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Abstract

The present article discusses the role of laughter in the much cited ‘laughter epidemic’ that occurred in Tanganyika in 1962. Despite its extraordinary nature, the veracity of the event is confirmed, crucially on the basis of similar reports. But most current representations are flawed by their exaggeration and misinterpretation of the role of laughter in the event, relating it to a humorous stimulus, a virus or environmental contaminant, or identifying it as contagious laughter. It is argued that the event is a motor-variant case of mass psychogenic illness of which laughter is one common symptom. Therefore it cannot serve as support for other arguments in humor research.
The laughter of the 1962 Tanganyika
‘laughter epidemic’
CHRISTIAN F. HEMPELMANN
Abstract
The present article
1
discusses the role of laughter in the much cited ‘laugh-
ter epidemic’ that occurred in Tanganyika in 1962. Despite its extraordi-
nary nature, the veracity of the event is confirmed, crucially on the basis of
similar reports. But most current representations are flawed by their exag-
geration and misinterpretation of the role of laughter in the event, relating
it to a humorous stimulus, a virus or environmental contaminant, or identi-
fying it as contagious laughter. It is argued that the event is a motor-variant
case of mass psychogenic illness of which laughter is one common symp-
tom. Therefore it cannot serve as support for other arguments in humor
research.
Keywords: Laughter; laughter epidemic; mass hysteria; mass psychogenic
illness; Tanganyika; Africa.
1. Introduction
In the literature on laughter, reference is often made to an instance of a
‘laughter epidemic’ that is reported from Tanganyika (now Tanzania),
East Africa, in 1962 (e.g., Banwell 2000; Boss 1997; Brottman 2002; Car-
doso 2003; Colligan et al. 1982; Conley 1963; Ebrahim 1968; Holden
1993; Kagwa 1964; Lambo 1965; Muhangi 1973; Provine 1992, 1996; Si-
rois 1982; Stearns 1972; Trump 2002; Wessely 1987). A recent citation
that spawned much attention can be found in Provine (2000: 113¤ ).
According to these accounts, the laughter epidemic originated in a girls’
Humor 20–1 (2007), 49 –71 0933–1719/07/0020–0049
DOI 10.1515/HUMOR.2007.aaa 6Walter de Gruyter
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school, where students started to laugh uncontrollably, and subsequently
spread to their communities to ultimately paralyze the whole country for
several months.
Because this extraordinary instance, originally reported by Rankin and
Philip (1963), is described and misinterpreted frequently and recently not
only in popular literature, but also in scientific work, a reassessment of its
general veracity and the reported circumstances in the light of similar
phenomena and their analyses — is warranted. This paper will argu e that
the event is much quoted for two reasons: On the one hand, it is a good
story with an ironic juxtaposition of a joyful symptom and a disease
event. On the other hand, it appears to provide support to several
common-sensical notions about laughter, in particular its contagious na-
ture, psychopathological correlates, and cultural universality.
The main misapprehension about the event arises from the central fact
that the epidemic involved laughter: The assumption is that it must thus
have been related to humor, on the one hand, and enjoyed, on the other.
In fact, the laughter had nothing to do with merriment or humor nor was
its contagiousness instrumental in the epidemic spread. Laughter, in this
case, was just one and a fairly common symptom of an uncommonly
large case of mass psychogenic illness (MPI ), or mass sociogenic ill-
ness, that will have to be reassessed to highlight these most common
misinterpretations of the ‘laughter epidemic.’ In general, despite the
size of the event, both in the unusually large population a¤ected and the
long duration, most re ports — except for the original one — are exagger-
ated, oversimplified and tendentiously ignore central facts and pertinent
interpretations.
It has to be cautioned that for these reasons, mainly the non-humorous
nature of the laughter involved, the ‘laughter epidemic’ itself may appear
to fall outside of the purview of humor research. But this article, which
aims to address this very point for the sake of humor research, is of
course well within its limits. Accordingly, the present discussion is rele-
vant mostly for humor scholars, but also psychologists and sociologists,
whose fields centrally contribute to an understanding of the likely circum-
stances of the event, as well sociologists and anthropologists of science,
who will find in the reception and distortion of the original report a fairly
typical case of misquoting motivated by wishful thinking. In short, the
good news is that there is a real event underlying the reports, but the
bad news is that it had nothing to do with humor and only very little
with laughter.
50 C. F. Hempelmann
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2. Current reception
I choose to introduce the epidemic by way of its more inaccurate, but
more recent citations. This reproduces the usual order in which the reader
becomes acquainted with the episode and underlines the intended empha-
sis of the present discussion, which lies not only on the event itself, but
also on its presentation and reception. The most detailed, carefully pre-
sented, and original source will be presented in depth in the following
section.
The aim of this paper is not to discredit the journalists, like Trump
(2002), who seems to have used the archive of his own paper that contains
Conley (1963), or Sebastian (2003), who interviewed this author at a
presentation of the present research. They largely depend on the work of
the researchers and their purposes are those of journalists: to report the
researchers’ results and opinions, and to entertain. But since they are a
main source, even for some academic approaches, their simplified ac-
counts of the event dominate its reception. Banwell (2000) is a typical
example:
2
It was 1962 in Tanganyika. A group of teenage girls were hanging out together.
Something made them giggle maybe someone told a joke, maybe they were
giddy after a long day of school? The giggles quickly escalated from gu¤aws to
belly laughs to shrieks to wild hysterics. The girls laughed, then cried, then
laughed some more. When they met up with neighbors, they started to laugh too.
The laughter spread from community to community. Soon, Tanganyika was
caught in a full-scale laughter outbreak. Those people who did get to sleep woke
up laughing again. Work halted; schools were shut down. The laughing in Tan-
ganyika lasted for six months!
As I do not want to develop the present discussion against the back-
ground of an obvious strawman, let us turn to a more typical example:
Holden (1993), referring to Rankin and Philip (1963), claims ‘‘[t]he au-
thors wrote an account of a delightful social phenomenon in which whole
African villages would be infected en masse by highly contagious bouts of
laughter.’’ While it would be desirable for an author of self-help literature
(cf. Holden’s webpage: http://www.happiness.co.uk/) to find evidence for
such a ‘‘delightful’’ phenomenon, delight is far from the feeling of despair
and confusion Rankin and Philip report the victims of the epidemic to
have experienced, as we will see soon. Holden’s misrepresentation con-
tinues (1993: 82; my emphasis):
The Tanganyika ‘laughter epidemic’ 51
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The laughter would occasionally reach such a point that work and schooling
would have to be postponed until the merriment died down. On one famous occa-
sion, one or two pupils at a Catholic girls’ school began to giggle. The giggling
gathered pace and soon the whole class was merry. Teachers were tickled by this
spontaneous, joyful outburst and joined in. Soon the whole school was swimming
in a tide of laughter. Word spread to the village, and when mothers came to col-
lect their children they too became dizzy with laughter and chuckles of delight.
In these sources we always find an emphasis on positive emotions that are
claimed to have accompanied the laugher symptom, e.g., ‘‘merriment,’’
‘‘joy,’’ ‘‘delight.’’ As we will see, these emotions were not underlying the
symptoms reported of the event.
Typical for a more reliable, yet still centrally flawed, account in scientific
literature is Provine (2000: 130–131) who presents an accurate summary
of Rankin and Philip (1963), with additional interpretations of his own:
The first symptoms appeared on January 30, when three girls started laughing.
The symptoms of laughing, crying, and agitation quickly spread to 95 of the 159
students [ . . . ] Although temporarily debilitating, the laugh attacks produced no
fatalities or permanent aftere¤ects, but teachers reported students being unable
to attend to their lessons for several weeks after a laugh episode. [ ...]
Before finally abating two and a half years later, in June 1964, this plague of
laughter spread through villages ‘like a prairie fire,’ forcing the temporary closing
of more than 14 schools and a¿icting about 1,000 people in tribes bordering lake
Victoria in Tanganyika and Uganda.
Provine focuses on the contagiousness of laughter, which he considers to
be the main factor in the epidemic (cf. Provine 1992, 1996; also Stearns
1972: 40). As we will see, the event rather illustrates the contagiousness
of hysteria, of which laughter may be a symptom, in a predisposed popu-
lation. Provine (2000) attracted much journalistic attention and when it is
reviewed, the Tanganyika episode is almost always among the quoted
topics, as a tale too good not to be told, a tale about laughter having
been too much of a good thing.
Finally, a typical attempt at an assessment of the event with a di¤erent
focus can be found in Cardoso (2003; cf. also http:// www.humourwise
.co.uk/). It aims to find physical causes for the symptoms reported of
the epidemic, again, centrally for the laughter involved:
I find it improbable that a purely psychological mass reaction would last so long
and be so widespread. [...] The American neurologists Hanna and Antonio
52 C. F. Hempelmann
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Damasio suggest that abnormal laughter occurs when structures in the basal part
of the brain are damaged. The pathways that normally automatically adjust the
execution of laughter to be appropriate to the stimulus for it are disrupted
and the brain gets incomplete information about the cognitive and situational
context of a potential stimulus — it gets it wrong about whether or not to
laugh — resulting in chaotic behaviour. Based on this model, I suggest that a viral
infection, probably some kind of encephalitis in the basal part of the brain, pro-
voked the 1962 epidemic.
I will not pursue such physical cause explanations further. The details of
the spreading pattern clearly exclude a viral infection as a potential expla-
nation, and pathological laughter and crying show no contagiousness and
a di¤erent progression (see 5.1).
Setting aside the information on details like location, a¤ected popula-
tion, and duration until their detailed report from the original source
in the next section, the interpretation of the events in current sources
presents the following picture, reflecting the most common notions about
the event: Young females laugh, possibly because of a humorous stimu-
lus, but they also cry, both with increasing intensity; these symptoms
spread, possibly by contagion or a viral infection, interrupting everyday
life and lasting between 6 and 30 months; despite their graveness and
duration the symptoms are accompanied or even caused by merriment.
The present paper aims to correct these notions and to suggest a di¤erent
interpretation of the events on the basis of the original and other contem-
porary sources and more convincing analyses of the ‘laughter epidemic’
as a case of mass psychogenic illness.
3. Contemporary sources
3.1. The original report
Since it is the central source on which all other accounts rely and the first
published description and careful assessment of the epidemic, I now turn
to the concise
3
report by Rankin and Philip (1963) in detail in this sepa-
rate subsection. Their reports begins as follows:
The disease commenced on 30th January, 1962, at a mission-run girls’ school at
Kashasha village, 25 miles from Bukoba [ . . . ] when three pupils commenced to
act in an abnormal manner. From that date until the 18th March, 1962, when
the school was forced to close down, 95 of the 159 pupils had been a¤ected.
The Tanganyika ‘laughter epidemic’ 53
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Fifty-seven pupils were involved from the 21st May, when the school was re-
opened, until it was again shut at the end of June. (1963: 167)
The further progression of the epidemic can be divided into five stages. As
the report is high in content of factual data, for the sake of clarity it is
best presented in tabular form:
3.1.1. Initial breakout
Kashasha (25 m north of Bukoba) boarding school for girls (dormitories)
prodromal group: 3 students
symptoms: Attacks of laughing and crying lasting for a few hours,
in a few cases up to a maximum of 16 days, with an
average of 7 days, followed by a respite and then a re-
currence in the majority of cases; general restlessness,
persecution complex; no clear physical symptoms.
1. First phase
beginning: 1/30/1962
end: 3/18/1962
duration: 48 days
number: 95/159 pupils
[school closed between phase 1 and 2]
2. Second phase
beginnning: 5/21/1962
end: ca. 6/31/1962
duration: ca. 47 days
number: 57/159 pupils
3.1.2. Spread through cases from A. who were sent or went home
1. Nshamba village (55 m west of Bukoba)
beginnning: ca. 3/28/1962
end: ca. 4/30/1962
duration: ca. 34 days
number: 217/10,000 villagers (school children, young adults of
both sexes)
2. Ramashenye girls’ middle school (outskirts of Bukoba)
beginning: 6/10/1962
end: 6/18/1962
duration: 8 days
number: 48/154 pupils
54 C. F. Hempelmann
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3. Kanyangereka village (20 m south of Bukoba)
concurrent with B.2.
number: 3 (family of a case from B.2. who was sent home)
4. Further spread at the time of the writing of report, 2 further school
closures (boys’ schools)
5. Milder occurrence in a Mbarara primary school ( Uganda, 100 m
north of Bukoba)
After the synopsis of the facts, Rankin and Philip turn to a preliminary
analysis. It is still relevant today as their argument proceeds cautiously,
refrains from speculation and, as I will argue, already points in the direc-
tion of a general explanatory model, which will be found most appropri-
ate. According to the report, in order to exclude potential physical causes,
selected subjects were tested for food poisoning and signs of toxic sub-
stances, with negative results. No known form of virus is assumed to
account for the symptoms. Although I consider it unlikely, the possibility
of a viral infection can, of course, never be excluded on clinical grounds.
Yet, in view of the further argumentation of the present paper will make
clear that it is an unlikely explanation.
Rankin and Philip conclude: ‘‘It is suggested that this is mass hysteria
in a susceptible population. This is probably a culturally determined dis-
ease.’’ (1963: 170). Accordingly, the next section will briefly present re-
lated and similar cases of culturally determined diseases, that is, MPI,
previously known as mass hysteria, before I will continue to outline the
relevant research on MPI in general and to analyze to what degree it per-
tains to the case at hand, including a focus on the cultural determinants
of the Tanganyika ‘laughter epidemic.’
3.2. Similar cases
This subsection presents similar contemporary cases of MPI in the vicin-
ity of the event under discussion here. This will serve two purposes: First,
as crucial support for its general veracity, it will establish that the Bukoba
case and its spread is not a singular and isolated event. Second, it will
show that laughter is just one of several symptoms in these additional
cases, as much as in the Bukoba event itself, all of which are common
for a specific variant of MPI.
Kagwa (1964), citing Rankin and Philip (1963), and Ebrahim (1968)
discuss the Bukoba case as an instance of three connected events, the
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other two being ‘‘running manias,’’ which broke out in the area around
Lake Victoria. One outbreak occurred in Kigezi (southwestern Uganda)
in July 1963 with ca. 600 a¤ected people. The second instance took place
in Mbale (eastern Uganda) in November 1963 involving about 300 vic-
tims. Both cases are characterized by aimless running, general hyperactiv-
ity, as well as violence, and these symptoms spread predominantly among
school populations in a pattern identical to the Bukoba event. A fur-
ther similar event is reported by Muhangi (1973) for Ankola (southwest
Uganda) in July 1971. Fifty of the 287 students of a Rugarama male pri-
mary school show grimacing, vulgar language, and aimless walking, as
well as laughing. Another similar, but much shorter, incident from neigh-
boring Zambia is reported by Dhadphale and Shaikh (1983).
With the help of these reports, it can be established that related events
took place in the same region in the same period and that additional sim-
ilar events are reported. In addition to placing Rankin and Philip’s report
into context, these reports point to the main problem with the alleged
laughter epidemic, namely that it didn’t just involve laughter, but ‘‘[t]he
epidemic was characterised by episodes of laughing and crying (Rankin
and Philip 1963: 167; my emphasis). That is, first of all, it is not a laugh
epidemic, but an event involving seeming expressions of strong emotional
disturbance in general and, in some specific cases, laughter in particular.
As such the laughter found in this event is clearly not elicited by humor,
but rather a symptom of mass psychogenic illness.
4. Mass psychogenic illness
4.1. General
This section will establish the complex of mass psychogenic illness (MPI),
its general features, populations typically a¤ected, patterns of spreading
from initial to later stages, general variants, and possible causes. All these
aspects are closely related so that the argument will repeatedly have to
anticipate certain points in later subsections. The focus in the discussion
will be on factors that pertain to the initial outbreak (A. in section 3.1).
Seminal surveys of cases have been compiled and analyzed by Sirois
(1974; reported in Sirois 1982), and a follow-up by Boss (1997), as well
as the work of Bartholomew and associates (e.g., Bartholomew and
Wessely 2002) and Wessely (e.g., 1987). In addition to numerous case
56 C. F. Hempelmann
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studies reporting events similar to our focal case, these surveys are the
main sources for this section. It will become obvious that MPI is a para-
digm example for Fleck’s (1981 [1935]) observation that diseases are con-
structed models on the basis of pseudo-theories of causes and symptoms;
that is, they are functionalist answers to urgent and often biased ques-
tions. Since the Bukoba case is an almost prototypical example of MPI,
and references abound in the work introduced in this subsection, it is as-
sumed necessary to introduce another additional detailed example in this
section.
The following list summarizes the characteristics of the typical course
of MPI (Seldon 1989: 893):
absence of physical findings about organic causes
preponderance in girls/women and (pre-)adolescents
transmission by sight/sound
– hyperventilation/syncope (as signs of anxiety)
rapid spread and remission of symptoms
relapses in original settings of outbreak
as well as the generally assumed underlying causes:
unusual physical/psychological stress in general
evidence of prior physical or mental stress of the prodromal cases in
particular
Based on these general observations, I will discuss, in turn, those charac-
teristics in more detail that are relevant for the Bukoba case.
4.1.1. A¤ected population. All surveys over case studies confirm that
‘‘the prevalence of illness is almost always higher in females than in
males.’’ (Boss 1997: 235). Sirois (1982), for example, observes that ‘‘[o]f
the 70 reviewed outbreaks [in Sirois 1974] 34 appeared in schools, [and]
[w]omen were almost exclusively involved (80%), [...] [t]hey were young,
below 20 years of age, often in the first years of adolescence’’ (104). The
reason for the prevalence of females in a¤ected populations is not com-
pletely obvious, but the general disenfranchisement of females in most
cultures leading to higher psychosocial stress is assumed. McGrath’s ar-
gument is typical:
Perhaps the high incidence of females, as both a¤ected and non-a¤ected members
of the settings in which MPI occur, simply reflects our tendency to put females in
low status and otherwise unrewarding jobs. If so, then ‘female,’ along with
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‘young’ and ‘poor,’ should be treated as a variable that signals ‘low social status,’
not some character flaw like ‘hysteria’ or ‘hypochondria.’ Perhaps the MPI symp-
toms represent a ‘last resort’ means for low-status persons (female, young, poor,
etc.), in high stress situations, to express their distress. (1982: 73)
The gender question is not central to the present study, but it can be
observed that the unequal gender and age distribution is reproduced in
the Bukoba case. I will return to the more general point that MPI is a
last resort to escape stress situations for powerless ‘‘low status’’ people
below, as it is a key part of the present argumentation.
4.1.2. Settings. It is not astonishing that school settings are often indi-
cated for MPI, as a population of young age is likely to congregate in
such a setting. But there are specific additional factors that make a school
population a likely breeding ground for MPI, independent of gender dis-
tributions and partially independent of age. Sirois observes that ‘‘some
outbreaks in the school setting occurring at the beginning of the school
year could be seen as ‘rites of passage.’ They would be useful to bind anx-
iety linked to the formation of the group and act as witness of collective
cohesiveness’’ (1982: 106). Furthermore, in the case of boarding schools,
where students are living together around the clock, stress is intensified
through the separation from family settings. An additional factor is
observed by Boss: ‘‘Outbreaks in schools may have been reported more
frequently than those that occur elsewhere because of the importance at-
tached to investigating outbreaks involving children’’ (1997: 239), an ar-
gument also valid for the many reported MPI cases in Western schools
(e.g., Helvie 1968; Jones et al. 2000; Small and Borus 1983). Yet another
reason may lie in the fact that in colonial settings, as in the Tanganyika
case, schools are the point of contact between the traditional local popu-
lation and Western teachers/missionaries. As we will see below (subsec-
tion 4.2) such a point of contact is also a point of friction, leading to
additional stress. Furthermore, the local population may in general be
susceptible to MPI, and may just be the fact that a Western observer hap-
pens to be present to document the outbreak.
4.1.3. Spread. In the initial or prodromal stage, before the epidemic
spread, the first or index cases involved are often ‘‘unusual [‘hysterical’]
personalities,’’ easily a¤ected by stress; this facilitates spread to ‘normal
personalities (Kerckho¤ and Back 1968: 40). In contrast to this, Sirois
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sees the typical pattern involving hysterics rather as second and third
cases after the index case (1982: 112), while the index case is not necessar-
ily susceptible to hysterical reactions, but more importantly of high social
status. Teoh and Yeoh (1973: 288) confirm that in the prodromal stage,
the index case is usually dominant in the given population, and the sec-
ond and third cases are troubled personalities in the orbit of the index
case (cf. also Benaim et al. 1973). This sociometric pattern, in which
‘‘the regressive e¤ect of crowd behavior on intellectual and emotional
processes — and a small minority of unstable or emotionally labile indi-
viduals which often can be found to gravitate around index cases’’ (Sirois
1982: 104) — plays an important role, can unfortunately not be confirmed
for the Bukoba event. The the relevant data has simply not been recorded
by Rankin and Philip, although ‘‘three pupils’’ were identified as the ini-
tial group a¤ected (1963: 167).
The general spreading pattern of MPI after the prodromal stage is
characterized by a snowballing e¤ect with early satiation, the quick
drop-o¤ being accelerated through outside forces ( Kerckho¤ and Back
1968: 35). At first sight, this appears not to be the case for the Bukoba
event, which lasted long without drop-o¤s, yet these are better under-
stood as relapses, in particular the case in the original population (A.2 in
subsection 3.1) and in individuals. Rather, Sirois identifies the Bukoba ep-
idemic as a case of ‘‘di¤use outbreak’’ (1982: 107) combining the spread
pattern of closed and open settings: ‘‘Its prodromal stage is obscure, but
the epidemic spread starts in the typical explosive manner in a closed set-
ting, the school, but then spreads into the community, and the subsequent
‘‘rebound stage is spectacular’’ (ibid.).
4
The Bukoba event started in the
school environment and then spread into the communities/families (cases
under B. in subsection 3.1), where it lingered. Thus, it appears to combine
the propelling factors of the two typical developments: ‘‘the most com-
mon outbreaks those in schools and places of business tended to be
of short duration, whereas those in communities and families tended to
last longer’’ (Boss 1997: 238).
The general problem of the lack of information on the social composi-
tion of the a¤ected population in the Bukoba case is grave and obvious,
as Sirois recognizes: ‘‘When the outbreak lasts longer ( Kagwa 1964; Ran-
kin and Philip 1963), it is often found that the reservoir of susceptible per-
sons is much larger than originally suspected. this meant that important
and more general aspects necessary for the understanding of the situa-
tion were missed and the original group was only instrumental in the
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outbreak’’ (1982: 108). This points to the importance of identifying not
only clinical aspects and the underlying triggering event of the epidemic,
if any, but also the sociocultural context, which Rankin and Philip (1963)
were not able to do su‰ciently. This is not so much a fault of oversight,
but the Bukoba case occurred when the model of MPI had not yet ma-
tured as a concept, and a main issue in ‘mass hysteria’ research was to
eliminate potential physical causes.
4.1.4. Anxiety vs. motor variant. In the previous paragraphs, di¤erent
types of MPI were described mainly with respect to their development.
But a more important variance is characterized by di¤erent types of
symptoms. This is reflected in Wessely’s (1987) convincing distinction of
two main types of MPI: ‘‘mass anxiety hysteria covers outbreaks demar-
cated by the phenomena of anxiety abdominal pain, chest tightness, dizzi-
ness, fainting, headache, hyperventilation, nausea and palpitation’’ (1987:
112) and ‘‘mass motor hysteria,’’ which such symptoms as seizures, drop
attacks, hysterical dancing, running, and, in three cases, described in
Dhadphale and Shaikh (1983), Ebrahim (1968), and Rankin and Philip
(1963), respectively, also laughing. Accordingly, Wessely classifies the
Bukoba outbreak as ‘‘mass motor hysteria’’ (1987: 112). A di¤erence cor-
roborating this classification is that, in contrast to anxiety types, motor
hysteria attacks ‘‘may persist for months or even years’’ (Wessely 1987:
113), which holds for the case under scrutiny here and makes the ac-
count of the episode appear less fantastic. A case described in (Nandi
et al. 1985) is assumed to have involved relapses over a period of ten
years.
The distinctive symptoms of motor-variant MPI must be discussed in
connection with the underlying causes, namely the possibility of escape
from stress situations, which will be attempted below (subsections 4.2).
The motor variant can be used for that purpose only if its more extreme
symptoms are accepted as symptoms of illness in the cultural context in
which they occur. This social acceptability of motor-variant symptoms
appears to be lower in Western cultures. These cultures have ‘clinicalized’
scripts of disease, into which symptoms like dancing, laughing and
running cannot be accommodated. This would also explain, why in the
motor-variant epidemic originating in Bukoba ‘‘[n]o literate and relatively
sophisticated members of society have been attacked’’ (Rankin and Philip
1963: 167). From a historical perspective, Boss points out that in the
period from 1872 to 1972, surveyed in Sirois (1974), motor-variant
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symptoms are more commonly reported, while in the period from 1973 to
1993 anxiety variant symptoms prevail (1997: 238). In short, today and
in so-called Western societies, dizziness and fainting can earn you a day
home from work, while laughing and dancing will earn you odd looks.
In the period until 1972 and in so-called traditional societies, laughing
and dancing will also have been considered as symptoms of disease.
4.2. Causes: Sociocultural transition and stress
Rankin and Philip stress that ‘‘[t]he type of mental disorder that a¤ects a
community is influenced by the culture of the particular community’’
(1963: 170). More specifically, as we saw in the previous subsection, the
culture of the community also strongly predicts the variant of MPI that
may occur in it. These observations about types of symptoms point in
the direction of a meaningful explanation for underlying causes of MPI,
which will turn out to be more complex and tentative than previous at-
tempts in humor-related and other literature that have aimed to reduce it
to contagion or viral infections. Sirois summarizes that a ‘‘state of ideo-
logical or cultural transition is frequently noted to be associated, as well
as periods of uncertainty and social stress like wars, endemic diseases, or
technological changes’’ (1982: 106). Tanganyika clearly underwent such a
period at the time of the epidemic. Therefore, the analysis of the Bukoba
event in terms of cultural factors and stressors will be facilitated by a brief
outline of the political situation in Tanganyika (cf. Ofcansky and Yeager
1997), before I will turn to the specific local factors at the mission-run
boarding school in Bukoba and similar settings.
The area of Tanganyika was a colony since the late 1880s. It was con-
trolled first by Germany, o‰cially as ‘‘Deutsch-Ostafrika’’ since 1891,
and after World War I became a mandate territory of Great Britain in
1919 and practically part of the British Empire. Like in other African
colonies, no strong independence movement developed until after World
War II, when the U.N. as the successor to the League of Nations renewed
the mandate to Britain with the obligation to prepare the country for
independence. The most prominent African figure in the intensifying
struggle for Tanganyikan independence, Julius K. Nyerere, formed the
openly anticolonial Tanganyika African National Union ( TANU ) with
collaborators in 1954. During Nyerere’s term as first Prime Minister, the
country achieved full independence on December 9, 1961. It appears
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likely that these political events, less than two months from the outbreak
of the Bukoba event on January 30, 1962, and in addition the abandon-
ment of racial division in schools since January 1, 1962, increased the so-
ciocultural stress situation in the young country in general (cf. Wessely
1987: 114). Very similar developments occurred to the neighboring
countries, mainly Uganda, independent since 1962, but also Rwanda, Bu-
rundi, Kenya, and Zambia, from which the related motor-variant epi-
demics are reported (cf. subsection 3.2).
As briefly mentioned above, the local situation in the school setting can
also increase stress as it is a point of friction and transition where the
students from the traditional tribal society are confronted with Western
methods of instruction, educational expectations, and religious-moral
values (Boss 1997: 234). In addition, the transition of the students through
adolescence takes place while they are separated from their families.
Stearns agrees that these factors result in ‘‘anxiety, guilt feeling, loss of
identity, feelings whose repression by schooling and discipline finally re-
sulted in aggressive-compulsive behavior or conversion hysteria’’ (1972:
43), his term for a specific type of MPI.
The high indication for MPI of the specific situation at boarding
schools in countries in transition is corroborated by the research on
motor-variant cases by Teoh and colleagues (e.g., Teoh and Yeoh 1973;
Teoh et al. 1975). Teoh and Yeoh (1973) focuses on cultural transition
as the central stress factor for a group of young college women involved
in a MPI episode in Malaysia. In particular the way these changes a¤ect
the educational system is considered a crucial environmental factor for
MPI (1973: 284):
[W]ith higher educational expectations of the Malay rural parents for their
children, greater pressure is imposed on these children [ ...] These adolescent
girls, away from home, seek alternative culturally-sanctioned modes of expressing
their frustration in this transitional period, in the form of outbreaks of epidemic
hysteria.
Sirois summarizes the general factors of this endemic propensity, which
correspond to observations of Muluka et al. (1985: 251) for a similar Ke-
nyan case, as follows: ‘‘outbreaks in Malaysia were detected in schools in
1970–1971, after the 1969 troubles and in a context of administrative and
educational changes’’ (1982: 109).
In sum, we find a transitional stress-inducing situation both in the
country, which is in the process of consolidating its recently gained
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independence, in general and in the specific circumstances of the a¤ected
population in particular, namely, separation from family, adolescence,
and confrontation with Western educational and other standards. Which
of these factors is more important, and which may not even pertain, and
which may have been overlooked, especially at the individual and prodro-
mal group level, can no longer be clearly decided for the Bukoba event.
But I argue that a combination of these factors creates a stress-inducing
context that is the indirect cause of the epidemic event described by Ran-
kin and Philip (1963).
4.3. Potential purpose: Advantages of the sick-role
Although it is neither instrumental for the assessment of the veracity of
the reports on the Bukoba case, nor for the analysis of the role of laughter
in the event, a central point for the general understanding of the epidemic
as a case of MPI is the question for possible motives of the a¤ected
population. Since they are experiencing a disease event, the victims are
normally not consciously aware of the reason for their symptoms: ‘‘The
common feature of the stressors underlying outbreaks of mass motor hys-
teria is an inability on the part of the subjects either to comprehend the
true nature of the threat facing them or to avoid it’’ (Wessely 1987: 115).
This subsection will accordingly be the most speculative and controver-
sial
5
of the present study.
As briefly mentioned above and in accordance with most research on
MPI (e.g., Boss 1997; Kerckho¤ and Back 1968; Wessely 1987), I see the
reason for people su¤ering from severe stress and anxiety to exhibit the
symptoms of MPI in that they may a¤ord them an escape from the situa-
tion that induces the stress and anxiety. ‘‘Outbreaks provide a temporary
escape from stress because factories, o‰ces, or schools close while inves-
tigations are under way’’ (Boss 1997: 237). This advantage of MPI is
identical to that of the sick-role in general: The su¤erer can evade a situ-
ation that they are otherwise expected to endure. The central case of
motor-variant MPI reported by Nandi et al. (1985) is remarkable in this
respect: The eight women a¤ected by the symptoms relapsed over more
than a decade (1985: 248), and the instrumental nature of their episodes
in escaping the beating by their alcoholic husbands is a shared stressor
rather directly addressed by their behavior.
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The symptoms must be socially acceptable in a given cultural context
for MPI to fulfill this function, which explains the di¤erence of MPI vari-
ants presented above in two ways. First, as Kerckho¤ and Back observe:
‘‘What occurs in cases of hysterical contagion is that physiological symp-
toms, which occur largely as a result of unresolved psychological stress,
are explained (and thus responded to) in terms of a newly invented label’’
(1968: 34). In other word s, the purported trigger — in Western societies
for example, nuclear fallout, viruses, or environmental contaminants, in
traditional societies for example, witchcraft and curses, poisoned food, or,
insect bites — as well as the symptoms — anxiety sympto ms and extreme
motor behavior, respectively —that provide a socially acceptable rational-
ization of the socially unacceptable behavior of leaving the workplace,
school, or any other stress-inducing situation, must be socially acceptable.
A very telling ‘confession’ by an index case of an epidemic was char-
acterized by a falling symptom among adolescent students of a London
school supports this escapism argument: ‘‘I enjoyed the attention this
malady a¤orded and the general concern of everyone around me. [...] I
used it as an escape from the problems I could not face at home and at
school, and became completely wrapped up in it’’ (Benaim et al. 1973:
369). In sum, there are ‘‘rewards to be gained from being sick’’ (Muluka
et al. 1985: 251). But these rewards can be reaped only if the sickness is
presented as evoked by a socially acceptable cause and expressed in so-
cially acceptable symptoms. Under these circumstances MPI can a¤ord
its victims the advantages of the sick-role. It must be cautioned, again,
that the rationalization presented in this section is the most speculative
part of the present discussion, and that the secondary sick-role advantage
is usually not an explanation for all individuals involved.
5. Potential additional explanations
On the basis of the previous sections, it should have become obvious that
the laughter involved in the Tanganyikan epidemic was one of the symp-
toms of motor-variant MPI. But before I can turn to a summary of the
argument that leads to this conclusion, I want to briefly address addi-
tional research and explanatory attempts besides MPI that can help clar-
ify what may have taken place in 1962 and what may not, both because
the explanations pertain to the case and because they are thought to per-
tain to it, but don’t.
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5.1. Pathological laughter
A di¤erent and obviously oversimplified explanation is to declare the
laughter involved in the Bukoba event to be pathological laughter of a
specific type reported in other cases (cf. Black 1982). This kind of laugh-
ter is inappropriate, unmotivated, as well as involuntary (cf. Shaibani
et al. 1994: 243) and continuous (Arlazaro¤ et al. 1998: 184). Apart from
brain lesions (cf. Parvizi et al. 2001) and other diseases with organically
distinct causes, psychiatric disorders that include pathological laughter
and crying (PLC) as a symptom include hysteria. Arlazaro¤ et al. (1998)
describe a patient who has fits of pathological laughter after hitting her
head in a car accident. While no social transmission is involved, the spells
of this patient occurred mainly in stressful or delicate situations [...].’’
(1998: 186). Thus, while PLC is a related symptom, it cannot account
for the epidemic dimensions of the Bukoba event.
5.2. Physiology of laughter
The extent to which the laughter symptom is reported to have lasted dur-
ing the epidemic event can also be evaluated from a physiological per-
spective, a research topic since Spencer (1860). Physiological aspects of
laughter — prominently respiration and phonati on — vary across genders,
individuals, and also in the output of one individual along various factors
(cf. Black 1984; Fry and Rader 1977; Hauser et al. 1997). In general it is
an extremely exhausting activity, resulting in a signal that is more compa-
rable in volume to shouting at up to 80 dB ( Rothga
¨nger et al. 1998) than
to normal speech at ca. 60 dB. The muscles involved in the exhalation
crucial for laughter diaphragm, abdominal and rib cage muscles are
usually not active in that part of the breathing cycle ( Ruch and Ekman
2001: 432) and thus not well trained for it. In addition, during laughter
there is a pronounced antagonism between the opposing sets of muscles
for inspiration and expiration, which are normally working alternately.
This produces the extraordinarily high levels of expiration and subglottal
air pressure in laughter, up to five times as much as in normal phonation
(Ohala 1990; Schroetter 1925), which are usually followed by long peri-
ods of apnea (Lloyd 1938). Because of all these factors, humans tire
quickly from the saccadic contractions required for laughter, as witnessed
by the soreness of abdominal and thoracic muscles after extensive laugh-
ing and, vice versa, the painfulness of laughter after exercising that has
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involved abdominal muscles. Laughing continuously for long stretches of
time as they are understood by some to be implied by the overall length
of the epidemi c event in Tanganyika — must be considered impossible.
These gelotological results indicate that only short episodes of laughter
can be symptoms of a the motor-variant of MPI. They could last for
seconds at a time, and only be repeated over short stretches for each indi-
vidual, but not over hours, weeks, or even months as claimed in some re-
ports on the ‘laughing epidemic.’
5.3. Contagious laughter
A seemingly plausible interpretation of the epidemic reduces the cause
to the contagiousness of laughter (cf. Black 1982). This argument is rep-
resented most prominently by Provine (1992, 1996), and has received
much attention since the publication of Provine (2000) and the subse-
quent resurgence of reports on the event: ‘‘The power of contagious
laughter as a social coupling process is suggested by a persistent epidemic
of laughter that began among 12- to 18-year-old girls in a boarding
school in Tanganyika and spread throughout a district, requiring the
closing of schools’’ (1992: 1). As we have seen in the preceding discussion,
the event cannot be reduced to laughter as the central symptom. Thus,
the undeniably contagiousness of laughter at short range, unsuccessfully
modeled by Provine’s laughter detector-generator (2000: 149), cannot
serve an explanation for an event of the extent of the motor-variant MPI
case that took place in Bukoba.
5.4. Viral infection and environmental contaminants
As we have seen above, there are attempts to explain the ‘laughter epi-
demic’ as a reaction to a virus (Cardoso 2003) or environmental contam-
inant. Rankin and Philip (1963) excluded a limited number of such possi-
ble causes. Since no blood samples are known to have been preserved, no
update of their falsification of such causes can be attempted. Yet, I would
argue that this is not necessary, as there are no known viruses or con-
taminants leading to the symptoms described for the event, while MPI
provides us with a plausible theory.
In oral communication, similarities in symptoms — and more tenta-
tively in cause to Kuru have been pointed out to me (cf. also Conley
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1963). Kuru, also called the ‘‘laughing sickness,’’ is a well-documented
(e.g., Gajdusek 1963, 1976) type of transmissible spongiform encephalo-
pathy, in which prions transmitted through the ritual eating of the brains
of recently deceased humans cause fatal brain deterioration. One com-
mon symptom in the final stages of Kuru are short episodes of laughter
(cf. also Virani and Jain 2001). Yet, there is only one connection between
the ‘‘laughter epidemic’’ and this ‘‘laughter disease’’: The ironic associa-
tion of a sad event, a disease, with a seemingly happy symptom, laughter,
in both cases leads to their analogous names.
6
This also reflected in
phrases like ‘‘plague of laughter’’ ( Provine 2000: 1313) and taken to the
extreme in the title of Zigas (1990): ‘‘Laughing Death.’’
6. Conclusion
The Tanganyika laughter epidemic is a case of motor-variant mass psy-
chogenic illness. This is the result of the present reassessment of the
original report on the event and corroborated by reports on similar events
under similar circumstances. Although emphasized in reports on the epi-
demic, laughter in this context is just one of several symptoms, even if it
makes a descriptive name based on the ironic contrast between a sign of
joy and merriment, on the one hand, and a painful disease event, on the
other. Laugher played a much smaller role in the event than most current
descriptions claim, not least because laughing on an epidemic scale is
physiologically impossible. The laughter in the event is not caused by a
humorous stimulus that transmits it. It is not a case of contagious laugh-
ter, neither as emotional or behavioral contagion, but only one of several
common symptoms of motor-variant MPI, none of which could be trig-
gered by or trigger laughter, e.g., running or seizures. For these reasons
it is suggested that the present article should be the last to discuss the
‘laughter epidemic’ in research on humor, other than to illustrate the dis-
sociation of laughter and humor.
Georgia Southern University
Notes
Correspondence address: hempelma@mac.com
1. The author would like to thank Robert E. Bartholomew, Willibald Ruch, and the two
anonymous referees for helpful comments on earlier versions of this paper.
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2. An even wilder account can be found in Shibles (n.d.): ‘‘Between 1962 and 1964 it is
reported that 1000 people in Tanganyika and Uganda (especially girls in Catholic con-
vent schools) died in a group laughing epidemic. The report, it would seem, would need
detailed checking.’’ Indeed.
3. It comprises only four pages, one of which is taken up by a map of the area around
Lake Victoria.
4. Sirois (1982: 110) ascribes a report on an episode of ‘‘collective running [that] shows an
underlying fantasy of being savagely attacked and contaminated by some atomic
power.’’ to ‘‘Rankin and Philip (1964) [sic!].’’ It is unclear which source he is referring
to as no such explanations are proposed by Rankin and Philip (1963) nor by Rawnsley
and Loudon (1964), the next entry in his bibliography that also corresponds in page
number to his citation.
5. Ascribing psychological motivations is always a speculative business as well as one sel-
dom well received by those whose role as su¤erers from a disease it evaluates. A prime
example for this is the controversy over the Joint Royal College Report on chronic
fatigue syndrome, one of the authors of which is Wessely (Royal College of Physicians
et al. 1996).
6. There is one further coincidental connection at the perimeter of Kuru that has no impact
on the present argument: ‘‘Five young females, they had allegedly been typical advanced
Kuru cases whose progressive symptoms had ceased. All five, like Teirari, were in close
contact with other Kuru victims, and being of emotional, somewhat hysterical tempera-
ment, had developed what was obviously a hysterical mimicry of Kuru’’ (Zigas 1990:
285).
References
Arlazaro¤, Aharon, Roberto Mester, Baruch Spivak, Colin Klein, and Paz Toren
1998 Pathological laughter: Common vs. unusual aetiology and presentation. The
Israel Journal of Psychiatry and Related Sciences 35 (3), 184–189.
Banwell, Wilson
2000 Laughing. University of Alberta Employee and Family Assistance Program
Quarterly 5 (1).
Bartholomew, Robert E., and Simon Wessely
2002 Protean nature of mass sociogenic illness. From possessed nuns to chemi-
cal and biological terrorism fears. British Journal of Psychiatry 180, 300–
306.
Benaim, Silvio, John Horder, and Jennifer Anderson
1973 Hysterical epidemic in a classroom. Psychological Medicine 3, 366–373.
Black, Donald W.
1982 Pathological laughter. Journal of Nervous and Mental Diseases 170, 67–71.
1984 Laughter. Journal of the American Medical Association 252 (21), 2995–
2998.
Boss, Leslie P.
1997 Epidemic hysteria: A review of the published literature. Epidemiologic Re-
views 19 (2), 233–243.
Brottman, Mikita
2002 Funny peculiar: Gershon Legman and the psychopathology of humor. MS,
Maryland Institute College of Art.
68 C. F. Hempelmann
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Cardoso, Silvia
2003 Interview by Sophie Petit-Zeman. Hypnomonthly. Available at: http://
hypnomonthly.com/articles/its_no_laughing_matter.htm
Colligan, Michael J., James W. Pennebaker, and Lawrence R. Murphy (eds.)
1982 Mass Psychogenic Illness: A Social Psychological Analysis. Hillsdale, NJ:
Lawrence Erlbaum.
Conley, Robert
1963 Laughing malady puzzle in Africa. The New York Times August 8, Lþ, 29,
55.
Dhadphale, Manohar, and S. P. Shaikh
1983 Epidemic hysteria in a Zambian school: The mysterious madness of Mwini-
lunga. British Journal of Psychiatry 142, 85–88.
Ebrahim, G. J.
1968 Mass hysteria in school children. Notes on three outbreaks in East Africa.
Clinical Pediatrics 7 (7), 437–438.
Fleck, Ludwik
1981 [1935] Genesis and Development of a Scientific Fact. Chicago: Chicago University
Press.
Fry, William F., Jr., and Con Rader
1977 The respiratory components of mirthful laughter. Journal of Biological Psy-
chology 19 (2), 39–50.
Gajdusek, D. Carleton
1963 Motor-neuron disease in natives of New Guinea. New England Journal of
Medicine 268, 474–476.
1976 Unconventional viruses and the origin and disappearance of Kuru. Nobel
Lecture, December 13. In Nobel Lectures, Physiology or Medicine 1971–
1980. Singapore: World Scientific Publishing, 305–354.
Hauser, Gertrud, Hartmut Rothga
¨nger, Aldo Carlo Cappellini, Assunta Guidotti, and
Alessandro Vienna
1997 The biology of laugher: Medical, functional, and anthropological-human
ethological aspects. In Ja
¨kel, Siegfried, Asko Timonen, and Veli-Matti Rissa-
nen (eds.), Laughter Down the Centuries, vol. 3. Turku: Turun Yliopisto, 9– 21.
Helvie, Carl O.
1968 An eEpidemic of hysteria in a high school. Journal of School Health 38,
505–509.
Holden, Robert
1993 Laughter: The Best Medicine. London: Thorsons.
Jones, Timothy F., Allen S. Craig, Debbie Hoy, Elaine W. Gunter, David L. Ashley, Dana
B. Barr, John W. Brock, and William Scha¤ner
2000 Mass psychogenic illness attributed to toxic exposure at a high school. New
England Journal of Medicine 342 (2), 96–100.
Kagwa, B. H.
1964 The problem of mass hysteria in East Africa. East African Journal of Medi-
cine 11 (41), 560–566.
Kerckho¤, Alan C., and Kurt W. Back
1968 The June Bug: A Study of Hysterical Contagion. New York: Appleton-
Century-Croft.
Lambo, Thomas A.
1965 Discussion contribution. In DeReuck, A. V. S., and Ruth Porter (eds.).
Transcultural Psychiatry. London: Churchill, 162–163.
The Tanganyika ‘laughter epidemic’ 69
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
(AutoPDF V7 6/12/06 11:08) WDG (148225mm) TimesM J-1662 Humor, 20:1 HC1: elo 5/12/06 pp. 49–72 1662_20-1_03 (p. 69)
Lloyd, E. L.
1938 The respiratory mechanism in laughter. Journal of General Psychology 19,
179–189.
McGrath, Joseph E.
1982 Complexities, cautions and concepts in research on mass psychogenic illness.
In Colligan, Michael J., James W. Pennebaker, and Lawrence R. Murphy
(eds.), Mass Psychogenic Illness: A Social Psychological Analysis. Hillsdale,
NJ: Lawrence Erlbaum, 57–85.
Muhangi, Joseph R.
1973 A preliminary report on ‘mass hysteria’ in an Ankole school in Uganda.
East African Medical Journal 50 (6), 304–309.
Muluka, E. A. P., M. Dhadphale, and J. M. Mwita
1985 Family hysteria in a Kenyan setting. Journal of Nervous and Mental Disease
173 (4), 249–252.
Nandi, Dhirenda Nath, G. Banerjee, Shibena Bera, Sabyasachi Nandi, and Parthasarathi
Nandi
1985 Contagious hysteria in a West Bengal village. American Journal of Psycho-
therapy 39, 247–252.
Ofcansky, Thomas P., and Rodger Yeager
1997 Historical Dictionary of Tanzania. Lanham, MD: Scarecrow.
Ohala, John J.
1990 Respiratory activity in speech. In Hardcastle, William J., and Alain Marchal
(eds.), Speech Production and Speech Modeling. Dordrecht: Kluwer, 23–53.
Parvizi, Josef, Steven W. Anderson, Coleman O. Martin, Hanna Damasio, and Antonio R.
Damasi Brain
2001 Pathological laughter and crying: A link to the cerebellum. Brain 124 (9),
1708–1719.
Provine, Robert R.
1992 Contagious laughter: Laughter is a su‰cient stimulus for laughs and smiles.
Bulletin of the Psychonomic Society 30, 1–4.
1996 Contagious yawning and laughter: Significance for sensory feature detection,
motor pattern generation, imitation, and the evolution of social behavior. In
Heyes, Cecilia M., and Bennett G. Galef, Jr. (eds.), Social Learning in Ani-
mals: The Roots of Culture. San Diego: Academic, 179–208.
2000 Laughter: A Scientific Investigation. New York: Viking.
Rankin, A. M., and P. J. Philip
1963 An epidemic of laughing in the Bukoba district of Tanganyika. Central Af-
rican Journal of Medicine 12 (9), 167–170.
Rawnsley, K., and Loudon, J. B.
1964 Epidemiology of mental disorder in a closed community. British Journal of
Psychiatry 110, 830–839.
Rothga
¨nger, Hartmut, Gertrud Hauser, Aldo Carlo Cappellini, and Assunta Guidotti
1998 Analysis of Laughter and Speech Sounds in Italian and German Students.
Naturwissenschaften 85, 394–402.
Royal College of Physicians, Royal College of Psychiatrists, and Royal College of General
Practicioners
1996 Chronic Fatigue Syndrome. Report of a Joint Working Group of the Royal
Colleges of Physicians, Psychiatrists, and General Practitioners. CR54. Lon-
don: Royal College of Physicians of London. Available at: http:// dspace
.dial.pipex.com/comcare/docs/brisrep.txt
70 C. F. Hempelmann
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
(AutoPDF V7 6/12/06 11:08) WDG (148225mm) TimesM J-1662 Humor, 20:1 HC1: elo 5/12/06 pp. 49–72 1662_20-1_03 (p. 70)
Ruch, Willibald, and Paul Ekman
2001 The expressive pattern of laughter. In Kaszniak, A. W. (ed.), Emotion,
Qualia, and Consciousness. Tokyo: World Scientific Publisher, 426–443.
Schroetter, H.
1925 Zur Kenntnis des Energieverbrauches bei emotiven A
¨ußerungen des See-
lenlebens. Monatsschrift fu
¨r Ohrenheilkunde und Laryngo-Rhinologie 59,
82–108.
Sebastian, Simone
2003 Examining 1962’s ‘laughter epidemic’.’’ Chicago Tribune July 29, 2, 1, 4.
Seldon, Brad S.
1989 Adolescent epidemic hysteria presenting as a mass casualty, toxic exposure
incident. Annals of Emergency Medicine 18 (8), 892–895.
Shaibani, Aziz Taher, Marwan N. Sabbagh, and Rachelle Doody
1994 Laughter and crying in neurological disorders. Neuropsychiatry, Neuropsy-
chology, and Behavioral Neurology 7 (4), 243– 250.
Shibles, Warren
n.d. Humor reference guide. A comprehensive classification and analysis. Avail-
able at: http://facsta¤.uww.edu/shiblesw/humorbook
Sirois, Francois
1974 Epidemic hysteria. Acta Psychiatrica Scandinavica. Supplementum 252, 1–
46.
1982 Epidemic hysteria. In Roy, A. (ed.), Hysteria. Chichester: Wiley, 101–115.
Small, Gary W., and Jonathan F. Borus
1983 Outbreak of illness in a school chorus: Toxic poisoning or mass hysteria?
New England Journal of Medicine 308 (11), 632–635.
Spencer, Herbert
1860 The physiology of laughter. Macmillan’s Magazine 1, 395–402.
Stearns, Frederic R.
1972 Laughing: Physiology, Pathophysiology, Psychology, Pathopsychology, and
Development. Springfield, IL: Thomas.
Teoh, J.-I., and K.-L. Yeoh
1973 Cultural conflict and transition: Epidemic hysteria and social sanction. Aus-
tralian and New Zealand Journal of Psychiatry 7, 283–296.
Teoh, J.-I., S. Soewondo, and M. Sidharta
1975 Epidemic hysteria in Malaysian schools: An illustrative episode. Psychiatry
38, 258–268.
Trump, Eric
2002 Got the giggles? Join the club. The New York Times July 27, L, B7, B9.
Virani, M. J., and S. Jain
2001 Trigeminal Schwannoma associated with pathological laughter and crying.
Neurology India 49, 162–165.
Wessely, Simon
1987 Mass hysteria: Two syndromes? Psychological Medicine 17, 109–120.
Zigas, Vincent
1990 Laughing Death: The Untold Story of Kuru. Clifton, NJ: Humana Press.
The Tanganyika ‘laughter epidemic’ 71
1
2
3
4
5
6
7
8
9
10
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... According to Krichtafovitch (2006), it is an inborn quality that is necessary for the survival and development of human beings. Humor and particularly jokes have been dealt with by various linguists and psychoanalysts such as Freud (1960), Hempelmann (2007), and Norrick (2009). Freud's Jokes and their Relation to the Unconscious, as Billig (2002) claims, is itself a product of Freud's personal interest in humor where the jokes result from discrimination. ...
... These daily insurrections begin with almost ritualistic anger but quickly become public shows -theater, beauty contests, fashion shows, and public displays of wit -in the hope that whoever is watching might be in need of extra hand, either in the office, at home, or in bed. (Hecht and Simone 1994, 179, emphasis added) Its ubiquity in African daily life notwithstanding, academic interest in humour has been extremely patchy (Hempelmann 2007;Hagberg 2007;Obadare 2009;Hammett 2010;Geshekter and Warsama 1996;Ayoade 1988;Verwoerd and Verwoerd 1994;Smith and Schalkwyk 2002;Barnard 2004). Until recently, to say something was a joke was to literally excise it from the purview of serious interrogation, and studies of humour have remained notably exiguous, even though the larger field of popular culture is relatively crowded. 1 The irony is that humour arguably ought to have stimulated academic interest for exactly the same reasons it appears to have been generally overlooked. ...
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Humour and environmental protection is the first comprehensive and interdisciplinary review focusing on the relationship between humour research and environmental protection, aimed at a wide audience. The book opens up the key characteristics of humour and creates an overall picture of the different humour theories and their links to environmental issues. The book summarises classic humour theories including incongruity, superiority and relief theory, as well as sociological, medical and evolutionary humour studies. Expressions of humour are analysed through different areas of environmental protection, including nature conservation, water protection and climate and energy debates. The book shows that different forms of humour are present in all areas of environmental protection, from urban nature to organic farming. Different parties of social debates utilise humour in various ways, as shown by debates over large carnivores, the protection of old forests and invasive species. The book is based on a summary of an extensive body of research and concrete examples from domestic and foreign environmental debates. In particular, the book examines how humour is utilised in parallel with expert knowledge and suggests that a solution to environmental problems may be found from ecological irony.
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Both psychologists and linguists have discussed the nature of linguistic humor as distinct from forms of humor based on such cultural categories as politics or obscenity or on cognitive categories such as the visual stimulus of slapstick. Linguists have been primarily concerned with manipulations of grammatical categories in producing humorous effect (Green & Pepicello, 1978; Hockett, 1977; Pepicello, 1980; Scott, 1965, 1969). Psychologists have primarily dealt with linguistic humor as an extension of the study of incongruity and its resolution (e.g., Shultz & Robillard, 1980; Suls, 1972). However, both types of study share a common focus, namely, that much of the linguistic humor that appears in traditional riddles and jokes is based on ambiguity, that is, on a word or phrase that has more than one possible meaning.
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[Claire Poppe - STS 901 - Fall 2006] Fleck focuses on the cognitive and social structures idea and fact development and acceptance. - All ideas stem from "proto-ideas" - hazy, unspecific, unscientific concepts accepted as truth in their time period and existing in a socio-cognitive system. - The social structure involved in cognition is conceived as the relationship between: 1) the knowing subject (individual) 2) the object to be known (objective reality) 3) the existing fund of knowledge (provided by the thought collective). - The thought collective is a community of persons mutually exchanging ideas; it is the bearer of collective knowledge and the historical developer of knowledge. The individual's role is to decide whether results fit within the conditions specified by the collective. In this, he/she is influenced by the "thought style," an ambiguous cloud which directs perception and limits the options for interpretation without the perceiver being aware that they are being influenced. - A scientific fact is a signal of resistance opposing free, arbitrary thinking. Facts are 1) in line with the interests of the collective, 2) accepted by the general membership of the collective, and 3) expressed in the style of the collective. - Truth is only true within a single collective. It changes as collectives gradually change with the incorporation/adaptation or rejection of challenges to the thought style. - Within a thought collective, there is a hierarchy consisting of two different groups: a) Esoteric: a small group of experts with specialized knowledge who develop exoteric, popular knowledge b) Exoteric: a larger, more "popular" group that creates public opinion, though not the entire public - Categories of science from more exoteric to esoteric, more concrete to more flexible: a) Popular science: attractive, lively, readable, artificially simplified science in which facts are reality and truth is objective b) Vademecum science: a closed, organized system of the "commonly held" view of science where facts become fixed c) Journal science: a personal, cautious and modest system open to contradictions and explorations
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Linguistic theory makes a vital contribution to humor research by explaining why some joke texts fail to fire for specific audiences, particular people. Much time and effort have been devoted to firing, or successful, joke texts, but it is the joke text not "gotten" that proves more interesting and provides a key to the linguistic processing of joke texts. The constructs of joke competence and humor competence as constituents of a native speaker's linguistic competence are necessary to explain what happens when a hearer processes a joke text.