Symptoms and Signs

1. Contralateral hemiplegia of the extremities (sparing the face) due to pyramidal tract involvement.
2. Ipsilateral lateral rectus palsy leading to diplopia that is accentuated when the patient looks towards the side of the lesion, internal strabismus (i.e., Esotropia) and loss of power to rotate the affected eye outward due to the involvement of CN VI.
3. Ipsilateral peripheral facial nerve paresis leads to flaccid paralysis of the muscles of the facial expression and loss of the corneal reflex due to cranial nerve VII involvement.[5]

Clinical Examination

The diagnosis of Millard-Gubler syndrome (MGS) is confirmed by a clinical examination of VI and VIII CN along with hemiplegia of upper and lower extremities. Because various etiologies might cause MGS, take a detailed history to exclude other causes like infection (fever) or vascular insult (presence of other neurologic deficits).

Imaging

Neurological Imaging, i.e., computed tomography (CT) and magnetic resonance imaging (MRI) are helpful in identifying the lesion. However, MRI of the brain is more sensitive and specific than CT scan to identify the infarcts at an early stage of onset, especially in the setting of small pontine lesions. Ischemic stroke of pons on CT brain shows a hypodense lesion in the anteromedial side of the pons. MRI brain shows a lesion in one side of the anteromedial pons, which is hypointense on T1 sequences and hyperintense on T2 /FLAIR sequences.[5] The Magnetic resonance imaging also shows diffusion restriction in the pontine ischemic lesion. However, there have been some reported cases presenting as MGS with no imaging findings.[6] Other associated lesions (tuberculoma, tumors, and cysticercus granulomas)[2] can also be identified using imaging.

Angiography

Vertebral angiography is helpful in cases if the lesion is caused due to the occlusion of the basilar artery.

Pontine-crossed syndromes are Foville, Raymond, Raymond–Cestan syndrome, Gasperini syndrome, and Brissaud-Sicard syndrome. These syndromes are unique as the lesion involves the brainstem above the decussation of the pyramidal tracts. Therefore, the clinical signs of the cranial nerve are ipsilateral to the lesion, and the long tract signs contralateral, resulting in crossed syndrome.

• Foville syndrome: This syndrome is caused due to a unilateral lesion involving the dorsal pontine tegmentum in the caudal third of the pons and manifests as ipsilateral facial palsy and horizontal gaze palsy, and contralateral hemiparesis, Hemi sensory loss, Internuclear ophthalmoplegia.

• Raymond syndrome: This syndrome is caused due to a lesion involving the ventral medial pons. It usually presents as two subtypes - Classical and common. Classical Raymond syndrome manifests as ipsilateral abducens palsy, contralateral central facial paresis, and contralateral hemiparesis. The common subtype of Raymond syndrome presents as ipsilateral lateral gaze paresis and contralateral hemiparesis sparing the face.[7]

• Raymond–Cestan syndrome: This syndrome is caused due to the lesion involving the upper dorsal pons. It manifests as ipsilateral ataxia and coarse intention tremor, ipsilateral paralysis of muscles of mastication and sensory loss in the face, contralateral sensory loss in the body and contralateral hemiparesis of the face and the body.

• Gasperini’s syndrome: This is a rare syndrome caused due to a lesion of the caudal pons tegmentum and mostly presents as ipsilateral impairment of the cranial nerves V, VI, VII, VIII and contralateral sensory loss.

• Brissaud-Sicard syndrome: This is a very rare pontine syndrome caused due to damage of the anterolateral and inferior pons involving the corticospinal tract and CN VII nucleus and the nerve root. Classically this syndrome presents as ipsilateral facial cramps and contralateral hemiparesis.

Treatment mainly depends on the etiology of the disease. In some cases, patients presenting with multiple deficits require early conservative measures together with multidisciplinary rehabilitation.

• Ataxic hemiparesis

• Dysarthria

• Locked-in syndrome

• Pure motor hemiparesis

• Raymond syndrome

• Ventral pontine syndromes

• Prognosis mainly depends on the extent and etiology of the disease.
• A vertebrobasilar stroke usually leaves a significant neurologic deficit.
• Patients with small lesions usually have a better prognosis.
• Patients with acute basilar artery occlusion have a high mortality. 

• Millard-Gubler syndrome (MGS) is one of the classical brainstem-crossed syndromes caused due to a unilateral lesion in ventral pons, manifesting as ipsilateral palsy of CN VI and VII with contralateral hemiplegia.
• Etiology varies with age. In younger people, the leading causes are tumors, infectious diseases (neurocysticercosis and tuberculosis), demyelinating disease (multiple sclerosis), and viral infection (Rhomb encephalitis). In older patients, it is more often due to hemorrhage and ischemic stroke.
• MGS clinical features are an ipsilateral weakness of eye abduction and ipsilateral facial muscle weakness along with contralateral upper and lower extremity weakness.
• Diagnosis of MGS depends on a detailed history and physical examination. Imaging studies such as CT and MRI are confirmatory.
• Other pontine-crossed brainstem syndromes include Foville syndrome, Raymond syndrome, Gasperini syndrome, Brissaud-Sicard syndrome, and Raymond–Cestan syndrome.
• Classical Raymond syndrome also has the same components as Millard-Gubler syndrome, but there is ipsilateral sixth nerve palsy along with contralateral facial paresis and hemiplegia.
• Management mainly depends on the etiology of the disease.
• Patients with small lesions usually have a better prognosis. However, MGS caused due to acute basilar artery occlusion has a high mortality rate.

MGS is best managed by an interprofessional team that also includes neurology nurses. There is no specific treatment for the neurological deficits but the condition causing the disorder has to be controlled. The prognosis depends on the severity of the neurological deficits, patient age, co-morbidity, and the cause.