War-related traumatic brain injuries

An article in the most recent Monitor on Psychology (published by the American Psychological Association) [here’s a link to the article that is accessible for free online: Link) reminded me of something one of my professors in graduate school told our class a couple years ago. He is a clinical neuropsychologist who occasionally does some consulting for the military. After he returned from a consultation with the military he told us that between the war in Afghanistan and the Iraq war there had been 18,000 central nervous system (brain and spinal cord) injuries of soldiers and contract employees serving in those two countries. The majority of the injuries were minor and many were not combat related but there are still thousands of people with moderate to severe CNS injuries that were acquired in war zones. Quoting from the Monitor article:

“Psychologists, particularly neuropsychologists, are stepping in to assess the damage, help patients learn new strategies to compensate while their brains recover, and raise public awareness of the increasing number of servicemen and women with TBIs. In fact, 1,977 service members were treated for them at Defense and Veterans Brain Injury Center (DVBIC) sites from January 2003 to February 2007.”Soldier Helmet

One reason for high rates of traumatic brain injury in the Iraq (and Afghanistan) war(s) is the improved (compared to previous wars) body armor and other life-saving devices. The downside to fewer fatalities is that there are higher rates of people with severe injuries who survive. The mild TBI rates are shown to be: “between 10 and 20 percent [in some surveys] of soldiers returning from deployments” (Source). It’s great to have fewer fatalities but TBIs can have profound effects on people. Clinical neuropsychologists can help people with TBIs learn how to best cope with their injuries as well as understand how their lives might be different and what they can do to compensate for any difficulties. Most people with mild to moderate TBIs seem to have complete or nearly complete recoveries; however, those with moderate to severe TBIs may have deficits, many very severe, that last the rest of their lives.

There can be myriad short-term problems associated with TBIs (e.g., mental slowing, memory problems, personality changes, concentration and attentional difficulties, etc.) but there are also long-term ones. Research has shown that a person with a history of multiple TBIs is more likely to get Alzheimer’s Disease in old age (well, the research actually shows that there is an over-representation of people with multiple TBIs in the Alzheimer’s population). There is a great need for clinical neuropsychologists currently and in the future to work with and help all of our war veterans who have acquired brain injuries.

Acute Respiratory Distress Syndrome

Acute respiratory distress syndrome is a common cause of mortality and morbidity, affecting an estimated 150,000 people per year in the United States (Rubenfeld, Doyle, & Matthay, 1995) however, recent evidence suggests the incidence may be higher (Rubenfeld, 2003). Compared to 20 years ago mortality has decreased from 80% to 30% of ARDS participants (Milberg, Davis, Steinberg, & Hudson, 1995; Brower et al., 2000) resulting in approximately 100,000 people who survive ARDS each year in the United States (Bersten, Edibam, Hunt, & Moran, 2002). Acute respiratory distress syndrome occurs in response to a variety of insults including sepsis, trauma, pneumonia, massive transfusion and other medical/surgical conditions. Treatment of ARDS requires aggressive supportive care including positive pressure ventilation (Brower et al., 2000) and increased oxygen concentrations with risks of barotrauma, oxygen toxicity, and nosocomial infection.

Acute respiratory distress syndrome may be a consequence of multiple organ system dysfunction, including the central nervous system (Bell, Coalson, Smith, & Johanson, 1983; Montgomery, Stager, Carrico, & Hudson, 1985). Participants who survive ARDS are at risk for neuropsychological deficits (Hopkins et al., 1999; Rothenhausler, Ehrentraut, Schelling, & Kapfhammer, 2001; Al-Saidi et al., 2003; Hopkins, Weaver, Chan, & Orme, 2004) 6 to 12 months following hospital discharge. Approximately 33% of general medical ICU survivors, some with ARDS, have cognitive impairments (Jackson et al., 2003) 6 months after hospital discharge. In 1999, Hopkins and colleagues found that 45% of ARDS survivors had neurocognitive impairments including impaired memory, attention, concentration, mental processing speed, and global intellectual decline one year post-discharge.

Others have since made similar observations (Marquis et al. 2000; Rothenhausler et al., 2001; Al-Saidi et al., 2003; Jackson et al., 2003). The prevalence of neurocognitive impairments varies from 25% (Rothenhausler et al., 2001) to 78% in participants with more severe ARDS (Hopkins et al., 1999). Neurocognitive impairments are a major determinant in return to work, work productivity, and life satisfaction following ARDS (Rothenhausler et al., 2001).


Al-Saidi, F., McAndrews, M. P., Cheunt, A. M., Tansey, C. M., Matte-Martyn, A., Diaz-Granados, N., et al. (2003). Neuropsychological sequelae in ARDS survivors. American Journal of Respiratory and Critical Care Medicine, 167, A737.

Bell, R. C., Coalson, J. J., Smith, J. D., & Johanson, W. G., Jr. (1983). Multiple organ system failure and infection in adult respiratory distress syndrome. Annals of Internal Medicine, 99, 293–298.

Bersten, A. D., Edibam, C., Hunt, T., & Moran, J. (2002). Incidence and mortality of acute lung injury and the acute respiratory distress syndrome in three Australian States. American Journal of Respiratory and Critical Care Medicine, 165, 443–448.

Brower, R. G., Matthay, M. A., Morris, A., Schoenfeld, D., Thompson, B. T., & Wheeler, A. (2000). Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. New England Journal of Medicine, 342, 1301–1308.

Hopkins, R. O., Weaver, L. K., Chan, K. J., & Orme, J. F. (2004). Quality of life, emotional, and cognitive function following acute respiratory distress syndrome. Journal of the International Neuropsychological Society, 10, 1005–1017.

Hopkins, R. O., Weaver, L. K., Pope, D., Orme, J. F., Bigler, E. D., & Larson-Lohr, V. (1999). Neuropsychological sequelae and impaired health status in survivors of severe acute respiratory distress syndrome. American Journal of Respiratory and Critical Care Medicine, 160, 50–56.

Jackson, J. C., Hart, R. P., Gordon, S. M., Shintani, A., Truman, B., May, L., et al. (2003). Six-month neuropsychological outcome of medical intensive care unit participants. Critical Care Medicine, 31, 1226–1234.

Marquis, K., Curtis, J., Caldwell, E., Davidson, T., Davis, J., Sanchez, P., et al. (2000). Neuropsychological sequelae in survivors of ARDS compared with critically ill control participants. American Journal of Respiratory and Critical Care Medicine, 161, A383.

Milberg, J. A., Davis, D. R., Steinberg, K. P., & Hudson, L. D. (1995). Improved survival of participants with acute respiratory distress syndrome (ARDS): 1983-1993. Journal of the American Medical Association, 273, 306–309.

Montgomery, A. B., Stager, M. A., Carrico, C. J., & Hudson, L. D. (1985). Causes of mortality in participants with the adult respiratory distress syndrome. American Review of Respiratory Disease, 132, 485–489.

Rothenhausler, H. B., Ehrentraut, S., Stoll, C., Schelling, G., & Kapfhammer, H. P. (2001). The relationship between cognitive performance and employment and health status in long-term survivors of the acute respiratory distress syndrome: Results of an exploratory study. General Hospital Psychiatry, 23, 90–96.

Rubenfeld, G. D. (2003). Epidemiology of acute lung injury. Critical Care Medicine, 31, S276–S284.

Rubenfeld, G. D., Doyle, R. L., & Matthay, M. A. (1995). Evaluation of definitions of ARDS. American Journal of Respiratory and Critical Care Medicine, 151, 1270–1271.

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”

Ventromedial prefrontal cortex damage results in impaired moral judgments

Click on the following link to read the news article from New Scientist: Moral judgment

The researchers found that people with ventromedial prefrontal cortex (which is involved in emotional regulation) damage have impaired judgment regarding moral dilemmas in which they are personally involved. Their judgment is not impaired compared to people without ventromedial prefrontal cortex (VMPC) damage in situations in which they are not personally involved. The likely pathway of this impairment is: damage to VMPC –> impaired emotional regulation –> impaired moral judgment in personal moral dilemmas.

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.

The basal ganglia and cognition

The basal ganglia are a collection of subcortical structures that were traditionally viewed as only being involved in movement. The basal ganglia include the caudate, globus pallidus, putamen, and nucleus accumbens (the subthalamic nucleus and the substantia nigra are also often included as part of the basal ganglia). Scientists have known about the basal ganglia’s role in movement for a number of years but have only recently really started studying their role in cognition, executive function, and memory.

Dissections of the brain have shown that there are a number of white matter “loops” exiting and entering the basal ganglia. We know that the striatum, which consists of the putamen and the caudate and is so named because there are connections between the two structures that look like stripes (striations), receives excitatory input from all over the cortex (Seger & Cincotta, 2002). The prefrontal cortex (roughly the very front of the brain) connects to the anterior putamen and the head of the caudate but the tail of the caudate and the posterior parts of the putamen receive inputs from parts of the temporal and parietal lobes. The frontal lobes are involved in tasks such as planning, remembering, organizing, and many other of the “higher-order” cognitive abilities. The parietal lobes are involved in visuo-spatial tasks and the temporal lobes are involved in memory and object recognition (these are gross simplifications of lobular function – all lobes have more functions than I wrote about). So if parts of the basal ganglia receive inputs from the frontal lobes, what are the basal ganglia doing if not just moderating movement?

Seger and Cincotta (2002) demonstrated that the striatum is involved in a type of learning. Lamar, Price, Libon, Penney, Kaplan, Grossman, and Heilman (2007) demonstrated that dementia patients with higher levels of white matter disruption (which likely interferes with basal ganglia connectivity) have poorer working memory performance. One example of what working memory is is performing a multiplication task in your head without using any paper – having to remember the digits and manipulate them is a process of working memory. Benke, Delazer, Bartha, and Auer (2003) reported on two clinical cases of patients with hematoma disrupting the left basal ganglia. Both patients had “executive function” disruption, short- and long-term memory impairment, and attentional difficulties. Many other researchers have demonstrated the role the basal ganglia has in cognition but we are still in the early stages of this area of research.

The study of brain-injured individuals

The brain is an interesting organ. Its complexity is far beyond any other part of the body, which is what makes studying it so difficult. Individual differences affect how the brain functions – to an extent – and how it reacts to stressors, damage, or decay. When the brain is injured or dysfunctions, we can learn about its normal functioning. There have been some widely publicized cases of brain damage and the effect that damage has on cognition and life. One such case was the Terry Schiavo case that caught widespread national attention two years ago. The lessons we learned from Terry were mostly political, legal, and moral ones. What about cases where there is more than minimal higher-order brain functioning as in Terry’s case?

A number of years ago some researchers reported the case of a man who had damage to his thalamus, a structure in the middle of the brain that is viewed as a “relay center” for the brain, among other functions. In this man’s case he had an anomia (i.e., lack of ability to name) for medical instruments and terms. He was not a doctor or other health care professional, he just had great difficulty naming medically-related terms. There have been other similar cases where people have had random category naming difficulties following brain injury. It is cases like this that make the study of the brain so interesting.

Over the years there have been a number of famous brain injury patients. Gage was a railroad foreman in the 1800s whose personality and emotionality changed after a tamping rod was blasted through his frontal lobes in a horrific accident. H.M. is a man whose medial temporal lobes were removed in surgery. Following the surgery he had severe anterograde amnesia (that roughly means he doesn’t remember anything that happened after his surgery) and mild retrograde amnesia (he doesn’t remember the few days prior to his surgery either). From HM researchers learned a lot about the memory system and how the medial temporal lobes are involved in memory processes (although the theories are still under development and some ideas about how information is processed into long-term memory are controversial). Then there have been cases of people with temporal lobe damage who have lost the ability to recognize objects or people. The study of brain dysfunction is fascinating and informative. Sometimes one doesn’t know what to expect.

Learn also: How personal injury affects employment.

Reference: Rear End Accident Attorney Louisiana.