RESUMEN
BACKGROUND: Costochondritis is commonly encountered in primary care, but is not routinely referred to PT. Costochondritis can last from several weeks to several months, limiting the patient's ability to perform tasks at work and home. PURPOSE: Identify common impairments and examine the effects of treatment in subjects with costochondritis. STUDY DESIGN: Retrospective case series. CASE DESCRIPTION: Eight subjects were referred to physical therapy for costochondritis (mean duration of condition 6.3 ± 1.3 months) and reported that their condition restricted their ability to participate in occupational and fitness activities. The numerical pain rating scale (NPRS) and patient-specific functional scale (PSFS) were administered at the initial evaluation and at discharge. The Global Rating of Change (GROC) scale was only administered at discharge. All subjects received treatment directed at the cervicothoracic spine and ribcage and consisting of manual therapy and exercise. OUTCOMES: Subjects were seen 4.8 ± 0.9 (mean±standard deviation) times. All subjects showed clinically meaningful changes at discharge. The mean NPRS decreased by 5.1 ± 1.7 points; the mean PSFS increased by 5.3 ± 1.4 points; and the mean GROC was 5.9 ± 1.1 points. All subjects were able to return to participation in previous activities without restrictions at discharge. DISCUSSION - CONCLUSION: The results of this case series suggests that PT utilizing an impairment based examination and treatment approach including manual therapy and therapeutic exercise may facilitate the resolution of costochondritis. LEVEL OF EVIDENCE: Level IV.
RESUMEN
Peripheral sensory diabetic neuropathy is characterized by morphological, electrophysiological and neurochemical changes to a subpopulation of primary afferent neurons. Here, we utilized a transgenic mouse model of diabetes (OVE26) and age-matched controls to histologically examine the effect of chronic hyperglycemia on the activity or abundance of the enzymes acid phosphatase, cytochrome oxidase and NADPH-diaphorase in primary sensory neuron perikarya and the dorsal horn of the spinal cord. Quantitative densitometric characterization of enzyme reaction product revealed significant differences between diabetic, compared to control, animals for all three enzymes. Levels of acid phosphatase reaction product were found to be significantly reduced in both small diameter primary sensory somata and the dorsal horn. Cytochrome oxidase activity was found to be significantly lower in small primary sensory somata while NADPH-diaphorase labeling was found to be significantly higher in small primary sensory somata and significantly lower in the dorsal horn. In addition to these observed biochemical changes, ratiometric analysis of the number of small versus large diameter primary sensory perikarya in diabetic and control animals demonstrated a quantifiable decrease in the number of small diameter cells in the spinal ganglia of diabetic mice. These results suggest that the OVE26 model of diabetes mellitus produces an identifiable disturbance in specific metabolic pathways of select cells in the sensory nervous system and that this dysfunction may reflect the progression of a demonstrated cell loss.
