Lateral pontine syndrome

Overview

Lateral pontine syndrome, also known as Marie–Foix syndrome, is a neurological condition resulting from an infarction (stroke) in the lateral part of the pons, a structure located in the brainstem. The syndrome occurs due to occlusion of specific arteries supplying the pons, leading to damage in the cranial nerve nuclei, motor tracts, and sensory pathways. Depending on the exact location and size of the infarct, the syndrome produces a distinct combination of ipsilateral cranial nerve deficits and contralateral sensory or motor impairments. It is less common than lateral medullary syndrome but shares some overlapping features.

Causes

Lateral pontine syndrome is most commonly caused by an ischemic stroke affecting one of the branches of the anterior inferior cerebellar artery (AICA), or occasionally the basilar artery. Common underlying causes include:

• Atherosclerosis – narrowing of arteries due to plaque buildup

• Embolism – blockage from a blood clot or debris originating from the heart or proximal arteries

• Arterial dissection – especially in younger patients with neck trauma

• Small vessel disease – due to hypertension or diabetes

Symptoms

The clinical presentation of lateral pontine syndrome depends on the structures involved in the infarct. Common signs and symptoms include:

• Facial weakness (ipsilateral) – due to involvement of the facial nerve (cranial nerve VII)

• Loss of taste (anterior two-thirds of tongue)

• Vertigo, nausea, and vomiting – due to vestibular involvement

• Hearing loss or tinnitus (ipsilateral) – from cochlear nerve involvement

• Ataxia and unsteady gait (ipsilateral) – due to damage to cerebellar connections

• Loss of pain and temperature sensation:

  • Contralateral body – due to damage to the spinothalamic tract

  • Ipsilateral face – from involvement of the spinal trigeminal nucleus

• Horner’s syndrome – ptosis, miosis, and anhidrosis on the same side of the lesion

Diagnosis

Diagnosis of lateral pontine syndrome is based on clinical signs, neuroimaging, and vascular studies. Key diagnostic steps include:

• Neurological examination – to identify the characteristic pattern of cranial nerve and sensory deficits

• MRI of the brainstem – most sensitive for detecting infarcts in the pons

• MRA or CTA – to visualize vascular anatomy and identify arterial occlusion or stenosis

• Cardiac workup – including ECG and echocardiogram to assess for embolic sources

• Laboratory testing – to evaluate risk factors like blood glucose, lipids, and clotting disorders

Treatment

Treatment of lateral pontine syndrome focuses on acute stroke management, secondary prevention, and symptom-specific rehabilitation. Therapeutic measures include:

• Thrombolytic therapy – such as tPA (tissue plasminogen activator), if within the treatment window and eligible

• Antiplatelet agents – like aspirin or clopidogrel to prevent further strokes

• Blood pressure and lipid control – to manage vascular risk factors

• Physical and occupational therapy – for motor coordination, strength, and daily activities

• Speech and swallowing therapy – if cranial nerve deficits affect communication or feeding

• Hearing aids or assistive devices – in cases with auditory loss

Prognosis

The prognosis for lateral pontine syndrome depends on the extent of the stroke and timeliness of medical intervention. Many individuals experience partial recovery with appropriate rehabilitation, though some may have persistent neurological deficits, including facial weakness, ataxia, or sensory disturbances. Early recognition, stroke unit care, and long-term management of risk factors are critical to improving outcomes and reducing the risk of recurrent strokes. Most patients can regain a good degree of independence with proper care and support.