Pons injury: Symptomatology

Most primary injuries to the midbrain and pons in particular are related to vascular insults or in the setting of osmotic demyelination.

The pons receives the majority of its blood supply from the basilar artery, which branches into the bilateral anterior inferior cerebellar arteries (AICA) and its paramedian and dorsolateral sub-branches. Complete basilar artery occlusion at the level of the pons can lead to ventral pontine damage and “locked-in syndrome.” The ventral pons includes the descending motor pathways, spinothalamic tract, medial lemniscus, facial nucleus (CN VII), Abducens nucleus (CN VI), the trigeminal nucleus (CN V), and vestibular nucleus (CN VIII), cochlear nucleus (CN VIII), as well as sympathetic tract.

Interruption of the bilateral descending motor pathways leads to quadraparesis, dysphagia, dsyparthria, interruption of the spinothalamic tract leads to loss of fine touch, and interruption of cranial nerve nuclei loss of facial movement, strabismus, facial anesthesia, vertigo, and potentially hearing loss.

Medial pontine syndrome, which may be caused from unilateral occlusion of paramedian branches of the anterior inferior cerebellar artery, leads to compromise of:

• Medial lemniscus: contralateral loss of touch, vibration, and proprioception from body
• Corticospinal tract: contralateral spastic (UMN) hemiparesis
• Abducens nucleus: ipsilateral lateral rectus paralysis and strabismus

Lateral pontine syndrome, which may be caused from unilateral occlusion of dorsolateral branches of the anterior inferior cerebellar artery, leads to compromise of:

• Trigeminal nucleus: ipsilateral facial hemianesthesia (loss of pain and temperature)
• Facial nucleus: ipsilateral paralysis of upper and lower face
• Vestibular nucleus: nausea, vertigo and nystagmus
• Cochlear nucleus: ipsilateral central deafness
• Lateral spinothalamic tract: contralateral loss of pain and temp sensation from body
• Descending sympathetic tract: ipsilateral Horner’s syndrome (ptosis, miosis and anhidrosis)

Occlusion of a unilateral AICA can lead to a combination of symptoms of both medial and lateral pontine syndromes.

Updated definition 2020:

The pons is a collection of tracts and nuclei in the brainstem that are vital for sensory, motor, and autonomic functions. The ventral pons houses the pontine nuclei, which is responsible for coordination of movement (synapse from the corticopontine fibers to middle cerebellar pedicle fibers that make their way to the cerebellum). The pontine tegmentum houses the pontine respiratory group (PRG) which include the upper pneumotaxic center (decreases depth of inspiration and signals the medulla’s dorsal respiratory group to increases respiratory rate) and the lower apneustic center (promotes depth of inspiration by stimulating the medulla’s dorsal respiratory group). Other nuclei include the motor and main sensory nuclei of the trigeminal nerve (sensory and motor function of the head and face), abducens nucleus (lateral eye movement), facial nucleus (facial expression muscles and sensory information from mouth), and vestibulocochlear nerve nuclei (in addition to nuclei in the medulla, carry information about hearing and vestibular senses). The pons also houses locus coeruleus’ norepinephrine neurons (responsible for regulating rapid eye movement sleep among other function) and the reticular formation (maintaining behavioral arousal and consciousness) including the raphe nuclei’s primarily serotonergic neurons (responsible for wakefulness, sleep-wake cycles, mood, and inhibition of pain). Finally, the pons carries sensory tracts up into the thalamus.

Lesions in the pons from a stroke or central pontine myelinolysis (now known as osmotic demyelination syndrome) may lead to locked-in syndrome, slow, deep, irregular breathing, and difficulties with hearing, balance or equilibrium, walking, sensing facial touch and pain, tasting, secreting saliva and tears, eye movement including during REM sleep, facial expressions, and swallowing and speaking.