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Alternatively, autobiographical memory loss may result from subtle changes in the temporal lobe which gives rise to temporal lobe epilepsy and to memory problems. The mechanism and etiology of this phenomenon remain controversial, especially as it is impossible to rule out prior subclinical epileptic activity which could be responsible for a ...
The hallmark symptom of LATE is a progressive memory loss that predominantly affects short-term and episodic memory. [1] This impairment is often severe enough to interfere with daily functioning and usually remains the chief neurologic deficit, unlike other types of dementia in which non-memory cognitive domains and behavioral changes might be noted earlier or more prominently. [1]
Amygdalohippocampectomy is a surgical procedure for the treatment of epilepsy.It consists of the removal of the hippocampus, which has a role in memory, spatial awareness, and navigation, [1] and the amygdalae, which have a role in the processing and memory of emotional reactions, [2] both structures forming part of the limbic system of the brain.
This is why after a stroke people have a chance of developing cognitive deficits that result in anterograde amnesia, since strokes can involve the temporal lobe in the temporal cortex, and the temporal cortex houses the hippocampus. Anterograde amnesia can be the first clinical sign that Alzheimer's disease is developing within the brain ...
SD is a clinically defined syndrome but is associated with predominantly temporal lobe atrophy (left greater than right) and hence is sometimes called temporal variant FTLD (tvFTLD). [7] SD is one of the three variants of primary progressive aphasia (PPA), which results from neurodegenerative disorders such as FTLD or Alzheimer's disease .
Frontal lobe epilepsy; Lacunar syndromes; Migraine variants; Posterior cerebral artery stroke; Syncope and related paroxysmal spells; Temporal lobe epilepsy; If the event lasts less than one hour, transient epileptic amnesia (TEA) might be implicated. [2] [30] If the condition lasts longer than 24 hours, it is not considered TGA by definition.
It is a symptom associated with temporal lobe changes in epilepsy and in Geschwind syndrome. [1] Structures that may have an effect on hypergraphia when damaged due to temporal lobe epilepsy are the hippocampus and Wernicke's area. Aside from temporal lobe epilepsy, chemical causes may be responsible for inducing hypergraphia.
The removed brain structures included the hippocampus, the amygdala, and the parahippocampal gyrus, now called the medial temporal lobe memory system. [28] HM was one of the most studied memory cases to date and started the examination of neurological structures in relation to memory.