Which means the presence of one or more herniated discs on an MRI is not a cause for alarm. It probably has nothing to do with your back or neck pain and it is DEFINITELY NOT an indication that you need surgery.
NEXT: Part Two:
Examine the clinical proof that herniated discs do in fact heal, and that they actually shrink up and totally disappear if given half a chance.
Christensen et al (2004) Clinical reasoning in the diagnosis and management of spinal pain. In : Boyling & Jull (2004) Grieves Modern Manual Therapy, The Vertebral Column, Churchill Livingston, ch27
Cholewicki & Silfies (2004) Clinical biomechanics of the lumbar spine. In : Boyling & Jull (2004) Grieves Modern Manual Therapy, The Vertebral Column, Churchill Livingston, ch7
Elvey & O'Sullivan (2004) A contemporary approach to manual therapy. In Boyling & Jull (2004) Grieves Modern Manual Therapy, The Vertebral Column, Churchill Livingston. Ch33
Bed rest can have deleterious effects on muscle function. Researchers have recently described a direct muscle afferent-pituitary axis whereby bio-assayable growth hormone (BGH) regulation is tightly coupled with muscle function rather than muscle fibre type. Unlike, exercise-induced increases in plasma immuno-assayable growth hormone (IGH), whose concentration peak occurs during or after longer duration aerobic or resistance exercise involving larger muscle mass, BGH is released after a brief series of isometric contraction (McCall et al 2001). The BGH response is absent , despite the maintenance of normal torque output and pre-exercise plasma BGH and IGH, when leg musculature is chronically unloaded, as after 2 days bed rest or space flight. They hypothesised that this was due to chronic alterations in proprioceptive inputs (McCall et al 2001). These responses normalised within approximately 8 days of ambulatory recovery. Furthermore, they suggested that BGH stimulates bone growth and that low threshold fibre activation through electrical stimulation, exercise and /or vibration may ameliorate the effects of chronic unloading (McCall et al 2001). Moreover, this is direct evidence for the existence of a muscle-pituitary functional pathway in the absence of inflammation. It also highlights the need not to underestimate the effects of bed rest when recommencing a training regime after a period of illness or trauma. Furthermore, it would appear that low threshold isometric contractions, as occur during the application of muscle energy techniques, may stimulate this growth hormone.
The dense C.T fibroblasts don't respond to stretch due to the stiff matrix preventing the fibroblasts from receiving any strain. Scarring due to injury causes an increase in dense C.T which can be pevented by 10minutes, 2 times per day for 1 week in a suspended tail animal model. The combination of reduced movement and inflammation is a recipe for fibrosis. R-T US can be used as feedback during dry needling to observe C.T movement. In people suffering low back pain the fascial layers are less fluid and less differentiated. Additionally, people with LBP have hicker perivascular C.T. Involuntary muscle spasms may decrease the relative C.T motion during passive movement. Conversely, increased C.T thickness, stiffness and/or viscosity may affect the passive stiffness and range of movement of adjacent muscles.
At the APA conference in Sydney during October 2009, Dr Helene Longevin presented her research into the effects of stretching subcutaneous tissue. Superficial and deep fascia are composed of loose and dense connective tissue layers. The loose layers allow dense layers to glide past one another. This tissue contains abundant fibroblasts, immune cells and neurovascular bundles. A 20% static stretch of loose connective tissue for 30minutes significantly increases the size of fibroblasts in vivo and in vitro. Although this mechanism remains unclear it is hypothesised to be due to microtubule reorganisation (Beta-tubulin). Inhibition of growth kinase and Roc prevents the cells from spreading out. Actine polymerisation occurs at the leading edge. Fibro-attraction occurs whereby fibroblasts push forward at it's front edge, whilst retracting the rear (through Rho). Both Rac and Rho are activated simultaneously. The fibroblasts microtubule assembly contributes to connective tissue (C.T) relaxation, which means that tense in connective tissue is actively regulated. Viscoelastic response of loose connective tissue is influenced by specific cytoskeletal inhibitors. Rac increases the equilibrium force. Active C.T tensioin regulation may occur normally in response to sustained chnages in tissue length (e.g. hift in body position). This role may be to prevent sustained mechanical stimulation of other cells within the C.T (immune cells, nerve fibres, blood vessels).
Intrinsic tension within C.T will have profound effects in the cells within it such as blood vessel precursors stimulating angiogenesis. Similarly, immune cells may be affected by this tension. High amplitude or repetitive tissue stretch may cause injury but can also increase C.T strength. Low amplitude stretch within or slightly beyond the usual ROM may help maintain appropriate mibility and dynamic tissue response. Hence this may represent strong eveidence for STM, dry needling, joint mobilisations, muscle energy technqiues, strain-counterstrain techniques and training with Whole Body Vibration.
Titan molecules span the gap between the ends of the thick filaments and Z-bands. At the 2007 MPA conference in Cairns, Rob Herbert, provided the AJP oration whereby he explained the significance of Titan as a major determinant of extensibility in muscle fibres. Additionally, he stated that Titan is differentially expressed in human skeletal muscle as short stiff fibres and long compliant fibres
However, a number of sites in the myofibrillar complex such as reduce binding sensitivity and capacity of Troponin C for calcium, altered troponin-tropomysosin interaction to impaired binding and force generation by actin and myosin have been implicated in impaired force generation (Green 1990). Indeed, in the absence of any association between relaxation rates and Calcium kinetics raises support for the notion of a rate-limiting process controlling the relaxation of fatigued muscles being located in the contractile proteins (Hill et al 2001). During fatigue the relaxation times can be prolonged as much as 50% (Bigland-Ritchie et al 1986) thus resulting in increased force generation during submaximal stimulation due to tetanic fusion despite a substantial fall in the maximum tetanic force (Bigland-Ritchie et al 1986).