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A Brief Introduction to Schizophrenia by Miguel A. Faria, MD
The journal article, “New concepts in the development of schizophrenia, autism spectrum disorders, and degenerative brain diseases based on chronic inflammation: A working hypothesis from continued advances in neuroscience research,”by Drs. Russell L. Blaylock and Miguel A. Faria, was published in Surgical Neurology International in 2021. The journal article was written and prompted, at least in part, following a discussion the authors had concerning the poignant film, Occupied. The movie plot centered on a young woman with schizophrenia who is babysitting an adolescent girl in an isolated cabin. Schizophrenia is an illness that the paper’s authors have an interest in and continue to study and investigate.[1]
There is now compelling evidence that schizophrenia is a very complex syndrome that involves numerous neural pathways in the brain, far more than just dopaminergic and serotonergic systems. One of the more popular theories in recent medical literature is that it represents a hypo-glutaminergic deficiency of certain pathways, including thalamic ones. After much review of the research and study in this area, we have concluded that most such theories contain a number of shortcomings. Most are based on clinical responses to certain drugs, particularly antipsychotic drugs affecting the dopaminergic neurotransmitters; thus, assuming dopamine release was the central cause of the psychotic symptoms of schizophrenia. The theory was limited in that dopamine excess could only explain the positive symptoms of the disorder. Antipsychotic medications have minimal effectiveness for the negative and cognitive symptoms associated with schizophrenia. It has been estimated that 20–30% of patients show either a partial or no response to antipsychotic medications. In addition, the dopamine hypothesis does not explain the neuroanatomic findings in schizophrenia.
The following is a short introduction to the historical background of the disease and its clinical symptomatology. Schizophrenia was originally named dementia praecox (“premature dementia”). In 1893, the German psychiatrist Emil Kraepelin separated the two psychoses with which this disorder had been confused—that is, dementia praecox and manic depression. It was renamed schizophrenia by the Swiss psychiatrist Eugen Bleuler in 1908, meaning in Latin “split mind or split personality.” It was not until the mid-20th century that true schizophrenia was further separated from split (or multiple) personality hysteria—the latter, subsequently categorized as either a conversion reaction or a dissociative, identity disorder. Hollywood, however, continues to confuse schizophrenia and hysteria in their motion pictures.[1]
As I wrote elsewhere, the two leading lights of psychiatry at the turn of the century—namely, Austrian psychoanalyst Sigmund Freud (1856–1939) and German psychiatrist Emil Kraepelin (1856–1926)—had conflicting approaches to mental illness, including schizophrenia. Freud recommended psychotherapy, which was almost always unsuccessful and unfeasible in severely mentally ill patients. Kraepelin, in contrast, preferred more aggressive intervention with electroconvulsive therapy (ECT) and insulin shock therapy—the former therapy was often ineffective and the latter too dangerous and therefore no longer used. Thus, psychosurgery came into vogue; fortunately, it was soon supplanted by psychotherapy, which proved to be safer and the most efficacious treatment in Schizophrenia in at least 75% of patients.[2]
Necessarily in the original descriptions of the disease, the behavioral and sociological aspects of schizophrenia have been emphasized, but not its anatomic, biochemical, or pathophysiological substrates. For example, schizophrenia has been described as a functional mental illness that begins gradually, occasionally very suddenly, striking in adolescence or young adulthood. No standard neuroimaging techniques disclosed any definitive pathological abnormalities in these patients. Moreover, there is no objective pathognomonic test that would confirm the illness, which is still diagnosed on the clinical symptomatology and observed behavior.
In his autobiography, Nobel-prize winner Eric R Kandel explains how, as a psychiatrist and research neuroscientist, he had attempted to apply the scientific method to psychiatry as a new “science of the mind.” He asserts that the human mind can be studied with biological tools to create this new science. He further asserts that in time all mental disorders, including those categorized as “functional” (or psychological, including schizophrenia by implication), will be found to have a structural, biochemical, and/or molecular basis, and that the old subjective criteria for psychiatric illnesses will completely give way to the new biological and scientific “science of the mind.”[3] We do not agree with this viewpoint, rather we agree with Sir John Eccles that the mind is a separate metaphysical entity from the material brain. This does not negate the idea that dysfunction of the brain can result in abnormal behavior and thought patterns of a psychological nature. The analogy of a radio fits here perfectly. The radio represents the brain with its complex of circuits, transistors, and other electronic components, while the mind would represent the invisible radio waves giving activity to the electronic contraption. Any abnormality of the “radio” would be manifested as a garbled radio message or static.
In medical school and in our psychiatry rotations, we learn about the four fundamental symptomatologies of schizophrenia, originally described by Dr. Bleuler as the four A’s of schizophrenia:
(1) looseness of associations, or disordered associations with a loss of contact with reality;
(2) autism, a disordered conception of the world with a preference for fantasy rather than reality; (3) a disorder of affect, or an abnormal emotional state or mood;
[4] ambivalence, a mixed feeling about a subject matter and contradictory attitudes that may be indirectly expressed. Schizophrenia is also characterized by cognitive impairments, delusions, and hallucinations that are most frequently auditory.[4]
Neurophysiological disorders of the central nervous system neurotransmission and biochemical defects of neurotransmitters production, transport, reuptake, blockage, and degradation have provided the best theories for explaining the good to excellent responses in schizophrenic patients to a variety of neuropharmacological agents. In addition, defects in working memory associated with disconnection of the hippocampal formation with the prefrontal cortex and in neurotransmission in the dorsolateral prefrontal cortex and frontotemporal disconnection have implicated both the frontal and temporal lobes in the neuropathology of schizophrenia.[5,6]
Those who have a further interest in this disorder and its scientific basis, including our hypothesis as to psychopathology, should read the original paper in Surgical Neurology International.[7]
References
1. Faria, M.A. Schizophrenia in the dramatic film “Occupied” (2011) and its critics. HaciendaPublishing.com, January 20, 2018. Available from: https://www.haciendapublishing.com/schizophrenia-in-the-dramatic-film-occupied-2011-and-its-critics-by-miguel-a-faria-md.
2. “Violence, mental illness, and the brain—A brief history of psychosurgery: From trephination to lobotomy,” In: Miguel A. Faria, Jr., Controversies in Medicine and Neuroscience: Through the Prism of History, Neurobiology and Bioethics (Newcastle upon Tyne, UK: Cambridge Scholars Publishing, 2023), 2-14.
3. “The neurobiology of learning and memory—As related in the memoirs of Eric R. Kandel,” In: Miguel A. Faria, Jr., Controversies in Medicine and Neuroscience: Through the Prism of History, Neurobiology and Bioethics (Newcastle upon Tyne, UK: Cambridge Scholars Publishing, 2023), 44-68.
4. Randel PM, McCurdy L. (eds.). The Psychiatry Learning System—A Multimedia Self-Instructional Course in Basic Psychiatry (Charleston, SC: Department of Psychiatry and Behavioral Sciences, Medical University of South Carolina; 1975).
5. “The temporal lobes and the limbic system in neuropsychiatry—A book review,” In: Miguel A. Faria, Jr., Controversies in Medicine and Neuroscience: Through the Prism of History, Neurobiology and Bioethics (Newcastle upon Tyne, UK: Cambridge Scholars Publishing, 2023), 90-93.
6. “Frontal lobe syndromes in neuropsychiatry—A book review,” In: Miguel A. Faria, Jr., Controversies in Medicine and Neuroscience: Through the Prism of History, Neurobiology and Bioethics (Newcastle upon Tyne, UK: Cambridge Scholars Publishing, 2023), 83-89.
7. Russell L. Blaylock, Miguel A. Faria, “New concepts in the development of schizophrenia, autism spectrum disorders, and degenerative brain diseases based on chronic inflammation: A working hypothesis from continued advances in neuroscience research,” Surgical Neurology International, 08-Nov-2021;12:556. Available from: https://surgicalneurologyint.com/surgicalint-articles/new-concepts-in-the-development-of-schizophrenia-autism-spectrum-disorders-and-degenerative-brain-diseases-based-on-chronic-inflammation-a-working-hypothesis-from-continued-advances-in-neuroscience/.
Written by Dr. Miguel Faria
Miguel A. Faria, MD is Associate Editor-in-Chief of neuropsychiatry; socioeconomics, politics, medicine, and world affairs for Surgical Neurology International (SNI). Author of several books on health care and medical history, including Controversies in Medicine and Neuroscience: Through the Prism of History, Neurobiology, and Bioethics (2023), published by Cambridge Scholars Publishing in Newcastle upon Tyne, United Kingdom.
This article may be cited as: Faria MA. A Brief Introduction to Schizophrenia. HaciendaPublishing.com, March 28, 2024. Available from: https://haciendapublishing.com/a-brief-introduction-to-schizophrenia-by-miguel-a-faria-md/.
Copyright ©2024 Miguel A. Faria, Jr., M.D.
4 thoughts on “A Brief Introduction to Schizophrenia by Miguel A. Faria, MD”
Great review. This disorder is one that Miguel and I share an interest in and a scientific curiosity of its etiology as well as its nature. It shares many aspects of autism. Both can be triggered by in-utero or early life alteration in immune stimulation. In both there seems to be either a neurodevelpmental component or an ongoing immunoexcitotoxic process. With autism spectrum disorders it is delayed until about age 6 and schizophrenia until adolescence. In both we see immunoexcitoxicity occurring in-utero or during early life. The most successful treatment appears to be attacking both. The immune reaction by galantamine, which activates the 7alpha-nicotinic receptors (an immune suppressor system within the brain) and the excitotoxicity by drugs ( such as memantine) that reduce excitotoxicity, of which includes N-acetyl-L-cysteine, that has been shown to lower quinolinic acid that activates the NMDA glutamate receptor (an excitotoxic receptor).
Excellent discussion of this enigmatic disorder. As Dr. Faria explains, this is a very complex disorder involving many systems in the brain. We know that schizophrenia and Autism Spectrum disorders have many characteristics alike and that both result from 3rd trimester immune stimulation with the later manifestations (schizophrenia) occurring after birth. Usually during adolescence with schizophrenia. There is now evidence, as we point out in our article in SNI, that we are seeing immunoexcitotoxicity in this disorder, as with many such neurological disorders. This is a direct connection between immune stimulation and excitotoxicity. The most effective treatments in this disorder require been addressing both systems with Memantine (NMDA receptor blocking) and galantamine (reducing the immune stimulation by stimulating the 7alpha-nicotinic cholinergic system, which suppresses immune over activation).
Interesting discussion. I have always felt the major difference between autism and the other enigmatic neuropsychiatric disorders is that in autism, the rate of epilepsy is increased by thirty times that of the general population. The seizures may be generalized tonic-clonic, or they may be complex partial, with behavioral disturbances. This indicates to me that there is a fundamentally different pathology in autism, since it is rare to find such a hard neurological symptom in schizophrenia, except perhaps if the seizure threshold had been lowered sufficiently by neurotropics, or the schizophrenia had been complicated by an unrelated brain tumor. With respect to that, the newer findings that malignant glioma may facilitate its growth by forming connections with normal neuronal synapses now suggests that disorders of thought with “intrusions” may increase malignancy of gliomas by facilitating their growth.
Overall, a slight decrease of cancer is seen in schizophrenia patients compared to the general population. This has been particularly noted with lung cancer, since a disproportionate number of schizophrenics are heavy smokers. Classic studies have shown a decrease in the rate of lung cancer associated with schizophrenia after correcting for the lesser number of heavy smokers in the general population. Depending on the study, one may find an slight increase or decrease in the rate of association between schizophrenia and malignant glioma. Now that linkage has been observed between the tumor suppressor gene P53 and schizophrenia, it remains to be seen if the differential rates of cancer in schizophrenics and “neurotypicals” might be explained on this basis.
The dysregulation of nicotinic acetylcholinergic receptors seen in schizophrenia has led several researchers to postulate that the schizophrenic derives some benefit in perception and/or behavior from nicotine; the short answer seems to be yes.