Decentralized cardiovascular autonomic control and cognitive deficits in persons with spinal cord injury

Abstract

Spinal cord injury (SCI) results in motor and sensory impairments that can be identified with the American Spinal Injury Association (ASIA) Impairment Scale (AIS). Although, SCI may disrupt autonomic neural transmission, less is understood regarding the clinical impact of decentralized autonomic control. Cardiovascular regulation may be altered following SCI and the degree of impairment may or may not relate to the level of AIS injury classification. In general, persons with lesions above T1 present with bradycardia, hypotension, and orthostatic hypotension; functional changes which may interfere with rehabilitation efforts. Although many individuals with SCI above T1 remain overtly asymptomatic to hypotension, we have documented deficits in memory and attention processing speed in hypotensive individuals with SCI compared to a normotensive SCI cohort. Reduced resting cerebral blood flow (CBF) and diminished CBF responses to cognitive testing relate to test performance in hypotensive non-SCI, and preliminary evidence suggests a similar association in individuals with SCI. Persons with paraplegia below T7 generally present with a normal cardiovascular profile; however, our group and others have documented persistently elevated heart rate and increased arterial stiffness. In the non-SCI literature there is evidence supporting a link between increased arterial stiffness and cognitive deficits. Preliminary evidence suggests increased incidence of cognitive impairment in individuals with paraplegia, which we believe may relate to adverse cardiovascular changes. This report reviews relevant literature and discusses findings related to the possible association between decentralized cardiovascular autonomic control and cognitive dysfunction in persons with SCI.

Figure 1

SBP over a 24-hour observation period in subjects with tetraplegia (C3–C8: closed circles), high paraplegia (T2–T5: open triangles), low paraplegia (T7–T12: closed triangles), and non-SCI controls (asterisks). The interaction effect was significant; P < 0.01, post hoc analysis revealed that SBP was significantly lower in the tetraplegic group compared to the non-SCI and high-paraplegic groups (P < 0.05). Recreated from Ref. 70.

Figure 2

The nocturnal dip in BP (SBPdip) among the non-SCI, low-paraplegic, high-paraplegic, and tetraplegic groups; *P < 0.05; **P < 0.01; ***P < 0.001 versus tetraplegic group. Reported in Ref. 70.

Figure 3

Seated SBP among the non-SCI, paraplegia, and tetraplegia groups. *P < 0.01 versus similar condition in paraplegic and non-SCI groups. Reported in Ref. 73.

Figure 4

Mean change in CBF from seated rest to seated cognitive testing. Recreated from Ref. 73.

Figure 5

Individual change scores in CBF (cm/second) from seated rest to seated cognitive testing among the non-SCI, paraplegia, and tetraplegia groups. Reported in Ref. 73.

Figure 6

Individual change scores in CVRi (cm/second) from seated rest to seated cognitive testing among the non-SCI, paraplegic, and tetraplegic groups. Recreated from Ref. 73.

Figure 7

The relationship between change in CVRi and t-score on the Stroop color task was significant in the non-SCI controls subjects (r = 0.579; P = 0.0187), but there was no significant association in either the paraplegic or tetraplegic groups. Recreated from Ref. 73.

Figure 8

HR over a 24-hour observation period in subjects with tetraplegia (C3–C8: open circles), high paraplegia (T2–T5: asterisks), low paraplegia (T7–T12: closed triangles), and non-SCI controls (open squares). The interaction effect was significant; P < 0.0001, post hoc analysis revealed that HR was significantly higher in the high- and low-paraplegic groups compared to the non-SCI (P < 0.05) and tetraplegic group (P < 0.01). Recreated from Ref. 70.