Palilalia (from the Greek πάλιν ("pálin") meaning "again" and λαλιά ("laliá") meaning "speech" or "to talk"), a complex tic, is a language disorder characterized by the involuntary repetition of syllables, words, or phrases. It has features resembling other complex tics such as echolalia or coprolalia, but, unlike other aphasias, palilalia is based upon contextually correct speech.

It was originally described by Alexandre-Achille Souques in a patient with stroke that resulted in left-side hemiplegia, although a condition described as auto-echolalia in 1899 by Édouard Brissaud may have been the same condition.

The exact cause of palilalia is unknown.

Palilalia also occurs in a variety of neurodegenerative disorders, occurring most commonly in Tourette syndrome, Alzheimer's disease, and progressive supranuclear palsy. Such degradation can occur in the substantia nigra where decreased dopamine production results in a loss of function. It can also occur in a variety of genetic disorders including Fragile X syndrome, Prader-Willi syndrome, Asperger's syndrome, autism, and the speaker has no difficulty initiating speech.

Echolalia (also known as echologia or echophrasia) is defined as the unsolicited repetition of vocalizations made by another person (by the same person is called palilalia). In its profound form it is automatic and effortless. It is one of the echophenomena, closely related to echopraxia, the automatic repetition of movements made by another person; both are "subsets of imitative behavior" whereby sounds or actions are imitated "without explicit awareness". Echolalia may be an immediate reaction to a stimulus or may be delayed.

The word "echolalia" is derived from the Greek , meaning "echo" or "to repeat", and ("laliá") meaning "speech" or "talk" (of onomatopoeic origin, from the verb ("laléo"), meaning "to talk").

Echolalia can be categorized as immediate (occurring immediately after the stimulus) vs. delayed (some time after the occurrence of a stimulus). Immediate echolalia results from quick recall of information from the short-term memory and "superficial linguistic processing". A typical pediatric presentation of immediate echolalia might be as follows: a child is asked "Do you want dinner?"; the child echoes back "Do you want dinner?", followed by a pause, and then a response, "Yes. What's for dinner?"

In delayed echolalia the patient repeats words, phrases, or multiple sentences after a delay that can be anywhere from hours to years later. Immediate echolalia can be indicative that a developmental disorder exists, but this is not necessarily the case. Sometimes echolalia can be observed when an individual echoes back a statement to indicate they are contemplating a response and fully heard the original statement.

Researchers observed the daily repetitions of an autistic six-year-old in order to examine the differences between triggers for delayed versus immediate echolalia. Researchers further distinguished immediate echos by the sequential context in which they occur: after corrections, after directives, or in indiscernible sequential positions. Delayed echos are distinguished on the basis of ownership: self-echos, other-echos, and impersonal echos. The results showed that nearly all immediate echos produced by the six-year-old were found in sequential contexts, while the delayed echoes also occurred in the basis of ownership.

Although echolalia can be an impairment, the symptoms can involve a large selection of underlying meanings and behaviors across and within subjects. "Mitigated echolalia" refers to a repetition in which the original stimulus is somewhat altered, and "ambient echolalia" refers to the repetition (typically occurring in individuals with dementia) of environmental stimuli such as a television program running in the background.

Examples of mitigated echolalia are pronoun changes or syntax corrections. The first can be seen in the example of asking the patient “Where are you going?” and with patient responding “Where am I going?” The latter would be seen in the clinician asking “Where are I going?” and the patient repeating “Where am I going?” In mitigated echolalia some language processing is occurring. Mitigated echolalia can be seen in dyspraxia and aphasia of speech.

A Japanese case report describes a 20-year-old college student who was admitted to the hospital complaining about headaches and meningitis; however, he also exhibited signs of ambient echolalia. The researchers stated that the young patient's repetition was occurring at approximately the same tempo as his normal speech rate. The patient did not simply repeat words he had heard one after another. The patient reported that his ambient echolalia appeared to be random but appeared when he was distracted. He was also aware of his echolalia, but said he is unable to stop the repetitions.

The U.S. Food and Drug Administration (FDA) has not approved any drug for the direct treatment of stuttering. However, the effectiveness of pharmacological agents, such as benzodiazepines, anticonvulsants, antidepressants, antipsychotic and antihypertensive medications, and dopamine antagonists in the treatment of stuttering has been evaluated in studies involving both adults and children.

A comprehensive review of pharmacological treatments of stuttering in 2006 concluded that few of the drug trials were methodologically sound. Of those that were, only one, not unflawed study, showed a reduction in the frequency of stuttering to less than 5% of words spoken. In addition, potentially serious side effects of pharmacological treatments were noted, such as weight gain, sexual dysfunctions and the potential for blood pressure increases. There is one new drug studied especially for stuttering named pagoclone, which was found to be well-tolerated "with only minor side-effects of headache and fatigue reported in a minority of those treated".

Altered auditory feedback, so that people who stutter hear their voice differently, has been used for over 50 years in the treatment of stuttering. Altered auditory feedback effect can be produced by speaking in chorus with another person, by blocking out the person who stutters' voice while talking (masking), by delaying slightly the voice of the person who stutters (delayed auditory feedback) or by altering the frequency of the feedback (frequency altered feedback). Studies of these techniques have had mixed results, with some people who stutter showing substantial reductions in stuttering, while others improved only slightly or not at all. In a 2006 review of the efficacy of stuttering treatments, none of the studies on altered auditory feedback met the criteria for experimental quality, such as the presence of control groups.

The treatment of Tourette's focuses on identifying and helping the individual manage the most troubling or impairing symptoms. Most cases of Tourette's are mild, and do not require pharmacological treatment; instead, psychobehavioral therapy, education, and reassurance may be sufficient. Treatments, where warranted, can be divided into those that target tics and comorbid conditions, which, when present, are often a larger source of impairment than the tics themselves. Not all people with tics have comorbid conditions, but when those conditions are present, they often take treatment priority.

There is no cure for Tourette's and no medication that works universally for all individuals without significant adverse effects. Knowledge, education and understanding are uppermost in management plans for tic disorders. The management of the symptoms of Tourette's may include pharmacological, behavioral and psychological therapies. While pharmacological intervention is reserved for more severe symptoms, other treatments (such as supportive psychotherapy or cognitive behavioral therapy) may help to avoid or ameliorate depression and social isolation, and to improve family support. Educating a patient, family, and surrounding community (such as friends, school, and church) is a key treatment strategy, and may be all that is required in mild cases.

Medication is available to help when symptoms interfere with functioning. The classes of medication with the most proven efficacy in treating tics—typical and atypical neuroleptics including risperidone (trade name Risperdal), ziprasidone (Geodon), haloperidol (Haldol), pimozide (Orap) and fluphenazine (Prolixin)—can have long-term and short-term adverse effects. The antihypertensive agents clonidine (trade name Catapres) and guanfacine (Tenex) are also used to treat tics; studies show variable efficacy, but a lower side effect profile than the neuroleptics. Stimulants and other medications may be useful in treating ADHD when it co-occurs with tic disorders. Drugs from several other classes of medications can be used when stimulant trials fail, including guanfacine (trade name Tenex), atomoxetine (Strattera) and tricyclic antidepressants. Clomipramine (Anafranil), a tricyclic, and SSRIs—a class of antidepressants including fluoxetine (Prozac), sertraline (Zoloft), and fluvoxamine (Luvox)—may be prescribed when a Tourette's patient also has symptoms of obsessive–compulsive disorder. Several other medications have been tried, but evidence to support their use is unconvincing.

Because children with tics often present to physicians when their tics are most severe, and because of the waxing and waning nature of tics, it is recommended that medication not be started immediately or changed often. Frequently, the tics subside with explanation, reassurance, understanding of the condition and a supportive environment. When medication is used, the goal is not to eliminate symptoms: it should be used at the lowest possible dose that manages symptoms without adverse effects, given that these may be more disturbing than the symptoms for which they were prescribed.

Cognitive behavioral therapy (CBT) is a useful treatment when OCD is present, and there is increasing evidence supporting the use of habit reversal (HRT) in the treatment of tics. There is evidence that HRT reduces tic severity, but there are methodological limitations in the studies, and a need for more trained specialists and better large-scale studies.

Relaxation techniques, such as exercise, yoga or meditation, may be useful in relieving the stress that may aggravate tics, but the majority of behavioral interventions (such as relaxation training and biofeedback, with the exception of habit reversal) have not been systematically evaluated and are not empirically supported therapies for Tourette's. Deep brain stimulation has been used to treat adults with severe Tourette's that does not respond to conventional treatment, but it is regarded as an invasive, experimental procedure that is unlikely to become widespread.

, studies on the impact of dietary interventions on the symptoms of Tourette's are scarce and methodologically poor, and a single dietary pattern has not been established. Anecdotal reports suggest that certain dietary interventions may relieve symptoms, such as gluten-free and low-sugar diets.

Tourette syndrome is found among all social, racial and ethnic groups and has been reported in all parts of the world; it is three to four times more frequent among males than among females. The tics of Tourette syndrome begin in childhood and tend to remit or subside with maturity; thus, a diagnosis may no longer be warranted for many adults, and observed prevalence rates are higher among children than adults. As children pass through adolescence, about one-quarter become tic-free, almost one-half see their tics diminish to a minimal or mild level, and less than one-quarter have persistent tics. Only 5 to 14% of adults experience worse tics in adulthood than in childhood.

Up to 1% of the overall population experiences tic disorders, including chronic tics and transient tics of childhood. Chronic tics affect 5% of children, and transient tics affect up to 20%. Prevalence rates in special education populations are higher.

The reported prevalence of TS varies "according to the source, age, and sex of the sample; the ascertainment procedures; and diagnostic system", with a range reported between .4% and 3.8% for children ages 5 to 18. Robertson (2011) says that 1% of school-age children have Tourette's. According to Lombroso and Scahill (2008), the emerging consensus is that .1 to 1% of children have Tourette's, with several studies supporting a tighter range of .6 to .8%. Bloch and Leckman (2009) and Swain (2007) report a range of prevalence in children of .4 to .6%, Knight et al. (2012) estimate .77% in children, and Du et al. (2010) report that 1 to 3% of "Western" school-age children have Tourette's.

Singer (2011) states the prevalence of TS in the overall population at any time is .1% for impairing cases and .6% for all cases, while Bloch and colleagues (2011) state the overall prevalence as between .3 and 1%. Robertson (2011) also suggests that the rate of Tourette's in the general population is 1%. Using year 2000 census data, a prevalence range of .1 to 1% yields an estimate of 53,000–530,000 school-age children with Tourette's in the US, and a prevalence estimate of .1% means that in 2001 about 553,000 people in the UK age 5 or older would have Tourette's.

Tourette syndrome was once thought to be rare: in 1972, the US National Institutes of Health (NIH) believed there were fewer than 100 cases in the United States, and a 1973 registry reported only 485 cases worldwide. However, multiple studies published since 2000 have consistently demonstrated that the prevalence is much higher than previously thought. Discrepancies across current and prior prevalence estimates come from several factors: ascertainment bias in earlier samples drawn from clinically referred cases, assessment methods that may fail to detect milder cases, and differences in diagnostic criteria and thresholds. There were few broad-based community studies published before 2000 and until the 1980s, most epidemiological studies of Tourette syndrome were based on individuals referred to tertiary care or specialty clinics. Individuals with mild symptoms may not seek treatment and physicians may not confer an official diagnosis of TS on children out of concern for stigmatization; children with milder symptoms are unlikely to be referred to specialty clinics, so prevalence studies have an inherent bias towards more severe cases. Studies of Tourette syndrome are vulnerable to error because tics vary in intensity and expression, are often intermittent, and are not always recognized by clinicians, patients, family members, friends or teachers; approximately 20% of persons with Tourette syndrome do not recognize that they have tics. Newer studies—recognizing that tics may often be undiagnosed and hard to detect—use direct classroom observation and multiple informants (parent, teacher, and trained observers), and therefore record more cases than older studies relying on referrals. As the diagnostic threshold and assessment methodology have moved towards recognition of milder cases, the result is an increase in estimated prevalence.

Tourette's is associated with several comorbid conditions, or co-occurring diagnoses, which are often the major source of impairment for an affected child. Most individuals with tics do not seek medical attention, so epidemiological studies of TS "reflect a strong ascertainment bias", but among those who do warrant medical attention, the majority have other conditions, and up to 50% have ADHD or OCD.

Immediate treatment of drug induced OGC can be achieved with intravenous antimuscarinic benzatropine or procyclidine; which usually are effective within 5 minutes, although may take as long as 30 minutes for full effect. Further doses of procyclidine may be needed after 20 minutes. Any causative new medication should be discontinued. Also can be treated with 25 mg diphenhydramine.

Thought disorder (TD) or formal thought disorder (FTD) refers to disorganized thinking as evidenced by disorganized speech. Specific thought disorders include derailment, poverty of speech, tangentiality, illogicality, perseveration, and thought blocking.

Psychiatrists consider formal thought disorder as being one of two types of disordered thinking, with the other type being delusions. The latter involves "content" while the former involves "form". Although the term "thought disorder" can refer to either type, in common parlance it refers most often to a disorder of thought "form" also known as formal thought disorder.

Eugen Bleuler, who named schizophrenia, held that thought disorder was its defining characteristic. However, formal thought disorder is not unique to schizophrenia or psychosis. It is often a symptom of mania, and less often it can be present in other mental disorders such as depression. Clanging or echolalia may be present in Tourette syndrome. Patients with a clouded consciousness, like that found in delirium, also have a formal thought disorder.

However, there is a clinical difference between these two groups. Those with schizophrenia or psychosis are less likely to demonstrate awareness or concern about the disordered thinking. Clayton and Winokur have suggested that this results from a fundamental inability to use the same type of Aristotelian logic as others. On the other hand, patients with a clouded consciousness, referred to as "organic" patients, usually do demonstrate awareness and concern, and complain about being "confused" or "unable to think straight"; Clayton and Winokur suggest that this is because their thought disorder results, instead, from various cognitive deficits.

In considering whether an individual has thought disorder, patterns of their speech are closely observed. Although it is normal to exhibit some of the following during times of extreme stress (e.g. a cataclysmic event or the middle of a war) it is the degree, frequency, and the resulting functional impairment that leads to the conclusion that the person being observed has a thought disorder.

- "Alogia" (also "poverty of speech") – A poverty of speech, either in amount or content; it can occur as a negative symptom of schizophrenia.

- "Blocking" – An abrupt stop in the middle of a train of thought; the individual may or may not be able to continue the idea. This is a type of formal thought disorder that can be seen in schizophrenia.

- "Circumstantiality" (also "circumstantial thinking", or "circumstantial speech") – An inability to answer a question without giving excessive, unnecessary detail. This differs from tangential thinking, in that the person does eventually return to the original point.

- "Clanging" or "Clang association" – a severe form of flight of ideas whereby ideas are related only by similar or rhyming sounds rather than actual meaning. This may be heard as excessive rhyming and/or alliteration. e.g. "Many moldy mushrooms merge out of the mildewy mud on Mondays." "I heard the bell. Well, hell, then I fell." It is most commonly seen in bipolar affective disorder (manic phase), although it is often observed in patients with primary psychoses, namely schizophrenia and schizoaffective disorder.

- "Derailment" (also "loose association" and "knight's move thinking") – Thought and/or speech move, either spontaneously or in response to an internal stimulus (distinguishing derailment from "distractible speech," "infra"), from the topic's track onto another which is obliquely related or unrelated. e.g. "The next day when I'd be going out you know, I took control, like uh, I put bleach on my hair in California."

- "Distractible speech" – During mid speech, the subject is changed in response to an external stimulus. e.g. "Then I left San Francisco and moved to... where did you get that tie?"

- "Echolalia" – Echoing of another's speech that may only be committed once, or may be continuous in repetition. This may involve repeating only the last few words or last word of the examiner's sentences. This can be a symptom of Tourette's Syndrome. e.g. "What would you like for dinner?", "That's a good question. "That's a good question". "That's a good question". "That's a good question"."

- "Evasive interaction" – Attempts to express ideas and/or feelings about another individual come out as evasive or in a diluted form, e.g.: "I... er ah... you are uh... I think you have... uh-- acceptable erm... uh... hair."

- "Flight of ideas" – a form of formal thought disorder marked by abrupt leaps from one topic to another, albeit with discernable links between successive ideas, perhaps governed by similarities between subjects or, in somewhat higher grades, by rhyming, puns, and word plays (clang associations), or innocuous environmental stimuli – e.g., the sound of birds chirping. It is most characteristic of the manic phase of bipolar illness.

- "Illogicality" – Conclusions are reached that do not follow logically (non-sequiturs or faulty inferences). e.g. "Do you think this will fit in the box?" draws a reply like "Well duh; it's brown, isn't it?"

- "Incoherence (word salad)" – Speech that is unintelligible because, though the individual words are real words, the manner in which they are strung together results in incoherent gibberish, e.g. the question "Why do people comb their hair?" elicits a response like "Because it makes a twirl in life, my box is broken help me blue elephant. Isn't lettuce brave? I like electrons, hello please!"

- "Loss of goal" – Failure to follow a train of thought to a natural conclusion. e.g. "Why does my computer keep crashing?", "Well, you live in a stucco house, so the pair of scissors needs to be in another drawer."

- "Neologisms" – New word formations. These may also involve elisions of two words that are similar in meaning or in sound. e.g. "I got so angry I picked up a dish and threw it at the geshinker."

- "Perseveration" – Persistent repetition of words or ideas even when another person attempts to change the topic. e.g. "It's great to be here in Nevada, Nevada, Nevada, Nevada, Nevada." This may also involve repeatedly giving the same answer to different questions. e.g. "Is your name Mary?" "Yes." "Are you in the hospital?" "Yes." "Are you a table?" "Yes." Perseveration can include palilalia and logoclonia, and can be an indication of organic brain disease such as Parkinson's.

- "Phonemic paraphasia" – Mispronunciation; syllables out of sequence. e.g. "I slipped on the lice and broke my arm."

- "Pressure of speech" – Unrelenting, rapid speech without pauses. It may be difficult to interrupt the speaker, and the speaker may continue speaking even when a direct question is asked.

- "Self-reference" – Patient repeatedly and inappropriately refers back to self. e.g. "What's the time?", "It's 7 o'clock. That's my problem."

- "Semantic paraphasia" – Substitution of inappropriate word. e.g. "I slipped on the coat, on the ice I mean, and broke my book."

- "Stilted speech" – Speech characterized by the use of words or phrases that are flowery, excessive, and pompous. e.g. "The attorney comported himself indecorously."

- "Tangentiality" – Wandering from the topic and never returning to it or providing the information requested. e.g. in answer to the question "Where are you from?", a response "My dog is from England. They have good fish and chips there. Fish breathe through gills."

- "Word approximations" – Old words used in a new and unconventional way. e.g. "His boss was a ."

Drugs that can trigger an oculogyric crisis include neuroleptics (such as haloperidol, chlorpromazine, fluphenazine, olanzapine), carbamazepine, chloroquine, cisplatin, diazoxide, levodopa, lithium, metoclopramide, lurasidone, domperidone, nifedipine, pemoline, phencyclidine ("PCP"), reserpine, and cetirizine, an antihistamine. High-potency neuroleptics are probably the most common cause in the clinical setting.

Other causes can include postencephalitic Parkinson's, Tourette's syndrome, multiple sclerosis, neurosyphilis, head trauma, bilateral thalamic infarction, lesions of the fourth ventricle, cystic glioma of the third ventricle, herpes encephalitis, kernicterus and juvenile Parkinson's.