Tail of the Caudate Nucleus

From: Neuropsychiatry, Neuropsychology, Clinical Neuroscience
by Rhawn Joseph, Ph.D.
(Academic Press, New York, 2000)

Tail of the Caudate Nucleus


By Rhawn Joseph, Ph.D.

Structural Overview

The caudate nucleus consists of three major subsections, the "head," "body" and the "tail" which merges with the amygdala. thus the caudate nucleus (which, together with the putamen) constitures the corpus striatum, responds to amygdala impulses, as they receive extensive amygdala projections (Gloor, 1955; Klingler & Gloor, 1960; Krettek & Price, 1978)--projections which are not reciprocated. The the right and left amygdala povides ipsilateral connections via the tail of the caudate to the corpus striatum.

The tail of the caudate thus could also be considered the "nose" of the amygdala, and the amygdala, via the "tail of the caudate" therefore is able to exert considerable influence on the basal ganglia which appears to have evolved out of the amygdala in order to serve as an emotional-motor interface so that amygdala needs and impulses may be acted on in a flexible manner These are functions the basal ganglia (the limbic striatum in particular) continues to perform in humans as well as other creatures (e.g., MacLean, 1990; Mogenson 1991).

For example, the basal ganglia is exceedingly important in the stereotyped and species specific motoric expression of social and emotional states such as running away in fear, biting defensively, or via ballistic movements (hitting, kicking) or as manifested through facial expression, posture, muscle tone, or gesture (Mogenson & Yang, 1991; MacLean, 1990; Rapoport 1991). Because humans possess basically the same basal ganglia and limbic system, when happy, sad, angry, and so on, the facial and body musculature assumes the same readily identifiable emotional postures and expression regardless of culture or racial orgins (Ekman 1993; Eibl-Ebesfedlt, 1990; However, see Russell 1994).


Because of this similarity in basal ganglia functional architecture, regardless of culture or race (and in many respects, mammalian species) if frightened, angry, or in the process of being assaulted, animals or humans may similarly engage in (ballistic) hitting and kicking, or biting, and/or all of the above, depending on context, mood and situational variables (including play). However, in contrast to the brainstem and cerebellum which provides reflexive and stereotyped motor programs that can be performed without thinking, the basal ganglia is capable of considerable flexibility in regard to motor-emotional expression, and is exceedingly responsive to the organisms motivational and emotional state -via its extensive interconnections with the limbic system.

Thus, the striatum contains cells which selectively respond to motivationally significant stimuli, including novel and familiar variables that are rewarding or punishing (Rolls & Williams, 1987; Schneider & Lidsky, 1981). Striatal neurons can also react differently to familiar stimuli depending on their reinforcement properties, and many neurons will in fact increase their responsiveness as stimuli approach the mouth, and/or touch the face and mouth (Rolls & Williams, 1987; Schneider & Lidsky, 1981). Some striatal neurons also respond when making tongue and lip movements (e.g. licking) and during arm movements toward a food item (Rolls & Williams, 1987).

These findings suggest the striatum is involved in orienting and guiding movements toward the mouth presumably so that a desired object can be licked, sucked on, chewed, and consumed. In this regard the striatum could be considered a primary motor center which enables various limbic desires, needs, and impulses such as hunger, to be satisfied.


Chorea ("dance") is characterized by jerky, writhing, twisting, and unpredictable movements of the extremities. The two main types are Sydenham's Chorea (St. Vitus dance) and Huntington's Chorea. Sydenham's Chorea involves choreiform movements of the facial, tongue, and extremities, and is accompanied by loss of nerve cells in the caudate and putamen, as well as within the cerebral cortex, substantia nigra, and subthalamic nucleus.

Huntington's chorea is a progressive deteriorative inherited genetic disorder which is passed on by an autosomal dominant gene located on chromosome 4. It is characterized by an insidious onset that may begin during childhood or old age, with the illness beginning earlier in those who have an affected father (reviewed in Folstein et al. 1990; Young 1995). Cognitive decline, however, is gradual.

Affected individuals tend to suffer from memory and visual-spatial deficits, depression, and reduced fluent output although aphasia is not typical. Difficulty with motor coordination, planning skills, decision making, and a reduced capacity to consider alternate problem solving strategies or to shift form one mental set to another, is not uncommon (reviewed in Folstein et al. 1990). Hence, in some respects this disorder is suggestive of frontal lobe abnormalities (see chapter 19).

This syndrome is also associated with widespread neuronal loss in the caudate, putamen, brainstem, spinal cord, cerebellum, and atrophy in the GP (see Vonsattel, et al. 1987; Young 1995). Degeneration is predominantly of small striatal neurons whereas larger neurons remain intact. Opiate neurons located in the striatum are also significantly effected (Reiner et al. 1988). It is believed that the degeneration of these corpus striatal neurons, as well as the loss of GABA influences, results in reduced striatal control over the GP (see Narabayashi, 1987), thereby producing excessive movement.

It is noteworthy that some reports indicate that the posterior caudate and putamen are more severely effected than the anterior regions (Vonsattel, et al. 1987). Indeed, the posterior caudate and it's tail is usually the earliest and most severely effected part of the brain -which implicates the amygdala as a factor in the development of chorea. Indeed, in the early stages of Huntingtons chorea, atrophy and degeneration begin in the tail and spreads dorsally and anteriorally thus effecting the striatum and lenticular nucleus (Young 1995).

In this regard it is noteworthy that affective disorders and personality and mood changes are prominent early signs suggesting amygdala involvement. Indeed, disturbances of emotion may precede any motor or cognitive decline by as much as 20 years, with some patients displaying mania, depression as well as antisocial tendencies (reviewed in Folstein et al. 1990). As noted, neural degeneration tends to begin in the amygdaloid tail of the corpus striatum (Young 1995).

As per disturbances of movement, those with Huntington's disease tend to suffer from either or both voluntary and involuntary abnormalities. The involuntary aspects include the jerking and unpredictable movements of the limbs, trunk and face which may occur when at rest, walking, or while actively engaged in some task such that they may appear to be intoxicated and/or attempting to dance about.

Voluntary disorders include rigidity, slowed, clumsy, or difficulty initiating movement. Those who suffer from voluntary movement disorders are the most likely to demonstrate cognitive decline (Folstein et al. 1990).

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