Horner’s syndrome is a condition—usually unilateral—that results from interruption of the sympathetic nerves to the face. The effects include vasodilation, ptosis, miosis, and loss of sweating on the affected side. The syndrome can be caused by either a preganglionic or a postganglionic lesion, and knowledge of the location of the lesion (preganglionic or postganglionic) helps determine the optimal therapy. A localized lesion in a nerve causes degeneration of the distal portion of that fiber and loss of transmitter contents from the degenerated nerve ending—without affecting neurons innervated by the fiber. Therefore, a preganglionic lesion leaves the postganglionic adrenergic neuron intact, whereas a postganglionic lesion results in degeneration of the adrenergic nerve endings and loss of stored catechol-amines from them. Because indirectly acting sympathomi-metics require normal stores of catecholamines, such drugs can be used to test for the presence of normal adrenergic nerve endings. The iris, because it is easily visible and responsive to topical sympathomimetics, is a convenient assay tissue in the patient. If the lesion of Horner’s syndrome is postganglionic, indirectly acting sympathomimetics (eg, cocaine, hydroxy-amphetamine) will not dilate the abnormally constricted pupil because catecholamines have been lost from the nerve endings in the iris. In contrast, the pupil dilates in response to phenylephrine, which acts directly on the αreceptors on the smooth muscle of the iris. A patient with a preganglionic lesion, on the other hand, shows a normal response to both drugs, since the postganglionic fibers and their catecholamine stores remain intact in this situation.
• Midodrine Activates phospholipase C, resulting in increased intracellular calcium and vasoconstriction Vascular smooth muscle contraction increasing blood pressure (BP)
Oral • prodrug converted to active drug with a 1-h peak effect • Toxicity: Supine hypertension, piloerection (goose bumps), and urinary retention
Phenylephrine: Can be used IV for short-term maintenance of BP in acute hypotension and intranasally to produce local vasoconstriction as a decongestant α-Methyldopa, guanfacine, and guanabenz: Also used as central sympatholytics
Dexmedetomidine: Prominent sedative effects and used in anesthesia
Tizanidine: Used as a muscle relaxant
Apraclonidine and brimonidine: Used topically in glaucoma to reduce intraocular pressure `2 AGONISTS •ClonidineInhibits adenylyl cyclase and interacts with other intracellular pathways Vasoconstriction is masked by central sympatholytic effect, which lowers BP Hypertension Oral•transdermal•peakeffect1–3h•t1/2 oforaldrug~12h•producesdrymouthand sedation •Dobutamine1 Activates adenylyl cyclase, increasing myocardial contractility Positive inotropic effect Cardiogenic shock, acute heart failure IV•requiresdosetitrationtodesiredeffect 1Dobutamine has other actions in addition to β1-agonist effect. See text for details.
Amphetamine, racemic mixture Generic 1:1:1:1 mixtures of amphetamine sulfate, amphetamine aspartate, dextroamphetamine sulfate, and dextroamphetamine saccharate Adderall
Dextroamphetamine Generic, Dexedrine
Dobutamine Generic, Dobutrex
Dopamine Generic, Intropin
Epinephrine Generic, Adrenalin Chloride, Primatene Mist, Bronkaid Mist, EpiPen, Auvi-Q
Hydroxyamphetamine Paremyd (includes 0.25% tropicamide)