Interruption of postganglionic sympathetic fibers at any point along the internal carotid arteries or a lesion of the superior cervical ganglion results in miosis, drooping of the eyelid, and abolition of sweating over one side of the face; this constellation is the Horner, or more properly, Bernard-Horner syndrome (see also “Horner Syndrome” in Chap. 13). The same syndrome in less-obvious form may be caused by interruption of the preganglionic fibers at any point between their origin in the intermediolateral cell column of the C8-T2 spinal segments and the superior cervical ganglion or by interruption of the descending, uncrossed hypothalamospinal pathway in the tegmentum of the brainstem or cervical cord. The common causes are neoplastic or inflammatory involvement of the cervical lymph nodes or proximal part of the brachial plexus, surgical and other types of trauma to cervical structures (e.g., jugular venous catheters), carotid artery dissection, syringomyelic or traumatic lesions of the first and second thoracic spinal segments, and infarcts or other lesions of the lateral part of the medulla (Wallenberg syndrome). There is also an idiopathic variety that is in some cases hereditary. If a Horner syndrome develops early in life, the iris on the affected side fails to become pigmented and remains blue or mottled gray-brown (heterochromia iridis; see Fig. 13-10).
A lesion of the stellate ganglion, for example, compression by a tumor arising from the superior sulcus of the lung (Pancoast tumor), produces the interesting combination of a Horner syndrome and paralysis of sympathetic reflexes in the limb (the hand and arm are dry and warm). With preganglionic lesions, facial flushing may develop on the side of the sympathetic disorder; this is brought on in some instances by exercise (harlequin effect). The combination of segmental anhidrosis and an Adie pupil is sometimes referred to as the Ross syndrome; it may be abrupt in onset and idiopathic, or it may follow a viral infection.
Keane has provided data as to the relative frequency of the lesions causing oculosympathetic (Horner) paralysis. In 100 successive cases, 63 were of central type caused by brainstem strokes, 21 were preganglionic from trauma or tumors of the neck, 13 were postganglionic from miscellaneous causes, and in 3 cases the localization could not be determined (see Chap. 13 for further discussion).
The pupillary disturbances associated with oculomotor nerve lesions, the Adie pupil, and other parasympathetic and pharmacologic testing for sympathetic abnormalities of pupillary function are considered fully in Chap. 13 and in Table 13-6 with the accompanying text. Apraclonidine, 0.5 percent, has become the favored drug for diagnostic testing as noted earlier.
Lesions of the C4 or C5 segments of the spinal cord, if complete, will interrupt suprasegmental control of both the sympathetic and sacral parasympathetic nervous systems. Much the same effect is observed with lesions of the upper thoracic cord (above T6). Lower thoracic lesions leave much of the descending sympathetic outflow intact, only the descending sacral parasympathetic control being interrupted. Traumatic necrosis of the spinal cord is the usual cause of these states, but they also may be a result of infarction, certain forms of myelitis, radiation damage, and tumors.