This conceptualization
suggests the existence of fatigue subtypes, each of which presumably
has distinct mechanisms. Studies are needed that better define
these subtypes and the fatigue syndromes with which they may
be linked, and clarify pathophysiology in relation to phenomenology.
This is fundamentally similar to pain research, in which phenomenology
has defined relevant subtypes (such as cramping visceral pain
caused by obstruction of a hollow viscus), which then become
targets for specific research approaches.
The likelihood of
fatigue subtypes gains credence from the diversity of mechanisms
that already have been proposed. Fatigue may be related to changes
in energy metabolism associated with increased requirement for
substrate (e.g. due to the metabolic activity caused by the
underlying disease, by infection or fever, or by tissue injury
such as surgery); decreased availability of substrate (e.g.
due to anemia, hypoxemia, or poor nutrition); or the abnormal
production of substances that impair metabolism or normal functioning
of muscles (e.g. cytokines or antibodies). Other proposed mechanisms
link fatigue to the pathophysiology of sleep disorders or major
depression. There is no definitive evidence in support of any
of these mechanisms and further research, linked to qualitative
differences in the fatigue experience, is needed.
The multidimensionality
of fatigue underscores the challenge of assessment in a research
setting. Although fatigue can be assessed unidimensionally (e.g.
by an intensity measurement alone), or as a dichotomous variable
(present or absent, according to some criterion definition),
the simplicity of these approaches must be balanced by the missed
opportunity to capture information about the other dimensions,
including qualitative differences that could potentially distinguish
clinically meaningful fatigue subtypes. The use of more sophisticated
assessment
methodologies can yield far more information.