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Anterior pathway vision loss due to subdural haematoma
  1. D A Hollander,
  2. J M Stewart
  1. Department of Ophthalmology, University of California, San Francisco, CA, USA
  1. Correspondence to: Jay M. Stewart MD, University of California, San Francisco, Department of Ophthalmology, 10 Koret Way, Suite K-301, San Francisco, CA 94143, USA; ne62yahoo.com

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Patients with vision loss associated with subdural haematomas typically present with homonymous hemianopias secondary to compression of the posterior cerebral artery during transtentorial herniation.1,2 In these cases, necropsy studies have demonstrated pregeniculate involvement in addition to occipital lobe lesions.2 We present a case illustrating a rarely reported phenomenon of anterior pathway vision loss associated with a subdural haematoma without any evidence of optic disc swelling, occipital lobe disease, or radiographic signs of chiasmal or optic nerve compression.

Case report

A 51 year old man, who had previously undergone two craniotomies (October 1992 and November 2000) for resection of an epidermoid tumour at the cerebellopontine angle, developed hydrocephalus and had a ventriculoperitoneal shunt placed in January 2001. Eleven months following placement of the shunt, the patient presented with ataxia and headaches but no visual complaints. A computed tomograph (CT) scan showed a right subdural haematoma measuring 2.8 cm on coronal section, and 150 ml of blood were drained via a burr hole.

One month following the drainage procedure, the patient presented to the hospital with a complaint of sudden, painless loss of vision in his left eye occurring 24 hours earlier. The patient had a left afferent pupillary defect with best corrected vision of 20/30 in his right eye and hand movements in his left eye. Extraocular movements were full, and the patient had normal colour vision in his right eye. Slit lamp examination showed only trace nuclear sclerosis cataracts bilaterally. Fundus examination was also normal, with no evidence of optic disc oedema or pallor in either eye (Figs 1A, B).

Figure 1

Fundus photograph with right (A) and left (B) optic nerves without oedema or pallor on initial presentation. Humphrey visual fields (C) on presentation and (D) 6 months following craniotomy with decompression of the subdural haematoma.

Automated perimetry revealed a constricted field in the right eye and severe, global depression in the left eye (Fig 1C). Magnetic resonance imaging (MRI) of the brain showed that the right subdural haematoma was still present but was decreased in size to 2.1 cm on coronal section (Fig 2A) compared to the study performed 1 month earlier. No intraorbital abnormalities were present, and the optic nerves and chiasm appeared free of direct compression by the haematoma. The blood did not appear to surround the optic nerves (Fig 2B). The patient’s haematocrit and blood pressure remained within normal limits during the initial presentation and subsequent treatment. The patient underwent craniotomy with further drainage of the subdural haematoma. After 6 months, the patient’s vision in the left eye improved to 20/200. Follow up perimetry showed less constriction on the right and improved performance on the left (Fig 1D). Funduscopic examination revealed mild optic nerve pallor in the left eye and a normal appearing right optic nerve.

Figure 2

Magnetic resonance imaging (T1 weighted coronal) of (A) right subdural haematoma with significant right to left midline shift but without direct compression of the prechiasmal optic nerves and (B) without compression of the intraorbital optic nerves.

Comment

This case represents a rare example of anterior pathway vision loss due to subdural haematoma. Most cases of vision loss with subdural haematoma affect the posterior visual pathway, with mechanisms including occipital infarct and compression of the posterior cerebral artery during transtentorial herniation.1,2 Posterior lesions may present with anterior signs—for example, optic atrophy was seen in three patients with occipital infarcts, two of whom initially presented with severe disc oedema.1 Necropsy studies have shown that transtentorial herniation can result in damage at the level of the optic tract, chiasm, or optic nerves.2

The anterior visual pathway can be compromised directly by gyrus herniation into the suprasellar cistern, a mechanism associated with meningiomas.3 Prechiasmal vision loss due to intracranial optic nerve infarction has also been reported in the setting of subdural haematoma; in this case the mechanism was presumably due to direct compression of the nerve against basal skull structures, although this specific radiographic finding was not described.4

The precise mechanism of anterior pathway vision loss due to subdural haematoma in our patient, as well as in the few previous reports, remains poorly understood.1,4 MRI showed no signs of blood in the orbits, direct compression of the optic nerves or chiasm, or gyrus herniation into the suprasellar cistern. The occipital lobes also appeared normal. Right to left midline shift due to the right sided haematoma was present, probably leading to vascular compromise or nerve compression that could not be visualised on MRI. Visual improvement following chiasmal decompression of mass lesions has been reported, and this mechanism may explain our patient’s improved visual acuity and peripheral fields following the drainage of the haematoma.5 Surprisingly, the subdural haematoma in our patient was smaller at the time of onset of visual symptoms than it had been 1 month earlier.

Subdural haematomas can affect vision through compression or vascular compromise at many points along the visual pathway. This case illustrates that optic neuropathy can occur late in the setting of a subdural haematoma, after the volume of the haematoma has begun to decrease. Because of the many ways in which patients with subdural haematomas can lose vision, they require close follow up, and a sudden change in vision necessitates immediate radiological testing, ophthalmological examination and, possibly, urgent surgical intervention and drainage.

References

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