Recovery of knee range of motion after total knee arthroplasty in the first postoperative weeks: poor recovery can be detected early.

PURPOSE: The aim of this study was to analyze in detail how knee flexion and extension progress in the first 8 weeks after primary total knee arthroplasty (TKA). The secondary goal was to compare knee range of motion (ROM) recovery patterns between patients with normal and delayed ROM recovery 8 weeks after TKA. METHODS: This prospective clinical trial included all patients who underwent a primary unilateral TKA between February and December 2016 with weekly ROM data documented by the treating outpatient physical therapists (n = 137). Goniometry was used to measure knee ROM preoperatively, postoperatively on day 1 and weekly until follow-up at the orthopedic clinic 8 weeks after surgery. ROM recovery patterns were compared between patients with sufficient (≥ 90°) or insufficient (< 90°) knee flexion 8 weeks after TKA. RESULTS: Knee flexion recovered from a median of 80° in the first postoperative week to 110° 8 weeks after surgery and knee extension from a mean of - 10.7° to - 3.2°. Recovery was nonlinear, with greatest improvements in the first 4 weeks for knee flexion. In contrast to patients with sufficient knee flexion 8 weeks postoperatively, the insufficient group (n = 8, 5.8%) had poor knee flexion on the first postoperative day and from week 4 to week 8 almost no improvement or even worsening of knee flexion. CONCLUSIONS: Both knee flexion and extension recover in a nonlinear manner after TKA surgery. Poor postoperative knee function can be detected early, using ROM data from the first postoperative day up to the fourth week.

Structural involvement of the glutamatergic presynaptic boutons in a transgenic mouse model expressing early onset amyloid pathology.

While the cholinergic depletion in Alzheimer's disease (AD) has been known for some time, a definitive involvement of other neurotransmitter systems has been somewhat more elusive. Our study demonstrates a clear involvement of both glutamatergic and, to a lesser extent, GABAergic neurons in an early onset transgenic mouse model of AD-like amyloid pathology. Immunohistochemical staining and subsequent quantification has revealed a statistically significant increased density of glutamatergic and GABAergic presynaptic boutons in both the plaque free and plaque adjacent cortical neuropile areas of transgenic mice as compared to non-transgenic controls. Furthermore, amyloid plaque size was shown to have a statistically significant effect on the relative area occupied by dystrophic glutamatergic neurites in the peri-plaque neuropile. These findings support our hypothesis that the amyloid pathology progresses in a time and neurotransmitter specific manner, first in the cholinergic system which appears to be most vulnerable, followed by the glutamatergic presynaptic boutons and finally the somewhat more resilient GABAergic terminals.