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The first-order neuronal projection extends from the hypothalamus to the upper thoracic spinal cord. Lesions in the hypothalamus are rare and usually cause other neurologic manifestations. Lesions in the brainstem that cause Horner syndrome usually lie in the medulla and never cause Horner syndrome alone. Spinal cord lesions would also be expected to cause other neurologic manifestations. The second-order neuronal projection extends from the spinal cord to the superior cervical ganglion in the neck. Lesions here could cause Horner syndrome in isolation, but almost never acutely. The third order neuronal projection extends from the superior cervical ganglion to the eye. Acute Horner syndrome with ipsilateral facial or neck pain is most commonly caused by cervical carotid dissection, which damages the oculosympathetic axons lying on the outer edge of the vessel wall. The deformation of the carotid artery wall also causes turbulent flow, which may generate emboli that can cause cerebral stroke. The risk of stroke rapidly declines within the first 10 days after the dissection. Patients are usually placed acutely on prophylactic aspirin. The ciliary ganglion and nerves do not lie within the oculosympathetic pathway.