Reticulospinal Tract

In primates, the corticospinal tract is the dominant pathway for control of movement, and has been much investigated. By contrast, pathways originating in the brainstem are often considered less important, and assumed to have a role primarily in posture or gross movements such as locomotion.

Recently, we have accumulated evidence that in primates the medial brainstem pathways (including vestibulospinal and reticulospinal tracts) may be involved in control of the distal muscles of the forelimb which are used in hand movements.

Why does this matter? Lesions such as stroke or spinal cord injury often affect the corticospinal tract. Patients initially are paralyzed on the side of the lesion, but then they recover function. We hypothesise that part of this recovery stems from strengthening the reticulospinal connections which already exist, and which provide a parallel pathway for hand control.

We are currently investigating the contribution of the reticulospinal tract to functional recovery by making experimental lesions of the corticospinal tract on one side (see figure). Although initially paralysed, animals rapidly recover function on the side contralateral to the lesion. After 6-8 months, we then assess the strength of reticulospinal connections. Our preliminary data shows that reticulospinal connections do appear to strengthen. However, this occurs only for motoneurons projecting to forearm flexor and intrinsic hand muscles. This suggests that the reticulospinal tract may underlie much of the functional recovery that is seen. The selective strengthening of connections to flexors, and failure to enhance activation of extensors, may underlie the extensor weakness and flexor spasticity which often form the main characteristics of disability in a stroke survivor in the chronically recovered phase.

Technique for unilateral pyramidal tract (PT) lesion in primates. Stimulating electrodes were inserted into the left and right PT, and antidromic field potentials recorded from epidural electrodes over left and right primary motor cortex (M1). A lesion probe was implanted in the left PT rostral to the stimulating electrode. The lesion probe temperature was raised to 60-70 C for 20s, using a radiofrequency generator. Between 1 and 4 such lesions were made. The traces show the antidromic potentials elicited from the stimulating electrodes before and after the lesions. The field on the right side was only slightly reduced, whereas that on the left was completely abolished.

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