Differentiating Central vs. Peripheral Facial Paralysis: Key Clinical Insights
Understanding Facial Paralysis: A Fundamental Overview
Facial paralysis can be broadly categorized into two primary types—central and peripheral—each with distinct neurological origins and clinical presentations. Accurate differentiation between the two is crucial for proper diagnosis, treatment planning, and patient prognosis. The key distinguishing factor lies in whether the upper portion of the facial muscles is affected, which reflects the underlying pathway involved in the nerve dysfunction.
Central Facial Paralysis: Characteristics and Symptoms
Neurological Basis and Muscle Involvement
Central facial paralysis, also known as upper motor neuron palsy, occurs due to a lesion above the facial nerve nucleus—typically within one hemisphere of the brain, such as from a stroke or traumatic brain injury. A critical feature of this condition is that the upper facial muscles remain functional because they receive bilateral cortical input. This means both brain hemispheres innervate the muscles responsible for forehead movement and eye closure.
As a result, patients with central facial paralysis typically retain the ability to raise their eyebrows and wrinkle their foreheads. The most noticeable symptoms appear in the lower face: when asked to smile or show teeth, the corner of the mouth on the affected side droops downward, and the nasolabial fold becomes markedly shallower. This asymmetric expression is often the first clinical clue pointing toward a central origin.
Associated Neurological Signs
In many cases, central facial paralysis does not occur in isolation. It is frequently accompanied by other neurological deficits, particularly central tongue paralysis. This manifests as deviation of the tongue toward the side of the lesion when protruded—a sign that further supports an upper motor neuron etiology. Additional symptoms may include weakness in the limbs on the contralateral side, depending on the location and extent of the brain lesion.
Peripheral Facial Paralysis: Comprehensive Muscle Impairment
Origin and Full Facial Involvement
In contrast, peripheral facial paralysis—also referred to as lower motor neuron palsy—affects the facial nerve (cranial nerve VII) after it exits the brainstem. Because the entire facial nerve is compromised, all facial muscles on the affected side become paralyzed, including those in the upper face. This results in a more dramatic and widespread loss of facial movement.
One of the hallmark signs is the inability to elevate the eyebrow or frown, indicating involvement of the frontalis muscle. Patients often cannot fully close their eye on the affected side due to orbicularis oculi muscle weakness, leading to incomplete blink reflexes and potential corneal exposure. This risk of dryness and ulceration necessitates immediate protective measures, such as artificial tears or eye patches.
Facial Asymmetry and Functional Impact
When smiling or showing teeth, individuals with peripheral facial paralysis exhibit a pronounced shift of the mouth toward the unaffected (healthy) side. The paralysis affects not only voluntary movements but also spontaneous emotional expressions, significantly impacting communication and social interaction. Other symptoms may include loss of taste on the anterior two-thirds of the tongue, hyperacusis (increased sensitivity to sound), and reduced salivation—all pointing to broader cranial nerve dysfunction.
Clinical Evaluation and Diagnostic Approach
Distinguishing between central and peripheral facial paralysis begins with a thorough physical examination focusing on facial muscle symmetry and function. Observing whether the patient can wrinkle the forehead or tightly close the eyes provides immediate insight into the level of the lesion. Imaging studies such as MRI or CT scans may be required to identify structural abnormalities in the brain or along the course of the facial nerve.
Early and accurate diagnosis enables timely intervention—whether through corticosteroids for Bell's palsy, antiviral therapy, or neurosurgical evaluation in cases of mass lesions. Understanding these differences empowers healthcare providers to deliver targeted care and improve long-term outcomes for patients experiencing facial nerve disorders.