Spinal high-velocity low amplitude manipulation in acute nonspecific low back pain: a double-blinded randomized controlled trial in comparison with diclofenac and placebo.
STUDY DESIGN: A randomized, double-blinded, placebo-controlled, parallel trial with 3 arms.
OBJECTIVE: To investigate in acute nonspecific low back pain (LBP) the effectiveness of spinal high-velocity low-amplitude (HVLA) manipulation compared with the nonsteroidal anti-inflammatory drug diclofenac and with placebo.
SUMMARY OF BACKGROUND DATA: LBP is an important economical factor in all industrialized countries. Few studies have evaluated the effectiveness of spinal manipulation in comparison to nonsteroidal anti-inflammatory drugs or placebo regarding satisfaction and function of the patient, off-work time, and rescue medication.
METHODS: A total of 101 patients with acute LBP (for <48 hr) were recruited from 5 outpatient practices, exclusion criteria were numerous and strict. The subjects were randomized to 3 groups:
(1) spinal manipulation and placebo-diclofenac;
(2) sham manipulation and diclofenac;
(3) sham manipulation and placebo-diclofenac. Outcomes registered by a second and blinded investigator included self-rated physical disability, function (SF-12), off-work time, and rescue medication between baseline and 12 weeks after randomization.
RESULTS: Thirty-seven subjects received spinal manipulation, 38 diclofenac, and 25 no active treatment. The placebo group with a high number of dropouts for unsustainable pain was closed praecox. Comparing the 2 active arms with the placebo group the intervention groups were significantly superior to the control group. Ninety subjects were analyzed in the collective intention to treat. Comparing the 2 intervention groups, the manipulation group was significantly better than the diclofenac group (Mann-Whitney test: P = 0.0134). No adverse effects or harm was registered.
CONCLUSION: In a subgroup of patients with acute nonspecific LBP, spinal manipulation was significantly better than nonsteroidal anti-inflammatory drug diclofenac and clinically superior to placebo.
Spine 2013 (Apr 1); 38 (7): 540–548
Some information obtained from www.chiro.org
The number of nonfatal injuries due to traumatic brain injury is estimated to be more than 2 million each year with an overall economic cost to society of about $25 billion per yeari. The incidence rate has been reported to be about 200 cases per 100,000 Americansii, however the true incidence and prevalence is difficult to determine because many such injuries, if sufficiently mild, are never seen by physicians. Motor vehicle trauma is the single most important agent in both fatal and mild brain injuries, causing from 60% to 67%iii. Many of these MVC-related injuries are the result of blunt head injury, most commonly due to contact of the head with some object, but without penetration of the skull.
High pressure gradients develop within the brain during rapid back and forth motion of the head during cervical acceleration/deceleration injury. At the time of injury, the brain is subjected to massive depolarization and tissues are damaged through transient shear forces that mechanically deform axons and microvessels. Various chemical changes throughout the brain begin to develop and areas of the brain that are vulnerable to injury lead to information processing difficulties, such as planning, anticipation and judgment. Injuries to these various parts of the brain also contribute to greater effects on a person’s social conditions, with some patients exhibiting impulsiveness, disinhibition and misinterpretation of others’ moods.
Most brain injuries are minor and the term mild traumatic brain injury is most useful. Within this subgroup of injuries, the spectrum ranges from concussion (without a loss of consciousness (LOC), but with some amnesia or confusion) to the classical concussion with brief LOC, amnesia, and mental changes that can be permanent. The post-concussion syndrome (PCS) can also develop from either. Post traumatic headaches are also very common residuals and may last anywhere from six months to several years and are an integral part of PCSiv,v.
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1. Goldstein M: Traumatic brain injury: a silent epidemic. Ann Neurol 27(3):327, 1990.
2. Elkind AH: Headache and head trauma. Clin J Pain 5:77-87, 1989.
3. Gennarelli TA: Biomechanics of head injury. Conference on the biomechanics of impact trauma. Assoication
for the Advancement of Automotive Medicine, Chicago Illinois, Novemeber 13-14, 1995.
4. Solomon S. Posttraumatic headache. Medical Clinics of North America. 2001:85:987.
5. Denker PG: The postconcussion syndrome: prognosis and evaluation of the organic factors. NY State J Med