The Taut Band and Other Mysteries of the Trigger Point: An Examination of the Mechanisms Relevant to the Development and Maintenance of the Trigger Point

Simons' integrated hypothesis proposed a model of trigger point (TrP) activation to explain known TrP phenomena, particularly endplate noise. We propose an expansion of this hypothesis to account for new experimental data and established muscle pathophysiology.

Monopolar needle electromyogram (EMG) was recorded simultaneously from trapezius myofascial trigger points (TrPs) and adjacent nontender fibers (non-TrPs) of the same muscle in normal subjects and in two patient groups, tension headache and fibromyalgia. Sustained spontaneous EMG activity was found in the 1-2 mm nidus of all TrPs, and was absent in non-TrPs. Mean EMG amplitude in the patient groups was significantly greater than in normals. The authors hypothesize that TrPs are caused by sympathetically activated intrafusal contractions.

Over recent years, it has become clear that mitochondria play a central role in many key aspects of animal physiology and pathophysiology. Their central and ubiquitous task is clearly the production of ATP. Nevertheless, they also play subtle roles in glucose homeostasis, acting as the sensor for substrate supply in the transduction pathway that promotes insulin secretion by the pancreatic -cell and that modulates the excitability of the hypothalamic glucose-sensitive neurons involved in appetite control. Mitochondria may also act as sensors of availability of oxygen, the other major mitochondrial substrate, in the regulation of respiration. Mitochondria take up calcium, and the high opacity mitochondrial calcium uptake pathway provides a mechanism that couples energy demand to increased ATP production through the calcium-dependent upregulation of mitochondrial enzyme activity. Mitochondrial calcium accumulation may also have a substantial impact on the spatiotemporal dynamics of cellular calcium signals, with subtle differences of detail in different cell types. Recent work has also revealed the centrality of mitochondrial dysfunction as an irreversible step in the pathway to both necrotic and apoptotic cell death. This review looks at recent developments in these rapidly evolving areas of cell physiology in an attempt to draw together disparate areas of research into a common theme.