Il Saing Choi

Parkinsonism after Carbon Monoxide Poisoning

Of 242 patients with carbon monoxide (CO) poisoning examined between 1986 and 1996, parkinsonism was diagnosed in 23 (9.5%). There were 11 men and 12 women. The age at onset ranged from 16 to 69 (mean 45.8) years, with the peak incidence during the 6th decade. The latency before the appearance of parkinsonism varied from 2 to 26 (median 4) weeks, but parkinsonism developed within 1 month after an acute insult in the majority of the patients. All showed encephalopathy with mildly to severely impaired cognitive functions during or immediately after delayed CO sequelae. The common symptoms were gait disturbance, impaired mentality, urinary incontinence, and mutism. The most frequent signs were short-step gait, hypokinesia, masked face, increased muscle tone (rigidity), glabella sign, grasp reflex, and retropulsion. Intentional tremor was occasionally found, but resting tremor could not be seen. There was no correlation between the neuroimaging findings and the development of parkinsonism. Levodopa and anticholinergic drugs were not effective. Of 16 patients followed up for 1 year, 13 (81.3%) recovered spontaneously within 6 months. In conclusion, parkinsonism after CO poisoning is not rare and usually appears as a part of delayed CO encephalopathy. Any drug is not effective, but the prognosis is good.

Delayed Movement Disorders after Carbon Monoxide Poisoning

Of 242 patients with carbon monoxide (CO) poisoning examined between 1986 and 1996, delayed movement disorders were diagnosed in 32 (13.2%). There were 15 men and 17 women. Ages at insult ranged from 9 to 69 years (mean 45.3 years). Of the 32 patients with delayed movement disorders, 23 (71.9%) had parkinsonism, 5 dystonia, 3 chorea and 1 myoclonus. All were associated with delayed CO encephalopathy. The median latency between CO poisoning and the onset of movement disorders was 4 weeks for parkinsonism, 51 weeks for dystonia, 4 weeks for chorea and 8 weeks for myoclonus. The latency of dystonia onset after CO poisoning was longer than that of other types of movement disorders. The CT findings in delayed movement disorders after CO poisoning were variable, and there was no correlation between the sites of imaging and the development of movement disorders. Abnormal dyskinesias disappeared within 8 weeks, and patients recovered from parkinsonism within 6 months. In conclusion, delayed movement disorders after CO poisoning are not rare, and usually appear as a part of delayed CO encephalopathy. The prognosis is good.

Idiopathic Hypertrophic Pachymeningeal Lesions

Nine patients with intracranial pachymeningeal thickening and enhancement on magnetic resonance imaging (MRI) completed a short-term clinical and MRI follow-up study. Based on clinical pictures, 4 of them were found to have spontaneous intracranial hypotension (SIH) and the remaining 5 had idiopathic intracranial pachymeningitis (IIP). Both groups were compared regarding their clinical and MRI characteristics. In 4 patients with SIH, gadolinium-enhanced T1-weighted images (WI) showed a diffuse and even enhancement of the entire intracranial and spinal dura mater. These thickened dura was slightly hyperintense on T2-WI. They had a favorable prognosis. In 2 patients with IIP, MRI demonstrated a relatively focal and even thickening and enhancement of the intracranial dura which was slightly hyperintense with a central hypointense area on T2-WI. These patients showed a very favorable course with or without steroid pulse therapy. In the remaining 3 patients with IIP, MRI depicted a focal, uneven enhancement of the intracranial dura which was relatively hypointense on T2-WI. Two of them with prolonged symptoms had a remitting and relapsing course, and 1 had a favorable outcome. In spite of current limitations in identifying the underlying causes of idiopathic pachymeningeal abnormalities, MRI can characterize the different patterns of pachymeningeal thickening. These findings may also correlate with the clinical picture and may be useful in predicting the response to treatment and prognosis.

Combined Therapy of Corticosteroid and Azathioprine in Hypertrophic Cranial Pachymeningitis

Hypertrophic cranial pachymeningitis (HCP) is a rare inflammatory disease of unknown origin in which recurrence is frequently observed in spite of the initial response to steroid therapy. Three patients, 1 man and 2 women, aged 63, 66, and 67 years, with severe intractable headache were evaluated by brain MRI. All patients were initially given prednisolone (60 mg/day, oral) or dexamethasone (20 mg/day, i.v.), and followed by long-term (at least 1 year) azathioprine therapy. All patients were evaluated by follow-up laboratory tests and brain MRI study, and completed the 2-year follow-up period. Symptoms including headache were initially improved with corticosteroid therapy, but patients became steroid-dependent. Azathioprine administration in these steroid-dependent patients permitted the complete cessation of corticosteroid and led to the clinical and radiological recovery. In conclusion, initial high-dose corticosteroid administration followed by long-term azathioprine therapy may be the ideal treatment of HCP at present.

Evaluation of Outcome of Delayed Neurologic Sequelae after Carbon Monoxide Poisoning by Technetium-99m Hexamethyl-propylene Amine Oxime Brain Single Photon Emission Computed Tomography

Using brain computed tomography (CT) and single photon emission computed tomography (SPECT) with technetium-99m hexamethylpropylene amine oxime (99mTc HM-PAO) in 13 patients with delayed neurologic sequelae after carbon monoxide poisoning, we tried to evaluate the clinical outcome of delayed CO sequelae. Among the 13 initial brain CTs, seven showed low density in the cerebral white matter and one revealed hypodensity in both globi pallidi. Of the 7 follow-up CT scans, 3 have remained unchanged, but in 4 cases more aggravating patterns with cortical atrophy without the clinical correlation were observed. There was no correlation between the CT findings and the outcome of delayed CO sequelae. All initial SPECTs in 13 patients with delayed CO sequelae showed diffuse patchy hypoperfusion throughout the cerebral cortex. Among the follow-up SPECTs in 7 patients, 6 patients showed increased cerebral perfusion with the concomitant clinical improvement, but the SPECT of a patient in bedridden state had remained unchanged, compared with the initial SPECT. There seemed to be good correlation between the findings of SPECT and the outcome of delayed CO sequelae. In conclusion, 99mTc HM-PAO brain SPECT is more sensitive than CT, and may be a useful test in evaluating the clinical outcome of delayed neurologic sequelae after CO poisoning.

Early Hypoperfusion of Technetium-99m Hexamethylprophylene Amine Oxime Brain Single Photon Emission Computed Tomography in a Patient with Carbon Monoxide Poisoning

Single photon emission computed tomography (SPECT) with technetium-99m (99mTc) hexamethylprophylene amine oxime (HM-PAO) were repeatedly performed in a 55-year-old woman with carbon monoxide (CO) poisoning. The initial brain SPECT 10 days after anoxic insult showed focal hypoperfusion which appeared 20 days prior to the onset of delayed neurologic sequelae, and the findings of follow-up SPECTs correlated with the clinical course of CO poisoning. The possibilities of early hypoperfusion on SPECT of acute CO poisoning were discussed.