• Tremor;
  • Movement disorders;
  • Cerebellum;
  • Inferior olive;
  • Red nucleus


This article is devoted to animal models of tremors that emerge from lesions in the Guillain-Mollaret triangle. Cerebellar intention tremor is caused by lesions in the brachium conjunctivum or in the interpositus nucleus, possibly in combination with damage to the dentate nucleus. Impaired feedforward motor control delays the braking of rapid movements, resulting in target overshoot and subsequent oscillation. Transcortical and transcerebellar sensorimotor loops undergo oscillation at a frequency that depends on the mechanical properties of the limb and the length of the sensorimotor loop (mechanical reflex oscillation). The crescendo quality of intention tremor may be a result of amplification of tremor in reverberating brain stem-cerebellar or thalamocortical loops. So-called rubral or midbrain tremor is caused by a combination of damage to the brachium conjunctivum and nigrostriatal pathways in the vicinity of the red nucleus. Secondary compensatory changes in the motor system are probably involved because midbrain tremor in people usually begins weeks or months after a midbrain stroke or trauma. Harmaline causes enhanced neuronal synchrony and rhythmicity in the inferior olive; this animal model, although as yet unproven, is the most popular one for essential tremor (ET). Additional studies in laboratory animals are needed to define the seemingly universal involvement of the cerebellum and ventrolateral thalamus (ventralis intermedius [Vim]) in virtually all human tremor disorders.