APOPLEXY

1. What happens in apoplexy?

Williss astonishing Disease, apoplexy, had of old intuitively been
attributed to some ill-define obstruction, whether from want of animal spirits
via the nerves in the tradition of Greek medicine, or, after Harveys time, by
deprivation of blood flow. Yet, it should be remembered that the notion of an
intrinsic nervous energy only slowly lost ground; even Boerhaave in the 18th
century still echoed ancient notions in his explanation of apoplexy as a
stoppage of the spirits (spiritus interceptio; Boerhaave, 1959). In the Table
2.1 we have provided a schematic representation of the development of ideas
abaout apoplexy, and its relationship to arterial lesions, throughout the ages.
Hat Wilis had found bony and impervious arteries in patients who actually
had not died from a stroke was probably the reason tha he was not outspoken
on the pathogenesis of apoplexy. His contemporaries, Wepfer, in
Schaffhausen, and Bayle, in Toulouse, only tentatively associated apoplexy
with corpora fibrosa (Wepfer, 1658) or with calcification of cerebral arteries
(Bayle, 1677).
Wepfer not only recognized arterial lesions, but he also made one of the
great advances in the knowledge about stroke by distinguishing between on
the one hand, arterial obstruction preventing the influx of blood into the
substance of the brain or the ventricular cavities, which were traditionally seen
as an important source of mental energy. What still largely escaped him was
the focal nature of apoplexia, which instead he mainly regarded as a process
of global stunning. The four cases of heamorrhage. Wepfer described were
massive, at the base of the brain or deep in the parenchyma, in back to
Byzantine medicine in the 7th century (Paulus Aeginita, 623-90, edition of
1884), Wepfer suspected dysfunction of the ipsilateral rather than the
contralateral side. He also observed patients who had recover from apoplectic,
and he noted that those most liable to apoplexy were the obese, those whose
face and hands are livid, and those whose pulse is constantly unequal.
That the paralysis was on the opposite side of apoplectic lesion was
clearly predicated by Domwnicio Mistichelli from Pisa (Mistichelli, 1709) on

the basis of his observation of the decussation of the anatomical substrate of

stroke was the work Morgagni. In 1768 he published an impressive series of
clinicopathological observation collected over a lifetime. In which he not only
confirmed the notion of crossed paralysis but also firmly divided apoplexy
into sanguineous apoplexy and serous apoplexy (and a third form which
was neither serous nor sanguineous; Morgagni, 1761). A decade later, Portal
rightly emphasized that it was impossible to distinguish between these two
forms during life (Portal, 1781). It would be a grave anachronism, however, to
assume that serous (non-haemorrhagic) apoplexy was recognized as being
the result of impaired blood flow, let alone of mechanical obstruction. Some
even linked the arterial lesions with brain haemorrhages and not with the
serous apoplexies (Baillie, 1973). Although we have seen that 17 th century
scientist such as Bayle and Wepfer associated some non-haermorrhagic cases
of apoplexy with obstruction of blood flow, in the 18 th century medical
opinion swayed towards vascular congestion, a kind of pre-haemorrhagic
state. That explanation was propounded not only by Morgagni (Morgagni,
1761), but also by may of his contemporaries and followers (Portal, 1781,
Hall, 1836; Burrows, 1846). Cheyne pointed out that, in patients who have
survived a stroke of apoplexy for a considerable time, autopsy may show a
cavity filled with serum which is rusty yellow in colour and which may have
been describing a residual lesion after cerebral harmorrhage rather than
infarction (chayne, 1812).

Figure 1. illustration of
the base of the brain from
williss cerebri anatome (1664),
showing the interconnections
between the right and left
carotid systems, and also
between these two and the
posterior circulation. (from
drawing by Christopher wren,
the architect of st pauls
cathedral in London.)

The anatomical organ based approach exemplified by Morgagni

reflected the Italian practice, in which the separation between physicians and
surgeons was much less strict than in northern Europe with its more
theoretical framework of medicine. The proponents of that school were
Boerhaave (1668-1738) in Leiden and later Cullen (1710-90) in Edinburgh,
both the most influential clinical teachers of their time. They established a
nosological classification that was based much more on holistic theory, in
terms of a disturbed system, than on actual observations at the level of the
organs, at least with 20th century hindsight (King 1991). Probably our own
time will be branded as the era of exaggerated reductionism! In the intellectual
tradition of the Dutch-Scottish school, purely clinical classification of
apoplexy were proposed in the early 19 th century by Serres (with and without
paralysis), by Abercrombie (primary apoplexy, with deprivation of sense and
motion, and sometimes with convulsions, a second type beginning with
headache, and a third type with loss of power on one side of the body and of
speech, often with recovery) and by Hope and Bennett (transient apoplexy,
primary apoplexy with death or slow recovery, ingravescent apoplexy with
parial recovery and relapse, and paraplexic apoplexy paralysis) (Serres, 1819;
Abercrombie, 1828; Hope et al 1840).

Figure 2. illustration
from mistichellis book on
apoplexy (1709) in which
he shows the decussation of
the pyramids and also the
outward rotation of the leg
on the paralysed side.

There are several reasons why the lesions in what we now call cerebral
infraction was not actually identified until the middle of the 19 th century. First,
it was impossible to recognize ischemic softening in patients who had usually
died not long after their stroke. Fixation methods were not available until the
end of the 8th century; Vicq dAzyr, Marie Antoinettes physician, was the first
to use alcohol as a tissue fixative (Vicq dAzyr, 1786) and formaldehyde
fixation was not employed until one-century later (Blum, 1893). Second, it is
probable that many patients diagnosed as having died from apoplexy in fact
had suffered from other conditions. If in our time the diagnosis can be wrong
in as many as 13% of patients referred and subsequently admitted with a
presumed stroke (Norris & Hachinski, 1982), the diagnostic accuracy was
presumably no better in centuries past.