The brain stem is a stalk-like structure at the base of the brain, acting as the communication bridge between the cerebrum, cerebellum, and spinal cord. It is composed of three sections: the midbrain, the pons, and the medulla oblongata. This region serves as the control center for many involuntary, life-sustaining functions that do not require conscious thought. Damage to the brain stem results in immediate and profound functional loss.
Compromise of Essential Autonomic Functions
Injury to the brain stem immediately threatens life by disrupting the centers that regulate involuntary physiological activities. The medulla oblongata and the pons house the nuclei responsible for controlling basic autonomic functions, including respiration and cardiovascular stability. Damage to these areas can lead to central dysautonomia, where the nervous system loses its ability to regulate the body’s internal environment.
The respiratory centers in the medulla and pons manage the rhythm and depth of breathing. Damage can cause irregular breathing patterns or complete cessation of breathing (apnea). This often necessitates mechanical ventilation, as the body can no longer initiate inhaling and exhaling on its own. The medulla also contains cardiovascular centers that reflexively adjust heart rate and blood pressure.
Destruction of these nuclei can cause severe fluctuations in blood pressure and irregular heart rhythms, compromising blood flow to the rest of the brain and body. The brain stem is also involved in thermoregulation, and injury can result in the body being unable to maintain a stable internal temperature. This instability in the cardiac and pulmonary systems requires immediate and intensive medical support.
Impact on Arousal and Wakefulness
The brain stem contains the Reticular Activating System (RAS), a network of nuclei that regulates consciousness, wakefulness, and alertness. Damage to this system interrupts the signals necessary to maintain an awake state, leading to altered awareness. The most severe outcome is a coma, a state of profound unconsciousness where the individual cannot be aroused and shows no evidence of awareness.
A patient may transition to a Persistent Vegetative State (PVS) if the brain stem remains relatively intact but the cerebral hemispheres suffer widespread damage. In PVS, the preserved RAS allows for sleep-wake cycles and eye opening, but the individual has no cognitive awareness of themselves or their surroundings.
A condition resulting from damage to the ventral pons is Locked-in Syndrome (LIS). LIS is distinct because the RAS and the cerebrum are spared, meaning the person is fully conscious and cognitively intact. However, the injury destroys the descending motor pathways, resulting in near-total paralysis of the body and face. The individual is unable to speak or move, with the only preserved movements typically being vertical eye movements and blinking.
Impairment of Movement and Sensory Pathways
The brain stem acts as the conduit for all major nerve tracts connecting the brain to the spinal cord, and damage causes widespread physical disability. The corticospinal tracts carry motor commands from the cortex to the body, traveling through the brain stem before crossing over (decussating) in the medulla. Injury above this decussation point typically results in weakness or paralysis (hemiparesis or hemiplegia) on the opposite side of the body.
Damage below the crossing, or bilateral damage, can lead to quadriplegia, paralysis affecting all four limbs. The brain stem also processes sensory information traveling via ascending pathways, such as the spinothalamic tract (pain and temperature) and the dorsal column pathway (touch and vibration). Disruption of these pathways results in a loss or alteration of sensation below the level of the lesion.
The brain stem contains pathways that connect to the cerebellum, the structure responsible for coordination and balance. Injury to these connections, particularly in the pons, can cause severe ataxia, characterized by a staggering gait and uncoordinated movements. Deficits involve the inability to initiate movement, loss of fine motor control, and poor postural stability.
Deficits in Speech, Swallowing, and Facial Control
Ten of the twelve pairs of cranial nerves originate from nuclei within the brain stem, controlling the muscles and sensations of the head and neck. Damage to these nuclei results in localized functional losses. The ability to speak is compromised by damage to the nerves controlling the tongue, pharynx, and larynx (CN IX, X, and XII).
This injury manifests as dysarthria (slurred, slow, or difficult speech) due to poor control over the muscles of articulation. Swallowing relies on the coordinated action of multiple cranial nerves:
- Trigeminal (CN V)
- Glossopharyngeal (CN IX)
- Vagus (CN X)
- Hypoglossal (CN XII)
Damage leads to dysphagia, where difficulty swallowing increases the risk of aspiration pneumonia.
Eye Movement and Facial Control
Eye movement is regulated by three cranial nerves (CN III, IV, and VI) originating in the midbrain and pons. Injury can cause diplopia (double vision) and gaze palsies, where the eyes cannot move together in a coordinated manner. Damage to the facial nerve (CN VII) nucleus in the pons results in facial weakness or paralysis. This causes drooping on one side of the face and an inability to make expressions or close the eye fully.