Page 134 - Migraine, the heart and the brain

Chapter 7
individuals suffering from impaired pegboard performance might accidently show ischaemic lesions in both the cerebellum and supratentorial regions (possibly even including whitematter lesions). Such a hypothesis would be compatible with ndings by Brighina and colleagues (7), who found in MA patients a signi cant de cit in cerebellar inhibition of cerebral cortical processing following conditioning with transcranial magnetic stimulation. However, several of the migraine patients with both cerebellar and supratentorial lesions had a good score on the pegboard task (supplemental table), whereas many with a bad score had no signs of cerebral cortical lesions. Studies at even higher MRI resolution and including even larger numbers of patients with possibly even more speci c tests and multivariate lesion symptom mapping approaches might help to resolve this issue (40).
Cerebellar function in FHM1
In contrast to migraine patients, FHM1 patients showed impaired cerebellar function with signi cant differences for all primary and most secondary outcome measures of all ve cerebellar function tests. As our group of FHM1 patients was small (n =13) and their average age was about 15 years younger (Table 1), the differences we found are likely to underestimate the true difference with non-hemiplegic migraine patients and controls. Our test ndings were in line with the ndings on physical examination and are in agreement with other studies on gural memory and executive function in FHM1 patients (41). Body-sway in FHM1 patients was particularly increased in the anterior-posterior direction, which is in line with ndings in spinocerebellar ataxia patients (42). The symptoms of impaired motor and non-motor cerebellar function in FHM1 patients probably initially result directly from a different calcium influx in their Purkinje cells, the simple spike output of which is highly irregular early on (43,44). These electrophysiological aberrations have been shown to be suf cient to cause ataxia (43,45,46), but they will also induce changes in energy consumption and contribute to cerebellar degeneration over time (47,48). Thus, the combination of these pathophysiological mechanisms following the FHM1 CACNA1A mutation increasingly affects the capabilities for motor learning and consolidation, and ultimately leads to motor performance problems and overt signs of ataxia (45). However, as we did not have (recent) MRI imaging of most FHM1 patients, any effect of possible macroscopical structural lesions on cerebellar function can also not be ruled out.
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