Spasticity: its physiology and management. Part I. Neurophysiology of spasticity: classical concepts.
Spasticity, seen so frequently in clinical situations, presents motor signs resembling those produced experimentally by transecting the brain stem of a cat at the intercollicular level. This paper reviews experimental results which elucidate the roles of different brain regions in the genesis of classical decerebrate rigidity and demonstrate the function of the gamma motor system in the maintenance of the rigidity. Interruption of the gamma-spindle loop of a muscle (i.e. interrupting the monosynaptic reflex arc subserving the stretch reflexes) abolishes rigidity in that muscle. This reflex-mediated gamma support of decrebrate rigidity is also a prominent feature of clinical spasticity, making classical decerebrate rigidity a useful model for studying the neural mechanisms underlying spasticity. Not all rididities, however, are gamma dependent. Those rigidities surviving dorsal root rhizotomy are called alpha rigidity. Alpha rigidity results when a brain lesion disrupts descending systems which normally exert a net inhibitory effect upon alpha motoneurons.
D000818:Animals; D001921:Brain / Q000503:physiopathology*; D002415:Cats; D003655:Decerebrate State; D005116:Extrapyramidal Tracts / Q000503:physiopathology; D006801:Humans; D009046:Motor Neurons / Q000502:physiology; D009127:Muscle Rigidity / Q000503:physiopathology; D009128:Muscle Spasticity / Q000503:physiopathology*; D009470:Muscle Spindles / Q000503:physiopathology; D011149:Pons / Q000503:physiopathology; D011712:Pyramidal Tracts / Q000503:physiopathology; D013116:Spinal Cord / Q000503:physiopathology