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Chapter 2 – Literature Review<br />
difficulties surround the ability to identify the pathology of ET including<br />
varying classifications, misdiagnosis and inadequate controls (R. J. Elble,<br />
2009; Lorenz & Deuschl, 2007). Furthermore, it is often difficult to<br />
separate effects of co-morbidities and general aging from ET on the<br />
neural system (Deuschl & Elble, 2009).<br />
Pathophysiology - Neural dysfunction<br />
Neural dysfunction can be thought of as comprising two subgroups, that<br />
of a central and peripheral pathology. Central pathology in this review<br />
examines alterations occurring in ET that relate to central areas such as<br />
that of the cerebellum or inferior olive while peripheral pathology<br />
identifies the influence of stretch reflex and motor unit entrainment in<br />
ET.<br />
Central pathology<br />
ET typically exhibits a kinetic tremor of 4-12Hz (E. Louis, 2005). Various<br />
possible sources for this oscillation have been suggested including the<br />
cerebellarthalamocortical pathway and olivocerebellar pathway (R. J.<br />
Elble, 2009; Pinto, Lang, & Chen, 2003).<br />
The possible involvement of the cerebellum in the pathology of ET has<br />
been identified through the use of imaging tools such as Positron<br />
Emission Tomography (PET), dysfunction in tasks related to cerebellar<br />
function (Trillenberg, et al., 2006), the disappearance of tremor after<br />
cerebellar stroke (Pagan, Butman, Dambrosia, & Hallett, 2003) and the<br />
use of DBS to successfully treat tremor (Jenkins, et al., 1993; Yu &<br />
Neimat, 2008). Jenkins, et al. (1993) assessed 11 ET patients and 8<br />
10