A case of dyskinetic cerebral palsy resembling post-anoxic action myoclonus

Sugama, Seiichi; Kusano, Kaoru

doi:10.1016/0387-7604(95)00030-f

Cited by 6 publications

(8 citation statements)

References 9 publications

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“…Some reports have suggested that the symptoms of myoclonus after perinatal anoxia of the ascending efferents of the basal ganglia to the thalamus and the thalamocortical pathways are not observed in the first decade of life, despite the development of pathological lesions specific to these symptoms [22,23] . Moreover, Sugama and Kusano [3] suggested that the development of movement disorder due to perinatal anoxia may be related to the maturation of the thalamus after birth. Our patient could thus have been in a thalamotomy-like state during the infantile period because of the immaturity of the thalamus.…”

Section: Discussionmentioning

confidence: 99%

“…Perinatal anoxia can, on rare occasions, induce myoclonus as the main neurologic abnormality [1][2][3] . The detailed pathophysiology of postperinatal anoxic myoclonus remains unknown.…”

Section: Discussionmentioning

confidence: 99%

“…Myoclonus is rarely the main neurologic sequela of perinatal anoxia [1][2][3] ; it is more commonly observed after brain anoxia in adults [1][2][3] . Deep brain stimulation (DBS) of the thalamus (thalamic DBS) is effective for the treatment of tremors [4][5][6][7][8][9][10][11][12][13] .…”

Section: Introductionmentioning

confidence: 99%

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Thalamic Deep Brain Stimulation for the Treatment of Action Myoclonus Caused by Perinatal Anoxia

Kobayashi

Katayama

Otaka

et al. 2010

Stereotact Funct Neurosurg

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Background: Perinatal anoxia rarely causes myoclonus as the main neurologic abnormality. The exact neuronal mechanism underlying myoclonus induced by perinatal anoxia remains unknown. Some studies have indicated that the development of involuntary movements may be related to the maturation of the thalamus after birth. Objectives and Methods: Here, we describe the first case of a patient who developed action myoclonus after experiencing perinatal anoxia and was successfully treated by chronic deep brain stimulation (DBS) of the thalamus (thalamic DBS). Results andConclusion: The effectiveness of chronic thalamic DBS in this patient supports the concept of involvement of the thalamus in postperinatal anoxic myoclonus.

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Section: Discussionmentioning

confidence: 99%

“…Perinatal anoxia can, on rare occasions, induce myoclonus as the main neurologic abnormality [1][2][3] . The detailed pathophysiology of postperinatal anoxic myoclonus remains unknown.…”

Section: Discussionmentioning

confidence: 99%

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Thalamic Deep Brain Stimulation for the Treatment of Action Myoclonus Caused by Perinatal Anoxia

Kobayashi

Katayama

Otaka

et al. 2010

Stereotact Funct Neurosurg

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“…Most patients who develop post-hypoxic myoclonus are between the ages of 15 and 60 years (Frucht 2002), whereas such movement disorders are very rarely reported in childhood. Obeso et al (1983) and Sugama and Kusano (1995) reported children with action myoclonus that appeared beginning a few years after perinatal asphyxia.…”

mentioning

confidence: 99%

“…From the day of admission, generalized clonic movements that could be elicited by tactile stimulation were observed frequently, especially during periods of wakefulness. These phenomena were easily Post-hypoxic myoclonus (Lance and Adams 1963;Obeso et al 1983;Sugama and Kusano 1995;Hallett 2000) is caused by hypoxicischemic brain injuries. There are two types of post-hypoxic myoclonus, acute and chronic.…”

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confidence: 99%

Neonatal-Onset Brainstem Reticular Reflex Myoclonus Following a Prenatal Brain Insult: Generalized Myoclonic Jerk and a Brainstem Lesion

Kakisaka

Haginoya

Togashi

et al. 2007

Tohoku J. Exp. Med.

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Brainstem reticular reflex myoclonus (BRRM) is characterized by sudden, generalized, shock-like movements that can be elicited by sensory stimulation. We present a boy, born after 35 weeks gestation, who was diagnosed with neonatal-onset BRRM. Within 1 hr of birth, the patient showed spasticity and generalized clonic movements of all limbs elicited with tactile stimulation anywhere on the body. Surface electromyography showed co-contraction of agonistic and antagonistic muscles, revealing that his generalized clonic movements were tremulous myoclonus in nature. Brain magnetic resonance imaging (MRI) at 21 hrs after birth disclosed highintensity lesions in the Rolandic area, thalamus, basal ganglia, and brainstem, including the dorsal pons and medulla, the center of BRRM, in T1-weighted images. Follow-up MRI at 1 month revealed dramatic improvement in the pontine lesion. The patient showed gradual remission of the characteristic movements, which disappeared at 1 year of age, but the patient died unexpectedly at 1 year and 3 months. In conclusion, neonatal BRRM arises as a result of severe brainstem injury, and the associated lesions may only be seen temporarily on MRI taken soon after birth. prenatal brain insult; brainstem lesion; brainstem reticular reflex myoclonus; stimulus-sensitive generalized clonic movement

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Deep Brain Stimulation in a Case of Mitochondrial Disease

Martínez-Ramírez

Hack

Vasquez

et al. 2015

Movement Disord Clin Pract

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Background DBS has proven to be an effective therapy for Parkinson's disease, essential tremor, and primary dystonia. Mixed results have been reported in case series for other hyperkinetic disorders, and sparse data are available regarding secondary movement disorders. We report on the clinical effects of bilateral globus pallidus internus (GPi) DBS, a progressive mitochondrial cytopathy. Methods A single patient with myoclonus and dystonia syndrome secondary to a mitochondrial cytopathy with history of perinatal hypoxia was identified from our University of Florida DBS database. Demographics, clinical, surgical, and DBS data were documented. Results At 6 months post‐DBS, we observed a 32% (361 to 527) improvement on quality of life (36‐item Medical Outcome Study Short‐Form Health Survey; SF‐36). Objective clinical scales revealed a 33% (143 to 96) improvement in the Unified Myoclonus Rating Scale (UMRS) total score. The UMRS action myoclonus subsection revealed a 29% (69 to 46) improvement. No significant changes were observed in the Burke‐Fahn‐Mardsen Dystonia Rating Scale (BFMDRS). After 1‐year follow‐up, a worsening of 59% (527 to 215) was observed in the SF‐36 scale, of 19% (28.5 to 35) in the BFMDRS, and of 23% (96 to 124) in the UMRS. However, the frequency and intensity of action myoclonus scores remained lower when compared to baseline scores. Conclusions Although we observed a loss of benefit in the long term for most quality‐of‐life and clinical outcomes, the DBS effects on action myoclonus seemed to remain stable. Longer follow‐up studies are necessary to confirm our short‐term and unblinded findings.

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A case of dyskinetic cerebral palsy resembling post-anoxic action myoclonus

Cited by 6 publications

References 9 publications

Thalamic Deep Brain Stimulation for the Treatment of Action Myoclonus Caused by Perinatal Anoxia

Thalamic Deep Brain Stimulation for the Treatment of Action Myoclonus Caused by Perinatal Anoxia

Neonatal-Onset Brainstem Reticular Reflex Myoclonus Following a Prenatal Brain Insult: Generalized Myoclonic Jerk and a Brainstem Lesion

Deep Brain Stimulation in a Case of Mitochondrial Disease

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