doi:10.

1093/brain/awl348 Brain (2007), 130, 1690 ^1703

OCC ASIONAL PAPER

Exploring the visual hallucinations of migraine aura:
the tacit contribution of illustration
G. D. Schott

National Hospital for Neurology and Neurosurgery, Queen Square, London, UK

Correspondence to: G D Schott, The National Hospital for Neurology and Neurosurgery, Queen Square, London, WC1N
3BG, UK. E-mail: geoffrey.schott@uclh.nhs.uk

Downloaded from http://brain.oxfordjournals.org by on April 12, 2010

The visual aura of migraine is a subjective phenomenon, and what the migraineur experiences is necessarily
inaccessible to others. Fortunately, however, the sufferer can occasionally reveal what is being seen by means
of graphic representation, enabling an otherwise closed ‘window’ to be opened on the transiently dysfunctioning
brain. This article explores the unique contribution that illustration has made to understanding mechanisms
subserving the visual aura. The most revealing illustrations are those made by the very few scientists who have
recorded and analysed the scotomas, and in particular the expanding fortification spectra, experienced during
their migraine attacks. It is solely through illustrations such as these that the uniform nature of many of these
hallucinations has been demonstrated. As a result, it follows that there is likely to be a similarly uniform reper-
toire of processes that generate the hallucinations in the occipital cortex. The precise form of the zigzags that
comprise the fortification spectrum, their shimmering appearance, and in particular the speed of the periph-
eral spread, all of which are entirely dependent on graphic display for their elucidation, enable conclusions to be
reached about a number of the underlying pathophysiological mechanisms, including the involvement of spread-
ing cortical depression, that likely occur. Illustration has been pivotal too in revealing uncommon and sometimes
curious, if not bizarre, visual hallucinations, the forms of which suggest that extrastriate and temporal lobe
involvement contributes to migraine aura in some instances. Illustration can also be valuable in differential diag-
nosis, depicting other forms of visual hallucination which result from a variety of non-migrainous causes.
Illustration, particularly when made during the attack, provides an unusual, little used but powerful tool
which uniquely allows the sufferer’s subjective visual experiences to inform objective analysis. In turn, this ana-
lysis leads to insights into some of the cerebral disturbances which subserve migraine aura.

Keywords: illustration; hallucination; visual aura; migraine

Received October 6, 2006. Revised November 12, 2006. Accepted November 15, 2006. Advance Access publication January 30, 2007

Introduction: ‘surveying the inner wall

of vision’
‘And you who want to demonstrate with words . . . do away
with such an idea, because the more minutely you describe the
more you will confuse the mind of the reader, and the more
you will remove him from knowledge of the thing described;
it is therefore necessary both to make a drawing of it as well as
to describe it’ (Leonardo da Vinci, c. 1509–1512).
The aim in this review is to draw attention to the primacy
of graphic illustration in the study of the visual aura of
migraine. Migraine with aura is an important, distressing and
common condition; it occurs in 8% of the general
population, and visual aura occurs in 99% of those patients
in at least some of their attacks (Kirchmann, 2006).
But because the aura is a subjective experience, there are
great difficulties not only in evaluating exactly what the
sufferer is experiencing, but also in exploring the underlying
mechanisms. This is where illustration unexpectedly proves to
be the unique method of overcoming many of these
difficulties. Thus, compared with the extensive written
accounts of migraine which date from antiquity, particularly
‘The rising fame of the visual aura’ during the 19th century
and later (Isler, 1987), the documentation and objectivity
attainable by means of illustration provide unique insights
into processes occurring in the transiently dysfunctioning
brain. This contribution considers the development and

ß The Author (2007). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Illustrating the migraine aura
pivotal role of illustration when ‘surveying the inner wall of
vision’ (Updike, 1964), and discusses its role in elucidating
the processes subserving the visual aura of migraine.
As unusual and ingenious scientific devices for translat-
ing symptoms into objective information, the most
revealing illustrations are those detailed graphic analyses
made by the migraineur during the time the visual
disturbance is actually being experienced. Considering the
high prevalence of migraine both with and without aura,
however, accurate illustrations are extremely few in
number. It is all the more remarkable, therefore, that it is
just these rare illustrations which have provided so much of
importance for understanding the underlying cerebral
disturbances. By comparison, illustrations made retrospec-
tively, or at second hand, provide less accurate but none the
less often valuable information.
It is obvious that the illustrations made by the migraineur
depend on the ability to represent accurately what is seen. For
example, children may have difficulty in expressing their
visual disturbances, although illustrations have confirmed
that even young children experience similar visual phenom-
ena to adults during migraine attacks (Hachinski et al., 1973;
Strafstrom et al., 2002). The ability to record what is being
seen may also be compromised by debilitating accompanying
symptoms such as impaired concentration and disturbed
cognition (Aring, 1972). Fortunately, however, these dis-
turbances may be minor or absent during the visual
prodrome—contrasting with the more profound cognitive
disturbances in drug-induced and various other hallucinatory
states sometimes accompanied by visual aura.
On occasions, and not attributable to impaired ability or
confusion, peculiar perceptual features appear in illustra-
tions made by migraine sufferers. These pictures, which
often also include features of distress or suffering, are well
represented by contributions from the public to the various
exhibitions of migraine art, and also by impressive
examples of some professional artists’ output. Important
as they may be to the sufferers, however, these illustrations,
which are briefly discussed later, only occasionally provide
insights into mechanisms. Thus it is to those few analytical
illustrations made by scientists that most attention must
turn when studying these visual phenomena.
The essential role of illustration in
demonstrating uniformity
A prerequisite for any study of the mechanisms subserving
migraine is that there should be at least some degree of
constancy and uniformity in the phenomena experienced. If
every sufferer’s experiences were entirely different, investiga-
tion would be almost impossible, and it would be equally
impossible to envisage any common or unifying mechanism.
It is, however, through illustration, rather than verbal
description, that the uniform nature of the various
hallucinations has been so unequivocally documented. In
passing, it has also been possible to demonstrate that, in spite
Brain (2007), 130, 1690 ^1703 1691
of what might be changing forms of verbal expression over
the years and indeed centuries, this visual constancy can be
shown to be uniform over time. Uniformity can readily be
demonstrated in two particular examples of the visual aura of
migraine: the scotoma and the fortification spectrum, and
these are discussed in the sections that follow.
A comment on the use of the term ‘hallucination’ is
apposite here. It should be clarified that the term is used
throughout in a rather loose and umbrella fashion,
following ffytche and Howard who deliberately had ‘not
differentiated between hallucinated (without afferent sen-
sory signals) and illusory percepts (false percepts with
afferent sensory signals) nor’ . . . ‘differentiated between the
perceptual experiences that are recognized as real by the
patient and those that are not’ (ffytche and Howard, 1999).
In the present article this means the term can encompass
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the great variety of visual experiences that have been
described during the aura, including reports of some
extremely bizarre perceptual phenomena, (e.g. Podoll and
Robinson, 1999, in which illustrative examples are
included), and a number of which are discussed in a later
section. Furthermore, some authors have reported that their
visual aura was influenced by retinal illumination, (e.g.
Fisher, 1999; Pöppel, 1973) this indicates that visual
phenomena that originate within the brain can yet be
modulated by such ‘afferent sensory signals’, thereby
blurring the distinction between internally and externally
triggered visual sensations. Nosological considerations aside,
‘hallucination(s)’ is a word now accepted and in widespread
use throughout the literature on migraine aura, and indeed
it even appears in titles of articles, (e.g. ffytche, 2004;
Panayiotopoulos, 1994, 1999; Reggia and Montgomery,
1996; Wilkinson, 2004).
The uniformity of the scotoma
A striking example of uniformity, impressively revealed by
graphic representation, is the illustration of certain
scotomas, some of which precede, trail or replace the
fortification spectrum. Interesting is the frequent use of
the printed page, superimposed on which is displayed the
central or paracentral and often jagged-edged scotoma, and
examples showing this technique have spanned a century
(Gowers, 1904; Jolly, 1902; Wilkinson and Robinson, 1985)
(Fig. 1). Using a fine detail and high-contrast background
such as print, or more recently a dynamic random-dot
noise pattern (Grüsser and Landis, 1991) (Fig. 2),
with which to reveal the scotoma and its borders in greater
detail is not surprising. This is because, as Ekbom noted,
his scotoma was ‘no larger than the fraction of a letter’
when he was reading a newspaper (Ekbom, 1975), a visual
field defect that would easily be missed in other
circumstances. Sufferers often report the scotomatous area
is grey and indistinct, rather than black, but colours
may also be observed (e.g. Airy, 1870; Grüsser and Landis,
1991).
1692 Brain (2007), 130, 1690 ^1703
Fig. 1 The use of the printed page to reveal the uniformity of migraine scotomas. Left to right: from Jolly (1902); from Gowers (1904);
exhibit from the first exhibition of migraine art, from Wilkinson and Robinson, 1985, reproduced with permission of the Migraine Action
Association and Boehringer Ingelheim UK Limited.
Fig. 2 Display of the scintillating migraine phosphene and its
trailing scotoma, as observed on a dynamic random-dot noise
pattern, from Gru«sser and Landis (1991). Reproduced with
permission of Palgrave Macmillan.
The uniform nature of the fortification
spectrum
Arguably the most dramatic and revealing visual aura that
accompanies an attack of migraine is the fortification
G. D. Schott
spectrum. This term comes from the resemblance of the
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zigzags to the fortified, star-shaped bastions and ravelins
of mediaeval town walls, and not to the appearance of
the crenellations that surmount fortified or decorated walls.
Another descriptive term, ‘teichopsia’, Greek for ‘town-wall
vision’, was introduced by Hubert Airy (1870), and an
account of the terminology of the fortification spectrum
and related hallucinations has been given by Plant (1986),
who also pointed out that ‘spectrum’ refers not to the
coloured spectrum of the rainbow but to the spectral or
ghostly apparition of the hallucination.
The fortification spectrum is so characteristic as to be
almost diagnostic of migraine. Its homonymous jagged
and shimmering, scintillating zigzags usually start central
or more often just paracentral to fixation (e.g. Airy, 1870;
Ekbom, 1975; Fisher, 1999; Grüsser, 1995; Pöppel, 1973);
the zigzags then move outwards, expanding and becoming
brighter as they proceed, and disappear in the periphery. As
noted earlier, the sufferer often first becomes aware that
there is something amiss when reading (e.g. Airy, 1870;
Ekbom, 1975), finding one or more individual letters has
disappeared, and the scintillating zigzags then develop soon
after. These move when the point of gaze is moved, they
affect both eyes simultaneously, and typically accompanying
the zigzags is an inner, characteristically bean-shaped
scotoma. The march of the hallucination takes 20 min,
and is often but not always followed by headache and the
other typical components of migraine.
But if, in summarizing numerous sufferers’ descriptions,
this account describes the fortification spectrum, it tells
little else, and merely emphasizes that, in investigating
the migraine aura, the ‘main constraints are imposed by
the subjective results from psychophysical recordings of the
symptoms’ (Dahlem and Müller, 2004). From the written
description of this hallucination it would be impossible to
envisage, let alone investigate, precisely what is being
experienced; one instinctively reaches for a pencil.
Exemplifying why illustration proves an essential inves-
tigative tool, and one often far superior to the written
account, are the supposedly earliest illustrations of a
migrainous visual aura. These appeared in Scivias, the
Illustrating the migraine aura Brain (2007), 130, 1690 ^1703 1693

mediaeval illuminated manuscript written around 1180 by
Hildegard of Bingen (1098–1180). It has been claimed that
this visionary German abbess suffered from migraine and
that her illustrations ‘indisputably’ represented migrainous
hallucinations (‘visions’), (e.g. Sacks, 1993). This view
originated from the influential paper by the medical
historian Charles Singer, who commented on the ‘often
definite fortification figures’ (Singer, 1917). However, even
cursory inspection of the illustrations shows they reveal
features entirely different from those characteristic of
migraine—rather, Hildegard’s ‘fortification figures’ resem-
ble the castellated tops of battlements, which are depicted
together with human figures. To the present writer, neither
Hildegard’s illustrations, nor her descriptions, are at all
suggestive of migraine aura, and others too have been
sceptical (Levene, 1975–6; Plant, 1986; Rose, 2004). Here
Revealing the characteristics of the fortification spectrum
started in earnest in the 19th century. The consistently
jagged outlines to scotomas, that recall the jagged periphery
of the fortification spectrum, have been referred to earlier.
However, probably the first but almost unknown illustra-
tion of the spreading scintillations of a migraine aura
appears in a remarkable letter from Sir George Biddell Airy,
the Astronomer Royal (Fig. 3, upper left). In 1865 he
described his own spreading zigzags as resembling ‘a
Norman arch’; the zigzags are deeper inferiorly, and they
‘tremble strongly’, again particularly inferiorly. Only one
arch is seen at a time, it expands as it spreads outwards,
and ‘finally passes from the visual field’, the duration of
‘this ocular derangement’ being 20–30 min (Airy, 1865).
However, undoubtedly the most famous and similarly
detailed, but entirely different, form of representation of the

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illustration has been instrumental in discriminating fact fortification spectrum was published by G. B. Airy’s son,
from fiction. Hubert, in 1870 (Fig. 3, upper right), and this important

Fig. 3 The 19th century and the first drawings of the fortification spectrum. Upper left: spreading zigzags resembling ‘a Norman
arch’çA is at the beginning, and lines Bb, Cc, etc. show the arch as it gradually increases in dimensions and moves peripherally, from Airy
(1865). Upper right: the upper two lines of sequences (1^ 4, 5^ 6) show the spread of two hallucinations, the white dot, o, being the
fixation point; the large figure, 9, shows the fortification pattern in more detail, from Airy (1870). Lower left: a colourful representation of
expanding spectra drawn by Babinski’s patient, from Babinski (1890). Lower right: Charcot’s marginal diagram of a scotoma with a
fortification-type outline, from Charcot (1887).
1694 Brain (2007), 130, 1690 ^1703
illustration is discussed in the following section. Later in
the 19th century others, too, illustrated fortification
spectra, another fine example being the numbered sequence
of coloured hallucinations drawn by the sufferer, a
professional etcher, and reproduced by Babinski in his
paper on hysteria and migraine (Babinski, 1890) (Fig. 3,
lower left). The visual hallucinations as depicted would be
consistent with migraine aura, even if other features of the
attacks were somewhat unusual.
Intriguingly, the patient was referred to Charcot in 1886,
and a year later Charcot himself illustrated a fortification
spectrum in his ‘Leçons du Mardi à la Salpêtrière’ for 22
November 1887 (Fig. 3, lower right). After interviewing ‘le
malade’ who suffered from ‘la migraine ophthalmique’,
Charcot not only illustrated the visual disturbance but also
commented that it ‘ressemble à une plan de fortifications
. . .’ (Charcot, 1887). Whether Charcot knew of the Airys’
papers and the various other descriptions of the fortifica-
tion appearance is unclear, but Charcot evidently appre-
ciated the analogy between the hallucination and its
resemblance to the architectural features. Non-scientists,
too, have left graphic records of what are probably their
fortification spectra, including Pascal, whose doodles in the
margins of his letters are thought to show his own
fortification spectra (Critchley, 1967).
If these illustrations of the fortification spectrum, as with
those of the scotoma, show how similar these hallucinations
are, and thus strongly suggest an equally similar repertoire
of underlying physiological processes, illustration was yet to
prove far more powerful in understanding those physiolog-
ical processes.
Representing the march of the
visual hallucination
It would be all but impossible to investigate the dynamic
cortical events taking place in the visual cortex without the
detailed graphic depictions of the expanding aura made
during the time of the migraine attack. As mentioned
earlier, the best known illustrations of this spreading visual
hallucination were those drawn in 1870 by Hubert Airy, son
of Sir George Airy, both of whom suffered from migraine.
Hubert Airy’s famous drawings, published by none other
than his father in the Philosophical Transactions of the Royal
Society of London, record the progress and expansion of his
own visual disturbances (Airy, 1870), and are arguably the
most beautiful scientific records of migraine aura ever made
(Fig. 3, upper right). However, although Airy stated that his
auras lasted ‘about 30 min’, his illustrations did not record
the timing of the successive images.
A later, similar graphic representation of the outward
rippling of the fortification spectrum was provided by
Aring, who, although stating the phenomenon lasted
20 min, again provided no further information (Aring,
1972). Thus the illustrations provided by the Airys (1865,
1870) and Aring (1972) documented the constant nature of
G. D. Schott
the spreading and expanding disturbance with its time
course of 20–30 min, and others during the past century
have made similar graphic recordings of their self-observed
spreading scotomas and fortification spectra, sometimes
using a series of images, (e.g. Hare, 1966; Jolly, 1902;
Pöppel, 1973). However, none of these illustrations, even
though they sometimes included sequences, provided the
detail necessary for further analysis of the temporal aspects.
In 1941 Lashley provided the first and remarkably
detailed quantitative records of the nature and temporal
spread of his own migrainous scotomas and fortification
spectra. In his classic illustrations Lashley plotted in detail
the movement of his hallucinations, enabling him to deduce
that the speed of its spread over the cerebral cortex was
3 mm/min (Lashley, 1941) (Fig. 4). Others came to a
similar conclusion, and recently Wilkinson, using subjects
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who drew their auras under controlled conditions, pro-
jected these changes of spreading aura on to a map of the
unfolded striate cortex, and confirmed a rate of spread of
2 mm/min (Wilkinson, 2004).
Even more detailed and analytical, self-drawn illustra-
tions of the evolving fortification-like patterns during
migraine attacks have been made by a small number of
scientists, including McCulloch (Bücking and Baumgartner,
1974), and Grüsser and his colleagues (Grüsser and Landis,
1991), and these illustrations have confirmed and developed
Lashley’s observations. Once again, it is solely illustrations
such as these, some examples of which are included in
Fig. 5, which enable these fortunately uniform and
consistent phenomena to be evaluated with precision, and
considerable quantitative information to be derived.
Not only do these illustrations reveal a striking inter-
observer consistency, but illustrations can reveal intra-
observer consistency as well, as exemplified by Grüsser’s
recordings of 11 of his own attacks over 15 years (Grüsser,
1995). From such recordings it has also been
confirmed that the speed of movement of the spreading
hallucination increases as the hallucination moves
peripherally.
Analysing the composition of the
fortification spectrum
An understanding of the composition of the fortification
spectrum is almost entirely dependent on its graphic
depiction. Drawings of the hallucination show that the
characteristic features comprise short stacks of jagged,
alternating black and white lines or bars, the stacks being
set at angles to each other, and arranged in an arc
surrounding a scotoma at the trailing border.
One of the most detailed early analyses resulted from the
illustrations reported by Richards (1971), although these were
not those recorded by the author during a migraine attack, but
were those ‘seen by the author’s primary subject (his wife)’
and redrawn from her sketches (Fig. 6, left). Whilst acknowl-
edging they are second-hand, these detailed illustrations
Illustrating the migraine aura Brain (2007), 130, 1690 ^1703 1695

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Fig. 4 The first analytical drawings of the spatiotemporal evolution of spreading migraine hallucinations. Left: a scintillating scotoma,
spreading at the intervals shown. The blindspot is shown as the dotted circle, and the fixation point as x; alternate outlines are solid and
dotted to avoid confusion; scintillations were confined to the region above the line s-s. Right: successive forms of a scintillating scotoma,
mapped at different time intervals as indicated; the fixation point is shown as x. From Lashley (1941). Copyright ß 1941 American Medical
Association. All rights reserved.

Fig. 5 Self-observed and recorded illustrations during migraine attacks, showing detailed temporospatial relationships of the
hallucinations. Left: drawn by W. S. McCulloch, from Bu«cking and Baumgartner (1974). Reproduced with kind permission of Springer
Science and Business Media. Centre 2 figures, from Gru«sser and Landis (1991). Reproduced with permission of Palgrave Macmillan. Right,
reprinted from Gru«sser O-J (1995). Copyright 1995, with permission from Elsevier.

of the ‘bars’ in the fortification arc show that they consist
of two parallel bright lines with a dark gap between. The
lines are described as shimmering and oscillating in bright-
ness, ‘with all the inside lines ‘‘on’’ when all the outside
lines are ‘‘off ’’, and vice versa’, producing ‘a ‘‘boiling’’ or
‘‘rolling’’ motion’. This appearance suggested to Richards that
there was a network of reciprocal inhibition, with depression
of activity enhancing the spontaneous neural activity in
adjacent regions.
The parallel lines of the fortification spectrum are
‘serrated’ or angulated, with an internal angle of 45 near
the centre of the visual field, increasing to 70 at the
periphery. Richards pointed out that his wife’s redrawn
illustrations showed there were no radial lines perpendicular
to the boundary of the fortifications, and that there were
often gaps separating the ends of the lines (Fig. 6, right). The
size of the individual phosphene ‘bars’ or ‘particles’, and the
width of the scotoma, increase with increasing eccentricity
1696 Brain (2007), 130, 1690 ^1703 G. D. Schott

Fig. 6 Left: Redrawn sketch of Richard’s wife’s spreading fortification spectrum; ordinarily one arc is seen at a time; the dot is the fixation

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point. Right: analysis of its component bars, showing the inner angle of the serrations are 45 near the centre, increasing to 70 at
the periphery; the radial lines, which are never seen, have been added to show the postulated underlying honeycomb pattern and hence
latticed structure of the visual cortex. From Richards (1971). Reproduced with permission of Jerome Kuhl.

from the centre. This had first been quantified by Hare

(1966), whose detailed self-observations were presented in a
graph that showed the increasing vertical diameter of the
visual disturbance as the attack progressed.
From Lashley’s drawings it has been possible to confirm
not only the expansion and spread of the scintillating
scotoma, but also that the detailed components of the
fortification pattern remain unaltered, although Lashley
noted that the pattern was coarser and more complicated
inferiorly (Lashley, 1941) (Fig. 7). The difference in the
appearance between the upper and lower parts of the
hallucination strikingly recalls G. B. Airy’s observations of
his own migrainous zigzags almost a century earlier (Airy,
1865), although such differences may simply relate to the
distance of the fortification patterns from the fovea
(Grüsser and Landis, 1991).
How many lines, their lengths, and the angles between
them vary to some extent between different individuals, and
because they move and shimmer, even the most detailed Fig. 7 The scotoma and different components of the fortification
drawings are at best approximations as to what is being outline, with the coarser and more complex features represented
seen. Nevertheless, the reproducibility of these observa- in the lower part. See text for further details. From Lashley
(1941). Copyright ß 1941 American Medical Association. All rights
tions (e.g. Grüsser, 1995) again strongly suggests that reserved.
there is likely to be constancy of pathophysiological
mechanisms which generate the various components of
the hallucinations.
(Lauritzen, 1994). It is now known that CSD can also be
induced by other stimuli, including high concentrations of
Cortical spreading depression (CSD): a likely potassium ion and glutamate, and, at least in animals, it can
mechanism revealed through illustration be blocked by NMDA antagonists. The interruption of cor-
In 1944, Leão described a new phenomenon: the wave of tical function is associated with profound changes in cortical
depression of cortical electrical activity that follows electrical ion homeostasis, in particular intracellular loss of potassium
or mechanical stimulation of the cerebral cortex (Leão, 1944). and hydrogen ions, and entry of sodium, calcium and
This spreading depression is a wave of short-lasting neuronal chloride ions together with water, but involvement of a host
and glial depolarization that moves across the cortex in of other chemicals and up-regulation of a variety of genes
all directions at a speed of 3–5 mm/min. It is accompanied are also known to occur (Sanchez-del-Rio and Reuter, 2004),
by a brief, marked increase in cerebral blood flow, which though the precise mechanisms mediating cortical spreading
is followed by a more prolonged phase of hypoperfusion depression remain unclear.
Illustrating the migraine aura
A year after his first paper on CSD, Leão himself had
speculated in passing that it might be associated with
epilepsy
‘and the presumably related condition of migraine. The latter
disease . . . is suggestively similar to the experimental phenom-
enon here described’ (Leão and Morrison, 1945).
It was Lashley’s illustrations of his migraine aura,
however, and his conclusion concerning the speed
of spread of the hallucination, that subsequently enabled
Milner to more clearly envisage the possible link between
CSD and migraine. In a prescient comment, he stated:
‘In brief, the writer thinks that attention should be drawn to
the striking similarity between the time courses of scintillating
scotomas and Leão’s spreading depression because, if there is
a true correspondence between these phenomena, there is hope
that some of the work done on spreading depression can be
brought to bear on the problem of migraine’ (Milner, 1958).
For two reasons the implications of Milner’s comments
proved a subject of much debate. First, theories that
postulated a primarily vascular basis for migraine and
its aura vied with theories invoking a primarily neural
basis (Spierings, 2004), even interictally (Kennard, 1996).
Second, although the involvement of CSD in migraine had,
as indicated earlier, been long proposed, and indeed
Lauritzen had noted ‘It appears that CSD displays
sufficiently important similarities to the migraine attack
that it can be considered a disease model’ (Lauritzen, 1994),
it was unclear whether the experimental findings in animals
that underpinned the concept of CSD also obtained in
humans—which it has recently been confirmed they do
(e.g. Fabricius et al., 2006).
This suggestion has been indirectly supported by
numerous imaging techniques including xenon, SPECT
and PET scanning, and MRI, and by magneto-
encephalography (MEG) (Hadjikhani et al., 2001).
However, further and compelling evidence was recently
provided by means of functional MRI studies on three
migraineurs. One of the subjects induced two of the attacks,
and two other subjects had three spontaneous attacks.
Admittedly, the spreading visual aura was not a fortification
spectrum but a white scintillating crescent, ‘like TV snow’,
that progressed peripherally in a similar fashion and was
followed by a central scotoma. Admittedly, too, the
illustration of the spreading hallucination was not drawn
by the migraineur during the scanning but was mapped by
noting the times of onset and cessation of the scintillations
(Fig. 8). Nevertheless, it was crucially the graphic display of
the migraineurs’ hallucinations during the aura that allowed
correlation with the changes in the blood oxygenation level-
dependent (BOLD) signal (Hadjikhani et al., 2001).
Hadjikhani and colleagues (2001) were able to confirm that
there was an initial increase in BOLD signal, possibly due to
vasodilatation, which progressed slowly and contiguously at a
Brain (2007), 130, 1690 ^1703 1697
rate of 3.5 mm/min, and this was congruent with the visual
aura. Following this progression was diminution in the BOLD
signal, perhaps due to vasoconstriction. These and other data
enabled the authors to conclude that the visual aura does
indeed have characteristics typical of CSD, and the vascular
changes appear to be secondary. Whilst both areas are
retinotopic, in one of their patients the aura appeared to arise
from the extrastriate area V3 rather than V1, and extrastriate
and temporal lobe involvement in migraine aura has also
been detected by MEG (Hall et al., 2004)—an aspect
commented on later.
The implications that structural elements of the brain,
or what would now be considered the specific cytoarchi-
tectonic composition of the visual cortex, might be crucial
for understanding the visual hallucinations in migraine,
was correctly foreshadowed over a century ago. Sir John
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Herschel, another famous 19th century astronomer, specu-
lated that his migraines might be due to ‘. . . a kaleidoscopic
power in the sensorium to form regular patterns by the
symmetrical combination of causal elements . . .’ (Herschel,
1866). Over the ensuing 150 years, as a result of detailed
analyses of the illustrations of the aura made during
migraine attacks, a number of likely neural processes at the
cellular level have been elucidated (for reviews, see, e.g.
Grüsser and Landis, 1991; Grüsser, 1995; Dahlem et al.,
2000; Dahlem and Chronicle, 2004; Silberstein, 2004). In
brief, a continuous and smooth wave of excitation probably
propagates across the primary visual cortex (Dahlem et al.,
2000); the zigzag pattern has been related to the functional
micro-structure of the hypercolumns in area V1 (Richards,
1971; Grüsser, 1995; Wilkinson, 2004); the flickering
phosphenes have been attributed to spreading waves of
cortical hyperactivity, with the scotoma at the trailing edge
of the fortification spectrum being attributed to neural
hypoactivity (Lashley, 1941; Grüsser and Landis, 1991);
and the peripheral spread of the hallucination has been
attributed to spreading diffusion of a variety of ions and
neurotransmitters, including potassium ions or glutamate,
or both, along the extracellular space along the stripe of
Gennari—the disappearance of the hallucination perhaps
being because this process stops at the area V1/V2 border
(Grüsser, 1995).
Furthermore, computational models of travelling waves
of neural activation as seen in CSD can generate corre-
sponding visual features that strikingly resemble the
hallucinations in migraine aura (Fig. 9). Such models also
satisfyingly predict an exponentially increasing speed of
the visual hallucinations as they spread peripherally (Reggia
and Montgomery, 1996).
Thus, in summary, it is now generally accepted that
neural processes which give rise to CSD are indeed likely to
account for the spreading aura of migraine (Silberstein,
2004; Teive et al., 2005): Leão and Milner were almost
certainly correct. This link could only have been made by
means of illustration, and it is striking that so many
scientific articles, including those dealing with theoretical
1698 Brain (2007), 130, 1690 ^1703 G. D. Schott

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Fig. 8 Spreading suppression of cortical activity during migraine aura, as shown by fMRI. (A) A drawing of the progression over 20 min
of the scintillating field defect, as described by the patient, with fixation point marked as small cross. (B) The spread of the BOLD signal
complex from the posterior pole towards more anterior regions representing the peripheral visual field; MR perturbations develop earlier
in the foveal regions than in the periphery, consistent with the progression of the aura from the centre to the periphery. (C) The MR
maps of retinotopic eccentricity acquired during interictal scans. See text for further details. From Hadjikhani et al. (2001) Copyright
2001 National Academy of Sciences, USA.

aspects, necessarily incorporate one or more of the
illustrations discussed in this review.
Illustrating the effect of haemodynamic
changes on the migraine visual aura
Hare plotted his own migrainous hallucinations in 12
attacks (Hare, 1966). On six occasions during three attacks
he was able to show that inhalation of ‘small doses
(3–5 breaths)’ of amyl nitrite temporarily reduced the
vertical diameter of the spectral pattern by 515% of the
expected diameter. Larger doses of amyl nitrite had
no effect. He speculated that the march of the visual
disturbances was either related to a steady state of
vasoconstriction with increasing spread of anoxia, or that
there was a gradually increasing spread of vasoconstriction
throughout the march. As an aside, he also speculated in
a later study whether ergot, presumably through its vaso-
constricting properties, altered the form of the visual
hallucination.
Hare’s graph recorded an effect that had previously been
shown but in a different form by observations made by
Cahan. During two episodes of migraine, Cahan made
‘accurate and rapid observations of his own visual field
defects’; he displayed his observations by means of serial
plots of his visual fields after inhaling amyl nitrite,
comparing the visual changes after an amount insufficient
to induce hypotension with an amount producing
symptomatic hypotension (Fig. 10). Schumacher and
Wolff, who reported these studies, concluded that cerebral
vasodilatation without hypotension caused the scotoma to
disappear, but hypotension that presumably resulted in
decreased cerebral blood flow exacerbated the visual
disturbances (Schumacher and Wolff, 1941). Neither
Hare, nor Schumacher and Wolff, took account of the
neural substrates that might also be involved and which are
considered today to be crucial.
Illustrating neurophysiological influences on
the fortification spectrum
Although Pöppel had reported that eye movements shifted
his fortification patterns by the angle of eye movement
(Pöppel, 1973), more extensive studies were published by
Illustrating the migraine aura
Fig. 9 Computer-generated simulation of the fortification
hallucination. From Dahlem et al. (2000). Reproduced with
permission of Blackwell Publishing.
Jung (1979). Whilst confirming Pöppel’s observation, Jung
also investigated the influence of induced nystagmus on the
fortification spectra seen during his own and a colleague’s
migraine attacks. He found that there was translocation of
the phosphene in the direction of the slow phase of the
nystagmus induced by optokinetic stimulation, but—in
contrast to voluntary eye movements—the phosphenes
induced did not cross the midline. Furthermore, he
depicted the effects of nystagmus induced by a rotating
chair: on rotation to the right, the phosphene moved to the
left in the direction of the slow phase of the nystgamus, and
became more elliptical. On stopping rotation, the phos-
phene moved to the right in the direction of the slow
phase, became flattened, and moved transiently beyond its
initial position.
Jung used illustrations to demonstrate the effects of these
vestibular influences on the spontaneous peripheral spread
of the fortification spectrum, and concluded that the
vestibular system has inhibitory effects on what would
otherwise be more marked movements of the visual
hallucination. However, the illustrations themselves lack
detail and have limitations; for example, it is unclear how
Brain (2007), 130, 1690 ^1703 1699
they were drawn, the distance of the screen from the
migraineur, and the timing of the normal outward drift of
the phosphene in relation to the induced nystagmus. The
illustrations therefore provide in some but not exhaustive
detail what would otherwise be unrecordable physiological
phenomena.
Illustrating visual perceptual changes
in migraine
Contrasting with the illustrations discussed earlier, and
which contribute much to the scientific analysis of the
migraine aura, are the numerous illustrations which simply
express distress. However, there are yet other illustrations
that reveal much more unusual perceptual visual distur-
Downloaded from http://brain.oxfordjournals.org by on April 12, 2010
bances, the processes causing them being ill understood.
Various disturbances of visual perception in migraine have
been reported over the past century, and 40 years ago Klee
and Willanger reviewed the available literature and added
eight cases of their own (Klee and Willanger, 1966)—
although their observations are limited by the lack of
graphic representation of these disturbances. It was,
however, and unexpectedly, through the advent of exhibi-
tions of migraine art that the extent of the visual
phenomena experienced by migraineurs first became
evident.
In the first British exhibition of migraine art in 1981, 32
of the 207 entries showed metamorphopsia or alterations of
shape or objects with distorted contours (Wilkinson and
Robinson, 1985). From larger numbers of pictures available
through further exhibitions, even more unusual perceptual
disturbances have been identified; for example, 7 illustra-
tions from a total of 562 pictures were recorded as showing
out-of-body features—including hallucinations of a dupli-
cate or parasomatic body (Podoll and Robinson, 1999).
Sufferers’ drawings of a corona around objects, Lilliputian
hallucinations, illusory splitting, and macro- and micro-
somatognosia are other examples in which illustration has
been the sole means by which these visual auras became
recorded and characterized, and even digital image
reconstruction of such disturbances has been employed
(Kew et al., 1998).
Unfortunately there is little if any information on when
the pictures were made in respect of the timing of the
migraine attack, and often specific elements of the visual
aura and expression of distress are combined in an
interesting but scientifically less useful way. Nevertheless,
despite their subjective nature, ‘the large number of similar
representations probably confirms their organic nature’
(Wilkinson and Robinson, 1985). Temporal lobe dysfunc-
tion during the visual aura of migraine in particular may be
relevant (Podoll and Robinson, 1999), and temporal lobe
changes detected by MEG (Hall et al., 2004) and by
functional MRI (Hadjikhani et al., 2001) have been referred
to earlier.
1700 Brain (2007), 130, 1690 ^1703 G. D. Schott

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Fig. 10 Cahan’s self-observations on his migrainous field defects when inhaling a small (upper figure) or larger (lower figure) amount of
amyl nitrite. In the former experiment, when blood pressure was maintained, the migraine scotoma disappeared, whereas in the
latter, when hypotension developed, the scotoma increased. See text for further details. From Schumacher and Wolff (1941). Copyright
ß 1941 American Medical Association. All rights reserved.

lesions. Some disorders, for example dementia, psychoses

The differential diagnosis of the visual aura
of migraine
Countless illustrations have recorded the great variety of
visual hallucinations in many non-migrainous disorders.
These disorders have been classified into those involving the
visual pathways, and those involving the brainstem/
cholinergic system. The former group is seen in ocular
disease, occipital infarcts and epilepsy, as well as migraine;
the latter group is variously attributable to anticholinergic
drugs, Parkinson’s disease, narcolepsy and peduncular
and delirium, may implicate both groups. In ‘matching
syndrome to aetiology’, it has been argued that ‘the palette
of hallucinations in a given patient thus reflects the location
and extent of their susceptible cortex’ (ffytche, 2004).
Particularly when visual hallucinations result from
disorders of the visual system, the disorder may be far
more clearly identified when revealed by self-illustration.
For instance, in another irritative cortical phenomenon, the
occipital epilepsy of childhood, Panayiotopoulos argued
that, whilst not invariable and whilst epilepsy and migraine
Illustrating the migraine aura
can coexist, colours and circular or spherical shapes are
typically encountered in the former, and jagged, and often
non-coloured hallucinations in the latter (Panayiotopoulos,
1994, 1999). Although comprising pictures made by
children after, rather than during, their epileptic attacks,
Fig. 11, left, shows the appearance of visual hallucinations
which clearly are quite different from the usual hallucina-
tions experienced during migraine aura.
When reviewing the various hallucinatory phenomena
encountered in eye disease, ffytche and Howard (1999)
commented on the similarity of certain forms of hallucina-
tions. For example, these authors drew attention to ‘the
consistency’ of tesselloptic hallucinations in patients with a
right occipital infarct, under the influence of LSD and
mescaline, ‘patients with eye disease’, and migraine.
The term ‘tesselloptic’ is derived from ‘tessellopsia’
(from the Greek ‘tesseres’ or tessares’, ‘four’ as in four-
sided, and thence a small tile used in mosaic); it was
proposed by ffytche and Howard (1999) to describe the
patterns of regular, repeating forms seen in brickwork,
lattices, mosaics, crazy paving, etc., and recalls what
Klüver called ‘form constants’ when describing the similar,
often geometric visual hallucinations experienced by
those under the influence of mescaline (Klüver, 1966).
Acknowledging there are often angulated features to
the drawings, to the present writer examination of the
graphic appearances often reveals dissimilar features. This
dissimilarity is hardly surprising, since it is likely that the
different disorders are subserved by equally different
underlying pathophysiological processes. Indeed, numerous
detailed illustrations testify to the very different visual
hallucinations recorded by patients whose disorders range
from psychotic disturbances (Guttmann and Maclay, 1937)
to the effects of hallucinogenic drugs (Maclay and
Guttmann, 1941); and to ophthalmic conditions which
affect structures as anterior as the lens (Hu and Scotcher,
Fig. 11 Illustration as an aid to differential diagnosis. Left: visual hallucinations as depicted by children suffering from occipital
seizures, from Panayiotopoulos (1994). Copyright ß 1994, BMJ Publishing Group. Right: zigzag lines depicted by an artist illustrating his
own hallucinations during mescaline intoxication. From Maclay and Guttmann (1941). Copyright ß 1941 American Medical Association.
All rights reserved.
Brain (2007), 130, 1690 ^1703 1701
2005) and retina (Burke, 2002), and as posterior as the
occipital cortex.
Exemplifying the value of illustration in revealing
different underlying causes is an example of mescaline-
induced hallucinations, described as comprising ‘spreading
of zigzag lines’ (Maclay and Guttmann, 1941) (Fig. 11,
right). Were these hallucinations migrainous? Recalling the
discrepancy between the written and visual accounts of
Hildegard’s auras, although the description might suggest a
migrainous disturbance, the illustration made during
mescaline intoxication immediately reveals a pattern of
hallucinations that is easily distinguishable from that
occurring in migraine—including the lack of a hemianopic
distribution and the far less regular and angulated form of
fortification pattern.
Illustration has also allowed detailed analysis of experi-
Downloaded from http://brain.oxfordjournals.org by on April 12, 2010
mentally induced visual hallucinations, including those
following stroboscopic (Smythies, 1959, 1960), electrical
(Brindley and Lewis, 1968), combined electrical and drug
(Knoll et al., 1963), and transcranial magnetic (Cowey and
Walsh, 2000) stimulation. Again, whilst the written
accounts may variously refer to tesselloptic hallucinations,
including those similar to the hallucinations reported with
hallucinogenic drugs (Klüver, 1966), the graphic records
show that experimentally-induced visual hallucinations are
in reality entirely different from those occurring during
migraine.
Conclusions
Probably the first scientific illustrator of the migrainous
visual aura, G. B. Airy rightly, although at the time
controversially, concluded that ‘the seat of the disease is
the brain’ (Airy, 1865), and graphic representation can
provide invaluable and sometimes the only method for
elucidating those underlying processes occurring in the
brain. Nevertheless, there have been remarkably few
1702 Brain (2007), 130, 1690 ^1703
accurate and detailed illustrations—and nearly all of them
have been made during the past 150 years by scientists,
notably first by astronomers and then by neuroscientists.
The paucity of scientifically useful illustrations contrasts
with the increasing numbers of illustrations of migrainous
phenomena provided by the public. It also contrasts
with the output of professional artists such as de Chirico
(Fuller and Gale, 1988); in these artists, migraine—
diagnosed with varying degrees of certainty—merely
seems to ‘expand the repertoire of visual forms’ available
to them, rather than reveal underlying mechanisms
(Chatterjee, 2004).
Illustration, particularly self-made during the attack,
remains a unique but neglected scientific method in an
age which prizes objectivity, and in the study of the visual
aura of migraine the use of illustration has enabled
subjective experience to inform objectivity and analysis.
To extend these studies further, Pöppel (1973) and later
Grüsser (1995) pleaded for migraine sufferers with visual
auras to communicate their observations to the respective
authors, and recently it has also been possible for patients
to compare their auras with computer-generated
animated simulations of fortification spectra. Since these
simulations can be ‘alarmingly realistic’ (Dahlem and
Chronicle, 2004), they may perhaps prove a valuable tool
for further research.
Finally, the ancients from the time of Plato to the albeit
wavering believer, Leonardo da Vinci, with whom this
account began, were sometimes right (Kemp, 1977): in
certain circumstances, what we see indeed emanates from
within rather than from without.
Acknowledgement
I am most grateful to Professor Ian McDonald for his
comments and encouragement.
Note added in the proof: This contribution is respectfully
dedicated to the memory of Professor Ian McDonald, who
died as the paper was going to press.
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