An Introduction to and Overview of the Brain

bi sang by seung ji baek

The human brain is a wondrous thing. It is the single most complex organ on the planet. It sits atop the spinal cord. Gazing upon the brain, one sees four main distinct areas – two roughly symmetrical hemispheres, a cerebellum stuck up underneath the posterior part of the brain, and a brainstem sticking out and down from the middle of the brain. Each cerebral hemisphere is divided into four visible lobes: frontal, temporal, parietal, and occipital. The frontal lobes jut out at nearly a 90 degree angle from the spinal cord and are the largest part of the human brain. The temporal lobes stick out the sides of the brain, like thumbs pointing forward at the side of a fist. The parietal lobes are harder to distinguish. They are just posterior to the frontal lobes and dorsal to (above) the temporal lobes. The occipital lobes are at the very back of the brain, like a caboose on a train.

The outside of the brain is covered with a series of bumps and grooves. The bumps are called gyri (sing. gyrus) whereas the grooves are called sulci (sing. sulcus). This outside part of the brain is filled with tiny cell bodies of neurons, the main functional cell of the brain. Some people estimate that there are 100 billion neurons in the central nervous system (brain + spinal cord). This outer layer of the brain is called the cortex (which means “bark”). The cortex is only about 5mm thick, or about the thickness of a stack of 50 sheets of copy paper, yet it is responsible for much of the processing of information in the brain.

At room temperature the brain is the consistency of warm cream cheese. If removed from the skull and placed on a table, it would flatten and widen out a bit, like jello that is warming up. The brain is encased in a series of protective sheaths called meninges. The outermost encasing is called the dura mater (L. “tough mother”), which is thick and tough and is attached to the skull. The next layer in is softer. It is called the arachnoid layer; it adheres to the brain. Just underneath this layer is where cerebrospinal fluid (CSF) flows. This fluid is produced in holes in the middle of the brain called ventricles. CSF helps cushion the brain as well as remove waste products from the brain. Underneath this is a very thin and fine layer called the pia mater (L. “soft mother”), which adheres directly to the cortex and is difficult or impossible to remove without damaging the cortex. These three layers of meninges serve to protect the brain.

The brain can be roughly split into three functional areas, each one more “advanced” than the previous. The brainstem (and midbrain), which includes such structures as the medulla, pons, and thalamus, activates and regulates the general arousal of the cortex. Damage to the brainstem often results in coma or death. The next rough functional area is the posterior portion of the brain (parietal and occipital lobes and portions of the temporal lobes). This area is heavily involved in sensory processing – touch, vision, hearing. It sends information to other parts of the brain largely through the midbrain structures. The last functional area includes the frontal lobes. This area can regulate all other parts of the brain but is essential for goal-setting, behavior inhibition, motor movements, and language. The frontal lobes are the most advanced area of the brain and arguably the most important for human functioning – for what makes us human. In summary the three areas roughly are responsible for:

  1. Overall arousal and regulation
  2. Sensory input
  3. Output, control, and planning

Underneath the cortex is a large area of the brain that looks white. This area is comprised of the axons of the neurons of the cortex and subcortical structures. These axons are the pathways between neurons – like superhighways connecting cities. The axons look white because the majority are covered with a fatty tissue called myelin. Myelin helps axons work more efficiently and transmit more quickly. The white matter of the brain is as important for normal brain functioning as the gray (neurons) matter is.

The brain is energy-hungry. It cannot store energy so it needs a constant supply of nutrients from blood. However, blood can be toxic* to neurons so the brain has to protect itself from the blood and other toxic materials through what is called the blood-brain barrier. This barrier keeps blood cells out of the brain but allows molecules of nutrients (e.g., glucose) to pass into or feed the cells. The entire surface of the brain is covered with blood vessels, with many smaller vessels penetrating deep into the brain to feed the subcortical structures. Deoxygenated blood must be removed from the brain. Veins take the blood out of the brain and drain into venous sinuses, which are part of the dura matter.

The brain works as a whole to help us sense, perceive, interact with, and understand our world around us. It is beautiful in its form and function.

*”Today, we accept the view that the BBB limits the entry of plasma components, red blood cells, and leukocytes into the brain. If they cross the BBB due to an ischemic injury, intracerebral hemorrhage, trauma, neurodegenerative process, inflammation, or vascular disorder, this typically generates neurotoxic products that can compromise synaptic and neuronal functions (Zlokovic, 2005Hawkins and Davis, 2005 and Abbott et al., 2006).” From Zlokovic, B. V. (2008). The blood-brain barrier in health and chronic neurodegenerative disorders. Neuron57(2), 178-201.

Image: Bi Sang by Seung Ji Baek

Brodmann’s Map of the Cortex

I’ll be writing some basic neuroanatomy posts over the coming months (I started with my previous post about the corticospinal tract). I recently finished an intense neuroanatomy course where I learned how much I love basic neuroanatomy. It’s exciting to look at a brain or brain slices and try to figure out what and where different structures are.

In the early 1900s Korbinian Brodmann studied the cytoarchitecture (organization of the cortical layers of neurons) of human and non-human brains. His work was painstaking and thorough. He created a topographic map of the cortex containing 52 (50 in humans) different areas. In my class we were not required to learn all of Brodmann’s cortical areas but had to learn some of the major ones. Brodmann’s Areas (BA) 3,1, and 2 compose the primary somatosensory area of the brain. BA 4 is the primary motor cortex. BA 5 is somatosensory association cortex just posterior to BA 3,1,2. BA 6 is pre-motor cortex, which connects directly to BA 4. BA 7 is more somatosensory association cortex that lies just posterior to BA 5. BA 8 is the frontal eye fields, which among other things is responsible for initiating horizontal eye saccades (i.e., quick movement to the left or right). BA 17 is the primary visual cortex, a credit card sized area that lies both dorsal and ventral to the calcarine fissure in the occipital lobe. This area processes most of the basic visual information. BAs 18 and 19 are visual association cortices. BA 22 is Wernicke’s Area, which is involved in the comprehension of language and is in the dorsal-posterior temporal lobe on the border between the temporal and parietal lobes. BAs 41 and 42 are the primary auditory cortex, which processes auditory information from the cochlea; this lies on the transverse temporal gyrus in the dorsal part of the temporal lobes (it is hidden from view unless the cortex around the Sylvian Fissure is pulled away). BAs 44 & 45 are Broca’s area, which is involved in the production of language and is in the lateral frontal lobes.

The Corticospinal Tract

The corticospinal tract is a descending motor pathway originating in the Primary Motor Cortex (Brodmann’s area 4) and terminating at various levels in the ventral horn of the spinal cord. The corticospinal tract descends through the posterior limb of the internal capsule then down through the cerebral peduncles into the brainstem. In the brainstem the corticospinal tract remains in the ventral portion, passing through the pyramids on its way down. In the caudal brainstem (just above where the spinal cord starts) 90% of the the corticospinal tract decussates (crosses) to the contralateral (opposite) side and continues down through the dorsolateral spinal cord. This portion controls limb movements. The remaining 10% remains in the ventral spinal cord and is largely responsible for bilateral axial (trunk) movement. From the dorsolateral spinal cord, the axon (that started in the cortex) enters the ventral horn of the spinal cord at the appropriate level (e.g., cervical for arms or lumbar for legs) then exits through the ventral root to terminate on the appropriate muscles.

Through this tract, the cortex controls much of the movement of the body; as such, it’s vitally important for our functioning. Damage to the tract results in an upper motor neuron disorder, with paresis (weakness instead of complete paralysis) and the Babinski reflex fairly common symptoms. Soon after damage, a patient might have flaccid paralysis though with little to no movement of the affected limb(s). As the body starts to recover slightly, spastic paralysis usually sets in with jerky, often uncontrolled limb movements. The corticospinal tract is one of the largest pathways in the central nervous system; it’s one of the most important for motor functioning as well.

Another anatomy site

I found a nice but very basic anatomy site (i.e., good for kids). It also has more anatomy than just the brain, with skeletal, heart, and digestive tract anatomy in English and Spanish.

Click on the image to visit the site.
Brain Site

Great Skull Anatomy Site

I stumbled across this wonderful anatomy site that focuses on the skull. You can move your mouse over different parts of the skull to highlight their names. You can also mouse over a structure and have the area of the skull highlighted. This is a wonderful study guide if you have to know the parts of the skull.

clipped from

Split-belt Treadmill as Therapy for Brain-injured Patients

CNN has an interesting article about a split-belt treadmill that is being used for stroke survivors and other people with brain injuries.

Story here

The treadmill’s two belts can move independently and even in opposite directions. Doctors and researchers are trying to find any underlying intact neural circuitry by providing unique motor challenges to brain injury patients.

The 3D brain

Technology Review has an interesting article about “new” 3D brain imaging software being developed at Thomas Jefferson University Hospital in Philadelphia, PA (I put “new” in quotation marks because there are other similar programs out there; they might not be as polished but some are even open source). Their software fuses MRI, fMRI, and DTI together to create a fairly comprehensive view of the brain: “The fusion of these different images produces a 3-D display that surgeons can manipulate: they can navigate through the images at different orientations, virtually slice the brain in different sections, and zoom in on specific sections.”

The software looks like it is aimed more at neurosurgeons than researchers (i.e., it probably isn’t free like a lot of MRI image processing software). It does produce amazing images (view the images here) and looks like it could be a very useful tool for at least a qualitative approach to brain imaging.

DTI fibers near a tumor

The software is focused a lot on DTI (diffusion tensor imaging) and how the white matter fibers in the brain interact with lesions or tumors. I think that one researcher’s word of caution is important:

“Bruce Fischl, an assistant in neuroscience at Massachusetts General Hospital, says that the idea is ‘interesting’ but cautions that there are a number of levels of ambiguity when talking about connectivity in imaging. ‘Just because you live next to the Mass Pike doesn’t mean that there is an exit,’ he says.”

In other words, don’t get too caught up in the fact that fibers are right by a tumor, they may not really have anything to do with the part of the brain the tumor is most affecting.

In any case, I think that the idea behind this software is amazing. The graphics renderings are impressive (but they are just the pretty pictures – the rendering details may be beneficial in clinical surgery settings but they are not particularly useful in research situations, other than producing nice pictures to go in your publication). This software is very similar to something that I envisioned using a few years ago and I’m glad to see it being developed.

Image credit: Song Lai, Thomas Jefferson University Hospital (borrowed via

Alternate assumptions to naturalism in neuroscience

Thinking ManThis post is very different than anything I’ve previously written; it’s more philosophical than psychological and is an example of Theoretical and Philosophical Psychology, a small but important niche within psychology that provides critical analyses of the underlying assumptions [philosophies] of psychology and the related sciences. My post is not meant to attack the neurosciences (after all, that is my field of specialization); rather, it is meant to expose the philosophical underpinnings of neuroscience. The alternative assumptions I write about are not necessarily superior, just different. Feel free to contact me with any questions or if you are interested in the references I cite.

This post is an exposition of the naturalistic assumptions in the article An fMRI Study of Personality Influences on Brain Reactivity to Emotional Stimuli by Canli et al. (2001). It will also focus on alternative assumptions. I will first explore the assumption of materialism, one half of Descartes’ dualism, and contrast this assumption with a holistic monism. Then I will discuss biological determinism as well as an alternative assumption to it, namely agency.

Materialism accounts for one half of the Cartesian dualism (and thus has been termed a one-sided dualism), the theorized split between mind and matter. It is defined as the notion that “biological explanations will (eventually) be able to fully account for and explain…psychological phenomena” (Hedges, p. 3). Materialism assumes that biology is sufficient to explain behavior. This article is focused on “the neural correlates of emotion [and personality] in healthy people” (p. 33) by using brain imaging techniques. This is an example of materialism in that the authors are looking for “the biological basis [or an objective foundation] of emotion [a subjective phenomenon]” (p. 33). The authors’ assumption of materialism will become clearer with another example. Canli et al. state: “The similarity in the dimensional structure of personality and emotion is due to a common neural substrate where personality traits moderate the processing of emotional stimuli” (p. 33; italics added). What they are saying is that neurons (the brain) are the base and that emotional processing in the brain is affected by personality traits (which they state have a “common neural substrate” with emotions). This is a one-sided dualism—the researchers attempt to explain the subjective experiences of the mind (i.e., emotion) in terms of the material, or biological, body while not including the mind in their methods.

The authors of this study sought to understand emotional responses in terms of neuroimaging. This is an example of method-driven science in that the researchers “ignored…[the] notion of the mind [being immaterial and unpredictable] and focused…on the body” (Slife, p. 13). There is no way to image emotions directly, but by assuming that they are centered in biological reactions, these researchers were able to use traditional scientific methods to measure those reactions. This materialism, or one-sided dualism, has its shortcomings. An alternative way to approach the hypothesis of how personality serves as a “middleman” between the brain and emotions is to use the assumption of a holistic monism. Whereas the authors assume that the brain (body) is the foundation of emotional experience and thus sufficient for that experience, with a monistic assumption the researchers would recognize both body and mind as necessary but not separately sufficient. This would change their study because they would look at a more inclusive picture of people, not just biology and mind but context as well. All of these conditions interact and are only understood in relation to one another. The authors would also consider qualitative measures of life experience and meaning and research those, taking a pluralistic approach.

Another prevalent assumption, which is inseparable from materialism and is in fact a subset of it, is that of biological determinism. Whereas my materialism section focused on the authors’ attempts to explain subjective experiences by their “objective” methods, this one will focus on how they explain varying emotions as caused by variations in biological factors. The authors end their paper on a strong deterministic note: “The different brain activation patterns that these pictures produce…may result in two different subjective interpretations of the identical objective experience” (p. 39). Although they hedge their statement with a may, what they are saying is that their subjects all had the same “objective experience” but because of apparent differences in how their brains responded, this difference caused the variation in subjective emotional interpretation. They imply that people’s interpretations are determined by biology, which rules out agency.

Alternately, when viewing this article according to holistic monism, specifically agency, there are would be many changes in it. First off, it would not be a problem to recognize the role agency plays in the body. The authors would assume that the body affects agency and vice versa–they constitute each other. Instead of “different brain activation patterns” (p. 39) causing different interpretations of emotion it could be that the interpretations affect the neuronal firing instead (or an interplay of both). Also, with an alternative assumption, the following hypothesis would no longer be deterministic: “Extraversion is associated with greater brain reactivity to positive” (p. 34). The authors imply that personality traits are biologically based (see paragraph 2 of this paper)–even if behaviorally influenced; therefore, biology causes personality which causes changes in brain reaction (which are experienced subjectively by people as emotions). Alternatively, this can be explained by “agentic factors” (Slife, p. 25), such as people choosing (even unconsciously) how to respond to the pictures. Also, instead of personality being determined by the brain, manifestations of agency (choices) in a context (e.g., experiences) could shape personality.

Hippocampal Volume Loss and Major Depression

Mood disorders range from major depressive disorders to major manic episodes. These disorders are both unipolar and bipolar. One main area of mood disorder research is that of unipolar major depression. Major depression can last just one episode or it can be a disorder, which can last for years with multiple depressive episodes over this extended period. The psychological aspects of depression are well understood but the biological foundations are less understood. As some evidence of this, the DSM-IV manual does not include any neurological information concerning major depression. In this handbook, depression is treated purely as a mental condition without an explanation of the biological aspects of the disorder. On the other hand, there are many psychopharmaceuticals prescribed to people with depression, which suggests that there is more than a cursory acknowledgment of the biological basis of this mental illness. However, this biological focus is mainly a focus on neurotransmitters and not anatomy. Recently, there have been numerous studies conducted to investigate the relationship between brain structure and depression (see Videbech & Ravnkilde, 2004). One of the structures most often studied in connection with depression is the hippocampus, which is a key structure for memory. The purpose of this paper is to investigate whether the hippocampus specifically is negatively impacted in depressed patients.

Frodl et al. (2002) investigated hippocampal changes in patients with first episode major depression. The authors had 30 adult depressed subjects (mean age = 40.3) and 30 matched controls (mean age = 40.6). The mean time of the depressive episode for the depression group was 0.71 years. The researchers collected MR images for all subjects. They compared the hippocampal volumes of the depressed group with the control group with ANCOVAs. Depressed men had significantly smaller left hippocampal volume than did healthy male subjects but right hippocampal volume was not significantly different. Female depressed subjects had significantly larger right hippocampal volume than did their matched controls and left volume did not differ, which implicates differing effects of depression on men and women. There was a significant left-right hippocampal volume disparity in the depressed patients but there was not one in the healthy subjects. Overall, the difference in hippocampal volume was not significant between the depressed and control groups though. There was also no significant correlation between age and hippocampal volume for either group but this finding goes against that of other research (Frodl et al.). On the other hand, between groups there was a significant reduction of hippocampal white matter volume. In other words, both male and female depressed patients had on average a reduction in the hippocampal white matter compared to the control subjects.

The authors concluded that there are likely physiologic gender differences in how males and females react to stress, which would explain why depressed males had smaller hippocampal volume and females did not. They believe this may be an example of the protective effects of estrogen against stress seen in other studies. In any case, there was a tendency for both depressed males and females to have significant left-right hippocampal asymmetry and reduced white matter. They concluded that this represents the beginning of left hippocampus volume loss and disrupted axonal transmission, respectively. The researchers could not conclude, however, that depression caused the volume loss. It may be that the loss came in response to stress or some other factor, which in turn predisposed the depressed subjects to major depression. Alternatively, the depression could have been the catalyst for the reduction (Frodl et al., 2002). Further longitudinal research is needed to uncover the causal relationship between depression and hippocampal volume.

Continue reading “Hippocampal Volume Loss and Major Depression”

Dopamine, the Basal Ganglia, and Learning

A significant proportion of dopamine (DA) is produced in the substantia nigra pars compacta (SNpc) and is carried to the striatum via the nigrostriatal pathway. While this pathway has been traditionally linked with motor functioning, recent research has implicated striatal DA involvement in language (Crosson, 2003) and learning (Seger, 2006). One disease in which there is considerable DA disruption is Huntington’s Disease (HD). In HD the head of the caudate is typically the first brain structure affected by neuronal cell loss. This cell loss not only affects connections with the SNpc but also affects the connections between the striatum and the prefrontal cortex. In HD the disruption of these dopaminergic pathways leads to disruptions in motor and cognitive functioning.

How DA disruptions affect cognition has been explained by theories that are modifications of Mink’s model (1996) of center and surround (i.e., direct and indirect) basal ganglia regulation. Within the caudate there are two main families of DA receptors – D1 and D2. These receptors have been shown to have different functioning within the basal ganglia (Seger, 2006) – the D1 receptor is involved with the direct pathway and the D2 receptor is involved in the indirect pathway. The D1, or direct pathway, can be viewed as increasing the strength of the signal of the desired response while the D2, or indirect pathway, serves to reduce the noise of the competing undesired responses. Dopaminergic systemic disruption in HD should thus decrease the signal-to-noise ratio, which results in the person having a greater difficulty selecting the desired response (see model below).

Center-surround model of basal ganglia-based learning and memory

*Model based on Mink (1996) and Frank, Seeberger, and O’Reilly (2004)

There is evidence that in early stages of Huntington’s disease, D2 receptors are the first to be affected, with less binding occurring at D2 receptors presumably due to receptor loss. As the disease progresses, the D1 receptors also start to become depleted, with the end result of widespread DA dysfunction (Glass, Dragunow, & Faull, 2000). This DA dysfunction possibly affects verbal learning and recall by impacting the indirect pathway in the early stages of HD and indiscriminately the whole direct and indirect system in later stages of the disease process.


Crosson (2003). Left and right basal ganglia and frontal activity during language generation: Contributions to lexical, semantic, and phonological processes. Journal of the International Neuropsychological Society, 9, 1061-1077.

Frank, M. J., Seeberger, L. C., & O’Reilly, R. C. (2004). By carrot or by stick: Cognitive reinforcement learning in Parkinsonism. Science, 306, 1940-1943.

Glass, M., Dragunow, M., & Faull, R. L. M. (2000). The pattern of neurodegeneration in Huntington’s disease: A comparative study of cannabinoid, dopamine, adenosine and GABAA receptor alterations in the human basal ganglia in Huntington’s disease. Neuroscience, 97(3), 505-19.

Seger, C. A. (2006). The basal ganglia in human learning. Neuroscientist, 12(4), 285-290.