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| Journal of the New Zealand Medical Association,
07-August-2009, Vol 122 No 1300
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Bilateral trochlear nerve palsies following dorsal
midbrain haemorrhage
Sumu Simon, Avninder Sandhu, Dinesh Selva, John L
Crompton
Acquired BSO palsy is extremely rare and constitutes 0.48%
of nerve palsies affecting the oculomotor, trochlear and abducens
nerves.1 One of the authors (JLC), in 30 years
of clinical practice has seen 34 patients with acquired BSO palsies. The
commonest cause of acquired BSOP is closed head
trauma.2 Dorsal midbrain haemorrhage with
resultant bilateral SOP is usually associated with other neuro- ophthalmic and
neurological manifestations with only 5% of fourth nerve palsies being truly
isolated.3
Case reportA 37-year-old man had a sudden onset of generalised
weakness, double vision, tinnitus, deafness, numbness over the right cheek and
tingling over his right arm. He had a history of alcohol abuse. On examination
he was found to be alert. Best corrected visual acuity was 6/6 bilaterally.
There was no significant head tilt. Cover test revealed slight right hypertropia
in primary gaze. Bielshowsky was positive to both sides.
Ocular motility examination revealed limitation of
depression in adduction in both the eyes (-2 in the right eye (RE) and -1 in the
left eye (LE)) and a V pattern esotropia. There was mild inferior oblique over
action in both eyes. He had vertical and torsional diplopia which worsened on
down gaze. Double Maddox rod examination demonstrated an excyclotorsion of 15
degrees. He had normal saccades and there was no papilloedema.
Visual field testing was normal. Systemic examination
revealed mild nuchal rigidity, bilateral sensorineural deafness, decreased
sensation in the maxillary division of the right trigeminal nerve to pain and to
light touch and tingling in the right arm. Blood pressure was normal and there
were no signs of chronic liver failure.
Computerised tomography showed a non-enhancing 15 mm
hyperdense mass in the region of the tectum, obliterating the aqueduct which was
consistent with acute haemorrhage. There was also early dilatation of the
lateral and third ventricle (Figure 1).
Figure 1. Axial section CT scan showing a well
circumscribed hyperdense lesion in the dorsal midbrain (arrow) suggestive of
acute haemorrhage.
 Magnetic resonance imaging confirmed the presence of acute
haemorrhage in the midbrain with perilesional oedema and obstructive
hydrocephalus. An audiogram revealed a mild high tone sensory neural loss with
the right side hearing slightly worse than the left. Routine blood
investigations were normal (platelet count 366x10
9/L). He had an altered lipid profile (total
triglycerides 4.1mmol/L, total cholestrol 8.4 mmol/L, HDL 1.1 mmol/L, LDL 5.4
mmol/L).
The liver function tests were normal except for elevated
levels of gamma glutamyl transpeptidase (116U/L). He was started on
dexamethasone 2 mg twice a day which was tapered over the next three days. His
diplopia resolved over five weeks. The facial numbness and upper limb tingling
improved over a week. The deafness and tinnitus resolved six months later. He
was followed up periodically with MRI over two years (Figure 2) which showed
near total resolution of the haemorrhage with no evidence of an underlying
lesion.
Figure 2. MRI scan at 2 years follow up. An
axial T1-weighted image shows near total resorption of the haemorrhage in the
dorsal midbrain (arrow) with normalisation of the ventricles
 DiscussionSpontaneous bilateral SOP from midbrain stroke with no other
associated ocular signs has been reported only once
before,4 and we are unaware of any other
detailed clinical description in the English literature. The cause of
spontaneous midbrain haemorrhage is often unclear; the commonest cause being
vascular malformation.5 The cause for the
haemorrhage in our patient may have been due to a bleed from a cavernous
haemangioma or cryptic arteriovenous malformation.
The bilateral sensorineural loss was probably due to the
involvement of the inferior colliculi.6
Although no cause for the other neurological deficits was detected on
imaging, a plausible explanation is that the bleed and resultant perilesional
oedema could have caused a restricted sensory syndrome. The diagnostic dilemma
in this case would be an alternating skew deviation but the arguments in favour
of double fourth nerve palsy are the impaired ductions in the domain of the
superior oblique, V pattern esotropia and significant excyclotorsion. The other
reported non traumatic causes of isolated double fourth nerve palsy include
intracranial inflammations, arachnoid cysts, neoplasms, post infectious
neuritis, mononeuritis multiplex, hydrocephalus and multiple
sclerosis.7–13
Both CT and MRI are accurate and non invasive
investigations, with CT being more useful to diagnose an acute haemorrhage while
MRI is the preferred investigation to monitor the evolution. Management is
usually conservative. Exploration and shunting can be done in patients with
progressive deterioration and hydrocephalus
respectively.5
In conclusion, non-traumatic isolated bilateral SOP are
indicative of pathology in the midbrain, specifically a dorsal midbrain lesion.
Appropriate imaging with CT and/ or MRI should be performed on a semiurgent
basis in order to make an accurate diagnosis and to lead to appropriate advice
and treatment.
Author information: Sumu
Simon1; Avninder
Sandhu2; Dinesh
Selva1;
John L Crompton1 South Australian Institute of Ophthalmology and Discipline
of Ophthalmology and Visual Sciences1 &
Department of Radiology2
Royal Adelaide Hospital, Adelaide, Australia
Correspondence: Sumu Simon, South
Australian Institute of Ophthalmology, Level 8, Royal Adelaide Hospital,
North Terrace, Adelaide-5000, Australia. Email: sumusimon@yahoo.co.in
References:
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