spinal cord injury

the ASIA scale goes from A which indicates no sensory or [blank] function at that level to E which is a normal individual

motor

during the acute phase of SCI (0-48 hours) there is a large increase of [blank] which increases nitric oxide and glutamate which can cause excitotoxicity

pro-inflammatory cytokines

in the sub-acute phase (2-14 days) the pro-inflammatory cytokines decrease [blanks] which decrease astrocyte end-feet binding and decrease glutamate transporters (EAAT1/2) which causes excitotoxicity

aquaporins

in the sub-acute phase (2-14 days) the pro-inflammatory cytokines increase reactive astrocytes which increase the amount of [blanks]

chondroitin sulfate proteoglycans (CSPGs)

in the subacute phase the continued ischemia and [blank] cell recruitment further increases amount of pro-inflammatory cytokines

immune

[blank] therapies are either neuroprotective (to limit damage from secondary injury) or pro-regenerative (favor “good plasticity”) and they increase gliosis, axon repair, and regeneration agents

Pharmacological

Modulation of monoamine neurotransmitters in the descending noradrenergic, serotonergic, and dopaminergic pathways to directly activate neurotransmission in the spinal cord can enhance [blank] feedback

proprioceptive

cell-based therapies may involve [blank] cells, oligodendrocyte precursor cells, umbilical cord derived stem cells, and bone marrow derived cells

Schwann

[blank] usually involves deep brain stimulation or spinal cord stimulation

neuromodulation

[blank] is the capacity of the CNS to undergo changes in function, structure and/or chemical profile

Neuroplasticity

acute reorganization involves unmasking of previously latent synapses while chronic reorganization improves synaptic [blank] and grows new synapses by axonal sprouting

efficacy

Synaptic [blank] occurs after some presynaptic terminals are lost due to accumulation of neurotransmitters

hyper effectiveness

Unmasking of a silent synapse occurs by [blank] receptors moving to post-synaptic membrane

AMPA

maladaptive plasticity can cause unintended [blanks], confusion in sensory modalities, and increased pain/nociception

movements

spinal cord injury leads to spasticity and hyperreflexia and frequency-dependent depression of the H-reflex is used as an estimation of spasticity and is [blanked] after SCI

decreased

maladaptive plasticity involves increased efficacy causing exaggerated stretch reflex, H-reflex, and monosynaptic EPSP and decreased [blank] for low frequency-dependent depression, reciprocal inhibition, presynaptic inhibition

modulation

four ways of improving functional plasticity include [blank] learning, pharmacology, activity-based therapies, and spinal cord stimulation

instrumental

the novel drug [blank] is a pharmacological agent that promotes plasticity after a SCI

NVG-291

Adaptive plasticity induced by activity-based therapies improves H-reflex reflex [blank] (actually see decrease)

depression

Activity-based therapies minimizes acute [blank] of hindlimb muscles, maintains muscle mass over the long term, restores muscle mass if delayed, improves reflex modulation, increases the expression of a number of neurotransmitters, neuromodulators and their receptors in the spinal cord

atrophy

[blank] stimulation increases excitability allowing motor pool recruitment with weaker descending commands (this strengthens connections)

epidural