OCD and Tourette Syndrome: Causes and Symptoms
Disorders including obsessions and compulsions arise from dysfunctions in the ancestral portion of our human brains and occur almost twice as often as schizophrenia. We humans have inherited many hard-wired, innate behaviors from animals including our primate cousins, chimpanzees. The neurocircuitry for these repetitive patterns remains intact within our human brains, susceptible to the pressures of human culture and vulnerable to automatic activation under certain other pressures we will discuss below.
In The Boy Who Couldn't Stop Washing: The Experience & Treatment of Obsessive-Compulsive Disorder (1989), Judith L. Rapoport writes: "It is one of psychiatry's great ironies that although obsessions and compulsions illustrate psychoanalytic ideas of conflict better than any other neurosis, the symptoms of obsessions and compulsions are not helped by psychoanalytic treatment."
The photograph to the right is from the Science Museum website, originating in the United Kingdom. As the image (links to source) illustrates, a person diagnosed with obsessive-compulsive cisorder is often trying to avoid a negative circumstance such as contamination or pimpled skin. He/she may be trying to make right something that is out of order, asymmetrical, or dirty. The OCD sufferer may have difficulty in knowing that the oven is turned off, that a routine is complete, so he/she keeps checking or repeating actions. The person with OCD lacks a sense of completion. He/she may feel as if trapped in a sequence of actions, a behavioral loop that has no exit option. A good way to describe OCD is the state of being disconnected from one's will.
In Obsessive Compulsive Disorder: Practical, Tried-and-Tested Strategies to Overcome OCD (2002), Frederick Toates and Olga Coschug-Toates point out an important distinction that is helpful in discussing the possible etiologies of obsessions and compulsions. They write: "Obsessive compulsive behavior is distinct from what we would call 'extreme appetitive urges' or, as some might call them, 'appetitive compulsions'. This term means such things as apparently compulsive gambling, drug addiction and some forms of sexual activity." Although the distinction can sometimes blur, Toates and Coschug-Toates point out that "Appetitive urges involve what we would call 'incentives' or 'positive reinforcer'. An 'incentive' is an object such as food or a drug, the gain of which forms the end-point of a bit of behavior."
It is certain, however, that the obsessions and compulsions that make for a diagnosis of OCD and the appetitive compulsions that make for a diagnosis of addiction involve at least some of the same brain structures and neurochemicals. Whether one suffers from OCD, ADHD, PTSD, Tourette syndrome, trichotillomania, compulsive skin picking, or from one of the addictions—whether it be for food, drug, or sex—our subcortical mammalian brain governing emotion and motivation is designed the same way. It seems to be the mix—of genetic, epigenetic (including trauma, chronic stress, and viral vectors), and/or cultural pressures—that cause one or the other distinct symptom picture to emerge.
Since we do not usually think of family dynamics as a part of our culture, I think it is important to point out the importance of family interactions. Within any given culture, family dynamics can be extremely variable. Even within what we call a nuclear family, one child may experience life much differently from siblings. I contend that in all families, however, young people often mature in such a way as to meet expectations, even when those expectations are expressed in a subtle way. Such expectations, along with feelings of either guilt or shame, can play a part in driving many kinds of behavior aimed at restoring confidence. Such negative feelings certainly sometimes exacerbate OCD. Although I do not know enough about addictions to say one way or the other, it seems possible that guilt and shame might also contribute to some cases of addiction.
In their article
"Toward a Neurobiology of Obsessive-Compulsive Disorder" (2000), Ann M. Graybiel and Scott L. Rauch provide the following succinct and illuminating information about obsessive-compulsive disorder (OCD):
The name, OCD, comes from the hallmark signs and symptoms of the disease, which affect both cognition and motor behavior: obsessions, thoughts that repeat over and over again, unwanted but insistent; and compulsions to act, to repeat fragments of behavior over and over in ritualistic, stereotyped succession. Typically, particular compulsive acts are carried out in response to a particular obsession, as if to neutralize the anxiety and negative affect associated with that obsession. The most common of these obsessions and compulsions involve checking (going back over a behavior repeatedly in response to obsessive self-doubts whether it was done, and done just right), washing (for example, washing the hands until they bleed in response to the "obsession" that they are dirty), ordering (straightening up, like a child having to line up the shoes in his closet over and over, or having to put them in sets of three), and fears of performing aggressive or untoward behaviors and repeated attempts to prevent this.
According to Graybiel and Rauch, estimates of the rate of OCD-like behavior in patients with Tourette syndrome are as high as 90%.
Many scientists think that OCD and Tourette syndrome are, as Rapoport puts it in The Boy Who Couldn't Stop Washing, "two sides of the same neurobiological coin." We will discuss similarities later in this section when we discuss the role of the corpus striata complex (basal ganglia) in producing obsessions, compulsions, and tics.
In the blocked quotation below, from Brainscapes: An Introduction to What Neuroscience Has Learned about the Structure, Function, and Abilities of the Brain (1995), neurologist Richard M. Restak sums up how Tourette syndrome was identified and given a name. I should note here that not all people with Tourette syndrome suffer from such overt and dramatic symptoms as those of the Marquise de Dampierre. The image below depicts Georges Gilles de la Tourette and links to source. Restak writes:
In 1825, Neurologist Jean Itard reported on the Marquise de Dampierre, who developed persistent symptoms of bodily tics, barking like a dog, and the uttering of uncontrollable obscenities. … Over sixty years later neurologist Georges Gilles de la Tourette wrote of the marquise and eight other people with multiple tics, involuntary movements, and the tendency to shout obscenities (coprolalia) and to echo back the spoken words of others (echolalia). Tourette believed the symptoms of the disorder occurred involuntarily, and thus exactly opposite of the way that obsessive-compulsive disorders were thought to happen. For this reason, the two disorders were "adopted" by different specialists of the human mind: OCD was appropriated by the psychiatrists who remained convinced of its psychological origins and spun elaborate theories to account for it; Tourette's remained under the banner of the neurologists who emphasized the motor tics and inquired little about their patient's inner experiences. During my own training years I don't recall any reference to OCD by my neurology professors, nor anything said about Tourette's by my psychiatric instructors.
National Institute of Neurological Disorders and Stroke provides a comprehensive summary of Tourette syndrome, explaining that tics, which include repetitive, stereotyped, involuntary movements and vocalizations, characterize the disorder. "The early symptoms of TS are almost always noticed first in childhood, with the average onset between the ages of 7 and 10 years," reports the National Institute. Symptoms can but do not always include coprolalia and echolalia, which Restak describes above. The National Institute report says that simple motor tics include eye blinking, grimacing, shoulder shrugging, and head or shoulder jerking. Complex tics include grimacing combined, perhaps, with a head twist and a shoulder shrug. Other complex tics may appear purposeful such as repeatedly touching objects, hopping, jumping, bending, or twisting. Simple vocalizations include repetitive throat-clearing, sniffing, snorting, grunting, or barking. Complex vocal tics include words or phrases.
There is evidence of a genetic component in both OCD and Tourette Syndrome. Of those at risk for such disorders because of family history, the National Institute says that "males are more likely to have tics and at-risk females are more likely to have obsessive-compulsive symptoms." Also, of all those affected with Tourette syndrome, "males are affected about three to four times more often than females." The report goes on to explain that although Tourette syndrome "can be a chronic condition with symptoms lasting a lifetime, most people with the condition experience their worst symptoms in their early teens, with improvement occurring in the late teens and continuing into adulthood."
It is important to remember, however, that as people with childhood-onset Tourette syndrome and/or OCD age, they may learn how to postpone or camouflage symptoms, finding ways to keep their obsessions, compulsions, or tics secret. While in their public lives, they may appear to function appropriately, in their private lives their secret symptoms may cause stress, embarrassment, and depression. For this reason, it is of utmost importance to address any shameful feelings associated with such unusual behavior. Feelings of shame can lead to secrecy and secrecy cuts off avenues for successful treatment.
In "Toward a Neurobiology of Obsessive-Compulsive Disorder," Ann M. Graybiel and Scott L. Rauch write:
There are also potential etiologic links between OCD and OC-spectrum disorders based on the possibility that OCD and OC-spectrum disorders can occur as a result of infection. This idea was proposed by von Economo, who described patients suffering from obsessions and compulsions in the wake of the great 1917 epidemic of viral encephalitis in Europe. This proposal has received new impetus from the work of Swedo and colleagues (Swedo et al., 1998), who have studied disorders precipitated by rheumatic fever, caused by type A ß-hemolytic streptococcal infection. Such infections can lead to Syndenham's chorea, itself characterized by symptoms including obsessions, compulsions, and tics, and to OCD-like syndromes. This group of disorders has been termed Pediatric Autoimmune Neuropsychiatric Disorders Associated with Strep (PANDAS). Their underlying pathology is thought to involve an autoimmune-mediated attack on the striatum [corpus striata] precipitated by the streptococcal infection.
The scanning electron micrograph image below (links to source) of streptococci bacteria is from a Pathogenic Microbiology Course resource. David M. Rollins and Sam W. Joseph of the University of Maryland, College Park, created the course.
For nonscientists including myself, "anti-nuclear antibodies" are antibodies directed against the nucleus of cells that make up the human body. These antibodies usually develop in auto-immune disease conditions (e.g., rheumatoid arthritis), where a person's immune system is activated against proteins in his/her own body. Such autoimmune activity may be directed only to certain organs or only to a particular type of tissue. It is possible that such anti-nuclear antibodies could attack the corpus striata complex, as Graybiel and Rauch suggest above.
In "An Animal Model of Tourette's Syndrome," available online from the American Journal of Psychiatry (2002), Jane R. Taylor and eight other distinguished scientists describe an interesting study infusing sera from Tourette syndrome patients into rats. (Sera is the plural of serum and refers to the clear yellowish fluid that remains from blood plasma after clotting factors have been removed.) The authors of this study discuss stereotypies, which we discuss early in Part 3 of MyBrainnotes.com, in Displacement, stereotypies, frustration, and perseveration—understanding ADHD, OCD, PTSD, and Tourette Syndrome). Taylor et al. write:
Method: Sera from 12 patients with Tourette's syndrome with high levels of antineural or antinuclear antibodies were infused bilaterally into the ventrolateral striatum of rats. Sera from 12 additional Tourette's syndrome patients and 12 normal subjects (both groups with low levels of autoantibodies) were infused for comparison. Rates of oral stereotypies were recorded by observers who were blind to the origin of the infused sera. Results: Oral stereotypies significantly increased in the rats infused with sera from the patients with high levels of autoantibodies. Conclusions: The results are consistent with an autoimmune etiology in a subset of cases of Tourette's syndrome.
Regarding grooming, Taylor et al. write: "Although the present study focused on oral stereotypy, other behaviors were also altered. For example, there was a marked increase in genital grooming in the rats infused with high-antibody Tourette's syndrome sera, compared with the other groups… .
The National Institute of Mental Health Science Update, "How Strep Triggers Obsessive Compulsive Disorder—New Clues" reports on research included in Kirvan et al., Antibody-Mediated Neuronal Cell Signaling in Behavior and Movement Disorders" (2006). The NIMH Science Update article appears below in full.
A likely mechanism by which a bacterial infection triggers obsessive compulsive disorder (OCD) in some children has been demonstrated by scientists at the National Institutes of Health's (NIH) National Institute of Mental Health (NIMH) and collaborators at California State University (CSU) and the University of Oklahoma (UO). Their research suggests that an antibody against strep throat bacteria sometimes mistakenly acts on a brain enzyme, disrupting communications between neurons and causing a form of obsessive compulsive and related tic disorder in children—pediatric autoimmune neuropsychiatric disorders associated with streptococci (PANDAS).
When added to cultured neurons, three fourths of blood samples from acute, symptomatic PANDAS cases boosted the brain enzyme to significantly higher levels than samples from recovering, non-symptomatic patients. Similarly, nearly three-fourths of the blood samples from symptomatic cases contained antibodies for strep, compared to only 23 percent of samples from recovering, non-symptomatic patients. PANDAS patients' cerebrospinal fluid (CSF), which bathes the brain and directly reflects its activity, contained highly elevated levels of the suspect strep-triggered enzyme, while CSF of non-PANDAS subjects contained little or none. NIMH's Drs. Susan Swedo and Lisa Snider, Christine Kirvan (CSU) and Madeleine Cunningham (UO) report on their discovery in the July 26, 2006 online edition of the Journal of Neuroimmunology.
Although Swedo and her team had long hypothesized such a strep-triggered process in which antibodies gone awry disrupt brain activity, the specific players involved were unclear. To identify them, the researchers followed up clues from their studies of Sydenham chorea, which is marked by involuntary movements and speech impediments, and is thought to be the neurological counterpart of rheumatic fever, which is known to result from a strep-triggered autoimmune process in which the body attacks itself.
All patients with the movement disorder had high levels of the strep antibody that induced activity of the enzyme, thought to play a role in making and releasing neurotransmitters, most notably glutamate, which is implicated in OCD. In addition to the above findings, the researchers showed that PANDAS blood samples cleansed of the antibody failed to activate the enzyme.
Swedo and colleagues propose that in PANDAS somewhat lower levels of enzyme activity than seen in chorea may contribute to OCD symptoms. Although how the antibodies cross the blood-brain barrier remains a mystery, the researchers say the new findings provide insights into how antibodies against strep may disrupt neuronal communications and cell function.
Doing the research to create MyBrainNotes.com has led me to conclude that there are several kinds of pressures that can affect the brain's neurotransmitter production and pathway function, resulting in obsessive and/or compulsive symptoms.
The first is evolutionary change involving mutations in DNA, over generations. These kinds of changes may result in a genetic vulnerability to develop certain kinds of symptoms, especially when that vulnerability is combined with another risk factor. For example, in
Part 2 of MyBrainNotes.com, we discuss how hypervigilance might be genetically encoded in certain individuals, prompting them to serve as sentinels for their group, and how hypervigilance along with chronic stress might lead to obsessions and compulsions (see Hypervigilance, depression, obsessions, and compulsions).
The second kind of pressure is epigenetics, which includes any environmental factor that influences gene expression (see The hippocampus, epigenetics, and PTSD). Epigenetic pressures may include prenatal stress on a developing fetus's brain chemistry. The caption for the image to the right (links to source) from the Jirtle Laboratory reads: "Despite their appearance, these mice are genetically identical. Their mothers ate different diets during pregnancy, which led to epigenetic changes in the Agouti gene that influenced coat color and body weight."
A third kind of pressure involves physical injury to the brain during accidents or attack. In "Obsessive-Compulsive Disorder Associated with Brain Lesions: Clinical Phenomenology, Cognitive Function, and Anatomic correlates," Marcelo L. Berthier, et al., studied patients who acquired OCD when they acquired brain lesions as well as those with idiopathic (of unknown cause) OCD. The authors write: "Neuroimaging in the acquired OCD group disclosed a variety of lesions involving exclusively the cerebral cortex (frontal, temporal, or cingulate regions), the basal ganglia, or both."
A fourth kind of pressure relates to the often permanent damage to neurocircuitry due to previous viral or bacterial infection. Regarding viral infection, we discuss postencephalitic disorders in Encephalitis, OCD symptoms, and Parkinsonism in Part 2 of MyBrainNotes.com. On this webpage, above, we discuss the role of streptococcal infections.
And a fifth kind of pressure involves stress-induced kindling (see Kindling and stress—how experience affects the brain and Fear processing, PTSD, and kindling). Kindling strengthens stress-response neurocircuits. Traumatic experiences, any kind of chronic stress, attachment deficits in childhood, and social isolation can contribute to kindling. One of the purposes of MyBrainNotes.com is to illustrate how, over time, often building on inculcated cultural concerns, kindling can commandeer or potentiate instinctual behavior patterns called fixed-action patterns (see Fixed-action patterns and OCD) in order to release frustration or restore confidence. The result of such action can be a hypersensitive neural network, or bioprogram, that generates uncontrollable, dangerous symptoms.
Regarding OCD, Tourette syndrome, or any other disorder involving subcortical brain structures, age of onset, duration, symptom manifestations, and as we discuss above, etiology, can be highly variable. For most people who suffer from obsessions, compulsions, and/or tics, several factors are likely at play in producing symptoms. And to complicate the issue, cultural conditioning may often play a role in determining the content of symptoms. We don't think about how to ride a bicycle. We just do it. The knowledge is inculcated within ancient structures responsible for sequencing and habit formation. Symptoms involving religious ritual illustrate the importance of culture in determining symptom content. In The Trouble with Testosterone and Other Essays on the Biology of the Human Predicament (1997), Robert M. Sapolsky asks "But why should religion be filled not only with ritual, but so often with the same types of ritual—cleansing, food preparation, entering and leaving, numerology—as carried out by the OCD patient?" Sapolsky observes: "The solace of religious ritual for the OCD patients is the structure."
As we will discuss below, it seems that when functions of the corpus striata complex, including sequencing functions, are overly active, motor and mental sequencing activity can play out in a variety of easily accessed innate or learned patterns, including those involving religious ritual, grooming, checking, cleaning, or punding.
We first discuss the corpus striata complex in Part 1 of MyBrainNotes.com (see The corpus striata (basal ganglia) complex. It is this collection of nuclei that governs everything from our ability to drink a cup of hot tea to our ability to use a keyboard to input information into a computer. Presented again here for review, the basic anatomical components of the corpus striata complex are illustrated to the right (links to source).
In addition to coordinating the precise physical movements of a surgeon, the corpus striata complex coordinates cortical information into coherent plans, such as determining the most efficient order in which home remodeling projects should be done.
Jaak Panksepp illustrates the importance of the corpus striata complex in Affective Neuroscience in his discussion of Huntington's Disease, a genetically determined disease in which "excessive levels of endogenous glutamate may gradually destroy the basal ganglia [corpus striata]." Panksepp points out that although "these patients eventually exhibit severe motor disabilities, their mental status is initially compromised by a schizoid type of disorder characterized by disjointed cognitive activity." Without a properly functioning corpus striata complex, imagine the difficulty a pilot would have in determining the correct sequence of actions required to navigate a plane from thousands of feet in the air to a smooth and ordered landing in a busy airport. So the corpus striata complex does not just coordinate physical movements, the corpus striata complex also coordinates thoughts, especially those related to sequencing. Given this understanding, it is easy to see how symptoms such as compulsive punding, counting, ordering, checking, and organizing might be related to hyperactive corpus striata activity. Regarding such activity, dopamine certainly plays a dominant role in at least some cases. We will discuss specifics regarding dopamine's role in producing symptoms in a separate webpage included in Part 3 of MyBrainNotes.com.
In The Boy Who Couldn't Stop Washing, Rapoport identifies dysfunction in the corpus striata complex (or basal ganglia) as a primary cause of OCD. Regarding these structures, she writes: "They serve as relay stations between all of our senses, our motor functions, and higher cortical centers." Regarding her work with patients who have OCD, Rapoport writes: "As we saw more and more patients with obsessions and compulsions, we noticed what a high proportion of them had, or had had, minor tics or twitches of the face of hands." In comparing symptoms of her patients with OCD with the symptoms of patients diagnosed with Tourete syndrome, Rapoport found that similar obsessions and compulsions appeared in "about one third of the cases with Tourette's Syndrome." She writes: "Tourette's disease is almost certainly a disease of the basal ganglia."
In Brainscapes, Restak refers to a study of Tourette syndrome patients in which 93% of patients reported "premonitory urges." Restak explains: "A similar percentage reported that their tics were either fully or partially a voluntary response to the premonitory urges and accompanied by a feeling of relief." These symptom descriptions, Restak concludes, "blurred the margins between Tourette's and obsessive-compulsive disorder, which is marked by a conscious-minded—indeed hyperconscious—awareness accompanying an internal demand to think a certain thought (obsession) or perform a certain act (compulsion)." Restak notes: "Indeed, some patients coming to the attention of psychiatrists or neurologists defied any exact classification under a single disorder."
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