Although peripheral trauma induced movement disorders have been rarely reported, diagnostic criteria for peripherally induced movement disorders (PIMD) have been established. Because preexisting subclinical movement disorders, or secondary gain for compensation and legal purposes are difficult to confirm, differential diagnosis for physicians still remains difficult.

We present four patients developed movement disorders after relatively various intervals after traffic accident. Three patients of them showed tremor and one patient presented propriospinal myoclonus. In this report, we investigate whether peripheral trauma can lead to movement disorders and describe the relationship between peripheral injury and movement disorders in four cases.

Injury was serious enough to develop involuntary abnormal movements with pain and the latency between injury and the onset of movements in all of cases was less than 1 year. Thus, our cases showed temporal and anatomical correlation between injury and the onset of movement disorder, strongly supporting the cause-and-effect relationship by previous diagnostic criteria for peripherally induced movement disorders.

Oromandibular dyskinesia (OMD) can occur spontaneously or they can be induced by the conventional dopamine receptor antagonists. Anticholinergic medications have rarely been reported to cause OMD in parkinsonian or non-parkinsonian patients.

We analyzed the clinical features of two parkinsonian and one non-parkinsonian patients who experienced OMD after anticholinergic medication.

Each patient of our cases developed oromandibular symptoms in the temporal regions that were related to the addition of anticholinergic agents, and the symptoms were relieved following the discontinuation of the causative anticholinergic drugs. In one of our case, levodopa alone did not cause dyskinesia but augmented dyskinesia associated with anticholinergics.

Here we report two parkinsonian and one non-parkinsonian patients with OMD induced by the use of anticholinergic agents. In our cases, we could not find any other precipitating or actual secondary causes for the OMD symptoms in our patients. Furthermore, the fact that the OMD in our cases were ameliorated with cessation of anticholinergics suggests that it may be anticholinergic-induced.

Ataxia associated with Hashimoto’s thyroiditis autoantibodies has been reported as acquired cerebellar ataxia. However, relationship between anti-thyroid antibodies and cerebellar ataxia has not been clarified yet.

We aimed to analysis the relibility of serum anti-thyroid antibodies screening in the diagnosis of Parkinson’s disease (PD) and multiple system atrophy (MSA).

We enrolled 105 patients with clinically diagnosed PD and 75 patients with probable MSA. Patients with PD were classified into 70 patients with early PD (Hoehn & Yahr stage I to II) and 35 patients with late PD (Hoehn & Yahr stage III to IV). In MSA, 28 patients were classified as MSA-p (parkinsonism predominant) and 47 MSA-c (cerebellar predominant). For analysis of thyroid function, serum free triiodothyronine (T3), free thyroxine (T4), anti-thyroglobuline (TG) antibodies and anti-microsomal antibodies were measured. Cut-off level for abnormal titers of anti-thyroid antibodies were defiend as above 100 U/ml.

Abnormally high titer of serum anti-TG antibodies and anti-microsomal antibodies was more frequently observed in MSA than in PD (p =0.001 and 0.003, respectively). However, there was no significant difference in the frequency of abnormal titer either between MSA-c and MSA-p (p>0.05) nor between early PD and late PD (p>0.05). Among clinical parameters, only ataxia was correlated with both titer of anti-TG antibody and anti-microsomal antibody (p=0.007 and 0.002, respectively).

These results suggest that high titer of anti-thyroid antibodies may be associated with MSA rather than PD and screening of serum anti-thyroid antibodies may be helpful for discrimiation of PD from MSA. However, anti-thyroid antibodies screening may not be helpful to differentiate MSA-c from MSA-p.

Parkinson’s disease (PD) is characterized by motor and non-motor symptoms including cognitive, autonomic, sleep, and sensory disturbances. Cognitive impairment may occur in up to 80% of PD patients, and dementia in approximately 30%. The purpose of this study is to evaluate the frequency of cognitive impairment and the characteristics of cognitive deficits and to know the possibility of early detection of cognitive deficits in outpatient clinics with the questionnaire for patients and caregivers.

A total of 129 consecutive patients with idiopathic Parkinson’s disease were visited movement clinic from March 2006 to August 2006. Eighty-five patients performed cognitive test and questionnaires. All patients had motor symptoms with Hoehn and Yahr stage 0.5 to 3 (mean: 1.98±0.617), and evaluated with cognition by K-MMSE (Korean version of Mini-mental status examination), 7-MS (7-minutes screen test), and demographic features.

The frequency of cognitive impairment in PD patients was 44.7% (38/85), among them thirty (78.9%) patients complained memory disturbance. The characteristics of cognitive test were retrieval defect in memory, visuospatial dysfunction and categorical word fluency. With questionnaire, the complaint of memory decline and difficulties in activity of daily living (ADL) w ere important points of cognitive deficit in PD patients. However questionnaire did not showed significant correlation between complain of memory decline and cognitive deficit, only regular check with cognitive function test revealed the patient’s early cognitive impairment.

The cognitive impairment was frequent in PD patients. The characteristics of cognitive testing w ere retrieval defect in memory function and frontal executive dysfunction.