would be predicted from the nigrostriatal dopaminergic pathology associated with DLB (53). FP-CIT SPECT can also differentiate DLB from AD (54).
Scintigraphy with [123I]metaiodobenzyl guanidine (MIBG) enables quantification of postganglionic sympathetic cardiac innervation. Cardiac MIBG scanning can differentiate DLB (where the signal is reduced) from AD (where the signal is similar to control values) (55,56).
The electroencephalogram (EEG) is diffusely abnormal in over 90% of DLB patients. Early slowing of the dominant rhythm, with 4- to 7-Hz transient activity over the temporal lobe area, is characteristic and correlates with a clinical history of loss of consciousness (57). It is not possible to reliably differentiate DLB and AD subjects on the basis of the EEG, however (58). The diagnostic significance of bursts of bilateral frontal rhythmic delta activity, reported to be more common in DLB than AD, has yet to be established (59).
Multifocal action myoclonus, which occurs in approx 15% of DLB patients, is clinically more severe than that associated with PD, although it has the same electrophysiologcal characteristics. The balance of evidence favors a cortical source for the myoclonus (60). Since myoclonus also occurs in AD, it will be interesting to determine whether concomitant cortical Alzheimer's-type pathology influences the presence and severity of the myoclonus in Lewy body disorders.
DLB patients have fewer and abnormally delayed auditory startle responses (ASRs) of low amplitude and short duration in extremity muscles compared with healthy controls (61). Virtually no responses may be elicited in the lower limbs. Interestingly, the reduced ASR probability in advanced DLB is similar to that found in PD patients with postural instability and recurrent falls, suggesting a common brainstem pathophysiological mechanism for both disorders.
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