Dysfunction of the temporal lobes accounts for several types of amnesia, aphasia, and the agnosias. The anatomy is a bit more complex conceptually than that of the other lobes because the cortex extends into the inferior surface and medial regions of the brain, and because limbic structures are so closely structurally related.
Amnesia
Amnesia, in the most general sense, is memory dysfunction. Memory can be divided along different characteristics. Memory for information within conscious awareness is termed explicit while information outside of awareness is termed implicit. In general, explicit information is termed declarative and it can be further subdivided into episodic memory, recall of specific events, and semantic memory, recall of facts, or knowledge. In contrast to declarative memory, procedural memory refers to changes in the ability to perform tasks as a result of experience. If declarative memory answers “what” queries, procedural memory deals with “how” to do tasks. Table 8.1 presents a clinically and conceptually useful classification system.
Diseases affecting these systems invariably involve the related anatomy and are listed in the following section by type of memory impaired (Table 8.2).
Tumors, strokes, hemorrhages, and other focal disease can affect all memory types as well, depending on the location of the dysfunction.
Two frequently encountered syndromes involving memory are transient global amnesia and Korsakov syndrome.
Clinically, transient global amnesia presents with patient disorientation and repetitive questioning on the patient’s part to solve that disorientation. It usually lasts hours, and patients should not have any recollection of that time later. Although vascular and epileptic theories both exist for the etiology, sequelae are typically minimal and recurrence is uncommon. A thorough workup is nevertheless indicated, although if negative, treatment is not indicated.
Patients with Korsakov syndrome seem conversationally normal but are unable to retain new information. They tend to guess and confabulate responses rather than deny their knowledge. Thiamine deficiency often presents acutely with Wernicke encephalopathy, with Korsakov syndrome occurring later. The nutritional imbalance is often due to the patient’s preference for the calories contained in ethanol to the exclusion of anything else. Pathologically, microhemorrhages occur in mammillary bodies and the medial dorsal nucleus of the thalamus, both parts of the Papez circuit (Fig. 8.1). While treatment of thiamine deficiency does not often reverse acute Wernicke encephalopathy, for Korsakov syndrome it will not reverse the damage.
TABLE 8.1 AMNESIA CLASSIFICATION
MEMORY TYPE (DEFINITION) AND DURATION
ANATOMY
EXAMPLES
AWARENESS
Episodic (events and experiences); minutes to years