Guillain-Barré syndrome (GBS) in spinal nerves and we read their previous studies with great interest. 3 Gallardo et al showed involvement of spinal nerves with electrophysiologic, ultrasonographic, and pathologic findings in patients with early GBS. 3 Correspondingly, magnetic resonance imaging (MRI) of our patient using short-tau inversion recovery (STIR) sequences showed edema of the spinal nerves and corresponding rami, demonstrating proximal demyelination. MRI using post-contrast T1 sequences helps to demonstrate the topography of nerve root enhancement in GBS, but it is not applicable to patients with kidney failure or contrast allergies. 4 We think that adding coronal STIR sequences to the imaging protocol is a useful method for the detection inflammatory edema of nerve roots and plexus. In STIR sequences, all structures with short T1 relaxation times are suppressed, whereas structures with high water content show a bright signal on a dark background and demonstrate the swollen spinal nerves and corresponding rami. The coronal plane is the most valuable plane in STIR images, because it demonstrates anatomic structures including proximal nerve segments in a familiar perspective. 5 Late-response alterations (F wave and H reflex) are the most common early electrophysiologic findings supporting proximal demyelination in early GBS. 6,7 In our case, the increased chronodispersion and decreased persistence of F waves in the median and ulnar nerves can be caused by demyelination in any segment of the peripheral nerve, because nerve conduction studies revealed conduction blocks of median and ulnar nerves in the wrist-elbow segment, and STIR images showed involvement of proximal nerve segments. More investigations with electrophysiologic, radiologic, and pathologic studies will help further our understanding of the pathophysiologic mechanisms of GBS and elucidate therapeutic strategies.

There are no studies on event-related cognitive potentials in frontotemporal dementia (FTD). In order to evaluate the aptitude and usefulness of the event-related P300 potential in this disease, we prospectively examined 60 cases: 11 patients with FTD diagnosed according to the Lund and Manchester criteria and Neary consensus criteria, 33 patients with a probable Alzheimer’s disease diagnosis following NINCDS-ADRDA criteria, and 16 normal controls. P300 latency, amplitude and reaction time were recorded using an auditory oddball paradigm. In this sample, P300 potential could be reliably performed by 10/11 FTD patients, notwithstanding their language or executive function deficiencies. The FTD group P300 mean latency was midway between the normal controls and the Alzheimer’s disease group (ANOVA F_2, 74199 = 16.5; p = 0.00003). The latency range of the FTD patients were within normal values (average plus 1.96 standard deviation of the values of the control group), except for one case with a latency of 448 ms. Post hoc Newman-Keuls analysis showed that the P300 latencies of the control and FTD groups did not differ significantly (p = 0.15) and that the Alzheimer’s disease group had a delayed P300 latency that differed significantly from that of the FTD (p = 0.002) and control group (p = 0.0002). However, there was overlapping in P300 latency values of the three groups. Despite these differences in latencies, the reaction time was significantly increased in the FTD and the Alzheimer’s disease groups. These findings indicate that the P300 potential is less affected in patients with FTD than those with Alzheimer’s disease. This fact could aid in FTD diagnosis, differential diagnosis with Alzheimer’s disease and possibly its clinical management.

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