Nonmicrocephalic Infants with Congenital Zika Syndrome Suspected Only after Neuroimaging Evaluation Compared with Those with Microcephaly at Birth and Postnatally: How Large Is the Zika Virus “Iceberg”?

BACKGROUND AND PURPOSE: Although microcephaly is the most prominent feature of congenital Zika syndrome, a spectrum with less severe cases is starting to be recognized. Our aim was to review neuroimaging of infants to detect cases without microcephaly and compare them with those with microcephaly. MATERIALS AND METHODS: We retrospectively evaluated all neuroimaging (MR imaging/CT) of infants 1 year of age or younger. Patients with congenital Zika syndrome were divided into those with microcephaly at birth, postnatal microcephaly, and without microcephaly. Neuroimaging was compared among groups. RESULTS: Among 77 infants, 24.6% had congenital Zika syndrome (11.7% microcephaly at birth, 9.1% postnatal microcephaly, 3.9% without microcephaly). The postnatal microcephaly and without microcephaly groups showed statistically similar imaging findings. The microcephaly at birth compared with the group without microcephaly showed statistically significant differences for the following: reduced brain volume, calcifications outside the cortico-subcortical junctions, corpus callosum abnormalities, moderate-to-severe ventriculomegaly, an enlarged extra-axial space, an enlarged cisterna magna (all absent in those without microcephaly), and polymicrogyria (the only malformation present without microcephaly). There was a trend toward pachygyria (absent in groups without microcephaly). The group with microcephaly at birth compared with the group with postnatal microcephaly showed significant differences for simplified gyral pattern, calcifications outside the cortico-subcortical junctions, corpus callosum abnormalities, moderate-to-severe ventriculomegaly, and an enlarged extra-axial space. CONCLUSION: In microcephaly at birth, except for polymicrogyria, all patients showed abnormalities described in the literature. In postnatal microcephaly, the only abnormalities not seen were a simplified gyral pattern and calcifications outside the cortico-subcortical junction. Infants with normocephaly presented with asymmetric frontal polymicrogyria, calcifications in the cortico-subcortical junction, mild ventriculomegaly, and delayed myelination

Focus on the management of thunderclap headache: from nosography to treatment

Thunderclap headache (TCH) is an excruciating headache characterized by a very sudden onset. Recognition and accurate diagnosis of TCH are important in order to rule out the various, serious underlying brain disorders that, in a high percentage of cases, are the real cause of the headache. Primary TCH, which may recur intermittently and generally has a spontaneous, benign evolution, can thus be diagnosed only when all other potential underlying causes have been excluded through accurate diagnostic work up. In this review, we focus on the management of TCH, paying particular attention to the diagnostic work up and treatment of the condition

Psychopharmacotherapy of panic disorder: 8-week randomized trial with clonazepam and paroxetine

The objective of the present randomized, open-label, naturalistic 8-week study was to compare the efficacy and safety of treat- ment with clonazepam (N = 63) and paroxetine (N = 57) in patients with panic disorder with or without agoraphobia. Efficacy assessment included number of panic attacks and clinician ratings of the global severity of panic disorders with the clinical global impression (CGI) improvement (CGI-I) and CGI severity (CGI-S) scales. Most patients were females (69.8 and 68.4% in the clonazepam and paroxetine groups, respectively) and age (mean ± SD) was 35.9 ± 9.6 years for the clonazepam group and 33.7 ± 8.8 years for the paroxetine group. Treatment with clonazepam versus paroxetine resulted in fewer weekly panic attacks at week 4 (0.1 vs 0.5, respectively; P < 0.01), and greater clinical improvements at week 8 (CGI-I: 1.6 vs 2.9; P = 0.04). Anxiety severity was significantly reduced with clonazepam versus paroxetine at weeks 1 and 2, with no difference in panic disorder severity. Patients treated with clonazepam had fewer adverse events than patients treated with paroxetine (73 vs 95%; P = 0.001). The most common adverse events were drowsiness/fatigue (57%), memory/concentration difficulties (24%), and sexual dysfunction (11%) in the clonazepam group and drowsiness/fatigue (81%), sexual dysfunction (70%), and nausea/vomiting (61%) in the paroxetine group. This naturalistic study confirms the efficacy and tolerability of clonazepam and paroxetine in the acute treatment of patients with panic disorder

Neuroanatomia do transtorno de pânico Neuroanatomy of panic disorder

OBJETIVOS: O Transtorno de Pânico (TP) é um transtorno de ansiedade que permite um estudo comparativo de modelos animais visando à elucidação dos circuitos cerebrais envolvidos na sua gênese, embora estes ainda tenham sido pouco discutidos. MÉTODOS: Os autores realizam uma revisão da literatura sobre neurobiologia e neuroanatomia do TP. RESULTADOS: Uma revisão de dados demonstra a existência de uma "rede de medo", que tem como ponto principal o núcleo central da amígdala e compreende o hipotálamo, o tálamo, o hipocampo, a substância cinzenta periaquedutal, o locus ceruleus e outras estruturas do tronco cerebral. Sua presença é evidenciada em estudos de modelos animais de estados emocionais e comportamentais, e sua presença e importância podem ser extrapoladas para o TP em humanos. CONCLUSÃO: Esta rede de medo pode permitir que novos avanços e estudos utilizando técnicas de neuroimagem e/ou psicofármacos possam auxiliar na maior elucidação da circuitos cerebrais do TP.<br>OBJECTIVES: Animal model studies may allow greater elucidation of the cerebral circuits involved in the genesis of panic disorder (PD), but these studies have not yet been fully analyzed. METHODS: The authors review recent literature on the neurobiology and neuroanatomy of PD. RESULTS: In this update, the authors present a revision of data that demonstrates the existence of a "fear network", which has as its main point the central nucleus of the amygdale and includes the hypothalamus, the thalamus, the hippocampus, the periaqueductal gray region, the locus ceruleus and other brainstem structures. Its existence is evidenced in animal studies of emotional and behavioral states, and its presence and importance can be extrapolated to the study of PD in humans. CONCLUSION: This fear network can allow new progresses and studies using neuroimaging techniques and/or psychopharmacological trials, further elucidating the cerebral circuits of PD