terms, if people want to protect their brains they best they can as they age, they need to remain physically and mentally active and in good physical and mental shape. Learn new things. Travel to new locations. Take up a physically demanding hobby or dedicated exercise. This won’t solve all our aging problems but it will help a lot.


Díez-Cirarda, M., Ojeda, N., Peña, J. et al. Brain Imaging and Behavior (2016). doi:10.1007/s11682-016-9639-x

Memory Problems in Some With Parkinson’s Disease

From a recent news release by Jill Pease at the University of Florida.

Using a combination of neuropsychological testing and brain imaging, University of Florida researchers have discovered that in a group of recently-diagnosed patients with Parkinson’s disease, about one quarter have significant memory problems.

Parkinson’s disease is commonly known as a movement disorder that leads to tremors and muscle rigidity, but there is growing recognition of cognitive problems associated with the disease. One of the most common is slower thinking speed that causes patients to have trouble quickly retrieving information. The UF study identifies a subset of patients who have a different kind of cognitive issue — memory problems, or difficulty learning and retaining new information.

The findings were published July 24 in the journal PLOS ONE.

“While a large proportion of people with Parkinson’s will experience slower thinking speed, which may make them less quick to speak or have difficulty doing two things at once, we now know that there are a subset of individuals with Parkinson’s disease who have memory problems,” said Catherine Price, Ph.D., the study’s senior author and an associate professor in the UF College of Public Health and Health Professions’ department of clinical and health psychology, part of UF Health. “It is important to recognize which people have issues with learning and memory so we can improve diagnostic accuracy and determine if they would benefit from certain pharmaceutical or behavioral interventions.”

For the UF study, 40 people in the early stages of Parkinson’s disease and 40 healthy older adults completed neuropsychological assessments and verbal memory tests.

About half the participants with Parkinson’s disease struggled with an aspect of memory, such as learning and retaining information, or recalling verbal information, said lead author Jared Tanner, Ph.D., an assistant research professor in the UF department of clinical and health psychology who conducted the study as part of his dissertation research for a UF doctoral degree in clinical psychology.

“And then half of those participants, or nearly one quarter of all participants with Parkinson’s, were really having a difficult time consistently with their memory, enough that it would be noticeable to other people,” said Tanner, adding that researchers were encouraged by the fact that most participants in the initial stages of Parkinson’s were not having significant memory problems.

All participants received brain scans, which used new imaging techniques that allowed the scientists to navigate the pathways of white matter fibers, the tissue through which messages travel across the brain. The methodology was developed by the research group ofThomas Mareci, Ph.D., a professor of biochemistry and molecular biology in the UF College of Medicine, and is described in a paper published July 14 in PLOS ONE.

Experts have theorized that cognitive problems in Parkinson’s are caused by a shortage of the brain chemical dopamine, which is responsible for patients’ motor issues. But with the help of imaging, the UF researchers were able to spot changes in the brain’s gray and white matter that appear unrelated to dopamine loss and are specific to those patients with Parkinson’s who have memory problems.

“Not only is gray matter important for memory, in Parkinson’s disease white matter connections between the temporal lobe and a region in the posterior portion of the brain called the retrosplenial cortex were particularly important in the recall of verbal information,” Tanner said. “People with Parkinson’s disease who had stronger connections between these areas of the brain did better at remembering information.”

Tanner’s study is part of a larger research project supported by a $2.1 million grant from the National Institute of Neurological Disorders and Stroke of the National Institutes of Health. Researchers led by Price are using imaging and cognitive testing to determine profiles for the cognitive problems that most commonly affect patients with Parkinson’s. The information gleaned from the research could help clinicians foreshadow the type of cognitive impairment a patient may experience over time, if any, and tailor treatment plans accordingly.

GABA receptor role in postoperative cognitive decline

About 20-30% of older adults (age greater than 60) undergoing major surgery experience temporary (generally reversed) memory and thinking deficits after major surgery, particularly heart and orthopedic. A small minority (<5%, probably much less) might not return to cognitive baseline (how they were before surgery). The cause of this decline in cognition is unclear, although many attribute it to the anesthesia used. So far, however, research has been inconclusive as to specific causes of cognitive difficulties after surgery. This is because surgeries are major events that affect most parts of the body, not just what is being operated upon. They are stressful – physically and emotionally.

Newly published research proposes one mechanism for causes of memory problems after surgery – anesthesia acting on ɣ-aminobutyric acid type A receptors (ɣ5GABAaR). This new research suggests that the function of these receptors does not return to baseline until much later than previously believed. This means that the normal function of chemicals in the brain, particularly ones important for memory, might be disrupted for longer than expected, and might play a role in memory problems that some individuals experience after major surgery.


Zurek, A. A., Yu, J., Wang, D. S., Haffey, S. C., Bridgwater, E. M., Penna, A., … & Orser, B. A. (2014). Sustained increase in ?5GABA A receptor function impairs memory after anesthesia. The Journal of clinical investigation, 124(12).

Modeling the Human Brain

Wired has an article about Dr. Henry Markram’s goal to simulate an entire human brain within 10 years. While his goal will not be met within that time-frame, this is important work to do. If we can have a way to simulate brain development or function, it can help us understand how brain disorders occur and help with the treatment of them.

One of the great things about the project is the collaborative nature of it: “‘But the only way you can find out is by building it,’ [Markram] says, ‘and just building a brain is an incredible biological discovery process.’ This is too big a job for just one lab, so Markram envisions an estimated 6,000 researchers around the world funneling data into his model…. Neuroscientists can spend a whole career on a single cell or molecule. Markram will grant them the opportunity and encouragement to band together and pursue the big questions.”

Read the Wired article for more information about the project and the 1 billion Euro grant Markham received.

Parkinson’s Disease and the Brain

The Michael J. Fox Foundation has a good, basic introduction to the neurobiology of Parkinson’s disease. The brief animate video provides an overview of affected parts of the brain as well as the role that dopamine, a neurotransmitter – a chemical in the brain that allows brain cells to communicate with each other – plays in Parkinson’s disease. Click on the link below and then click on the video link titled PARKINSON’S AND THE BRAIN to learn more about how Parkinson’s disease affects the brain.

Learn More

Modems and White Matter

Yesterday my connection to the Internet decided to stop working. I tried restarting the cable modem, the wireless router, and other attached devices. That didn’t fix the problem. That’s usually a good first step though. I saw that the internet connectivity light was lit on the modem but the PC/Activity light was not lit. That told me that maybe the router was bad. I tried plugging my computer directly into the modem via ethernet and my computer did not recognize that a cable was plugged in. I had discovered what was wrong. While it hadn’t taken me long to figure out the problem, I did what many people do and look for solutions in the hardware first rather than in the connections. That’s not necessarily wrong, cables are more hardy than electronic components, but it did reveal my biases. So what was the problem?

The components were all okay – modem, router – but the connections were not. Wiring was the problem. Being interested in the brain, I immediately knew this would make  great brain analogy.

When someone’s cognitive functioning changes, one of the first things clinicians usually jump to is which part of the cortical or subcortical gray matter went bad, so to speak. While those components can and do go bad, we often overlook, just as I did at first, the connections. In my case, the ethernet cable had gone bad. There are many times when what’s affected in the brain are not the components but rather, the wiring – the axons. White matter might be just as important or even more important than the gray matter for cognition, even if its contribution might be more subtle. Much of my current research revolves around this idea.

So the moral of the story is that when things are not working correctly, the wiring might be the culprit.

How did my ethernet cable get damaged? Maybe it just stopped working spontaneously but it also had experienced a bit of acute stress earlier in the day (the modem fell off its stand). Something might have happened to the cable during this time. The white matter of our brain can similarly be affected by traumatic injury, nontraumatic injury (anoxia, hypoxia, etc.), stroke, or a long history of cerebrovascular problems. Just as we can take care of our electronic equipment (by not dropping it or knocking it off its home or stepping on it or whatever else we can do to our technology), we can take care of our white matter by avoiding similar injuries.

Exercise, weight control, managing diabetes, managing blood pressure, and managing cholesterol, can all help protect white matter from going bad and disconnecting different brain areas. We can’t connect to the Internet if our wiring is bad.

Common Misconceptions about Parkinson’s Disease

This brief video provides an overview of some of the common misconceptions about Parkinson’s disease, including causes, course, and outcome. For example, a single head injury will not cause Parkinson’s disease, at least there is no scientific evidence of it occurring. However, repeated head injuries might result in someone who is predisposed to Parkinson’s appear with symptoms earlier than they otherwise would be. This is the same with any environmental factors, such as pesticides or heavy metals (researchers have not shown a solid link between environmental hazards and Parkinson’s disease).

Watch this brief video for a few other misconceptions about Parkinson’s disease.

Donate to Brain Research

The American Academy of Neurology (AAN) has a site where you can donate to help fund brain research. All overhead for the donations are covered by AAN so all of your donated money will go directly to fund research into neurologic disorders. If you or a loved one suffer from a brain disorder or disease, this is a great way to potentially help others with neurologic disorders.

The minimum donation is $5.

Note: I am not affiliated with AAN or the donation site; I just think it is a great cause.

In Memory of H.M. – Live Video

The Brain Observatory – In Memory of H.M..

Click on the above link to watch H.M.’s brain being sliced into histological sections at the University of California – San Diego. The cutting resumes today (Thursday, December 3, 2009) at 11 AM EST. The researchers expect to cover the medial temporal lobes (including what is left of H.M.’s hippocampi). This is a historical event involving the brain of the most studied person in psychology and neuroscience. Who is H.M.? Click here to read my short post about him.

The Relationship Between Executive Function and Processing Speed

Understanding the relationship between brain (specifically subcortical structures) and cognitive processes is a field still in its infancy. The rise of structural and functional neuroimaging that started in the 1970s and really began to mature in the 1990s (with even greater changes and advancements being made today), led to the ability to measure the structure and function of various brain regions in vivo. This was and is important for neuropsychologists because it allowed them to more accurately assess the relationship between the brain and cognitive and behavioral functions.

Processing speed is a basic cognitive or brain processes that subserves many other higher-order cognitive domains. Among those higher domains is executive functioning, a somewhat broad construct that involves the organization of behaviors and behavior responses, selective attention of pertinent information and suppression of unnecessary information, and maintenance and shifting of cognitive sets. Thus, executive functioning is dependent on processing speed but processing speed is not dependent on executive functioning. If executive functioning is a car, processing speed is the engine. Having a faster or more powerful engine means that the car can go faster. More efficient engines allow the car to function at a higher level of efficiency. Thus, while processing speed and executive functions are distinct, they are related with processing speed as one of the basic cognitive processes driving executive functions.

As an example of the interaction between executive functions and processing speed in clinical applications we can look at the Stroop Color-Word task. A person who is not only able to read the words or name the colors quickly but also able to inhibit the undesired but automatic process (namely, word reading on the incongruent color-word task) will receive a higher score on the Stroop task. This would, in combination with other executive function tests, be evidence for intact or even good executive functioning.

Even on non-speeded executive tasks those with fast processing speed can benefit because they can sort through information more quickly and hopefully, efficiently – speed and efficiency are related but not exactly the same. However, not all tests of executive function rely on processing speed. A person, for example, could be slow on the Wisconsin Card Sort Test, yet not exhibit any “executive dysfunction” in that they could complete all the categories and not have an abnormal number of perseverative errors. This simply demonstrates that “executive functions” are diverse and varied.

As a basic process that is dependent on basic neuronal function and glial support, any sort of focal or diffuse injury to the brain can affect processing speed. An example of this is traumatic brain injury, which frequently results in diffuse axonal injury; this diffuse injury negatively affects cognitive processing speed. Any time the white matter is focally or grossly disrupted, processing speed is in danger of disruption itself. This disruption of white matter could be anything from axonal damage, loss of oligodendroglia (which form the myelin), or even low levels of neurotransmitters.

White matter disruption also occurs in multiple sclerosis where diffuse lesions are apparent in the white matter. This disruption also occurs more often in people with heightened vascular risk factors, such as hypertension, diabetes, and cardiovascular disease. People who have these vascular risk factors and subsequent damage to their white matter (this damage or disruption is frequently termed leukoaraiosis) have reduced processing speed and attention (Viana-Baptista et al., 2008). Lesions to subcortical structures, such as the caudate, also result in reduced processing speed (Benke et al., 2003) in addition to executive dysfunction.

In subcortical disease processes such as Huntington’s disease, which usually starts with atrophy of the caudate nuclei, or Parkinson’s disease, which starts with a loss of the majority of dopaminergic cells in the substantia nigra, processing speed is consistently affected. Some common symptoms of Parkinson’s disease are freezing and a shuffling gait; even though these symptoms are motoric, they can be indicative of the global cognitive slowing that also occurs. However, it seems that processing speed is heavily dependent on the integrity of white matter.

Because of the diffusivity of processing speed, I am not aware of any areas of the brain shown to be necessary for processing speed, outside of global white matter. As I mentioned above, damage to the caudate has been shown to affect processing speed but damage to almost any area of the brain, especially if the white matter is disrupted results in slowed processing speed. Neuropsychologists often talk about a patient who has executive dysfunction, slowed speed of processing, as well as some other cognitive deficits as exhibiting signs of a frontal-subcortical disruption – a frontal-subcortical profile. So far, no one has localized processing speed to a single area – many brain structures or areas affect it.

At this point, processing speed and executive functions cannot be “mapped” to separate basal ganglia structures or loops. Of the three classically recognized cortico-striato-thalamo-cortical loops involved in cognitive and emotional processes rather than basic motor processes, which were first introduced by Alexander, Delong, and Strick (1986), the dorsolateral prefrontal cortex circuit appears to be most correlated with processing speed (Mega & Cummings, 1994). This is also the circuit most strongly linked with executive functioning. It appears that rather than utilizing different circuits processing speed and executive functions utilize the same circuits; however, processing speed is much more globalized.


Alexander, G. E., DeLong, M. R., & Strick, P. L. (1986). Parallel organization of functionally segregated circuits linking basal ganglia and cortex. Annual Review of Neuroscience, 9, 357-381.

Benke, T., Delazer, M., Bartha, L., Auer, A. (2003). Basal ganglia lesions and the theory of fronto-subcortical loops: Neuropsychological findings in two patients with left caudate lesions. Neurocase, 9, 70-85.

Mega, M. S., & Cummings, J. L. (1994). Frontal-subcortical circuits and neuropsychiatric disorders. The Journal of Neuropsychiatry and Clinical Neurosciences, 6, 358-370.

Viana-Baptista M, Bugalho P, Jordão C, Ferreira N, Ferreira A, Forjaz Secca M, Esperança-Pina JA, Ferro JM. (2008). Cognitive function correlates with frontal white matter apparent diffusion coefficients in patients with leukoaraiosis. Journal of Neurology, 255, 360-366.