SUMMARY: RCVS is a clinical condition of recurrent severe headaches that may be associated with ischemic or hemorrhagic stroke and that is defined by the presence of segmental vasoconstriction in multiple cerebral arteries. The angiographic appearance resembles vasculitis, except that the abnormalities resolve during the course of several months. Because the treatment of RCVS differs from that for vasculitis, radiologists must understand the clinical and radiologic features so as to better guide imaging algorithms and facilitate diagnosis. We present a series of 6 cases of RCVS that highlight the imaging features across multiple modalities.ABBREVIATIONS: IPH ϭ intraparenchymal hemorrhage; MIP ϭ maximum intensity projection; NSAID ϭ nonsteroidal anti-inflammatory drug; PACNS ϭ primary angiitis of the CNS; PRES ϭ posterior reversible encephalopathy syndrome; RCVS ϭ reversible cerebral vasoconstriction syndrome; SDH ϭ subdural hematoma; TCD ϭ transcranial Doppler R CVS is an under-recognized clinical-radiologic entity characterized by a history of sudden severe headaches, sometimes associated with ischemic or hemorrhagic stroke, focal neurologic deficits, or seizures. First described by Call et al in 19881 , RCVS encompasses a wide variety of entities previously described by other names, including postpartum angiopathy, migrainous vasospasm, migrainous stroke, druginduced angiopathy, and benign angiopathy of the CNS. 2,3The condition is defined by reversible segmental cerebral vasoconstriction on angiography.1-3 The angiographic findings are similar to those of other vasculopathies, including PACNS.4 Unlike PACNS, the vascular abnormalities of RCVS resolve within several months. 1,2,5,6 RCVS typically occurs following exposure to a trigger, commonly sympathomimetic or vasoactive agents, including amphetamines, phenylpropanolamine, pseudoephedrine, serotonergic antidepressants, nicotine, caffeine, cannabis, and triptan-or ergot-containing medications.2,7-9 Other triggers include the peripartum period, 10 eclampsia, strenuous physical activity, bathing or showering, sexual activity, and binge alcohol drinking.2 Most patients with RCVS are young and middle-aged women. 3Patients with RCVS exhibit a range of parenchymal abnormalities, including convexal SAH, IPH, ischemic infarcts, and PRES.2,9,11-13 Alternatively, imaging findings may be normal.2,9 Findings of CSF analysis are usually normal or nearnormal.3 Because of the overlap with other causes of headache and stroke in adults and because the vascular abnormalities early in the course of the disease may be subtle or absent, the diagnosis of RCVS is easily missed. Early recognition of RCVS allows appropriate clinical management aimed at reducing the frequency, duration, and severity of vascular complications, primarily through identification and removal of triggers. Because management and outcome of RCVS differ from those of other vasculopathies, it is critical that radiologists recognize its typical imaging appearance, time course, and clinical features. Case Series...

The role of a neuron in neural processing is ultimately determined by whether or not it fires an action potential in a given context. Studies on synaptic plasticity have focused primarily on changes in EPSPs, and not on whether plasticity translates into changes in firing. However, this issue has been addressed by examining EPSP-spike (E-S) potentiation, which enhances the ability of an EPSP of a fixed slope to elicit spikes after long-term potentiation (LTP). Although LTP is thought to underlie learning and memory, E-S potentiation could play an equally important role by potentiating the neuronal input-output function. Here, we used a combined experimental and theoretical approach to examine both the mechanisms underlying E-S potentiation as well as the role of inhibition in shaping the input-output function of neurons. Whereas previous studies examined tetanus-LTP, in which inhibitory synapses may have undergone plasticity, here we examined pairing-induced associative LTP. We determined that although intact inhibition was necessary for pairinginduced E-S potentiation, inhibitory plasticity was not. We further established using computer simulations that a primary mechanism of E-S potentiation was a change in the relative recruitment and latency of inhibitory neurons. Although these studies do not exclude the presence of additional mechanisms of E-S potentiation that may be engaged depending on the induction protocol, they do establish that under intact pharmacology, LTP of the Schaffer collateral to CA1 pyramidal neuron synapses will produce E-S potentiation as a result of changes in the balance and timing of excitation and inhibition.

For the purposes of this review, we classify SAH into three main patterns, defined by the distribution of blood on unenhanced CT: diffuse, perimesencephalic, and convexal. The epicenter of the hemorrhage further refines the differential diagnosis and guides subsequent imaging. Additionally, we review multiple clinical conditions that can simulate the appearance of SAH on CT or MRI, an imaging artifact known as pseudo-SAH.

Long-term potentiation (LTP) in the hippocampus enhances the ability of a stimulus to produce cell firing, not only by increasing the strength of the EPSPs, but also by increasing the efficiency of the input/output (I/O) function of pyramidal neurons. This means that EPSPs of a given size more easily elicit spikes after LTP, a process known as EPSP-spike (E-S) potentiation. In contrast to LTP, it is not known whether the synaptic strengthening produced by paired-pulse facilitation (PPF) also results in changes in the I/O function. We have addressed this question by examining E-S curves from rat hippocampal area CA1 in response to both PPF and LTP. We describe a novel form of I/O modulation in which PPF produces E-S depression; that is, the E-S curve is shifted to the right, indicating a decreased ability of EPSPs to elicit action potentials. Consistent with the notion that E-S potentiation observed with LTP is caused by long-term increases in the excitatory-inhibitory ratio, we show that PPF-induced E-S depression relies on short-term decreases in this ratio. These results indicate that different forms of synaptic plasticity that produce the same degree of EPSP potentiation can result in dramatically different effects on cell firing, because of the dynamic changes in the excitatory-inhibitory balance within local circuits.

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