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Neurophysiol Clin (1990) 20, S, 85s 87s © Elsevier, Paris 85s Communications affich4es Posters SESSION 14 Stimulation corticale Brain stimulation P140 TRANSCRANIAL MAGNETIC STIMULATION OF THE FACIAL NERVE IN PATIENTS WITH BELL'S PALSY I.Rimpil~inen (i), J, Laranne (2), E. Eskola (i), V. K. H~kkinen (i), P. Karma (2). Dept. of Clinical Neurophysiology (i), and Dept. of Otolaryngology (2), Tampere University central Hospital, SF-33520 Tampere, Finland Transcranial magnetic stimulation (TMS) provides access to intracranial stimulation of cranial nerves. The stimulation of the nerve takes place on its course between the brain stem and the meatus acousticus interna. Seventy eight patients with acute Bell's palsy were examined. TMS to the proximal part of the facial nerve was delivered on each side with the coil center positioned parietally. Conventional electric extracranial facial nerve stimuli were given near the stylomastoid foramen. Motor evoked potentials were recorded on the nasolabial fold, which according to our experience, reveals the most distinguished responses. The patients could be divided into four different groups according to achieved responses. In the first group (30 patients) there were abnormal electrically induced responses on the affected side (amplitude 1.0 ± 0.9 mV, latency 4.1 ± 0,4 ms) and the responses on magnetic stimulation were not elicitable. In the second group of patients (no - 8) the magnetically evoked responses could not be evoked on the paralyzed side but the electric responses did not significantly differ from that on the healthy side. In eight patient neither electric nor magnetic could produce motor responses on the affected side. The fourth group consisted of 32 patients in whom both the electrically and magnetically evoked motor responses could be elicited (amplitude 1.3 ~ 0.9 mV and 0.5 ± 0.4 mV , latency 4.4 ± 0.5 ms and 4.8 ± 0.7 ms, respectively). Motor evoked responses with TMS of the facial nerve could be evoked in 41 % of the patients with acute Bell's palsy, indicating nerve conduction through the affected site of nerve lesion in the bony canal of facial nerve. Of the patients, 59% showed total conduction block with varying degree of nerve degeneration as indicated with electric stimuli distal to the site of nerve lesion. PI41 MAGNETIC STIMULATION OF MOTOR CORTEX IN THE DEMENTIA OF ALZHEIMER TYPE. G. Galardi, S. Amadio, M. ALberoni, M. Franceschi, G. Comi. Department of Neurology - Scientific Institute H San Raffaele University of Milan - Via Olgettina, 60 - 20132 Milan - Italy Motor disturbancies in dementia of Alzheimer type are usually considered absent or mostly related only to the late stage of the disease, in spite of the findings of neuronal and neurotransmitter loss in midfrontal cortex. In this study we have quantified the involvement of the central nervous system considering motor evoked potentials by Magnetic Stimulation in 20 patients with diagnosis of Alzheimer Disease according to NINCDS-ADRDA criteria (McKhann et al, 1984). Patients age was between 55 and 86 years and the disease was lasting between 1 and 8 years. Right and left motor cortex responses were recorded from abductor pollicis brevis. The following parameters were taken into account; I) cortical excitability threshold (as percentage of the highest intensity of the magnetic field - 1.9T) with and without muscle contraction; 2) central motor conduction time; 3) morphology of motor responses. Nine of our patients showed an increase of cortical excitability threshold (bejond the normal mean value +3 S.D.) motor threshold was abnormal bilaterally in four and unilaterally in five cases. In four patients the elevation Of motor threshold was associated to an increase of the central motor conduction time. Absence or poor definition or motor evoked responses was frequently observed. Results of this study suggest an involvement of motor cortex in patients with Alzheimer disease. The possible pathophysio- logic mechanisms will be discussed.

P141 Magnetic stimulation of motor cortex in the dementia of Alzheimer type

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Page 1: P141 Magnetic stimulation of motor cortex in the dementia of Alzheimer type

Neurophysiol Clin (1990) 20, S, 85s 87s © Elsevier, Paris

85s

Communications affich4es Posters

SESSION 14

Stimulation corticale Brain stimulation

P140

TRANSCRANIAL MAGNETIC STIMULATION OF THE FACIAL NERVE IN PATIENTS WITH BELL'S PALSY

I.Rimpil~inen (i), J, Laranne (2), E. Eskola (i), V. K. H~kkinen (i), P. Karma (2). Dept. of Clinical Neurophysiology (i), and Dept. of Otolaryngology (2), Tampere University central Hospital, SF-33520 Tampere, Finland

Transcranial magnetic stimulation (TMS) provides access to intracranial stimulation of cranial nerves. The stimulation of the nerve takes place on its course between the brain stem and the meatus acousticus interna. Seventy eight patients with acute Bell's palsy were examined. TMS to the proximal part of the facial nerve was delivered on each side with the coil center positioned parietally. Conventional electric extracranial facial nerve stimuli were given near the stylomastoid foramen. Motor evoked potentials were recorded on the nasolabial fold, which according to our experience, reveals the most distinguished responses.

The patients could be divided into four different groups according to achieved responses. In the first group (30 patients) there were abnormal electrically induced responses on

the affected side (amplitude 1.0 ± 0.9 mV, latency 4.1 ± 0,4 ms) and the responses on magnetic stimulation were not elicitable. In the second group of patients (no - 8) the magnetically evoked responses could not be evoked on the paralyzed side but the electric responses did not significantly differ from that on the healthy side. In eight patient neither electric nor magnetic could produce motor responses on the affected side. The fourth group consisted of 32 patients in whom both the electrically and magnetically evoked motor responses could be elicited (amplitude 1.3 ~ 0.9 mV and 0.5 ± 0.4 mV , latency 4.4 ± 0.5 ms and 4.8 ± 0.7 ms, respectively).

Motor evoked responses with TMS of the facial nerve could be evoked in 41 % of the patients with acute Bell's palsy, indicating nerve conduction through the affected site of nerve lesion in the bony canal of facial nerve. Of the patients, 59% showed total conduction block with varying degree of nerve degeneration as indicated with electric stimuli distal to the site of nerve lesion.

PI41

MAGNETIC STIMULATION OF MOTOR CORTEX IN THE DEMENTIA OF ALZHEIMER TYPE. G. Galardi, S. Amadio, M. ALberoni, M. Franceschi, G. Comi. Department of Neurology - Scient i f ic Inst i tute H San Raffaele University of Milan - Via Olgettina, 60 - 20132 Milan - I t a l y

Motor disturbancies in dementia of Alzheimer type are usually considered absent or mostly related only to the late stage of the disease, in spite of the findings of neuronal and neurotransmitter loss in midfrontal cortex. In this study we have quantified the involvement of the central nervous system considering motor evoked potentials by Magnetic Stimulation in 20 patients with diagnosis of Alzheimer Disease according to NINCDS-ADRDA cr i te r ia (McKhann et al , 1984). Patients age was between 55 and 86 years and the disease was lasting between 1 and 8 years. Right and l e f t motor cortex responses were recorded from abductor pol l ic is brevis. The following parameters were taken into account; I ) cortical exc i tab i l i ty threshold (as percentage of the

highest intensity of the magnetic f ie ld - 1.9T) with and without muscle contraction;

2) central motor conduction time; 3) morphology of motor responses. Nine of our patients showed an increase of cortical exc i tab i l i t y threshold (bejond the normal mean value +3 S.D.) motor threshold was abnormal b i la te ra l ly in four and uni la tera l ly in f ive cases. In four patients the elevation Of motor threshold was associated to an increase of the central motor conduction time. Absence or poor def in i t ion or motor evoked responses was frequently observed. Results of this study suggest an involvement of motor cortex in patients with Alzheimer disease. The possible pathophysio- logic mechanisms wil l be discussed.