Neurologic complications of 2009 influenza-a H1N1 infection in children.

Little is known about the neurologic complications of the 2009 Influenza-A H1N1 epidemic in children. We present a retrospective analysis of children evaluated at a tertiary children's hospital who tested positive for H1N1 with neurologic complications. A total of 164 children tested positive for H1N1. Thirty-one of these patients (19%) were evaluated and discharged from the emergency department. Thirty-nine (24%) were treated in the intensive care unit, the remaining 94 (57%) were treated in medical in-patient units. Six subjects died (3.7%). Neurologic complications identified included headache, encephalitis, polyneuropathy, seizures, and malignant hyperthermia. The rate of neurologic complications in this cohort of patients who tested positive for H1N1 was 19%. The incidence of serious neurologic complications was 3%, with another 3% of patients who experienced rapid clinical deterioration and subsequently died. Our observation of neurologic complications associated with 2009 influenza-A H1N1 epidemic suggests the need for clinical vigilance during future influenza epidemics.

Detection of coronavirus in the central nervous system of a child with acute disseminated encephalomyelitis.

We present a case in which human coronavirus was detected in the cerebrospinal fluid of a child presumed to have acute disseminated encephalomyelitis. In murine models, coronavirus has been found to cause a chronic demyelinating condition that resembles multiple sclerosis. Additionally, there is in vitro evidence of human coronavirus's ability to infect neural cells. This case report provides additional support for the hypothesis that coronavirus may be an important etiologic factor in the pathogenesis of demyelinating disease in humans.

Hyperkinetic seizures in children.

The objective of this study was to delineate the clinical and video-electroencephalographic (EEG) manifestations of children with complex partial seizures with a predominant "hyperkinetic" presentation. Certain types of partial seizures can be difficult to differentiate from nonepileptic seizures because of their intense motor presentation and, at times, lack of alteration of consciousness. Based on a published semiologic seizure classification, this type of seizures can be described as "hyperkinetic," characterized by intense motor activity involving the extremities and trunk. We report five children diagnosed with hyperkinetic seizures by video-EEG monitoring. All patients were referred for video-EEG evaluation because of an initial suspicion of pseudoseizures. Presented in this study is a review of the patients' clinical data, including video-EEG evaluation. There were three boys and two girls; the mean age at presentation was 10 +/- 3 years. In four patients, there was a history of behavioral disorder, with two patients carrying a diagnosis of attention-deficit hyperactivity disorder (ADHD). One girl had significant developmental delay and an abnormal neurologic examination. Brain magnetic resonance imaging was normal in three patients and abnormal in two. The semiology of the seizures consisted of stereotypic intense motor activity, mainly upper extremity flailing and kicking. Screaming and shouting were noted in three cases, and intense fear was present in two patients. The hyperkinetic ictal activity progressed to tonic-clonic seizures in two patients. Seizures occurred out of sleep or on awakening in four patients. The interictal EEG activity was normal in one patient and revealed a continuous generalized slowing and slowing of the posterior dominant rhythm in two patients. One of the latter patients had interictal epileptiform activity in the frontal and midline regions. An intermittent rhythmic slow activity of the left hemisphere with superimposed bifrontal sharp waves was noted in the fifth patient. The ictal EEG revealed profuse superimposed electromyographic (EMG) activity in all patients, making some of the EEG interpretation difficult to analyze, particularly a longitudinal bipolar montage. However, with digital manipulation of the ictal EEG data, such as changes in EEG sensitivity, application of fast frequency filters, and use of different EEG montages, it was possible to discern an ictal EEG pattern or postictal slowing following the diffuse EMG artifact in all patients. On clinical follow-up, adequate seizure control was achieved in three patients. Based on the clinical history, one patient was diagnosed with autosomal dominant nocturnal frontal lobe epilepsy. Diagnosis of hyperkinetic seizures can be difficult because of the similarity of the clinical manifestations with nonepileptic events such as certain parasomnias and pseudoseizures. Video-EEG is the most effective way of diagnosing this type of seizure.

Acute disseminated encephalomyelitis in children.

OBJECTIVE: To describe the epidemiologic, clinical, neuroimaging, and laboratory features; treatment; and outcome in a cohort of children with acute disseminated encephalomyelitis (ADEM). METHODS: A 6-year retrospective chart review of children with the diagnosis of ADEM was conducted. RESULTS: Eighteen cases were identified. Sixteen patients (88%) presented in either winter or spring. Thirteen children (72%) had a recent upper respiratory tract illness. Patients presented most often with motor deficits (77%) and secondly with altered consciousness (45%). Spinal fluid abnormalities occurred in 70%. Despite rigorous microbiologic testing, a definite microbiologic diagnosis was established only in 1 child with Epstein-Barr virus disease and probable or possible diagnoses in 3 children with Bartonella henselae, Mycoplasma pneumoniae, or rotavirus disease. Brain magnetic resonance imaging identified lesions in the cerebral cortex in 80%, in subcortical white matter in 93%, in periventricular white matter in 60%, in deep gray matter in 47%, and in brainstem in 47% of patients. Eleven patients (61%) were treated with corticosteroids, and 2 were treated with intravenous immunoglobulins. All patients survived. Three patients (17%) had long-term neurologic sequelae. CONCLUSIONS: Epidemiologic evidence from this study suggests an infectious cause for ADEM. The agent is most likely a difficult-to-diagnose winter/spring respiratory virus. Magnetic resonance imaging was the neuroimaging study of choice for establishing the diagnosis and for following the course of the disease. Prognosis for survival and outcome was excellent. Recurrent episodes of ADEM must be differentiated from multiple sclerosis.

Pseudomigraine with prolonged aphasia in a child with cranial irradiation for medulloblastoma.

We report a 12-year-old child with episodes of migraine-like headaches with visual and motor auras a year after the surgical resection and radiation therapy for medulloblastoma The patient presented with an episode of headache, prolonged aphasia, right hemiparesis, status epilepticus, and salt wasting. There was no evidence of a structural lesion. The neurologic deficits resolved over a period of 6 weeks. Because of the progressive deterioration in neurologic deficits, the patient underwent an extensive battery of laboratory tests and multiple neuroimages, all of which were normal. The unusually prolonged neurologic deficit in this patient without demonstrable structural lesions and his eventual complete recovery were most likely caused by ischemia in the left hemisphere secondary to vasospasm. This presentation mimics migraine headache. Evidence suggesting that this represents a long-term complication of treatment of children with central nervous system neoplasia is presented.

Diffuse magnetic resonance imaging white-matter changes in a 15-year-old boy with mitochondrial encephalomyopathy.

We report a 15-year-old boy who presented with recurrent headaches associated with numbness, confusion, and speech difficulty. Brain magnetic resonance imaging (MRI) revealed diffuse bilateral white-matter hyperintensity on fluid-attenuated inversion-recovery and T2-weighted images in the internal capsule, periventricular and subcortical white matter, base of the pons, and middle cerebellar peduncles. Lesions were isointense on T1-weighted images and nonenhancing. Muscle biopsy showed changes consistent with a mitochondrial myopathy. Mitochondrial respiratory chain enzyme activity analysis revealed a significant reduction in complex II activity. Genetic testing was negative. We conclude that mitochondrial encephalomyopathy may present with unusual diffuse supratentorial and infratentorial white-matter changes on MRI.