Secondary parkinsonism after subdural hematomas: Presynaptic dopaminergic deficit as possible mechanism?

Parkinsonism is a rare consequence of chronic subdural hematomas (SDH). Since 1963 twenty cases have been published in the literature. Typical is the subacute development within several weeks and the marked symptom improvement after hematoma evacuation. The pathomechanism of parkinsonism after SDH as well as the question why it is such a rare consequence of such a common disorder is still subject to discussion. A compression of the mesencephalon and the basal ganglia as well as an affection of frontal premotoric areas and fronto-pallidal connections is discussed. We present a case of an 84-year-old male who developed marked parkinsonism within three months. Predominant was a gait disorder with small steps, abrogated arm movements while walking, bound posture and severe postural instability. There was no brain trauma in his medical history. Cerebral computed tomography (CCT) showed marked bilateral chronic SDH. The symptoms resolved rapidly and completely within weeks after burr hole trepanation and hematoma drainage. Preoperative 99TC ECD SPECT showed a marked bifrontal and biputaminal hypoperfusion which improved after neurosurgical intervention. Interestingly, a postoperatively performed 123I FP-CIT SPECT showed a significant reduction of presynaptic dopaminergic connections. 2.5 years after this episode, the patient developed a dopa-responsive parkinsonism without recurrence of SDH. We hypothesize that SDH leads in only in a small number of patients to parkinsonism, because a, so far compensated, presynaptic dopaminergic deficit, that decompensates by compression induced hypoperfusion of the basal ganglia, may be required for symptom development. This theory could also explain single reports about dopa-responsiveness of SDH induced parkinsonism.