References of "Electroencephalography and Clinical Neurophysiology"
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See detailMotor and somatosensory evoked potentials in cervical spondylotic myelopathy
MAERTENS DE NOORDHOUT, Alain ULg; MYRESSIOTIS, Sophie ULg; DELVAUX, Valérie ULg et al

in Electroencephalography and Clinical Neurophysiology (1998), 108

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See detailNumber and relative size of thenar motor units in ALS patients: application of the adapted multiple point stimulation method.
Wang, François-Charles ULg; Delwaide, Paul ULg

in Electroencephalography and Clinical Neurophysiology (1998), 109(1), 36-43

In the present study, the adapted multiple point stimulation (AMPS) method was first applied to median innervated thenar muscles in 22 amyotrophic lateral sclerosis (ALS) patients who did not received any ... [more ▼]

In the present study, the adapted multiple point stimulation (AMPS) method was first applied to median innervated thenar muscles in 22 amyotrophic lateral sclerosis (ALS) patients who did not received any treatment. In all patients, a motor unit number estimate (MUNE) and an average surface-recorded motor unit action potential (S-MUAP) size have been derived even if the denervation was severe; and the results were reproducible. The thenar MUNE was less than the normal lower limit for age in 17 patients, and the mean MUNE (67.1 +/- 90.6) was significantly different from that estimated in control subjects (263.3 +/- 116.8). The mean S-MUAP size in the 22 ALS patients was 352.9 +/- 328.4 microV x ms versus 94.1 +/- 30.3 microV x ms in healthy volunteers. A control AMPS was achieved in 8 patients after 2 and 6 months of a glutamate-release antagonist (riluzole) treatment. The mean loss of motor units, based on control thenar MUNEs realized after 6 months of treatment, was 53%. In conclusion, we propose AMPS as a manageable, reproducible and non-invasive procedure which permits one to quantify peripheral denervation and to appreciate the effectiveness of collateral reinnervation in ALS patients. [less ▲]

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See detailCatecholaminergic function and P300 amplitude in major depressive disorder (P300 and catecholamines).
Hansenne, Michel ULg; Pitchot, William ULg; Gonzalez Moreno, A. et al

in Electroencephalography and Clinical Neurophysiology (1995), 96(2), 194-6

The neurobiology of P300 is still a subject of controversy. P300 amplitude appears to be modulated by multiple neurotransmitter systems, especially dopaminergic, noradrenergic as well as cholinergic and ... [more ▼]

The neurobiology of P300 is still a subject of controversy. P300 amplitude appears to be modulated by multiple neurotransmitter systems, especially dopaminergic, noradrenergic as well as cholinergic and GABAergic. In this study, we investigated the relationship between P300 amplitude and catecholaminergic neurotransmission as assessed by the growth hormone (GH) response to clonidine and apomorphine challenges in 20 major depressive patients. Results showed a correlation of P300 amplitude with the apomorphine test (r = 0.54; P = 0.01), but not with the clonidine test (r = 0.22; NS). This study supports a role for dopamine in the neurobiological modulation of P300 amplitude. [less ▲]

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See detailCatecholaminergic function and P300 amplitude in major depressive disorders.
Hansenne, Michel ULg; PITCHOT, William ULg; Gonzalez Moreno, Antonio et al

in Electroencephalography and Clinical Neurophysiology (1995)

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See detailPercutaneous Magnetic Stimulation of the Motor Cortex in Migraine
MAERTENS DE NOORDHOUT, Alain ULg; Pepin, Jean-Louis ULg; Schoenen, Jean ULg et al

in Electroencephalography and Clinical Neurophysiology (1992), 85(2), 110-5

We have used transcranial magnetic stimulation of the motor cortex interictally in 12 patients with unilateral classic migraine with sensorimotor auras and 10 patients with common migraine and unilateral ... [more ▼]

We have used transcranial magnetic stimulation of the motor cortex interictally in 12 patients with unilateral classic migraine with sensorimotor auras and 10 patients with common migraine and unilateral headache. In classic migraine, the threshold of activation of the FDI muscle by the cortical stimulus was significantly increased on the side of the auras, when compared to the unaffected side (P less than 0.01) and to normal subjects (P less than 0.01). The amplitude of EMG responses was also reduced in FDI on the affected side when compared to normals (P less than 0.02). Responses obtained in common migraine patients were normal on both sides. We suggest that some permanent subclinical dysfunction of the motor cortex might play a role in the pathogenesis of attacks of classic migraine with sensorimotor auras. [less ▲]

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