Abstract

WHAT DO WE MEAN BY SUBCONSCIOUSNESS?
When you are driving your car in the traffic jam, you manage not to hit others cars or run down your fellow citizens. Even though you are thinking to other things, you are able to turn the steering wheel as you should, and to brake in time. Your ability to do this is surprising given that you are unaware of what you are doing. You are not paying attention to the task. It seems as if these actions happen all by themselves, automatically. This means that you are adapting perfectly to your environment. In this sort of situation, you do things subconsciously: “you don’t think you are doing something, perceiving or thinking, but you do, you perceive or you think automatically”.
Nevertheless, you can modify this behavior at will. All you have to do is make the decision. For instance, if you have to adapt to a changing environment, your behavior is not entirely subconscious: “you don’t think you are doing something, but you do it … non-automatically”. This is what we call “preconsciousness” (a mental function which is interpreted as consciousness by many authors). Besides these automatic and non-automatic behaviors, you can reflect on what you are doing. In this case, “you think you are doing something”. You can also “think you are feeling or you are thinking, or even you are existing … This is what we can call “consciousness” (or reflexive consciousness by some authors).
WHY SUBCONSCIOUSNESS IS SUCH AN IMPORTANT CONCEPT?
Your brain continuously receives a vast amount of information over time and space. Some of this information is stored in the brain but not all fortunately … In the case of subconsciousness, you are in the position to sort through the mass of information you are continuously receiving. Subconsciouness is working as an autopilot. More than consciousness and preconsciousness, subconsciousness needs to be carefully taken into account for three main reasons: 1) this subconscious behavior is present in all animals, at least in mammals, allowing them to ensure their survival; 2) the subconscious is permanent, at difference from consciousness and preconsciousness; 3) because subconsciousness is natural and irrepressible, it is difficult or even impossible to hide, meaning that it is an excellent reflection of your personality. Since subconsciousness, whatever its complexity, is expressed as an observable motor behavior, it reflects our intellect and emotions. Much can be learnt from looking to people by observing the way they walk, by looking at their gesture, the way they speak (a bucco-lingual and laryngeal motor function), their facial expression.
WHICH BRAIN REGIONS PLAY A ROLE IN THE SUBCONSCIOUS PROCESSING?
When the cerebral cortex is damaged, dysfunction of its posterior part leads to perceptual disorders, and frontal cortical dysfunction leads to a loss of strategic planning. These brain regions are damaged in patients with memory, linguistic, perceptual anddysexecutive symptoms. Patients can become anosognosic or anosodiaphoric, but, interestingly, routine behaviors, i.e., procedural skills (in other word subconsciousness) remain intact when subcortical brain regions are spared. In contrast, dysfunction of the basal ganglia leads to alteration in automatic behaviors (i.e., subconsciousness), whereas intellectual abilities are spared as a result of the integrity of the cerebral cortex. This strongly suggests that the basal ganglia play an important role in the processing of subconsciousness. As a matter of fact, we know that the basal ganglia participate: 1) in the automatic execution of motor behaviors [1], 2) in the selection of motor programs of cortical origin; to the learning of motor behaviors (walking, riding a bicycle, dancing, playing tennis, etc …) as shown experimentally in the rat [2] and by neuroimaging in humans [3].
If subconscious automatic motor behaviors reflect emotional abilities, does this mean that emotional behaviors are also mediated by the basal ganglia? This is indeed the case. Several studies have shown a preferential activation of the limbic territories of the basal ganglia in subjects observing emotionally charged images sometimes under the most subtle conditions [4]. To be sure that the limbic basal ganglia circuits play a major role in the processing of emotional information we need to manipulate the corresponding brain territory to see whether it is possible to elicit the same emotional behavior. A first step in this direction is illustrated by retrospective post-mortem histopathological studies of patients who had suffered a variety of basal ganglia lesions [5], but these retrospective studies lack specificity. To further confirm and refine the role of the basal ganglia in emotions, the use of brain high frequency stimulation is of particular interest since it enables to modulate the neuronal activity of restricted limbic territories of the basal ganglia. For instance, it is possible to trigger an inappropriate laughter or a manic state when stimulating the limbic territory of the sub-thalamic nucleus in patients with Parkinson’s disease who are in other respects treated effectively for their disorder [6]. Even more surprising, it is possible to trigger an acute transient depression when the simulation is performed with an electrode placed in restricted limbic regions of the basal ganglia, in this case the substantia nigra [7]. These observations suggest that stimulating a limbic territory within the basal ganglia might improve severe psychiatric disorders resistant to all known medical treatments. This is the case for patients with Gilles de la Tourette disease, whether the target is the thalamus or the pallidum [8]. This type of operationis now currently performed in the most severe cases of Gilles de la Tourette disease. Several interesting results have been obtained in patients suffering from obsessive compulsive disorder whom obsessions and compulsions can be attenuated by stimulation of the limbic territory of the sub-thalamic nucleus [9]. All these studies, and many others which have been published recently, indicate that the basal ganglia play an important role in the processing of automatic not only of motor but also of intellectual and emotional behaviors, which corresponds to the definition of subconsciousness.
In normal subjects, subconsciousness (“I don’t think I am thinking … but I think … automatically”) is an interesting concept which allows to describe not only automatic motor but also intellectual and emotional behaviors. There is no doubt that this mental function is essentially processed within the different structures of the basal ganglia, the striatum being the “hub” of this physiological ensemble. Whether the major function of the basal ganglia is to bind intellectual and emotional abilities into subconscious motor behavior still remains to be answered, however. Nevertheless, the basal ganglia are not totally isolated in the center of the brain. They are closely linked to the cerebral cortex, thus forming a close cortico-subcortico-cortical neuronal loop, where the basal ganglia are mainly involved in the processing of subconsciousness, whereas the cerebral cortex is mainly implicated in the control of preconsciousness and consciousness.
THE CONCEPT OF SUBCONSCIOUSNESS IN NEUROLOGICAL AND PSYCHIATRIC DISORDERS
When the subconscious is ill, abnormal involuntary movements (akinetic-rigid syndrome, dystonia, chorea, etc …) are observed when the sensori-motor pathways are implicated. Similarly, “abnormal involuntary thoughts” (slowness of thought, dysexecutive symptomatology, a syndrome which was called “sub-cortical dementia” in the past) and “abnormal involuntary emotions” (depression, disinhibition, obsessions, seen in patients with psychiatric disorders) are observed when associative and limbic neuronal systems are dysfunctioning within the basal ganglia. But when the cerebral cortex is intact (for example in levodopa-responsive parkinsonian patients), preconsciousness and consciousness, which depend upon the integrity of cortical territories, are spared. The moderate frontal lobe-like symptomatology and emotional symptoms (depression, anxiety) often observed at this stage of Parkinson’s disease very likely result from the demodulation of the cerebral cortex (frontal associative and limbic territories) consecutive to the degeneration of the ascending meso- cortical and nigro-striatal dopaminergic systems). If we assume, for the purpose of simplification, that the clinical picture of Alzheimer’s disease is a mirror image of Parkinson’s disease, then we can understand that mental symptoms (memory, language, disorders, irritability …) resulting from the loss of neurons in different areas of the cerebral cortex (entorhinal cortex, hippocampus, temporal cortex, etc …) remain relatively isolated, simply because the basal ganglia are not yet damaged. At this stage of the disease, automatic behaviors (subconsciousness) expressing motor, cognitive, and emotional abilities are preserved. Unfortunately, dysfunction of the subconscious will appear later during the course of the disease, at a time when the loss of neurons progressively involve first the striatum then the remaining parts of the basal ganglia.
Whereas neuronal networks on the cerebral cortex still remain a difficult target for medical and surgical treatment to improve symptoms characteristic of Alzheimer’s disease, this is less the case for disorders of the basal ganglia. Indeed, as a result of the extreme convergence of the different circuits within the basal ganglia, this structure represents an excellent therapeutic target, not just for the improvement of motor disorders such as essential tremor (thalamus), Parkinson’s disease (motor territory of the sub-thalamic nucleus) and dystonia (motor territory of the pallidum), but also psychiatric disorders such as tics or obsessive compulsive disorders (limbic territories of the basal ganglia). The basal ganglia have thus become a therapeutic target of choice for both scientists and pharmaceutical industry for the development of new drug treatments in order to improve the condition of patients with not only motor but also cognitive and psychiatric disorders.
This paper is inspired by a short text published as a Hypothesis in the Annals of Neurology.
