Since the first description of Wallenberg's syndrome more than 100 years ago, clinical and pathological findings of lateral medullary infarction (LMI) have been sporadically reported. Dizziness and ataxia are one of the most common symptoms/signs of lateral medullary infarction (LMI). Other symptoms/signs include nystagmus and ocular motor abnormality, dysphagia, dysarthria, hoarseness, nausea/vomiting, and hiccup. In patients with normal angiographic findings, atherothrombotic occlusion of a perforating artery itself seems to be the mechanism of infarction. Medial medullary infarction is usually caused by occlusion of penetrating branches associated with an atherosclerotic distal vertebral artery (VA) or vertebral arteries-basilar artery (VA-BA) junction. Lateral and medial medullary infarction may occur simultaneously or consecutively. Spontaneous primary medullary hemorrhage is rare. Although the causative role of hypertension is controversial, autopsy and imaging studies illustrate that hypertensive medullary hemorrhage does exist. Cavernous angiomas are a relatively frequent cause of medullary hemorrhage.

Cerebral venous thrombosis (CVT), a rare variety of cerebrovascular disease, is a well-established cause of intracerebral hemorrhage (ICH). Cerebral venous thrombosis in neonates is a condition that widely differs from CVT in children and adults because of the frequent association with an acute illness at time of diagnosis and the clinical presentation with seizures and lethargy. The diagnosis of CVT is based on neuroimaging but, even though some locations of hemorrhages can be suggestive of CVT, brain imaging by itself is of little positive value. Computerized tomography scan remains often the first investigation performed on an emergency basis. Antiepileptic drugs are usually prescribed only in patients who present with seizures. Patients with ICH frequently have severe headaches that may require strong analgesics such as morphine, but these usually rapidly decrease after initiation of heparin treatment. The follow-up of patients with H-CVT is similar to that of patients with non-H-CVT.