Expanding lesions of the temporal fossa.

Brain-stem Compression Expanding lesions in the temporal fossa readily displace the brain-stem towards the opposite side where it is forced against the edge of the tentorium. At the same time a wedge formed by the uncus and hippocampal gyrus is forced downward between the midbrain and the edge of the tentorium on the side of the lesion (Fig. i). These two mechanisms produce the various stages of midbrain compression. The downward herniation of the uncus and hippocampal gyrus also compresses the homolateral oculomotor nerve. Rarely the ncrve is at first stimulated and therefore the pupil is constricted, but as pressure on the nerve increases paralysis ensues and the pupil becomes dilated. Usually, however, the pupil dilates as soon as the nerve is compressed. If the patient is conscious, ptosis and paralysis of the external ocular muscles supplied by the oculomotor nerve may be observed. The posterior cerebral artery prolapses through the tentorial notch with the herniated brain and occasionally a contralateral homonymous hemianopia is produced by kinking of the artery or its calcarine branch over the free edge of the tentorium. Increased intracranial pressure is produced by expansion of the lesion itself, pressure on the midbrain and consequent obstruction of the aqueduct of Sylvius, and often also by associated cerebral oedema. The increasing pressure, if not too rapid, may produce papilloedema. It also causes descent of the brain-stem through the tentorial opening sometimes resulting in sufficient traction on one or both abducens nerves to cause unilateral or bilateral external rectus palsy. If descent of the brain-stem continues, ' coning' of the cerebellar tonsils occurs at the foramen magnum and compression of the medulla oblongata results. Midbrain compression may be roughly classified into the following stages: Stage i. Clouding of consciousness, normal pupils or occasionally contraction of the pupil on :ii.ii$iiliiiri;