Parinaud Syndrome: Comprehensive Imaging Guide and Clinical Overview
Overview
Parinaud syndrome, also known as dorsal midbrain syndrome, is named after French ophthalmologist Henri Parinaud, who first described the characteristic ocular findings in the late 19th century.
The naming rationale stems from Parinaud’s detailed observations of patients with upward gaze palsy and associated eye movement disorders due to lesions in the dorsal midbrain.
Brief clinical findings include upward gaze palsy present in 87-100% of cases, convergence-retraction nystagmus, light-near dissociation, and Collier’s sign with bilateral lid retraction in 20-40% of patients.
Parinaud syndrome is typically sporadic and not associated with an inheritance pattern, arising from acquired lesions such as tumors, infarcts, or hemorrhages rather than genetic factors.
Key Imaging Features
- MRI demonstrates intrinsic midbrain signal abnormality (IMSA) in 85% of Parinaud syndrome cases with pineal masses, appearing as hyperintensity on T2-weighted and FLAIR sequences in the dorsal midbrain tectum.
- Bilateral infarction of third nerve nuclei and mesial thalami on MRI indicates artery of Percheron infarct, a key feature in vascular Parinaud syndrome, with restricted diffusion on DWI sequences.
- Pineal region masses on MRI cause midbrain compression or displacement, often with hydrocephalus in 80-84% of cases, regardless of syndrome presence.
- T1 post-contrast MRI shows heterogeneous enhancement in pineal tumors associated with Parinaud syndrome, with IMSA predicting symptom likelihood.
- Lesions in the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF) and interstitial nucleus of Cajal (INC) on high-resolution MRI correlate with vertical gaze palsy, typically measuring 5-10 mm in the dorsal midbrain.
- Pretectal nucleus involvement appears as T2 hyperintensity crossing the posterior commissure, explaining light-near dissociation in Parinaud syndrome.
- Hydrocephalus with aqueductal compression evolves over days to weeks on serial CT or MRI, with tectal plate thickening greater than 5 mm signaling progression.
Pathophysiology
Lesions in the dorsal midbrain tectum disrupt the vertical gaze center, including the riMLF for vertical saccades and INC for gaze holding, leading to upward gaze palsy on MRI as T2 hyperintensity in these nuclei.
Compression or intrinsic signal changes in the pretectal nuclei and posterior commissure impair the pupillary light reflex while sparing near response pathways, manifesting as light-near dissociation visible on dedicated midbrain MRI sequences.
Pineal masses cause intrinsic midbrain signal abnormality through direct invasion or edema, with IMSA on FLAIR MRI reflecting gliosis or ischemia that mechanistically produces convergence-retraction nystagmus.
Vascular insults like artery of Percheron infarction involve bilateral paramedian thalami and rostral midbrain, showing cytotoxic edema on DWI MRI, which extends beyond classic pretectal involvement to include oculomotor subnuclei.
Over time, chronic lesions evolve to atrophy of the tectal plate on follow-up MRI, with measurements decreasing from acute 8-12 mm swelling to stable 3-5 mm, correlating with persistent gaze deficits.
Differential Diagnosis
Progressive supranuclear palsy shows midbrain atrophy with hummingbird sign on sagittal MRI, distinguished from Parinaud syndrome by symmetric horizontal gaze preservation and lack of IMSA.
Pineal cyst mimics mass effect but lacks IMSA and enhancement on MRI, with no hydrocephalus evolution, unlike symptomatic Parinaud syndrome pineal tumors.
Brainstem glioma presents with diffuse pontomesencephalic expansion on MRI, differing from focal tectal IMSA in Parinaud syndrome by progressive cranial nerve involvement beyond oculomotor pathways.
Artery of Percheron infarct features acute DWI restriction in thalami and midbrain, unique from tumor-related Parinaud syndrome by cardioembolic history and lack of mass effect.
Tectal plate glioma causes aqueductal stenosis with transependymal edema on MRI, but Parinaud syndrome is distinguished by prominent IMSA and light-near dissociation absent in isolated hydrocephalus.
Imaging Protocols and Techniques
Initial non-contrast CT head assesses hydrocephalus and pineal calcification, followed by MRI brain with thin-slice (2-3 mm) axial T2/FLAIR through midbrain for IMSA detection.
Recommended MRI protocol includes pre- and post-contrast T1, DWI/ADC for infarct, SWI for hemorrhage, and sagittal reconstructions to evaluate tectal plate and posterior commissure anatomy.
For pineal lesions, add coronal MRI sequences to measure midbrain displacement, with 3T preferred for riMLF/INC resolution; avoid routine CT perfusion unless vascular etiology suspected.
Follow-up MRI at 3-6 months monitors lesion evolution, hydrocephalus resolution post-ventriculostomy, and IMSA changes predicting Parinaud syndrome persistence.
Pearls: IMSA strongly predicts Parinaud syndrome (85% sensitivity); pitfalls include overcalling displacement without IMSA, as it lacks specificity; measure tectal thickness for progression tracking.
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