Pathophysiology of AD

AD is most commonly triggered by urinary bladder issues or colon irritation. However, many other causes have been reported in the literature (Mathias & Frankel 2002; Teasell et al. 2000). AD is caused by a widespread sympathetic response triggered by either noxious or non-noxious stimuli below the level of injury (Krassioukov & Claydon 2006). AD episodes are usually short-lived either due to treatment or inherently self-limiting. However, there are reports of AD triggered by a specific stimulus, which continued to be present days up to weeks (Elliott & Krassioukov 2006).

Numerous mechanisms have been proposed for the development of AD. It is known from animal studies that autonomic instability following SCI results from plastic changes occurring within the spinal cord and peripheral autonomic circuits in both the acute and chronic stages following injury (Krassioukov, 2006; Mathias & Frankel 1988; Mathias & Frankel 2002; Teasell et al. 2000). Currently, unstable blood pressure control following SCI can be attributed to the destruction of the descending vasomotor pathways, resulting in the loss of inhibitory and excitatory supraspinal input to the sympathetic preganglionic neurons (Furlan et al. 2003). Moreover, there is significant animal and human evidence suggesting that plastic changes within the spinal cord (specifically spinal sympathetic neurons and primary afferents) underlies the abnormal cardiovascular control and the development of AD following SCI. Further, altered sensitivity of peripheral alpha-adrenergic receptors (receptors in the sympathetic nervous system) may contribute to AD (Arnold et al. 1995; Karlsson, 1999; Krassioukov et al. 1999; Krassioukov et al. 2002; Osborn et al. 1990).

Discussion

Individuals who have SCI and AD often experience increases in HR along with BP (Calderón-Juárez et al. 2024). Walter et al. (2018) also found neurogenic detrusor overactivity to be predictive of AD during urodynamic investigation.

Furthermore, events of AD commonly occur during urination, where longer restoration times (the time from initiation of voiding until BP returns to resting value) are correlated with higher peak sBP and change in sBP (Huh et al. 2024).

Conclusion

There is level 4 evidence (from one pre-post) (Calderón-Juárez et al. 2024) that sBP increased as urodynamic studies progressed, and the highest HR was reached 60 seconds after maximal sBP.

There is level 4 evidence (from one pre-post) (Cívicos Sánchez et al. 2021) that most individuals with AD presented neurogenic orthostatic hypotension (NOH) concomitantly, but none of SCI participants without AD had NOH.

There is level 4 evidence (from one pre-post) (Currie et al. 2019) that AD parameters are not significantly correlated with arterial stiffness.

There is level 4 evidence (from one pre-post) (Huh et al. 2024) that restoration time is strongly correlated with peak sBP and change in sBP.

There is level 4 evidence (from one pre-post) (Walter et al. 2018) that the presence of neurogenic detrusor overactivity may predict AD during UDS.