Where is the lesion localized in a patient with reduced consciousness, left sided conjugate gaze limitation, reduced left sided horizontal saccade, left sided facial weakness, gag weakness, and left sided body weakness?

Lesion Localization: Left Paramedian Pontine Tegmentum

The lesion is localized to the left paramedian pontine tegmentum, specifically involving the left abducens nucleus, medial longitudinal fasciculus (MLF), and the facial nerve fasciculus as it courses around the abducens nucleus. 1, 2, 3

Anatomical Basis for Clinical Findings

The constellation of symptoms localizes to a specific pontine region through the following mechanism:

Left-Sided Conjugate Gaze Limitation and Reduced Horizontal Saccades

• The abducens nucleus in the pons serves as the horizontal gaze center, coordinating both the ipsilateral lateral rectus (via CN VI) and the contralateral medial rectus (via MLF connections to CN III nucleus). 3, 4
• A lesion involving the left abducens nucleus produces ipsilateral (left) conjugate gaze palsy because this nucleus generates all horizontal eye movements to that side. 2, 3
• This differs from a peripheral CN VI palsy, which would only affect the lateral rectus muscle without conjugate gaze limitation. 5

Left Facial Weakness

• The facial nerve fasciculus curves around the abducens nucleus (forming the "facial colliculus" or "facial nerve knee") before exiting the brainstem. 1, 2
• Pontine lesions affecting the abducens nucleus frequently involve the facial nerve due to this intimate anatomical relationship, producing ipsilateral peripheral facial weakness with forehead involvement. 6, 7

Contralateral (Right) Body Weakness

• The corticospinal tracts descend through the ventral pons (basis pontis) before decussating in the medulla. 1, 7
• A paramedian pontine lesion affecting these descending motor pathways produces contralateral hemiparesis. 1, 7
• This creates the classic "alternating hemiplegia" pattern: ipsilateral cranial nerve deficits with contralateral body weakness. 1

Gag Weakness and Reduced Consciousness

• Gag weakness suggests involvement of CN IX/X nuclei or their connections in the medulla, which may indicate extension of the lesion caudally or separate medullary involvement. 1
• Reduced consciousness suggests either bilateral pontine involvement affecting the reticular activating system or increased intracranial pressure from mass effect. 1

Specific Syndrome Classification

This presentation is consistent with Millard-Gubler syndrome (ventral pontine syndrome) with possible extension to involve the pontine tegmentum and potentially the medulla. 7

Classic Millard-Gubler Triad:

• Ipsilateral CN VI palsy (conjugate gaze palsy when nucleus involved). 3, 7
• Ipsilateral CN VII palsy (peripheral pattern). 7
• Contralateral hemiparesis. 7

Additional Features Suggesting Extended Involvement:

• Gag weakness indicates caudal extension to involve CN IX/X nuclei in the medulla. 1
• Reduced consciousness suggests either bilateral involvement or significant mass effect requiring urgent evaluation. 1

Diagnostic Imaging Recommendations

Brain MRI with diffusion-weighted imaging (DWI) is the diagnostic modality of choice, with thin-section coronal DWI detecting nearly 25% more acute brainstem infarcts than standard axial DWI. 1

Key Imaging Considerations:

• Ischemic and hemorrhagic infarcts are the most frequent cause of acute brainstem syndromes affecting this region. 1
• False-negative DWI can occur with very small ischemic brainstem infarcts, necessitating thin-section protocols. 1
• The lesion should be visible in the left paramedian pontine tegmentum on T2-weighted and FLAIR sequences. 2, 7

Clinical Pitfalls to Avoid

• Do not mistake this for a peripheral CN VI palsy alone: The presence of conjugate gaze limitation (not just isolated lateral rectus weakness) indicates nuclear involvement. 3, 5
• Do not overlook the alternating pattern: Ipsilateral cranial nerve deficits with contralateral motor deficits are pathognomonic for brainstem localization. 1, 7
• Consider vascular etiology first: In acute presentation, pontine infarction from paramedian perforator occlusion is the most common cause. 1, 7
• Assess for bilateral involvement: Reduced consciousness may indicate bilateral pontine pathology or complications requiring immediate intervention. 1

Prognosis

The small size of isolated pontine infarcts and lack of hemorrhagic transformation typically suggest favorable prognosis with early diagnosis and management. 1, 7