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In spinal cord injured adult mammals, neutralizing the neurite growth inhibitor Nogo‐A with antibodies promotes axonal regeneration and functional recovery, although axonal regeneration is limited in length. Neurotrophic factors such as BDNF stimulate neurite outgrowth and protect axotomized neurons. Can the effects obtained by neutralizing Nogo‐A, inducing an environment favorable for axonal sprouting, be strengthened by adding BDNF? A unilateral incomplete hemicord lesion at C7 level interrupted the main corticospinal component in three groups of adult macaque monkeys: control monkeys (n = 6), anti‐Nogo‐A antibody‐treated monkeys (n = 7), and anti‐Nogo‐A antibody and BDNF‐treated monkeys (n = 5). The functional recovery of manual dexterity was significantly different between the 3 groups of monkeys, the lowest in the control group. Whereas the anti‐Nogo‐A antibody‐treated animals returned to manual dexterity performances close to prelesion ones, irrespective of lesion size, both the control and the anti‐Nogo‐A/BDNF animals presented a limited functional recovery. In the control group, the limited spontaneous functional recovery depended on lesion size, a dependence absent in the combined treatment group (anti‐Nogo‐A antibody and BDNF). The functional recovery in the latter group was significantly lower than in anti‐Nogo‐A antibody‐treated monkeys, although the lesion was larger in three out of the five monkeys in the combined treatment group.

The aim of this study was to evaluate whether the six-spot-step test (SSST) is more suitable for monitoring walking ability in patients with chronic inflammatory polyneuropathy than the timed 25-foot-walking test (T25FW). In the SSST, participants have to walk as quickly as possible across a field measuring 1 × 5 m, while kicking blocks out of five circles on the floor. Sixty-two patients and 61 controls performed the SSST and T25FW. Patients also performed the overall disability sumscore, INCAT sensory sumscore, Medical Research Council sumscore, and 9-hole-peg-test. Twenty-one patients treated with intravenous immunoglobulin (IVIG) every 4–6 weeks were tested prior to and 2–3 weeks after treatment and judged change in their own clinical condition using the patient global impression of change (PGIC) scale. In patients, SSST ranged from 5.7 to 26.8 s and T25FW ranged from 3.6 to 12.9 s. Intra-class correlation between repeated tests was 0.97 for SSST and 0.95 for T25FW. Correlation with the additional tests was stronger for SSST than T25FW. In IVIG-treated patients, the mean change in walking time was −2.3 s for SSST and −0.6 s for T25FW. The SSST showed larger responsiveness in terms of effect size, standardized response means, and relative efficiency. Both ambulation tests correlated moderately to PGIC. The SSST may be superior to the T25FW in terms of dynamic range, floor effect, and responsiveness which makes the SSST a possible alternative for monitoring walking ability in patients with chronic inflammatory polyneuropathy.

Background: Central nervous system involvement in primary Sjögren’s syndrome is a matter of controversy, and its diagnosis remains difficult. Methods: We report 3 patients with primary Sjögren’s syndrome and central nervous system involvement in whom we assessed intrathecal immunoglobulin G synthesis and the presence of cerebrospinal fluid anti-SSA and anti-SSB autoantibodies. Results: We found intrathecal immunoglobulin G synthesis and presence of cerebrospinal fluid anti-SSA autoantibodies in all patients, with demonstration for the first time of specific anti-SSA autoantibody intrathecal synthesis in 2 patients. Conclusion: We suggest that cerebrospinal fluid anti-SSA autoantibodies could serve as a biomarker for Sjögren’s-syndrome-related central nervous system involvement.

Background Stroke remains one of the most common diseases with a serious impact on quality of life but few effective treatments exist. Mild hypothermia (33°C) is a promising neuroprotective therapy in stroke management. This study investigated whether a delayed short mild hypothermic treatment is still beneficial as neuroprotective strategy in the endothelin-1 (Et-1) rat model for a transient focal cerebral ischemia. Two hours of mild hypothermia (33°C) was induced 20, 60 or 120 minutes after Et-1 infusion. During the experiment the cerebral blood flow (CBF) was measured via Laser Doppler Flowmetry in the striatum, which represents the core of the infarct. Functional outcome and infarct volume were assessed 24 hours after the insult. In this sub-acute phase following stroke induction, the effects of the hypothermic treatment on apoptosis, phagocytosis and astrogliosis were assessed as well. Apoptosis was determined using caspase-3 immunohistochemistry, phagocytic cells were visualized by CD-68 expression and astrogliosis was studied by glial fibrillary acidic protein (GFAP) staining. Results Cooling could be postponed up to 1 hour after the onset of the insult without losing its positive effects on neurological deficit and infarct volume. These results correlated with the caspase-3 staining. In contrast, the increased CD-68 expression post-stroke was reduced in the core of the insult with all treatment protocols. Hypothermia also reduced the increased levels of GFAP staining, even when it was delayed up to 2 hours after the insult. The study confirmed that the induction of the hypothermia treatment in the Et-1 model does not affect the CBF. Conclusions These data indicate that in the Et-1 rat model, a short mild hypothermic treatment delayed for 1 hour is still neuroprotective and correlates with apoptosis. At the same time, hypothermia also establishes a lasting inhibitory effect on the activation of astrogliosis.

BACKGROUND AND PURPOSE: Several studies have investigated outcomes after disc surgery. However, the occurrence of kinesiophobia has not been investigated previously in patients after disc herniation surgery. In this cross-sectional study, we investigated kinesiophobia in patients who had been treated surgically for lumbar disc herniation, and we related the results to established outcome measures. PATIENTS AND METHODS: 10-34 months after surgery, questionnaires were sent to 97 patients who had undergone standardized open discectomy. Outcome measures included Tampa scale for kinesiophobia (TSK); Oswestry disability index (ODI); European quality of life in 5 dimensions (EQ-5D); visual analog scale (VAS) for leg and back pain, work disability, and patient satisfaction; Zung self-rating depression scale (ZDS); pain catastrophizing scale (PCS); and a self-efficacy scale (SES). RESULTS: 36 of 80 patients reported having kinesiophobia. There were statistically significant differences in ODI, EQ-5D, VAS leg and back pain, ZDS, PCS, and SES between patients with and without kinesiophobia. INTERPRETATION: Half of the patients suffered from kinesiophobia 10-34 months after surgery for disc herniation. These patients were more disabled, had more pain, more catastrophizing thoughts, more symptoms of depression, lower self-efficacy, and poorer health-related quality of life than patients without kinesiophobia.