The concept of neglected tropical diseases (NTDs) emanated from the meetings convened in Berlin by the World Health Organization (WHO) and Deutsche Gesellschaft für Technische, now Internationale Zusammenarbeit in 2003 and 2004 (WHO 2004). Following these developments, Weiss (2008) and Hotez (2008) recently reviewed the issues of stigma in NTDs. Historically leprosy has been a major focus of stigma studies and literature. Other NTDs that generate stigma overtones include onchocerciasis, lymphatic filariasis, plague, Buruli ulcer, leishmaniasis, African trypanosomiasis and Chagas’ disease. The numbers of existing cases of selected NTDs estimated by WHO (2010) and which cause stigma and disablement have increased sharply (Table 1).

In many NTDs stigma results from external deformations such as scars, physical manifestations of leprosy, or physical disabilities (Table 1). Furthermore, the impact of the meaning of the name of the disease may be as great, or even greater, source of suffering as symptoms of the disease. For example, paucibacillary leprosy may present at an early stage as a painless depigmented or anaesthetic patch. Receiving the announcement of the diagnosis is likely to be far more troubling than these symptoms per se (Weiss et al. 2006; Corrigan 2007). The emotional impact of the social and cultural meanings of illness indicates another way by which stigma operates. For example, in settings where arranged marriages are a major concern of families for their children, the impact of a health problem on the ability to marry is troubling. For example, men with hydrocele suffer from embarrassment, ridicule and frustration due to their inability to perform sexual intercourse (Ahorlu et al. 2001).

We are, by nature, a highly affiliative species craving social contact. When social experience becomes a source of anxiety rather than a source of comfort, we have lost something fundamental – whatever we call it. (Insel 2002).

Thomas R. Insel, Editor of Biological Psychiatry, concluded that findings from various neuroscience disciplines appear to suggest that the brain has a special way of processing social behavioral information (Yizhar et al. 2011; Greimel et al. 2012; Tate et al. 2006). It would even appear that special genes determine whether some animals that do not have brains exhibit solitary or social behavior (Dreller and Page 1999). We have attempted to summarize the current data in trying to answer the following questions:

Is there any such neural network as a stigma centre in the brain? How does the brain develop social norms and are these ‘programmes’ fixed in time and space and if not, what modulates them? These questions are clearly very difficult to answer. The young growing discipline of behavioural or social neuroscience is going to hopefully enable us to gain a better understanding of these issues. Derks et al. (2008) have reviewed data obtained with electroencephalography, event-related potentials, or functional magnetic resonance imaging (fMRI) methods to examine neural correlates of stereotype and social identity threat. The findings that brain activation is related to the experience of being stereotyped have shed light on the cognitive processes underlying the social identity processes (Derks et al. 2008). Stereotype threat is a situational predicament in which individuals are at risk, by dint of their actions or behaviours, of confirming negative stereotypes about their group (Steele and Aronson 1995). For example, data obtained using fMRI suggest that stereotype threat affects women’s mathematics performance in two ways: first, it disrupts normal recruitment of cognitive areas required for high math performance (the inferior prefrontal cortex, left inferior parietal cortex, and bilateral angular gyrus) and, second, it increases the recruitment of areas which allow for the processing and regulation of emotions (ventral anterior cingulate cortex). This implicates that women perform more poorly under stereotype threat because valuable cognitive resources are spent on emotional regulation instead of on the task at hand (Derks et al. 2008). Although this approach has limitations, it has the merit of providing some leads to the understanding of the complex phenomenon of stigma, which may in future contribute to its reduction in the targeted populations.

With regards to the second question, social neuroscience research has focused more on people who stereotype others rather than on the stigmatized individuals (see Dickter and Bartholow 2007; Ito et al. 2006). Brain imaging and electrophysiology have been applied to research on stereotyping from the perpetrator’s perspective and this approach has yielded some insights into the processes that underlie prejudice and racial bias. For example, race effects have been observed in two brain areas traditionally associated with face perception, the fusiform gyrus and the posterior cingulate cortex. While these brain areas are considered to be responsible for face encoding and person knowledge respectively, evaluation and behaviour regulation appears to occur in the amygdala and anterior cingulate cortex, respectively (Ito and Bartholow 2009). This model, however, still has many unanswered questions such as the brain mechanisms of stereotype activation and regulation of stereotypic responses, and the psychological mechanisms involved.