A case of parkinson's disease with L-dopa-evoked catalepsy

Catalepsy is a generalized condition of diminished responsiveness shown by a trance-like state, posturing, or maintenance of physical positions for a prolonged period of time. It is an internal reaction to escape from stress and one of the characteristic symptoms of catatonia. Interactions among various neurotransmitters such as dopamine, serotonin, and γ-aminobutyric acid (GABA) are involved in the onset of catalepsy, but the mechanism has not yet been completely elucidated. An 87-year-old man with Parkinson's disease on l-dopa therapy showed catalepsy. Eight years after the onset, he developed episodes of akinetic mutism with catalepsy, which gradually became prolonged. He became almost unable to take oral medication, so was admitted to our department, where intravenous l-dopa injection therapy was started. At 20min after l-dopa injection, catalepsy was evoked. Suspecting that l-dopa was involved in catalepsy, we reduced the dose. With a reduction in l-dopa, the frequency of akinetic mutism with catalepsy decreased. In addition, single-photon emission computed tomography (SPECT) with three-dimensional stereotactic surface projection (3D-SSP) demonstrated decreased cerebral blood perfusion in the prefrontal cortex and increased perfusion in the motor cortex. Some reports have shown that stress can increase dopamine release in the medial prefrontal cortex, and excessive dopamine causes dopamine receptor down-regulation. In this case, besides chronic stress, l-dopa was a factor in causing excessive dopamine in the prefrontal cortex. Moreover, increased perfusion in the motor cortex is suspected of being associated with continuous movement. Some reports have shown that various modulations originate in the prefrontal cortex and affect the motor area, and that disturbance of such modulation is involved in the onset of catalepsy. In conclusion, we speculate that stress and l-dopa caused the down-regulation of dopamine receptors in the prefrontal cortex and subsequent dysfunction of this area. As a result, modulation originating in the prefrontal cortex and affecting the motor area did not function appropriately.