From the Research
Lesions in the internal capsule lead to contralateral facial paresis because the internal capsule contains the corticobulbar tract fibers that control facial movements, which originate in the motor cortex of one hemisphere and cross to the opposite side in the brainstem before synapsing with the facial nucleus. When a lesion occurs in the internal capsule, it interrupts these descending motor pathways before they cross, resulting in weakness or paralysis of the face on the side opposite to the brain lesion. Importantly, in internal capsule lesions, the entire contralateral face is affected (both upper and lower portions) because the corticobulbar fibers controlling the lower face cross to the opposite side while those for the upper face have bilateral innervation, as suggested by a study on the location of emotional corticobulbar tract in the internal capsule 1. This pattern differs from lower motor neuron lesions of the facial nerve itself, which would cause ipsilateral facial weakness affecting both upper and lower face. The internal capsule is a common site for strokes, particularly lacunar infarcts, which can produce this characteristic contralateral facial weakness as part of a broader hemiparesis syndrome, and recent studies have provided insights into the specific location of the emotional corticobulbar tract within the internal capsule 1. Some studies have reported cases of pontine infarction-induced contralateral central facial palsy, which may present with similar symptoms to internal capsule lesions 2. However, the most recent and highest quality study on this topic is from 2023, which reported a case of "uncrossed central facial paralysis" caused by pontine infarction, highlighting the complexity of facial paralysis and the need for careful diagnosis and treatment 2. In terms of treatment, botulinum toxin injections have been shown to improve quality of life in patients with long-standing facial palsy, but this is not directly related to the question of why lesions in the internal capsule lead to contralateral facial paresis 3. Overall, the evidence suggests that lesions in the internal capsule can cause contralateral facial paresis due to the interruption of corticobulbar tract fibers, and this is supported by recent studies on the location of the emotional corticobulbar tract in the internal capsule 1.
Some key points to consider include:
- The internal capsule contains the corticobulbar tract fibers that control facial movements
- Lesions in the internal capsule can cause contralateral facial paresis
- The entire contralateral face is affected (both upper and lower portions) in internal capsule lesions
- The internal capsule is a common site for strokes, particularly lacunar infarcts
- Recent studies have provided insights into the specific location of the emotional corticobulbar tract within the internal capsule 1
- Pontine infarction can also cause contralateral central facial palsy, which may present with similar symptoms to internal capsule lesions 2