Abstract
In relation to mechanisms involved in functional recovery of manual dexterity from cervical cord injury or from motor cortical injury, our goal was to determine whether the movements that characterize post-lesion functional recovery are comparable to original movement patterns or do monkeys adopt distinct strategies to compensate the deficits depending on the type of lesion? To this aim, data derived from earlier studies, using a skilled finger task (the modified Brinkman board from which pellets are retrieved from vertical or horizontal slots), in spinal cord and motor cortex injured monkeys were analyzed and compared. Twelve adult macaque monkeys were subjected to a hemi-section of the cervical cord (n = 6) or to a unilateral excitotoxic lesion of the hand representation in the primary motor cortex (n = 6). In addition, in each subgroup, one half of monkeys (n = 3) were treated for 30 days with a function blocking antibody against the neurite growth inhibitory protein Nogo-A, while the other half (n = 3) represented control animals. The motor deficits, and the extent and time course of functional recovery were assessed. For some of the parameters investigated (wrist angle for horizontal slots and movement types distribution for vertical slots after cervical injury; movement types distribution for horizontal slots after motor cortex lesion), post-lesion restoration of the original movement patterns (“true” recovery) led to a quantitatively better functional recovery. In the motor cortex lesion groups, pharmacological reversible inactivation experiments showed that the peri-lesion territory of the primary motor cortex or re-arranged, spared domain of the lesion zone, played a major role in the functional recovery, together with the ipsilesional intact premotor cortex.
Highlights
Primates are characterized by an outstanding capability to perform fractionated finger movements, representing the exquisite behavioral attribute of manual dexterity [see e.g., Ref. [1, 2]]
PHARMACOLOGICAL DATA In contrast to intact monkeys in which PMd was reversibly inactivated without an effect on manual dexterity of the contralesional hand [38], the present study demonstrates that reversible inactivation of PMd in monkeys subjected several months earlier to a permanent lesion of the hand representation in M1 provokes a loss of the recovered manual dexterity, irrespective of whether the recovery was spontaneous or enhanced with an anti-Nogo-A antibody treatment
We compared the functional recovery after a unilateral SCI and motor cortex lesion in adult macaque monkeys using a sensitive manual dexterity task as a test system
Summary
Primates (humans and non-human) are characterized by an outstanding capability to perform fractionated finger movements, representing the exquisite behavioral attribute of manual dexterity [see e.g., Ref. [1, 2]]. The CS projection comprises the socalled corticomotoneuronal (CM) connection, forming a direct projection of CS neurons in layer V onto spinal cord motoneurons. This CM system is a specialty of primates, and believed to be for the most part the anatomical support of manual dexterity [e.g., Ref. A lesion located at the origin of the CS-CM projection, in the hand area of the primary motor cortex, from which about 50% of the CS projection originates in the frontal lobe [3] Both types of lesion were followed by an immediate dramatic, and generally complete, loss of manual dexterity, which persisted for a few weeks. In our two models of CS-CM lesion, recovery of manual dexterity was incomplete
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