Intelligence and Neurological Conditions

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.

Frontotemporal Dementias

The New York Times has a very nice article about Frontotemporal demetia (FTD). This type of dementia is interesting, affecting personality, inhibition, attention, and language. It is similar to Alzheimer’s Disease but has a different progression and manifestation. Anyway, the article provides a nice picture of the disease.

Recent alcohol research


There was an interesting recent news story from Reuters. Researchers at the University of Missouri-Columbia found that, “Young adults who binge drink frequently are more likely to show disadvantageous decision-making patterns than their peers who don’t drink as heavily” (from the news article). You can’t assume that just because drinking and poor decision making are correlated that the drinking causes the poor decisions (because people who are poorer at decision making in general may drink more) but as I like to say, “Correlation does not imply causation but neither does does it deny causation.”

On the other hand, there is some evidence that drinking alcohol might slow down the progression and/or onset of dementia (e.g., Alzheimer’s Disease): Alcohol and dementia article. Again, the study is correlational so firm causations should not be inferred.

These two articles demonstrate that there is still a lot of  uncertainty about the long-term effects of alcohol consumption.

Anosognosia and Dementia

Anosognosia is a word that means unawareness of functional deficit. It is a common condition in people with Alzheimer’s Disease (AD) – they are not fully aware of their deficits. We can’t state that people with AD never have awareness of their deficits because there is a fair amount of evidence that in the earlier stages of AD there is at least some awareness of memory problems and slowed cognition. The relative anosognosia in AD patients can be contrasted with Parkinson’s patients who are all too aware of their deficits. Theirs is mainly a motoric disorder, which is brought about by neuronal death in the substantia nigra, an area of the brain that produces dopamine (a neurotransmitter). The resting tremors and slowed movements can been extremely frustrating to people with Parkinson’s disease because they are completely aware of their problems.

On Alzheimer’s Disease and other dementias

There are two general classes of dementias: cortical and subcortical. A cortical dementia is one like Alzheimer’s Disease (AD) where the outer layer (the “bark”) of the brain is first affected. AD typically affects the ventromedial frontal and dorsomedial temporal lobes first. The medial portions of the temporal lobes (e.g., hippocampus and parahippocampal gyrus) are heavily involved in memory processes. So typically with AD we first see atrophy (or volume loss) in those regions; the gray matter (bodies of neurons) die off and the brain shrinks. We are still not entirely sure what causes AD – we know genetics plays a part as do environmental factors such as exercise, nutrition, and education but we don’t know the specific pathology of the disease. AD also is related to swelling to some degree; so an adult who is approaching old age can likely reduce the chances of getting AD simply by taking a “baby aspirin” daily. At the very least it will likely delay the onset and slow down the progression of the disease.

There are also subcortical dementias. These can occur as a result of stroke, Huntington’s disease, or Parkinson’s disease. These types of dementias can occur and worsen rapidly (in the case of strokes) or can be fairly mild initially (as in Parkinson’s-type dementias). Subcortical dementias will over time and in the latest stages of the disease become indistinguishable from AD. Another type of subcortical dementia is Dementia with Lewy Bodies (DLB, or Lewy-body dementia). This is a disease that appears to combine aspects of Parkinson’s, Alzheimer’s, and schizophrenia. People with DLB often have vivid visual hallucinations and other psychoses. It is a terrible disease for the person with it as well as caretakers and family.