How often do neurological disorders lead to dizziness in childhood?

OBJECTIVE: The aim of the study was to determine the features and differential diagnosis of childhood dizziness and find out the prevalence of neurological diseases in children who were referred to the pediatric neurology outpatient clinic. A secondary aim was to evaluate the outcome of dizziness after 12 months. MATERIAL AND METHODS: The records of children with a complaint of dizziness that were referred to the pediatric neurology outpatient clinic were retrospectively reviewed, and detailed medical and family history, clinical characteristics, laboratory investigations including vitamin B12 levels, and neuroimaging tests were analyzed. Patients were grouped as neurological disorders and non-neurological disorders. Neurological disorders included vestibular migraine, benign paroxysmal vertigo, and epilepsy, and non-neurological disorders contained the remaining disorders. RESULTS: The study consisted of 60 children (36 females, 24 males) with a mean age of 11.7±4.1 years. The most common diagnoses were vestibular migraine (21.7%) and orthostatic hypotension (20%). We found that the incidence of neurological diseases was 40% (vestibular migraine, 21.7%; epilepsy, 10%; benign paroxysmal vertigo, 8.3%). When we compared the neurological disorders with non-neurological disorders, there was a significant difference in terms of age at onset and duration of attacks (p=0.001 for both), whereas no significant difference was detected in terms of gender, frequency of attacks, and vitamin B12 levels. We detected ongoing symptoms in 10% of the patients who were diagnosed with vestibular migraine and psychogenic dizziness. CONCLUSION: Both non-neurological and neurological diseases are common in etiology of children with dizziness.

Interictal epileptiform discharges on electroencephalography in children with methylenetetrahydrofolate reductase (MTHFR) polymorphisms.

OBJECTIVE: Methylenetetrahydrofolate reductase (MTHFR) is an important enzyme involved in folate metabolism. MTHFR C677T and A1298C polymorphisms are best-defined variants of MTHFR that were reported to be associated with epilepsy development. The aim of the study was to determine the incidence of interictal epileptiform discharges on electroencephalography (EEG) in asymptomatic children with C677T and A1298C polymorphisms who had no history of seizure. METHODS: Children with MTHFR C677T or A1298C polymorphisms who had normal neurological examination without a history of seizure were included in the study. Blood samples for serum folate, vitamin B12, and homocysteine levels were analyzed. Sleep and awake electroencephalograms (EEG) were recorded. RESULTS: A total of 102 children (50 girls and 52 boys) with a mean age of 59.4 ± 58.7 months were included in the study. Interictal epileptiform EEG discharges were detected in 3 children (2.9%). CONCLUSION: There was no increase in the prevalence of interictal epileptiform discharges in seizure-free and asymptomatic children with MTHFR C677T and A1298C polymorphisms.

Risk factors associated with epilepsy development in children with cerebral palsy.

OBJECTIVES: Epilepsy is one of the most common and important comorbidity among patients with cerebral palsy (CP). The purpose of this study was to determine the risk factors predicting the development of epilepsy considering prenatal, perinatal, and natal characteristics; associated impairments; and cranial imaging findings in our patient population with cerebral palsy at a tertiary center in Istanbul, Turkey. METHODS: This retrospective study consisted of 234 children aged between 3 and 18 years of age. Children were divided into two groups as CP patients with epilepsy (126 patients) and CP patients without epilepsy (108 patients). Demographic features and clinical and cranial magnetic resonance imaging (cMRI) findings were compared between the two groups. RESULTS: Presence of family history of epilepsy, history of neonatal seizure especially in the first 72 h of life, quadriplegic type of CP, severe degree of gross motor function and fine motor disorders, and moderate to severe mental retardation or psycho-social developmental delay were determined as risk factors for the development of epilepsy in CP patients. Also, an increased risk of epilepsy was detected in term infants and appropriate for gestational age (2500-4000 g) infants. On the other hand, presence of parental consanguinity, being born from a primiparous mother, age of mother at birth, mode of delivery, presence of multiple gestation and labor problems, history of follow-up in neonatal intensive care unit and intubation, and cMRI findings were not significant risk factors for the development of epilepsy in CP. CONCLUSION: Predicting epilepsy development by determining the risk factors in patients with CP might be useful because knowing the risk factors could provide close follow-up of these patients for epilepsy.

The frequency of late-onset Pompe disease in pediatric patients with limb-girdle muscle weakness and nonspecific hyperCKemia: A multicenter study.

The aim of this multicenter study was to screen for late-onset Pompe disease in high-risk children with limb-girdle muscle weakness and nonspecific hyperCKemia using the dried blood spot (DBS) test. Seventy-two children from four pediatric neurology departments in Turkey were enrolled in the study: 37 with limb-girdle muscle weakness and 35 with nonspecific hyperCKemia. Acid α-glucosidase (GAA) activity was measured on DBS by tandem mass spectrometry. Six patients tested positively for Pompe disease. In three patients, one with the limb-girdle muscle weakness and two with nonspecific hyperCKemia, this was confirmed by genetic analysis. The overall frequency of late-onset Pompe disease in the study population was 4.2%. The c.1784C>T mutation found in one patient is a new mutation whereas the c.1655T>C mutation detected in the other two patients is not novel. In conclusion, Pompe disease should be suspected in patients with limb-girdle muscle weakness and nonspecific hyperCKemia. The DBS test is a safe and reliable method of diagnosis but must be confirmed by genetic analysis. In patients with a positive DBS test and negative genetic analysis, tissue assay of GAA should be considered.