Ipsilateral Hemiparesis from Brainstem Lesions: Yes, Through Alternating Syndromes
Yes, brainstem lesions can cause ipsilateral hemiparesis, but this occurs through specific "alternating" or "crossed" syndromes where ipsilateral cranial nerve deficits accompany contralateral hemiparesis—not true ipsilateral hemiparesis of the limbs. The classic mechanism involves damage to both cranial nerve nuclei/fascicles and the adjacent corticospinal tracts before they decussate.
Understanding the Anatomical Basis
The key to understanding this phenomenon lies in the unique anatomy of the brainstem:
Pontine lesions produce alternating syndromes because cranial nerve VI courses through the corticospinal tracts within the pons, resulting in contralateral hemiparesis with ipsilateral cranial nerve deficits 1
The facial nerve (CN VII) frequently accompanies CN VI deficits because it curves over the abducens nucleus, leading to ipsilateral facial paralysis alongside contralateral limb weakness 1
Classic pontine alternating syndromes include Millard-Gubler syndrome, Foville syndrome, locked-in syndrome, and facial colliculus syndrome 1
Specific Brainstem Syndromes
Midbrain Lesions (Weber's Syndrome)
Weber's syndrome demonstrates the classic pattern: ipsilateral oculomotor nerve (CN III) palsy with contralateral hemiparesis due to damage to the cerebral peduncle 2
This results from midbrain infarction affecting paramedian branches of the posterior cerebral artery or perforating branches of the basilar bifurcation 2
Despite being a brainstem stroke, Weber's syndrome carries a favorable prognosis with early treatment and risk factor control 2
Medullary Lesions (Avellis' Syndrome)
Avellis' syndrome presents with ipsilateral palatolaryngeal paresis and contralateral hemiparesis/hemihypesthesia due to nucleus ambiguus involvement 3
This syndrome is rare and caused by medullary infarction affecting both the nucleus ambiguus and adjacent corticospinal tract 3
Important Clinical Distinctions
What This Is NOT:
True ipsilateral limb weakness from ipsilateral brainstem lesions is extremely rare and typically requires previous contralateral injury with functional reorganization of motor pathways 4
Schmidt's and Vernet's syndromes (multiple lower cranial nerve palsies with contralateral hemiparesis) appear not to exist as true brainstem syndromes—they represent extracerebral lesions of multiple cranial nerves 5
Diagnostic Approach
Key Clinical Features to Identify:
Look for the "crossing" pattern: ipsilateral cranial nerve deficit(s) with contralateral motor/sensory findings 6
Ischemic and hemorrhagic infarcts are the most frequent cause of acute brainstem syndromes affecting cranial nerves 6, 1
Associated neurological deficits suggest brainstem involvement and require prompt evaluation 7
Imaging Recommendations:
MRI with DWI is the preferred modality for investigating brainstem processes leading to cranial nerve palsies 6
Thin-section coronal DWI detects nearly 25% more acute brainstem infarcts than standard axial DWI, as false-negative DWI occurs with very small ischemic brainstem infarcts 6, 1
Pre- and post-contrast imaging with high-resolution techniques through the affected cranial nerve courses provides the best opportunity to identify and characterize lesions 6
MRA or CTA may be complementary to characterize the vasculature in acute brainstem syndromes 6
Critical Pitfalls to Avoid
Do not confuse alternating syndromes with true ipsilateral hemiparesis—the limb weakness is contralateral to the brainstem lesion, while only the cranial nerve deficit is ipsilateral 1, 2, 3
Bilateral CN VI palsy suggests increased intracranial pressure or clival chordoma, not a simple brainstem lesion 7
Papilledema indicates increased intracranial pressure and necessitates immediate further investigation 7
The small size of many brainstem infarcts and lack of hemorrhagic transformation generally suggest favorable prognosis 1