C. Butera

Churg Strauss syndrome presenting as acute neuropathy resembling Guillain Barré syndrome: case report.

JO N 3035 by rapidly progressive weakness of the lower limbs. She had a two year history of asthma and rhinitis with positive atopic tests for Parietaria and Dermatophagoides pteronyssinus (two of the most important pollen and house dust allergen sources); the year before she underwent surgical treatment for nasal polyposis. General examination was unremarkable, neurological examination revealed bilateral weakness of ankle dorsiflexion [right: Medical Research Council grade (MRC) 4, left: MRC 3], knee jerks were diminished and ankle jerks were absent. Joint position sense was markedly reduced in the feet and ankles (left > right). Lumbosacral MRI was normal. Nerve conduction studies (NCS) were normal in the upper limbs, while the lower limbs showed normal sensory action potentials (SAPs) and reduced amplitude of the left peroneal compound motor action potential (CMAP); F waves could not be elicited from left peroneal and tibial nerves. Cortical and spinal motor evoked potentials (MEPs) recorded from the left foot muscles were absent, while central and peripheral conduction times to the right foot muscles were normal Table 1). A working diagnosis of GBS was made. Intravenous immunoglobulin (IVIG) therapy was started. The next day motor examination revealed paralysis of the left leg distal muscles and marked weakness (MRC: 3) of the right leg distal muscles. Hematochemical investigations revealed: Hemoglobin: 11.1 g/dL, eosinophils 28 %, C-reactive protein: 31.4, absent antineutrophil cytoplasmic antibodies (ANCA). Chest-X-ray and CSF analysis were normal. Retrospective evaluation of nasal polyps histology revealed an eosinophilic infiltrate. A diagnosis of CSS was made, high-dose steroid therapy was started, with subsequent partial improvement of the neurologiNilo Riva Federica Cerri Calogera Butera Stefano Amadio Angelo Quattrini Raffaella Fazio Mauro Comola Giancarlo Comi

Sensory tricks and brain excitability in cervical dystonia: A transcranial magnetic stimulation study

Sensory tricks such as touching the face with fingertips often improve cervical dystonia [CD]. This study is to determine whether sensory tricks modulate motor cortex excitability, assessed by paired‐pulse transcranial magnetic stimulation [p‐pTMS].

P6.6 Effect of sensory tricks on brain excitability in cervical dystonia: TMS study

controls and remained so (except for CV) after DBS. The postoperative Low Frequency (LF) band was lower than the preoperative and the controls’ LF. A significant decrease in Total Power (TP) in the patients after the implantation as opposed to controls was also noted. Pre and post DBS values of High Frequency (HF) band and ratio LF/HF were not significant different. Conclusions: Unlike motor improvement, DBS does not offer a clear benefit to cardiovascular dysautonomia. The reduced postoperative LF, an index of sympathetic activity, might be explained by the LEDD reduction.

62. Sensory Tricks in cervical dystonia: A neurophysiological study with short latency afferent inhibition

A classic hallmark of cervical dystonia (CD) is the improvement of dystonic symptoms during a specific maneuver, defined ‘sensory trick’ (ST). Even if the mechanism by which ST improves dystonia is not well understood, it is likely that cortical sensorimotor integration processes are involved. In a previous preliminary study, we evaluated the short latency afferent inhibition (SAI) in a group of CD patients and the effects of ST on the SAI profile. To date, we have increased our sample including 28 patients with primary CD (18 with ST, CD+, and 10 without ST, CD-) and 11 controls. The analysis of variance showed no significant differences between CD- patients and controls. On the contrary, a remarkable trend toward a reduced SAI was observed in CD+ patients when they did not perform ST. Interestingly, SAI was further reduced in CD+ patients when they performed ST, reaching a strong statistical relevance. Our results show the presence of an abnormal sensorimotor integration in CD+ patients. Furthermore, they prove that ST acts by modulating the abnormal link between sensory input and motor output.