Chapter 2. Prehension

218 THE PHASES OF PREHENSION
nonnervous stimuli.
The periodicity of insensible eccrine sweating has been attributed
to a central source of innervation. The secretory portion of the duct
has myoepithelial cells, arranged with their long axes parallel to the
tubule, and it is generally assumed that their contraction promotes
delivery of sweat to the surface (Kuno, 1934, cited in Rothman,
1954). Although the pathways for this innervation are not clearly
established, Guttmann and List (1928, cited in Rothman, 1954),
suggest 5 main connections on the efferent pathway for generalized
reflex sweating: cortex, hypothalamus, medulla, lateral horn of cord,
sympathetic ganglia” to sweat glands. These authors indicate that
“the adequate stimuli are psychic for the first neuron, thermal for the
second, gustatory for the third and nonthermal skin stimuli for the
fourth and fifth.”
Innervation of the eccrine sweat glands is through sympathetic
neurons which release acetylcholine. The sympathetic dermatomes for
sweat fibers span T4-T7. The eccrine sweat glands are innervated by
sympathetic cholinergic fibers, which originate from the paravertebral
ganglia (Dale & Feldberg, 1934, cited in Gabella, 1976). This
apparent contradiction is explained as follows. Most postganglionic
fibers originating from the sympathetic ganglia are adrenergic. A
minority of fibers are cholinergic, emerging from non-adrenergic
sympathetic ganglion cells. Other sypathetic cholinergic fibers are
vasodilator fibers to skeletal muscles and to the muscles of the tongue
(Gabella, 1976). With thermal sweating, active vasodilation and
sweating onset occur at about the same time. Eccrine sweat glands
respond to both cholinomimetic and adrenomimetic drugs, leading
some authors to argue that they have a double innervation or that the
same nerves can respond to either stimulation (Montagna & Parakkal,
1972).
With respect to neural control of sweating, several points are of
particular interest. One is that the cortical innervation for sweating
may involve some of the same cortical areas as for grasping (see
Chapters 4 and 5). Cortical lesions in the parietal area of humans
often cause contralateral hyperidrosis (excessive sweating on the side
of motor paresis). This has been considered due to irritation of the
diseased cortical center or to the release of cortical inhibition (Linder,
1947, cited in Rothman, 1954). Cortical lesions in the premotor area
(Brodmann’s area 6) of cats leads to lack of sweating on the
11A ganglion is a mass of nerve cells serving as a center from which nerve
impluses are transmitted.