Oculomotor Palsy in Spontaneous Intracranial Hypotension: Case Report and Review of the Literature

Magnetic resonance imaging (MRI) of the brain (Figure 1C,D) showed such features of intracranial hypotension as diffuse bilateral convexity, dural thickening and enhancement, downward displacement of the midbrain through the incisura with decreased pontine–midbrain angle and distended dural sinuses. CSF plays a suspensor role for the cranial content, preventing downward traction.2 With loss of CSF in SIH, structures are subject to traction.2 Most commonly, loss of CSF is due to such iatrogenic causes as lumbar puncture.2,5 Traumatic causes also have to be excluded for the intracranial hypotension to be considered spontaneous.2,5 Pathophysiology is thought to be due to microruptures of the dura at weak points along spinal root sleeves, through perineural cysts.2 Traction on cortical or bridging veins can cause subdural haematomas. In comatose patients, lumbar infusion of saline may be needed to improve the level of consciousness while the epidural blood patch is arranged.5 Typically, SIH presents with postural headaches.3 About 12% of patients can present with visual deficits other than diplopia, such as visual acuity and field deficits, nystagmus and photophobia.5 Associated ophthalmoplegia has been reported in about 30–35% of cases, with the abducens nerve being most frequently implicated in 83% of cases.5 This may be explained by the sixth cranial nerve’s prolonged intracranial course along the clivus and through Dorello’s canal as well as attachment to the Gruber ligament.5 A review of the pertinent literature on oculomotor palsy in SIH revealed eight reported cases.1-5 Bilateral third nerve palsies were reported in two patients.4 Two patients presented with both oculomotor and trochlear nerve palsies.5 One patient presented with oculomotor palsy associated with abducens nerve palsy.