A stroke occurs when blood flow to a part of the brain is disrupted, either by a blockage (ischemic stroke) or bleeding (hemorrhagic stroke). This interruption starves brain cells of oxygen and nutrients, causing them to die rapidly. The resulting facial droop is a highly visible sign of this neurological damage, pointing to an interruption in the brain’s control over the facial muscles. Understanding this symptom requires tracing the path of the motor signals from the brain down to the face.
How the Brain Directs Facial Muscle Movement
Voluntary movement of the face, such as smiling or raising an eyebrow, begins in the primary motor cortex of the brain, located in the frontal lobe. This area contains the “command signals” for movement, which are carried by specialized nerve cells called upper motor neurons (UMNs). The UMNs for the face travel downward from the cortex through a major white matter tract toward the brainstem.
These signals must ultimately reach the facial nerve (Cranial Nerve VII), which emerges from the brainstem and directly innervates the muscles of facial expression. The motor signals cross over, meaning UMNs originating in the right motor cortex control the muscles on the left side of the face, and vice versa. This contralateral arrangement ensures that damage to one side of the brain affects the opposite side of the body.
The UMNs synapse onto the lower motor neurons (LMNs) within a structure in the brainstem called the facial nucleus. These LMNs then exit the brain and travel through the skull to reach their specific target muscles, commanding them to contract. This entire pathway, from the motor cortex down to the facial nucleus, is the mechanism that allows for deliberate, coordinated facial expressions.
The Interruption of Signal Transmission by Stroke
A stroke causes damage to brain tissue by cutting off the blood supply to a specific region, which destroys nerve cells within minutes. When the stroke occurs in a region supplied by the middle cerebral artery, it commonly damages the motor cortex or the descending UMN pathway responsible for controlling the face. This destruction immediately stops the transmission of the volitional motor command.
Because the UMN pathway crosses over, a stroke in the left hemisphere of the brain will abolish the motor signals intended for the muscles on the right side of the face. The affected muscles no longer receive the command to maintain tone or move, leading to the characteristic facial weakness and drooping. This results in the inability to lift the corner of the mouth or cheek on the side opposite the brain lesion.
The location and size of the stroke determine the severity of the droop and whether other body parts are affected, but the mechanism remains the same: the physical loss of the nerve pathway. The sudden cessation of blood flow creates a zone of death in the brain tissue that was relaying the signal to the face. This interruption is the direct cause of the loss of muscle function observed in a stroke.
The Anatomical Reason for Partial Facial Droop
Facial drooping from a stroke is often described as “partial” because it affects the lower half of the face much more severely than the upper half. This pattern is due to a unique anatomical arrangement known as dual innervation in the upper face. The lower facial muscles, responsible for movements like smiling, receive motor commands only from the contralateral (opposite side) motor cortex.
In contrast, the upper facial muscles, which control eyebrow raising and eye closure, receive motor signals from UMNs originating in both the left and right motor cortices. This dual supply provides a built-in redundancy. If a stroke damages the UMN pathway on one side of the brain, the upper facial muscles can still receive a functional signal from the undamaged side of the brain.
Therefore, when a stroke occurs, the lower face loses its sole source of motor command and droops noticeably, while the upper face retains function due to the surviving input from the healthy brain hemisphere. This difference in innervation explains why a stroke patient may be unable to smile fully on one side but can still wrinkle their forehead or close their eyes somewhat symmetrically. This presentation of weakness primarily in the lower face is a hallmark sign of a central nervous system injury, distinguishing it from other causes of facial paralysis.