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Query: UMLS:C0004352 (autism)
32,579 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Psychiatric patients are significantly more often smokers than the general population, the only known exception being obsessive-compulsive disorder (OCD) and catatonic schizophrenia. We have investigated nicotine use in subjects with autism spectrum disorders (ASD). Ninety-five subjects (25 females and 70 males) consecutively diagnosed with any ASD and of normal intelligence were included in the study. Only 12.6% were smokers, compared with 19% in the general population and 47% in a control group of 161 outpatients diagnosed with schizophrenia or a schizophreniform disorder. The results suggest that smoking is rare among subjects with ASD, while the opposite was shown for schizophrenia. If replicated, this finding could suggest biological differences between non-catatonic schizophrenia and ASD, and support the theory of a biological link between ASD and a subtype of OCD, and between ASD and catatonic schizophrenia.
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PMID:Low prevalence of smoking in patients with autism spectrum disorders. 1286 Mar 73

Evidence supports the hypothesis that normalization of cholinergic tone by selective antagonism of neuronal nicotinic acetylcholine receptors (NNRs) may ameliorate the core symptoms of autism. As often is the case, epidemiology has provided the first important clues. It is well recognized that psychiatric patients are significantly more often smokers than the general population. The only known exceptions are obsessive-compulsive disorder (OCD), catatonic schizophrenia and interestingly, autism. In this regard, clinical studies with nicotine have demonstrated amelioration of symptoms of a number of diseases and disorders, including Alzheimer's disease, Parkinson's disease, ADHD and Tourette's syndrome. Nicotine's agonist properties at CNS NNRs have been implicated in these effects and support the concept of self-medication as a strong motivation for smoking in cognitively compromised individuals. On the other hand, the inverse correlation between autism and smoking suggests that smoking does not provide symptomatic relief and may actually be indicative of an active avoidance of nicotine's agonist effects in this disorder. Neuroanatomical evidence is consistent with this idea based on the presence of hypercholinergic architecture in the autistic brain, particularly during the first few years of development, making the avoidance of further stimulation of an already hyperactive cholinergic system plausible. This may also explain why stimulants (known to increase dopamine levels as do NNR agonists) appear to aggravate autistic symptoms and why studies with cholinesterase inhibitors that increase acetylcholine levels in the brain have yielded variable effects in autism. Taken together, the evidence suggests the possibility that nicotinic cholinergic antagonism may in fact be palliative. Pharmacological evidence supports this hypothesis. For example, antidepressants, many of which are now known to be non-competitive NNR antagonists, have been used successfully to treat a number of autistic symptoms. More specifically, there is anecdotal evidence from at least one medical practitioner that mecamylamine, a non-selective NNR antagonist, is effective in treating many autistic symptoms, particularly those that are refractory to most other treatments. Clearly there is a need for carefully controlled clinical studies with novel selective NNR antagonists to explore their potential as a new and exciting approach for the treatment of autism.
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PMID:Nicotinic cholinergic antagonists: a novel approach for the treatment of autism. 1640 87

Background: Catatonic phenomena such as stupor, mutism, stereotypy, echolalia, echopraxia, affective flattening, psychomotor deficits, and social withdrawal are characteristic symptoms of both schizophrenia and autism spectrum disorders (ASD), suggesting overlapping pathophysiological similarities such as altered glutamatergic and dopaminergic synaptic transmission and common genetic mutations. In daily clinical practice, ASD can be masked by manifest catatonic or psychotic symptoms and represent a diagnostic challenge, especially in patients with unknown or empty medical history. Unclear diagnosis is one of the main factors for delayed treatment. However, we are still missing diagnostic recommendations when dealing with ASD patients suffering from catatonic syndrome. Case presentation: A 31-year-old male patient without history of psychiatric disease presented with a severe catatonic syndrome and was admitted to our closed psychiatric ward. After the treatment with high-dose lorazepam and intramuscular olanzapine, catatonic symptoms largely remitted, but autistic traits persisted. Following a detailed anamnesis and a thorough neuropsychological testing, we diagnosed the patient with high-functioning autism and catatonic schizophrenia. The patient was discharged in a remitted state with long-acting injectable olanzapine. Conclusion: This case represents an example of diagnostic and therapeutic challenges of catatonic schizophrenia in high-functioning autism due to clinical and neurobiological overlaps of these conditions. We discuss clinical features together with pathophysiological concepts of both conditions. Furthermore, we tackle social and legal hurdles in Germany that naturally arise in these patients. Finally, we present diagnostic "red flags" that can be used to rationally select and conduct current recommended diagnostic assessments if there is a suspicion of ASD in patients with catatonic syndrome in order to provide them with the most appropriate treatment.
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PMID:Two Sides of the Same Coin: A Case Report of First-Episode Catatonic Syndrome in a High-Functioning Autism Patient. 3103 60