This review summarizes current information regarding the changes in structure or function that occur in skeletal muscle secondary to spasticity. Most published studies have reported an increase in fiber size variability in spastic muscle. There is no general agreement regarding any shift in fiber type distribution secondary to spasticity. Mechanical studies in whole limbs as well as in isolated single cells support the notion of an intrinsic change in the passive mechanical properties of muscle after spasticity in addition to the more widely reported neural changes that occur. Evidence is presented for changes within both the muscle cell and extracellular matrix that contribute to the overall changes in the tissue. Taken together, the literature supports the notion that, although spasticity is multifactorial and neural in origin, significant structural alterations in muscle also occur. An understanding of the specific changes that occur in the muscle and extracellular matrix may facilitate the development of new conservative or surgical therapies for this problem.

Spasticity, a neurological problem secondary to an upper motor neuron lesion, has a significant effect on skeletal muscle. The upper motor neuron lesions may be secondary to a cerebral vascular accident, head injury, spinal cord injury, or degenerative diseases such as multiple sclerosis, or perinatal brain injuries such as cerebral palsy. Functional ability in these patients can be severely compromised but the basic mechanisms underlying these deficits are not clearly understood. In this review we evaluate the current evidence in the literature that suggests that skeletal muscle tissue itself is altered in spastic conditions. Experimental studies were evaluated that included a variety of methods encompassing joint mechanics, tissue mechanics, and muscle morphology. Taken together, the literature strongly supports the assertion that 'spastic muscles' are altered in a way that is unique among muscle plasticity models and inconsistent with simple transformation due to chronic stimulation or disuse. Further studies are required to detail the intra- and extracellular modifications of skeletal muscle that occur secondary to spasticity so that novel therapeutic treatments can be developed for this impairment.

Purpose A recent study reported a higher incidence of pre-operative ulnar nerve symptoms in patients with flexion-type supracondylar fractures than in those with the more common extension supracondylar fractures and a greater need for open reduction (Kocher in POSNA paper #49 2006). We have encountered a specific pattern of flexion supracondylar fractures that often require open reduction with internal fixation (ORIF) due to entrapment of the ulnar nerve within the fracture. Methods Medical records and X-rays from 1997 to 2005 at our children's hospital were examined to identify flexion supracondylar fractures that required open reduction. The operative reports were reviewed to identify cases that had the ulnar nerve blocking the reduction. Results During the 8 years examined, 1,650 supracondylar fractures had been treated by means of closed reduction and percutaneous pinning. Of these, only 1.8% or 30 cases could not be reduced closed and required open reduction internal fixation, excluding 11 open fractures. Of the 30 fractures requiring open reduction internal fixation, 24 were of the extension type needing ORIF because of interposed periosteum/muscle. The other 6 patients had flexion-type supracondylar fractures that failed closed reduction. All had a persistent medial gap at the fracture site. All 6 fractures had interposed periosteum or muscle, while in 3 cases the ulnar nerve was also entrapped within the fracture site (Figs. 1, 2) Conclusion Flexion-type supracondylar fractures remain a relatively uncommon variant (2-3%) of supracondylar fractures. Recent reports have noted that open treatment of these fractures is required more frequently than for extension fractures. In our series, 20% of the open cases were flexion-type fractures and in half of these the ulnar nerve was found to be entrapped in the fracture, preventing reduction.

Spasticity, a neurological problem secondary to an upper motor neuron lesion, has a significant effect on skeletal muscle. The upper motor neuron lesions may be secondary to a cerebral vascular accident, head injury, spinal cord injury, or degenerative diseases such as multiple sclerosis, or perinatal brain injuries such as cerebral palsy. Functional ability in these patients can be severely compromised but the basic mechanisms underlying these deficits are not clearly understood. In this review we evaluate the current evidence in the literature that suggests that skeletal muscle tissue itself is altered in spastic conditions. Experimental studies were evaluated that included a variety of methods encompassing joint mechanics, tissue mechanics, and muscle morphology. Taken together, the literature strongly supports the assertion that 'spastic muscles’are altered in a way that is unique among muscle plasticity models and inconsistent with simple transformation due to chronic stimulation or disuse. Further studies are required to detail the intra‐ and extracellular modifications of skeletal muscle that occur secondary to spasticity so that novel therapeutic treatments can be developed for this impairment.

BACKGROUND The purpose of the study was to investigate whether a safety checklist could be used consistently in an academic center, and, whether its presence correlates with a decreased rate of complications, and therefore, improved overall patient safety. METHODS Data from 3 years before and after the implementation of the checklist were compared. Pre-checklist data from August 2008 through August of 2011, including all operative supracondylar humerus fractures treated at our institution, were retrospectively reviewed. Post-checklist data, from August 2011 to August 2014 were prospectively collected. Patients’ charts and their imaging were all reviewed for: fracture type, nerve injury, placement of a medial pin, infection, loss of alignment, loss of fixation, and return to the operating room. Patients who were within the checklist group were reviewed for checklist compliance and concordance of resident and attending-attested checklists. RESULTS 931 operative supracondylar humerus fractures were reviewed - 394 in the pre-checklist group and 537 in the post-checklist group. There was no significant difference in fracture type between the pre- and post-checklist groups. No significant differences were found between pre- and post-checklist patients in regards to loss of fixation, loss of alignment, infection, or nerve injury. In the post-checklist group, the number of medial pins placed was significantly less than in the pre-checklist group [p = 0.0001], but this was not found to have clinical significance. In the pre-checklist group, 11 patients returned to the operating room for a second procedure whereas 4 in the post-checklist group had a return to the operating room. This finding was significant [p = 0.015], but the returns to the operating room were not related to checklist parameters. The checklist compliance of the attending physicians was 85.85% and the residents were compliant 83.11% of the time. There were documented discrepancies between resident and attending checklists in 7.38% of all total checklists. CONCLUSIONS Our patient safety checklists are not necessarily affecting patient care in a clinically significant manner. It is important that we validate and refine these specialty-specific checklists before becoming reliant on them. LEVEL OF EVIDENCE III