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Chapter 2 – Literature Review
Gait ataxia has also been identified in ET and is associated with
cerebellar dysfunction (Lundy-Ekman, 2007). Klebe, et al., (2005)
investigated gait ataxia in ET patients and how ingesting ethanol may
reduce this effect. After ingestion of alcohol ET participants showed a
significant improvement in gait measures, with no comparable change in
the control group. Klebe, et al. (2005) also noted that there was no
relation between levels of ataxia and self-rated severity of tremor. The
authors hypothesised that alcohol may have a mediatory effect on
cerebellar receptors or complex spike activity generated by the inferior
olive. It was also suggested that due to the ability of alcohol to alter the
ataxia it seemed more likely that ET reflects central dysfunction as
opposed to neural degeneration.
The inferior olive has been implicated as a possible oscillatory source of
ET, propagating though the olivocerebellar pathway and resulting in the
associated cerebellar dysfunctions noted in ET (Deuschl, Raethjen,
Lindemann, & Krack, 2001; R. J. Elble, 2009; Lorenz & Deuschl, 2007).
The olivocerebellar network may act to control motor timing and have a
role in motor correction (Llinás, 2009). Structurally, inhibitory afferent
impulses from the inferior olive travel via climbing fibres to Purkinje cells
found in the cerebellum (Velarde, Nekorkin, Makarov, Makarenko, &
Llinás, 2004). Inferior olive oscillatory activity is evoked by the action of
normal sodium and potassium conductors and three membranous ion
channels (Rothwell, 1998). These channels include a low threshold
calcium somatic membrane ion channel, a high threshold calcium
dendritic ion channel and a calcium-dependant potassium conductance
channel (Llinás, 2009; Rothwell, 1998; Velarde, et al., 2004). Olive
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