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Paul J. Schwartz, MD
National Institute of Mental Health Clinical Psychobiology Branch Room 45239 9000 Rockville Pike Bethesda, MD 20892

Arch Gen Psychiatry. 1991;48(3):279-280.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.—

Drs Kupfer and Ehlers¹ propose a new theoretical framework for understanding the phenomenon of shortened rapid eye movement (REM) latency in depression. In their schema, REM sleep occurs earlier in the type 1 mechanism secondary to a primary weakening in the non-REM (especially slow-wave sleep) processes and in the type 2 mechanism "because of so-called increased REM pressure." "The type 2 REM latency mechanism is envisioned to be more closely related to changes in arousal and REM sleep physiology itself."

Their synthesis adds appreciably to our understanding of REM latency mechanisms in depression. However, the proposed type 2 mechanism confounds key concepts and requires considerable clarification and expansion. Specifically, they have mistakenly related increased REM pressure to decreased REM latency and have neglected the contributions of the desynchronization data and phase theories of mood disorders. In doing so, important theoretical constructs having major pathogenetic significance . . . [Full Text PDF of this Article]

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