A small number of syndromes that initially were correlated, more or less convincingly, with relevant lacunes observed at subsequent autopsy have come to be regarded as the classical lacunar syndromes (LACS), pure motor stroke (PMS), pure sensory stroke (PSS), homolateral ataxia and crural paresis (HACP), dysarthria-clumsy hand syndrome (DCHS), ataxic hemiparesis (AH), and sensorimotor stroke (SMS). The original cases of HACP were described as having weakness of the lower limb, particularly the ankle and toes, a Babinski sign, and striking dysmetria of the arm and leg on the same side. The classical LACS are clinical paradigms that should be fine-tuned by clinicians. They have been shown to be simple and reasonably valid markers for a numerically significant and pathophysiologically distinct subgroup of patients with cerebral infarction. Clinical and research utility of the classical LACS will have to be kept under review in the era of hyperacute stroke assessment and treatment.

The arterial system supplying the midbrain is terminal for the midbrain itself, arising from the basilar artery and from the bifurcation of the basilar artery. According to magnetic resonance imaging (MRI)-based stroke registries, the midbrain was involved in 0.9% of strokes and 3% to 8% of posterior circulation infarcts. Oculomotor palsies are frequent in midbrain strokes and dominate the neurological picture. Combined upward- and downward-gaze palsy has been related to bilateral or unilateral midbrain infarcts. A lacunar infarct of the lateral midbrain affecting the pyramidal tract in the cerebral peduncle can cause pure motor stroke. Midbrain hematomas or infarcts that involve the sensory lemniscus have been reported as causes of pure sensory strokes. Bilateral, isolated small infarcts in the lateral midbrain involving the corticospinal tracts have been responsible for tetraplegia and mutism, leaving conscious patients with only gaze movements as a means to communicate.