Both excessive sweating (hyperhidrosis) and decreased sweating are commonly reported in PD. These involve thermoregulatory eccrine sweat glands which are distributed over most of the body surface. Sweating is controlled by sympathetic signals originating in the hypothalamic preoptic sweat center, synapsing with neurons in the intermediolateral cell columns which project to unmyelinated post-ganglionic class C fibers in the paravertebral ganglia that form peripheral nerves to reach the sweat glands. In addition to PD pathology in sympathetic interomediolateral nuclei of the spinal cord[4
], skin biopsies have also demonstrated lower cutaneous autonomic innervation in blood vessels, sweat glands and erector pili muscles in PD[22
]. Autopsy studies have demonstrated α-synuclein to be present in unmyelinated fibers of the dermis in 20/85 cases with CNS Lewy body pathology[23
]. Another autopsy study found no α-synuclein skin staining in 0/11 cases of PD, ILDB and dementia with Lewy bodies[5
]. In vivo
skin biopsies in PD patients found 2/20 (10%) to stain for α-synuclein. There were several methodological differences among these studies that could account for the differing percentages of positive biopsied cases[24
], though heterogeneity within PD may also play a role.
The sympathetic skin response (SSR) is recorded by electrodes on the palmar and plantar surfaces. SSR is evoked electrodermal activity (EDA) that originates from sweat glands and adjacent skin. A peripheral nerve afferent is electrically stimulated and the EDA is recorded. The EDA is generally biphasic with an initial negativity followed by a positive potential. The initial negativity is from the sweat gland[7
]. Positivity varies with circulation, chest pressure, cholinergic activity and arousal. The presence of EDA depends on the integrity of cutaneous innervation, hydration and perspiration, making the EDA difficult to interpret. Many, but not all studies report the SSR in PD to be abnormal (often with a longer latency and diminished amplitude in PD)[21
]. It has been postulated that excessive sweating in PD may occur as a compensatory reaction to lower sympathetic function in the extremities[31
Sweat function can also be measured by thermoregulatory sweat testing (TST) and the quantitative sudomotor axon-reflex test (QSART). The TST assesses the sweat response mediated by preganglionic and post ganglionic pathways. Subjects are induced to sweat by heat and, causing an indicator powder on the skin to change color. Percent anhidrosis in PD is less than those with multisystem atrophy[32
]. The QSART assesses the reflex mediated by the postganglionic sympathetic sudomotor axon. An impulse is delivered antidromically from the sweat gland until reaches a branch point where another axon also meets the same peripheral nerve. The impulse then travels orthodromically down that axon to evoke a sweat response which is recorded. In PD patients with confirmed sympathetic cardiac denervation, the QSART was found to be normal suggesting selective loss of post-ganglionic catecholaminergic but not cholinergic nerves[35
], while another study found QSART responses to be lower in PD compared to controls[36
]. Skin sympathetic peroneal nerve activity has also been found to be lower in PD compared to controls[37
], suggesting postganglionic sympathetic sudomotor lesions in PD.