The Stiff-Person Syndrome: An Autoimmune Disorder Affecting Neurotransmission of γ-Aminobutyric Acid

Figure 1. Impairment of intracortical inhibitory neurons causes corticospinal neurons in the motor cortex to discharge heavily to the α motor neurons. The increased excitation to the spinal cord causes excessive firing by α motoneurons ( ). The loss of spinal inhibitory circuits, represented by two inhibitory motor neurons (illustrated with solid dots in center), enhances the motoneuron hyperexcitability and may increase discharges from γ motor neurons to the muscle spindles ( ). Excessive responses to afferent impulses from muscle spindles ( ) and skin afferents ( ), caused by impaired inhibitory interneurons, may explain the increased stiffness after sudden tactile stimuli.
Figure 1. Impairment of intracortical inhibitory neurons causes corticospinal neurons in the motor cortex to discharge heavily to the α motor neurons. The increased excitation to the spinal cord causes excessive firing by α motoneurons ( ). The loss of spinal inhibitory circuits, represented by two inhibitory motor neurons (illustrated with solid dots in center), enhances the motoneuron hyperexcitability and may increase discharges from γ motor neurons to the muscle spindles ( ). Excessive responses to afferent impulses from muscle spindles ( ) and skin afferents ( ), caused by impaired inhibitory interneurons, may explain the increased stiffness after sudden tactile stimuli. Proposed mechanism of development of stiffness in the stiff-person syndrome.abcd

This Article

  1. Ann Intern Med October 5, 1999 vol. 131 no. 7 522-530
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