[Loss of sight in the postpartum period]. / Verminderd zicht in het kraambed.

BACKGROUND: Vision problems in case of pre-eclampsia or Hemolysis, Elevated Liver, Low Platelets syndrome (HELLP) occur in 25-40% of the cases. Ablatio retinae as a complication occurs in only 0,1-2%. CASE DESCRIPTION: This article describes the case of a healthy 31-year-old woman who gave birth to her first child. A few hours after delivery she experienced vision loss. HELLP was diagnosed. Because of persistent vision loss combined with headache, the ophthalmologist and neurologist were consulted. A bilateral ablatio retinae as a complication of HELLP was diagnosed. Headache was most likely due to the side effect of nifedipine tablets, tension headache or a symptom of HELLP. Vision loss recovered spontaneously within a few weeks. CONCLUSION: Ablatio retinae due to preeclampsia or HELLP is very rare. For all concerned health care providers it is essential to pay attention to vision loss being the first symptom of possible acute underlying diagnosis postpartum.

Interaction of Cortical and Amygdalar Synaptic Input Modulates the Window of Opportunity for Information Processing in the Rhinal Cortices.

The perirhinal (PER) and lateral entorhinal (LEC) cortex function as a gateway for information transmission between (sub)cortical areas and the hippocampus. It is hypothesized that the amygdala, a key structure in emotion processing, can modulate PER-LEC neuronal activity before information enters the hippocampal memory pathway. This study determined the integration of synaptic activity evoked by simultaneous neocortical and amygdala electrical stimulation in PER-LEC deep layer principal neurons and parvalbumin (PV) interneurons in mouse brain slices. The data revealed that both deep layer PER-LEC principal neurons and PV interneurons receive synaptic input from the neocortical agranular insular cortex (AiP) and the lateral amygdala (LA). Furthermore, simultaneous stimulation of the AiP and LA never reached the firing threshold in principal neurons of the PER-LEC deep layers. PV interneurons however, mainly showed linear summation of simultaneous AiP and LA inputs and reached their firing threshold earlier. This early PV firing was reflected in the forward shift of the evoked inhibitory conductance in principal neurons, thereby creating a more precise temporal window for coincidence detection, which likely plays a crucial role in information processing.

Excitation-Inhibition Dynamics Regulate Activity Transmission Through the Perirhinal-Entorhinal Network.

The perirhinal (PER) - lateral entorhinal (LEC) network plays a pivotal role in the information transfer between the neocortex and the hippocampus. Anatomical studies have shown that the connectivity is organized bi-directionally: the superficial layers consist of projections running from the neocortex via the PER-LEC network to the hippocampus while the deep layers form the output pathway back to the neocortex. Although these pathways are characterized anatomically, the functional organization of the superficial and deep connections in the PER-LEC network remains to be revealed. We performed paired recordings of superficial and deep layer principal neurons and found that a larger population of superficial neurons responded with action potential firing in response to superficial cortical input, compared to the deep layer population. This suggested that the superficial network can carry information from the cortex towards the hippocampus. The relation between the excitatory and inhibitory input onto the deep and superficial principal neurons showed that the window of net excitability was larger in superficial principal neurons. We performed paired recordings in superficial layer principal neurons and parvalbumin (PV) expressing interneurons to address how this window of opportunity for spiking is affected in superficial principal neurons. The PV interneuron population initiated inhibition at a very consistent timing with increasing stimulus intensity, whereas the excitation temporally shifted to ensure action potential firing. These data indicate that superficial principal neurons can transmit cortical synaptic input through the PER-LEC network because these neurons have a favorable window of opportunity for spiking in contrast to deep neurons.

Parvalbumin interneuron mediated feedforward inhibition controls signal output in the deep layers of the perirhinal-entorhinal cortex.

The perirhinal (PER) and lateral entorhinal (LEC) cortex form an anatomical link between the neocortex and the hippocampus. However, neocortical activity is transmitted through the PER and LEC to the hippocampus with a low probability, suggesting the involvement of the inhibitory network. This study explored the role of interneuron mediated inhibition, activated by electrical stimulation in the agranular insular cortex (AiP), in the deep layers of the PER and LEC. Activated synaptic input by AiP stimulation rarely evoked action potentials in the PER-LEC deep layer excitatory principal neurons, most probably because the evoked synaptic response consisted of a small excitatory and large inhibitory conductance. Furthermore, parvalbumin positive (PV) interneurons-a subset of interneurons projecting onto the axo-somatic region of principal neurons-received synaptic input earlier than principal neurons, suggesting recruitment of feedforward inhibition. This synaptic input in PV interneurons evoked varying trains of action potentials, explaining the fast rising, long lasting synaptic inhibition received by deep layer principal neurons. Altogether, the excitatory input from the AiP onto deep layer principal neurons is overruled by strong feedforward inhibition. PV interneurons, with their fast, extensive stimulus-evoked firing, are able to deliver this fast evoked inhibition in principal neurons. This indicates an essential role for PV interneurons in the gating mechanism of the PER-LEC network.

Distinct Spatiotemporal Activation Patterns of the Perirhinal-Entorhinal Network in Response to Cortical and Amygdala Input.

The perirhinal (PER) and entorhinal cortex (EC) receive input from the agranular insular cortex (AiP) and the subcortical lateral amygdala (LA) and the main output area is the hippocampus. Information transfer through the PER/EC network however, is not always guaranteed. It is hypothesized that this network actively regulates the (sub)cortical activity transfer to the hippocampal network and that the inhibitory system is involved in this function. This study determined the recruitment by the AiP and LA afferents in PER/EC network with the use of voltage sensitive dye (VSD) imaging in horizontal mouse brain slices. Electrical stimulation (500 µA) of the AiP induced activity that gradually propagated predominantly in the rostro-caudal direction: from the PER to the lateral EC (LEC). In the presence of 1 µM of the competitive γ-aminobutyric acid (GABAA) receptor antagonist bicuculline, AiP stimulation recruited the medial EC (MEC) as well. In contrast, LA stimulation (500 µA) only induced activity in the deep layers of the PER. In the presence of bicuculline, the initial population activity in the PER propagated further towards the superficial layers and the EC after a delay. The latency of evoked responses decreased with increasing stimulus intensities (50-500 µA) for both the AiP and LA stimuli. The stimulation threshold for evoking responses in the PER/EC network was higher for the LA than for the AiP. This study showed that the extent of the PER/EC network activation depends on release of inhibition. When GABAA dependent inhibition is reduced, both the AiP and the LA activate spatially overlapping regions, although in a distinct spatiotemporal fashion. It is therefore hypothesized that the inhibitory network regulates excitatory activity from both cortical and subcortical areas that has to be transmitted through the PER/EC network.

Complement C1q-C3-associated synaptic changes in multiple sclerosis hippocampus.

OBJECTIVE: Multiple sclerosis (MS) is a demyelinating disease of the central nervous system, leading to memory impairment in up to 65% of patients. Memory dysfunction in MS has been associated with loss of synapses in the hippocampus, but its molecular basis is unknown. Accumulating evidence suggests that components of the complement system, C1q and C3, can mediate elimination of synapses. METHODS: To investigate the involvement of complement in synaptic changes in MS, gene and protein expression and localization of C1q and C3 were analyzed in relation to neuropathological changes in myelinated and demyelinated hippocampi from postmortem MS brains. Findings were compared to hippocampi of Alzheimer disease (AD) and non-neurological controls. RESULTS: C1q expression and C3 activation were increased in myelinated and demyelinated MS hippocampi, mainly in the CA3/2 and CA1 subfields, which also showed a marked decrease in synaptic density and increased neuronal staining for the mitochondrial heat shock protein 70 (mtHSP70) stress marker. Neurons were the major source of C1q mRNA. C1q protein and activated C3 localized at synapses within human leukocyte antigen-positive cell processes and lysosomes, suggesting engulfment of complement-tagged synapses by microglia. A significant association (p < 0.0001) between the density of C1q and synaptophysin-positive synapses or mtHSP70 was seen in myelinated MS hippocampi, further pointing toward a link between the complement pathway and synaptic changes. In contrast to AD, MS hippocampi were consistently negative for the terminal complement activation complex C5b9. INTERPRETATION: These data support a role for the C1q-C3 complement axis in synaptic alterations in the MS hippocampus.