The purpose of our study was to investigate gait dynamics and kinematics in patients with Parkinson’s disease (PD) and to correlate these features with the predominant clinical features and with the presence of the freezing of gait (FOG). We measured the temporospatial and kinematic parameters of gait in 30 patients with PD (M:F=12:18, age=68.43±7.54) using a computerized video motion analysis system.

We divided the subjects into subgroups: (1) tremor-dominant (TD) group and postural instability and gait disturbance (PIGD) group and (2) FOG group and non-FOG group. We compared the gait parameters between the subgroups.

The walking velocity and stride length were reduced significantly in the PIGD group compared to the TD group. The PIGD group showed a significantly reduced range of motion in the pelvic and lower extremity joints by kinematics. Stride time variability was significantly increased and the pelvic oblique range was significantly reduced in the freezing gait disorder group.

Our findings suggest that there are differences in the perturbation of the basal ganglia-cortical circuits based on major clinical features. The reduction of the pelvic oblique range of motion may be a compensatory mechanism for postural instability and contributes to stride time variability in patients with FOG.

Status of the disease is the one of main concerns of clinicians, especially in the course of primary degenerative disorders. In Parkinson’s disease (PD), Unified Parkinson’s Disease Rating Scale (UPDRS) is an useful clinical score that can express severity of parkinsonian symptoms, but L-DOPA treatment and motor fluctuations can change the UPDRS scores. Even in the best ‘on’ state, there can be residual motor deficits, and it is very difficult to estimate the worst ‘off’ state due to long duration effect of L-DOPA.

To find relevant examination scores of ‘on’ or ‘off’ state of PD patients which correlates with clinical and demographic variables those can represents the status of Parkinson’s disease.

Sixty-four patients with PD (24 male, age 63.0±8.6 years, Hoehn and Yahr stage (HY) 2.8±0.5) were examined UPDRS at ‘on’ and practically defined ‘off’ (12 hours after last medication) state. We evaluated the association between the ‘on’ and ‘off’ scores of UPDRS and duration of disease and treatment, and equivalent L-DOPA dose of the patients. Patients were grouped according to the presence of motor fluctuation to find the differences in those associations.

There were significantly strong correlations between UPDRS ‘off’ scores and clinical variables such as duration of disease and treatment. In ‘on’ state, only complication part of UPDRS was correlated with duration of disease and treatment, but activity of daily living (ADL) and motor part of UPDRS were correlated well with age of the patients. Age at disease onset showed significant negative association with the difference between ‘off’ and ‘on’ state UPDRS scores. Thirty-one patients who had motor fluctuation (9 male, age 62.7±9.3 years, HY 3.0±0.6) showed significantly increased duration of the disease, duration of L-DOPA treatment and equivalent DOPA dose compared to those of 33 patients without motor fluctuation (15 male, age 63.3±8.1 years, HY 2.6±0.3). In patients without motor fluctuation, both ‘off’ and ‘on’ UPDRS showed association with duration of disease and treatment, but ‘off’ and ‘off’ – ‘on’ difference of UPDRS were better correlated with duration of disease and treatment in patients with motor fluctuation.

We found that the UPDRS scores of practically defined ‘off’ state significantly correlated with the duration of the disease and treatment. Patients with motor fluctuation revealed better responsiveness to medication than those without motor fluctuation. In patients without motor fluctuation, UPDRS scores of ‘on’ state can reflect the clinical presentation as much as those of ‘off’ state.

The cause of idiopathic Parkinson’s disease (IPD) is unknown, but reduced activity of complex I of the electron-transport chain has been implicated in the pathogenesis of IPD. Hyperhomocysteinemia is a well-established risk factor for cardiovascular and cerebrovascular diseases. However, recent evidence suggests that changes in the metabolic fate of homocysteine, leading to hyperhomocysteinemia, may also play a role in the pathophysiology of IPD.

Age and sex-matched 41 drug-naive IPD patients (16 men and 25 women) and 161 healthy controls (66 men and 95 women) were included in this study. Their fasting plasma homocystein and folate level, and the genotypes of methylenetetrahydrofolate reductase (MTHFR) were analyzed.

The plasma level of homocysteine was higher in untreated IPD patients (12.0±2.9 μmol/L) compared to the controls (9.0±2.6 μmol/L) (p =0.001). The frequencies of MTHFR C677T genotypes were not different between patients (CC:CT:TT=7:23:11) and controls (CC:CT:TT=27:86:48) (p =0.930). The adjusted odds ratio of homocysteine was remarkable (adjusted OR=1.149, 95% confidential interval=1.66–2.28, p =0.004).

IPD patients have higher plasma homocysteine level than healthy controls but MTHFR C667T genotype was not related to the homocysteine level. It can be suggested that increased plasma homocysteine level may contribute to the pathogenesis of IPD.

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.