CLINICAL MEDICINE
Papilloedema (Choked Disc)
AK Agarwal*, Pushpa Yadav**, RK Sharma**, Ratnesh Singh Kanwar***
Papilloedema simply means oedema of the optic
disc, without reference to its underlying cause. It
may be due to different pathological states, of
which the most important ones are mentioned in
Table I.
This article mainly concentrates on papilloedema
due to raised intracranial pressure.
Table I: Causes of Optic Disc Oedema and
Papilloedema
I. Increased intracranial pressure (tumour,
haemorrhage, infarction, abscess, oedema,
benign intracranial hypertension).
II. Inflammatory optic neuropathy (optic or
retrobulbar neuritis).
III. Infiltrative optic neuropathy (sarcoidosis,
leukaemia and other malignancies).
IV. Optic nerve tumours (angioma, meningioma,
childhood optic nerve glioma, malignant optic
nerve glioma, metastatic carcinoma).
V. Compressive optic neuropathy (Grave’s disease,
sphenoid wing meningioma).
VI. Vasculopathies (anterior ischaemic optic
neuropathy, central retinal vein occlusion,
malignant hypertension).
VII. Intra-ocular disease (posterior uveitis, posterior
scleritis).
VIII. Venous obstruction (due to space occupying
lesions in the orbit, cortico-cavernous fistula,
intrathoracic venous obstruction as by
neoplasms, aneurysm of aorta).
IX. Conditions associated with a massive increase
in the protein content of CSF (e.g., some cases
of Guillain Barre syndrome and spinal tumours).
X. Pseudopapilloedema (optic disc drusen,
hyperopia and other anomalies).
* Consultant in Medicine
** Senior Specialist
*** Postgraduate student
Department of Medicine, Dr Ram Manohar Lohia
Hospital, New Delhi–110 001, India.
Papilloedema due to raised intracranial
pressure
Recognition of papilloedema is of great clinical
importance because it is the classic and most
important clinical sign of raised intracranial
pressure. Modern diagnostic methods have
advanced to such an extent that the recognition
and treatment of raised intracranial pressure is
usually undertaken before papilloedema
appears.
The following are the principal causes of
increased intracranial pressure:
1. Intracranial tumours: Not all intracranial
tumours cause papilloedema 1 . In many
cases it is not seen early in the course of the
tumour. Its occurrence depends upon
whether the tumour is so placed as to cause
a rise in the tension of the CSF and also
upon its rate of growth. It may not even be
present with slowly growing tumours despite
their enormous size. Infratentorial tumours
that arise from the cerebellum and the fourth
ventricle tend to raise the intracranial
pressure early by obstructing the flow of the
CSF through the aqueduct of sylvius. In
contrast it may be absent in many cases of
tumour at the base of the skull, temporal,
subcortical, and pontine region (Pontine
glioma). Among the supra-tentorial tumours,
third ventricle tumours cause papilloedema
frequently. It is less common with
parasagittal, parietal, or occipital tumours.
Papilloedema is rarely seen in pituitary
adenomas. Overall 60% of patients with
cerebral tumours have papilloedema
sometimes during the course of illness with
a distinctly higher frequency with infra-
tentorial tumours2.
Papilloedema may be observed at almost any
age, but it is relatively uncommon in infants,
 because the fontanelle are not obliterated and
the cranial sutures are not fused at this age;
therefore they bulge and split, and the head
circumference increases, providing more room
for the enlarging tumour mass. Papilloedema
occurs more frequently between age of two and
ten years3,4. The high frequency in this age group
is related to high frequency of infra-tentorial
tumours. About two-thirds of intracranial
tumours of childhood are located in the
cerebellum, fourth ventricle, or brain stem.
As a rule, papilloedema is bilateral. Unilateral
papilloedema may be encountered under
following circumstances:
(i) A frontal lobe tumour may compress the
ipsilateral nerve, eventually producing optic
atrophy, while simultaneously increasing the
intracranial pressure and producing
papilloedema in the other eye (Foster-Kennedy
syndrome)5.
(ii) There is pre-existing unilateral optic disc
anomaly or optic atrophy4.
(iii) When the transmission of increased pressure
from the intra-cranial subarachnoid space into
the peri-optic meningeal space is interrupted
by either compression and obliteration of the
space by the tumour or the presence of a
congenital anomaly of the surrounding sheaths
themselves, unilaterality may occur.
If papilloedema is asymmetric, the difference
in degree does not necessarily indicate the
laterality of the tumour.
2. Cerebral Abscess: Papilloedema may not always
be present and generally appears late. It is more
common in chronic than in acute abscess, seen
in about 25-30% of cases; abscess in temporal
lobe being the most frequent.
3. Hydrocephalus: Hydrocephalus from any
cause may lead to papilloedema. Various skull
malformations that alter the size of the cranial
vault may cause rise in intracranial pressure.
Permanent closure of the cranial sutures, tower
skull, and craniofacial dysostosis are examples
Journal, Indian Academy of Clinical Medicine
Vol. 1, No. 3
of such entities. Pressure of the distended floor
of the third ventricle upon the optic chiasma
may cause optic atrophy. Papilloedema due
to hydrocephalus is rarely seen in infants
because of ability of the cranial cavity to
expand.
4. Intracranial infections: Intracranial infections
whether focal or diffuse may cause
papilloedema. Meningoencephalitis due to any
cause may produce papilloedema. Obstruction
to the CSF pathway may cause raised intracranial
pressure and papilloedema. Occasionally it may
be seen in chronic meningitis due to tuberculosis
or cryptococcus infection and in the past was
observed in cases of syphilitic meningitis. Herpes
simplex encephalitis is a rare cause of
papilloedema. Neurocysticercosis deserves
special mention as a cause of papilloedema.
5. Intracranial sinus thrombosis: This increases the
pressure of the CSF by diminishing its rate of
absorption. Lateral sinus thrombosis secondary
to middle ear disease was initially a common
cause of the syndrome of benign intracranial
hypertension5. It is now becoming apparent that
a significant proportion of patients with benign
intracranial hypertension have sinus thrombosis6.
6. Cerebral oedema: Generalised brain swelling
as in:
(a) Head injury – papilloedema may appear within
a few hours after trauma or may be delayed
upto 10 days. Acute subdural or intracerebral
haematomas may be associated with
papilloedema.
(b) Focal oedema as after massive infarction or
cerebral haemorrhage. In subarachnoid
haemorrhage, papilloedema has been observed
to occur within 60 minutes of the occurrence of
haemorrhage.
(c) Benign intracranial hypertension.
Review of literature indicates that in our country
nearly 40% of all cases presenting with
papilloedema without localising neurological
signs have inflammatory and parasitic lesions

October-December 2000 271
 of the brain 7 . Neurotuberculosis and
neurocysticercosis account for a large number
of such cases. In contrast to this, several
western authors have emphasised that patients
with papilloedema without localising signs
most commonly have lateralised or midline
space-occupying lesions8.
Benign intracranial hypertension (BIH)
Synonyms: Pseudotumour cerebri, Idiopathic
intracranial hypertension
It is an idiopathic syndrome of raised intracranial
pressure manifesting as headache, papilloedema,
sixth nerve palsies, and progressive visual loss. The
diagnostic criteria include the following:
1. Symptoms and signs restricted to those of
elevated intracranial pressure.
2. Normal neuro-imaging studies (excluding non-
specific findings of raised intracranial pressure).
3. Increased cerebrospinal fluid pressure with a
normal composition.
Pathophysiology: The pathophysiology of this
disorder although unclear, is a relative resistance to
the absorption of cerebrospinal fluid across the
arachnoid villi. Other theories support an
abnormality in the cerebral circulation with a resulting
increase in the brain’s water content. The subsequent
increase in the intracranial pressure is transmitted
to the structures within the intracranial cavity including
the optic nerves.
This disorder is often seen in obese, adolescent
females. The role of obesity in this disorder is unclear.
The cardiac filling pressures are raised due to
increased intra-abdominal pressure as a result of
obesity. The rise in pressure impedes venous return
from the brain with a subsequent elevation in
intracranial venous pressure.
There is a strong predilection of this disease for
women, the female to male ratio ranging from
2:1-10:1 in literature. Most patients with this
disease present in the third decade of life.
Patients usually present with symptoms related to
raised intracranial pressure, which include a
272 Journal, Indian Academy of Clinical Medicine
combination of headache, visual obscuration, and
diplopia due to unilateral or bilateral sixth nerve
palsy. Occasionally, patients with diplopia will present
with oculomotor or trochlear nerve palsy. Rarely it
may be asymptomatic. The most significant finding
in these patients is bilateral papilloedema. It may at
times be asymmetric. The syndrome may resolve
spontaneously over several months or it may take
as long as two years. However, there can be clinically
significant visual loss, if left untreated.
Although the majority of cases are of unknown cause,
there are many associated clinical settings as shown
in Table II.
Bilateral papilloedema is presumed to be due to
increased intracranial pressure secondary to an
intracranial tumour. Until proven otherwise, it is also
worthwhile to first rule out malignant hypertension.
The CT or MRI scan of the brain shows small “slit
like” lateral ventricles in cases of pseudotumour
cerebri. CT and MRI are quite effective in ruling out
both a mass lesion as well as potential dural sinus
thrombosis. Once an intracranial mass lesion is ruled
out, lumbar puncture is performed to demonstrate
opening pressure of CSF. Orbital sonography allows
for precise measurement of the optic nerve sheath
diameter.
The medical management consists of weight control
for obese patients, treatment of underlying
diseases(s), or cessation of exogenous agent(s)
implicated in the causation of increased pressure.
Repeated lumbar punctures daily initially to lower
pressure to less than 180 mm H2O is advocated by
some. Lumbo-peritoneal shunting or optic nerve
sheath fenestration may be required when vision is
seriously threatened. Steroids, acetazolamide,
furosemide and oral glycerol have been tried alone
or in combinations with varying success.
The visual prognosis, in timely and appropriately
treated patients, can be encouraging in cases of
pseudotumour cerebri. Since the increase in
intracranial pressure tends to be chronic in nature,
all patients with this disorder must be followed for
years after presentation. Medical treatment may
have to be continued on long term basis.

Vol. 1, No. 3
October-December 2000
Pathogenesis of papilloedema
It has been a matter of controversy for many years.
Much of our knowledge about it has been
contributed by the research work of Hayreh9.
The optic nerve is developmentally and histologically
a part of the brain. It is surrounded immediately by
the piamater and superficial to that is the arachnoid.
Both extend forward to fuse with the sclera.
Duramater lies outside both and is continuous
anteriorly with the orbital periosteum. Therefore, the
optic nerve is surrounded by a subarachnoid space.
The continuity of this space is necessary for the
development of papilloedema. Increased pressure
in the subarachnoid space surrounding the optic
nerve is the essential element in the production of
papilloedema as demonstrated by Hayreh. The
increased pressure in the intracranial subarachnoid
space is easily transmitted to the perineural space10.
A rise in the pressure in the subarachnoid space has
a double effect causing compression of the central
vein of the retina and thereby stasis of venous return
and impeding lymphatic drainage from the retinal
and optic nerve which in turn increases the pressure
in the central retinal vein and causes passive oedema
of the optic nerve head. It is also proposed that
increased pressure in the vein impedes the blood
supply to the optic nerve and produces ischaemia,
which is an additional mechanism contributing to
the disk swelling.
Recently it has been proposed that elevated
intracranial pressure leads to impaired axoplasmic
flow and blockage of extra-axonal centripetal
transport of tissue fluid11. The stasis takes place at
the level of the lamina cribrosa, leading to
accumulation of axoplasm and swelling of optic
nerve fibres in the optic nerve head. The swollen
axons compress the fine vessels in the prelaminar
region, causing venous stasis and dilatation,
microaneurysm formation and haemorrhages in the
disc and the neighbouring retina.
Ophthalmoscopic appearance
papilloedema
Fully developed papilloedema has the following
Journal, Indian Academy of Clinical Medicine
Vol. 1, No. 3
features when observed ophthalmoscopically.
1. The disc margins are blurred due to swelling
and elevation. The oedema is most distinct in
the superior and inferior margins. This blurring
extends to the nasal side before the temporal.
2. The optic nerve fibres appear striated.
3. In the earliest stages the retinal veins are
congested. The vessels are obscured as they
cross the disc margin.
4. In the earliest stages the optic disc is pinker
than normal. It is hyperaemic.
5. There are capillary and venous dilatations.
Distension of retinal vein is extreme, and the
haemorrhages may develop in the retina and
on the disc itself. Microaneurysms may
develop.
6. Spontaneous venous pulsation is absent – The
absence of central venous pulsations in a
person with no other sign of raised intracranial
pressure should not be considered evidence
of papilloedema. They are absent in 20% of
normal individuals. The presence of
spontaneous venous pulsations at the disc
suggests that the CSF pressure is 220 mm H2O
or less at that moment of observation. Because
intracranial pressure is subject to cyclic changes
even in patients with significant intracranial
disease, it is not uncommon to see venous
pulsations in the presence of papilloedema.
7. The central cup is obliterated – increasing
oedema fills the physiological cup, and later
the nerve head becomes elevated above the
retina, sometimes by as much as 8 or even 10
dioptres. The oedema in severe cases spreads
into the retina, causing a macular fan. This
does not occur until the very late stage of
papilloedema.
If chronic papilloedema ensues, the condition
may progress to so-called secondary optic
atrophy. The swelling of the disc diminishes, it
becomes paler, and the arteries become
of
constricted. Finally, in a typical case the disc is
pale and flat, the physiological cup remains
filled, and the edges of the disc are less distinct

October-December 2000 273
 than formerly. The arteries are constricted, but
the veins often remain congested for sometime.
Haemorrhages and exudates begin to
disappear. The glial elements proliferate in
reaction to nerve fibre degeneration.
Malignant hypertension often associated with
raised intracranial pressure practically always
causes bilateral disc oedema. This type of disc
swelling is characterised by less venous
distension and more marked narrowing of
retinal arterioles than when the disc swelling
is caused by expanding intracranial mass.
Figure 1.
Retinal vascular sclerosis as reflected by
abnormalities of A-V crossings and heightened
vascular reflexes is often conspicuous. In
Symptoms of papilloedema
addition, retinal haemorrhages and exudates
are more diffuse and are less likely to be In majority of patients vision remains normal,
confined to the immediate vicinity of the optic even if papilloedema is of long duration. The
disc. preservation of central vision serves to

Table II : Systemic and latrogenic Disorders associated with Benign Intracranial Hypertension
Commonly prescribed drugs
Nalidixic acid Penicillin Indomethacin
Nitrofurantoin Carbidopa Growth hormone
Phenytoin Levodopa Steroid therapy/withdrawal
Sulphonamides Cyclosporine Ketoprofen
Tetracycline Danazole
Vit. A (>100,000 units per day)
Endocrine and metabolic disorders
Addison’s disease
Cushing’s syndrome
Hypoparathyroidism
Levothyroxine therapy
Menarche, pregnancy, oral contraceptives
Obesity, irregular menses
Haematological disorders
Cryoglobulinaemia
Iron deficiency anaemia
Miscellaneous disorders
Dural venous sinus obstruction/thrombosis Familial Mediterranean fever
Head trauma Chronic respiratory insufficiency
Internal jugular vein ligation Multiple sclerosis
Lupus erythematosus Psittacosis
Middle ear disease Sarcoidosis
Reye’s syndrome

From Cecil’s Textbook of Medicine 1992; 19: 2222.

274 Journal, Indian Academy of Clinical Medicine
Vol. 1, No. 3
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differentiate papilloedema from other
conditions that produce disc swelling in which
loss of visual acuity is usually the first
m a n i f e s ta t i o n . H o w e v e r, t h i s i s n o t a n
absolute rule and patients may seek medical
attention because of transient or permanent
failure of vision related to papilloedema.
Recurrent attacks of transient obscuration of
vision may occur in one eye, alternate
between the two eyes, or (rarely) affect both
eyes simultaneously 12. The duration of each
fleeting attack is about 5 seconds and rarely
exceeds 30 seconds. The obscuration begins
and ends abruptly and the vision is usually
restored completely at the termination of the
attack. The attacks come at irregular
intervals, ranging from only a few a week to
as many as 50 times a day 13. Standing up
from sitting position, stooping, and turning
the head abruptly may trigger an attack 13 .
Visual loss is variable during each attack.
T h e r e m a y b e f o g g i n e s s , s l i g h t b l u r,
descending veil, or obscuration of patient’s
surroundings.
Transient obscuration of vision is usually
associated with either moderate or severe
papilloedema 1 . These symptoms demand
urgent measures to reduce intracranial
pressure as they indicate ischaemia due to
pressure upon the central retinal artery, which
may become permanently occluded if
unchecked, thereby causing irreversible
blindness. Transient blindness which occurs
in amaurosis fugax due to occlusive disease
of the carotids lasts ordinarily 5 to 15 minutes
and examination of fundus may show emboli.
In retinal migraine, transient mono-ocular
visual loss may occur but these episodes last
for only 15-20 minutes and fundus
examination is normal.
Sometimes in cases of papilloedema, vision
may not be restored and permanent blindness
may occur either after an attack of transient
blindness or after a period of days or weeks.
Journal, Indian Academy of Clinical Medicine
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Vision in papilloedema may also be reduced
due to retinal haemorrhages or macular
oedema and development of chronic atrophic
papilloedema. On an average, chronic
atrophic papilloedema develops in six to nine
months. Visual loss with central scotoma is
significant in fully developed cases. With the
advent of neuroimaging techniques, space
occupying lesions are diagnosed early and
chronic atrophic papilloedema is rarely seen
nowadays.
The pathogenesis of visual disturbances in
papilloedema is not clear. Various proposed
mechanisms include development of
hydrocephalus, herniation of temporal lobe
producing ischaemia of the visual cortex by
compressing the same sided posterior cerebral
artery, spasm of retinal arteries, and strangulation
of the optic nerve behind the disc.
The visual fields in papilloedema
In the earlier stages, enlargement of the blind
spot is the only finding. Later on, concentric
constriction of the visual fields occurs. There
may be other field changes due to lesions
involving other parts of the visual system.
Differentiation of blurred optic disc is shown in Table
III. Optic neuritis causes visual loss usually with a
central scotoma, loss of colour vision and a relative
afferent pupillary defect. Anterior ischaemic optic
neuropathy is usually associated with altitudinal field
defect. Papilloedema due to infarction of the nerve
head is characterised by extension of the swelling
beyond the nerve head, whereas the papilloedema
of raised intracranial pressure is associated with
peripapillary haemorrhages. Often this distinction
cannot be made on the basis of fundoscopic
appearance alone, in which case the most reliable
distinguishing feature is the presence or absence of
visual loss. Infarction of the nerve head is associated
with loss of vision, severe as a rule, whereas
papilloedema is characterised by enlargement of
the blind spots and constriction of visual fields with
retention of visual acuity and normal pupillary
reflexes.

October-December 2000 275
Differential diagnosis
Slight elevation of the optic disc due to increased
myelin anterior to the lamina cribrosa is
sometimes seen in hypermetropic individuals
and is one of the causes
pseudopapilloedema. Optic disc drusen are a
major source of confusion and should be
considered when disc swelling is not associated
with any visual disturbance or symptoms of
raised intracranial pressure. Exposed optic disc
drusen may be obvious clinically or can be
demonstrated by their autofluorescence. Buried
or exposed drusens are best detected by CT
scanning. Other family members may be
similarly affected. The absence of venous
congestion is a valuable sign in distinguishing
this change from true papilloedema but, when
doubt persists, fluorescein retinal angiography
is helpful as in true papilloedema it shows
swollen and proliferated capillaries around the
disc margin and fluorescence in the swollen disc
itself.
Table III : Differentiation of Blurred Optic Discs
Papilloedema
Visual acuity Normal
Visual fields Enlarged
Haemorrhages May be present
Pupils Normal
Investigations
Imaging studies
Neuro-imaging: Evaluation of papilloedema
requires a patient to undergo urgent neuro-
imaging to rule out an intracranial mass or dural
sinus thrombosis. Although computerised axial
tomography is certainly adequate in most
instances, magnetic resonance imaging is quite
effective in ruling out both a mass lesion as well
as a potential dural sinus thrombosis. MR
angiography is done in selected cases to
investigate the possibility of a dural venous sinus
occlusion or an arteriovenous shunt.
276 Journal, Indian Academy of Clinical Medicine
Lumbar puncture: If neuroradiologic studies are
normal, the subarachnoid opening pressure
should be measured by lumbar puncture to
confirm that it is elevated. The opening pressure
should be taken with the patient relaxed in order
of
to avoid falsely elevated readings. Besides the
value of opening pressure the clarity and colour
of the cerebrospinal fluid should be remarked
upon. In addition, assessment of the fluid’s cell
count, cytology, cultures, glucose, protein, and
electrolyte concentrations are also done. If the
opening pressure of cerebrospinal fluid is elevated
without explanation, the diagnosis of
pseudotumour cerebri is made by exclusion.
Ultrasonography: Standardised A-Scan orbital
ultrasonography allows for precise measurement
of the optic nerve sheath diameter. If this diameter
is noted to be increased in primary gaze and
diminishes by 25% in eccentric gaze (30 degree
test) then increased subarachnoid fluid
surrounding the optic nerve is presumed to be
present. This finding is consistent with
Neuritis Pseudo-papilloedema
Reduced Normal
Central scotoma Normal
May be present None
Often abnormal Normal
papilloedema if it is bilateral. This investigation
requires a highly skilled clinician in order to obtain
reproducible results.
Fluorescein angiography, red free fundus photo
which highlights the retinal nerve fibres, and
stereoscopic fundus photography may be
helpful in detecting early oedema of optic discs.
Treatment
Treatment begins with a correct diagnosis. Most
importantly, it is crucial to distinguish between
papilloedema and many other forms of optic
disc oedema, including pseudopapilloedema.

Vol. 1, No. 3
October-December 2000
If the signs indicate an optic neuropathy,
management is aimed at treating the underlying
disorder. Neurological consultation and co-
management is obligatory in all cases of
papilloedema. The treatment may be medical
or surgical depending on the disorder.
All patients with chronic papilloedema must be
monitored carefully. The treatment goal for
these patients is to preserve optic nerve function
while managing their underlying cause. Optic
nerve function should be monitored with
assessment of visual acuity, colour vision, optic
nerve head observation, and perimetry.
Those patients with progressive visual failure
not controlled by medical therapy should be
considered for optic nerve sheath
fenestration. The local filtering effect of
fenestration acts as a safety valve and
eliminates the pressure from being
transmitted to the optic nerve. Lumbo-
peritoneal shunt is quite effective in lowering
the intracranial pressure.
Conclusions
The key points to be considered carefully:
a) Not all swollen discs constitute optic disc
oedema and,
b) Not all cases of optic disc oedema constitute
papilloedema.
Malinserted discs, congenitally full discs
(seen often in hypermetropes), or
especially buried drusen may at times be
mistaken for optic disc oedema even by
the most experienced clinicians. All of
these conditions are essentially non-
pathological.
Many primary inflammations of the optic
nerve which are treatable and in some cases
Journal, Indian Academy of Clinical Medicine
Vol. 1, No. 3
self limiting are often misdiagnosed as
papilloedema, a condition which constitutes
a medical emergency to the internists.
Therefore utmost care, to distinguish these
disorders, should be taken; so that
appropriate and early steps towards proper
management can be initiated.
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