There is no pharmacological test to differentiate between a first and second order neuron lesion. Dilation lag testIt is important to distinguish the ptosis caused by Horners syndrome from the ptosis caused by a lesion to the oculomotor nerve. In the former, the ptosis occurs with a constricted pupil (due to a loss of sympathetics to the eye), whereas in the latter, the ptosis occurs with a dilated pupil (due to a loss of innervation to the sphincter pupillae). In a clinical setting, these two ptoses are fairly easy to distinguish. In addition to the blown pupil in a CNIII (oculomotor nerve) lesion, this ptosis is much more severe, occasionally occluding the whole eye. The ptosis of Horner syndrome can be quite mild or barely noticeable (partial ptosis).When anisocoria occurs and the examiner is unsure whether the abnormal pupil is the constricted or dilated one, if a one-sided ptosis is present then the abnormally sized pupil can be presumed to be on the side of the ptosis. History
The syndrome is named after Johann Friedrich Horner, the Swiss ophthalmologist who first described the syndrome in 1869. Several others had previously described cases, but "Horners syndrome" is most prevalent. In France and Italy, Claude Bernard is also eponymized with the condition (Claude Bernard–Horner syndrome, abbreviated CBH). In France, Francois Pourfour du Petit is also credited with describing this syndrome. Children
The most common causes in young children are birth trauma and a type of cancer called neuroblastoma. The cause of about a third of cases in children is unknown.
They are however a diagnosis of exclusion.Neurological conditions such as spinal cord injury, phrenic nerve injuries, Guillain–Barré syndrome, amyotrophic lateral sclerosis, multiple sclerosis and muscular dystrophy can all cause an individual to experience shortness of breath. Shortness of breath can also occur as a result of vocal cord dysfunction (VCD).Sarcoidosis is an inflammatory disease of unknown etiology that generally presents with dry cough, fatigue, and shortness of breath, although multiple organ systems may be affected, with involvement of sites such as the eyes, the skin and the joints. Pathophysiology
Different physiological pathways may lead to shortness of breath including via ASIC chemoreceptors, mechanoreceptors, and lung receptors.It is thought that three main components contribute to dyspnea: afferent signals, efferent signals, and central information processing. It is believed the central processing in the brain compares the afferent and efferent signals; and dyspnea results when a "mismatch" occurs between the two: such as when the need for ventilation (afferent signaling) is not being met by physical breathing (efferent signaling).Afferent signals are sensory neuronal signals that ascend to the brain. Afferent neurons significant in dyspnea arise from a large number of sources including the carotid bodies, medulla, lungs, and chest wall. Chemoreceptors in the carotid bodies and medulla supply information regarding the blood gas levels of O2, CO2  and H+. In the lungs, juxtacapillary (J) receptors are sensitive to pulmonary interstitial edema, while stretch receptors signal bronchoconstriction. Muscle spindles in the chest wall signal the stretch and tension of the respiratory muscles.