Chon-Haw Tsai

Movement related cortical potentials of cued versus self-initiated movements: Double dissociated modulation by dorsal premotor cortex versus supplementary motor area rTMS

The dorsal premotor cortex (PMd) is thought to play a significant role in movement preparation cued by sensory information rather than in self‐initiated movements. The evidence in humans for this contention is still circumstantial. Here we explored the effects of modulation of PMd by excitability decreasing 1 Hz repetitive transcranial magnetic stimulation (rTMS) versus excitability increasing 5 Hz rTMS on two forms of movement related cortical potentials: contingent negative variation (CNV) versus Bereitschaftspotential (BP) reflecting externally cued versus self‐triggered movement preparation. Ten healthy right‐handed subjects performed visually cued or self‐triggered simple sequential finger movements with their right hand. CNV and BP were recorded by 25 EEG electrodes covering the fronto‐centro‐parietal cortex and divided into an early (1500–500 ms before a go‐signal or movement onset) and a late potential (500–0 ms). MRI‐navigated 1 Hz rTMS of the left PMd resulted in significant increase of the late CNV over the left central region predominantly contralateral to the prepared right hand movement, while 5 Hz rTMS had no effect on CNV. In contrast, 1 and 5 Hz rTMS did not modify BP. Control experiments of 1 Hz rTMS of the supplementary motor area (SMA) and of low‐intensity 1 Hz rTMS of the left primary motor cortex did not change CNV, but 1 Hz SMA‐rTMS increased late BP. This double dissociation of effects of PMd‐rTMS versus SMA‐rTMS on CNV versus BP provides direct evidence that the left PMd in humans is more involved in preparatory processes of externally cued rather than self‐initiated movements, contrasting with an opposite role of the SMA. Hum Brain Mapp 2012.

Medical and non-medical correlates of carpal tunnel syndrome in a Taiwan cohort of one million

Background:  Carpal tunnel syndrome (CTS), with unclear etiology, is the most common entrapment neuropathy. Its occurrence is related to lots of medical and non‐medical conditions with uncertain causality. With a large population, we characterized selected demographical and clinical factors to add more information on CTS‐correlated factors and new insight into future CTS prevention.

Cerebellum to motor cortex paired associative stimulation induces bidirectional STDP-like plasticity in human motor cortex

The cerebellum is crucially important for motor control and adaptation. Recent non-invasive brain stimulation studies have indicated the possibility to alter the excitability of the cerebellum and its projections to the contralateral motor cortex, with behavioral consequences on motor control and adaptation. Here we sought to induce bidirectional spike-timing dependent plasticity (STDP)-like modifications of motor cortex (M1) excitability by application of paired associative stimulation (PAS) in healthy subjects. Conditioning stimulation over the right lateral cerebellum (CB) preceded focal transcranial magnetic stimulation (TMS) of the left M1 hand area at an interstimulus interval of 2 ms (CB→M1 PAS2 ms), 6 ms (CB→M1 PAS6 ms) or 10 ms (CB→M1 PAS10 ms) or randomly alternating intervals of 2 and 10 ms (CB→M1 PASControl). Effects of PAS on M1 excitability were assessed by the motor-evoked potential (MEP) amplitude, short-interval intracortical inhibition (SICI), intracortical facilitation (ICF) and cerebellar-motor cortex inhibition (CBI) in the first dorsal interosseous muscle of the right hand. CB→M1 PAS2 ms resulted in MEP potentiation, CB→M1 PAS6 ms and CB→M1 PAS10 ms in MEP depression, and CB→M1 PASControl in no change. The MEP changes lasted for 30–60 min after PAS. SICI and CBI decreased non-specifically after all PAS protocols, while ICF remained unaltered. The physiological mechanisms underlying these MEP changes are carefully discussed. Findings support the notion of bidirectional STDP-like plasticity in M1 mediated by associative stimulation of the cerebello-dentato-thalamo-cortical pathway and M1. Future studies may investigate the behavioral significance of this plasticity.

Two novel mutations of the glycine receptor gene in a Taiwanese hyperekplexia family

The authors report a Taiwanese family with autosomal recessive hyperekplexia. Two novel mutations, W96C (from the paternal allele) and R344X (from the maternal allele), which are located in exon 4 and exon 7 of the GLRA1 gene, were identified in this family. A series of electrophysiologic investigations were conducted in one of the probands, and the results suggest that the “startle center” is located subcortically.

VBM Reveals Brain Volume Differences between Parkinson’s Disease and Essential Tremor Patients

Symptoms of essential tremor (ET) are similar to those of Parkinson’s disease (PD) during their initial stages. Presently, there are few stable biomarkers available on a neuroanatomical level for distinguishing between these two diseases. However, few investigations have directly compared the changes in brain volume and assessed the compensatory effects of a change in the parts of the brain associated with PD and with ET. To determine the compensatory and/or degenerative anatomical changes in the brains of PD and ET patients, the present study tested, via two voxel-based morphometry (VBM) approaches (Basic vs. DARTEL VBM processing), the anatomical brain images of 10 PD and 10 ET patients, as well as of 13 age-matched normal controls, obtained through a 3T magnetic resonance scanner. These findings indicate that PD and ET caused specific patterns of brain volume alterations in the brains examined. In addition, our observations also revealed compensatory effects, or self-reorganization, occurring in the thalamus and the middle temporal gyrus in the PD and ET patients, due perhaps in part to the enhanced thalamocortical sensorimotor interaction and the head-eye position readjustment, respectively, in these PD and ET patients. Such a distinction may lend itself to use as a biomarker for differentiating between these two diseases.

Bi-directional Modulation of Somatosensory Mismatch Negativity with Transcranial Direct Current Stimulation: An event Related Potential Study

Sensory mismatch negativity is impaired in patients with cerebellar lesions, suggesting that the cerebellum may play an important role in this form of sensory processing. Anodal transcranial direct current stimulation over the right cerebellar hemisphere increased the amplitude of sensory mismatch negativity to stimuli delivered to the right hand while cathodal transcranial direct current stimulation reduced it. The cerebellum appears to be an important node in the network mediating sensory mismatch negativity, and tDCS is a useful method with which to manipulate sensory mismatch negativity for experimental studies.

Neuropsychiatric Manifestations in Vascular Cognitive Impairment Patients with and without Dementia

BACKGROUND Neuropsychiatric profile has less been well recognized in all subtypes of vascular cognitive impairment (VCI). The aim of this study is to explore the neuropsychiatric manifestations in patients with different subtypes of VCI. METHODS A consecutive series of 157 patients with VCI visited the dementia clinic in a regional hospital in mid-Taiwan were investigated in this study. All patients were examined with the Cognitive Abilities Screening Instrument (CASI), the Hachinskis Ischemic Scale (HIS), and the Clinical Dementia Rating (CDR) scale. The Neuropsychiatric Inventory (NPI) was used to assess neuropsychiatric symptoms. RESULTS Of the 157 participants with VCI, 41 (26.1%) had VCI, without dementia (vascular CIND), 95 (60.5%) had vascular dementia (VaD), 21 (13.4%) had Alzheimers disease (AD) with a vascular component (mixed AD/VaD). Sleep disturbance was the most common symptom in all patient groups. Apathy is significantly lower in VCI without dementia compared with VCI with dementia. Patients with VaD had the highest mean composite NPI scores in most domains and vascular CIND patients had the lowest composite scores in most domains. CONCLUSIONS Neuropsychiatric symptoms were common in patients with VCI with and without dementia. It deserves attention that neuropsychiatric symptoms as well as cognitive deficits frequently arise from cerebrovascular disease regardless of the development of dementia.

Reversible paraneoplastic limbic encephalitis caused by a benign ovarian teratoma: report of a case and review of literatures

Paraneoplastic limbic encephalitis (PLE) is widely believed to be a remote, irreversible neurological complication of small cell lung carcinoma and other malignancies [1]. PLE caused by a mature ovarian teratoma is extremely rare; in fact, only three cases have been reported [2–4]. We report a patient with a reversible PLE caused by a benign ovarian teratoma. A 35-year-old married saleswoman had been well until October 2001 when she had one episode of tonic deviation of the tongue toward left cheek followed by numbness of the left-sided of her face and clonic convulsion of both upper limbs. These symptoms lasted for approximately 2 min before completely resolving. She went to work as usual the next day. However, 3 days after the neurological insult, she was hospitalized because of fluctuating paraesthesia of the left-sided of her face and the right lower limb. Physical and neurological examinations revealed a large palpable mass in the pelvic region. Two days after admission, bursts of agitation, irritation, confusion, and focal seizures developed. After initial conservative treatment, the patient’s condition deteriorated rapidly. Inattention, incoherent speech, hand tremor, dystonia, and sweating were noted. Furthermore, her blood pressure and heart beats were in fulminant fluctuation. A brain MRI preand post-gadolinium on 10 October, 2001 was normal. Electroencephalograms (EEG) on 29 October, 2001 and November 5, 2001 disclosed diffuse, continuous delta and theta waves with intermittent sharp-wave complexes in both frontal lobes. A HMPAO SPECT 1 week after admission in 2001 revealed regional cerebral hypoperfusion involving both frontal lobes and the left temporal lobe. A lumbar puncture yielded clear CSF under normal pressure containing 9 white counts per microliter, 75 mg/dl of glucose, and 18 mg/dl of protein. The bacterial and TB cultures for microorganisms, cryptococcal antigen test, venereal disease research laboratory test, and the herpes simplex virus PCR of the CSF were negative. No malignant cells were identified by the CSF cytological examination. Serum complete blood cell counts disclosed anemia (Hb: 11 gm/dl). The results from the following serologic tests of erythrocyte sedimentation rate, blood ammonia, thyroid function, vitamin B12, and folic acid were within normal range. Antinuclear Antibody test, HIV antibody, and anti-Japanese B virus antibody were negative. Serum immunoglobulin levels, including IgG, IgA, IgM, C3, and C4, were also within normal range. A mildly elevated serum tumor marker CA-125 [50.04 U/ml ( <35)] was noted. Pelvic Y.-W. Yang Æ C.-H. Tsai Æ F.-C. Chang Æ M.-K. Lu Department of Neurology, Neuroscience Laboratory, China Medical University Hospital, Taichung, Taiwan

Diminution of basal ganglia dopaminergic function may play an important role in the generation of akinetic mutism in a patient with anterior cerebral arterial infarct.

We report the clinical features and dopamine transporter [2-[[2-[[[3-(4-chlorophenyl)-8-methyl-8-azabicyclo[3.2.1]oct-2-yl]methyl](2-mercaptoethyl)amino]ethyl]amino]ethanethiolato(3-)-N2,N20,S2,S20]oxo-[1R-(exo-exo)]-[99mTc] technetium([99mTc]TRODAT-1) image finding in an 86-year-old woman with akinetic mutism due to infarction of bilateral anterior cerebral arterial territories. TRODAT-1 is a cocaine analogue that can be labeled with technetium-99m and bound to the dopamine transporter (DAT) site. It reflects primarily the integrity of presynaptic dopamine neuron terminals. With the evolution of the clinical features, the TRODAT SPECT images change from bilateral diminution of radioactivity uptake at the 81st-day check point to normal pattern at the 6-month one when the akinetic mute manifestations were nearly gone. This novel illustration suggests that the akinetic mutism caused by anterior cerebral arterial infarct is closely linked to the perturbation of the subcortical dopaminergic system. And the amelioration of the clinical features concordantly evolved with the restoration of the dopaminergic function.

Nonapnea sleep disorders are associated with subsequent ischemic stroke risk: a nationwide, population-based, retrospective cohort study

BACKGROUND AND OBJECTIVES Obstructive sleep apnea (OSA) is related to an increased risk for stroke and cardiovascular disease. However, studies investigating the relationship between nonapnea sleep disorders (NSD) and the risk for subsequent ischemic stroke are scant. The objective of our study was to assess the association between NSD and the risk for acute ischemic stroke among patients in Taiwan. METHODS We conducted our longitudinal nationwide, population-based, retrospective study using Taiwans National Health Insurance Research Database (NHIRD) from January 1997 to December 2001. All study participants were followed until the incidence of ischemic stroke, or until censoring due to death; until withdrawal from the insurance program; or until they were lost to follow-up by the end of 2010. Cox proportional hazard regression analysis was used to assess the association between NSD and subsequent ischemic stroke risk. RESULTS We analyzed the data collected from 94,160 participants as a comparison cohort and 47,080 participants as a NSD cohort with the diagnosis date as the index date. The age range of cohorts was 20.0-101.7years and 64% were women. The average follow-up duration was 9.61years for the NSD cohort and 9.42years for the reference cohort. Overall, the ischemic stroke incidence was 1.48-fold higher in the NSD cohort than in the reference cohort (8.87 vs 6.00/1000 individual-years), with an adjusted hazard ratio (HR) of 1.19 after controlling for age, sex, and comorbidities. Our study also showed a 1.35-fold significantly higher risk for developing ischemic stroke in men compared to women. The adjusted HR was 31.2 for elderly patients compared with participants aged ⩽35years. CONCLUSIONS Our nationwide, population-based, retrospective cohort study provides evidence that patients with NSD were at increased risk for developing ischemic stroke compared to patients without diagnosed sleep disorder, with men and the elderly being at greatest risk.