Limbic System 11

MEDI CAL 475

Section IV • Neuroscience

Clinical Correlate

Olfactory deficits may be incomplete (hyposmia), distorted (dysosmia), or complete (anosmia). Olfactory deficits are caused bytransport problems or by damage to the primary olfactory neurons or to neurons in the olfactory pathway to the central nervous system (CNS). Head injuries that fracture the cribriform plate can tear the central processes of olfactory nerve fibers as they pass through the plate to terminate in the olfactory bulb, orthey may injure the bulb itself. Because the olfactory bulb is an outgrowth ofthe CNS covered by meninges, separation ofthe bulb from the plate may tearthe meninges, resulting in cerebrospinal fluid (CSF) leaking through the cribriform plate into the nasal cavity.

LIMBIC SYSTEM

The limbic system is involved in emotion, memory, attention, feeding, and mat­ ing behaviors. It consists of a core of cortical and diencephalic structures found on the medial aspect of the hemisphere. The limbic system modulates feelings, such as fear, anxiety, sadness, happiness, sexual pleasure, and familiarity.

The Papez Circuit

A summofarythe simplified connections of the limbic system is expressed by the Papez circuit (Figure IV-11-1). The Papez circuit oversimplifies the role ofthe lim­ bic system in modulating feelings, such as fear, anxiety, sadness, happiness, sexual pleasure, and familiarity; yet, it provides a useful starting point for understanding the system. Arbitrarily, the Papez circuit begins and ends in the hippocampus. Ax­ ons of hippocampal pyramidal cells converge to form the funbria and, finally, the fornix. The fomix projects mainly to the mammillarybodies in the hypothalamus. The mammillary bodies, in turn, project to the anterior nucleus of the thalamus by way ofthe mammillothalamic tract. The anterior nuclei project to the cingulate gyrus through the anterior limb of the internal capsule, and the cingulate gyrus communicates with the hippocampus through the cingulum and entorhinal cortex.

The amygdala functions to attach an emotional significance to a stimulus and helps imprint the emotional response in memory.

476 MEDICAL

Section IV • Neuroscience

Clinical Correlate

Anterograde Amnesia

Bilateral damage to the medial temporal lobes including the hippocampus results in a profound loss ofthe ability to acquire new information, known as anterograde amnesia.

KorsakoffSyndrome

Anterograde amnesia is also observed in patients with Korsakoff syndrome. Korsakoff syndrome is seen mainly in alcoholics who have a thiamine deficiency and often follows an acute presentation ofWernicke encephalopathy. Wernicke encephalopathy presents with ocular patsies, confusion, and gait ataxia and is also related to a thiamine deficiency. In Wernicke-Korsakoffsyndrome, lesions are always found in the mammillary bodies and the dorsomedial nuclei ofthe thalamus.

In addition to exhibiting an anterograde amnesia, Korsakoffpatients also present with retrograde amnesia. These patients confabulate, making up stories to replace past memories they can no longer retrieve.

Klilver-Bucy Syndrome

KlUver-Bucy syndrome results from bilateral lesions of the amygdala and hippocampus. These lesions result in:

•Placidity-there is marked decrease in aggressive behavior; the subjects become passive, exhibiting little emotional reaction to external stimuli.

•Psychic blindness-objects in the visual field are treated inappropriately.

For example, monkeys may approach a snake or a human with inappropriate docility.

•Hypermetamorphosis-visual stimuli (even old ones) are repeatedly approached as though they were completely new.

•Increased oral exploratory behavior-monkeys put everything in their mouths, eating only appropriate objects.

•Hypersexuality and loss of sexual preference

•Anterograde amnesia

478 MEDICAL

Chapter u • Limbic System

AlzheimerDisease

• . Alzheimer disease accounts for 60% of allcases of dementia. The inci­ dence increases with age.

•Clinical: insidious onset, progressive memory impairment, mood altera­ tions, disorientation, aphasia, apraxia, and progression to a bedridden state with eventual death

•Five to 10% of Alzheimer cases are hereditary, early onset, and transmit­ ted as an autosomal dominant trait.

Table IV-11-1. Genetics ofAlzheimer Disease (AD)

Lesions involve the neocortex, hippocampus, and subcortical nuclei, including forebrain cholinergic nuclei (i.e., basal nucleus of Meynert). These areas show atrophy, as well as characteristic microscopic changes. The earliest and most se­ verely affected areas are the hippocampus and temporal lobe, which are involved in learning and memory.

Table IV-11-2. Pathology of Alzheimer Disease