Location of Pupillomotor and Accommodation Fibres in the Oculomotor Nerve: Experimental Observations on Paralytic Mydriasis.

Hutchinson (1867-68) in his 'Lectures on compression of the brain' was the first to indicate that with an acutely expanding intracranial mass, the ipsilateral pupil frequently dilated and became unresponsive to light. This he attributed to compression of the third nerve. Von Bergmann (1880) and subsequently Macewen (1887) came to similar conclusions regarding the significance of paralytic mydriasis in determining on which side such lesions were to be found. These authors and most subsequent writers on the subject have favoured compression ofthe third nerve as the most likely mechanism. A number of reports over the years, however, have suggested another basis for this sign. Cushing (1908) expressed the view that compression of the cerebral hemisphere was responsible and that brief narrowing of the pupil preceded progressive mydriasis. Adrogue and Balado (1925) said that compression of some structure other than the third nerve should be considered, at least in some instances, since in their experimental and clinical studies the nerve occasionally showed no evidence of trauma. Schorcher (1937), on the basis of experimental and clinical data, stated categorically that compression of the oculomotor nerve was not a factor in the early phases of paralytic mydriasis and that irritation of sympathetic pathways in the brain-stem should be regarded as the predominant mechanism. Reid and Cone (1939) concluded that pressure on the third nerve was the cause of the dilated pupil and pointed out that because of the close association of pupilloconstrictor centres in the midbrain it was highly improbable that unilateral mydriasis would occur from pressure there. Nelson (1942) and Penfield and McEachern (1949), however, attributed paralytic mydriasis to compression of the brain-stem. Current opinion favours trauma to the third nerve, and among more recent studies sponsoring this view-