The eye muscles are responsible for all movements of the eyes including the functional eye adjustment. In addition to six outer, the human has three inner eye muscles. The inner eye muscles carry smooth muscles and are subject to control by the autonomic nervous system. All eye muscles of the inner area serve to resize both pupils. This process is also known as adaptation.
In addition to the adaptation, the inner eye muscles are responsible for the regulation of refractive power and thus control the visual acuity. The sphincter pupillae muscle is one of the inner eye muscles. The muscle is a sphincter that can narrow the pupils. Like all circular muscles of the human body, the sphincter pupillae muscle has a circular fiber course. Its fibers are ring-like around the pupil and form the posterior part of the iris stroma.
Due to its functions, the muscle in the medical literature is also called the constrictor pupillae muscle. Nerve fibers from the ciliary ganglion innervate the circular muscle parasympathetic. The antagonist of the sphincter pupillae muscle is the dilator pupillae.
The individual fibers for the innervation of the lattice-like sphincter pupillae muscle originate from the Edinger-Westphal nucleus and extend via the oculomotor nerve to the ciliary ganglion. The Edinger-Westphal-Kern is a part of the midbrain and corresponds to the core area for the control of the pupillary reflex or the eye adaptation.
The nucleus receives afferents via the optic nerve and the optic tract, which project directly into the epithalamus and are switched in the nucleus pretectalis to so-called interneurons with bilateral connection to the Edinger-Westphal nucleus. The efferents of the nucleus reach the pupil constrictor and the ciliary muscle via the ciliary ganglion. The fibers of the sphincter pupillae muscle originate from the nucleus accessorius n. Oculomotorii, the nucleus of the III. Cranial nerves. In the ganglion ciliare, an interconnection takes place from the pre- to the postganglionic neuron. From there the fibers pass through in the form of the Nn. ciliares breves the white eye skin and pull towards the inside of the eye.
The sphincter pupillae muscle is involved in the adaptation of the eyes by contracting the pupils. The circular muscle receives the commands for contraction via efferents (descending pathways) from the midbrain in the form of bioelectric excitation and then sets the so-called miosis in motion. Based on the average eye hole diameter, this constriction of the pupils may be subject to different degrees of severity.
Not only the active contraction of the sphincter pupillae muscle, but also the failure or limitation of its antagonist. The dilator pupillae muscle induces miosis. Physiologically, parasympathetic nerve fibers mediate the constriction of the pupils. Light incidence as well as the Naheinstellungstrias from Nahfixation, accommodation and convergence movement condition the adaptation movement automatically. Specifically, in the case of miosis, the nerve fibers originating from the accessory nucleus of the oculomotor nerve are connected in the ciliary ganglion. Via the Nervi ciliares breves they reach the musculus sphincter pupillae.
The reflex arc begins at the retina, from where it is connected on both sides via the optic nerve in the area pretectalis. The main task of the sphincter pupillae muscle is therefore a reflex movement, which is primarily initiated by light stimuli. In unilateral light irritation, both pupils narrow. This is also a consensual or indirect light reflex the speech. On the other hand, the pupil constriction in the accommodative lens curvature amplification always takes place when close objects are focused.
The contraction of the sphincter pupillae muscle in the sense of a miosis can be brought about by opiates or opioids. Pathologically constricted pupils are therefore often interpreted as a sign of intoxication. Also, pharmacological agents such as miotics (pilocarpine) can cause a narrowing of the pupils.
The administration of these drugs usually takes place in a therapeutic or diagnostic context. The therapeutic steps are used, for example, in glaucoma or for the differential diagnostic clarification of pharmacodynamic pupillotonia. A pronounced miosis even improves the visual acuity of lensless people. The narrowing of the viewing hole increases the depth of field and has a similar effect to a stenotic gap. Miotics thus cause an increase in visual acuity through the stimulation of the pupil-narrowing muscle.
Unlike the substances mentioned, mydriatics such as atropine do not stimulate the sphincter pupillae muscle, but cause paralysis of the circular muscle. By administering the funds, the miosis can be prevented for a limited period of time. Active substances such as parasympatholytics in turn cause a complete loss of accommodation due to a temporary paralysis of the parasympathetic innervated ciliary muscle. Paralysis of the sphincter pupillae muscle is gaining clinical relevance, not only in diagnostics and therapy. Sudden paralysis of the muscle usually manifests itself in pupillary rigidity with an inability to accept.
The cause of this phenomenon is traumatic and inflammatory lesions of the supplying nerves as well as nerve compression by tumors. Miosis is scarcely or not at all possible with a paralysis of the sphincter pupillae muscle. In contrast, pathological pupil constrictions occur in disorders of sympathetic care, for example in the context of Horner syndrome or Argyll-Robertson syndrome.Tags: