What is lateral infarct?

Lateral Medullary Infarct or lateral medullary syndrome , the term used for a clinical condition resulting from damage to lateral part of the medulla oblangata. Lateral medullary syndrome is also known as Wallenberg syndrome or posterior inferior cerebellar artery (PICA) syndrome.[1]

Causes

Lateral medullary syndrome can result from occlusion or a critical narrowing of the posterior inferior cerebellar artery (PICA) – that can occur either because of a thromboembolism originating from the vertebral or basilar arteries, or the artery of origin narrowing due to atherosclerosis or dissection [2] resulting in inadequate blood supply and subsequent ischemia.

Risk factors for lateral medullary infarction include:

hypertension

diabetes

hypercholesterolemia

smoking

atrial fibrillation

carotid artery stenosis

Less commonly, the lateral medullary syndrome can result from: trauma, vertebral artery dissection or embolic events due to a cardiogenic cause.[2]

Signs and symptoms

The lateral medullary syndrome characteristically presents with the combination of:

Ipsilateral Horner syndrome (ptosis, miosis, anhidrosis) resulting from damage to the descending sympathetic fibers that have their nuclei in the hypothalamus and terminate at the level of T1/T2

Impaired pain and temperature sensation on the contralateral side of the body because of damage to lateral spinothalamic tract axons conveying impulses of pain and temperature, from the body up to the level of C2.

Dysphagia due to damage to the nucleus ambiguus – which gives rise to axons forming the pharyngeal branch of vagus nerve.

Nystagmus resulting from damage to vestibular nucleus and its connection within medulla and pons.

Vertigo and ataxia due to damage to the vestibular nucleus.

Weakness of ipsilateral trapezius muscle and palate muscles due to damage to the nucleus ambiguus.

Hoarseness of voice due to damage to the recurrent laryngeal nerve which has a nucleus within medulla.

Impaired sensation of taste over the posterior one third of the tongue (ipsilateral side) due to damage to the nucleus solitarius that receives sensory information from the posterior one third of the tongue; this is conveyed by way of the glossopharyngeal nerve .[2]

Posterior inferior cerebellar artery syndrome

Wallenberg syndrome is due to injury of the lateral medulla supplied by the posterior inferior cerebellar artery (PICA). The clinical consequences are as follows:[3]

Ipsilateral Horner's syndrome consisting of miosis, ptosis and anhidrosis resulting from damage to ipsilateral descending sympathetic fibres which arise from the hypothalamus. Their cell body lies in the intermediolateral column from T1-T2. Therefore, damage to these fibres anywhere along their course may lead to Horner's syndrome.

Nystagmus which is predominantly rotatory and horizontal and occasionally a gaze palsy resulting from damage to the medial longitudinal bundle (MLF).

Vertigo and ataxia from lesion to the lateral vestibular nucleus and cerebellar connections.[4][5]

Impaired pain and temperature sensation on the contralateral side of the face and body due to damage to the contralateral spinothalamic tract.

Ipsilateral dysphonia and dysphagia from nucleus ambiguus lesion affecting the vagus and glossopharyngeal nerves.[4]

Sometimes hemiparesis and athetoid movements resulting from damage to corticospinal and rubrospinal tracts. This is uncommon as those tracts are supplied by the anterior spinal artery.[6]

Impaired taste sensation (ageusia) over the posterior one-third of the ipsilateral tongue since taste fibres from the posterior third are carried via the glossopharyngeal nerve. Lesion to the nucleus of tractus solitarius also impairs taste sensation.[4]

Wallenberg syndrome is classically associated with a PICA infarction but in rare cases can be caused by infarction in the territory of the anterior inferior cerebellar artery (AICA).[7][8]