Perusing Psychology

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.

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.

Parkinson’s disease (PD) affects an estimated 1.5 million Americans and about 2% of people over 65 in the U.K. Its prevalence increases with age, although roughly 15% of Americans with Parkinson’s disease are 50 or younger. Parkinson’s disease is part of a broader spectrum of disorders known as parkinsonism. While it was viewed as fairly homogeneous in the past, researchers and clinicians now recognize the complexity of the disease and its related diseases.

The defining neurological marker of Parkinson’s disease is the destruction of the substantia nigra pars compacta, a small nucleus in the brain that is one of the major dopamine-producing brain areas. Symptoms of PD are not evident until around 80% of the neurons in the substantia nigra (literally translated as “black substance”) are destroyed. Because the substantia nigra produces dopamine, which is an important neurotransmitter, the depletion of dopamine in the brain that is associated with PD affects the striatum, which in part suppresses the subthalamic nucleus. This in turn results in more activity in the globus pallidus and substantia nigra pars reticulata, which in the end leads to more activation of the inhibitory thalamic nuclei that are involved in motor functioning. To summarize, decreased dopamine results in decreased motor activation as well as other motor problems.

The common features of Parkinson’s disease are easily remembered by the mnemonic TRAP.

1. T – Tremor, specifically resting tremor. Tremor that occurs when moving (e.g., reaching for an object) is called essential tremor and is not a defining characteristic of PD; in fact, it is a different but related disorder.
2. R – Rigidity. Difficulty moving and stiff arms and limbs.
3. A – Akinesia. No or slow movements.
4. P – Postural instability. Posture problems.

Gait abnormalities is also one of the common features of PD. It is especially useful for detecting the disease early in the process. The common gait problems are decrease height and length of step and less arm swing (i.e., walking more with a shuffle than a normal gait). People with PD also often take very small steps when turning around.

PD patients often have difficulty swallowing saliva so they often drool. They also often have micrography (very small writing) that progressively gets smaller with prolonged writing. Depression is common in PD patients as well. If given levodopa (L-dopa) they will respond. Symptoms of dementia often occur as well but they usually occur after a few years post diagnosis. However, there are often more mild cognitive changes early on in the disease process, such as slowed processing speed and slowed reaction time.

Reference

Approach to diagnosis of Parkinson disease (C. Frank, G. Pari, & J. P. Rossiter, 2006). Canadian Family Physician, 52, 862-868.