Cefepime-induced encephalopathy: Neural mass modeling of triphasic wave-like generalized periodic discharges with a high negative component (Tri-HNC).

AIM: Cefepime, a fourth-generation cephalosporin, acts as a GABAA receptor antagonist. Cefepime-induced encephalopathy (CIE) is frequently overlooked. We aimed to clarify the clinical features, characteristic electroencephalography (EEG), and mechanisms of CIE to aid in its early recognition. METHODS: CIE cases documented by a single-center consultation-liaison team between April 2015 and March 2017 were retrospectively reviewed. For further investigation, neural mass modeling was performed in silico. RESULTS: Three patients with CIE refused medication/examination and showed overt pain, palilalia, and much greater deterioration of eye and verbal response than the motor response, which was possibly related to GABAergic dysfunction. Triphasic wave-like generalized periodic discharges with a high negative component (Tri-HNC) were identified on the EEG of all three cases. The simulation reproduced the characteristic feature of 2-3 Hz Tri-HNC and recovery course on EEG, and a possible involvement of individual differences in pharmacological intervention. It also suggested that auto-inhibition (synaptic inputs from interneuron to interneuron) dysregulation contributed to generating Tri-HNC in CIE. CONCLUSION: As CIE is iatrogenic and continues unless cefepime is stopped, early recognition is crucial. Physicians should be vigilant about altered mental status, pain, and verbal changes in patients taking cefepime. Tri-HNC on EEG can expedite the diagnosis of CIE, and the association between Tri-HNC and CIE suggests that an excitatory and inhibitory imbalance due to the dysfunction of GABAergic interneurons is the underlying mechanism. This modeling may offer a new method of investigating disorders related to GABAergic dysfunction.

Quantum critical point of an itinerant antiferromagnet in a heavy fermion.

A quantum critical point of the heavy fermion Ce(Ru(1-x)Rh(x))2Si2, (x = 0,0.03) has been studied by single-crystalline neutron scattering. By accurately measuring the dynamical susceptibility at the antiferromagnetic wave vector k3 = 0.35c*, we have shown that the inverse energy width gamma(k3), i.e., the inverse correlation time, depends on temperature as gamma(k3) = c1 + c2T((3/2)+/-0.1), where c1 and c2 are x dependent constants, in a low temperature range. This critical exponent 3/2 +/- 0.1 proves that the quantum critical point is controlled by that of the itinerant antiferromagnet.