Abnormalties of Ocular Motor Movement in Patients with Parkinson's Disease

OBJECTIVE : We investigated the relationship between the severity of the disease and the abnormality of some ocular movements in parkinson's disease. BACKGROUND: Disorders of eye movements have been described in diseases of the basal ganglia for over a century and ocular motor deficits of the saccadic and pursuit system have been reported in parkinsonian patients. METHOD : We studied the electro-oculography of the eye tracking and saccadic movement in 26 patients (11 males, 15 females) with Parkinson's disease. The severity of the disease was divided into two groups by Hoehn & Yahr(H-Y) staging, H-Y stage 1, 2(group A) and H-Y stage 3, 4 (Group B). Some patients antiparkinsonian drugs of L-dopa, dopamine agonist and anticholinergics. RESULT : The velocity of smooth pursuit and the velocity and latency of saccade were calculated and compared between two groups. Eye tracking test revealed decreased pursuit velocity leading to catch-up saccades, but normal phase relationship between eye and target movement, while saccadic eye movement had increased latency. These results showed more profound severity in more advanced stages of the disease. CONCLUSION : We suggest that ocular movement be often chosen as a simple but relevant example of general motor function, as well as criteria for staging of Parkinson's disease and basal ganglia play significant role in ocular movement.

Three Cases of Chronic Cerebral Paragonimiasis

Although CNS involvement of paragonimiasis is not frequently encountered, it has been reported in 10-25% of clinical cases of all paragonimiasis. It causes various symptoms and signs including epilepsy, headache, hemiparesis, visual field defect or other neurologic deficits. Infestation usually occurs by ingestion of freshwater crabs or crayfish infected with Paragonimus metacercariae. We report three patients with chronic cerebral paragonimiasis, which were diagnosed by history, neurologic examination, radiological and serological evaluations, Two of them had history of ingestion of freshwater crabs or crayfish in childhood. Only one patient showed a positive enzyme-linked immunosorbent assay reaction for Paragonimus specific antibody in serum and CSF. Their clinical manifestations were seizure, headache, and visual field defect. In their plain skull X-rays, congregated round oval calcifications were recognized. Brain computed tomography of patients revealed pathognomonic findings of multiple, variable sized, round, calcified lesions surrounded by low density areas together with cortical atrophy in occipital, parietal, and temporal lobes.

Raeder's Syndrome

Raeder's syndrome, or Raeder's paratrigeminal syndrome, is a painful Horner's syndrome characterized by unilateral head pain, oculosympathetic paralysis (miosis, ptosis) and anhydrosis over the forehead with otherwise normal facial sweating. We report two cases of Raeder's syndrome whose cause had not been found despite of intensive investigation and one case associated with nasopharyngeal tumor. The first case had a headache, miosis, ptosis but had not cranial nerve palsy. The second case had a unilateral facial headache, oculosympathetic paralysis, aoydrosis of forehead and sensory change in the ipsilateral ophthalmic division of the trigeminal nerve. The third case had a headache, miosis, ptosis, anhydrosis of forehead and sensory change in the whole territory of the trigeminal nerve.

Two Cases of Thoracic Myelopathy Secondary to Ossification of the Ligamentum Flavum

Hypertrophied ligamentum flavum is not a common cause of myelopathy. Only a minority of cases in the previous reports of myelopathy or radiculopathy secondary to thickening of the ligamentum f lavum had calcification of the ligamentum. We report two cases of thoracic myelopathy caused by ossified ligamentum flavum. One case was a twenty-five year old female who complained of weakness of lower limbs. The other was a fifty-three year old male who complained of tingling sensation on both lower extremities and weakness of right leg. These two patients showed weakness of lower extremities associated with hypesthesia below the level of calcified ligamentum flavum, positive ankle clonus, extensor plantar response, and hyperreflexia. Magnetic resonance imaging (MRI) showed clearly the spinal cord compression at the second to fourth thoracic level by a low-intensity-signal lesion. Metrizamide myelography with computerized tomography showed precise preoperative diagnosis and anatomic localization of the lesion. About one month after laminectomy and removal of the ossified ligaments flava, there was improvement of weakness, hypesthesia and ankle clonus.

Cyanide-induced Parkinsonism

Since cyanide poisoning is almost always fatal, reports of surviving patients to develop neurologic signs are rare. Systemic hypoxemia was not documented with arterial blood gases : however, significant tissue hypoxia most likely occurred from the action of cyanide. A38-year-old man ingested cyanide in a suicidal attempt. He was treated and survived the poisoning episode. But one week later, he showed classic extrapyramidal symptoms and signs, characterized by pit disturbance, bradykinesia, increased muscle tone, micrographia, tremor, apraxia of eyelid opening, palilalia. These symptoms and signs continued to progress, and response to levo-dopa and anticholinergics was poor, except apraxia of eyelid opening. About 3 months later, brain MRI showed abnormal signals (increas ed signal intensity on T2WI, decreased signal intensity on TIWI) in both globus pallidus and a part of putamen, but hippocompus and substantia nigra was normal. After 16 months, follow-up brain MRI showed the same findings. Although brainstem auditory evoked potential(BAEP) was normal, motor evoked potential(MEP) showed prolongation of central motor conduction time(CMCT) in right upper and lower extremities, then wecould suspect subtle changes in pyramidal tract. We report a patient as cyanide-induced parkinsonism by history, neuroimaging finding, and clinical parkinsonian symptoms and signs.

A Case of Circling Seizure

Circling seizure in which the patient walks repetitively in samall circles is relatively uncommon and may either represent a benign form of primary generalized epilepsy or occur secondary to a focal epileptic activity. Especially circling due to focal seizure activity has been regarded as rare. The authors report 6-year old boy who showed many repetitive circling behavior toward the left side, running automatism, vocalization and mental confusion for 6 hours. He had a history of relatively intractable epilepsy for 3 years of adversive seizures(turning to the right side), staring and vocalzation followed by tonic fencing posturing with cyanosis. The electroencephalography demonstrated frequent focal spikes in the left fronto-temporal area.