Abstract

Developmental amnesia (DA) is a selective episodic memory disorder associated with hypoxia-induced bilateral hippocampal atrophy of early onset. Despite the systemic impact of hypoxia-ischaemia, the resulting brain damage was previously reported to be largely limited to the hippocampus. However, the thalamus and the mammillary bodies are parts of the hippocampal-diencephalic network and are therefore also at risk of injury following hypoxic-ischaemic events. Here, we report a neuroimaging investigation of diencephalic damage in a group of 18 patients with DA (age range 11–35 years), and an equal number of controls. Importantly, we uncovered a marked degree of atrophy in the mammillary bodies in two thirds of our patients. In addition, as a group, patients had mildly reduced thalamic volumes. The size of the anterior-mid thalamic (AMT) segment was correlated with patients' visual memory performance. Thus, in addition to the hippocampus, the diencephalic structures also appear to play a role in the patients' memory deficit.

Highlights

  • Situated within the medial-temporal lobe, the hippocampus is vulnerable to damage during hypoxic-ischaemic episodes due to its high oxygen requirement and susceptibility to glutamate-induced neurotoxicity (Schmidt-Kastner & Freund, 1991)

  • We reported a causal sequence from exposure to neonatal hypoxia-ischaemia leading to significant hippocampal pathology, in turn resulting in a pronounced deficit in episodic recall in the absence of deficits in semantic memory, working memory, academic attainments and intelligence

  • In patients with amnesia resulting from hypoxicischaemic events, the hippocampus is the structure predicted to exhibit the largest degree of atrophy

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Summary

Introduction

Situated within the medial-temporal lobe, the hippocampus is vulnerable to damage during hypoxic-ischaemic episodes due to its high oxygen requirement and susceptibility to glutamate-induced neurotoxicity (Schmidt-Kastner & Freund, 1991) These systemic events are associated with a cascade of direct and secondary neuropathology (Faro & Windle, 1969) affecting multiple brain regions Caine and Watson's (2000) survey of neuropathological studies revealed that the thalamus was affected in 56% of anoxic patients In addition to these direct effects, the mammillary bodies and nuclei of the thalamus can become damaged after injury to the hippocampus by anterograde degeneration (Bachevalier & Meunier, 1996). Hippocampal injury is known to produce degeneration of both the mammillary bodies (Loftus, Knight, & Amaral, 2000; Schubert & Friede, 1979) and the thalamus (Kodama et al, 2003)

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