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Parinaud's syndrome in a patient with thalamic infarction due to cerebral venous thrombosis

Menon, Ashok DM; Sreedhar, Ani MS; Anilkumar, D MD; Ittyerah, T P MS

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Indian Journal of Ophthalmology: May–Jun 2007 - Volume 55 - Issue 3 - p 237-238
doi: 10.4103/0301-4738.31954
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Dear Editor,

The dorsal midbrain syndrome, characterized by upward gaze paralysis, convergence-retraction nystagmus and light-near dissociation owes its eponym to the French ophthalmologist, Henri Parinaud. Pineal tumors, intrinsic midbrain lesions and hydrocephalus or aqueductal enlargement compressing the posterior commissure are frequently implicated causes. We report a patient with thrombosis of the deep cerebral venous system (CVT) who presented with Parinaud's syndrome. Isolated eye signs are seldom discussed in CVT and Parinaud's syndrome has not been described.

A diagnosis of "benign" intracranial hypertension (BIH) was proffered in a 30-year-old man with blurred vision, papilledema and normal brain magnetic resonance imaging (MRI). Lumbar puncture tapped clear cerebrospinal fluid (CSF) under opening pressure of 350 mmH2O; CSF analysis was normal. Obtaining no relief, he was referred for re-evaluation. Visual acuity was 20/20 and perimetry mapped full visual fields without blind spot enlargement. Bilateral papilledema and convergence-retraction nystagmus was noted; equal pupils constricted well during accommodation but sluggishly to light. Upgaze was absent, eyelids retracted on looking up (Collier's sign), downward saccades and pursuit were normal. Neurological examination was otherwise unremarkable.

The lesion was clinically localized to the dorsal mesencephalon and MRI was repeated [Fig. 1]. Cerebral venogram revealed unilateral posterior thalamic infarction with thrombosis involving multiple cerebral venous sinuses [Fig. 2]. The third ventricle and aqueduct were not enlarged.

Figure 1
Figure 1:
T2 weighted axial MR image depicting altered hyperintense signal involving the right thalamus. The signal was hypointense on T1 and suggests infarction. To the right, a T2 weighted sagittal MR image shows a hyperintense signal replacing the normal flow void in the great cerebral vein of Galen (arrowhead), straight sinus, torcula (short arrow) and superior sagittal sinus (long arrow)
Figure 2
Figure 2:
MR venogram sagittal view shows absent flow in superior sagittal, straight, lateral and sigmoid sinuses and poor filling of the deep venous system

Premotor structures mediating vertical gaze lie in the periaqueductal paramedian nuclei of the midbrain reticular formation. The nuclei responsible are the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF), posterior commissure and its nucleus, nucleus of Darkschewitsch and interstitial nucleus of Cajal (INC). Medium-lead burst neurons in riMLF generate vertical saccades1 while INC controls vertical slow movements and gaze integration. The posterior commissure is particularly important in mediating upward gaze. Although typically caused by bilateral involvement, upgaze paresis may result from unilateral midbrain lesions that disrupt posterior commissural connections.2

Intracranial hypertension could arguably cause upgaze palsy and papilledema even before ventricular dilatation is apparent.3 However, gaze palsy developed despite cerebral decongestant measures and persisted after CSF pressure had normalized.

Our subject had venous thalamic infarction without obvious midbrain involvement but vertical gaze disturbances could result from concomitant undetected microinfarcts in dorsal mesencephalic structures that share a common vascular supply.45 Arterial thalamic infarcts may be associated with upgaze paresis, probably because of interruption of supranuclear pathways mediating vertical gaze.5 Patients with venous thalamic infarction are often obtunded and isolated eye signs are rarely reported.

Thrombosis involving dural venous sinuses and deep cerebral veins may masquerade as BIH. MRI with venography is the technique of choice to diagnose CVT but may miss partial or early disease as described here. Thrombosis appears as absent flow void on spin-echo images and lack of signal in angiographic images. Decreased signal on T2 weighted imaging in early CVT may be confused with normal flow void and imaging at intermediate field strengths becomes necessary. We emphasize caution in diagnosing BIH when ocular motility disturbances are present and advocate repeated scanning directed by a high index of clinical suspicion.

1. Buttner-Ennever JA, Buttner U, Cohen B, Baumgartner G. Vertical glaze paralysis and the rostral interstitial nucleus of the medial longitudinal fasciculus Brain. 1982;105:125–49
2. Smith MS, Laguna JF. Upward gaze paralysis following unilateral pretectal infarction Arch Neurol. 1981;38:127–9
3. Chou SY, Digre KB. Neuro-ophthalmic complications of raised intracranial pressure, hydrocephalus and shunt malfunction Neurosurg Clin N Am. 1999;10:587–608
4. van der Graaff MM, Vanneste JA, Davies GA. Unilateral thalamic infarction and vertical gaze palsy: Cause or coincidence? J Neuroophthalmol. 2000;20:127–9
5. Clark JM, Albers GW. Vertical gaze palsies from medial thalamic infarctions without midbrain involvement Stroke. 1995;26:1467–70
© 2007 Indian Journal of Ophthalmology | Published by Wolters Kluwer – Medknow