Due to the very ambiguities and difficulties cited by the correspondents, we elected to group all our patients with primary autonomic failure together, hoping thereby to avoid the introduction of unnecessary bias, Presumably, we all hope to determine whether these syndromes represent a spectrum of abnormalities based on common pathogenetic and etiological mechanisms, or whether, alternatively, they are composed of distinct entities. Premature subclassification can only obscure the answer to this critical question. Since our studies were directly concerned with the role of transsynaptic dysfunction in disease pathogenesis, it was particularly important not to assign o u r cases prematurely to Jifferent categories. In tact, as reported 141, no signiticant transsynaptic dysfunction was observed in any of the patients in the autonomic failure group. Subclassification of patients within this group does not alter that conclusion. We thank Drs Rajput and Rozdilsky for their laudatory comments and regret that space restrictions prevented us from citing their article. We included only those reports immediately relevant to o u r studies, since ours was not, after all, a review article. Many of Dr Oppenheimer’s comments arise from speculations, some of which are based on inadequate or misinterpreted data [2]. Drs Bannister and Oppenheimer attempted to estimate numbers of neurons in the spinal intermediolaterd column (ILC) in patients dying with autonomic failure [2]. Unfortunately, the apparent methods employed were inadequate, containing serious errors that resulted in virtually uninterpretable data [2]. First, essential and standard morphometric techniques [ 1, 31 were not described as being employed, and the authors apparently did not correct raw data for the relationship between object (cell) diameter and section thickness. This is particularly important since larger objects appear o n multiple histological sections and since, without correction, data may be several-fold in error [ 1, 31. Such considerations are immediately relevant to any disease process that may alter neuron size. Unaccountably, the authors did not describe the methods they employed [2]. Second, Drs Bannister and Oppenheimer presented no statistical analysis of the data, rendering their contentions at best speculative [2]. Third, since the ILC contains a heterogeneous group of cells, nonpreganglionic cells may have been included in their samples. The foregoing oversights limit the value of their work. To avoid these difficulties, we based our conclusions on parallel biochemical, ultramicroscopic, and light microscopic observations. Normal activity of presynaptic choline acetyltransferase activity in sympathetic ganglia correlated very well with findings on light microscopic examination of spinal cord perikarya and was entirely consistent with ultrastructural abnormalities indicating primary adrenergic degeneration [4]. W e submit that such an interdisciplinary approach to the biology of human disease increases the probability of success in defining pathogenetic mechanisms.

2. Bannister R, Oppenheimer DR: Degenerative diseases o f the nervous system associated with autonomic failure. Brain 951457-474, 1972 3. Konigsmark BW: Methods for the counting of neurons, in Nanta WJH, Ebbeson SOE (eds): Contemporary Research Methods in Neuroanatomy. New York, Springer. 1970, pp 3 15-340 4 . Petito CK, Black IB: Ultrastructure and biochemistry of sympathetic ganglia in idiopathic orthostatic hyporension. Ann Nrurol 4:6-17, 1978

Unusual Phenomenon in Parkinson Disease James A. McCarthy, M D

I recently saw an interesting phenomenon which I would like to share. A 63-year-old man who has had Parkinson disease for eight years has been doing reasonably well taking Sinemet, 25/250, four times a day, and amantadine, 100 mg twice a day. The only major problem the patient has experienced is a marked “on-off’ phenomenon-at times he has been totally unable to initiate walking. About one month before this writing the patient noted one day that he was unable to move while standing in his home-he felt as if his feet were “glued” to the floor. At that moment, on the radio, a Sousa march started to play, and the patient found that he was suddenly able to walk. Since that time, the patient has repeated this phenomenon on numerous occasions. He is now considering carrying with him a small tape recorder with march music on a cassette. Accepted for publication Nov 30. 1978. Author’s address: Neurological Associates of Cape Cod. 119 Cedar St, Hyannis, MA 02601.

Developmental Reflexes and Cortical Atrophy Joseph J. Moylan, PhD, and Carlos A. Saldias, MD In our clinic we routinely assess all patients for the developmental reflexes of suck, snout, grasp, glabellar blink, and palmomental reflexes using the Paulson method [11. This letter concerns 3 3 patients so evaluated whose common feature was dementia of varying severity with no signs of focal or lateralited cortical dysfunction; no effort was From the Dororhea Dix Hospital, Raleigh. NC.

References

Accepted for publication Oct 3 1. 1978.

1 . Abercrombie M: Estimation of nuclear population from microtome sections. Anat Rec 94:239-247. 1946

Address reprint requests to Dr Moylan. Dorothea Dix Hospital, Raleigh, N C 2761 1 .

Notes and Lcttcrs

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