Aripiprazole Can Improve Apraxia of Eyelid Opening in Parkinson's Disease.

We herein report three cases of Parkinson's disease associated with difficulty in eyelid opening, referred to as apraxia of eyelid opening (AEO), which improved after aripiprazole treatment. In case 1, aripiprazole was administered as a psychiatric treatment. It proved to be effective in AEO with blepharospasm. In case 2 and case 3, the patients experienced AEO without blepharospasm, and a significant improvement was observed after aripiprazole treatment. In this study, the aripiprazole dosage ranged between 3 and 9 mg/day. This is the first report of aripiprazole as a potentially effective treatment for AEO in Parkinson's disease.

Modifications of excitatory and inhibitory transmission in rat hippocampal pyramidal neurons by acute lithium treatment.

The acute effects of high-dose Li(+) treatment on glutamatergic and GABAergic transmissions were studied in the "synaptic bouton" preparation of isolated rat hippocampal pyramidal neurons by using focal electrical stimulation. Both action potential-dependent glutamatergic excitatory and GABAergic inhibitory postsynaptic currents (eEPSC and eIPSC, respectively) were dose-dependently inhibited in the external media containing 30-150 mM Li(+), but the sensitivity for Li(+) was greater tendency for eEPSCs than for eIPSCs. When the effects of Li(+) on glutamate or GABAA receptor-mediated whole-cell responses (IGlu and IGABA) elicited by an exogenous application of glutamate or GABA were examined in the postsynaptic soma membrane of CA3 neurons, Li(+) slightly inhibited both IGlu and IGABA at the 150 mM Li(+) concentration. Present results suggest that acute treatment with high concentrations of Li(+) acts preferentially on presynaptic terminals, and that the Li(+)-induced inhibition may be greater for excitatory than for inhibitory transmission.

Midbrain infarction causing oculomotor nerve palsy and ipsilateral cerebellar ataxia.

We herein report the case of an 81-year-old woman with midbrain infarction causing pupil-sparing oculomotor nerve palsy with ipsilateral cerebellar ataxia. The lesion was located at the rostral end of the decussation of the superior cerebellar peduncle touching the dorsal side, further caudal and dorsal to causal lesions of Claude's syndrome, which presented as oculomotor palsy and contralateral cerebellar ataxia. This is the third report of midbrain infarction causing partial oculomotor nerve palsy with ipsilateral cerebellar ataxia. It may be possible to establish this entity as a new syndrome following the accumulation of more cases.

Longitudinal changes of motor cortical excitability and transcallosal inhibition after subcortical stroke.

OBJECTIVE: A general lack of longitudinal studies on interhemispheric interactions following stroke led us to use transcranial magnetic stimulation (TMS) to examine changes in corticospinal/intracortical excitability and transcallosal inhibition over a 1-year period following subcortical stroke. METHODS: We measured TMS parameters such as motor threshold (MT), short-interval intracortical inhibition (SICI), and ipsilateral silent period (iSP) and evaluated clinical scores at three time-points (T1, T2, and T3) in 24 patients and 25 age-matched healthy subjects. RESULTS: At T1, we observed reduced MTs and SICIs with prolonged iSPs in the unaffected hemisphere (UH). In contrast, increased MTs and reduced SICIs were observed in the affected hemisphere (AH). These abnormalities gradually reduced and no MEP response to TMS at T1 predicted a worse prognosis. The prolonged iSP at T1 was associated with more severe impairments, but it did not necessarily predict a worse prognosis after 1year. CONCLUSIONS: UH excitability was increased at the post-acute time-period, which may have resulted in enhanced transcallosal inhibition to the AH. However, it is unclear whether there was a causal relationship between the enhanced transcallosal inhibition and the extent of clinical recovery. SIGNIFICANCE: This is the first study to demonstrate changes in transcallosal inhibition over a longitudinal period following stroke.

Parallel inhibition of cortico-muscular synchronization and cortico-spinal excitability by theta burst TMS in humans.

OBJECTIVE: To investigate the after-effects of theta burst TMS (TBS) on cortico-muscular synchronization, and on cortico-spinal excitability, in humans. METHODS: We studied 10 healthy subjects using a continuous paradigm of TBS (cTBS), i.e. 600 pulses in 40s. Before and after the cTBS, coherence function was computed as a measure of cortico-muscular synchronization by recording electroencephalogram (EEG) from 19 scalp sites and electromyogram (EMG) from right first dorsal interosseous (FDI) muscle during the isometric contraction. In a separate experiment, motor-evoked potentials (MEPs) in response to single TMS pulses were recorded from the FDI muscle before and after the cTBS, to measure cortico-spinal excitability. RESULTS: When the cTBS was applied over the left primary motor cortex (M1), the beta-band cortico-muscular coherence for the C3 scalp site, as well as the MEP amplitude significantly decreased in 30-60 min, and then recovered to the original levels in 90-120 min. Neither sham stimulation nor cTBS applied over 2 cm posterior to M1 produced significant effects. CONCLUSIONS: cTBS-over-M1 can inhibit the cortico-muscular synchronization in parallel with the decline of cortico-spinal excitability. SIGNIFICANCE: Our results provide the first evidence that TBS can efficiently alter the functional cortico-muscular coupling in humans.

Effect of theta burst stimulation over the human sensorimotor cortex on motor and somatosensory evoked potentials.

OBJECTIVE: To study the after-effect of theta burst stimulation (TBS) over the left sensorimotor cortex on the size of somatosensory as well as motor evoked potentials evoked from both hemispheres in healthy human subjects. METHODS: We used a continuous TBS paradigm for 40 s (600 pulses) in which a burst of 3 transcranial magnetic stimuli at 50 Hz is repeated at 5 Hz [Huang YZ, Edwards MJ, Rounis E, Bhatia KP, Rothwell JC. Theta burst stimulation of the human motor cortex. Neuron 2005;45:201-6]. Somatosensory evoked potentials (SEPs) following electrical stimulation of right or left median nerve and motor evoked potentials (MEPs) in the right or left first dorsal interosseous (FDI) muscles were recorded before and after TBS over the left motor cortex (M1) or a point 2 cm posterior to left M1. RESULTS: Amplitudes of P25/N33 (parietal components) following right median nerve stimulation were significantly increased for at least 53 min after TBS over the left M1, whereas this component was suppressed for 13 min after TBS over a point 2 cm posterior. MEPs in right as well as left FDI muscles were suppressed with a similar time course after TBS over the left M1. CONCLUSIONS: A single-session of TBS over the sensorimotor cortex can induce a short-lasting change in the size of ipsilateral cortical components of SEPs as well as MEPs evoked from both hemispheres. SIGNIFICANCE: TBS is an interventional tool that can induce rapid reorganization within cortical somatosensory as well as motor networks in humans.

Effects of wheelchair training on VO2 kinetics in the participants with spinal-cord injury.

PURPOSE: We tested the hypothesis that, in eight participants (seven males, one female; 46.5 +/- 8.3 years) with spinal-cord injury (complete lesions, T7-L1), the effects of exercise training on pulmonary O2 uptake (VO2) on- and off-kinetics would appear early in this pilot study. METHODS: The subjects underwent the wheelchair-training program (3 day/w, 30 min/day, and 50% HRreserve), and were evaluated before training ("time 0", T0), and after 7 (T7), 15 (T15), 30 (T30), and 60 (T60) days of training. Breath-by-breath peak VO2 was determined during the incremental exercise until their exhaustion. At another day following the incremental exercise, the subjects performed three repetitions of a constant exercise at 50% peak VO2 workload so that VO2 could be determined for both on- and off-kinetics. RESULTS AND CONCLUSION: Peak VO2 showed a tendency to increase with training; the increases became significant at T30. The time constants (tau 2) during "phase II" of the VO2 on-kinetics were 62.4 +/- 13.0 (s) (T0), 51.2 +/- 8.7 (T7), 46.1 +/- 7.4 (T15), 45.0 +/- 7.2 (T30), and 43.4 +/- 6.4 (T60); a significant difference compared to T0 was observed from T7 onward. The same pattern of change as a function of training was described for the VO2 off-kinetics. It is concluded that in SCI participants, the acceleration of VO2 kinetics at the onset of exercise was observed over a short term.

Increased corticospinal excitability after 5 Hz rTMS over the human supplementary motor area.

Transcranial magnetic stimulation (TMS) can produce effects not only at the site of stimulation but also at distant sites to which it projects. Here we examined the connection between supplementary motor area (SMA) and the hand area of the primary motor cortex (M1(Hand)) by testing whether prolonged repetitive TMS (rTMS) over the SMA can produce changes in excitability of the M1(Hand) after the end of the stimulus train. We evaluated motor-evoked potentials (MEPs) and the cortical silent period (CSP) evoked by a single-pulse TMS, short-interval intracortical inhibition (SICI) and intracortical facilitation (ICF) produced by a paired-pulse TMS, and forearm flexor H reflexes before and after 750 pulses of 5 Hz rTMS over SMA at an intensity of 110% active motor threshold (AMT) for the first dorsal interosseous (FDI) muscle. The amplitude of MEPs recorded from the right FDI muscle at rest as well as during voluntary contraction increased for at least 10 min after the end of rTMS, although the duration of the CSP, SICI and ICF did not change. There was no effect on H reflexes in the flexor carpi radialis muscle, even though the amplitude of the MEP obtained from the same muscle increased after rTMS. The effects on MEPs depended on the intensity of rTMS and were spatially specific to the SMA proper. We suggest that 5 Hz rTMS over SMA can induce a short-lasting facilitation in excitability of the M1(Hand) compatible with the anatomical connections between SMA and the M1(Hand).