Possible Diagnosis
Question: I am a psychotherapist involved with the geriatric population. One fellow who has been referred three times in the past year for possible depression has a unique but recurrent set of symptoms. He is 74 y.o with Parkinson’s of long standing nature, he has a history of NPH which was not intervened upon but is thought not to be needing surgical intervention. Each time preceding my referral (and from all prior medical records I could find) he has a shift in his sedimentation rate, with a higher rate being accompanied by more severe behavioral sequel. The symptoms include: more pronounced ataxia of gait, a loss of interest in food primarily to increased sense of nausea, increased episodes of incontinence, occasionally headache, and more pronounced confusion. From his history these episodes have been characterized as an atypical anorexia which spontaneously resolves. I believe there is a causal relationship between an inflammatory process and the behaviors observed. As such we have not treated him for depression but secondary frustration due to his change in physical status. It would seem that his behaviors mimic those of increasing pressure or those seen in some NPH individuals. Would an inflammatory process be causal in this symptomolgy? He was given a diagnosis of temporal (giant cell) arteritis and has been receiving prednisone 10 mg since 5/97, however, his symptoms have again reoccurred with a sed rate at 80 (in 4/97 prior to prednisone it was 88, symptoms quite severe then). The attending isn't quite convinced that this is a syndrome but I'd hate to begin aggressive anti-depressant treatment with such clear metabolic correlation, over time, to the behavior. Could an arteritis affect the ability of the brain to maintain normal pressure? Your thoughts would be helpful and I know that it would not be a diagnosis or prescription for care.

Answer: I doubt the NPH theory; but, there is clear cerebritis seen in many inflammatory arteritis. Temporal arteritis clearly affects the mentation of some patients. I would correlate his sed rate over time with some measurable part of the mini mental status exam. However, if his sed rate is 80 he is not receiving adequate prednisone dosing. Checking an antinuclear cytoplasmic antibody( P-ANCA and C-ANCA) might be helpful. Also, this cerebral inflammation is more common in lupus than TA-has he had an ANA to test for lupus? CNS involvement is difficult to diagnose;but, fairly common(10% or so) of many of the vasculitis syndromes.
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