Use of calcitonin to prevent complex regional pain syndrome type I in severe hemiplegic patients after stroke.

PURPOSE: To evaluate the effects of calcitonin in preventing complex regional pain syndrome type I (CRPS) in patients with severe hemiplegia following stroke. METHODS: In this observer-blinded, controlled study comparison with historical controls between April 2003 and May 2004, subjects comprised consecutive patients with post-stroke hemiplegia admitted between June 2004 and September 2005, with any upper limb or finger graded as Brunnstrom stage (BrST) III or below. One group was administered intramuscular injection of 20 units of elcatonin (EL) (Asu(1-7) eel calcitonin) weekly from immediately after admission to discharge, together with rehabilitation therapy. The control group received rehabilitation therapy alone. Patients were observed during the in-hospital rehabilitation period. The main outcome measure was onset of CRPS. RESULTS: Incidence of CRPS in all patients with post-stroke hemiplegia during the control period was about 8.2%, similar to recent studies. Limited to serious hemiplegic patients graded as BrST III or below, incidence of CRPS was significantly lower in the EL group (12.5%) than in controls (57.1%). No significant differences in patient background were seen between groups. CRPS was completely prevented when EL injection was started 6 weeks after stroke. CONCLUSION: Intramuscular calcitonin appears to suppress onset of CRPS after stroke, particularly when started early after stroke.

Actions of brain-derived neurotrophic factor on spinal nociceptive transmission during inflammation in the rat.

The aim of the current study was to investigate whether, and if so how, brain-derived neurotrophic factor (BDNF) acts to develop the spinal sensitization underlying inflammation-induced hyperalgesia. In spinal cord slice preparations from rats with inflammation induced by complete Freund's adjuvant (CFA), BDNF, but not nerve growth factor (NGF) or neurotrophin-3 (NT-3), acted presynaptically to increase the frequency of excitatory miniature EPSCs in substantia gelatinosa (SG) neurones of the CFA-treated, but not untreated rats, through activation of lidocaine (lignocaine)-sensitive, TTX-resistant Na+ channels. This effect was observed in the spinal cord slices of the CFA-treated rat only 2-4 days after the CFA injection. On the other hand, the number of monosynaptic Abeta afferent inputs to the SG significantly increased 1 week after the onset of the inflammation, and this increase was significantly suppressed by treatment with anti-BDNF antiserum administered 1 day before and just after the CFA injection. In addition, the treatment with anti-BDNF antiserum significantly attenuated the CFA-induced hyperalgesia and/or allodynia. These findings, taken together, suggest that BDNF, which is considered to be released from the sensitized primary afferents, increases the excitability of SG neurones through its action on the presynaptic terminals. BDNF may thereafter induce monosynaptic Abeta afferents to the SG, thereby developing hyperalgesia and/or allodynia during inflammation.

Induction of myogenin messenger ribonucleic acid in rat skeletal muscle after 1 hour of passive repetitive stretching.

OBJECTIVE: To investigate the effect of repetitive passive stretch of living rat muscle on myogenin messenger ribonucleic acid (mRNA) expression. DESIGN: Case-controlled study. SETTING: University laboratory. ANIMALS: Seventeen female 8-week-old Wistar rats. INTERVENTIONS: Repetitive stretch (15 times/min) was performed manually on gastrocnemius muscle of anesthetized rats for 15, 30, and 60 minutes. MAIN OUTCOME MEASURES: Total RNA was extracted, after the animals were killed, from the gastrocnemius muscle, and Northern blotting was performed using oligonucleotide complementary to myogenin. RESULTS: Repetitive stretch to gastrocnemius muscles of anesthetized rats for 1 hour induced a 21.5% increase in the expression of myogenin mRNA. CONCLUSIONS: Repetitive passive stretch of the rat skeletal muscle for 60 minutes induced the expression of myogenic transcription factor myogenin mRNA. These findings suggest the clinical utility of passive repetitive stretch to maintain muscle strength in patients who are unconscious or paralyzed.

Repetitive stretch induces c-fos and myogenin mRNA within several hours in skeletal muscle removed from rats.

OBJECTIVE: To investigate what effect repetitive stretch has on gene transcription in muscle tissues removed from rats. DESIGN: Case-control study. SETTING: University laboratory. ANIMALS: Eight female 8-week-old Wistar rats. INTERVENTIONS: Rat anterior tibial and soleus muscles were removed and repetitively stretched about 20% of the muscle length by using the Magnus method in Krebs-Ringer solution. Stretch-relax cycles 15 times per minute were continued for 2 hours in 1 group and 4 hours in another group. Contralateral muscles removed from the same rat were incubated without stretch as the control. MAIN OUTCOME MEASURES: After repetitive stretch, total ribonucleic acid (RNA) was extracted from the muscles and Northern blotting was carried out using c-fos and myogenin oligonucleotide as probes. RESULTS: Repetitive stretch during 2 hours significantly increased the expression of c-fos messenger RNA (mRNA) in both the tibialis anterior and soleus muscles. Increased expression of myogenin mRNA in both muscles was observed with repetitive stretch for 4 hours. Because of the initial increase of immediate early gene c-fos mRNA and the subsequent increase of myogenic transcription factor myogenin mRNA, it appears that repetitive muscle stretch induces sequential progression of gene transcription toward muscle hypertrophy. CONCLUSIONS: Mechanical repetitive stretch for a few hours would be one of the stimulating factors for muscle growth and should be available for muscle training in clinical rehabilitation.