Publications by authors named "Scott P Falci"

3 Publications

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Neuroprotective effects of human spinal cord-derived neural precursor cells after transplantation to the injured spinal cord.

Exp Neurol 2014 Mar 8;253:138-45. Epub 2014 Jan 8.

Division of Neurodegeneration, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Geriatric Clinic Res Lab., Novum, S-14186 Stockholm, Sweden; Stockholms Sjukhem Foundation, Mariebergsgatan 22, S-11235 Stockholm, Sweden. Electronic address:

To validate human neural precursor cells (NPCs) as potential donor cells for transplantation therapy after spinal cord injury (SCI), we investigated the effect of NPCs, transplanted as neurospheres, in two different rat SCI models. Human spinal cord-derived NPCs (SC-NPCs) transplanted 9 days after spinal contusion injury enhanced hindlimb recovery, assessed by the BBB locomotor test. In spinal compression injuries, SC-NPCs transplanted immediately or after 1 week, but not 7 weeks after injury, significantly improved hindlimb recovery compared to controls. We could not detect signs of mechanical allodynia in transplanted rats. Four months after transplantation, we found more human cells in the host spinal cord than were transplanted, irrespective of the time of transplantation. There was no focal tumor growth. In all groups the vast majority of NPCs differentiated into astrocytes. Importantly, the number of surviving rat spinal cord neurons was highest in groups transplanted acutely and subacutely, which also showed the best hindlimb function. This suggests that transplanted SC-NPCs improve the functional outcome by a neuroprotective effect. We conclude that SC-NPCs reliably enhance the functional outcome after SCI if transplanted acutely or subacutely, without causing allodynia. This therapeutic effect is mainly the consequence of a neuroprotective effect of the SC-NPCs.
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http://dx.doi.org/10.1016/j.expneurol.2013.12.022DOI Listing
March 2014

Caudal granular insular cortex is sufficient and necessary for the long-term maintenance of allodynic behavior in the rat attributable to mononeuropathy.

J Neurosci 2011 Apr;31(17):6317-28

Department of Psychology and Neuroscience, University of Colorado, Boulder, Colorado 80309-0345, USA.

Mechanical allodynia, the perception of innocuous tactile stimulation as painful, is a severe symptom of chronic pain often produced by damage to peripheral nerves. Allodynia affects millions of people and remains highly resistant to classic analgesics and therapies. Neural mechanisms for the development and maintenance of allodynia have been investigated in the spinal cord, brainstem, thalamus, and forebrain, but manipulations of these regions rarely produce lasting effects. We found that long-term alleviation of allodynic manifestations is produced by discreetly lesioning a newly discovered somatosensory representation in caudal granular insular cortex (CGIC) in the rat, either before or after a chronic constriction injury of the sciatic nerve. However, CGIC lesions alone have no effect on normal mechanical stimulus thresholds. In addition, using electrophysiological techniques, we reveal a corticospinal loop that could be the anatomical source of the influence of CGIC on allodynia.
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http://dx.doi.org/10.1523/JNEUROSCI.0076-11.2011DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3089761PMC
April 2011

Posttraumatic spinal cord tethering and syringomyelia: surgical treatment and long-term outcome.

J Neurosurg Spine 2009 Oct;11(4):445-60

Department of Neurosurgery, Craig Hospital, Englewood, Colorado 80113, USA.

Object: Permanent neurological loss after spinal cord injury (SCI) is a well-known phenomenon. There has also been a growing recognition and improved understanding of the pathophysiological mechanisms of late progressive neurological loss, which may occur after SCI as a result of posttraumatic spinal cord tethering (SCT), myelomalacia, and syringomyelia. A clinical study of 404 patients sustaining traumatic SCIs and undergoing surgery to arrest a progressive myelopathy caused by SCT, with or without progressive myelomalacia and cystic cavitation (syringomyelia) was undertaken. Both objective and subjective long-term outcomes were evaluated. To the authors' knowledge, this is the first series of this size correlating long-term patient perception of outcome with long-term objective outcome analyses.

Methods: During the period from January 1993 to November 2003, 404 patients who had previously sustained traumatic SCIs underwent 468 surgeries for progressive myelopathies attributed to tethering of the spinal cord to the surrounding spinal canal, with or without myelomalacia and syrinx formation. Forty-two patients were excluded because of additional pathological entities that were known to contribute to a progressive myelopathy. All surgeries were performed by the same neurosurgeon at a single SCI treatment center and by using a consistent surgical technique of spinal cord detethering, expansion duraplasty, and when indicated, cyst shunting.

Results: Outcome data were collected up to 12 years postoperatively. Comparisons of pre- and postoperative American Spinal Injury Association sensory and motor index scores showed no significant change when only a single surgery was required (86% of patients). An outcome questionnaire and phone interview resulted in > 90% of patients self-assessing arrest of functional loss; > 50% of patients self-assessing improvement of function; 17 and 18% self-assessing improvement of motor and sensory functions to a point greater than that achieved at any time postinjury, respectively; 59% reporting improvement of spasticity; and 77% reporting improvement of hyperhidrosis.

Conclusions: Surgery for spinal cord detethering, expansion duraplasty, and when indicated, cyst shunting, is a successful treatment strategy for arresting a progressive myelopathy related to posttraumatic SCT and syringomyelia. Results suggest that surgery leads to functional return in ~ 50% of patients, and that in some patients posttraumatic SCT limits maximal recovery of spinal cord function postinjury. A patient's perception of surgery's failure to arrest the progressive myelopathy corresponds closely with the need for repeat surgery because of retethering, cyst reexpansion, and pseudomeningocele formation.
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http://dx.doi.org/10.3171/2009.4.SPINE09333DOI Listing
October 2009