What are the clinical manifestations of pontine infarction?

The impact of pontine infarction is relatively large, so it is important to pay attention to the understanding of the symptoms. Common patients may experience dizziness, headache, vertigo, or total disorder and hemiplegia, which seriously affect the patient's life and work.

(1) Pure motor hemiplegia resembling cerebral hemisphere lesions accounts for 60.9% of pontine infarctions. This is because the vertebral tract is located at the base of the pons, and the base is supplied with blood by the paramedian deep perforating branches of the basilar artery. The arteries in this area are prone to arteriosclerotic changes and hyaline degeneration. When the proximal end is occluded, it causes median infarction at the base, causing damage to the uncrossed vertebral tract.

(2) Two-thirds of patients with pontine infarction present with bilateral limb paralysis during the course of the disease. Therefore, if bilateral limb paralysis occurs during the course of the disease, it indicates the possibility of pontine infarction.

(3) Crossed palsy and cranial nerve paralysis are not common in pontine infarction because the cranial nerve nuclei of the pons are mostly located in the tegmentum and are supplied with blood by the relatively abundant long circumflex arteries and superior cerebellar arteries. The posterior communicating artery, posterior cerebral artery and superior cerebellar artery have collateral circulation, so the cranial nerves are not affected.

(4) Typical ventrolateral pontine damage is rare in patients with crossed facial nerve palsy and dysarthria-clumsy hand syndrome, which may be related to the fact that the lateral edge of the pons base is supplied with blood by the short circumflex artery and is less affected.

(5) Pontine infarction may cause ataxic hemiplegia. The ataxic hemiplegia is not obvious because the cortical pontocerebellar bundle is affected by the occlusion of the deep paramedian perforating branches.

(6) Pontine infarction may cause contralateral hemisensory disturbance, which may be caused by occlusion of the paracentral deep perforating branch, affecting the medial lemniscus located at the junction of the base and the tegmentum.

(7) Pontine infarction may cause symptoms such as vertigo, headache, dizziness, and slurred speech, but there are no definite positive signs. This may be due to the fact that the pyramidal tracts are divided into bundles by the pontine nuclei, and the lesions are small and do not involve or only involve a small part of the pyramidal tracts and other functional structures. Impairment of consciousness may also rarely occur because the lesion is small, with a maximum diameter of 1.1 cm and does not involve the reticular structure.

(8) Pontine infarction is often accompanied by basal ganglia or paraventricular infarction. This may be caused by atherosclerosis affecting multiple large arteries at the base of the brain. Due to insufficient blood supply from the internal carotid artery, the posterior communicating artery fails to compensate, thus triggering vertebrobasilar artery occlusion. Or long-term hypertension may cause hyalinization of the deep perforating arterioles of the vertebral basilar artery and internal carotid artery systems, resulting in microinfarction.