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Several structures, located at different levels in the Central Nervous System (CNS), collaborate to the control and realization of ocular movements (O.M.) Therefore, alterations of oculomotricity, of varying degree and of different kinds, may be found in a lot of diseases of the CNS. The study of O.M., expecially when carried out by means of specific techniques such as electro-oculography, may represent an useful tool in the diagnosis (both from a topographic and an etiological standpoint) and in the follow-up of patients, possibly also allowing a precise evaluation of therapy effectiveness. In this review the Authors briefly examine the role of the supranuclear structures mostly involved in the control and in the execution of oculomotricity and the characteristics of the different types of O.M. (rapid and slow, vergence movements). Successively, they analyze the semeiological features of supra-nuclear disturbances of O.M., describing alterations of saccadic movements (slowing, dysmetria) and of smooth pursuit, fixation instability (square waves, flutter, opsoclonus, nystagmus,...) and other alterations of O.M. (ocular bobbing, see-saw nystagmus, skew deviation,...). Successively, disturbances of O.M. are analyzed in relation to their topodiagnostic significance, describing oculomotor involvements due to focal lesions of different areas of CNS (frontal cortex, parieto-occipital cortex, basal ganglia, cerebellum, brainstem) and particular syndromes (Foville syndromes, locked-in syndrome, Parinaud syndrome, anterior internuclear ophthalmoplegia, "one and a half" syndrome, Balint syndrome,...). Finally, particular attention is drawn to the oculomotor disturbances observed in degenerative cerebellar and multisystemic diseases, and several abnormal "oculomotor patterns", which seem to be specifically related to particular diseases, are described. In particular, the oculomotor patterns of Steele-Richardson-Olszewsky disease (slowing and hypometria of horizontal saccades, loss of upward saccades with preservation of reflex movements) and of Friedreich ataxia (fixation instability mostly due to the occurrence of square waves, saccadic dysmetria, impairment of smooth pursuit) are stressed.

Cerebral toxoplasmosis is the most common cause of focal CNS disease complicating AIDS and may afflict 10% to 33% of such patients. We present the clinical, neuroradiological and immunological findings in 5 cases with cerebral toxoplasmosis complicating the acquired immune deficiency syndrome. All patients had focal neurological signs and symptoms; CT scan findings included single or multiple lesions with ring contrast enhancement, mass effect and oedema. CSF analysis showed increased protein levels, decreased glucose levels and pleocytosis; CSF IgG antitoxoplasma antibodies were positive in 4 patients; serum IgG antitoxoplasma antibodies were positive in all patients, while IgM resulted always negative in serum and in CSF. After therapy, in 2 cases CT scans showed small areas of encephalomalacia replacing the abscesses. We think that non-invasive techniques (CT scans, CSF and serum immunochemical tests) together with the finding of a favourable response to therapy may be useful for the diagnosis of cerebral toxoplasmosis, allowing to avoid invasive technique such as cerebral biopsy.

Employing optical density methods, platelet aggregation in response to increasing concentration of ADP was tested in 24 patients with migraine and 15 controls. The migraine patients don't demonstrate platelet hyperaggregability when compared with controls. Platelet aggregate ratio (P.A.R.) was measured in 13 patients and 15 controls by the method of Wu and Hoak: a significant difference was found between and controls. The hyperaggregability found here, even if only for the P.A.R., may help explain the increased incidence of stroke and heart attack in migraine patients that has been reported elsewhere.

Central nervous system diseases occur frequently in patients with AIDS. From 20 to 40% of all these patients develop neurological symptoms and in about 10% of AIDS patients the onset of the disease is characterized by neurological symptoms. These may be related to primary HIV infection or to any of a large number of opportunistic viral and non-viral infections. Moreover, the observation of multiple central nervous system infections is frequent, making the diagnosis difficult. AIDS-related opportunistic infections of the central nervous system are discussed, presenting both a review of the literature and several case reports.