Crossed cerebellar diaschisis.

The term "diaschisis," as originally used by Von-Monakow (1), implies an immediate decrease in neuronal activity in a region due to an interruption of its afferent axonal supply. Experimental studies, in animals , of unilateral ischemia in which neuronal function in the contralateral hemisphere was demonstrated to be impaired, provided evidence for such a mechanism (2). The corpus callosum appeared to play a role in this process. Changes in cerebral blood flow in the hemisphere opposite a cerebral infarction were first demonstrated by Kempinsky et al in 1961 (3), and Hoedt-Rasmussen and Skinhoj in 1964 (4). Several theories have been proposed to explain these remote alterations in blood flow, postulating neurogenic, vasogenic, and chemical mechanisms (3-1 0). The remote blood flow changes observed, according to the neurogenic theory, are presumed to be secondary to metabolic alterations produced by the decreased axonal input to the region. Such decreased metabolism in the nonischemic hemisphere and in the contralateral cerebellum of patients with infarcts has been documented (8, 11-13). Little data is available concerning the time course of these cerebral blood flow changes in the nonischemic hemisphere. -A. progressive decline in cerebral blood flow in the nonischemic hemisphere has been observed during the first week after an acute infarction (14). This decline in flow could be partially explained by a loss of autoregulation, but suggested a process more complex than destruction of axonal afferents to the nonischemic region. Vasoactive substances released from ischemic tissue have been postulated to play a role in these remote effects (15). Experimental data have demonstrated the release of vasoactive substances and neurotransmitters from infarcted brain (16). While the release of such vasoactive substances might play a role in a more generalized depression of flow and metabolism, the more focal effects seen in the cerebellar hemisphere contralateral to various types of lesions make this less likely to be an important factor in the production of crossed cerebellar diaschisis. Crossed cerebellar diaschisis has been observed not only following cerebral ischemic events (12, 13), but in patients with brain tumors (13, 17) and following the injection of intracarotid sodium Amytal (18). One of the earliest studies demonstrating the importance of the pathways between the cerebrum and cerebellum on the function of the latter was that of von Monakow in 1885 in which he noted hypoplasia of the contralateral cerebellar hemisphere following experimental cortical ablation (19). In the clinical literature, one of the earliest reports of similar findings was that of Hassin in 1935, in which atrophy of the contralateral cerebellum was observed in a patient with cerebral atrophy secondary to presumed birth injury (20). Ataxic hemiparesis (21) and other ataxic syndromes have been noted secondary to cortical insults (22, 23). False localized limb ataxia has been found to occur contralateral to cerebral tumors located either anteriorly or posteriorly in the cerebral hemispheres (24). Although such syndromes have been considered to occur mainly from contralateral frontal lesions (25), they also occur with lesions limited to the parietal lobe (22). The cerebellum has a significant input from the cerebral hemispheres, the bulk of which is contained in the cortico-ponto-cerebellar pathway (26). This pathway arises in the motor, premotor, parietal association, and occipital cortices (27). Other cerebro-cerebellar connections are relayed through the inferior olive and reticular formation (28). The contribution of different regions of the cortex to the cortico-ponto-cerebellar pathway varies in different species. Parietal areas project most heavily to the cerebellum in the cat