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Chapter 1: Introduction to the Research

Previous research has not considered a link between Sensory Modulation Disorder (SMD) and substance abuse. Literature is predominantly American in origin and involves the child population. This project can add to the adult South African SMD research base.

1.1: Statement of the problem

Sensory Modulation Disorder (SMD) affects the central nervous system (CNS) [6, pg 4]. The commonly abused substances have their effects on the CNS, as well as other systems of the body [3]. The limbic system is mentioned under both topics. Therefore, the area of affect seems to correlate. No research has been found that has considered such a link. This is a pilot study into a possible link between the two subjects. SMD is a relatively new topic with no standardised means of assessment. There is limited research into SMD in the adult population. From reviewing literature, it is evident that if such a link does exist, it is not a straight forward one. The correlation may occur through the primary (for example, stress/anxiety) or secondary effects (for example, learnt behavioural responses) of both topics. In general, both topics are multi-factorial in presentation. Up to now, the treatment of substance abuse has not been optimal and the relapse rates are high. The usage of SMD treatment together with conventional substance abuse treatment methods could improve the end results.

1.2: Purpose of the study

1.3: Null Hypothesis

There is no link between SMD and substance abuse.

1.4: Definitions of terms

Sensory integration: The neurological process that organises sensation from the body and from the environment making it possible to function effectively within the environment. The brain must select, enhance, inhibit, compare and associate the sensory information in a flexible, constantly changing pattern [6, pg 3-4].

Sensory Modulation Disorder (SMD): Failure of the higher central nervous system structures to modulate incoming sensory information (Fisher and Dunn, 1983 in [6, pg 120]). This leads to either too much or too little inhibition (Larson, 1982 in [6, pg 120]), causing a behavioural manifestation including sensory defensiveness, sensory dormancy and a combination of these two [6, pg 120].

Sensory defensiveness: A tendency to react negatively or with alarm to sensory input that is generally considered harmless or non-irritating [20, pg 3]. It can occur across one or more sensory modalities [19, pg 1]. Common symptoms may include over-sensitivity to light or unexpected touch, sudden movement or over-reaction to unstable surfaces, high frequency noises or visual stimuli and certain smells [20, pg 3]. It may lead to the sensory affective disorder discussed further on. It is thought to be due to too little inhibition of sensory information with a consequent flood of information reaching the higher central nervous system structures [12, pg 32]. It includes:

a)Tactile Defensiveness: An over-reaction to touch experiences. This may result in avoiding touch from others, dislike of crowds, irritation when having hair washed or cut, avoidance of certain types of clothing and many other similiar reactions to touching and being touched [19, pg 1].

b)Oral Defensiveness: An avoidance of certain textures of foods and irritation with certain activities using the mouth in general [19, pg 1].

c)Gravitational Insecurity: An emotional fear reaction that is out of proportion to the actual threat/danger of the vestibular-proprioceptive stimuli or the position of the body in space (especially those body positions in which the feet are no longer in contact with the ground) [6, pg 101].

d)Auditory Defensiveness: An over-sensitivity to certain sounds, which can trigger an alarm or defensive response [19, pg 1].

e)Visual Defensiveness: An over-sensitivity to light, visual distractability and/or gaze avoidance [19, pg 1].

f)Aversive Response to Movement: Includes a history of inordinate autonomic nervous system reactions to movement stimuli; characterised by nausea, vomiting, dizziness, or vertigo and other feelings of discomfort associated with sympathetic nervous system stimulation [6, pg 102].

g)Postural Insecurity: Fear and avoidance of certain movement activities due to poor postural mechanisms [13, pg 7].

h)Olfactory Defensiveness: Aversive reaction of over-sensitivity to certain odours [13, pg 7].

i)Proprioceptive Defensiveness: Aversion to any part of the body being moved passively [13, pg 8].

Levels of Severity of Sensory Defensiveness:

Level 1: Mild: While appearing quite normal, the individual might be described as "pricky", "over-sensitive", "slightly over-active", "resistant to change", or "slightly controlling". They will be able to achieve age appropriate levels and have good social relationships but may have to use enormous control and effort to succeed in these areas [20, pg 3].

Level 2: Moderate: Affects two or more aspects of the child's life. The individual usually has difficulty with social relationships and many self-care skills [20, pg 3]. There is severe stress and anxiety build-up [19, pg 2].

Level 3: Severe: Disruption in every aspect of the individual's life, leading to strong avoidance of some sensations and intense sensory-seeking of others [20, pg 3].

Sensory Dormancy: A result of excessive inhibition of incoming sensory inputs and a lack of sensory arousal [12, pg 32].

Self Regulation: The ability to achieve, monitor and change arousal state to match the demands of the environment. Essential for homeostasis [13, pg 2].

Sensory Affective Disorder: A hypothesised disorder involving emotional difficulties that may result from SMD (Wilbarger and Royeen, 1987 in [6, pg 120]). It involves a pattern of learnt behaviours which create habits and interaction which are protective and defensive in nature [13, pg 1].

Avoidance Patterns Precipitated by either Defensive or Dormant Behaviour:

a)Primary Avoidance: Patterns of behaviour which are directly related to the hyper- or hyposensitive response, are further identified here as a sensory defensiveness or sensory dormancy.

b)Secondary Avoidance: This refers to behaviour in motor output, social interaction or academic performance which is disorganized or disrupted due to the individual's sensory defensive or dormant response.

c)Tertiary Avoidance: This term implies the more serious emotional disturbances that exist; these may be related in part or originate in large measure from the primary sensory defensive and/or the sensory dormancy responses [12, pg 34].

Limbic System: Plays a role in affective or emotional tone, the perception and expression of emotion, arousal, drive states, memory and autonomic regulation or homeostasis [13, pg 1].

Neural Plasticity: The ability of the brain structure to change or to be modified [6, pg 15].

Substance Abuse: Should an individual use a chemical agent when there is no legitimate medical need to do so, or drink in excess of accepted social standards, that person could be said to be abusing the substance (Schuckit, 1989; in [3, pg 6].

Drug addiction: Dependency on a substance. It consists of two aspects: (1) an increasing tolerance to the drug's effects and (2) a withdrawal syndrome when the drug is discontinued [3, pg 6].

Tolerance: Is defined by either of the following (according to DSM IV criteria):

a)A need for markedly increased amounts of the substance to achieve intoxication or the desired effect.

b)Markedly diminished effect with continued use of the same amount of the substance [20, pg 387].

Psychological Dependency: This refers to a pattern of repeated self-administration of a substance because an individual finds it rewarding [3, pg 36].

Physical Dependency: This occurs once the body adapts to the effects of the drug and results in a withdrawal syndrome if it is discontinued [3, pg 36].

Withdrawal: Manifested by either of the following (according to DSM IV criteria):

a)A characteristic withdrawal syndrome for the substance.

b)The same/closely related substance is taken to relieve or avoid withdrawal symptoms [20, pg 387].

Central Nervous System Depressants: Act as sedatives, tranquillizers, hypnotic agents and/or anaesthetics at high dosages [3, pg 31]. The substances act in decreasing the functional power of the cells [7, pg 6].

Central Nervous System Stimulants: Act on brain structures to increase cell activity [7, pg 5].

Delinquent: A juvenile whose action deviates from social norms. He is labeled delinquent when he is detected and then encounters court and law enforcement authorities (Jacobson, 1974; in [5, pg 631]).

1.5: Limitations of the study

Chapter 2: Literature Review

Playground of Fear

"My life unfolded on the playground

With all of its pain and joy.

The fears and doubts of myself

Come into play--there in that make-believe, all too real world.

I jump on a swing

Prepared for an exhilarating experience--flying.

When the others pushed me beyond my security--laughing--the speed blurring all chance for reason,

And no laughter came from me,

As I clung to the hope of a speedy end to my anguish.

So I ran from the playground of fear--

This make-believe, all too real world,

Home where these games of life continued to be played out.

And no laughter came from me."

{a few verses from [1, pg 85], written 29 April 1973}

Sensory integrative problems have their roots in early childhood. Many authors consider disorders during this time, neglecting the adult years. SMD does persist into later life [6, pg 22]. Difficulties in childhood have detrimental effects on the individual's future life and therefore need to be considered. The literature reviewed considered SMD or substance abuse. Some confusion exists concerning the nature of SMD. The following review is a collaboration of current literature.

2.2: Anatomy of Sensory Modulation Disorder

SMD occurs when the brain is unable to select the most appropriate sensory information to be sent to the higher CNS areas [6, pg 3]. Either too much information reaches these areas, resulting in sensory defensiveness or too little information, resulting in sensory dormancy [6, pg 120]. The following are hypothesised precursors of both defensiveness and dormancy. Ayres [1, pg 54] discussed the possible hereditary predisposition for certain types of minimal brain damage, the contribution of environmental toxins, genetic factors making one part of the brain more vulnerable than usual, the effect of insufficient oxygen at birth and the possibility of leading a sensory-deprived life. Kinnealey, Oliver and Wilbarger [11, pg 449] cite environmental chemical abuse, physical sexual abuse, and prematurity as important precursors. They also refer to the precursors mentioned by Ayres. This list is not conclusive. The important precursors are in bold print above. The authors do not elaborate further, so substance abuse could be a precursor to SMD.

This disorder is theoretically based on sensory integration theory. Even though it is caused by irregular activity in the brain, most neurologists would find nothing structurally wrong with an individual suffering from SMD [1, pg 52]. We are unable to observe the physical functioning of the central nervous system (CNS), but are able to observe and evaluate defective behaviour that results from it. This is based on the first and second postulates of the theory [6, pg 15]. The first postulate specifies that "normal individuals take in sensory information derived from the environment and from movement of their bodies, process and integrate these inputs within the CNS, and use this sensory information to plan and organise behaviour". The second postulate specifies that "deficits in integrating sensory inputs result in deficits in conceptual and motor learning". We still cannot assume that defective behaviour is the result of poor sensory integration [6, pg 5].

Fisher [6] and Oetter [15] postulate the limbic system as the modulator of sensory information to the brain. Limbic structures include the limbic lobe, hippocampal formation, amygdaloid nucleus, the hypothalamus (especially the mamillary bodies) and the anterior nucleus of the thalamus [15, pg 15]. These structures appear to play a role in learning and memory, eating and drinking behaviours, aggression, sexual behaviour and the expression of emotions [6, pg 123]. Emphasis on the limbic system can help explain the emotional and social difficulties that often accompany SMD, the presence of SMD across the sensory systems and the extreme shifts in responsiveness in one or more sensory systems that may be observed in an individual [6, pg 123]. Involvement of the limbic system has been shown through animal studies [6, pg 123]. Lesions of the septal region of the limbic system demonstrate transient hyper-emotionality with possible exaggerated defense reactions and hyper-responsiveness to handling. The hyper-responsiveness leads to increased motor activity. It is, however, important not to generalise this behaviour to humans. There are a variety of responses that can occur. Stimulation studies of the same area indicate that it plays an important role in modulation of pleasure. This will be discussed in greater detail in the substance abuse section. Hippocampal lesions may result in animals that fail to persist in new tasks [6, pg 123]. We observe certain parallel behaviours in some humans experiencing SMD. The hippocampus appears to act as gate-keeper between sensory and motor activities. Through the hippocampus, the limbic system has connections with the autonomic nervous system for the visceral component to emotional experience [15, pg 15]. It is useful in maintaining "suitable conditions for mental actions and for behaviour" [6, pg 123].

Sensory dormancy and defensiveness were thought to be on opposite poles on the sensory responsiveness continuum [6, pg 120]. When the individual's variation in responsiveness is extreme and excessive time is spent at one end of the continuum or the other, or there is a shift from one extreme to the other , a problem may be indicated. Currently, the continuum is viewed as circular with sensory dormancy and defensiveness adjacent to one another [6, pg 123]. This would support the quick shift between dormancy and defensiveness or vice versa in some individuals, without passing through normal responsiveness. The individual will have problems maintaining or attending to the midrange.

The individual who has a non-defensive sensory system will be able to maintain arousal at the optimal level most of the time [13, pg 3]. The sensory dormant individual will function below this optimal level. The sensory defensive individual has difficulty lowering their arousal level to the optimum and easily goes into sensory overload. Both extremes show poor learning and attention levels [19, pg 8].

Finally, stress and anxiety can amplify SMD's [20, pg 16]. The manifestations of stress and anxiety have been associated with limbic system structures [6, pg 123]. Anxiety occurs when our expectations do not match the real situation [6, pg 124]. We find ourselves with increased arousal and uncertainty concerning future sensation expectations. This theory is fairly well accepted. Stress and anxiety are also postulated as outcomes of SMD's, especially sensory defensiveness [20, pg 3]. This is linked to the levels of arousal stated earlier. Ayres (1964, in [6, pg 118]) theorised that anxiety could be both cause and effect of the disorder and that the problem was self-perpetuating. Anxiety seems to have an effect on the neurotransmitters norepinephine, epinephine and serotonin (Ashton, 1987 in [6, pg 124]. "Anti-anxiety drugs that disrupt the action of these neurotransmitters reduce anxiety-induced behaviours" [6, pg 123].

The above mentioned comments are largely hypothetical and require more research.

2.3: The effects of SMD on the individual

There are varying effects of the disorder on an individual. Literature refers to generalised responses, but these do not occur in every individual. A sensory-defensive individual is often characterised as "disorganised", "overly active", "hyper-verbal", and "distractable" [12, pg 32]. In particular, the disorganised sensory input causes the individual to respond excessively and immaturely to sensory stimuli [12, pg 32]. There may be differing patterns of "avoidance", "sensory-seeking", "fear", "anxiety" or even "aggression" involved [19, pg 1]. Ayres [1, pg 56] characterises the sensory-defensive individual as "running instead of walking", executing purposeless activity and having an inability to reach his/her potential. Bauer (1977, in [6, pg 113]) has substantiated a relationship between tactile sensitivity and increased levels of activity. The sensory dormant individual is also thought of as "disorganised" and "immature"[12, pg 32]. Characteristics also include being "less alert than one would normally expect", difficult to arouse, "quiet and compliant" and "slow and sluggish". [12, pg 32-33]. Most research has been done on children. "With growth and maturity some of these aberrant forms of behaviour will have decreased or disappeared" [12, pg 33]. The severity of behavioural effects will depend on the severity of the SMD [20, pg 3].

SMD may be isolated to one type of sensation (for example, sensitivity to touch is tactile defensiveness) or to many types of sensations [20, pg 1]. Knickerbocker [12, pg 31] found there to be a relationship between the olfactory, tactile, auditory systems (which she named the OTA Triad) and the vestibular, visual systems (which she named the Visuo-Vestibular Dyad). According to her theory, dysfunction of one modality in the triad or dyad is often accompanied by dysfunction of the other modalities. The correlation is usually sensory defensiveness or dormancy. In particular, "the greater the number of sensory systems functioning in a hypo-sensitive manner, the less information the (individual) will receive from his environment to stimulate, or direct, a response" [12, pg 33]. It is, however, possible for one system to be in a defensive mode, while the other one/two may be dormant [12, pg 38]. If two or three of these sensory systems are performing on a defensive mode, the individual usually presents with the generalised sensory defensive behavioural responses mentioned earlier.

Authors distinguish between primary and secondary behavioural deficits [6, pg 113]. When an individual's behaviour is dominated by sensory defensiveness, for example, other social and emotional symptoms can appear [20, pg 1]. These secondary effects become a separate but related problem. They result in habits and learnt fears, that may need to be treated separately [20, pg 1]. It is important to be able to distinguish between the primary and secondary effects in order to establish a clear picture of the individual. Knickerbocker [12, pg 34] refers to primary, secondary and tertiary avoidance patterns. The avoidance behaviours are discussed below in point form and consider the OTA Triad elements. "It is essential to be able to trace as directly as is possible the relationship between the early primary or sensory avoidance patterns of behaviour and those forms of adaptive motoric, social and academic responses which are thus influenced" [12, pg 34].

Avoidance Behaviours [12, pg 35-48]:

1)Primary avoidance behaviours:

a)Due to tactile defensiveness: Characterised by a withdrawal from touch, aggressive behaviour towards others, excessive ticklishness, movements that are fast and erratic and/or the fight or flight response to touch.

b)Due to auditory defensiveness: Characterised by an individual who either immediately initiates a continuing, sometimes intense verbal response or requires others to stop talking in their presence. This usually subsides when talking stops. Excessive talking is seen as a protection against auditory input. The individual is distracted by sounds, even those in the distance. These become an all-encompassing focus of attention. He/she is extremely restless, has poor concentration and a poor ability to carry out instructions.

c)Due to olfactory defensiveness: Characterised by an acute awareness of "even the faintest suggestion of an offensive odour". The individual is unlikely to endure the smell for very long, over reacts to bathroom odours, to personal hygiene and to scents which are not recognised as offensive by most people.

d)Due to tactile dormancy: The individual appears to be sluggish, uncertain of action, insensitive to touch and pain, oblivious to his/her bruises, unaware of movement, exerts great effort to move, tires easily from exertion, requires more sleep than others, has hypotonic muscles, becomes easily overweight and lacks appropriate affect, becoming depressed at times.

e)Due to auditory dormancy: The individual seems to be unable to comprehend verbal communication at the appropriate age level.

2)Secondary avoidance patterns (due to sensory defensiveness or dormancy):

a)In Motor Skills: Results in poor manual dexterity, awareness of spatial relations, gross grasp, finger movements, hand dominance, directionality, hand writing, fine movement sequence patterns and gross motor activity.

b)In Social Interaction: Is usually accompanied by failure, frustration and rejection by others. The individual is often unable to form good social ties and withdraws from such events. The individual may associate with a predominantly younger age group, as this group will offer less competition. Aggressive behaviour may result from tactile defensiveness. This further alienates the individual from social interaction.

c)Of Academic Performance: The individual's short attention span and hyper-kinetic behaviour makes performance difficult, leading to poor completion of tasks and assignments. The individual may try to postpone or escape academic demands.

3)Tertiary avoidance patterns (for sensory defensiveness and dormancy):

a)Demonstrated Through Focal Symptoms: These include anxiety, irritability and depression.

b)Demonstrated Through a Phobic Response: This involves "avoiding the requested performance or preventing contact with the offending source of sensory stimulation" [12, pg 47]. This is necessary for emotional survival.

c)Through Global Response: This occurs if the individual "finds the sensory stimulation to one or more sensory systems overwhelming, he may be unable to react to it in a purposeful, productive manner, therefore he feels compelled to withdraw from his contact with the environment in order to protect himself" [12, pg 48].

Kinnealey, Oliver and Wilbarger [11] conducted a phenomenological study of sensory defensiveness in adults. According to this study, the subject's defensiveness led to behavioural strategies used to cope with the discomfort. The "coping strategies" included avoiding uncomfortable situations, maintaining predictability in routines (by organising/controlling these), using mental preparation prior to exposure or talking themselves through traumatic situations, counteracting the effects of the sensory input with something else or calming themselves after overstimulation and confronting their fears to allow the development of a plan to overcome these fears [11, pg 445]. The important strategy is counteraction. This involves using various sensory experiences to counteract the effects of sensory defensiveness [11, pg 449]. Could substance abuse be a counteraction technique? All these strategies have negative impacts on the formation of intimate adult relationships, for example [11, pg 445]. The coping strategies may help the individual survive the day's experiences, but do not decrease the defensiveness. They are energy and time-consuming, as well as emotionally exhausting. If severe enough, they have an effect on every aspect of the individual's life [11, pg 450]. They influence choices of leisure and work activities [11, pg 445]. Could this cause substance abuse? This article supports the concept of sensory defensiveness in the adult population [11, pg 449].

2.4: Specific research into SMD

Research identifies sensory integrative problems in children with learning difficulties [8; 1, pg 53]. Similiarly, studies have indicated a link between delinquency, criminality, alcoholism, drug abuse and learning disabled children [8; 5, pg 631; 1, pg 58]. In severe cases, the result may be academic failure and school drop-out [8; 1, pg 58]. In less severe cases, smaller problems such as difficulty remembering a sequence of numbers can occur [1, pg 58]. The teenager may avoid dancing or even clapping to a rhythm [1, pg 58]. This would cause misery. The result could be a vicious cycle of failure that extends into adulthood if no treatment is provided [8]. Fanchiang, Snyder, Zobel-Lachiusa, Loeffler and Thompson [5, pg 631] state that a child may become frustrated and angry by their incompetence at times and act out with behaviours that incorrectly label him/her as a delinquent. Lombard [13, pg 16] states that adolescents suffering from SMD may opt for alcohol or other substances to numb their feelings. It is, however, only one of the coping strategies they may opt to use.

Sensory integrative problems that appear in childhood are not usually outgrown [18, pg 2]. This is especially true when the problem is inaccurately diagnosed and the appropriate treatment is not provided. "A sensory system can develop only if it is exposed to the forces that activate its receptors" [1, pg 45]. Neural connections add new elements to sensory perceptions and motor abilities [1, pg 45]. The greater the number of neural connections, the greater the capacity to learn [1, pg 45]. Sensory integration theory is only applicable to adults who continue to demonstrate the manifestations of dysfunction that were present during childhood [6, pg 22]. The theory is not meant to explain adult onset dysfunction.

2.5: The treatment of SMD

The first step involves gaining awareness of a possible problem [19, pg 3]. A sensorimotor history assessment is conducted to gain insight into past and present defective behaviours [19, pg 10]. The therapist searches for test score correlations and 'meaningful clusters' [6, pg 128, 14]. There is usually a combination of sensory avoiding and sensory seeking behaviours [20, pg 4]. The identification of a problem should not be based on information from one source [6, pg 128]. The symptoms may be very individualised. It is only possible to list common symptoms that may point towards a problem [20, pg 4]. The symptoms will differ in mild, moderate and severe cases. Although a correlation between sensorimotor history assessment test scores may exist, this does not show how the constructs are related [6, pg 14].

The second step involves a sensory diet. Use will be made of specific activities designed to decrease the problem [19, pg 3]. Timing, intensity and sensory qualities of the activities are highlighted [19, pg 3]. The third step includes a programme of direct treatment in the clinic and specifically designed home programmes [19, pg 3]. Research indicates that neural plasticity persists into adulthood [6, pg 15]. This validates the usage of sensory integrative treatment techniques with the adult [6, pg 15].

2.6: What is Substance Abuse

According to the DSM IV [4] substance dependency is a "maladaptive pattern of substance use, leading to clinically significant impairment or distress" in three or more of the following: tolerance, withdrawal, substance ingestion in large amounts or over a longer period than was intended, a persistent desire coupled with unsuccessful efforts to discontinue its usage, a great deal of time expenditure in activities related to its abuse, a reduction or cessation of social, occupational or recreational activities, and/or continual usage of the substance even with medical knowledge of the consequences.

2.7: Risk Factors and Precursors to Substance Abuse

There are many reasons for substance abuse. The following are most commonly cited. Dependency is more common in men than women [16, pg 43; 10, pg 387]. Monozygotic twins show a higher rate of abuse than dizygotic twins and children of abusers are more likely than those of non-abusers to develop substance-related problems later in life [16, pg 43]. An association between drug usage and social disadvantage (including unemployment) has been shown [16, pg 43]. Accessibility to drugs and peer pressure or attitude plays a role [16, pg 43]. Substance abuse is more common among medical professionals than among non-medical professionals of equal levels of education [10, pg 387]. This is linked to the relative ease of access of drugs to certain individuals. There is little evidence to support the existence of a specific addictive personality [16, pg 43].

Other common cues to drinking include anxiety, tension, loneliness, boredom, bereavement, anger, frustration, relationship problems, family problems, sexual problems, work problems, difficulties with children, problems related to unemployment, losses (e.g. self confidence, self respect), fear of the future and a desire to escape from pressure and responsibility [2, pg 172]. Anxiety and tension have been cited as causes and effects of SMD. Reference to marital, occupational and social problems have been mentioned as results of SMD. Once again, an indirect link between SMD and substance abuse is evident.

2.8: Physiology of Substance Abuse

Substances are usually divided into stimulants and depressants. Central nervous system stimulants increase brain activity [7, pg 5] and are divided further into the psychomotor stimulants and the psycho-mimetic drugs/hallucinogens [14, pg 99]. The first group causes excitement and euphoria, decreases feelings of fatigue, and increases motor activity. They include amphetamines, caffeine, cocaine and nicotine [14, pg 99]. The psycho-mimetic drugs (lysergic acid dithylamide-LSD, Phencyclidine-PCP and Tetrahydrocannabinol-THC) produce profound changes in thought pattern and mood, with little effect on the brainstem and spinal cord [14, pg 99]. Nervous system stimulants may be given to hyperactive children with short attention spans [17, pg 84]. Central nervous system depressants sedate brain structures [7, pg 5]. They include: barbiturates, benzodiazepines, volatile inhaled substances, sedatives, tranquillizers, hypnotic agents, opioids, alcohol and anaesthetics (depending on the dose) [3, pg 31]. Drug usage is highly dependent on how it makes the indivdual feel. This may be subjective and/or objective in origin.

"Some behavioural models of substance abuse focus on "substance-seeking behaviours" [10, pg 391]. Accordingly, the abuser will continue taking drugs that give him/her pleasure and discontinue those that are perceived as unpleasant. This is related to positive and negative reinforcement. As stated previously, the limbic system is viewed as the pleasure centre.

Researchers have identified particular neurotransmitter receptors which are affected by specific substances. An abuser may have an abnormal endogenous receptor function or neurotransmitter concentration and self medicate using particular substances. This leads to substance dependency [10, pg 392]. They may, however, have completely normal levels. "The long term use of a particular substance of abuse may eventually modulate those receptor systems in the brain, so that the brain requires the presence of the exogenous substance to maintain homeostasis" [10, pg 392]. "Modulation of neurotransmitter release and neurotransmitter function has proved difficult to demonstrate" [10, pg 392]. The opiate, catecholamine (particularly dopamine) and GABA systems are cited as important. "Of particular (concern) are the dopaminergic neurons of the ventral tegmental nucleus accumbens. That particular pathway is thought to be involved in the sensation of reward and is thought to be the major mediator of the effects of such substances as amphetamine and cocaine" [10, pg 392]. The substances abused by the subjects of this study include: Cocaine, LSD, Estacy, Mandrax, Cannibus, alcohol, Valium, Demetrin, Librium, Enderol, pain-killers, Heroin, sleeping pills, Xanor, Rohypnol, Activan, benzodiazopines, hypnotics and Welconal. These are discussed below. Arorix, Tensin, prescribed medication, Magnin and diet tablets are also mentioned. There is insufficient information to research them.

"Chronic alcohol use can significantly reduce the brain's production of a group of opiate-like neurotransmitters: the endorphins, the enkephalins and the dynorphins (Trachtenberg and Blum, 1987; in [3, pg 37]). "These neurotransmitters function in the brain's pleasure centre to help moderate an individual's emotions and behaviours" [3, pg 37]. A sense of well-being will be experienced initially. Animal research on chronic alcohol abuse shows diminishing dopamine and serotonin levels in the brain [3, pg 37]. A common reason for alcohol usage is it's potential to reduce anxiety [10, pg 397]. A childhood history of attention-deficit/hyperactivity disorder increases the risk of an alcohol-related disorder in adulthood [10, pg 399].

Caffeine ingestion of 50-100 mg is associated with increased alertness, a mild sense of well-being, and a sense of improved verbal and motor performance [10, pg 418].

Cannabis can result in euphoria with drowsiness, distorted and heightened images, colours and sounds, altered tactile sensations and depersonalisation [16, pg 73]. According to Kaplan and Saddock [10, pg 420] the "cannabinoid receptor" is found in high concentrations in the hippocampus. There is some debate whether or not cannabinoids stimulate the so-called reward centres of the brain [10, pg 420]. "Cannabis intoxication commonly heightens the user's sensitivity to external stimuli, reveals new details, makes colours brighter and richer than in the past, and subjectively slows down the appreciation of time" [10, pg 421]. The appearance of anxiety symptoms is the most frequent adverse reaction to moderate cannabis usage [10, pg 422]. This usually occurs in inexperienced users.

Cocaine is one of the most commonly abused, addictive and dangerous substances [10, pg 423]. Clinical features of mild cocaine intoxification include euphoria, agitation and hallucinations [16, pg 75]. The primary neuro-pharmocological effect of cocaine is competitive blockade of dopamine re-uptake by the dopamine transmitter [10, pg 424]. This increases the concentration of dopamine in the synaptic cleft with intensified dopamine receptor activation [10, pg 424; 14, pg 102]. Dopamine is a chemical messenger associated with pleasure and movement, having a great effect on the extended amygdala (part of the limbic system) [9, pg 2]. The extended amygdala is involved in transforming the memories related to drug abuse into future craving for the drug [9, pg 2; 14, pg 102].

The benzodiazepines (therapeutically used as anti-anxiety drugs) selectively inhibit the neural circuits of brain structures, including the limbic system [14, pg 90]. They should not be used to alleviate the normal everyday stress, but should be reserved for continued severe anxiety [14, pg 90]. They include: Diazepam (Valium), Alprazolam (Xanor), Flunitrazepam (Rohypnol), Chloridiazepoxide (Librium), Activan and Prazepam (Demetrin) [17, pg 79]. They may be used as sleeping pills [17, pg 78]. Other drugs used to induce sleep include the barbiturates [17, pg 78]. Clinical features of barbiturate use includes reduction of anxiety, nervous tension and insomnia; drowsiness, impaired concentration, and mental and physical sluggishness [14, pg 90]. Other drugs that decrease anxiety are the beta-blockers, for example: Enderol [17, pg 79].

The hallucinogens include LSD and Ecstacy. They induce hallucinations, loss of contact with reality, and an expanding and heightening of consciousness [10, pg 429]. The abuser might believe that he/she has new insight into reality. The drugs do not generate new thoughts so much as alter one's perception of existing sensory stimuli [3, pg 142]. With hallucinogen usage, perceptions become unusually "brilliant and intense" [10, pg 432]. "Colours and textures seem to be richer than in the past, contours sharpened, music more emotionally profound, and tastes and smells heightened" [10, pg 432]. Changes in body image, intense and labile emotionality, and an altered sense of self (sometimes to the point of depersonalisation) can occur [10, pg 432].

Glue, chlorinated hydrocarbons (e.g. cleaning fluids, laquers and dyes), fluorocarbons (e.g. aerosol propellants and fire extinguishers), petrol, acetone (e.g. nail varnish remover and polystyrene cements), butane, propane, and amyl-, butyl- and isobutyl-nitrites are commonly inhaled substances [16, pg 73]. Clinical features are similar to those of alcohol intoxication and include euphoria, excitation and hallucinations [16, pg 74].

The most common form of nicotine is the tobacco in cigarettes [10, pg 436]. Nicotine is an agonist at the nicotinic subtype of acetylcholine receptors [10, pg 437]. It activates the dopaminergic pathway projecting from the ventral tegmental area to the cerebral cortex and the limbic system [10, pg 437]. It results in improved learning, reaction time and problem-solving ability. Tobacco is also reported to decrease tension [10, pg 438] and mediate pleasurable sensations [3, pg 156].

The opioid analgesics include heroin and morphine [16, pg 76]. They seem to mimic the action of the natural painkillers of the body, namely the endorphins, the enkephalins and the dynorphins [3, pg 108]. The substances moderate the emotions and help manage stress [3, pg 110]. Without stress or pain, euphoria is usually experienced. The hypothalamus and limbic system may be affected by this class of drug (along with other CNS areas) [14, pg 134]. The greatest concentration of opioid receptors is located in the amygdala [14, pg 135]. These receptors probably do not exert analgesic action, but may influence emotional behaviour.

The active ingredient in marijuana is THC. "Chronic exposure to THC damages and destroys nerve cells and causes other pathological changes in the hippocampus" [3, pg 101]. This portion of the brain is thought to be involved with processing sensory information. Research on the effects of THC suggests that it changes the way sensory information is handled by the brain [3, pg 100].

2.9: Traditional Treatment Approaches for Substance Abuse

An adapted programme might include: withdrawal from substances under medical supervision and frequent doses of vitamin supplements; social skills training; analysis of substance abuse behaviour and help in finding alternatives to drinking [2, pg 171]. Alternatives to anxiety, for example, may include learning relaxation techniques, setting aside time to practise these daily, using meditation if this is useful and/or trying to avoid dependency on another substance [2, pg 172].

2.10: Conclusion

Literature considers either SMD or substance abuse. Through the anatomy, causes and effects of both topics, an indirect link can be established. SMD may result from environmental toxins or chemical abuse. The modulator of sensory information is thought to be the limbic system. The limbic system plays a role in the modulation of pleasure and has shown changes in chronic substance abuse cases. Stress and anxiety have been postulated as part of the cause and effect of SMD. Similarly, anxiety can cause substance abuse and chronic substance abuse has been linked to increased levels of anxiety. Specific neurotransmitters are mentioned in both sections. An important coping strategy to SMD is counteraction. Could substance abuse be a form of counteraction? Importantly, SMD has little concrete evidence of its existence. It is clear that if a link is possible between SMD and substance abuse, it is a complicated one with many factors involved.

Chapter 3: Research methodology

3.1: Research Design

A descriptive research design was used.

3.2: Selection of subjects

The sample number was based on the maximum number of voluntary clients available. No random selection was done. Clients chosen were:

3.3: Materials and methods

Each patient who consented to undertake the project was asked to complete two questionaires, which took approximately half-an-hour to complete.

The first questionaire consisted of background information (see appendix 1 a). It considered the type of substance abused, how many days/weeks/months it was used and how frequently it was taken. The subjective effects of the substance were taken into consideration and the reason for the initial abuse was questioned; this aiding factors, besides SMD, that could have led to the substance abuse problem.

The second questionaire formed the sensorimotor history assessment (see appendix 1 b). This was adapted from Patti Oetter's original questionaire. Section A examined the health of the client's mother during pregnancy, any complications that occurred during the birth process and any diagnosed visual, auditory, muscle tone and/or co-ordination problems. It investigated past and present problems which may have led to SMD/substance abuse. "Yes", "No" or "I Don't Know" (D/K) reply columns were used. Section B questioned current behaviour concerning tactile, vestibular, visual, taste/smell and auditory information, muscle tone, co-ordination, behaviour and learning styles. The nine sub-sections to this component helped recognise the presence of hypo/hypersensitivity in an individual. Never (N), Sometimes (S) and Often (O) reply columns were used.

One to four fourth year O.T. students evaluated +/-10 patients per session. The number was dependent on the availability of patients at any one time. Patient numbers available for the research diminished over time. Each evaluation took place on a Friday afternoon, at Riverfield Lodge. The assessments were done every third week, from mid-February through to the end of July 1997. 70 clients were assessed and issued with client numbers.

The following method was used by all the students. The clients were seated round a table. The consent forms and questionaires were handed out, together with writing implements. The importance of confidentiality was explained. Each client was asked to fill out the consent form first and hand this back to the student before continuing. The client's name only appeared on the consent form. Any individuals not wishing to disclose their names on this form were allowed to continue the assessment if they so wished, but the information supplied was not included in the final analysis of the data. The importance of directing all questions to the student only and not to their fellow patients was stressed. The patients were requested to complete the questionaires and to ask for help if confused. There was no time limit or correct answer. If the answer was not known, it was more accurate to tick the D/K column than to guess. Once the questionaire was completed, it was checked by the student to determine any ambiguous answers. These could be addressed. Finally, the patients were thanked for their participation in the research project and informed that the outcome of the research would be made available to Riverfield Lodge on completion.

3.4: Control of Variables

The population and selection criteria outlined above were adhered to. The general structure of the assessment and the method of administration, as outlined above, was maintained during each evaluation session. An attempt was made to formulate a set of standardised answers to possible questions. Client questions were, however, not standardized and this attempt could not be adhered to.

The predominant extraneous variables included:

3.5: Collection of Data

70 clients were assessed and were issued with client numbers. Of these 70 clients, six were eliminated from the data analysis: three clients were under age and three had answered the questionaires insufficiently. The data from the sensorimotor history and background information questionaires were collected separately.

3.5.1: Sensorimotor history assessment

There is no standardized rating system available for this assessment. Knickerbocker had formulated a rating system for some of the questions [12]. This rating system was used together with information from other sensory integration references to formulate the most appropriate rating system (see literature review, chapter 2). The rating system is shown in appendix 2.

During this process it was noticed that some of the questions were inappropriately placed in the assessment. Adaptation of the form was necessary prior to the rating. The adaptation involved relocating the following section B questions into section A (under the original headings): I (8), II (8,9), III (1-3,5-7), V (1), VI (1-5), VII (1-11), VIII (1-4,9-11,13-19) and IX (1-8). The following questions were eliminated from the questionaire due to ambiguity in meaning: section A--F(1,2), section B--VI(6) & VIII(8). Section A was rated according to the possibility of a problem occurring in the past and/or present. This problem may have been linked to SMD and/or substance abuse. Section B was rated according to the presence of hyper- or hypo-sensitivity in any of the modalities. The researchers have defined hypersensitivity as referring to insufficient modulation of information in the limbic system, while hypo-sensitivity referred to too much modulation at the same area. The hypersensitivity responses were sensory-avoiding in nature. The hypo-sensitivity responses were sensory-seeking in nature.

Section A was rated as follows (see appendix 2a):

Did you 3)Sit, stand or walk late?--NO REPLY
4)Sit, stand or walk early?--NO
5)Crawl for an extended period?--NO
6)Crawl on your tummy?--YES
7)Crawl on your bottom?--NO

From the scoring system and the above formula:

Section B was rated as follows (see appendix 2b & 2c):

3--for a hypersensitive response

2--for a "sometimes" response

1--for a non-hypersensitive response

3.5.2: Background Information Assessment

3.5.3: Computer Spreadsheet

3.6: Data Analysis

The information was analysed using two computer programmes, namely: Corel Presentation and the Kolmogorov-Smirnov two sample test. Corel Presentation was used in the formulation of the pie graphs, bar graphs and data spreadsheets. The Kolmogorov-Smirnov two sample test was used to formulate the cumulative distribution frequencies between the groups of subjects mentioned later. This assisted in deciding whether the information gained was significant or not. The analysis began with the raw data spreadsheet (see appendix 4).

The demographics of the total sample was produced by means of pie graphs. Appropriate rating systems were decided on.

The spreadsheet columns relating to section A & B of the sensorimotor history assessment were analysed to extract client percentages that were high in each case (see appendix 5). For section A, all values greater than or equal to 50% were extracted. These subjects presented with problems in one or more areas. This value was chosen to represent the mid-way point. For section B, all values greater than 66,6% were extracted. This value was chosen to extract the upper third of cases. The result was hyper- or hypo-sensitivity in one or more modalities. In the case of tactile hypersensitivity and auditory hypo-sensitivity, a lowering of this level to 60% was necessary in order to obtain any sample. By means of this new table, all problem cases could be compared with one another and an idea of the number of individuals affected could be given. Bar graphs plotting the affected individuals of each modality against the effects of the abused substance were constructed from this table. It was also possible to discover the overall sensitivity of each affected individual by comparing the problems present. The individual presenting with only hyper- or hypo-sensitivity in one or more modalities would be said to have an "overall hyper- or hypo-sensitivity". The individual with a combination of sensitivities, would be classed as "neither" (see appendix 5).

The Kolmogorov-Smirnov two sample method was used to compare the relative difference between two sample sets of data, with respect to a third set. With reference to this project, the vestibular hyper- and hypo-sensitive groups (gained via the extraction of problem cases as stated above) were compared with each other or each was compared separately with the remaining sample. The remaining sample was defined by the researchers as the individuals who remained behind after the extraction of the vestibular hyper- or hypo-sensitive subjects. By comparing these groups with one another, the presence or absence of significant difference can be obtained. The two sets thus formed were compared with respect to their experiences in other areas (as mentioned later in the following chapter).

Chapter 4: Results

The results from the analysis of the total sample, clients with problems in any area, vestibular hyper/hypo-sensitivity and substance abuse are mentioned in this project. There were too many results to mention in one research project. For information on SMD's involving the other modalities, refer to Gill Bosch's, Kerry Maree's and Lee-Ann Mountjoy's respective projects.

4.1: Total sample results

4.1.1: Gender

4.1.2: Home Address

4.1.3: Client's Current Age

4.1.4: Occupation

4.1.5: Marital Status

4.1.6: Length of time at Riverfield

4.1.7: Voluntary/forced admission

4.2: Results related to all clients who presented with problems in any area

4.2.1: Mother's age at Delivery of the client:

Of the five people in the sample who had mother's aged 35 years or older at delivery, the following simultaneous problems were evident:

The following percentages represent the simultaneous problems in this group:

NOTE: All forms of hyper-, hypo-sensitivity and general problems in any of the modalities are defined according to the rating sheet formulated in Chapter 3 (see appendix 2).

4.2.2: Client's Birth Weight

4.2.3: General Results (see appendix 5)

4.3: Results specific to Vestibular Hypersensitivity

Five people presented with vestibular hypersensitivity (see appendix 5). This represents 8% of the sample. The following simultaneous problems were present in the number of people shown:

The following percentages represent the simultaneous problems in this group:

4.4: results specific to Vestibular Hypo-sensitivity

Thirteen subjects presented with vestibular hypo-sensitivity (see appendix 5). This represented 20% of the sample. The following simultaneous problems were present in the number of people shown:

A behavioural hyposensitive individual is defined in this project as "clingy". A behavioural hypersensitive individual is defined in this project as "hyperactive, an early riser, distractible, having irregular sleeping patterns and a short attention span, with frequent mood changes".

The following percentages represent simultaneous problems in the vestibular hyposensitive individuals:

4.5: Results related to the Substance Abuse Problem

4.5.1: Total sample analysis

The following represents the percentage of people in the total sample abusing the particular drug classes:

There was bias towards the depressant category. Additionally, all clients were abusing the substances on a daily basis.

Sixty two percent of the sample began substance abuse before thirty years of age. The percentage for age of onset became progressively smaller as the age increased. No significant difference in age of onset of substance abuse was evident between the vestibular hypersensitive, hyposenssitive and the remaining group.

39% o the sample had been abusing substances for under five years. No significant difference in duration of substance abuse was evident between the vestibular hypersensitive, vestibular hyposensitive and remaining groups.

Each individual from the total sample was analysed to determine their general sensitivity across all modalities. The sample was divided into people who presented with general hypersensitivity, hyposensitivity or a combination of the two. The sample was then analysed according to the drug class. Of the general hypersensitive group, the following percentage of people fell into each class:

Of the general hyposensitive group, the following percentages of people fell into each class:

Of the group that presented with both hyper- and hyposensitivity, the following percentages of people fell into each class:

The results are shown graphically below. Overall, The hypersensitive group abused more depressant substances than the other groups and the hyposensitive group abused more stimulant substances than the other groups. However, the hyposensitive group shows an overall higher abuse of depressants than stimulants.

4.5.2: Analysis related to vestibular hyper- and hyposensitivity groups

The percentage of vestibular hyposensitive people in the sample who abused specific drug classes is shown below:

There is no real bias towards any particular drug class as the percentages are quite similar.

The percentage of vestibular hypersensitive people in the sample who abused specific drug classes is as follows:

There is a definite bias towards the depressant drug class in the vestibular hypersensitive group.

A significant difference in drug classes was found when comparing the vestibular hyper- and hyposensitive individuals. The hypersensitive group showed a greater use of depressant substances, while the hyposensitive group showed a greater use of stimulant substances. This is shown graphically below. It is important to note that the hyposensitive group is larger than the hypersensitive one.

A significant difference in drug class configuration is evident between the vestibular hyposensitive group with the remaining sample. The percentage in the remaining sample who abused the specific drug classes is as follows:

Overall, the hyposensitive group abused a higher percentage of stimulant substances than the remaining sample. It is important to note that the vestibular hyposensitive group is much smaller than the remaining group. This is also true when comparing the later group with vestibular hypersensitive individuals also.

A significant difference in drug class configuration is also evident between the vestibular hypersensitive group and the remaining sample. The percentage in the remaining sample who abused the specific drug classes is as follows:

Overall, the hypersensitive group abused more depressants than the remaining group.

4.5.3: Subjective Reasons for Abusing Substances

The following reasons were mentioned by the members of this study, namely: pleasure, social influence (especially peer pressure), experimentation, escapism, loneliness/boredom, pain removal, stress removal and other varied responses. These are shown graphically below. The predominant reasons include the social influence, loneliness/boredom and other varied reasons.

4.5.4: Subjective Effects of Substance Abuse, after Substance Abuse and any other Side-effects

Information concerning this was too individualistic and complex to analyse objectively.

4.6: Conclusions

Chapter 5: Discussion

This chapter follows the same format as the previous one. Only sections that can be discussed, will be discussed. Literature concerning a link between SMD and substance abuse is lacking. The discussion is focused on increasing awareness into the possibility of a link.

5.1: Total sample discussion

5.1.1: Gender

5.1.2: Home Address

5.1.3: Current Age

5.1.4: Occupation

5.1.5: Marital Status

5.2: Discussion related to clients who presented with problems in any area

5.2.1: Mother's age at delivery of the client

5.2.2: General Results (see appendix 5)

5.3: Discussion specific to Vestibular Hypersensitivity

5.4: Discussion specific to Vestibular Hyposensitivity

5.5: Discussion related to the Substance Abuse Problem

5.5.1: Total Sample analysis

5.5.2: Discussion related to the Vestibular Hyper- and Hyposensitive Groups

5.5.3: Subjective Reasons for Abusing Substances

5.6: Conclusion

Chapter 6: Conclusions

6.1: Summary of the research

This research project aimed to increase awareness into the possibility of SMD occurring in the adult population, specifically the substance abuse population. Many problems were encountered while doing the research. These included a large percentage of extraneous variables, human error during the analysis process and the need to formulate rating systems specific to this project prior to analysis of the raw data. All of these would have a detrimental effect on the results. Additionally, limited literature was available.

However, through the analysis of the results certain conclusions could be reached. A large proportion of the substance abuser sample presented with simultaneous problems in one or more sections of the sensorimotor history assessment. The link between Section A of this assessment and SMD/substance abuse was not as direct. Additionally, the hypersensitive groups presented with a bias towards the depressant substances. The hyposensitive groups presented with the highest usage of stimulant substances, when compared to the hypersensitve groups.

In general, there appears to be sufficient evidence to support the need for continued research.

6.2: Recommendations

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