What do cortical signs indicate in a neuro examination?

Cortical Signs in Neurological Examination

Cortical signs refer to clinical findings on neurological examination that indicate dysfunction of the cerebral cortex, manifesting as deficits in higher-order functions such as language, memory, praxis, visuospatial processing, executive function, and complex sensory integration—essentially representing impairment of functions beyond basic motor and sensory pathways. 1, 2

Core Definition and Clinical Significance

Cortical signs represent dysfunction of primary cortical areas (motor, sensory, visual) or more complex associative cortical regions that integrate and modulate these primary functions. 1 The key distinction is that cortical signs reflect damage to the cerebral cortex itself rather than subcortical structures, brainstem, or peripheral nervous system. 1

Primary Cortical Signs Include:

• Motor cortex dysfunction: Weakness with characteristic upper motor neuron pattern, including preserved forehead function in supranuclear facial palsy due to bilateral cortical innervation of upper facial muscles 3
• Sensory cortex dysfunction: Loss of discriminative touch, two-point discrimination, graphesthesia, and stereognosis 1
• Visual cortex dysfunction: Homonymous visual field defects, cortical blindness 1

Higher-Order Cortical Signs Include:

• Language dysfunction (aphasia): Expressive, receptive, or mixed language impairment indicating dominant hemisphere cortical involvement 1, 2
• Memory deficits: Particularly encoding and retrieval problems suggesting temporal lobe cortical dysfunction 1, 2
• Apraxia: Inability to perform learned motor tasks despite intact motor and sensory function 1
• Agnosia: Failure to recognize objects, faces, or sounds despite intact primary sensory pathways 1
• Neglect: Inattention to one side of space, typically indicating non-dominant parietal cortex damage 1
• Executive dysfunction: Impaired planning, organization, and problem-solving reflecting frontal cortex involvement 2

Anatomical Localization

Each cognitive domain tested during neuropsychological evaluation has a specific anatomical substrate in the cortex, making neuropsychological testing essentially an extension of the neurological examination applied to higher-order cortical function. 2 This anatomical correlation allows precise localization of cortical pathology based on the pattern of deficits observed.

Distinguishing Cortical from Subcortical Pathology

The critical distinction between supranuclear (cortical) and nuclear/infranuclear lesions is forehead involvement: preserved forehead function indicates supranuclear cortical pathology, while complete forehead paralysis including inability to wrinkle the forehead indicates lower motor neuron pathology. 3 This occurs because upper facial muscles receive bilateral cortical input, providing redundancy that protects against unilateral cortical lesions. 3

Common Pitfalls in Assessment

• Confusing cortical signs with metabolic encephalopathy: Triphasic waves on EEG and generalized slowing can occur in hepatic encephalopathy and other metabolic conditions, representing transient subcortically or metabolically induced cortical dysfunction rather than primary structural cortical pathology 4
• Overlooking subtle cortical malformations: Focal cortical dysplasia may show only minimal blurring of the cortex-white matter junction on MRI, requiring high-resolution imaging and correlation with clinical seizure patterns 4
• Misinterpreting developmental cortical abnormalities: Polymicrogyria appears as an excessive number of abnormally small gyri with irregular "pebbled" cortical surface and "stippled" grey-white matter boundary, which can be mistaken for acquired pathology 4

Clinical Context and Implications

Identifying cortical signs requires systematic examination of higher cortical functions beyond routine motor and sensory testing. 1 The presence of cortical signs indicates pathology affecting the cerebral cortex from various etiologies including vascular disease, inflammatory conditions, tumors, infections, genetic disorders, and malformations of cortical development. 5 The specific pattern of cortical dysfunction guides both anatomical localization and differential diagnosis, directly impacting management decisions including surgical candidacy for refractory epilepsy. 6