Approach to differentiating lesions (cerebral cortical and subcortical structures): Clinical sciences

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Approach to differentiating lesions (cerebral cortical and subcortical structures): Clinical sciences

NEUROLOGY

NEUROLOGY

Approach to differentiating lesions (cerebral cortical and subcortical structures): Clinical sciences
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Decision-Making Tree

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Cortical and subcortical lesions represent injury to the cerebral cortex and deeper structures of the cerebral hemispheres. Cortical lesions are associated with cortical signs and symptoms, such as aphasia, homonymous anopsia, agnosia, and neglect. On the other hand, subcortical lesions are associated with motor symptoms, like weakness and involuntary movements, and sensory loss, as well as cognitive and behavioral changes.

Now, if your patient presents with chief concerns suggestive of a cortical or subcortical lesion, first, perform an ABCDE assessment to determine if they are unstable or stable. If unstable, stabilize the airway, breathing, and circulation. Sometimes, you might have to intubate the patient and start mechanical ventilation. Next, obtain IV access, consider starting IV fluids, and put your patient on continuous vital sign monitoring, including heart rate, blood pressure, and pulse oximetry; as well as cardiac telemetry. Finally, if needed, be sure to manage high intracranial pressure.

Now, let’s go back to the ABCDE assessment and discuss stable patients. First, obtain a focused history and physical examination. Depending on the lesion location, the patient may have cognitive and behavioral changes, difficulty identifying objects, and trouble speaking or understanding speech. Some individuals may report vision changes or motor symptoms like weakness or numbness.

Next, the physical exam might demonstrate cognitive impairment and abnormal behavior, agnosia, aphasia, neglect, and visual field deficits. Also, you might identify weakness and sensory loss. Keep in mind that there will be no contralateral findings, such as weakness in the face and contralateral weakness in the limbs. With these findings, you should consider a cortical or subcortical lesion.

At this point, your next step is to differentiate between the two by assessing for signs and symptoms that usually indicate a cortical lesion. These include aphasia, homonymous anopsia, agnosia, and neglect.

If any of these signs or symptoms are present, the patient likely has a cortical lesion, so be sure to assess the dominant feature to further localize the lesion. If aphasia, or language impairment, is the dominant feature, determine the type of aphasia. Broca aphasia, which is also known as expressive aphasia, is characterized by non-fluent speech, impaired written language, and impaired repetition, with language comprehension largely intact. This presentation indicates a lesion in the left posterior inferior frontal lobe.

On the other hand, Wernicke aphasia is associated with fluent, nonsensical speech, along with paraphasic errors, which refer to using a word that is phonetically similar or similar in meaning. Also, these individuals will present with impaired repetition and language comprehension. These findings indicate a lesion in the left posterior superior temporal lobe.

Next, let’s discuss presentations where the dominant feature is a homonymous anopsia, meaning that there is a visual field loss on the same side of the visual field for each eye. In order to figure out the location of the lesion, further assess the type of field cut.

If you identify the right superior quadrantanopia, you should think of a lesion to the inferior optic radiations that pass through the left temporal lobe. In other words, the underlying cause is probably a left temporal lobe lesion.

Here’s a clinical pearl to keep in mind! A lesion limited to either above or below the calcarine fissure in the occipital lobe can also cause a contralateral quadrantanopia.

On the other hand, right hemianopsia with macular sparing, meaning sparing of the center of the visual field, suggests a lesion in the left occipital lobe, which is often seen with a stroke of the posterior cerebral artery. In this case, macular sparing occurs due to the collateral supply of the occipital pole by the middle cerebral artery.

Here are a few more clinical pearls to keep in mind! Another cause of homonymous hemianopsia is a lesion to the optic tract or lateral geniculate nucleus. However, in this case, the visual field deficit between the two eyes is usually not as equal as is seen with occipital lobe lesions.

A lesion in the left occipital lobe that also affects the splenium of the corpus callosum causes an interesting disconnection syndrome called alexia without agraphia, or impairment of reading without impairment in writing. This is because the patient has lost their right visual field due to the occipital lobe lesion, and while the left visual field is intact, the right occipital lobe is unable to transmit visual information through the corpus callosum to the language area in the left hemisphere.

Alright, let’s switch gears and discuss patients with agnosia, which is an inability to recognize or identify an object, person, or sensory stimulus despite retaining the primary function of processing that sensory input. For example, the patient might have difficulty recognizing faces, or a particular sound, despite having intact vision and hearing.

Sources

  1. "Chapter 10: Cerebral hemispheres and vascular supply; Chapter 16: Basal ganglia; Chapter 18: Limbic system: Homeostasis, olfaction, memory, and emotion" Neuroanatomy Through Clinical Cases, 3rd ed. (2010)
  2. "Chapter 10: Integrative functions of the nervous system" Berne & Levy Physiology, 8th ed. (2024)