Eight-and-a-Half Syndrome is a syndrome combining ipsilateral horizontal gaze palsy, internuclear ophthalmoplegia (INO), and peripheral (lower motor neuron) facial nerve palsy. It was first named by Eggenberger in 1998 1).
One-and-a-half syndrome is derived from the sum of horizontal gaze palsy (1) and INO (0.5), totaling “1.5.” Eight-and-a-half syndrome is this one-and-a-half syndrome plus ipsilateral seventh cranial nerve (facial nerve) palsy, named as VII (7) + 1.5 = 8.5 1).
The incidence is extremely rare. No large-scale epidemiological studies exist, and reports are mainly case reports 2)5). The most common cause is cerebrovascular disease, followed by demyelinating diseases (e.g., multiple sclerosis) 2)4).
It is derived by adding the “7” of the seventh cranial nerve (facial nerve) to the “1.5” of one-and-a-half syndrome (horizontal gaze palsy + internuclear ophthalmoplegia), totaling 8.5. It was named by Eggenberger in 1998.
When caused by cerebrovascular disease, onset is sudden. The main subjective symptoms are as follows.
The three findings that constitute the 8.5 syndrome are shown below.
Horizontal Gaze Palsy
Inability to gaze conjugately to the ipsilateral side: Horizontal eye movement toward the affected side is limited in both eyes.
Conjugate deviation: In the acute phase, there may be a brief deviation toward the healthy side when looking straight ahead.
Gaze-evoked nystagmus: Appears when looking toward the affected side.
Internuclear Ophthalmoplegia
Limited adduction on the affected side: Characterized by a marked decrease in adduction speed, which tends to persist even after the limitation of movement resolves.
Nystagmus in the abducting eye on the healthy side: This is a monocular nystagmus called dissociated rhythmic nystagmus.
Convergence preservation: Convergence is possible even with MLF lesions.
Facial nerve palsy
Peripheral (LMN type): Inability to wrinkle the forehead, accompanied by incomplete eyelid closure. Unlike the upper motor neuron type, there is forehead paralysis.
Nasolabial fold flattening and mouth angle deviation: The nasolabial fold on the affected side disappears, and the mouth angle deviates to the healthy side.
The only remaining horizontal eye movement is abduction of the contralateral eye. In primary position, the affected eye is exotropic, called paralytic pontine exotropia.
It is not completely lost. Only abduction of the contralateral eye remains. Also, adduction during convergence is preserved, so adduction during near vision is possible.
The causative diseases are as follows:
The main risk factors are arteriosclerotic risk factors such as hypertension, diabetes, and dyslipidemia2)3).
8.5 syndrome is primarily a clinical diagnosis. Detailed eye movement examination and neurological assessment of cranial nerves are essential.
It cannot be ruled out. CT has low sensitivity for acute cerebral infarction, and a normal finding may miss brainstem infarction. If clinically suspected, MRI is necessary.
Treatment is based on the underlying disease.
In isolated 8.5 syndrome, the prognosis for diplopia and facial nerve palsy is good. Abducens palsy tends to persist longer than adducens palsy.
Muhammad et al. (2024) reported a case of 8.5 syndrome due to brainstem infarction in a 55-year-old man. After treatment with antiplatelet drugs, the ophthalmoplegia completely recovered within 3 months, and only slight residual facial nerve palsy remained2).
Ingle et al. (2021) reported a case of pontine infarction combined with acute myocardial infarction in a 54-year-old man. Dual antiplatelet therapy and physical therapy were administered, and improvement was observed at the 2-month follow-up3).
In isolated 8.5 syndrome, the prognosis is good, and eye movements improve within a few months in most cases. However, abducens palsy tends to recover more slowly than adducens palsy.
The responsible lesion in 8.5 syndrome is the dorsal tegmentum of the caudal pons. In this area, the abducens nucleus, medial longitudinal fasciculus (MLF), and facial nerve fibers are in close proximity.
The structures and pathways involved in controlling horizontal gaze are as follows.
Through this circuit, when the PPRF on one side is excited, the ipsilateral lateral rectus and contralateral medial rectus contract, establishing conjugate gaze toward the same side.
The facial nerve nucleus is located in the dorsal pons. The fibers of the facial nerve run dorsomedially from the nucleus, loop around the abducens nucleus dorsally, then turn ventrally to exit the pons (facial nerve genu). Due to this course, lesions near the abducens nucleus often involve the facial nerve fibers.
| Structure affected | Symptoms |
|---|---|
| PPRF / abducens nucleus | Ipsilateral horizontal gaze palsy |
| MLF | Ipsilateral internuclear ophthalmoplegia |
| Facial nerve fibers | Ipsilateral peripheral facial nerve palsy |
One-and-a-half syndrome results from simultaneous damage to the PPRF (or abducens nucleus) and the MLF. Eight-and-a-half syndrome is this plus involvement of the facial nerve fibers.
Blood flow to the affected area originates from the paramedian pontine arteries (branches of the basilar artery), which supply one side of the midline. In elderly individuals, branch artery infarction due to arteriosclerosis is the main cause, while in younger individuals, demyelination due to multiple sclerosis is more common.
