Different criteria in the assessment of visuospatial neglect.

mg/kg). Endotracheal intubation was performed during muscle relaxation with pancuronium (01 mg/kg). Anaesthesia was maintained with nitrous oxide, oxygen, and isoflurane (0-7-1-2%). Case 1 was a 51 year old man who, since 1986, had had a progressive spastic paraparesis and who complained of cervicobrachial pain. Neuroradiological investigations showed cervical spondylosis with a narrow canal from C3 to C7. The patient underwent a C3-C7 posterior laminectomy. After operation he complained of weakness and paraesthesiae in both hands. Motor and sensory functions in the arms were restored after three to four weeks. Before laminectomy, the potential recorded epidurally at Cv5 after median nerve stimulation was characterised by a normnal P10 followed by an Nil wave with a peak latency of 12-3 ms, and an N13 wave at 13 -9 ms. Amplitude (P1O-N13: 12 X8,pv) and waveform were normal. After laminectomy, the disappearance of the N13 wave was noticed. The P10 and N 1l waves were unchanged (figure). Case 2 was a 56 year old man who presented in 1984 with progressive spastic tetraparesis and hypoaesthesia below C4. An MRI of the cervical spine showed spondylotic stenosis of the canal from C3 to C5. He underwent a C3-C5 posterior laminectomy. After operation, he showed a transient (seven days) decrease of motor performance in the distal segments of the arms. Before laminectomy, the potential evoked by median nerve stimulation at Cv5 consisted of a slightly delayed PlO (peak latency: 11-2 ms), Nl (peak latency: 13-6 ms), N13 (latency: 14-9 ms), followed by a slow positive wave (P18 at 25-8 ms). Amplitude (P10-N13: 15 pv) and waveform were normal. After laminectomy a decreased amplitude (P10-N13: 10-7 pv) and a longer duration (I1-8 ms v a prelaminectomy value of 4 ms duration) of the main negative wave (N13) were evident (figure). Case 3 was a 67 year old man with spastic tetraparesis and hypoaesthesia of both hands. Cervical MRI showed a multisegmental spondylosis from C4 to C7. The patient underwent a C3-C7 posterior laminectomy. After operation a transient (four weeks) increase of the paresis and hypoaesthesia of upper extremities was evident. Before laminectomy, the epidural evoked potentials consisted of a slightly delayed P10 (peak latency 11i3 ms) followed by a negative wave peaking at 14 ms. The amplitude was normal from ThI to Cv6 (P1ON13: 10 ,uv), whereas it was decreased above Cv5-6 (PI0-N13 at Cv5-6: 5 puv). After laminectomy a decrease in amplitude or disappearance of the main negative wave (N13) was evident (figure). In these three cases, laminectomy was followed by an alteration in the postsynaptic component (N13) of the median nerve evoked potential, whereas the root component (NI 1) was unchanged.2 This is consistent with grey matter damage. The genesis of this damage is probably a vascular insult in an already hypoperfused area.34 Indeed, in cervical spondylotic myelopathy the osteophytic process may impinge on the anterior spinal artery and cause hypoperfusion with loss of the haemodynamic autoregulation in the spinal cord watershed areas.5 The decompression by posterior laminectomy may increase the blood supply, but as a consequence of the previously mentioned loss of haemodynamic autoregulation, it may cause hyperaemia in these areas and induce the paradoxal effect of a further ischaemia. Other mechanisms of damage such as cervical spine instability, a local concussion of the cord, or a temporary oedema caused by mechanical interference, cannot be excluded. In conclusion, this neurophysiological study shows that neurological deterioration after posterior laminectomy in these patients was due to grey matter damage and not to nerve root stretching. It is important to stress that the damage reversed spontaneously. B CIONI M MEGLIO L PENTIMALU M VISOCCHI Istituto di Neurochirurgia, Universita Cattolica, Roma, Italy