Vascular Abnormalities in Acute Reflex Sympathetic Dystrophy (CRPS I)

Abstract

Demonstrated for the first time is a complete functional loss of cutaneous sympathetic vasoconstrictor activity in an early stage of RSD/CRPS I with recovery. The origin of this autonomic dysfunction is in the central nervous system.

Diagnostic criteria in patients with complex regional pain syndrome assessed in an out‐patient clinic

“…Wasner et al found three types of vascular regulation, termed warm, cold, and intermediate. In the latter, the extremity can be warmer, colder, or may show no difference, depending on the state of sympathetic activity 23 . As we did not use a dynamic test to analyse the function of the vascular regulation system under different states of sympathetic activity, 11 the number of patients with confirmed CRPS might actually have been higher than reported here.…”

Diagnostic criteria in patients with complex regional pain syndrome assessed in an out‐patient clinic

“…Wasner et al found three types of vascular regulation, termed warm, cold, and intermediate. In the latter, the extremity can be warmer, colder, or may show no difference, depending on the state of sympathetic activity 23 . As we did not use a dynamic test to analyse the function of the vascular regulation system under different states of sympathetic activity, 11 the number of patients with confirmed CRPS might actually have been higher than reported here.…”

Clinical features and pathophysiology of complex regional pain syndrome

“…Even massive body cooling failed to activate sympathetic vasoconstrictor neurons. 81 Consistently, norepinephrine levels from the venous effluent above the painful area were lower in the affected limb than in the contralateral one. 81 (ii) An ‘intermediate type’ where temperature and perfusion were either warmer or colder, depending on the degree of sympathetic activity.…”

“…81 Consistently, norepinephrine levels from the venous effluent above the painful area were lower in the affected limb than in the contralateral one. 81 (ii) An ‘intermediate type’ where temperature and perfusion were either warmer or colder, depending on the degree of sympathetic activity. (iii) In those with greater than 6 months duration, the ‘cold’ type, temperature and perfusion on the affected limb were consistently lower than those on the contralateral limb.…”

Thoracic sympathetic block with botulinum toxin A for complex regional pain syndrome: a retrospective case series

“…Sympathetic involvement in CRPS is complex and may vary with disease duration, vasomotor phenotype, and peripheral tissue changes. Early warm or vasodilatory presentations may reflect impaired cutaneous sympathetic vasoconstrictor activity rather than sympathetic overactivity [ 8 , 19 ]. Later cold presentations may involve secondary neurovascular changes [ 5 , 8 ].…”

“…Later cold presentations may involve secondary neurovascular changes [ 5 , 8 ]. At the peripheral tissue level, altered adrenergic responsiveness has also been demonstrated in CRPS subgroups, including upregulation of α1-adrenoceptors on epidermal cells and cutaneous nerve fibers [ 6 , 8 , [19] , [20] , [21] ]. This peripheral adrenergic sensitization may allow sympathetic signaling to remain coupled to pain, even without increased sympathetic outflow [ 7 , 21 ].…”

Diagnostic criteria in patients with complex regional pain syndrome assessed in an out‐patient clinic

“…Wasner et al found three types of vascular regulation, termed warm, cold, and intermediate. In the latter, the extremity can be warmer, colder, or may show no difference, depending on the state of sympathetic activity 23 . As we did not use a dynamic test to analyse the function of the vascular regulation system under different states of sympathetic activity, 11 the number of patients with confirmed CRPS might actually have been higher than reported here.…”

Clinical features and pathophysiology of complex regional pain syndrome

“…Even massive body cooling failed to activate sympathetic vasoconstrictor neurons. 81 Consistently, norepinephrine levels from the venous effluent above the painful area were lower in the affected limb than in the contralateral one. 81 (ii) An ‘intermediate type’ where temperature and perfusion were either warmer or colder, depending on the degree of sympathetic activity.…”

“…81 Consistently, norepinephrine levels from the venous effluent above the painful area were lower in the affected limb than in the contralateral one. 81 (ii) An ‘intermediate type’ where temperature and perfusion were either warmer or colder, depending on the degree of sympathetic activity. (iii) In those with greater than 6 months duration, the ‘cold’ type, temperature and perfusion on the affected limb were consistently lower than those on the contralateral limb.…”

Thoracic sympathetic block with botulinum toxin A for complex regional pain syndrome: a retrospective case series

“…Sympathetic involvement in CRPS is complex and may vary with disease duration, vasomotor phenotype, and peripheral tissue changes. Early warm or vasodilatory presentations may reflect impaired cutaneous sympathetic vasoconstrictor activity rather than sympathetic overactivity [ 8 , 19 ]. Later cold presentations may involve secondary neurovascular changes [ 5 , 8 ].…”

“…Later cold presentations may involve secondary neurovascular changes [ 5 , 8 ]. At the peripheral tissue level, altered adrenergic responsiveness has also been demonstrated in CRPS subgroups, including upregulation of α1-adrenoceptors on epidermal cells and cutaneous nerve fibers [ 6 , 8 , [19] , [20] , [21] ]. This peripheral adrenergic sensitization may allow sympathetic signaling to remain coupled to pain, even without increased sympathetic outflow [ 7 , 21 ].…”

Diagnostic criteria in patients with complex regional pain syndrome assessed in an out‐patient clinic

“…Wasner et al found three types of vascular regulation, termed warm, cold, and intermediate. In the latter, the extremity can be warmer, colder, or may show no difference, depending on the state of sympathetic activity 23 . As we did not use a dynamic test to analyse the function of the vascular regulation system under different states of sympathetic activity, 11 the number of patients with confirmed CRPS might actually have been higher than reported here.…”

Clinical features and pathophysiology of complex regional pain syndrome

“…Even massive body cooling failed to activate sympathetic vasoconstrictor neurons. 81 Consistently, norepinephrine levels from the venous effluent above the painful area were lower in the affected limb than in the contralateral one. 81 (ii) An ‘intermediate type’ where temperature and perfusion were either warmer or colder, depending on the degree of sympathetic activity.…”

“…81 Consistently, norepinephrine levels from the venous effluent above the painful area were lower in the affected limb than in the contralateral one. 81 (ii) An ‘intermediate type’ where temperature and perfusion were either warmer or colder, depending on the degree of sympathetic activity. (iii) In those with greater than 6 months duration, the ‘cold’ type, temperature and perfusion on the affected limb were consistently lower than those on the contralateral limb.…”

Thoracic sympathetic block with botulinum toxin A for complex regional pain syndrome: a retrospective case series

“…Sympathetic involvement in CRPS is complex and may vary with disease duration, vasomotor phenotype, and peripheral tissue changes. Early warm or vasodilatory presentations may reflect impaired cutaneous sympathetic vasoconstrictor activity rather than sympathetic overactivity [ 8 , 19 ]. Later cold presentations may involve secondary neurovascular changes [ 5 , 8 ].…”

“…Later cold presentations may involve secondary neurovascular changes [ 5 , 8 ]. At the peripheral tissue level, altered adrenergic responsiveness has also been demonstrated in CRPS subgroups, including upregulation of α1-adrenoceptors on epidermal cells and cutaneous nerve fibers [ 6 , 8 , [19] , [20] , [21] ]. This peripheral adrenergic sensitization may allow sympathetic signaling to remain coupled to pain, even without increased sympathetic outflow [ 7 , 21 ].…”