Entrapment partly participates in the longitudinal progression of neuropathy with anti-MAG antibodies.

Neuropathy with anti-myelin-associated glycoprotein (MAG) antibodies commonly demonstrates distal-dominant prolongation of nerve conduction. However, recent electrophysiological studies have shown that distal motor demyelination is not always a distinct feature. We aimed to elucidate whether the longitudinal progression of nerve impairment occurs in a distal-dominant manner. Seven patients with neuropathy with anti-MAG antibodies were enrolled. Sequential nerve conduction studies revealed nerve conduction reduction only at the wrist segment in the median nerve of the patients, but not in the ulnar nerve. Median nerve entrapment at the wrist may play a role in longitudinal disease progression in neuropathy with anti-MAG antibodies.

Somatosensory-evoked cortical potential during attacks of paroxysmal dysesthesia in multiple sclerosis.

Paroxysmal dysesthesia is considered to be one of the characteristic symptoms of multiple sclerosis (MS), but the lesion responsible and the pathophysiology of this dysesthesia are not known. We report the interesting finding of somatosensory-evoked potentials (SEPs) in a patient with MS during a paroxysmal dysesthesia attack.

High voltage electrical stimulation of the proximal hypoglossal nerve in normal subjects.

OBJECTIVES: It is often difficult to stimulate the proximal hypoglossal nerve by magnetic occipital stimulation, even in normal subjects. Therefore, we tested an improved method of stimulating the proximal hypoglossal nerve, using high voltage electrical stimulation. METHODS: The proximal hypoglossal nerve was activated by high voltage electrical stimulation using surface electrodes over the occipital skull. The compound muscle action potential (CMAP) was recorded from the lingual muscles using surface electrodes in 10 normal subjects. CMAP and F waves produced by distal hypoglossal nerve stimulation and motor evoked potentials produced by transcranial magnetic stimulation were also recorded. RESULTS: When the anode electrode was placed at the mastoid process and the cathode below the inion, the unilateral proximal hypoglossal nerve was readily stimulated supramaximally in all the subjects. The CMAP latency was the same as that obtained with magnetic occipital stimulation. The central motor conduction time (CMCT) calculated from the proximal CMAP was 4.1+/-0.4 ms in the contralateral corticobulbar tract and 4.4+/-0.4 ms in the ipsilateral. The CMCT calculated from the minimal F wave latency was 3.3+/-0.2 ms. CONCLUSIONS: The high voltage electrical stimulation is a useful method for stimulating the proximal hypoglossal nerve to estimate the CMCT of the corticobulbar tract.

Role of the ipsilateral motor cortex in mirror movements.

The mechanism of mirror movements in two patients was investigated; one with congenital mirror movement, the other with schizencephaly. Transcranial magnetic stimulation on one side elicited motor evoked potentials (MEPs) in their thenar muscles on both sides with almost the same latencies, minimal thresholds, and cortical topographies. During voluntary contraction of the thenar muscle on one side, contralateral transcranial magnetic stimulation induced a silent period not only on the voluntary contraction side but on the mirror movement side and of the same duration. By contrast, ipsilateral transcranial magnetic stimulation elicited MEPs without silent periods in both muscles. With intended unilateral finger movements, an H2(15)O-PET activation study showed that the regional cerebral blood flow increased predominantly in the contralateral sensorimotor cortex, as seen in normal subjects, although mirror movements occurred. It is considered that the ipsilateral motor cortex plays a major part in the generation of mirror movements, which may be induced through the ipsilateral uncrossed corticospinal tract.

Central pathway of photic reflex myoclonus.

Direct, new evidence for the cortical origin of photic reflex myoclonus in a patient with "posterior cortical atrophy" is provided. Photic stimulation elicited myoclonic jerks in the right upper limb muscles. An H2(15)O-PET activation study with photic stimulation showed increased regional cerebral blood flow not only in both striate cortices but in the left premotor and primary motor areas as well. Transcranial magnetic stimulation over the area of the left occipital cortex elicited motor evoked potentials in the right upper limb muscles. It is concluded that in the central pathway of photic reflex myoclonus the contralateral occipital cortex is activated first, then the impulses propagate intrahemispherically to the primary motor cortex, to elicit myoclonic jerks.

The F wave disappears due to impaired excitability of motor neurons or proximal axons in inflammatory demyelinating neuropathies.

OBJECTIVES: Investigation of pathophysiology of F wave disappearance in demyelinating neuropathies. METHODS: The peripheral motor nerve conduction was studied by motor evoked potential (MEP) on transcranial magnetic stimulation as well as conventional nerve conduction studies before and after the treatment in 26 patients with inflammatory demyelinating neuropathies. In addition, serum antiganglioside antibodies in the acute or active stage were examined. RESULTS: The F wave was abolished in 10 patients. Seven of the 10 patients showed motor evoked potentials (MEPs) on transcranial magnetic stimulation that ranged from 1-4 mV. In six of them the F wave reappeared in the recovery stage, but the MEP size did not change. This may be caused by humoral factors, because the F wave reappeared immediately after plasma exchange or intravenous immunoglobulin treatment. A correlation of F wave disappearance with the presence of serum antiganglioside antibodies was found. CONCLUSIONS: The major pathophysiology of F wave disappearance in demyelinating neuropathies is impairment of motor neuron excitability or prolonged refractoriness of the most proximal axon for backfiring. The conventional interpretation that absent F waves suggest a conduction block at the proximal site is often inadequate.

Preserved leftward movement in left unilateral spatial neglect due to frontal lesions.

Three patients with left unilateral spatial neglect after predominantly frontal lobe lesions were asked to extend a horizontal line leftwards to double its original length. In this line extension task, they readily executed movements in or towards the contralesional left space. They performed the task in the left and right hemispaces as well as in the midline. The mean extension lengths did not differ significantly among these three spatial conditions. These results suggest that directional hypokinesia takes little part in left unilateral spatial neglect due to frontal lobe lesions. It is considered that the patients could execute leftward movements as the task oriented their attention sufficiently to the left. Two of the three patients, like reported cases with frontal neglect, showed a typical exploratory deficit for the left space in the line cancellation test. Such a deficit found in the traditional tasks, however, does not mean the presence of directional hypokinesia. All three patients showed visual extinction on double simultaneous stimulation. An attentional mechanism seems to play a predominant part in unilateral spatial neglect due to frontal lesions.