This report suggests a correlation between human cognitive performance and cellular capacity to activate RSK2. It provides additional evidence that the CREB kinase, RSK2, and CREB phosphorylation may play important roles in human learning and memory, as they do in lower animals.

The following article is the second in this series. It reviews genes and metabolic pathways involved in learning and memory in lower animals and in humans. These new, exciting studies will contribute to greater understanding of the molecular abnormalities responsible for cognitive disorders in children. Cognitive disorders in children have traditionally been described in terms of clinical phenotypes or syndromes, chromosomal lesions, metabolic disorders, or neuropathology. Relatively little is known about how these disorders affect the chemical reactions involved in learning and memory. Experiments in fruit flies, snails, and mice have revealed some highly conserved pathways that are involved in learning, memory, and synaptic plasticity, which is the primary substrate for memory storage. These can be divided into short-term memory storage through local changes in synapses, and long-term storage mediated by activation of transcription to translate new proteins that modify synaptic function. This review summarizes evidence that disruptions in these pathways are involved in human cognitive disorders, including neurofibromatosis type I, Coffin-Lowry syndrome, Rubinstein-Taybi syndrome, Rett syndrome, tuberous sclerosis-2, Down syndrome, X-linked ␣-thalassemia/ mental retardation, cretinism, Huntington disease, and lead poisoning. More than a thousand types of mental retardation are listed currently in Online Mendelian Inheritance in Man (OMIM, 2002) and many milder learning disorders are seen in clinical practice. Many of these disorders are associated with syndromes, chromosomal disorders, or metabolic diseases, but it is unclear how most of them disrupt the brain's chemical machinery for learning and memory. Experimental work over several decades makes it clear that long-term memory storage, which is essential for cognition, involves activity-dependent synaptic plasticity and transcription of genes to synthesize synaptic proteins (1, 2). Recently, several genetic forms of mental retardation have been linked to mutations in intracellular pathways that mediate synaptic plasticity, learning, and memory in lower animals (3). These discoveries suggest that a Alvin Zipursky Editor-in-Chief

The authors present a case of "surfer's myelopathy," a rarely described syndrome characterized by nontraumatic paraparesis/paraplegia in novice surfers and theorized to result from spinal cord ischemia secondary to surfing-related positional hyperextension. Imaging and clinical course of the youngest known affected individual are discussed, including evidence of acute spinal cord infarction on diffusion-weighted magnetic resonance imaging, a finding not previously described in the literature.