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Pathogenesis of Fatigue
The exact mechanism that causes or promotes fatigue in patients with cancer is
not known. It is likely that many different mechanisms play a role.[1,2]
Various models have been proposed for the study of fatigue. Prolonged stress
that produces a stress response may be used as a model for fatigue.[3] People
with cancer frequently suffer from extreme stress over a long period of time,
causing them to expend energy and experience a high level of fatigue. In
contrast, one study demonstrated that energy requirements vary in people with
cancer.[4] This suggests that factors other than energy requirements contribute to fatigue.
A neurophysiologic model has been proposed to study fatigue. This model has
both central and peripheral components. The central component consists of the
psyche/brain and spinal cord. The peripheral system consists of peripheral
nerves, muscle sarcolemma, transverse tubular system, calcium release,
actin/myosin interaction, cross-bridge tension and heat, and force/power
output. Impairment of the central component causes lack of motivation,
impaired spinal cord transmission, and exhaustion or malfunction of brain cells
in the hypothalamic region. Damage to the peripheral component can cause
impaired peripheral nerve function in transmission at the neuromuscular
junction, thereby affecting fiber activation. Both types of damage may play a
role in chronic fatigue. The central mechanism may be the key to explaining
the extreme fatigue of biotherapy-treated patients.[5] It remains to be
established whether potentially neurotoxic chemotherapeutic regimens cause
fatigue through this mechanism. Additionally, many individuals with cancer may
be concurrently receiving analgesics, hypnotics, antidepressants, antiemetics,
or anticonvulsants. Because many of these drugs exert their effect on the
central nervous system, they can significantly compound the problem of fatigue.
Another perspective in the study of fatigue focuses on the reduction in
skeletal muscle protein stores that may result from endogenous tumor necrosis
factor (TNF) or from TNF administered as antineoplastic therapy. This muscle
wasting would require individuals to exert an unusually high amount of energy
to generate adequate contractile force during exercise performance or during
extended periods of sitting or standing.[6]
Last, a fatigue framework has been proposed that encompasses biochemical,
physiologic, and behavioral factors that cause manifestations of fatigue.
These factors are modified by the perception of fatigue. Thirteen patterns are
thought to influence fatigue:[7]
- Accumulation of metabolites.
- Changes in energy
and energy substrate.
- Activity/rest.
- Sleep/wake.
- Disease/treatment.
- Symptoms.
- Psychologic.
- Oxygenation.
- Changes in regulation/transmission.
- Environmental.
- Life events.
- Social.
- Unique circadian rhythm.
References
-
Miaskowski C, Portenoy RK: Update on the assessment and management of cancer-related fatigue. Principles and Practice of Supportive Oncology Updates 1 (2): 1-10, 1998.
-
Morrow GR, Andrews PL, Hickok JT, et al.: Fatigue associated with cancer and its treatment. Support Care Cancer 10 (5): 389-98, 2002.
[PUBMED Abstract]
-
Aistars J: Fatigue in the cancer patient: a conceptual approach to a clinical problem. Oncol Nurs Forum 14 (6): 25-30, 1987 Nov-Dec.
[PUBMED Abstract]
-
Kaempfer SH, Lindsey AM: Energy expenditure in cancer: a review. Cancer Nurs 9 (4): 194-199, 1986.
-
Funk SG, Tornquist EM, Champagne MT, et al., eds.: Key Aspects of Comfort: Management of Pain, Fatigue and Nausea. New York: Springer Publishing, 1989.
-
St Pierre BA, Kasper CE, Lindsey AM: Fatigue mechanisms in patients with cancer: effects of tumor necrosis factor and exercise on skeletal muscle. Oncol Nurs Forum 19 (3): 419-25, 1992.
[PUBMED Abstract]
-
Piper BF, Lindsey AM, Dodd MJ: Fatigue mechanisms in cancer patients: developing nursing theory. Oncol Nurs Forum 14 (6): 17-23, 1987 Nov-Dec.
[PUBMED Abstract]
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