Nonconvulsive status epilepticus in pediatric populations: diagnosis and management.

The diagnosis and management of nonconvulsive status epilepticus (NCSE) pose special challenges in childhood. NCSE can be defined as a condition of ongoing or intermittent clinical epileptic activity without convulsions, for at least 30 minutes, with electroencephalographic evidence of seizures. NCSE accounts for approximately one-quarter of all cases of status epilepticus. NCSE should be suspected in children with epilepsy who undergo an otherwise inexplicable change in behavior and in children with recent onset change in speech, memory, school performance. NCSE can be observed in acute neurological injuries, specific childhood epilepsy syndromes, individuals with learning difficulties and other neurological conditions. NCSE is not uncommon in pediatric patients with an altered state of consciousness. NCSE in children is thought to be under-recognized. It is a highly heterogeneous clinical condition that is understudied in the pediatric population. Prompt recognition and treatment may be necessary to improve neurological outcome. Based on clinical semiology alone, diagnosis is difficult and requires emergent EEG. Management is often difficult, with highly variable response to treatment. Here I describe the diagnosis and management of NCSE in children.

Extrapulmonary tuberculosis: tuberculous meningitis new developments.

Tuberculosis (TB) can involve any organ system in the body. Extrapulmonary involvement can occur in isolation or along with a pulmonary focus as in the case of patients with disseminated tuberculosis. Tuberculosis meningitis (TBM) is the most severe form of extrapulmonary tuberculosis. TBM a medical emergency, is still a major cause of serious illness in many parts of the world. TBM remains difficult to diagnose, and it is usually due to hematogenous dissemination of the tubercle bacillus. The exact incidence and prevalence are not known. The clinical spectrum is broad and may be non-specific making early diagnosis difficult. Improved outcome requires early recognition and treatment of these conditions. Clinical features included fever for more than 7 days, headache, or neck stiffness. While TBM is a disease of childhood, tuberculomas and spinal tuberculosis are invariably an adult manifestation. In HIV infection, TB is often atypical in presentation, frequently causing extrapulmonary disease, and patients have a high incidence of TBM. Clinical response to antituberculous therapy in all forms of neurotuberculosis is excellent if the diagnosis is made early before irreversible neurological deficit is established. Diagnosis is based on the characteristic clinical picture, neuroimaging abnormalities, cerebrospinal fluid changes and the response to anti-tuberculosis drugs. Diagnosis is best made with lumbar puncture and examination of the cerebrospinal fluid (CSF). Suspect TBM if there is a CSF leucocytosis (predominantly lymphocytes), the CSF protein is raised, and the CSF plasma glucose is <50%. Rapid techniques based on nucleic acid amplification such as PCR are more sensitive and specific as they attempt to detect specific DNA sequences of the organism. The hallmark pathological processes are meningeal inflammation, basal exudates, vasculitis and hydrocephalus. Treatment delay is strongly associated with death and empirical anti-tuberculosis therapy should be started promptly in all patients in whom the diagnosis of TBM is suspected. Corticosteroids reduce the number of deaths. Development of an effective vaccine against tuberculosis hinges on an improved understanding of the human immune response to Mycobacterium tuberculosis (Mtb). The emergence of drug resistant tuberculosis poses a serious threat to the control of this pathogen, and the development of drugs that are active against the resistant strains is vital. Further research into the epidemiology, immune mechanisms, diagnosis, treatment, and prevention of TBM is urgently needed.

Factor V Leiden mutation and patent foramen ovale in ischemic stroke.

We report a 47-years-old male with ischemic stroke, whose arteriographic and echocardiographic investigations did not reveal any steno-occlusive arterial disease or embolic source from the left cardiac chambers. A transesophageal echocardiogram showed a patent foramen ovale (PFO), whilst laboratory screening for coagulation abnormalities showed heterozygosity for factor V Leiden mutation. The significance of the association of PFO with factor V Leiden mutation is discussed as a possible cause of ischemic stroke through paradoxical embolism from a venous source. The high prevalence of these two conditions in the general population is emphasized and the indication for anticoagulant therapy is discussed.