No abstract available.
Animals ; Hypokinesia* ; Immobilization* ; Muscle, Skeletal* ; Rats*

Parkinsonism is a very rare complication of phenytoin. The authors experienced a 71-year-old man who presented progressive cognitive decline, postural tremor, bradykinesia and gait disturbance. Laboratory test and brain imaging revealed no abnormality that commonly causes parkinsonism. The only abnormal finding was elevation of serum phenytoin above the therapeutic level. The patient showed marked improvement of symptoms by reduction of phenytoin dosage. Here we report a case of phenytoin induced parkinsonism.
Aged ; Gait ; Humans ; Hypokinesia ; Neuroimaging ; Parkinsonian Disorders ; Phenytoin ; Tremor

Changes in the individual symptomatology were analyzed on twenty-nine patients with Parkinson's disease who underwent thirty-five stereotaxic thalamotomies to evaluate the influence of each symptom on the surgical results. The thalamotomy could obviously improve and prevent progression of tremor and rigidity but not bradykinesia and axial symptoms. Long-term follow-up wtudy with statistical analysis suggested that progressive worsening after surgery was due not to recurrence of tremor and rigidity but aggravation of bradykinesia and axial symptoms in the natural course of the disease. We believe that timely surgical treatment should be encouraged in patients presenting symptoms of tremor and rigidity.
Follow-Up Studies ; Humans ; Hypokinesia ; Parkinson Disease* ; Recurrence ; Tremor

Whilst rare, the acute development of involuntary movements with characteristic lesions of the bilateral basal ganglia in a diabetic uremic patient is a well-demarcated clinical syndrome. Most patients with this syndrome present with either parkinsonism or chorea; however, concurrent chorea with bradykinesia or parkinsonism is rarely reported. We report herein two diabetic uremic patients who developed acute chorea and bradykinesia with characteristic MR images.
Basal Ganglia ; Chorea ; Dyskinesias ; Humans ; Hypokinesia ; Parkinsonian Disorders

Stereotactic thalamotomy has traditionally provided good relief of tremor for patients with intractable tremor dominant in Parkinson's disease. However bradykinesia, dyskinesia and rigidity are less reliably treated with this technique. Although posteroventral pallidotomy(PVP) can alleviate dyskinesias appendicular bradykinesia and rigidity, tremor may not be completely ameliorated. Between January 1993 and May 1997, the authors performed posteroventral pallidotomy(PVP) on 69 patients with Parkinson's disease who had bradikinesia, rigidity, drug induced dyskinesia and tremor. Of these patients who had only PVPs 17(25%) patients had severe tremor, 20(29%) patients moderate tremor and 32(46 %) patients mild or no tremor after the surgery. We have combined ventrolateral thalamotomy(VLT ) and PVP in 37 patients with moderate to severe tremor. Of the 37 patients, who had both PVP and VLT, 27(73%) patients showed good improvement, and fair improve-ment in 10(27%). Except for 6 cases with transient dysarthria we did not encounter any other operative complications from the ipsilateral combined PVP and VLT. The combination of the two procedures appear to provide excellent relief for the majority of symptoms in patients suffering from advanced Parkinsons disease with rigidity bradykinesia, dyskinesia and tremor.
Dysarthria ; Dyskinesias ; Humans ; Hypokinesia ; Pallidotomy* ; Parkinson Disease* ; Tremor

A woman developed a slowly progressive speech disturbance at age 51. Three years latter she showed difficulty in calculation, reading and writing. At age 57, she complained of right shoulder pain. At age 58, neurological examination revealed rigidity, bradykinesia and ideomotor apraxia in the right upper extremity. This case demonstrats a clinical overlap between progressive nonfluent aphasia and corticobasal degeneration.
Apraxia, Ideomotor ; Female ; Humans ; Hypokinesia ; Neurologic Examination ; Primary Progressive Nonfluent Aphasia ; Shoulder Pain ; Upper Extremity ; Writing

BACKGROUND: Drug-induced Parkinsonism(DIP) is the second commonest cause of Parkinsonism, after idiopathic Parkinson's disease(IPD). DIP is frequently produced by antipsychotic drugs. But the clinical characteristics of DIP did not get attention by neurologist. So we studied the clinical profiles of DIP patients. METHODS: We studied the clinical profiles of thirthone patients who showed parkinsonism after antipsychotic drug treatment. We compared the score of motor part of the Unified Parkinson's Disease Rating Scale(UPDRS) between trihexyphenidyl(n=15) & amantadine(n=16) monotherapy group(initial & 4 week after treatment). RESULTS: The mean age of patients was 45 years. Bradykinesia was the 1st symptom in 26 patients(94%), tremor in 5 patients(6%). In 25 patients(81%), the first symptom appeared within 1 week after sntipsychotic treatment. There was a statistical significant negative correlation between the dosage of antipsychotic drug and the symptom-onset interval following treatment with antipsychotic drugs(simple correlation analysis, p>0.01). Bradykinesia and rigidity were appeared in all DIP patients, symmetric distribution was more common(94%, 87%) Tremor occurred in 27 patients (87%). In patients with tremor, postural or action tremor was dominant in 15 patients(56%) asymmetric distribution was more common(16/27, 59%). There are no statistical difference in motor score of UPDRS between trihexyphenidyl & amantadine monotherapy group(student t-test, p<0.05) CONCLUSIONS: Bradykinesia was the most common 1st symptom in DIP patients. Asymmertrical postural or action tremor was relativelly common in DIP. Amantadine showed the same efficacy in the treatment of DIP compared to anticholinergics.
Amantadine ; Antipsychotic Agents ; Cholinergic Antagonists ; Humans ; Hypokinesia ; Parkinson Disease ; Parkinsonian Disorders* ; Tremor ; Trihexyphenidyl

BACKGROUND AND OBJECTIVES: Data on the usefulness of a combination of different electrocardiography (ECG) abnormalities in risk stratification of patients with acute pulmonary embolism (PE) are limited. We thus investigated 12-lead ECG patterns in acute PE to evaluate the role of the ECG score in risk stratification of patients with acute PE. SUBJECTS AND METHODS: One hundred twenty-five consecutive patients (63+/-14 years, 56 men) with acute PE who were admitted to Kyungpook National University Hospital between November 2001 and January 2008 were included. We analyzed ECG patterns and calculated the ECG score in all patients. We evaluated right ventricular systolic pressure (RVSP) (n=75) and RV hypokinesia (n=80) using echocardiography for risk stratification of acute PE patients. RESULTS: Among several ECG findings, sinus tachycardia and inverted T waves in V(1-4) (39%) were observed most frequently. The mean ECG score and RVSP were 7.36+/-6.32 and 49+/-21 mmHg, respectively. The ECG score correlated with RVSP (r=0.277, p=0.016). The patients were divided into two groups {high ECG-score group (n=38): ECG score >12 and low ECG-score group (n=87): ECG score < or =12} based on the ECG score, with the maximum area under the curve. RV hypokinesia was observed more frequently in the high ECG-score group than in the low ECG-score group (p=0.006). Multivariate analysis revealed that a high ECG score was an independent predictor of high RVSP and RV hypokinesia. CONCLUSION: Sinus tachycardia and inverted T waves in V(1-4) were commonly observed in acute PE. Moreover, the ECG score is a useful tool in risk stratification of patients with acute PE.
Blood Pressure ; Echocardiography ; Electrocardiography ; Heart Ventricles ; Humans ; Hypokinesia ; Multivariate Analysis ; Pulmonary Embolism ; Tachycardia, Sinus

The purpose of this study was to investigate the frequency of depression and the relationships between various clinical features and depression in the patients with idiopathic parkinsonism. We included 113 patients of idiopathic parkinsonism who had any three of resting tremor, rigidity, bradykinesia, impaired postural reflexes or any one of the first three displaying asymmetry without definite brain lesion on brain imaging studies or metabolic derangement. We used Beck depression inventory, and the results were compared with those of 70 normal controls. The following results were obtained: 1.The patients with idiopathic parkinsonism had more severe depression than normal controls. If we@ consider the cut-point scores for depression as more than 21points of Beck depression inventory scores, the frequency of depression in idiopathic parkinsonism was 44. 1%. 2.The scores of the BDI questionare representing somatic symptoms were increased in the patient group, whether they had mild or severe parkinsonian deficits. The patients who had more severe parkinsonian deficits had higher scores. However, those representing mood and self-reproach symptoms were increased only in the late stage of idiopathic parkinsonism. 3.The severe motor symptoms, particularly bradykinesia and rigidity, poor responsiveness to L-dopa treatment, longer the duration of disease, were the factors correlated with severe depression. However the current age, age of onset, whether treated or untreated, and whether sy7rnptonis affected predominantly right or left side of the body, were not correlated with the severity of depression. On the basis of the results, when we regard no tremorous symption and the poor responsiveness to L-dopa treatment as the clinical features of idiopahtic parkinsonism, we suspect the tendency that the patients with idiopathic parkinsonism may have more severe depression than those with idiopathic P-qrkinson's disease.
Age of Onset ; Brain ; Depression* ; Humans ; Hypokinesia ; Levodopa ; Neuroimaging ; Parkinsonian Disorders* ; Reflex ; Tremor

A variety of toxins cause parkinsonism and the lesions are primarily in the pallidostriatum. It usually does not respond to levodopa. We experienced a patient whose parkinsonian features developed after accidental acetone ingestion. She had rigidity, bradykinesia, gait disturbance and her speech was sluggish. Brain MRI showed bilateral basal ganglionic lesions. She was treated with levodopa and her neurological symptoms improved. To our knowledge, there has not been any previous reports of acetone causing parkinsonism. Acetone may cause parkinsonism by damaging the basal ganglia.
Acetone* ; Basal Ganglia ; Brain ; Eating ; Gait ; Ganglion Cysts ; Humans ; Hypokinesia ; Levodopa ; Magnetic Resonance Imaging ; Parkinsonian Disorders*