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Clinical spectrum of secondary parkinsonism in childhood: a reversible disorder
M R Pranzatelli1, S H Mott, S G Pavlakis
1Department of Neurology, George Washington University, Washington, D.C. 20010.
Insights
Acquired parkinsonism in children is rare but treatable. Diverse etiologies, including infections and medications, can cause this movement disorder, with most patients showing significant improvement.
Area of Science:
- Pediatric Neurology
- Movement Disorders
- Neuroscience
Background:
- Parkinsonism is infrequently observed in pediatric populations.
- This study details six unique cases of acquired parkinsonism in hospitalized children.
Observation:
- Clinical presentations varied, including akinetic-rigid syndromes, tremor, parkinsonism with dystonia, and parkinsonism-plus syndromes.
- Associated symptoms frequently included altered mental status, mutism, dysphagia, and sialorrhea.
- Identified etiologies encompassed hypoxic-ischemic encephalopathy, medication toxicity (haloperidol, chemotherapy agents), viral encephalitides, and a pineal tumor.
Findings:
- Cranial MRI findings ranged from normal to severe cerebral and cerebellar atrophy.
- Despite initial severity requiring pharmacotherapy, all patients demonstrated dramatic improvement, with some achieving complete symptom resolution.
- Two patients improved without specific treatment, and none required long-term antiparkinsonian medication.
Implications:
- Recognizing diverse causes of childhood parkinsonism is crucial for accurate diagnosis and timely treatment.
- Prompt diagnosis and management can lead to significant recovery, challenging the notion of irreversible neurological deficits in these cases.
- The findings highlight that causes of parkinsonism in pediatric hospitals are often more common than rare genetic forms like Segawa syndrome.
Abstract:
Parkinsonism is an uncommon movement disorder in childhood. Six unusual cases of acquired parkinsonism in hospitalized children are described. Clinical manifestations included an akinetic-rigid syndrome with and without tremor, the combination of parkinsonism and dystonia, and a parkinsonism-plus syndrome. Altered mental status, mutism, dysphagia, and sialorrhea were frequent associations. Etiologies included hypoxic-ischemic encephalopathy; haloperidol treatment with and without neuroleptic malignant syndrome; toxicity of cytosine arabinoside, cyclophosphamide, amphotericin B, and methotrexate; St. Louis encephalitis and other encephalitides; and a pineal tumor with hydrocephalus. Cranial magnetic resonance imaging results ranged from normal to profound cerebral and cerebellar atrophy with chemotherapeutic toxicity. The illnesses usually were severe enough to require pharmacotherapy. Incorrect diagnoses of depression or catatonia delayed treatment or aggravated the problem. Acute treatment included amantadine, levodopa/carbidopa with or without selegiline, diphenhydramine, or benztropine. The concentration of CSF homovanillic acid was normal in a neuroleptic-associated patient, but the level was low in an encephalitic patient. All patients demonstrated dramatic improvement, including two who were not treated; some had complete resolution of symptoms and none required continued antiparkinsonian drugs despite poor scores on the Unified Parkinson's Disease Rating Scale and the Modified Hoehn and Yahr Rating Scales. The causes of parkinsonism described are more common in a general pediatric hospital than the parkinsonism associated with the popularized Segawa syndrome.