Psychogenic amnesia: syndromes, outcome, and patterns of retrogradeamnesia. There are very few case series of patients with acute psychogenic memory loss (also known as dissociative/functional amnesia), and still fewer studies of outcome, or comparisons with neurological memory-disordered patients. Consequently, the literature on psychogenic amnesia is somewhat fragmented and offers little prognostic value for individual patients. In the present study, we reviewed the case records and neuropsychological findings in 53 psychogenic amnesia cases (ratio of 3:1, males:females), in comparison with 21 consecutively recruited neurological memory-disordered patients and 14 healthy control subjects. In particular, we examined the pattern of retrogradeamnesia on an assessment of autobiographical
Silent memory engrams as the basis for retrogradeamnesia Recent studies identified neuronal ensembles and circuits that hold specific memory information (memory engrams). Memory engrams are retained under protein synthesis inhibition-induced retrogradeamnesia. These engram cells can be activated by optogenetic stimulation for full-fledged recall, but not by stimulation using natural recall cues in engram cells. These results indicate that memory information is retained in a form of silent engram under protein synthesis inhibition-induced retrogradeamnesia and support the hypothesis that memory is stored as the specific connectivity between engram cells.
the injury, if they have any of these risk factors: • age 65 or over • any current bleeding or clotting disorders • dangerous mechanism of injury (a pedestrian or cyclist struck by a motor vehicle, an occupant ejected from a motor vehicle or a fall from a height of more than 1 m or 5 stairs) • more than 30 minutes' retrogradeamnesia of events immediately before the head injury. [2023] People under 16
patient outcomes and is the largest study of its kind. Results are forthcoming. TraumaTraumaADULT Advanced imaging is considered medically necessary in the diagnosis and management of head trauma in EITHER of the following scenarios: * Acute trauma when ANY of the following risk factors are present: * Age 65 years or older * Retrogradeamnesia * At least 2 episodes of emesis * Evidence of open
are present: * Age 65 years or older * Retrogradeamnesia * At least 2 episodes of emesis * Evidence of open, depressed, or basilar skull fracture * Focal neurologic findings * Glasgow coma scale less than 15 or altered mental status * High-risk mechanism of injury * Seizure * Bleeding diathesis/coagulopathy * Intracranial shunt * Non-acute trauma in EITHER of the following scenarios: * Focal neurological
after the accident, as assessed in the emergency department1 Psychomotor retardation: e.g., slower verbal response time, slower motor reaction time, etc.2 Retrogradeamnesia: amnesia of events prior to the accident. Anterograde amnesia: amnesia of events after the accident.3 Transient central cause of neurological impairment: consider any abnormality with a central neurological appearance – not just
response time, slower motor reaction time, etc.2 Retrogradeamnesia: amnesia of events prior to the accident Anterograde amnesia: amnesia of events after the accident.3 Transient central cause of neurological impairment: consider any abnormality with a central neurological appearance – not just lateralizing or very focal signs.4 Identifiedbalance/coordinationproblems: identified abnormality using
Trauma Trauma ADULT Advanced imaging is considered medically necessary in the diagnosis and management of head trauma in EITHER of the following scenarios: • Acute trauma when ANY of the following risk factors are present: o Age 65 years or older o Retrogradeamnesia o At least 2 episodes of emesis o Evidence of open, depressed, or basilar skull fracture o Focal neurologic findings o Glasgow coma scale
to the results of the multiple logistic regression analysis, GCS scores of ≤14 (OR 3.72, 95% CI 1.89-7.30), high-risk mechanisms of injury (OR 2.80, 95% CI 1.39-5.64), vomiting (OR 5.01, 95% CI 1.19-21.1), and retrogradeamnesia (OR 6.90, 95% CI 3.37-14.1) were identified as risk factors. In older patients with minor head injury, GCS ≤14, high-risk mechanisms of injury, vomiting, and retrogradeamnesia
) for injury situation, certainty of diagnosis, prolonged recovery, recurrent injuries, mental status alterations, loss of consciousness (LOC), posttraumatic amnesia (PTA), retrogradeamnesia (RGA), motor impairments, delayed symptom presentation, and immediate reporting. Concussions from varsity/intercollegiate sports [IPR of 1.73, 95% confidence interval (CI) 1.43-2.10] and intramurals (IPR of 1.53, 95% CI
The effects of treatment, clinical and demographic factors on recovery of orientation after ECT: A care network study. Time to reorientation after electroconvulsive therapy (ECT) has been shown to predict retrogradeamnesia and is a useful measure for monitoring patients over the acute treatment course. This study investigated the effects of treatment, clinical and demographic factors
. Any history of bleeding or clotting disorders. Dangerous mechanism of injury (a pedestrian or cyclist struck by a motor vehicle, an occupant ejected from a motor vehicle or a fall from a height of greater than 1 metre or 5 stairs). More than 30 minutes' retrogradeamnesia of events immediately before the head injury. A provisional written radiology report should be made available within 1 hour disorders. Current anticoagulation treatment. Dangerous mechanism of injury (a pedestrian or cyclist struck by a motor vehicle, an occupant ejected from a motor vehicle or a fall from a height of greater than one metre or five stairs). More than 30 minutes’ retrogradeamnesia of events immediately before the head injury. Patients who had a witnessed fall and did NOT hit their head, do NOT need a CT
and the implica-tions of not having the treatment. Details should also be provided about the treatment methodology and process, any side-effects or possible adverse events, including the risk of transient anterograde and retrograde cognitive impairment and, less commonly, irreversible retrogradememoryloss particularly if bitemporal (BT) techniques are utilised at 1.5 times sei-zure threshold are usually sufficient.It is important to note that ECT can cause retrogradeamnesia (including for autobiographical memories) that can be persistent (Sackeim et al., 2007). The severity and risk of this occurring and persisting depend on the ECT treatment approach (electrode placement, pulse width and dosing level), number of treatments and patient
characteristics across sexes included differences in the incident loss of consciousness (male: 5.9%, female: 2.6%; p < 0.001), post-traumatic amnesia (male: 13.6%, female: 5.1%; p < 0.001), and retrogradeamnesia (male: 6.8%, female: 2.8%; p < 0.001). A greater proportion of contact-sport student athletes experienced an altered mental status (52.7%) than limited contact (36.2%) and non-contact (48.6%) [p
endpoints were the recall of a numeric character patients had been shown just before anesthetic induction, as an assessment of retrogradeamnesia 24 h after surgery. Sixty-six patients (propofol, 32; remimazolam, 34) were assessed. Patients in the remimazolam group remembered significantly fewer posters shown to them after surgery than those in the propofol group (0 [0 - 2] vs. 2 [1 - 3], p < 0.001
divided into high- and low-stress groups according to the Amsterdam Preoperative Anxiety and Information Scale. Then, both groups were randomly divided into three subgroups receiving 0, 0.02, or 0.04 mg/kg of midazolam. Recall cards were shown to patients at 4 minutes, 2 minutes, and immediately before injection to determine retrogradeamnesia and at 2 minutes, 4 minutes, and 6 minutes after injection to determine anterograde amnesia. Hemodynamic changes were recorded during intubation. The chi-square and multiple regression tests were used to analyze the data. Midazolam injection was associated with the development of anterograde amnesia in all groups (P < 0.05); however, it had no effect on the development of retrogradeamnesia (P < 0.05). Midazolam could decrease the systolic and diastolic blood