# Clinical Cases: Brainstem ## Case 1: Lateral Medullary Syndrome (Wallenberg Syndrome) ### Patient Presentation **Demographics:** 58-year-old male **Chief Complaint:** Sudden dizziness, difficulty swallowing, and facial numbness **History of Present Illness:** A 58-year-old man with a history of hypertension and hyperlipidemia suddenly developed severe vertigo while at work. He describes the room spinning and immediate nausea and vomiting. He also noticed numbness on the left side of his face and difficulty swallowing, with liquids coming out of his nose. He reports that his voice sounds hoarse. He feels off-balance and tends to fall to the left. His left eye appears smaller than usual according to his coworker. He denies limb weakness, headache, or change in consciousness. **Physical Examination:** - Vital signs: BP 175/105, HR 78, RR 16 - General: Alert, nauseated, dysphonic - Neurological: - Mental status: Alert, oriented, normal cognition - Cranial nerves: - Left Horner syndrome (miosis, ptosis, anhidrosis) - Nystagmus (direction-changing) - Decreased sensation to pain and temperature on LEFT face (V1-V3) - Absent left gag reflex; left palate droop; left vocal cord weakness (hoarseness) - Tongue midline - Motor: 5/5 strength in all extremities - Sensory: Decreased pain and temperature on RIGHT body (arm, trunk, leg); normal on left body; light touch and proprioception intact bilaterally - Coordination: Left-sided limb ataxia (finger-to-nose dysmetria); truncal ataxia with falling toward left - Gait: Wide-based, falls to left **Workup:** - **CT head:** No hemorrhage - **MRI brain with DWI:** Acute infarct in left lateral medulla - **MR angiography:** Left vertebral artery occlusion - **CT angiography (neck):** Left vertebral artery dissection - **Echocardiogram:** Normal; no cardioembolic source **Diagnosis:** Left lateral medullary syndrome (Wallenberg syndrome) secondary to vertebral artery dissection **Treatment:** - Antiplatelet therapy (aspirin) initiated; anticoagulation considered for dissection - NPO initially with video swallow evaluation; modified diet after improvement - Speech therapy for dysphagia - Physical therapy for vestibular rehabilitation and ataxia - Aggressive secondary prevention (statin, blood pressure control) - Spontaneous improvement in swallowing over 2-3 weeks - Persistent mild ataxia and sensory symptoms at 6 months **Clinical Pearl:** Lateral medullary syndrome results from occlusion of the vertebral artery or its branch (PICA), affecting structures in the lateral medulla. The classic findings include ipsilateral facial sensory loss (descending trigeminal tract), ipsilateral Horner syndrome (descending sympathetic fibers), ipsilateral cerebellar ataxia (inferior cerebellar peduncle), dysphagia and hoarseness (nucleus ambiguus), vertigo and nystagmus (vestibular nuclei), and CONTRALATERAL body pain/temperature loss (spinothalamic tract). Notably, motor pathways are spared because the pyramids are located medially. This "crossed" sensory pattern (ipsilateral face, contralateral body) is the hallmark of a lateral brainstem lesion. --- ## Case 2: Weber Syndrome - Midbrain Stroke ### Patient Presentation **Demographics:** 65-year-old female **Chief Complaint:** Double vision and right-sided weakness **History of Present Illness:** A 65-year-old woman with poorly controlled diabetes, hypertension, and a recent diagnosis of atrial fibrillation (not yet on anticoagulation) experienced sudden onset of double vision and right-sided weakness while watching television. Her daughter noticed that her left eye was deviated outward and she could not move it inward. The patient also has right-sided facial droop and weakness of her right arm and leg. **Physical Examination:** - Vital signs: BP 162/94, HR 92 (irregular), RR 14 - General: Awake, alert, left eye visibly deviated - Neurological: - Mental status: Alert, oriented, normal cognition - Cranial nerves: - LEFT CN III palsy: Complete ptosis, eye deviated "down and out" (superior oblique and lateral rectus unopposed), dilated pupil (6 mm) non-reactive to light; right pupil 3 mm reactive - Right lower facial droop (upper motor neuron pattern - forehead spared) - Motor: Right arm 3/5; right leg 3/5; left side 5/5 - Tone: Increased on right - Reflexes: Right-sided hyperreflexia; right Babinski present - Sensory: Intact - NIHSS: 12 **Workup:** - **CT head:** No hemorrhage - **MRI brain:** Acute infarct in left ventral midbrain (cerebral peduncle and CN III fascicle) - **CT angiography:** Patent basilar artery; posterior communicating artery aneurysm excluded - **Echocardiogram:** Dilated left atrium, no thrombus visualized **Diagnosis:** Weber syndrome (left ventral midbrain infarct) - cardioembolic etiology (atrial fibrillation) **Treatment:** - IV thrombolysis not given (outside window) - Aspirin bridging to anticoagulation - Anticoagulation with apixaban started after appropriate interval - Eye patch for diplopia management - Physical therapy for hemiparesis - Glycemic and blood pressure optimization - Partial recovery of CN III function over months; persistent mild hemiparesis **Clinical Pearl:** Weber syndrome localizes to the ventral midbrain (basis pedunculi) and produces an ipsilateral CN III palsy with contralateral hemiparesis. The lesion affects the CN III fascicle as it exits the midbrain ventrally and the adjacent cerebral peduncle carrying the corticospinal tract. The "crossed" motor pattern (ipsilateral CN III, contralateral body) is characteristic of brainstem lesions. Other midbrain syndromes include Benedikt syndrome (CN III palsy plus contralateral tremor/ataxia from red nucleus involvement) and Claude syndrome (CN III plus contralateral ataxia from superior cerebellar peduncle involvement). The pupil is typically involved in Weber syndrome because the parasympathetic pupillary fibers travel on the outside of CN III. --- ## Case 3: Internuclear Ophthalmoplegia ### Patient Presentation **Demographics:** 32-year-old female **Chief Complaint:** Double vision when looking to the right **History of Present Illness:** A 32-year-old woman presents with horizontal double vision that is worse when looking to the right. She noticed it 3 days ago when driving and had difficulty changing lanes because of the visual disturbance. She recalls having an episode of visual blurring in her right eye that lasted 2 weeks about 18 months ago, which she attributed to stress and did not seek evaluation. She also mentions occasional tingling in her feet over the past year. She has no other medical history. **Physical Examination:** - Vital signs: Normal - General: Healthy-appearing young woman - Neurological: - Mental status: Normal - Cranial nerves: - Pupils: Equal, reactive - Eye movements: On RIGHT gaze - failure of LEFT eye adduction with nystagmus of abducting right eye; convergence intact; LEFT gaze normal - Motor: 5/5 throughout; no weakness - Sensory: Mildly decreased vibration sense at ankles bilaterally - Reflexes: 3+ bilateral lower extremities; bilateral Babinski responses - Coordination: Mild intention tremor on finger-to-nose - Gait: Mildly ataxic **Workup:** - **MRI brain:** Multiple periventricular, juxtacortical, and callosal white matter lesions; T2 hyperintense lesion in left medial longitudinal fasciculus (MLF); several lesions enhance with gadolinium, others do not (dissemination in time) - **MRI cervical spine:** Two short-segment T2 hyperintense lesions - **Lumbar puncture:** 3 WBC; protein 55 mg/dL; glucose normal; positive oligoclonal bands (present in CSF, not serum) - **Visual evoked potentials:** Prolonged P100 latency right eye (evidence of prior optic neuritis) **Diagnosis:** Multiple sclerosis with internuclear ophthalmoplegia **Treatment:** - IV methylprednisolone 1 g daily for 5 days for acute relapse - Initiation of disease-modifying therapy (ocrelizumab) after discussion of options - Neuro-ophthalmology follow-up - INO improved significantly after steroids - Long-term MS monitoring plan established **Clinical Pearl:** Internuclear ophthalmoplegia (INO) results from a lesion of the medial longitudinal fasciculus (MLF), which connects the CN VI nucleus to the contralateral CN III nucleus, coordinating lateral gaze. The syndrome consists of impaired adduction of the ipsilateral eye (the eye on the side of the MLF lesion) with nystagmus of the contralateral abducting eye on lateral gaze. Convergence is typically preserved because it uses a different pathway. In young patients, bilateral INO is highly suggestive of multiple sclerosis. In older patients, brainstem stroke is more common. The adducting eye fails because the MLF normally carries the command from the contralateral CN VI nucleus to the CN III nucleus controlling medial rectus function. --- ## Clinical Image ![Lateral medullary syndrome anatomy](case_01_image.jpg) **Image Description:** Cross-sectional diagram of the medulla showing the structures affected in lateral medullary syndrome (Wallenberg syndrome), including the vestibular nuclei, nucleus ambiguus, spinal trigeminal nucleus and tract, spinothalamic tract, sympathetic fibers, and inferior cerebellar peduncle, with the lateral territory supplied by PICA highlighted. **Attribution:** Image from Wikimedia Commons (https://commons.wikimedia.org/), Creative Commons Attribution-ShareAlike license.