Supranuclear Cortical Lesions
Supranuclear cortical lesions refer to pathological abnormalities affecting the cerebral cortex that result in dysfunction of neural pathways controlling cranial nerve nuclei from above (supranuclear), most commonly manifesting as upper motor neuron patterns of weakness that spare certain muscle groups due to bilateral cortical innervation.
Anatomical Definition and Clinical Significance
Supranuclear lesions are distinguished from nuclear or infranuclear lesions by their characteristic pattern of sparing upper facial muscles due to bilateral cortical innervation, whereas lower motor neuron (nuclear/infranuclear) lesions cause complete ipsilateral facial weakness including forehead involvement 1, 2, 3.
- Supranuclear facial palsy preserves forehead movement (ability to wrinkle forehead and raise eyebrows) because upper facial muscles receive bilateral cortical input 2, 3.
- This contrasts with peripheral facial nerve lesions where complete ipsilateral facial paralysis occurs, including inability to close the eye or wrinkle the forehead 1, 2.
Pathological Context in Multiple Sclerosis
In the context of demyelinating disease, cortical lesions represent focal abnormalities completely within the cortex or spanning cortex and subjacent white matter 4.
- Cortical lesions in multiple sclerosis are classified histopathologically into four types: Type I (leukocortical, affecting both grey and white matter), Type II (small perivenous intracortical), Type III (subpial demyelination extending inward from pial surface—the most frequent type), and Type IV (extending through full cortical width without crossing into white matter) 4.
- These lesions appear as hyperintensity on DIR sequences compared to normal grey matter, requiring at least 3mm size along the main axis 4.
- Curvilinear/worm-shaped cortical lesions following sulcal and gyral contours are pathognomonic for multiple sclerosis and not seen in other conditions 4.
Localization in Brainstem Pathology
Supranuclear lesions affecting facial nerve pathways can occur at the pontine level, where corticofacial fibers take a separate course from the main pyramidal tract 5.
- Pontine supranuclear facial palsy presents with contralateral facial weakness and may be accompanied by dysarthria, with MRI documenting the pontine lesion 5.
- Upper medullary infarctions can produce ipsilateral facial weakness through supranuclear (corticofacial) tract lesions, distinguishable from nuclear lesions through electrophysiological testing with transcranial magnetic stimulation 6.
Progressive Supranuclear Palsy Context
In progressive supranuclear palsy (PSP), cortical pathology involves tau-positive neurofibrillary tangles predominantly in deepest cortical layers, with highest density in precentral and angular gyri 7.
- Cortical degeneration in PSP is often circumscribed to premotor and motor cortex, characterized by neuronal loss, gliosis, and distinctive tufted astrocytes (not seen in other tauopathies) 8.
- The cortical lesions in PSP are linked to the pedunculopontine nucleus, suggesting this structure plays a prominent role in lesion spread 7.
Critical Diagnostic Distinctions
The key clinical distinction is forehead involvement: preserved forehead function indicates supranuclear (central) pathology, while complete forehead paralysis indicates nuclear or infranuclear (peripheral) pathology 2, 3.
- Multiple cranial nerve involvement (CN V, VI, VII, VIII together) suggests pontine lesion location 2.
- Combined CN VII and CN XII palsy with ipsilateral tongue deviation indicates skull base or extracranial pathology, not supranuclear cortical lesions 1, 2.
- MRI with contrast is mandatory for localizing lesions when multiple cranial nerves are involved or when clinical examination suggests central pathology 1, 2, 3.