The Occipital Emissary Vein: A Possible Marker for Pseudotumor Cerebri.

BACKGROUND AND PURPOSE: Transverse sinus stenosis can lead to pseudotumor cerebri syndrome by elevating the cerebral venous pressure. The occipital emissary vein is an inconstant emissary vein that connects the torcular herophili with the suboccipital veins of the external vertebral plexus. This retrospective study compares the prevalence and size of the occipital emissary vein in patients with pseudotumor cerebri syndrome with those in healthy control subjects to determine whether the occipital emissary vein could represent a marker of pseudotumor cerebri syndrome. MATERIALS AND METHODS: The cranial venous system of 46 adult patients with pseudotumor cerebri syndrome (group 1) was studied on CT venography images and compared with a group of 92 consecutive adult patients without pseudotumor cerebri syndrome who underwent venous assessment with gadolinium-enhanced 3D-T1 MPRAGE sequences (group 2). The presence of an occipital emissary vein was assessed, and its proximal (intraosseous) and distal (extracranial) maximum diameters were measured and compared between the 2 groups. Seventeen patients who underwent transverse sinus stent placement had their occipital emissary vein diameters measured before and after stent placement. RESULTS: Thirty of 46 (65%) patients in group 1 versus 29/92 (31.5%) patients in group 2 had an occipital emissary vein (P < .001). The average proximal and distal occipital emissary vein maximum diameters were significantly larger in group 1 (2.3 versus 1.6 mm, P <.005 and 3.3 versus 2.3 mm, P < .001). The average maximum diameters of the occipital emissary vein for patients who underwent transverse sinus stent placement were larger before stent placement than after stent placement: 2.6 versus 1.8 mm proximally (P < .06) and 3.7 versus 2.6 mm distally (P < .005). CONCLUSIONS: Occipital emissary veins are more frequent and larger in patients with pseudotumor cerebri syndrome than in healthy subjects, a finding consistent with their role as collateral venous pathway in transverse sinus stenosis. A prominent occipital emissary vein is an imaging sign that should raise the suspicion of pseudotumor cerebri syndrome.

Reelin, an extracellular matrix protein linked to early onset psychiatric diseases, drives postnatal development of the prefrontal cortex via GluN2B-NMDARs and the mTOR pathway.

Defective brain extracellular matrix (ECM) is a factor of vulnerability in various psychiatric diseases such as schizophrenia, depression and autism. The glycoprotein reelin is an essential building block of the brain ECM that modulates neuronal development and participates to the functions of adult central synapses. The reelin gene (RELN) is a strong candidate in psychiatric diseases of early onset, but its synaptic and behavioral functions in juvenile brain circuits remain unresolved. Here, we found that in juvenile reelin-haploinsufficient heterozygous reeler mice (HRM), abnormal fear memory erasure is concomitant to reduced dendritic spine density and anomalous long-term potentiation in the prefrontal cortex. In juvenile HRM, a single in vivo injection with ketamine or Ro25-6981 to inhibit GluN2B-N-methyl-D-aspartate receptors (NMDARs) restored normal spine density, synaptic plasticity and converted fear memory to an erasure-resilient state typical of adult rodents. The functional and behavioral rescue by ketamine was prevented by rapamycin, an inhibitor of the mammalian target of rapamycin pathway. Finally, we show that fear memory erasure persists until adolescence in HRM and that a single exposure to ketamine during the juvenile period reinstates normal fear memory in adolescent mice. Our results show that reelin is essential for successful structural, functional and behavioral development of juvenile prefrontal circuits and that this developmental period provides a critical window for therapeutic rehabilitation with GluN2B-NMDAR antagonists.

Persistence of amygdala gamma oscillations during extinction learning predicts spontaneous fear recovery.

Extinction of auditory fear conditioning induces a temporary inhibition of conditioned fear responses that can spontaneously reappear with the passage of time. Several lines of evidence indicate that extinction learning relies on the recruitment of specific neuronal populations within the basolateral amygdala. In contrast, post-extinction spontaneous fear recovery is thought to result from deficits in the consolidation of extinction memory within prefrontal neuronal circuits. Interestingly, recent data indicates that the strength of gamma oscillations in the basolateral amygdala during auditory fear conditioning correlates with retrieval of conditioned fear responses. In the present manuscript we evaluated the hypothesis that post-extinction spontaneous fear recovery might depend on the maintenance of gamma oscillations within the basolateral amygdala by using single unit and local field potential recordings in behaving mice. Our results indicate that gamma oscillations in the basolateral amygdala were enhanced following fear conditioning, whereas during extinction learning gamma profiles were more heterogeneous despite similar extinction learning rates. Remarkably, variations in the strength of gamma power within the basolateral amygdala between early and late stages of extinction linearly predicted the level of post-extinction spontaneous fear recovery. These data suggest that maintenance of gamma oscillations in the basolateral amygdala during extinction learning is a strong predictive factor of long term spontaneous fear recovery.

Midazolam in neonatal seizures with no response to phenobarbital.

The outcome of 45 neonates with EEG-confirmed seizures (ESz) was analyzed with regard to treatment. ESz persisted in 17 of 32 neonates receiving phenobarbital/phenytoin (13 had a poor outcome, 4 died). In contrast, ESz were rapidly controlled in 13 of 13 nonresponders to phenobarbital/phenytoin treated with midazolam (4 had poor outcome, 2 died). Nonresponders to phenobarbital/phenytoin had a significantly worse outcome than responders did. Midazolam effectively controlled ESz in nonresponders to phenobarbital/phenytoin and correlated with significantly improved long-term neurodevelopment.

[Neonatal convulsions: influence of the electroencephalographic pattern and the response to treatment on the outcome]. / Convulsiones neonatales: influencia del patrón electroencefalográfico en su evolución y en la respuesta al tratamiento.

INTRODUCTION: Neonatal convulsions continues being motive for multiple controversies: the diagnosis only by clinical approaches, the necessity to confirm with EEG record and their treatment and control. OBJECTIVE: To establish the incidence of type of clinical neonatal seizures and the correspondence of these to the EEG trace background and the EEG epileptic activity, the underlying etiology, the response to antiepileptic treatment, and their prognosis. PATIENTS AND METHODS: Retrospective study of admitted newborns with the diagnosis of neonatal seizures in our hospital, during the period included between January 1993 and October 2001. Some of variables collected were: birth and gestational age, Apgar, clinical pattern, duration of the convulsions, critical and intercritical EEG traced, EEG background, etiological diagnosis, treatment used and response of the same, evolution and neurological state at hospital discharge and at one year of age (corrected age in preterm infants). RESULTS: 74 children were admitted with neonatal convulsion diagnosis, of these only 56 EEG convulsions were confirmed (42% presented subtle seizures, 33.9% tonic, 64.3% clonic multifocal, 10.7% clonic focal, and 16.1% myoclonic multifocal). 55.4% of the infants had 2 or more types of clinical convulsions, 25% of all had an epileptic state, and 42.9% had at some time of the EEG record, electroclinical dissociation. The more frequent critical EEGs abnormalities was multifocal discharges (64.3%), and together with the focal discharges of low frequency had significant (p<0.01) worse pharmacological control, and also unfavourable outcome. The infants having had EEGs background moderately and markedly abnormal showed unfavourable outcome in 72.2% and 100% respectively, while it was only in 15.4% of the infants who had EEGs background normal or lightly abnormal. With the antiepileptic treatment the clinical control of the convulsions was obtained in more than 80% of the cases, while control of the electrical convulsions was only in 62.5%. There was a higher significant association between favourable response to treatment and normal neurological examination at hospital discharge and at 1 year of age. CONCLUSIONS: The necessity to confirm by means of EEG record the neonatal clinical convulsions, before and after having established the anticonvulsant treatment, due to the control of electrical convulsions improves their neurological outcome.

Convulsiones neonatales: influencia del patrón electroencefalográfico en su evolución y en la respuesta al tratamiento / Neonatal convulsions: influence of the electroencephalographic pattern and the response to treatment on the outcome

Introducción. Existen controversias sobre las convulsiones neonatales (CNN): fiabilidad del diagnóstico únicamente por criterios clínicos, necesidad de la confirmación electroencefalográfica y tratamiento. Objetivo. Estudiar la incidencia de los tipos clínicos de CNN y su correspondencia con el trazado electroencefalográfico de fondo y la actividad convulsiva del EEG, la respuesta al tratamiento anticonvulsivo y su pronóstico. Pacientes y métodos. Estudio retrospectivo de los casos ingresados con el diagnóstico de CNN en nuestro hospital, entre enero de 1993 y octubre de 2001. Se registraron las siguientes variables: patrón clínico, duración de las convulsiones, trazado electroencefalográfico crítico e intercrítico, trazado electroencefalográfico de fondo, diagnóstico etiológico, tratamiento y respuesta al mismo, y estado neurológico al alta y después del año de edad (edad corregida para los pretérmino). Resultados. De un total de 74 niños, en sólo 56 se confirmaron convulsiones electroencefalográficamente, y, de ellas, un 42 por ciento correspondió a convulsiones sutiles, 33,9 por ciento tónicas, 64,3 por ciento clónicas multifocales, 10,7 por ciento clónicas focales y 16,1 por ciento mioclónicas multifocales. El 55,4 por ciento presentó dos o más tipos clínicos de convulsiones, el 25 por ciento desarrolló un estado epiléptico, y el 42,9 por ciento mostró disociación electroclínica. Las anomalías electroencefalográficas críticas más frecuentes fueron las descargas multifocales (64,3 por ciento), que, junto con las descargas focales de baja frecuencia, eran las de peor control farmacológico y peor pronóstico. El trazado electroencefalográfico de fondo moderada y marcadamente anormal fue un indicador de mala evolución. Con tratamiento se consiguió el control clínico en más del 80 por ciento de los casos, y el control electroencefalográfico en sólo el 62,5 por ciento. Hubo una asociación significativa ( p < 0,01) entre la respuesta favorable al tratamiento y la exploración neurológica normal al alta de la unidad neonatal y después del año de edad. Conclusiones. Se deben monitorizar las CNN mediante EEG, antes y después de instaurado el tratamiento anticonvulsionante, ya que con el control de las convulsiones electroencefalográficas se mejora el pronóstico neurológico de estos niños (AU)

Introduction. Neonatal convulsions continues being motive for multiple controversies: the diagnosis only by clinical approaches, the necessity to confirm with EEG record and their treatment and control. Objective. To establish the incidence of type of clinical neonatal seizures and the correspondence of these to the EEG trace background and the EEG epileptic activity, the underlying etiology, the response to antiepileptic treatment, and their prognosis. Patients and methods. Retrospective study of admitted newborns with the diagnosis of neonatal seizures in our hospital, during the period included between January 1993 and October 2001. Some of variables collected were: birth and gestational age, Apgar, clinical pattern, duration of the convulsions, critical and intercritical EEG traced, EEG background, etiological diagnosis, treatment used and response of the same, evolution and neurological state at hospital discharge and at one year of age (corrected age in preterm infants). Results. 74 children were admitted with neonatal convulsion diagnosis, of these only 56 EEG convulsions were confirmed (42% presented subtle seizures, 33.9% tonic, 64.3% clonic multifocal, 10.7% clonic focal, and 16.1% myoclonic multifocal). 55.4% of the infants had 2 or more types of clinical convulsions, 25% of all had an epileptic state, and 42.9% had at some time of the EEG record, electroclinical dissociation. The more frequent critical EEGs abnormalities was multifocal discharges (64.3%), and together with the focal discharges of low frequency had significant (p < 0.01) worse pharmacological control, and also unfavourable outcome. The infants having had EEGs background moderately and markedly abnormal showed unfavourable outcome in 72.2% and 100% respectively, while it was only in 15.4% of the infants who had EEGs background normal or lightly abnormal. With the antiepileptic treatment the clinical control of the convulsions was obtained in more than 80% of the cases, while control of the electrical convulsions was only in 62.5%. There was a higher significant association between favourable response to treatment and normal neurological examination at hospital discharge and at 1 year of age. Conclusions. The necessity to confirm by means of EEG record the neonatal clinical convulsions, before and after having established the anticonvulsivant treatment, due to the control of electrical convulsions improves their neurological outcome (AU)