Spasticity as the First Manifestation of Ischaemic Lesions Involving the Cingulum

Background and Purpose. Spasticity is a positive sign of upper motor neuron syndrome that usually develops weeks after a stroke. The mechanisms that lead to its appearance are not completely understood, namely, the cortical regions whose lesion may induce spasticity. Summary of Cases. We report two patients with an ischaemic stroke entailing the anterior cingulate gyrus (pericallosal artery territory), who presented with acute hemiplegia and spasticity since symptom onset. Spasticity resolved within days after onset. Conclusions. The acute destruction of the anterior cingulate region, interrupting inhibitory projections towards lower motor centres, probably explains the acute onset of spasticity that occurred in these two patients. Further studies addressing the role of this region in acute and chronic disturbances of muscular tone are necessary. 1. Background and Purpose Ischaemic damage to the corticospinal tract may induce both negative (muscle weakness, impaired coordination, motor planning, and fatigue) and positive signs (rigidity, spasticity, exaggerated deep tendon reflexes, Babinski signs, and clonus) [1]. Spasticity is only one of those positive features and it was defined by Lance as a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes [2]. Usually, spasticity is expected to develop only weeks after an acute ischaemic lesion. The mechanisms that mediate its appearance are not completely understood. It is known that some descending motor pathways (from higher centres and brainstem) indirectly influence the excitability of anterior horn cells. In particular, the dorsal reticulospinal tract, arising in ventromedial reticular formation, is the main inhibitory tract for spinal reflex activity [1, 3]. Cortical motor regions facilitate this area, augmenting the inhibitory drive down to the spinal cord. However, the cortical areas involved in this feature are mostly undiscovered [3]. Some patients were described, in whom spasticity appeared as an acute sign of stroke, namely after subcortical basal ganglia injury [4], but not in cortical lesions. Moreover, some case series whose aim was to describe the clinical and radiological patterns of the anterior cerebral artery infarction [5–7] point several hypertonia phenomena. In Lausanne stroke registry [6], the appearance of spasticity within less than 10 days in those with motor deficit is referred and Alonso et al. [5] and Kumral et al. [7] articles indicate that a spastic muscle tone emerged rapidly in most patients, but not as early as being one of the first