Intraventricular administration of interferon and administration of methisoprinol by mouth in the treatment of adult‐onset subacute sclerosing panencephalitis

Mg, Harbord; Jones, Tyler S; Ep, Hicks; Blumbergs, P. C.

doi:10.5694/j.1326-5377.1988.tb139573.x

Cited by 5 publications

(2 citation statements)

References 8 publications

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“…This is a previously undescribed adverse effect of IFN-a-2a (which cannot be attributed to inosiplex, because the drug was not administered in case 2), probably caused by the prolonged administration of the drug and the higher doses than used in other studies [4,5,8,9,12,14]. For the upper motor neurons, these included Babinski signs in an early stage of the disease (both cases), with reduced amplitude and normal latency of the motor response to cortical stimulation, as well as pyramidal hypertonus, appearing after a reduction in lower motor neuron signs (Case 1).…”

Section: Discussionmentioning

confidence: 99%

“…Recent reports suggest that the course of subacute sclerosing panencephalitis (SSPE) can be improved by the intraventdcular (IVC) administration of interferon-alpha (IFN-c0 [2,4,5,8,9,12,14], although the persistent neurotoxicity of both systemic (see review in [7]) and IVC IFN-ct administration has also been reported. Impairment of vigilance, confusional state, cognitive and mnesic deficits, affective disorders, parkinsonian symptoms and EEG slowing are the most commonly described effects, and they have not always proved to be easily reversible after the discontinuation of treatment.…”

Section: Introductionmentioning

confidence: 99%

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Toxic effect of intraventricular interferon-alpha in subacute sclerosing panencephalitis

et al. 1994

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Intraventricular interferon (IFN) administration has been shown to improve the course of SSPE. However, in 2 patients treated with intraventricular IFN-alpha-2a over a long period, we observed the appearance of clinical and EMG signs suggestive of upper and lower motor neuron pathology. These signs improved slightly in one patient after the discontinuation of IFN. It is suggested that this poly-peptide may act on specific kinds of nervous cells which selectively suffer together in various well-known neurological diseases.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Toxic effect of intraventricular interferon-alpha in subacute sclerosing panencephalitis

et al. 1994

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Neurotoxicity of intraventricularly administered alpha-interferon for leptomeningeal disease

Meyers

Obbens

Scheibel

et al. 1991

Cancer

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Nine patients with leptomeningeal disease are reported who were treated with intraventricular alpha-interferon (alpha-IFN). In seven of these patients, a progressive vegetative state developed during treatment. The patients became unresponsive to verbal commands but opened their eyes with auditory or tactile stimulation. It took an average of 3 weeks for these patients to become verbally responsive after treatment was discontinued. Electroencephalographic findings showed evidence of irritative involvement of the deep midline nuclei in 80% of patients. Periventricular white matter changes developed during treatment in three of six patients who underwent computed tomographic scans. All patients with this severe neurotoxicity received whole-brain irradiation before treatment. Possible mechanisms for the development of this neurotoxic syndrome are discussed. The neurotoxicity of alpha-IFN and brain irradiation may be additive, suggesting a cautious approach when using this combination for treatment.

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Progressive Multifocal Leukoencephalopathy in a Patient with Hypogammaglobulinemia

et al. 1998

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We describe a child with congenital hypogammaglobulinemia that was diagnosed at 13 months of age. When he was 4 years old, gait disturbances began. The main neurological manifestations were progressive spastic tetraparesis and intellectual and speech deterioration. No infectious agent was identified. A magnetic resonance imaging scan of the central nervous system revealed periventricular demyelinating areas in the frontal, temporal, and parietal lobes with cortical atrophy. Stereotactic brain biopsy confirmed the diagnosis of progressive multifocal leukoencephalopathy caused by JC virus. He was treated with intravenous and intraventricular cytarabine and interferon-alpha, and there was clinical improvement. We emphasize the need for brain biopsy as soon as a neurological complication is suspected in patients with congenital hypogammaglobulinemia for whom cerebrospinal cultures or polymerase chain reaction analyses are negative.

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Intraventricular administration of interferon and administration of methisoprinol by mouth in the treatment of adult‐onset subacute sclerosing panencephalitis

Cited by 5 publications

References 8 publications

Toxic effect of intraventricular interferon-alpha in subacute sclerosing panencephalitis

Toxic effect of intraventricular interferon-alpha in subacute sclerosing panencephalitis

Neurotoxicity of intraventricularly administered alpha-interferon for leptomeningeal disease

Progressive Multifocal Leukoencephalopathy in a Patient with Hypogammaglobulinemia

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