Journal of child neurology · 2011
Late infantile neuronal ceroid lipofuscinosis and dopamine deficiency.
Клинический случайСтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Le Ngoc Minh D, Parikh Sumit
Аннотация
Neuronal ceroid lipofuscinosis is a severe neurodegenerative lysosomal storage disorder. Gamma-aminobutyric acid and glutamate deficiency have been reported with CLN1, CLN3, and CLN6. Isolated biopterin/neopterin without dopamine deficiency has been reported in 1 patient with a CLN2 mutation. This report describes a patient with a CLN2 mutation with symptomatic biopterin and dopamine deficiency. A 4-year-old boy presented with intractable epilepsy and developmental regression starting 1 year previously. His exam showed retinopathy, scanning speech, dysmetria, and ataxic fenestrating gait with stooped posture. Electroencephalogram showed generalized spikes with occipital spikes on slow photic stimulation. Brain magnetic resonance images 1 year apart showed significant diffuse atrophy. CLN2 gene sequencing showed pathogenic compound heterozygous mutations. Cerebrospinal fluid neurotransmitters showed low homovanillic acid and tetrahydrobiopterin. Levodopa-carbidopa resulted in dramatic improvement of gait. Dopamine/biopterin deficiency is a possible secondary manifestation of CLN2 mutations. Levodopa and dopamine agonists might be useful in treating these secondary abnormalities and improving quality of life in these patients.