Several case reports have ascertained the coexistence of idiopathic Parkinson’s disease (IPD) and schizophrenia1–4 predominantly in post-mortem analysis, while during lifetime motoric symptoms were interpreted as drug-induced parkinsonism.1,2,4 An in vivo distinction though is desirable, since it allows appropriate treatment. This case confirms IPD in a patient with chronic schizophrenia in vivo by the use of two independent methods.
Imaging with specific striatal DA transporter (DAT)- ligands for single photon emission computed tomography (SPECT) provides a marker for presynaptic nigral neurodegeneration. Reduced striatal DAT is typical for IPD and allows differentiation from drug-induced parkinsonism.5 Transcranial neurosonography (TCS) demonstrates characteristic changes of echogenicity in basal ganglia and brainstem nuclei. More than 90% of IPD patients present with increased nigral echogenicity indicating nigral neurodegeneration.6
The patient presented here was diagnosed as having paranoid schizophrenia, according to the 4th edition of the Diagnostic and Statistical Manual, in 1982 when he was 22. Symptoms included auditory hallucinations, suspicions about other people and feelings of his thoughts being influenced. During the first year of the disease, he was intermittently treated with haloperidol, promethazine, and chlorpromazine. Later, medication was changed to clozapine. He was admitted to the neurological unit of the Charité, University Medicine Berlin, Germany, in 2003 for evaluation of slowly progressing levodopa-responsive hypokinetic-rigid symptoms, which he developed at the age of 35 under stable neuroleptic medication: clozapine (250 mg/d), biperidine (2 mg/d), carbidopa/levodopa (900 mg/d), amantadine (300 mg/d), and lorazepam (1.5 mg/d). He had masked facies, stiff posture, oromandibular dyskinesia, marked symmetric cogwheel rigidity of arms and legs and moderate bradykinesia. Unified Parkinson disease Rating Scale motor score with DAergic medication was 24. He continued to have auditory hallucinations with retained insight. SPECT using DAT tracer 123I-FP-CIT demonstrated a significant bilateral decrease of striatal DAT (binding ratios striatum/frontal lobe: 2.1 [right], 2.3 [left], normal >2.6).5 TCS demonstrated increased nigral echogenicities of 26 mm2 (right) and 20 mm2 (left; normal <19 mm2).6
The presented case demonstrates two in vivo methods confirming IPD in a patient with chronic paranoid schizophrenia by quantifying (i) reduced striatal DAergic innervation and (ii) increased nigral signal extension. The findings support the hypothesis that the nigostriatal and mesolimbic DAergic pathways largely function independently, suggesting that patients with schizophrenia are not necessarily less likely than other patients to develop IPD as they age.