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Vigilance can get stuck at too high or too low values, thereby causing learning problems in autism and medial temporal amnesia.
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These data may have relevance to research into medial temporal lobe amnesia.
The mortality rate of HSE exceeds 70% in patients who had no or incomplete treatment and fewer than 3% of all patients return to normal function after recovering from their illness [27]. is an autoimmune-mediated paraneoplastic or non-paraneoplastic syndrome characterized by the subacute onset of confusion, anterograde amnesia, temporal lobe seizures and behavioural changes.
Temporally graded retrograde amnesia is observed in human patients with medial temporal lobe lesions as well as in animal models of medial temporal lobe lesions.
The generality of these results is further underlined by clinical studies of both temporal lobe and diencephalic amnesia that have again found dissociations between recognition memory and recency memory (Huppert & Piercy, 1978; Sagar, Gabrielle, Sullivan, & Corkin, 1990; Shaw & Aggleton, 1995), findings further supported by studies of monkeys (Charles et al., 2004).
In a previous study, we found that electrolytic lesions of the PRh produced retrograde amnesia, without a temporal gradient, for water-maze problems acquired 4 weeks and 2 days before surgery [Behav. Brain. Res. 114 (2000) 114].
Of the 6 cases in which both the severity of retrograde and anterograde amnesia and the temporal gradient of the retrograde amnesia were noted, 4 had a more severe retrograde amnesia with no temporal gradient and 2 had a less severe retrograde amnesia with a temporal gradient.
Because it is caused by a deficit in access to stored visual material and not by an impaired ability to encode or retrieve new material, it has the otherwise infrequent properties of a more severe retrograde than anterograde amnesia with no temporal gradient in the retrograde amnesia.
Molaison's groundbreaking case established that bilateral medial temporal lobe lesions cause severe amnesia (Scoville and Milner 1957).
Antibodies to voltage-gated potassium channels are often associated with limbic encephalitis, presenting with seizures, amnesia and medial temporal lobe inflammation.
In the peak-interval with a gap procedure, in which trials with a duration retention period are additionally introduced to study working memory temporal functions, hippocampal lesions caused amnesia for the interval prior to the gap [ 10].
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