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Intelligence and Neurological Conditions

April 29th, 2013 No comments

Intelligence is an interesting concept. We have tests that measure what we call intelligence but such tests are limited and culture-centric (not that that is necessarily a negative thing). However, for the sake of discussion I will operationally define aptitude (i.e., intelligence) as Intelligence Quotient so as to have a standard metric as foundation for this post.

I spend time assessing people’s memory and thinking abilities. I almost always try to get some measure of baseline aptitude either by estimating it (e.g., years of education, vocabulary knowledge, word reading ability) or by formally measuring via an intelligence test. Granted, this has limitations but it allows me to estimate how well an individual’s brain should function across multiple domains of thinking (e.g., problem-solving, reasoning, memory, language, and so forth). In other words, the higher a person’s general aptitude (abilities), the better he generally will do across most cognitive domains barring brain insult. This is certainly not a rule codified in stone and in triplicate but it serves as a rubric to follow.

Intelligence as measured by IQ is generally quite stable across the lifespan but can improve modestly with  diligence in informal or formal education. Intelligence as denoted by IQ can also decrease modestly if people are intellectually inactive, although such declines are slight. What can happen though is as brains age or if damaged by a pathological process or an injury, components of IQ can decrease. My primary clinical and research focus is in understanding how brains and cognition change in old age – both naturally and in the presence of neurological (brain) insult. Remarkably, the measures we use for intelligence tend to be rather insensitive to aging and even neurological insult, at least some of the components of intelligence are generally insensitive to brain insult. However, this leads to one area where our conceptualization of intelligence as IQ starts to break down.

As they age, the brains of people almost universally slow down. Wear and tear on the brain over decades of life affects how well and quickly we can think. Blood, which is essential for life and for the functioning of the brain, happens to be toxic to brain cells. Sometimes the protections in the brain that keep blood far enough from brain cells (neurons) to protect them but near enough to feed and maintain brain cells start to break down over time. This can injure the brain and start to reduce how well the brain works, even lowering IQ. Now, does that mean that a person’s intelligence decreases? If IQ = intelligence, then yes, it does. Contrary to how I operationalized intelligence earlier, intelligence is not synonymous with IQ. IQ can be a useful concept but it is far from perfect, particularly if by using it one argues that someone is less intelligent simply because his head was injured in an accident or because she developed dementia or suffered a stroke.

This is an area that demonstrates the limitations of our current research and clinical conceptualizations of intelligence. However, understanding how IQ changes over time and how it is affected by neurological conditions is important information to have, as it can help localize areas of pathology.

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.

Aphasia Syndromes

February 17th, 2009 No comments

Aphasia is an acquired disorder of language. It can manifest in various ways, including difficulty speaking or difficulty understanding speech or language. Stroke is the most common cause of aphasia with up to 40% of stroke patients experiencing some sort of aphasia. Depending on the nature of the injury (e.g., stroke, tumor, trauma), aphaisa can be temporary or permanent. Even in cases of severe stroke, some types and aspects of aphasia are treatable, with language improving over time. While language does not usually return to pre-morbid functional levels, many people with aphasia benefit greatly from speech therapy.

The following videos demonstrate two different types of aphasia – Broca’s aphasia (or non-fluent) and Wernicke’s aphasia (or fluent). Notice the differences between the aphasias.

Here is a patient with Broca’s aphasia.

Here is a patient with Wernicke’s aphasia.

PBS Frontline Explores Parkinson’s Disease

February 7th, 2009 2 comments

Here is the video PBS recently made about Parkinson’s disease called My Father, My Brother, and Me. From what I’ve watched so far, it’s done a good job putting a face to Parkinson’s disease while also focusing on the research and clinical aspects of it.

Patient HM’s Passing

December 4th, 2008 No comments

On Tuesday, December 2, 2008, Henry M., the most famous patient in modern neuroscience research and literature, passed away. He was 82. In 1953, H.M. had an experimental brain operation to try to stop his frequent seizures; his medial temporal lobes were resected bilaterally, with significant portions of his amygdalas and hippocampi in both cerebral hemispheres removed (parts of the brain are still resected in intractable epilepsy cases, however neurosurgeons do not perform that exact surgery any more because of the negative effects). His seizures stopped but immediately after the operation he had a severe anterograde amnesia. This means that from when he received the operation at age 27, he was unable to establish new memories for world events and for general information.

His amnesia became the focus of much scientific study from after his operation until the present. No one patient has been studied more in the 20th and 21st centuries than H.M. His memory impairment was also interesting because his overall intellectual abilities were still intact as was his personality. Neuropsychologists and neuroscientists will forever be grateful for the things they learned from H.M.

The New York Times has a very nice article about H.M.

Revisiting Clive

November 20th, 2008 No comments

Yesterday I posted a video clip about Clive Wearing. Here is the first part of a different documentary about Clive. This video goes more in-depth about his condition. Clive is sometimes referred to as the man with the shortest memory. Not only were his two hippocampi destroyed, but also surrounding areas of the his temporal lobes as well as portions of his left frontal lobe. He also remembers very little from before his illness, which is quite rare; this condition is called retrograde amnesia. Clive lives in an ever-present now, without connection to past or future. Other parts to this video can be found on YouTube.

The Unusual Case of Clive Wearing

November 19th, 2008 No comments

Clive Wearing is a 70 year old British man who contracted herpes simplex encephalitis in 1985. The virus destroyed his hippocampi bilaterally (as well as surrounding areas). He has complete anterograde amnesia and can only remember up to about 20 seconds. He retained the ability to play the piano and conduct a choir (which he did previously to his illness); this is because this procedural memory involves different areas of the brain, including the basal ganglia and the cerebellum. I’ll revisit this case over the coming days. Meanwhile, here is a clip from a BBC production that presents part of Clive’s story.

Epilepsy – Social and Cognitive Considerations

September 6th, 2008 No comments

A few days ago I wrote another post for Brain Blogger about some of the issues people who have been diagnosed with epilepsy face.

Sen. Kennedy’s Brain Tumor

May 22nd, 2008 1 comment

Sen. Ted Kennedy, one of the last of the siblings of JFK and Bobby who is alive recently was diagnosed with a malignant brain tumor in his left parietal lobe. His first symptom was a seizure. As soon as I heard that he had had a seizure I started wondering about a tumor. There aren’t too many reasons someone would have a seizure out of the blue at the age Sen. Kennedy is. Too much stress possibly could cause a seizure as could an adverse reaction to certain medications but those are not likely. Children often can have a seizure at random with no other symptoms or no specific underlying problems but it’s very rare for older adults to experience seizures without very specific reasons, such as a brain tumor (it’s very common to have seizures if you have a brain tumor).

Sen. Kennedy’s tumor, as stated earlier, is in his left parietal lobe. Depending on its specific location and size, the tumor could disrupt his ability to comprehend language (if it disrupts Wernicke’s Area). It could also affect his ability to integrate visual and motor information as well as affect his motor or sensory functioning on his right half of his body. All of those symptoms are speculative without neurological testing, of course, but the parietal lobes are involved in a number of functions, including sensory and cognitive integrative functions.

The good news is that this form of cancer – a glioma – does not spread to other parts of the body (although it could continue to grow in the brain). It is also treatable by resection and chemotherapy. Chemotherapy is far from an enjoyable process (it’s a treatment that practically kills people) but it can be very successful. While Sen. Kennedy’s prognosis is uncertain he could survive the cancer with relatively few lasting effects. I don’t think anyone can survive brain surgery and chemotherapy without at least some lasting cognitive deficits (although the deficits might be very hard to detect) but the outcome of gliomas is not always grim.