A case of anti-aquaporin-4 and anti-glutamate receptor antibodies positive myelitis presented with modest clinical signs.

We present a case of anti-aquaporin-4 antibody-positive myelitis, which suggests the high-risk syndrome of neuromyelitis optica, whose modest clinical signs were in conspicuous contrast to the extensive spinal cord lesions demonstrated on magnetic resonance (MR) imaging. Follow-up MR imaging showed marked improvement of lesions. Interestingly, an anti-glutamate receptor antibody, which has been suggested to cause dysfunction of N-methy-D-aspartate receptor on neuron, was detected in the cerebrospinal fluid of the patient. We discuss the case and related literature.

Extensive and temporally ungraded retrograde amnesia in encephalitis associated with antibodies to voltage-gated potassium channels.

BACKGROUND: Encephalitis associated with antibodies to voltage-gated potassium channels (VGKC-Ab) is characterized by epilepsy, behavioral changes, and anterograde memory impairment. Magnetic resonance imaging reveals abnormal signal predominantly restricted to the mediotemporal lobes. OBJECTIVE: To determine the temporal extent and potential reversibility of retrograde amnesia in 3 patients with VGKC-Ab-associated encephalitis. DESIGN: Case report. SETTING: Clinical. Patients Three patients diagnosed as having VGKC-Ab-associated encephalitis underwent cognitive testing before and after immunotherapy. MAIN OUTCOME MEASURES: In addition to standard neuropsychological tests, retrograde memory was assessed using 2 novel tests. Memory for past newsworthy events was assessed using a public events test; test material was divided into epochs of 5 years and spanned approximately 25 years. This was complemented by a famous faces test in which patients were required to identify individuals from the recent and remote past. RESULTS: All 3 patients were found to have temporally ungraded retrograde amnesia dating back more than 20 years. Magnetic resonance imaging in all patients revealed high-signal abnormalities predominantly affecting the hippocampi. Subsequent testing performed after immunotherapy revealed subjective improvement but no evidence of a temporal gradient in the recovery of past memories. CONCLUSIONS: Encephalitis associated with VGKC-Ab results in extensive and temporally ungraded retrograde amnesia that is partially reversible with immunotherapy. Magnetic resonance imaging high-signal abnormalities were primarily restricted to the hippocampi. These data are supportive of theories postulating a role for the hippocampus in the storage and retrieval of all past memories, irrespective of age, rather than theories of memory consolidation that propose an involvement of the hippocampus only in the temporary storage of memories.

A behavioural characterization of neonatal infection-facilitated memory impairment in adult rats.

We have reported that exposure to bacteria (Escherichia coli) during the neonatal period in rats is associated with impaired memory for a novel context in adulthood. However, impairment is only observed if a peripheral immune challenge (bacterial lipopolysaccharide (LPS)) is administered immediately following context exposure. The goal of the current study was to more fully characterize this phenomenon. In Experiment 1, memory impairment as a result of neonatal infection and subsequent LPS challenge was observed in juvenile rats, indicating that the changes induced by infection occur early on and are then manifest throughout the lifespan. In Experiment 2, infection in juvenile rats did not lead to LPS-induced memory impairment in adulthood, suggesting there is a critical period for early infection-induced alterations. In Experiments 3 and 4, memory for a novel context was impaired in neonatally infected rats, a task that is dependent on the hippocampus, whereas cued memory for a tone, which does not depend on the hippocampus, was not impaired. Furthermore, long-term, but not short-term contextual memory was impaired in adult rats infected as neonates following an LPS challenge either 24 h before or immediately after conditioning. Finally, in Experiment 5, no neonatal group differences were observed in corticosterone or open field behaviour, suggesting that decreased freezing to a conditioned context reflects impaired memory, and not simply hyperactivity or altered stress reactivity. Taken together, we have demonstrated that neonatal infection results in robust hippocampal-dependent memory impairment following an immune challenge in adulthood using a number of conditioning paradigms.