Organophosphate intoxication causing the extrapyramidal symptom is not frequent. A case of Parkinson's syndrome caused by organophosphate intoxication was observed, of which is reported with the quantitative measurement of tremor using Tri-axial accelerometry. A fifty nine year-old male was admitted to Wonju Christian Hospital after the intake of organophosphate for the purpose of suicide and three days after the accident, involuntary movements were detected. The encephalography and MRI showed no abnormality. With Tri-axial accelerometry, we detected less than 4 Hz resting tremor. The tremor did not response to L-dopa, and in the follow up examination performed 149 days after the accident, an increase in amplitude was detected. Gait disturbance and dysarticulation became more severe. In a case of the organophosphate intoxication patient, very rare Parkinson's syndrome findings were detected, and the tremor during the resting period was measured quantitatively by electromyography and Tri-axial accelerometry. (J Korean Acad Rehab Med 2010; 34: 110-113)
Organophosphate is known to damage both the peripheral and central nervous system. We report a case of organophosphate-induced peripheral polyneuropathy with myelopathy. A 46 years old woman who had ingested a large amount of insecticide (organophosphate) was transported to our hospital. Following medical treatment, she was transferred to the Department of Rehabilitation Medicine 1 month later. Upon admission to rehabilitation medicine, the patient was quadriplegic with markedly decreased muscle tone and strength. Electrodiagnostic examination revealed low amplitude of sensory nerve action potential (SNAP), unevokable compound muscle action potential in distal muscles and abnormal spontaneous activities with needle
electromyography, which were compatible with peripheral polyneuropathy. Three months later, motor and sensory function of upper extremities were normalized. The muscle tone of lower extremity increased to Ashworth grade II. Follow-up electrodiagnostic examination revealed normalization of SNAP and disappearance of spontaneous activities, but somatosensory evoked potential which were initially normal, revealed prolonged P40 latencies in the lower extremities. These electrophysiological findings were thought to result from the spinal cord lesion and correlated with clinical findings. We diagnosed the patient as peripheral polyneuropathy with delayed myelopathy induced by organophosphate. (J Korean Acad Rehab Med 2002; 26: 113-116)