Clemente Mendes (1819–75), who went on to describe his find-
ings in his Estudo sobre a Hemeralopia [Study on Haemeralopia
(Clemente Mendes, 1862)]. All cases resolved spontaneously and
without sequelae within a month. Roughly 2 years after the end of
the first epidemic the third outbreak occurred: between March
1863 and September 1864, 87 out of the 96 resident orphans
developed ‘spasmodic’ vomiting of poorly digested food, some-
times up to 30 or 40 times per day. Apparently no other clinical
manifestations accompanied the vomiting, and all cases resolved
when the patients were removed from the asylum and relapsed on
their return to the institution.
Finally, in March 1864 the paralyses reappeared temporarily in
seven of the patients also suffering from vomiting; five of these
had been affected in the first epidemic. The clinical manifestations
were identical to the ones in the original outbreak, with the ex-
ception that no secondary behavioural phenomena were found.
Barbosa provides an extensive description of one of these patients,
a 17-year-old girl called Maria Ina´cia (Barbosa, 1865). He found
her in good general condition, with an asymmetric paraparesis
(more severe on the right side) and requiring bilateral support
for walking ‘[. . .] to make a few steps she needs to be held up
[and then] will lift slightly each foot, dragging it behind her, keep-
ing it involuntarily turned inwards [. . .]’ (Barbosa, 1865). There
were no signs of atrophy in her lower limbs, no reflex reaction
to thermal or tactile stimuli, but only to electricity; pain, touch and
thermal sensory modalities were deficient from her lower extremi-
ties up to her waistline, and she complained of deep, almost con-
stant pain in the gluteal regions. There were no other findings in
her neurological or physical exam. When last observed, after leav-
ing the asylum, the patient was reported as being slightly im-
proved, but unfortunately, there is no report of a long-term
follow-up.
The controversy: conflicting
pathophysiological concepts
The two central questions debated by the authors were the direct
cause and the pathophysiological nature of these epidemics. As to
the first, Jorda˜o put great emphasis on the poor hygienic and
dietary conditions in the asylum: ‘[The diet consisted of] a quart
of bread at lunch and some tea, some beans and rice at dinner,
and some salad and bread at supper [. . .] Often I complained
about such a dietary system, and managed after a long time to
get them to put in 8 pounds of meat in the dinner pot. Because of
this state of affairs, I was forced in most occasions to resort to cod
liver oil to compensate for nutritional deficiencies and correct lym-
phatism. [After some time] ulcerative stomatitis rapidly developed
and became epidemic [. . .]’ (Jorda˜o, 1865). On the other side,
both Gomes and Barbosa reject such accusations, and the latter
described in exhaustive detail the daily diet the orphans received
e.g. ‘[. . .] Bread 416 grams per day. Meat 131 grams five times a
week. Codfish 69 grams two times a week. Sugar 30 grams per
day [. . .]’ (Barbosa, 1865). He also commented on the building’s
condition and the state of conservation of the copper cooking
equipment and measured the level of plumb in the drinking
water to conclude that in his opinion ‘[. . .] Searching for each of
the circumstances that most directly influence the life and health
of individuals, air, water, food [. . .] nothing stands out which is
not found to a much larger extent in the dispersed poor popula-
tion of Lisbon [. . .]’ (Barbosa, 1865). These two apparently con-
flicting visions probably just reflect differences in the time of
observation; Jorda˜o’s description is most relevant for the earlier
years of the institution and therefore bears a more direct causal
relationship with the start of the epidemics.
Beyond dietary problems, Gomes also pointed to several ‘moral
causes’, such as the life of confinement, overcrowding and the
effects of religious education. As we saw, Jorda˜o was extremely
critical of what he called the ‘excessive religious pressure’ to which
the orphans were subjected. Barbosa was also in agreement with
the negative effects of overcrowding and co-habitation on several
young and impressionable young patients. In their joint opinion,
these were sufficient to induce a ‘state of susceptibility to nervous
disease’ which Gomes and Jorda˜o called ‘hystericism’ while
Barbosa preferred the term ‘nervosism’. At that time, as we will
see, this distinction was more than just semantic.
The second set of questions relate to the nosological classifica-
tion of the paralyses. Barbosa provided the best systematization
and an overview of the contemporary conceptual framework.
Paralyses could have organic causes e.g. direct spinal cord lesions,
(‘material lesions [. . .] which attack the spinal cord primarily or
secondarily, either in its sheathing or the spinal tissue itself’), is-
chaemic causes (‘lack of irrigation of the spinal cord and nerves
[. . .] the organic condition for ischaemic paraplegia is the obstruc-
tion in the abdominal aorta artery which interrupts the access of
blood to the lower spinal cord and lower limb nerves’), dyscrasic
causes (‘alterations in the qualities of the blood’, such as ‘chlor-
osis’, intoxications with mineral—‘lead, mercury, arsenic’—and
vegetal—‘poison mushrooms, tobacco, camphor, ergot, lathyrus
sativus’—substances) and functional or ‘nervous’ causes (‘para-
lyses due to a functional perversion, that is, in which there is no
appreciable material lesion of the nervous centres, or a qualitative
or quantitative alteration in the blood’). This last category did not
refer, as today, to purely psychosomatic diseases, but brought
together paralyses caused by pyrexia and acute diseases, cachexia,
neurosis and hysteria, and the recently described reflex and per-
ipheral paralyses caused by ‘prolonged excitation transmitted to
the spinal cord by the peripheral nerves of the excited organs
such as the genito-urinary tract, abdominal organs, the skin,
etc.’ (Barbosa, 1865).
All authors agree that the events in the Ajuda asylum should be
classified within the functional category. The diagnosis of chlorosis,
or chloro-anaemia, was also briefly considered; this disease,
described for the first time in 1615 by Jean Colliot de Varanda
(c. 1563–1617) was later identified in part with hypochromic an-
aemia. It was thought to attack predominantly young adolescent
virgin women of ‘weak constitution’ (Mercer and Wangensteen,
1985), but for Thomas Sydenham (1624–89) and Armand
Trousseau (1801–67) chlorosis was a nervous disease that sup-
posedly caused a variety of symptoms, such as alterations in skin
tone (giving it a green tinge, hence the name, khloros—!o—
meaning ‘greenish-yellow’), lack of energy, dyspnoea, dyspepsia,
headaches and amenorrhea, and might cause paralysis by altering
The ‘Ajuda Paralyses’
Brain 2010: 133; 3141–3152
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