A 62-year-old man from Mumbai presents with acute onset of bilateral ptosis, bilateral ophthalmoplegia (CN III palsy), and preserved sensation but weakness of the right arm and leg. MRI shows an acute infarct in the ventromedial midbrain. What is the most appropriate next step in management?

Explanation

## Clinical Diagnosis: Weber Syndrome (Ventromedial Midbrain Infarct) ### Anatomical Localization The combination of **bilateral CN III palsies (ptosis, ophthalmoplegia)** with **contralateral motor weakness (right-sided hemiparesis)** localizes the lesion to the **ventromedial midbrain**. This is Weber syndrome, caused by infarction in the territory of the **penetrating branches of the proximal basilar artery** or the **superior cerebellar artery**. ### Brainstem Cross-Section at Midbrain Level ```mermaid flowchart TD A[Ventromedial midbrain lesion]:::outcome --> B[Damages CN III nerve fibers]:::outcome B --> C[Bilateral ptosis + ophthalmoplegia]:::outcome A --> D[Damages corticospinal tract]:::outcome D --> E[Contralateral hemiparesis]:::outcome A --> F{Vascular territory?}:::decision F -->|Basilar perforators| G[Acute ischemic stroke]:::outcome F -->|Hemorrhage| H[Acute hemorrhagic stroke]:::outcome G --> I[IV thrombolysis if time window met]:::action H --> J[Supportive care + neurosurgical consultation]:::action ``` ### Pathophysiology 1. **Oculomotor nerve (CN III) fascicles** pass through the ventromedial midbrain → bilateral involvement causes ptosis and ophthalmoplegia 2. **Corticospinal tract** lies medial to CN III → damage causes contralateral hemiparesis 3. **Medial longitudinal fasciculus (MLF)** may be involved → internuclear ophthalmoplegia (INO) if bilateral **Key Point:** Weber syndrome is characterized by the combination of **ipsilateral CN III palsy + contralateral motor weakness**. When bilateral CN III involvement is present, the lesion is midline and ventromedial. ### Management of Acute Midbrain Stroke | Step | Action | Rationale | |------|--------|----------| | **1. Time assessment** | Determine exact time of symptom onset | Thrombolytic window is 0–4.5 hours | | **2. Neuroimaging** | MRI (or CT if MRI unavailable) to exclude hemorrhage | Mandatory before thrombolysis | | **3. Vascular imaging** | CTA/MRA to identify large vessel occlusion | Guides decision for thrombectomy | | **4. Thrombolysis** | IV alteplase if ischemic, within window, no contraindications | First-line acute stroke therapy | | **5. Monitoring** | ICU-level care; monitor for complications | Brainstem strokes carry high morbidity | **High-Yield:** Midbrain infarcts are often supplied by the **proximal basilar artery** and its penetrating branches. These are high-risk lesions because: - Bilateral CN III involvement indicates midline pathology - Corticospinal tract involvement causes significant motor disability - Risk of extension to pons or medulla is high **Clinical Pearl:** Unlike unilateral Weber syndrome (CN III on one side + contralateral hemiparesis), bilateral CN III involvement suggests a midline basilar artery occlusion with potential for rapid deterioration. This warrants urgent vascular imaging and consideration of mechanical thrombectomy if large vessel occlusion is confirmed. **Warning:** ~~Mannitol and head elevation~~ are temporizing measures for increased intracranial pressure but do NOT address the underlying ischemia. In acute ischemic stroke, reperfusion therapy (thrombolysis or thrombectomy) takes priority over osmotic therapy. ### Why IV Thrombolysis Is the Best Next Step - Acute ischemic stroke within potential thrombolytic window - No hemorrhage on imaging (assumed from clinical presentation) - Restores blood flow to ischemic midbrain and prevents further neuronal death - Guideline-recommended first-line therapy - Mechanical thrombectomy is considered AFTER IV thrombolysis if it fails or is contraindicated [cite:Harrison 21e Ch 297]