Sen. Kennedy’s Brain Tumor

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.

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.

Frontal Lobes and Memory

I’ve been developing an interest in the role that the frontal lobes play in memory. We traditionally think of memory as heavily based in the medial temporal lobes. At least, the medial temporal lobes are larely responsible for the creation of new memories. Without the hippocampus and the surrounding area people have anterograde amnesia, which is the inability to form new memories. The classic and most well known example of this is the patient H.M. Researchers recognize the role that other areas of the brain have in memory but most memory research has focused on the medial temporal lobes – at least until recently (with recently being the last 20 years or so). New ideas take a while to develop and gain acceptance so some of these ideas about the role of other brain areas in memory creation are still developing.Man's Brain

For example, we now know that when information needs to be organized, such as in something like the Rey-Osterrieth Complex Figure (read here for a short description of the test) or with a list learning task with words from specific semantic categories, the frontal lobes are involved.

If the frontal lobes are heavily involved in the organization of information it follows that memory tests that require more organization of material should be affected by dysfunctioning of the frontal lobes. Some researchers are now trying to place certain functions with greater specificity within the frontal lobes. This isn’t really phrenology because the methods of phrenology were entirely suspect. Phrenologists extrapolated personality and cognitive characteristics of people based of measurements of their skulls. Many researchers who are interested in localizing brain functions do so by testing people with specific brain

lesions (injuries). If enough patients have damage to X part of the brain and subsequently have Y deficits, then we can assume that X is necessary for Y to occur (but is not necessarily sufficient for Y to occur). Phrenologists never looked at the brain or the head in this manner. Paul Broca was one of the first, with his patient Tan, to systematically look at the relationship between brain injury and behavior.

For a long time many people believed (and many still do) that certain areas of the frontal lobes, specifically the most anterior areas of the frontal lobes, are essentially superfluous. They base this idea on cases where

people have had damage to this area of the brain but apparently suffered no ill effects. Research has consistently not supported that view. We don’t have any non-necessary brain. What we do have are tests and measures that are not sufficiently sensitive nor specific. The brain is also very complex and most functions rely on networks of brain structures. We are also learning that the white matter in the brain is very involved in behavior and cognition (this is my own area of research). The more we learn, the more we realize our ignorance about the brain. There are layers upon layers to be unwrapped and understood about the brain.

Image by Debbi in California.

Leukoaraiosis and Lacunes – A Very Brief Overview

As people age, it is common for their brain white matter to change. These changes often appear as bright white spots on T2-weighted MR scans. These areas or spots of hyperintensity (i.e., white matter hyperintensities {WMH}) are also called leukoaraiosis (LA). Researchers are still investigating the exact nature and pathology of these abnormalities but our understanding of them is increasing. They most often seem to start around the lateral ventricles and spread from there, although it is possible to have punctate WMH throughout the brain white matter (i.e., WMH that are not connected to other regions). WMH on brain MRIs represent rarefaction of the white matter, including swelling, demyelination, and damage, although the exact nature and combination of the white matter changes is not known. These WMH can interfere with normal cognitive functioning, including processing speed, attention, inhibition, as well as global executive functioning (although these claims are still being investigated).

Other damage to white matter includes lacunes, which are little holes in the brain, much like the holes in Swiss cheese. They are caused by mini infarcts, or strokes, or other processes. Most of the time they are due to “silent strokes”, or strokes that are small enough that the person does not have any noticeable stroke symptoms. These lacunes can have similar impact on cognition as WMH. Both WMH and lacunes are related to vascular risk factors, such as hyper- or hypo-tension, diabetes, etc.

Symptoms of Parkinson’s Disease

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.


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

Hypothalamic Hamartomas

I saw an interesting case today. It was a child with a hypothalamic hamartoma, a tumor (likely present from birth or shortly thereafter) right on the midline of the brain by the hypothalamus and the third ventricle. These tumors are quite rare and result in some interesting behaviors. A common result of these hamartomas is what is called precocious puberty – very early puberty onset; this early puberty often occurs before age 2. This can occur because the hypothalamus is one of the major brain areas that creates hormones and modulates the endocrine system.

Another common result of these hamartomas is gelastic seizures. Gelastic seizures are laughing seizures. The seizure manifests with the child (or adult) having sudden laughing fits for no apparent reason. They can occur many times a day. Some people also have dacrystic seizures, or crying seizures. Developmental delays are also common in this type of brain disorder as is hyperactive behavior.

Hypothalamic hamartomas are sometimes treatable by resection. This surgery has the possibility of eliminating the seizures and stopping most or all of the hormonal abnormalities.

Dealing with TBIs from the Iraq War

I read a good article on CNN that details some of the problems that veterans and health professionals face when dealing with TBIs acquired during military action. The article provides a good perspective of the “human side” of TBI.

Link to the story

I’ve posted about this topic before but felt that we should revisit it because so many veterans are affected by TBIs (as well as mental health issues). I don’t know the exact number of veterans affected by TBIs but studies have shown that >30% of soldiers and Marines have some sort of psychological issue related to their service in Iraq and/or Afghanistan. The military and the government are realizing how salient this problem is and will be.

“Congress included $900 million in the DoD’s supplemental budget fir fuscal years 2007 and 2008 to fund more mental health services, as well as more research on the effects of traumatic brain injuries (TBI) and treatments for TBI and post-traumatic stress disorder (PTSD)” (Monitor on Psychology, Sep. 2007, pp. 38-39).

Clinical Neuropsychology Defined

If you were like me a few years ago I had no idea what clinical neuropsychology was. I guess I should first start out with what clinical psychology is and how it differs from other disciplines. One common misconception that I run across is that I am studying to be a psychiatrist. Nope, psychologists are different from psychiatrists. Psychiatrists go to medical school, receive an MD, and specialize in psychological disorders after that. Since they are MDs they can prescribe drugs (and often believe – if I can stereotype – that drugs are pretty close to panaceas). Psychologists earn PhDs (or, PsyDs) in the United States from clinical psychology programs. After grad school and an internship, psychologists need to pass the licensing exam in a state to be able to see clients and patients.

Neuropsychologists specialize in brain functioning and typically see clients with brain disorders. The problems can range from epilepsy to autism to learning disorders to traumatic brain injuries to dementias. Neuropsychologists generally want to understand how brain (dys)function affects performance on various tests. Conversely, they believe that test performance reaveals much about how the brain is or isn’t working and where any damage might be. Neuropsychologists also commonly use MRIs and other brain imaging techniques to provide more information about their clients.

What are the job options for someone with a PhD in Clinical Psychology (emphasizing neuropsychology)? There is always academia, where research and teaching are king. Many neuropsychologists in academia also see patients clinically. Neuropsychologists can also work in hospitals, clinics, or private practice. A number conduct forensic evaluations for legal cases (e.g., work-related injuries, automobile collisions, etc.). The military also employs a number of neuropsychologists. Some neuropsychologists also work for business or governmental agencies as consultants, statisticians, or psychologists. While psychologists do not make as much money as MDs, they generally are paid well, have good hours, and good job security.

Time for an OCD Post

Time has a nice article about obsessive-compulsive disorder (OCD) titled “When worry hijacks the brain.” Like most articles by journalists, it’s a bit melodramatic (e.g., “Even the most stable brain operates just a millimeter from madness”) at times but overall it is a nice introduction to OCD and the biology (neuroscience) behind the disorder.

The charitable accumbens

CharityCNN posted an interesting article about how when people choose to be charitable (i.e., give money away) that the nucleus accumbens, which is termed the “pleasure center” of the brain, and the caudate nucleus showed heightened activity. It’s turning out that the nucleus accumbens is involved in far more activities than we’ve ever realized. It’s an area of the brain that is heavily tied to the dopaminergic system and is directly tied to drug use, eating, sex, and pretty much anything else that people can enjoy. In addition, assumed dysfunction or dysregulation of the nucleus accumbens is tied to addictive behaviors. It’s not surprising then that a behavior that is enjoyable to so many – being charitable – is related to activity in the nucleus accumbens. Maybe some people are just Scrooges because they have too little dopamine in their brains [pure speculation and meant to be slightly humorous but it is a hypothesis that could be worth testing].

Image courtesy of benevolink