pupillestyringen

Pupillestyringen refers to the regulation of pupil size in the eye, a process driven by the autonomic nervous system to balance light intake and focus. The pupil size reflects the opposing actions of two smooth muscle groups: the sphincter pupillae, which constricts the pupil, and the dilator pupillae, which enlarges it.

Anatomy and pathways: The parasympathetic pathway controlling constriction originates in the retina and signals travel to the Edinger–Westphal nucleus in the midbrain, then via the oculomotor nerve to the ciliary ganglion and short ciliary nerves to the sphincter pupillae. The sympathetic pathway, which promotes dilation, begins in the hypothalamus, descends through the brainstem and spinal cord (ciliospinal center), ascends to the superior cervical ganglion, and reaches the dilator pupillae through long ciliary nerves. The two systems primarily act in opposition to regulate pupil diameter in response to light and to accommodation demands.

Reflexes and function: The pupillary light reflex involves both direct and consensual constriction in response to light, mediated by the parasympathetic pathway. The near response or accommodation combines lens adjustment with pupil constriction to enhance near vision.

Clinical relevance: Abnormal pupillestyring can indicate neurological or systemic issues. Anisocoria is a difference in pupil size between eyes. Horner syndrome involves ptosis and miosis due to disrupted sympathetic input. A dilated pupil may indicate third nerve palsy or pharmacological mydriasis. Pupillometry—quantitative measurement of pupil size and reactivity—serves as a tool in neurology and anesthesiology to assess brain function and autonomic status.

Pharmacology and testing: Cholinergic agonists (e.g., pilocarpine) induce constriction, while anticholinergics or adrenergic agents (e.g., phenylephrine) induce dilation. Pupil size varies with age, iris color, lighting, medications, and disease.