It has been commonly interpreted as a motor speech defect.
Palilalia (from the Greek πάλιν (pálin), which means “again” and λαλιά (laliá), which means “speak” or “speak”), a complex tic, is a language disorder characterized by the involuntary repetition of syllables, words or phrases.
Palilalia, a speech disorder characterized by compulsive repetition of utterances, has been found in various neurological and psychiatric disorders.
Palilalia can be seen in untreated schizophrenic patients, in paramedic thalamic damage, in later degenerative brain diseases such as Alzheimer’s disease, and during electrical stimulation of left hemisphere sites.
History of Palilalia
It was initially described by Alexandre-Achille Souques in a patient with a right-brain stroke, which resulted in hemiplegia on the left side.
In Palilalia, the patient repeats the last word or two of a sentence, often with increasing speed and decreasing volume.
Palilalia is frequently seen in stroke patients, especially with pseudobulbar palsy and postencephalitic parkinsonism. Palilalia is produced as quickly in response to the first as to the second stimulus.
Although a condition described as autoecholalia in 1899 by Édouard Brissaud may have been the same condition.
Classification of palilalia
Palilalia is considered aphasia, a language disorder, and should not be confused with speech disorders, as there is no difficulty in forming internal speech.
Palilalia is similar to speech disorders such as stuttering or clutter. It tends to express itself only in spontaneous speech, such as answering basic questions, and not in automatic speech, such as reading or singing; however, it distinctively affects words and phrases rather than syllables and sounds.
Palilalia can appear in conditions that affect the prefrontal cortex or the basal ganglia, whether due to physical trauma, neurodegenerative disorders, genetic disorders, or a loss of dopamine in these brain regions.
Palilalia occurs most commonly in Tourette syndrome and can be present in neurodegenerative disorders such as Alzheimer’s disease and progressive supranuclear palsy.
Symptoms and characteristics of Palilalia
Palilalia is the compulsive repetition of the speaker’s commonly spoken words, phrases, or syllables, often for several repetitions.
Palilalia has been described in various neurological disorders such as cerebrovascular and degenerative diseases, encephalitis, or tic syndromes. It has rarely been associated with seizure disorders such as ictal or postictal phenomena.
It resembles other complex tics such as echolalia or coprolalia, but unlike other aphasias, Palilalia relies on contextually correct speech.
In most cases, Palilalia and aphasia are separate disorders, but Palilalia with anterior and posterior aphasia has been reported. Basal ganglia involvement has been suggested as the cause of some cases of Palilalia.
Repeating units are generally entire sections of words and are larger than one syllable, with words repeating more frequently, followed by phrases and then by syllables or sounds.
Repetitions by Palilalia are often spoken in decreasing volume and speed up over time. It frequently occurs among people with autism and developmental disabilities.
A 2007 case study by Van Borsel et al. examined the acoustic characteristics in the Palilalia. AB, a 60-year-old man, was diagnosed with idiopathic Parkinson’s disease and noticed changes in his gait, posture, writing, and speech.
Observation of his perceptual speech characteristics and French’s dysarthria and the evaluation results suggested AB suffered from hypokinetic dysarthria with marked Palilalia.
It was determined to initiate speech therapy with passive (metronome) and active (stimulation plates) stimulation techniques to reduce the number of palilalic repetitions. Unfortunately, AB was unable to deliver despite extensive training.
AB’s speech therapy analysis showed that his repetitions lasted from 1 minute 33 seconds to 2 minutes 28 seconds, varying from 1 to 32 repetitions in some words, and differed from test to test.
Pauses were present between each repetition, ranging from 0.1 to 0.7 seconds. Van Borsel et al. concluded that the polysyllabic repeats of AB did not follow any pattern:
The duration of each repetition train did not decrease with time, the number of repetitions per train did not increase, and the course of each word did not fall in duration.
Such results indicated that not all polysyllabic repeats show an increasing rate with decreasing volume, and they challenged the two distinct subtypes of Palilalia as suggested by Sterling.
Sterling type A, sometimes called spasmodic palatalize, is characterized by rapid repetitions and decreasing volume. In contrast, Sterling type B, sometimes called atonic palatalise, is characterized by repetitions at a constant rate with interspersed periods of silence.
AB did not show a systematic increase (Sterling Type A) or a constant duration (Sterling Type B) and instead fell between the two.
It has been theorized that Palilalia is produced in writing and sign language. A case study by Tyrone and Moll examined a 79-year-old right-hand deaf man named PSP who showed abnormalities in his signature.
PSP had learned British Sign Language (LSB) by the age of seven and had developed left-sided weakness and dysphagia by age 77. PSP showed involuntary movements and repetitions in its signature.
Tyrone and Moll reported that their movements were malarial, as whole signs were repeated, and the repetitive movements became smaller and smaller in amplitude.
Causes of Palilalia
The exact cause of Palilalia is unknown.
Palilalia also occurs in various neurodegenerative disorders, most commonly occurring 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 various genetic disorders, including Fragile X syndrome, Prader-Willi syndrome, Asperger syndrome, autism, and logoclonia.
In contrast to stuttering or logoclonia, Palilalicense repetitions consist of entire sections of words or phrases, are often repeated many times, and the speaker has no difficulty initiating speech.
These observations suggest that Palilalia results from a malfunction of control at the articulator level. In contrast, other variants of pathological verbal iterations result from an alteration of the formulator or dysfunctions of both the articulator and the formulator.
Treatment for palilalia
Behavioral research suggests that antecedent conditions can be manipulated to decrease the occurrence of Palilalia and that they can be replaced with appropriate responses.
Consequently, various interventions designed to empower sponges have been investigated, including scripts, command training, and rule-governed or self-control tactics.
Research also shows that Palilalia was controlled by contextual conditions (i.e., audiences) that diminished Palilalia when self-control procedures caused the speaker to avoid the emission of the behavior.
Still, another investigation showed that Palilalia was under the control of competitive reinforcements. Greer et al. suggested that Palilalia may serve a role similar to stereotypy or self-stimulating “behavior” for speakers.
This finding was consistent with Sundberg, Michael, Partington, and Sundberg’s reports. They found that a stimulus-stimulus pairing procedure resulted in the emission of repetitive speech sounds, a process replicated by Yoon.
Like babbling, a typical response for typically developing babies, Palilalia may have a similar automatic reinforcement function for some people.
In reference sessions, students A, B, C, and D sit individually at a table containing the materials used to participate in an activity such as coloring or building blocks, or on the floor in a “free play” area where the Opportunities to participate in games were present.
Student E was seated at a table with a teacher, and regular academic instruction was delivered in the form of learning units. The instructor began each session by presenting the background, “It’s time for (name an activity),” and timing the session.
If Palilalia was issued, the instructor ignored the behavior. If correct touches were published, the instructor gave verbal praise to the student. If the proper operations occurred, the instructor delivered the requested item to the student.
When the participant emitted Palilalia during the treatment, the instructor immediately modeled a touch associated with the activity in which the student was engaged without the student being prevented from participating in the activity.
For example, if the student said, “Little wolf, little wolf, let me in,” while coloring or during instructions, the instructor immediately said, “I’m coloring,” or pointed to an object (for example, a book) and said, ” That’s a book,” while the student continued coloring.
If the student echoes the teacher’s touch, the experimenter gives the student words of verbal praise such as “That’s correct. That is a book. If the student did not echo the teacher’s touch but stopped emitting Palilalia, the teacher did not continue to model the communication, and the activity or instruction continued.
When the response was stable, the participants returned to baseline and treatment conditions identical to the initial baseline and treatment sessions.
Palilalia vs Ecolalia
Palilalia is an unsolicited reiteration of utterances recognized as motor perseverance involving the speech mechanism.
It frequently occurs with stereotypical prosody, accelerated rhythm, elevated tone, or decreasing volume (aphonic Palilalia), while echolalia is defined as the involuntary repetition of the utterances of others.
Echolalia and Palilalia are two disorderly language patterns common in children with autism and Asperger syndrome. These verbal symptoms can sometimes contribute to the early diagnosis of these disorders.
Echolalia is a term used to describe a child’s non-functional repetition of specific phrases, such as those heard on television shows or from a parent. For example, when an adult asks:
“How are you today?” a child using echolalia will respond with “How are you today?” instead of saying, “I’m fine.”
The echo of a phrase or question asked to the child directly is known as immediate echolalia, a prevalent trait in people with autism and Asperger’s syndrome.
Delayed echolalia occurs when a child spontaneously repeats a sequence of words that were heard earlier, for example, while watching a movie or TV show, in a way that is out of context with a typical conversation.
Palilalia is a speech tic characterized by the quick repetition of a child’s words in conversation. Often, repeated words are spoken in a whisper or murmur.
A child using Palilalia may say, “I want to go to the store,” and then immediately whisper, “to go to the store.”
This disorganized speech pattern is among the common characteristics of autism. Along with echolalia, it is often an indication that a child is not acquiring or using verbal communication in a neurotypical way.
Echolalia and Palilalia in children on the autism spectrum
Echolalia and Palilalia are classified as pragmatic speech disorders or a developmental deficit concerning conducting a two-way conversation or using verbal language in the appropriate context.
Children with Asperger syndrome or high-functioning autism often qualify for speech therapy based on these pragmatic disorders, as their general vocabulary skills can be extensive.
Speech therapists work with these children in an individual or small group setting to strengthen pragmatic language so that instances of echolalia and Palilalia can be reduced over time.
Parents of autistic children with echolalia should be aware not to fall into a trap when assessing their child’s understanding of communication. For example, a traditional method of testing whether the other person has understood is to ask them to repeat what was said.
You can then accept that the communication was understood or make corrections to help the other person better understand what you are saying.
However, this technique will not work and can be misleading when used with a child with echolalia. They are simply “repeating” the words back to you without a fundamental understanding of what was said or the meaning of the communication.
These parents must alert others who interact with caregivers and early childhood educators that the child has echolalia and may or may not have understood a particular conversation or question.
Children who are lower functioning on the autism spectrum may have poor verbal functioning beyond echolalia, but therapists can still encourage communication through sign language or picture boards.
Although rarely reported, repetitive speech behaviors, such as Palilalia and echolalia, have presented as ictal or postictal manifestations in seizure disorders.
However, the neuroanatomical correlates of these speech behaviors as ictal phenomena have not been determined.
This case with ictal Palilalia, echolalia, and echopraxia-palipraxia arising from the left frontal lobe, was successfully documented by video-electroencephalography (EEG) monitoring and neuroimaging modalities.
A 55-year-old right-handed man was admitted to the neurology department and complained of frequent bouts of rapid repetition of nonsense syllables.
Her medical history was unremarkable except for chronic alcohol addiction, and she had head trauma with a laceration of the scalp while intoxicated six years ago.
He did not lose consciousness or show any neurological abnormalities, such as confusion or aphasia, at that time.
The patient had experienced a generalized tonic-clonic seizure episode 7 months before admission but refused a medical examination and continued to drink.
Four months before admission, she began having stereotypical episodes of repeating syllables or words three to four times a day.
His family physician diagnosed conversion disorder and alcohol withdrawal syndrome; however, the episodes became more frequent and had occurred more than ten times a day at the time of admission.
During the interictal period, the patient was fully awake, and the bedside neurological examination showed no significant neurological dysfunction except for mild memory and short-term calculus impairment.
His language functions, including speaking, reading, writing, naming, repeating, and understanding, were intact.
Video electroencephalography monitoring for approximately half a day revealed 37 seizures of stereotypic ictal episodes of Palilalia, lasting 1–2 minutes each.
During the ictal episodes, he began a short and immobile gaze, followed by a slight rotation of the head to the right and a bilateral flexion of the arm for several seconds. He then repeated one or two nonsense syllables dozens of times, such as:
Da-Da-Da. Ma-Ma-Ma ”and“ Kirkuk-Kirkuk-Kirkuk ”(all seizures) and other significant but inappropriate words such as:
“Saram-Saram-Saram” (“human” in Korean) for tens of seconds (15 seizures) with or without a rhythmic head of 1-2 Hz, body rocking, or rhythmic posture of the right arm.
The involuntary repetitions were spoken at variable frequencies (1-5 Hz) and showed alteration of their rhythm, frequency, and volume during each episode.
He showed echolalia-palilalia consisting of an initial copy of a word or phrase followed by palilalic repetitions, partially responding to external verbal stimuli (11 seizures).
He even showed more complex behaviors, such as echolalia-palilalia-echopraxia-palipraxia (executing several times the examiner’s orders to “stretch your arms” and at the same time reiterate “stretch your arms, stretch your arms, stretch your arms …”) (three seizures).
Interictal EEG revealed an almost continuous irregular theta and delta frequency in the left frontocentral region.
Ictal electroencephalography showed an abrupt onset of diffuse electromyographic activity with glossokinetic artifacts.
This is followed by decreasing and decreasing rhythmic beta frequency activities over the left frontocentral region.
Then intermittent theta and delta activities interspersed with superimposed sharp waves appeared in the same region, which slowly evolved into semi-rhythmic repetitive, intense waves, with a maximum appearance at the F3-C3 electrodes.
Brain MRI revealed an encephalomatous lesion along the left superior frontal gyrus with hemosiderin deposits and subcortical atrophy, suggesting sequelae of previous head trauma.
The photon emission computed tomography scan was taken during the palilalia-echolalia episode 10 seconds after the ictal clinical onset, and an ictal interictal single-photon emission added tomography subtraction analysis co-recorded with magnetic resonance imaging.
It showed significantly increased blood flow on the medial surface of the left superior frontal gyrus, affecting the supplementary motor area above the encephalomalacia lesion.
Increased blood flow was also evident in the bilateral basal ganglia, thalamus, occipital lobes, and cerebellar vermis. Co-enrolled MRI was performed using Analyze (imaging software) 5.0.
Ictal hyperperfusion from single-photon emission computed tomography was considered significant.
But only when the regional cerebral blood flow difference in each pixel of brain photon emission computed tomography imaging between ictal and interictal states was more significant than two standard deviations of the distribution of subtraction pixel intensities.
4 mg intravenous lorazepam administration relieved ictal episodes immediately for approximately 6 hours. The patient has been seizure-free with antiepileptic treatment.
Palilalia or echolalia has been associated with various disorders involving cortical or subcortical structures, including autism, Alzheimer’s dementia, Tourette’s syndrome, Parkinson’s disease, and cerebrovascular diseases.
However, these unique behaviors have rarely been reported to be associated with epilepsy disorders.
As a postictal manifestation, mixed transcortical aphasia, including Palilalia and echolalia, was reported in one case with resection of a left frontal parasagittal meningioma.
Although performed after language functions returned to standard, single-photon emission computed tomography revealed left lateral hypoperfusion, anterior cingulate, and left insular cortical.
Linetsky et al. presented a case of echolalia-palilalia associated with non-convulsive status epilepticus.
Because the patient demonstrated generalized polypod and slow-wave activity with an occasional predominance of epileptic activity in the left frontal leads on EEG and lack of focal lesions on computed tomography.
It was not sure whether the patient had generalized or focal non-convulsive status epilepticus. The neuroanatomical correlates of Echolalia-palilalia are not yet clear, but the findings in this patient agree with several lines of evidence.
Rubens described echolalia in association with supplemental motor area infarction. Electrical stimulation of the supplementary motor area has been reported to cause repetitive vocalizations.
On the other hand, Bogousslavsky et al. reported a patient with mixed transcortical aphasia accompanied by echolalia caused by two areas of infarction in the left hemisphere.
One in the upper and posterior part of the frontal lobe and one in the parietotemporal-occipital junction suggested that mixed transcortical aphasia occurs due to the isolation of the perisylvian speech area, avoiding the repetitive circuit.
The infarct size in the frontal lobe is similar to that of the encephalomalacia lesion in our patient, which can disrupt the connections between Broca’s area and the supplementary motor area, the initiating supra motor speech center.
Palilalia-echolalia occurred in our patient with partial seizures from the left frontocentral region.
Co-enrolled to MRI showed a significant increase in blood flow in the medial aspect of the superior frontal gyrus corresponding to the supplementary motor zone, unique to the encephalomalacia lesion.
Consequently, we could postulate that ictal activity from the supplementary motor area would initiate speech or vocalization.
However, disconnection with the speech motor zone from the supplementary motor zone due to injury and subsequent isolation of the speech motor zone can disrupt the everyday reciprocal interactions between the additional motor zone and the speech motor zone during the speech process. Speaks and leads to Palilalia and Echolalia.
The echopraxia-apraxia, which occurred with external stimuli in this patient, could be related to the interaction between the supplementary motor area and the disconnected motor centers.
Hyperperfusion was also found in the subcortical nuclei on co-recorded MRI images in this patient.
Palilalia and echolalia can arise from dysfunction or injury of the subcortical nuclei, as seen in Tourette’s disease and other diseases that affect the basal ganglia.
The exact mechanism in the genesis of Palilalia and echolalia due to dysfunction of the subcortical nuclei is unclear.
Tongue alterations in association with lesions in the basal ganglia are explained by various mechanisms, such as alteration of language functions, disconnection of the cortical area, deterioration of modulator function, and functional diaschisis.
Rhythmic ictal movements, such as head nodding, body rocking, and arm posture in this patient, may be related to ictal activation of the subcortical nuclei.
The lateralizing value of ictal vocalization without speech quality has been reported in previous studies, emphasizing the location of this alteration in the left hemisphere, particularly in the frontal area.
The patient’s palilaginal reiterations of unspoken sounds also suggest that ictal vocalization may be a clinical manifestation indicating left frontal lobe epilepsy. However, he intermittently also showed different vocal vocalizations.
In conclusion, this patient presented rare ictal manifestations of partial epilepsy consisting of Palilalia, echolalia, and echopraxia-palipraxia, whose ictal origin was in the left frontocentral region demonstrated by electroencephalography and functional neuroimaging.
Immediate activation of the supplemental motor area and loss of inhibition in disconnected language and motor centers with a structural failure of connectivity in the frontal association area may generate unique repetitive motor and linguistic behaviors in this patient.