Various studies and approaches agree that autism begins in fetal development, and almost always involves the cerebellar vermal lobes VI-VII (and to a lesser extent VIII-X). Additionally, other areas of the brain are affected in different sub-types of autistic individuals, giving compounding presentations of the disorder. Biochemical, genetic and EEG studies have also attempted to show consistent differences in the autistic patient, but with disputed and limited success.

There are various strategies of treatment of autism, based mainly on controlling the particular symptoms of the individual autistic. The major treatable symptoms are seizures, tics, attention deficits, behavior problems, depression, anxiety and obsessive-compulsive-like behaviors, which are all treated by standard measures (Burg, p. 29-31). Other therapies have been hypothesized for the more characteristic symptoms of autism, but which have no standard pharmacological treatment, such as self-mutilation, social withdrawal, and language deficits. We will consider each of these treatments in the rest of this paper.

Seizures, tics and attention disorder are not uncommon in many kinds of neurological developmental disorders. Standard seizure medication is indicated in the autistic with seizures, as in the non-autistic patient. In addition, the anticonvulsants may be useful in increasing language skills. Valproate, carbamezapine and phenytoin have been shown to increase language skills in autistic patients who show sleeping epileptiform EEG’s, even though the patient may not present with seizures (Burg). One study with valproic acid had such good results, the researcher claims his autistic patients no longer qualify for a DSM diagnosis of autism because their language and social skills have improved so dramatically (Plioplys).

Tics, similarly, are treated as with the non-autistic patient, but have the same treatment side-effects. Haloperidol (together with benzotropine), clonazepam, or clonidine are the drugs of choice for this presentation. Attention disorders with hyperactivity must be treated with caution in the autistic, because amphetamines often cause severe exacerbation of autistic symptoms. The standard therapy here is methylphenidate and dextroamphetamine (Burg; Tonge).

Severe behavior problems and aggression have been successfully treated with thioridazine. This drug also reduced SIB and is somewhat beneficial for hyperactive children. Haloperidol, carbamezapine and valproate are three other options for behavior problems in the autistic. Depression is typically treated with imipramine, nortriptyline or desipramine (Burg). Carbamezapine and lithium carbonate are alternate treatments for depression (Tonge). Anxiety in the autistic is typically treated with lorazepam or alprazolam. These benzodiazepines, as well as carbamezapine have also been shown to be effective treatments for aggression and SIB. This paradoxical effect (both treat aggression and SIB, while one also treats depression and the other is for anxiety) is typical of autistic disorder, in that many unexpected effects are seen in the autistic patient with pharmacological treatment.

Obsessive-compulsive-like ordering behaviors are common among the autistic. Clomipramine, which is a standard treatment of OCD, is also effective in decreasing the ordering and compulsions of the autistic (McDougle; Gordon; Brasic). In addition to decreasing OCD-like symptoms, clomipramine has a number of other surprising effects, such as reducing SIB, aggression and motor stereotypies, as well as increasing social reciprocity. These effects have led some to believe autism is tightly linked to the serotonergic system, and that newer therapies should focus on these findings. I found nothing testing fluoxetine’s effects on the autistic patient.

Other novel pharmacological approaches to characteristic autistic symptoms are ascorbic acid, propanolol, naltrexone, fenfluramine, and LSD. LSD, which of course works on the serotonin system, has been shown to increase the autistic’s response to their environment, but is still accompanied by hallucinations (Cook). Fenfluramine, with its antiserotonergic effects, improved the cognitive, intellectual and social disorders of autism, but only on certain, few patients, and is fairly neurotoxic, so its use is not widespread (Burg, Cook, Tonge). Naltrexone, an opiate antagonist, was expected to reduce SIB, and has had some positive trials showing decreased SIB and social withdrawals (Tonge). One very rigorous study, however, indicates naltrexone’s only effect is to decrease hyperactivity (Campbell).

The ascorbic acid and propanolol treatments seek to effect the catecholaminergic systems, as opposed to the serotonergic. Double-blind ascorbic acid treatments indicate an increase in social activity in groups. The authors of this study hypothesized a dopaminergic role for autism, and believe the ascorbic acid effect substantiates this hypothesis (Dolske). Propranolol, a beta-adrenergic-blocker, affects the norepinephrine receptors, and has been used effectively to treat explosive behavior and major temper-tantrums. Use of propanolol with desipramine is believed to be more effective than propanolol alone (Burg). While data showing decreased dopamine or norepinephrine data is lacking, there is correlative evidence incriminating serotonin. In one study, serotonin levels were increased in 30-50% of autistic patients, and severity of increase was correlated to decreased IQ (Ritvo).

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Tonge, BJ, et al. “Autism: fifty years from Kanner (review).” Journal of Paediatrics and Child Health 1994, 30 (2): 102-7.

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