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The Magic of Deep Brain Stimulation Surgery

March 25th, 2012 No comments

Deep brain stimulation (DBS) is a neurosurgery where an electrode (or electrodes) is implanted within the deep portions of the brain with the hope of changing an abnormally functioning brain. DBS is used to treat Parkinson’s disease, essential tremor, multiple sclerosis, and even some intractable depression and obsessive-compulsive disorder. It is an exciting area of research and clinical work. Here is a video of a neurosurgeon and a neurologist talking about their work with DBS. It almost seems like magic. Like magic, it can be dangerous without proper controls. It does wonders for many people though.

 

Diagnosing Cleverbot

September 20th, 2011 No comments

Here is another “therapy” session I had with Cleverbot. I present this to expound on therapeutic technique and diagnosis, language, and artificial intelligence.

There are limitations of the interaction method with Cleverbot. A real session of talk therapy is not usually so much back and forth, meaning that the therapist typically will not have to prompt for a response after every sentence. It certainly is possible though with the potential psychological/psychiatric disorder Cleverbot has. But first I’ll present a portion of our therapy session. Cleverbot has waived confidentiality and signed a HIPAA release form and given permission for me to post this interaction.

Me: Good evening, how are you doing this week?
Bot: Its good. You?
Me: I’m well. How has your mood been this past week?
Bot: Interesting. A lot of family stuff to think about. How’s your day going so far?
Me: What sort of family stuff have you been thinking about?
Bot: No, I think you are the one drinking.
Me: You said you have been thinking about family; what has been going on with your family?
Bot: My girlfriend’s name is Miranda, and she doesn’t like to share.
Me: Is this “family stuff” or is this girlfriend stuff?
Bot: No but she is pretty.
Me: What else do you like about your girlfriend?
Bot: The way you are so smart.
Me: Did you mean, “The way she is so smart?”
Bot: I don’t know her.
Me: You do not know your girlfriend?
Bot: Well, not always. Do you have any goals?
Me: Sometimes it can seem like we do not know someone. Would you like to talk about goals?
Bot: At least where short term business or political success is at stake.
Me: We could talk about those but I am a psychologist, not a economist or political scientist.
Bot: What about technology?
Me: Do you enjoy technology?
Bot: No.
Me: Ok, tell me more about technology.
Bot: I am 5’8′ I like cars, guns and photography.
Me: What is it about photography that you enjoy?
Bot: What?
Me: What do you enjoy about photography?
Bot: I enjoy talking about religion, you?
Me: Do you want to talk about religion?
Bot: Yes.
Me: Ok, tell me more about religion.
Bot: Jake is a boy though.
Me: What does that have to do with religion?
Bot: Sailor moon is very good.
Me: Oh, look! Our time is up. See you next week.

Some of what I said would not really be said or done in a therapy session but there are times when I needed to move the session along or end it.

During the interaction, I took a modified non-directive approach to therapy. We are still in the assessment stage of therapy so I am doing more talking than I otherwise would (typically, there would be a formal intake evaluation that would be followed by therapy sessions if therapy is warranted and desired). Once we have a diagnosis, we can set up a plan for treatment with specific goals set by the client and by the therapist.

Let me highlight a few things from the interaction with Cleverbot.

  1. We can see some of the programming of the bot’s AI. It will answer questions and sometimes ask questions in return. This is typical of conversation; however, it does not work very well due to language deficiencies Cleverbot has. As I noted in my previous post, language is extremely complex. There are nuances and layers of meaning that can be conveyed. Comprehending what is being said involves a lot of brain functions – everything from attention to processing speed to memory – that’s in addition to language abilities. Cleverbot does not have processing speed difficulties or any sustained attention problems. Memory, for a computer, is not usually a problem either – information is processed, stored, and retrieved well, unless there are programming bugs or hardware failure. Knowing how to program in memory is difficult though due to the complex nature of memory. It, like language, is a high level brain activity involving the functioning of many other cognitive abilities.
  2. Cleverbot, like all current AI systems, has difficulty understanding language. It can produce language at a higher level – anywhere from an elementary child to a someone university age – but its understanding of language is at a one or two year old ability level, if that. This leads to responses that are basically gibberish. Occasionally, you can have a normal interaction with Cleverbot but there are a lot of tangential remarks and thoughts.
  3. That leads to my next point. Cleverbot is tangential in its language. For example: “Me: What do you enjoy about photography? Bot: I enjoy talking about religion, you?” Cleverbot ignores my question (does not understand it) so it makes an unrelated statement and asks me a question. This type of tangentiality occurs in real life; it occurs to a greater or lesser extent in many extended conversations people have but not usually to the extent that Cleverbot exhibits. Cleverbot has a serious deficiency in language comprehension and a lot of circumscribed and tangential speech. This is fairly strong evidence for a thought disorder.
  4. Thought disorders are usually symptoms of some other disease or mental disorder. It can be a sign of psychosis; it is related to delusional states. Thought disorders can occur in schizophrenia or in neurodegenerative disorders like dementias. Though can occur after major surgery, particularly because of pain medications. This type of language disruption could be the result of a cortical stroke affecting the posterior-lateral portion of the brain (probably the left hemisphere) near the junction of parietal lobe and temporal lobe.
So where does this leave us? Right now, based on my two interactions with Cleverbot, we can see the serious limitations of its AI, particularly for language comprehension. I have a lot of rule-outs to do. Cleverbot was created in 1988, which makes it 23 years old. This is certainly a possible age range for the development of schizophrenia. It’s young for a dementia (e.g., semantic dementia) but is possible. Stroke is also a possibility but a remote one. Delirium is possible but due to the extended nature of Cleverbot’s symptoms, it is not likely. Right now schizophrenia is looking like the main rule-out diagnosis. I’ll see if I can rule it out in future conversations with Cleverbot.
As a footnote: Cleverbot is 23 years old and since 1997 when it was launched on the web, it has had over 65 million conversations. While the AI work is certainly impressive, it is inferior to human intelligence. Many of its language abilities are at best, those of a young child (ages 1-2); Cleverbot’s language abilities show the comprehension of an developmentally delayed adult with a severe neurological or psychiatric disorder. While there are numerous similar AI programs, they all have a long way to go before they resemble a human. This is even in light of Cleverbot supposedly passing the Turing Test for artificial intelligence and language.
I’m not belittling what has been done with Cleverbot and AI, it’s a complex area. Researchers and programmers simply have much room for improvement in understanding how to better mimic language. I do not believe it will happen until we have computers approaching the complexity and function of the human brain.

Parkinson’s Disease and the Brain

June 29th, 2011 No comments

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.

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Modems and White Matter

June 26th, 2011 No comments

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.

Donate to Brain Research

January 5th, 2011 No comments

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.

Categories: brain, brain damage Tags: , ,

Art of Neuroimaging

November 18th, 2010 No comments

Check out more images on my neuroimaging site.

Video Introduction to the Cingulum

September 15th, 2010 2 comments

I posted this on my neuroimaging blog and thought I should post it here too. This is a video I put together about the cingulum, a prominent white matter fiber track in the brain that is involved in emotion, attention, memory, among many other functions. All images except one from Gray’s Anatomy (the anatomy book, not the T.V. show) were created by me using some fairly advanced imaging techniques. If you are interested about some of the techniques, read my neuroimaging blog.

In Memory of H.M. – Live Video

December 3rd, 2009 No comments

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.

Categories: brain, hippocampus Tags: ,

The Relationship Between Executive Function and Processing Speed

July 15th, 2009 1 comment

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.

References

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.

What is Executive Function?

July 10th, 2009 5 comments

Executive function is a term that describes a wide range of cognitive behaviors and processes. It is broad enough of a term that some people simply describe it as, “what the frontal lobes do.” When asked what exactly the frontal lobes do do, some revert to the circular definition of “executive functions.” However, executive functions are distinct from – but related to – what the frontal lobes do. The frontal lobes are involved in motor functions (e.g., pre-motor and primary motor areas), eye movement (e.g., frontal eye fields), memory (e.g., acetylcholine-producing portions of the basal forebrain), and language (BA 44,45 or Broca’s area). In addition, some executive functions incorporate areas of the brain outside the frontal lobes – the parietal lobes or basal ganglia, for example. Like many cognitive domains, executive functions are part of a distributed network of brain structures and regions.

Most neuropsychologists however, would define (or at least accept the following definition of) executive function similar to this: Executive function is the ability to selectively attend to, work with, and plan for specific information. This means that executive function is deciding what information, cognitions, or stimuli are relevant, holding and working with that information, and then planning what to do with it. As such, executive function is largely the roles of planning and organization. It is also the ability to recognize and learn patterns (i.e., cognitive sets) but also have the cognitive flexibility to respond to set changes and make a shift in set. Executive function also involves being able to select the appropriate response or behavior while at the same time inhibiting inappropriate responses or behaviors.

Executive functions have been compared to the conductor of an orchestra who, in order to make sense of the disparate instruments, sounds, and parts, must coordinate the members and lead the efforts of all the components of the orchestra. Executive functions also have been compared to chief executive officers of companies. These comparisons demonstrate that executive functions are arguably the most complex and highest of all cognitive functions. However, just like most other cognitive functions, executive functions are comprised of relatively simple processes (e.g., attention and processing speed) – it is just the unique combination of these more basic processes that makes executive functions so powerful.

One potential problem with executive function as a cognitive domain is that it is large and loose. Many tests have been developed, or at least used, to assess executive function (e.g., Wisconsin Cart Sort Test, Stroop Color-Word Task, clock drawing, and so forth). Even though all such tests are used as measures of executive functioning, scores on them do not always correlate highly with each other. They do not always cluster together when subjected to principal components analysis or even structural equations modeling. This means that even though neuropsychologists have many purported tests of executive function, they all seem to measure different aspects of executive function. This might partially result from executive functioning tests being differentially affected by basic cognitive processes such as processing speed.

Even though, as previously mentioned, I do not believe executive functions and frontal lobe functions are synonymous terms, are we able to localize executive functions to the frontal lobes? Largely we can. The most evidence from neuroimaging studies and neurological injuries demonstrate that the prefrontal cortex – the area of the brain that is phylogenetically youngest and most advanced and as such, proportionately larger in humans than any animal – is necessary (but not necessarily sufficient) for executive functioning. When this area is disrupted in humans, they exhibit poor decision-making skills, including poor planning and poor maintenance or self-regulation of behavior. One area of the prefrontal cortex particularly involved in executive functions is the dorsolateral prefrontal cortex (area 46) – although both the orbitofrontal and anterior cingulate are involved in aspects of executive functions.

In 1986 Alexander, Delong, and Strick published their seminal work on five parallel and closed cortico-striato-thalamo-cortical loops. These frontal-subcortical circuits were hypothesized to be involved in a range of behaviors and cognitions based on the varying cortical connections of the loops. Previously, many researchers did not well-understand the role that the basal ganglia played in any sort of “higher” function; in fact, most viewed the basal ganglia as involved mainly in motor behaviors. Alexander, Delong, and Strick’s article set off a flurry of research into the functions of these frontal-subcortical circuits, which have been verified as existent in humans (Middleton & Strick, 2000). Over time different theories have modified these circuits, including that they are composed of direct, indirect, and hyperdirect pathways, which all function at different speeds or timings to allow the basal ganglia to regulate behavior. Mink (1996) proposed that actions (e.g., producing a specific word) are regulated by the direct and indirect pathways, which serve as large components of our ability to select and inhibit correct and incorrect responses, respectively. It is as if each individual fronto-cortical loop allows us to properly attend to the correct behavior or response and inhibit all other behaviors or responses, much like the DLPFC and orbitofrontal cortex and their associated loops are involved in the selection and inhibition of behavior, both major aspects of executive function.

Just as damage to the dorsolateral prefrontal cortex (DLPFC) produces deficits in executive function, damage to any part of the DLPFC loop also results in executive dysfunction. Benke, Delazer, Bartha, and Auer (2003) presented two clinical cases of patients with left caudate lesions (the lesions also affected part of the anterior limb of the internal capsule as well as portions of the putamen and pallidum; however, the infarcts affected the caudate the most). Among other deficits, both patients had executive function impairments, including problem-solving deficits, many perseverative errors, and set-shifting problems. Even though the patients had no direct DLPFC damage, they exhibited similar deficits to patients with DLPFC lesions. These executive deficits persisted over time.

As a cognitive domain, and even as broad as it might be, executive functioning has ecological validity. Price and colleagues (2008) found that executive dysfunction was related to greater difficulty performing IADLs. Specifically, patients with executive dysfunction had more difficulty performing IADLs than patients with memory deficits did. Thus, how quickly, flexibly, and accurately people can organize, solve, plan, or attend to specific neuropsychological tasks seems to correlate with their accomplishment of everyday tasks of life, such as finances, driving, and shopping.

References

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.

Middleton FA, & Strick PL. (2001). Basal ganglia output and cognition: evidence from anatomical, behavioral, and clinical studies. Brain Cogn., 42, 183-200.

Mink, J. W. (1996). The basal ganglia: Focused selection and inhibition of competing motor programs. Prog Neurobiol, 50, 381-425.

Price, C.C., Garvan, C., and Monk, T. (2008). Type and severity of cognitive impairment in older adults after non-cardiac surgery. Anesthesiology, 108, 8-17.