Amnesia is the total or partial inability to recall past experiences back into the memory. It can be caused by traumatic brain injury, degeneration, metabolic disorders, seizures and mental disorders. The diagnosis is made clinically, but often includes a neuropsychological testing and brain imaging (eg. As CT, MRI) tools. The treatment depends on the particular cause.
The processing of memories includes:
Amnesia is the total or partial inability to recall past experiences back into the memory. It can be caused by traumatic brain injury, degeneration, metabolic disorders, seizures and mental disorders. The diagnosis is made clinically, but often includes a neuropsychological testing and brain imaging (eg. As CT, MRI) tools. The treatment depends on the particular cause. The processing of memories includes: registration (recording new information) Encoding (forms of associations, temporal markers and other processes that are necessary for the recollection) and the recollection. Retrieval deficits in each of these steps can cause amnesia. Amnesia resulting definition of limitations on memory function and not from the impairment of other functions that can cause similar symptoms (eg. As attention, motivation, thought, language). can amnesia be classified as follows: Retrograde: amnesia concerning events before the event causing anterograde: inability new memories after the causative event to save sense specific: amnesia for events that are processed by a z-sense. B. a agnosia Amnesia may Transient (like after a brain trauma) Ongoing (as occurs after a severe damage, for. Example, encephalitis, global ischemia or cardiac arrest) progressive (if it occurs with degenerative dementias, such as Alzheimer’s disease ) memory deficits rather using mostly the facts (declarative memory) and less frequently skills (procedural memory). An amnesia etiology may result from diffuse impairment of the brain of bilateral lesions or multifocal lesions involving the memory storage areas, and the cerebral hemispheres. Predominant paths for declarative memory are located along the medial parahippokampalen region and the hippocampus and temporal lobe in the inferomedial, the orbital surface of the frontal lobe (basal forebrain) and in the diencephalon (thalamus and hypothalamus that contains). Of these structures, the following are critical: Hippocampal gyri hypothalamus ganglia basal forebrain dorsomedial thalamic nuclei, the amygdala contributes to emotional reinforcement of memory. The intralaminar thalamic nuclei and the reticular formation in the brainstem stimulate the impression of memory contents. Bilateral damage to the thalamic nuclei affected mediodorsal strong new memories and the ability to form new memory content. Amnesia can be caused by: thiamine deficiency head injury seizures Global anoxia or ischemia of the brain encephalitis Embolic closure at the top of ((by Wernicke encephalopathy or Korsakoff’s psychosis) in patients with chronic alcohol abuse or severe malnutrition basilar artery Degenerative tip of the basilar artery embolism) dementias such as Alzheimer’s disease Various drug / Arzneimittelintoxikationen (z. B. chronic sniffing of solvents, amphotericin B or lithium toxicity) Hypothalamic tumors psychic trauma or stress posttraumatic amnesia for the time immediately before and after a concussion or a mild or severe head trauma appear to be caused by damage to the medial temporal lobe. Mild or severe damage may include larger areas of memory storage and -abrufs, the same is true for many diffuse cerebral disorders that cause dementia. Mental disorders of memory can from extreme psychological trauma or stress resulting (dissociative amnesia). Benign forgetfulness age (age-related memory impairment) refers to the memory loss that occurs with normal aging. People with benign forgetfulness age gradually develop significant memory problems, often first for name, for events and occasionally for spatial relationships. Benign age forgetfulness has no proven relation to dementia, although some similarities are obvious. Amnesic, weak cognitive impairment (amnestic MCI) may be present in people who have a subjective memory problem that perform poorly on objective memory tests, but otherwise have an intact cognition and daily function. People with amnestic MCI are at greater risk of developing Alzheimer’s disease than age-matched people without memory problems. Diagnostic test at the bedside Simple clinical studies (eg. As remembering three terms, retrieval of objects that were previously hidden in the room) and formal tests (z. B. word list learning tests such as the California Verbal Learning Test and the Buschke Selective Reminind test) can help to identify linguistic memory loss. The investigation of the non-verbal memory is more difficult and can playback visual pattern or a sequence of tones comprise. The clinical findings often suggest the cause and thus the necessary tests. Treatment Treatment is causal aligned. Each underlying disorder or psychological cause needs to be treated. Nevertheless, some patients improve with acute amnesia spontaneous. Certain disorders that cause amnesia (. Eg Alzheimer’s disease, Korsakoff’s syndrome, herpes encephalitis) may be treated; However, the treatment of the underlying disorder may not always improve the amnesia. Cholinergic drugs (eg. As donepezil) memory can easily and temporarily improve in patients with Alzheimer’s disease. These drugs are often tried if an other dementias is the cause. On the other hand, there are no specific measures to speed recovery or improve the chances of recovery. Important points amnesia have various causes, including traumatic brain injury, degenerative dementia, metabolic rStörungen, seizures and psychological trauma or stress. Amnesia was clinically with simple tests (eg. As remembering three terms) or formal tests (eg. As word list learning tests). There is a causal treatment of amnesia.