Hubbry Logo
AlogiaAlogiaMain
Open search
Alogia
Community hub
Alogia
logo
7 pages, 0 posts
0 subscribers
Be the first to start a discussion here.
Be the first to start a discussion here.
Alogia
Alogia
Alogia
View on Wikipedia
from Wikipedia

In psychology, alogia (/ˌeɪˈloʊdʒiə, əˈloʊdʒiə, əˈlɒdʒiə, -dʒə/; from Greek ἀ-, "without", and λόγος, "speech" + New Latin -ia)[1][2][3] is poor thinking inferred from speech and language usage.[4] There may be a general lack of additional, unprompted content seen in normal speech, so replies to questions may be brief and concrete, with less spontaneous speech. This is termed poverty of speech[4] or laconic speech.[5] The amount of speech may be normal but conveys little information because it is vague, empty, stereotyped, overconcrete, overabstract, or repetitive.[4][6] This is termed poverty of content[4] or poverty of content of speech.[6] Under Scale for the Assessment of Negative Symptoms used in clinical research, thought blocking is considered a part of alogia, and so is increased latency in response.[7]

This condition is associated with schizophrenia, dementia, severe depression, and autism.[8][9] As a symptom, it is commonly seen in patients with schizophrenia and schizotypal personality disorder, and is traditionally considered a negative symptom. It can complicate psychotherapy severely because of the considerable difficulty in holding a fluent conversation.

The alternative meaning of alogia is inability to speak because of dysfunction in the central nervous system,[10][3] found in mental deficiency and dementia.[11][3] In this sense, the word is synonymous with aphasia,[3] and in less severe form, it is sometimes called dyslogia.[10]

Characteristics

[edit]

Alogia may be on a continuum with normal behaviors. People without mental illness may have it occasionally including when fatigued or disinhibited, when writers use language creatively, when people in certain disciplines—such as politicians, administrators, philosophers, ministers, and scientists—use language pedantically. Hence, deciding if an individual has alogia depends on contextual clues. Is the person in control? Can the person moderate the effect if asked to be specific or concise? Is it better with another topic? Are there other significant symptoms?[12]

Alogia is characterized by a lack of speech, often caused by a disruption in the thought process. Usually, an injury to the left side of the brain may cause alogia to appear in an individual.[citation needed] While in conversation, alogic patients will reply very sparsely and their answers to questions will lack spontaneous content; sometimes, they will even fail to answer at all.[13][failed verification] Their responses will be brief, generally only appearing as a response to a question or prompt.[14][failed verification]

Apart from the lack of content in a reply, the manner in which the person delivers the reply is affected as well. Patients affected by alogia will often slur their responses, and not pronounce the consonants as clearly as usual. The few words spoken usually trail off into a whisper, or are just ended by the second syllable.[citation needed] Studies have shown a correlation between alogic ratings in individuals and the amount and duration of pauses in their speech when responding to a series of questions posed by the researcher.[15] The inability to speak stems from a deeper mental inability that causes alogic patients to have difficulty grasping the right words mentally, as well as formulating their thoughts.[15] A study investigating alogiacs and their results on the category fluency task showed that people with schizophrenia who exhibit alogia display a more disorganized semantic memory than controls. While both groups produced the same number of words, the words produced by people with schizophrenia were much more disorderly and the results of cluster analysis revealed bizarre coherence in the alogiac group.[16]

If the condition is assessed using a language other than the individual's primary language, the medical professional needs to make sure that the problem is not from language barriers.[17]

This condition is associated with schizophrenia, dementia, and severe depression.[8]

Example

[edit]

The following table shows an example of "poverty of speech" which shows replies to questions that are brief and concrete, with a reduction in spontaneous speech:

Example of "poverty of speech"[18]
Poverty of speech Normal speech

Q: Do you have any children?
A: Yes.
Q: How many?
A: Two.
Q: How old are they?
A: Six and sixteen.
Q: Are they boys or girls?
A: One of each.
Q: Who is the sixteen-year-old?
A: The boy.
Q: What is his name?
A: Edmond.
Q: And the girl's?
A: Alice.

Q: Do you have any children?
A: Yes, a boy and a girl.
Q: How old are they?
A: Edmond is sixteen and Alice is six.

The following example of "poverty of content of speech" is a response from a patient when asked why he was in a hospital. Speech is vague, conveys little information, but is not grossly incoherent and the amount of speech is not reduced. "I often contemplate—it is a general stance of the world—it is a tendency which varies from time to time—it defines things more than others—it is in the nature of habit—this is what I would like to say to explain everything."[19]

Causes

[edit]

Alogia can be brought on by frontostriatal dysfunction which causes degradation of the semantic store, the center located in the temporal lobe that processes meaning in language. A subgroup of chronic schizophrenia patients in a word generation experiment generated fewer words than the unaffected subjects and had limited lexicons, evidence of the weakening of the semantic store. Another study found that when given the task of naming items in a category, schizophrenia patients displayed a great struggle but improved significantly when experimenters employed a second stimulus to guide behavior unconsciously. This conclusion was similar to results produced from patients with Huntington's and Parkinson's disease, ailments which also involve frontostriatal dysfunction.[20]

Treatment

[edit]

Medical studies conclude that certain adjunctive drugs effectively palliate the negative symptoms of schizophrenia, mainly alogia.[citation needed] In one study, Maprotiline produced the greatest reduction in alogia symptoms with severity reduction in 50% of patients (out of 10).[21] Of the negative symptoms of schizophrenia, alogia had the second best responsiveness to the drugs, surpassed only by attention deficiency.[21] D-amphetamine is another drug that has been tested on people with schizophrenia and found success in alleviating negative symptoms. This treatment, however, has not been developed greatly as it seems to have adverse effects on other aspects of schizophrenia such as increasing the severity of positive symptoms.[22]

Relation to schizophrenia

[edit]

Although alogia is found as a symptom in a variety of health disorders, it is most commonly found as a negative symptom of schizophrenia.

Previous studies and analyses conclude that at least three factors are needed to cover both the positive and negative symptoms of schizophrenia; the three are: psychotic, disorganization, and negative symptom factors. Studies suggest that an inappropriate affect is strongly associated with bizarre behavior and positive formal thought disorder on a disorganization factor; attention impairment correlates significantly with psychotic, disorganization, and negative symptom factors. Alogia contains both positive and negative symptoms, with the poverty of content of speech as the disorganization factor, and poverty of speech, response latency, and thought blocking as the negative symptom factors.[23]

Alogia is a major diagnostic sign of schizophrenia, when organic mental disorders have been excluded.[19]

In schizophrenia, negative symptoms including flattening of affect, avolition, and alogia are responsible for the considerable morbidity of the disease compared with other psychotic disorders.[24] Negative symptoms are common in the prodromal and residual phases of the disease and can be severe.[25] During the first year, negative symptoms can progress, especially alogia, which may start off from a relatively low rate. Within 2 years, up to 25% of patients will have significant negative symptoms.[26] Psychotic symptoms tend to diminish as the individuals age, but negative symptoms tend to persist.[27] Prominent negative symptoms at disease onset, including alogia, are good predictors of worse outcomes.[26][28]

Negative symptoms can arise in the presence of other psychiatric symptoms. Positive symptoms are a common cause of apathy, social withdrawal, and alogia. Secondary causes of negative symptoms, such as depression and demoralization, often remit within a year, which helps distinguishing them from primary negative symptoms. Symptoms that don't diminish over a year with medications should be reconsidered as possible primary negative symptoms.[26]

See also

[edit]

References

[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Alogia

View on Grokipedia
from Grokipedia
Alogia, commonly referred to as poverty of speech, is a negative symptom characterized by a marked reduction in the quantity, fluency, and informative content of verbal output, often manifesting as brief replies, delayed responses, or a lack of spontaneous . It is most prominently associated with , where it contributes to social and functional impairments, but can also appear in other conditions such as , , autism spectrum disorder, and . In , alogia falls under the broader category of negative symptoms in diagnostic frameworks like the , where it is described as decreased speech output and is often accompanied by diminished or . This symptom arises from disruptions in brain regions involved in language processing, motivation, and executive function, potentially linked to and imbalances, though the exact mechanisms remain under investigation. Unlike positive symptoms such as hallucinations, alogia reflects an absence or diminution of normal speech behaviors, which can severely limit and daily functioning. Management of alogia primarily targets the underlying disorder; for instance, medications like second-generation agents (e.g., or ) may alleviate symptoms in by modulating activity, while and social skills training can help improve verbal engagement. In non-psychotic contexts, such as , supportive interventions focus on environmental adaptations and speech therapy to mitigate communication challenges. Early identification and intervention are crucial, as persistent alogia is associated with poorer long-term outcomes, including increased risk of and reduced .

Definition and Characteristics

Definition

Alogia refers to a form of poverty of speech in , characterized by a marked reduction in both the quantity and informative content of an individual's verbal output, often stemming from underlying impairments in thought processes rather than mechanical speech difficulties. This manifests as brief, empty responses that lack depth or elaboration, reflecting diminished verbal productivity. The term "alogia" derives from the Greek roots "a-" (without) and "" (speech or reason), denoting an absence or paucity of expressive . It was first described in psychiatric in the late by , who identified poverty of speech as a core negative feature within his conceptualization of , a precursor to modern diagnoses. Alogia must be distinguished from , a neurological involving deficits in comprehension, production, or word retrieval due to brain damage, and from mutism, which entails a total refusal or inability to speak. Unlike these, alogia preserves basic but is driven by motivational or cognitive . Alogia is commonly associated with the negative symptoms of psychotic disorders.

Key Features

Alogia is characterized by quantitative poverty of speech, which manifests as a marked reduction in the overall amount of verbal output. This includes decreased speech volume in terms of quantity, such as producing fewer words or shorter utterances, often limited to brief, monosyllabic responses during interactions. Additionally, individuals exhibit increased latency in replying, with prolonged pauses before initiating speech, reflecting a diminished and spontaneity in communication. Qualitative poverty further distinguishes alogia, involving a lack of spontaneous speech and content that is typically empty, , or overly simplistic without meaningful elaboration or abstract detail. Speech may appear vague or repetitive, conveying minimal substantive information even when the quantity is marginally adequate, which underscores the impoverishment in expressive depth rather than mere brevity. Unlike positive symptoms such as disorganized speech, alogia does not involve , tangentiality, or neologisms, but instead represents a core negative symptom marked by reduction and paucity without the distortions or excesses seen in formal thought disorders. In diagnostic frameworks like the , alogia is recognized as a key negative symptom of , contributing to impaired social and functional outcomes.

Clinical Presentation

Symptoms

Alogia, a core negative symptom in psychiatric disorders such as , is characterized by a marked reduction in the quantity and fluency of speech. Primary manifestations include monosyllabic or brief responses to questions, a to initiate conversations spontaneously. These features reflect not only decreased verbal output but also impoverished content, with individuals often exhibiting increased latency in responding and pauses during speech. The impact of alogia on social functioning is profound, as the minimal verbal engagement hinders effective communication and fosters isolation from others. Interactions become strained, leading to frustration for both the affected individual and their interlocutors, which can exacerbate withdrawal from social and professional activities. This diminished expressiveness contributes to broader impairments in daily relationships and overall . Alogia often overlaps with other negative symptoms, such as , amplifying functional deficits. In terms of progression, it may emerge subtly as reduced verbosity in early stages and worsen to near-silence in severe cases, with symptoms tending to remain stable or intensify over time, particularly in primary forms of the disorder.

Examples

Alogia manifests in clinical interactions through markedly reduced verbal output, often evident in responses to open-ended questions. For instance, when a asks a , "How have your days been going lately?", a typical response might be limited to a single word like "Fine" rather than providing details about activities or feelings. Similarly, in response to "What do you do for work?", the patient may reply simply with "Mow," omitting elaboration on their role or daily routine. In therapeutic settings, alogia appears as persistently short answers to prompts designed to elicit narrative responses. A therapist inquiring, "Can you tell me about a recent challenge you've faced?", might receive only "Work" after a long pause, lacking further context or emotional insight. This pattern hinders the therapeutic process, as the patient provides minimal spontaneous content despite encouragement. In social environments, such as group discussions, individuals with alogia often remain silent or contribute only brief affirmations like "Yes," avoiding engagement in conversations about shared experiences or plans. Alogia varies in severity, influencing the degree of communicative impairment. In mild cases, responses consist of short sentences that convey basic information but lack depth, such as answering "Do you have a job?" with "Yes, janitor at the ," without additional details on satisfaction or responsibilities. Severe alogia, by contrast, may involve even scantier output, or offering no reply at all, effectively resembling mutism in prolonged interactions. These examples are commonly observed in chronic settings among patients with .

Etiology and Pathophysiology

Causes

Alogia can arise from factors that disrupt verbal expression and . has been linked to the exacerbation of negative symptoms, including reduced speech output, as ongoing psychological pressure impairs motivation for communication. Social withdrawal often creates a reinforcing cycle with alogia, where diminished speech leads to further isolation, perpetuating poverty of speech through lack of practice and interaction. Childhood adversity, including trauma and , is associated with the development and persistence of negative symptoms such as alogia in conditions like . Developmental factors, such as , may contribute to the persistence of alogia by establishing patterns of limited verbal output from childhood. Neglectful environments deprive children of sufficient linguistic stimulation, fostering communicative deficits that can endure into adulthood, especially when compounded by later psychiatric vulnerabilities. These early disruptions highlight how inadequate caregiving can lay the groundwork for enduring communicative deficits. Iatrogenic causes of alogia include side effects from certain medications, notably sedatives and antipsychotics, which induce or that mimic or worsen speech reduction. High doses of first-generation antipsychotics, for instance, can produce akinesia, leading to decreased verbal fluency as a secondary effect. Additionally, alogia frequently co-occurs with mood disorders, where depressive withdrawal amplifies speech poverty.

Neurological Mechanisms

Alogia is associated with hypoactivity in key regions of the prefrontal cortex, particularly the (DLPFC) and , which impair the initiation and production of speech. The DLPFC plays a critical role in such as planning and monitoring verbal output, and its reduced activity disrupts the cognitive processes necessary for generating coherent speech. Similarly, hypoactivity in , located in the , contributes to diminished verbal fluency and poverty of speech by affecting the motor aspects of language articulation. These prefrontal deficits are thought to underlie the motivational and cognitive barriers that limit spontaneous verbal expression in alogia. Dopaminergic dysregulation in the further contributes to alogia by reducing transmission to prefrontal regions, leading to motivational deficits that diminish verbal output. The , originating from the and projecting to the , modulates reward processing and initiation of goal-directed behaviors, including speech; hypoactivity here results in and reduced drive for communication. This is mediated by decreased D1 receptor activation in the , which impairs the signaling necessary for sustaining verbal engagement. Genetic predispositions, such as variants in the COMT gene that accelerate breakdown, may exacerbate this prefrontal deficit. Glutamatergic imbalances, particularly hypofunction of NMDA receptors, have also been implicated in the of alogia and other negative symptoms. This dysregulation disrupts cortical excitatory-inhibitory balance, affecting processing and motivation in prefrontal regions, as evidenced by studies on glutamate levels and linguistic impairments in . Neuroimaging studies, particularly functional MRI (fMRI), provide evidence of decreased brain activation in individuals with alogia during tasks, with reduced BOLD signals in regions. For instance, patients exhibit lower activation in the DLPFC and compared to healthy controls when performing verbal fluency or sentence comprehension tasks, reflecting impaired neural recruitment for processing. These findings highlight the hypofrontality characteristic of alogia, where frontal underactivation correlates with the severity of speech poverty.

Diagnosis and Assessment

Diagnostic Criteria

Alogia is classified as a negative symptom within the diagnostic framework for in the , where negative symptoms are defined as diminished emotional expression or , encompassing reductions in speech quantity and content that persist for a significant portion of time during a 1-month period of active symptoms, with overall signs of the disorder continuing for at least 6 months. In this context, alogia manifests as poverty of speech, characterized by decreased verbal output or impoverished thought content, and must be present alongside at least one other characteristic symptom (such as delusions or hallucinations) to contribute to the . In the , alogia is explicitly listed as a core negative symptom of spectrum disorders, described as poverty of speech or thought with reduced quantity or content of verbal output, requiring the presence of at least two characteristic symptoms (including at least one core psychotic feature like delusions or hallucinations) for a significant portion of at least 1 month, accompanied by functional impairment persisting for 3 to 6 months or more. Severity of alogia and other negative symptoms in can be rated on a scale from none to severe, such as mild (noticeable but not markedly impairing) or severe (profoundly limiting communication and daily functioning). Diagnosis of alogia requires exclusion of alternative explanations, ensuring it is not attributable to , which involves global rather than isolated speech poverty; substance use or effects, which may induce transient speech reductions; or primary neurological conditions such as , a stemming from injury or that affects comprehension and production differently from alogia's content emptiness. Alogia is typically integrated with other negative symptoms, like or blunted affect, to assess the full negative symptom syndrome in , though it alone does not constitute a standalone .

Evaluation Methods

The evaluation of alogia primarily relies on standardized clinical scales that quantify the severity of speech poverty through structured interviews and observations. The Scale for the Assessment of Negative Symptoms (SANS), developed by Nancy Andreasen, includes a dedicated alogia subscale comprising items such as poverty of speech (assessed via quantity and rate of speech), poverty of content (evaluating the emptiness or vagueness of responses), blocking (unprompted interruptions in speech flow), increased latency of response, and a global rating of alogia. This subscale rates each item on a 6-point from 0 (none/not at all) to 5 (severe), allowing clinicians to derive a composite score for alogia's intensity based on the patient's verbal output during a . Observational methods complement these scales by providing quantifiable metrics of speech production during natural or prompted conversations. Clinicians often record the duration of patient responses and calculate speech rate as , where typical rates exceed 100 words per minute in unaffected individuals, while rates below 50 words per minute may indicate significant alogia in severe cases. These measures, such as total word count divided by speaking time, help capture reductions in spontaneous speech elaboration and overall verbal productivity without relying solely on subjective judgment. To minimize bias and enhance reliability, objective computerized speech tools have been developed for assessing alogia through automated ing of audio recordings. These systems measure parameters like response latency (time from prompt to speech onset), speech (frequency and duration of pauses), and overall (e.g., words or syllables per second), correlating strongly with clinical ratings of alogia severity. Such tools naturalistic speech samples, providing precise, reproducible that support consistent evaluation across sessions. These methods are particularly useful in longitudinal studies to monitor alogia's progression over time.

Associated Disorders

Schizophrenia

Alogia manifests as a core negative symptom in , characterized by reduced speech output and impoverished thinking, and is observed in a significant proportion of affected individuals. Negative symptoms, encompassing alogia, occur in up to 90% of patients during the initial psychotic episode, with persistence rates ranging from 35% to 70% following acute treatment. This symptom frequently appears early in the disease course, often during the prodromal phase or as one of the initial signs preceding full psychotic onset, with approximately 73% of patients experiencing negative symptoms before positive ones emerge. Within subtypes, alogia is particularly prominent in the deficit form, where it represents a primary, enduring feature intrinsic to the disorder, as opposed to secondary manifestations in non-deficit that may arise from comorbid depression or other transient factors. The deficit subtype, defined by stable negative symptoms enduring for at least 12 months, affects 15% to 25% of patients and is distinguished by its idiopathic nature and resistance to interventions targeting secondary causes. In contrast, secondary alogia in non-deficit cases is often reversible upon addressing underlying contributors like mood disturbances. The prognostic implications of alogia in are substantial, as it strongly correlates with diminished functional outcomes, including elevated and challenges in social and occupational domains. Patients with prominent alogia exhibit greater overall , with negative symptoms accounting for a major portion of long-term impairments in daily living and stability. Alogia shares neurobiological mechanisms with other negative symptoms, such as and blunted affect, contributing to the overall burden of the disorder.

Other Conditions

Alogia manifests in as a secondary negative symptom, primarily driven by and diminished motivation, leading to reduced verbal output that typically improves as depressive symptoms are addressed. In this context, individuals may exhibit brief responses or prolonged silences during interactions, reflecting broader emotional flattening rather than a primary impairment. In autism spectrum disorder, alogia overlaps with pragmatic language deficits, such as challenges in social reciprocity and contextual interpretation, but presents less as outright poverty of speech and more as literal, concrete expressions that limit conversational depth. These features stem from neurodevelopmental differences affecting communication flexibility, distinguishing them from the motivational deficits seen in other conditions. Alogia in , particularly , emerges in late stages due to progressive cognitive decline, characterized by profound verbal fluency loss alongside memory impairment, often progressing to near-mutism. This form differs from earlier manifestations by its inextricable link to global neurodegeneration, with reduced speech output reflecting eroded semantic and syntactic abilities. Alogia can also occur following (TBI), where damage to brain regions involved in , , and language processing leads to reduced verbal output and responsiveness. This manifestation is often part of broader or cognitive impairments and may improve with rehabilitation, though persistent cases can contribute to long-term communication challenges.

Treatment and Management

Pharmacological Interventions

Atypical antipsychotics, such as and , represent the primary pharmacological approach for managing alogia as part of negative symptoms in , primarily through modulation of D2 receptors and serotonin 5-HT2A antagonism, which may enhance prefrontal cortical activity and reduce hypodopaminergia associated with poverty of speech. , typically dosed at 200-600 mg/day, has demonstrated efficacy in improving core negative symptoms, including alogia, in treatment-resistant cases, with studies, including one open trial, showing approximately 30% improvement in negative symptom severity. , at doses of 4-8 mg/day, has shown comparable efficacy to in alleviating negative symptoms in some RCTs, with meta-analyses suggesting modest advantages for atypical antipsychotics overall. These agents are preferred over typical antipsychotics due to lower risk of extrapyramidal side effects (EPS), though monitoring for metabolic changes and remains essential. For secondary alogia linked to comorbid depression, adjunctive selective serotonin reuptake inhibitors (SSRIs) like (20 mg/day) can augment therapy by targeting serotonergic pathways to indirectly enhance tone in limbic regions. Meta-analyses of RCTs support this approach, revealing small-to-medium improvements in negative symptoms (SMD around -0.4). 's efficacy appears particularly pronounced in patients with residual depressive features exacerbating alogia, though benefits are less consistent for primary negative symptoms. As of 2025, recent meta-analyses continue to indicate modest effect sizes for these interventions on negative symptoms, with Cohen's d values around 0.3-0.6 for atypical antipsychotics and adjunctive SSRIs compared to or standard care, underscoring the need for individualized dosing and regular assessment of EPS and metabolic risks, alongside emerging augmentations like . Pharmacological strategies may yield better outcomes when combined briefly with psychotherapeutic approaches to reinforce communicative skills.

Psychotherapeutic Approaches

Psychotherapeutic approaches to alogia primarily target the enhancement of communication skills and , focusing on behavioral and cognitive techniques to address poverty of speech as a negative symptom often associated with . These interventions emphasize skill-building without relying on pharmacological agents, aiming to improve verbal expression and reduce isolation through structured therapeutic support. For alogia in other conditions, such as or , speech-language therapy and environmental adaptations are recommended to support communication. Cognitive behavioral therapy (CBT) is a key psychotherapeutic method for managing alogia, employing techniques such as verbal elaboration exercises and linking thoughts to speech to encourage more detailed and spontaneous communication. Sessions typically involve identifying cognitive barriers to expression, like negative beliefs about social interactions, and practicing behavioral experiments to build fluency, often structured over 8-12 weeks in individual or group formats. A meta-analysis of randomized controlled trials demonstrated that CBT significantly reduces negative symptoms, including those related to diminished speech, with a mean difference of -1.65 on the Positive and Negative Syndrome Scale (PANSS) negative subscale compared to treatment as usual, indicating moderate improvements sustained across short- to long-term follow-ups. Social skills training (SST) addresses alogia through role-playing scenarios that simulate everyday conversations, helping individuals practice initiating and maintaining to counteract speech poverty. Delivered in group settings to foster real-time feedback and peer interaction, SST focuses on breaking down complex social exchanges into manageable steps, such as greeting others or elaborating on responses. Evidence from clinical trials shows that SST, particularly cognitive-behavioral variants, improves social functioning and experiential negative symptoms by up to 0.72 at 21 months, with notable gains in conversation initiation rates among participants with . Family therapy plays a supportive role by educating relatives on strategies to prompt speech gently, such as open-ended questions and , without exerting pressure that could exacerbate withdrawal. This approach reduces family-expressed and isolation, promoting a communicative home environment through joint sessions that include problem-solving and empathy-building exercises. Long-term studies indicate sustained benefits, with family interventions yielding moderate reductions in negative symptoms (e.g., via the Scale for the Assessment of Negative Symptoms) and improved social outcomes over 12-24 months. These psychotherapeutic methods often serve an adjunctive function alongside other treatments to optimize overall of alogia.

References

  1. https://www.psychiatry.org/patients-families/schizophrenia/what-is-schizophrenia
  2. https://my.clevelandclinic.org/health/symptoms/25223-alogia
  3. https://www.medicalnewstoday.com/articles/alogia-schizophrenia
  4. https://pmc.ncbi.nlm.nih.gov/articles/PMC6953551/
  5. https://psychcentral.com/schizophrenia/alogia-poverty-of-speech
  6. https://www.verywellmind.com/overview-of-alogia-4797519
  7. https://academic.oup.com/book/60900/chapter/530759693
  8. https://journals.lww.com/armh/fulltext/2015/03020/negative_symptoms_of_schizophrenia__a_historical%2C.33.aspx
  9. https://pmc.ncbi.nlm.nih.gov/articles/PMC5479085/
  10. https://www.frontiersin.org/journals/psychiatry/articles/10.3389/fpsyt.2021.766692/full
  11. https://www.sciencedirect.com/topics/neuroscience/alogia
  12. https://pmc.ncbi.nlm.nih.gov/articles/PMC8480175/
  13. https://pmc.ncbi.nlm.nih.gov/articles/PMC8761803/
  14. https://pmc.ncbi.nlm.nih.gov/articles/PMC4254038/
  15. https://study.com/learn/lesson/alogia-poverty-of-speech.html
  16. https://psychcentral.com/schizophrenia/schizophrenia-speech-patterns
  17. https://www.webmd.com/mental-health/what-is-alogia
  18. https://pmc.ncbi.nlm.nih.gov/articles/PMC7041437/
  19. https://www.ncbi.nlm.nih.gov/books/NBK594231/
  20. https://pmc.ncbi.nlm.nih.gov/articles/PMC4694548/
  21. https://pmc.ncbi.nlm.nih.gov/articles/PMC8165195/
  22. https://psychiatryonline.org/doi/full/10.1176/appi.ajp.159.2.227
  23. https://www.nature.com/articles/s41537-021-00141-8
  24. https://pmc.ncbi.nlm.nih.gov/articles/PMC7315891/
  25. https://link.springer.com/article/10.1007/s12264-021-00740-6
  26. https://www.pnas.org/doi/10.1073/pnas.111134598
  27. https://www.frontiersin.org/journals/human-neuroscience/articles/10.3389/fnhum.2022.954898/full
  28. https://pmc.ncbi.nlm.nih.gov/articles/PMC2212592/
  29. https://www.sciencedirect.com/science/article/abs/pii/S0920996413003630
  30. https://www.jci.org/articles/view/19166
  31. https://www.ncbi.nlm.nih.gov/books/NBK519704/
  32. https://www.who.int/publications/i/item/9789240077263
  33. https://awspntest.apa.org/doi/10.1037/t12696-000
  34. https://pmc.ncbi.nlm.nih.gov/articles/PMC9371299/
  35. https://pmc.ncbi.nlm.nih.gov/articles/PMC2488151/
  36. https://www.nature.com/articles/s41398-023-02594-0
  37. https://www.sciencedirect.com/science/article/abs/pii/S0278584619308103
  38. https://psychiatryonline.org/doi/10.1176/ajp.155.3.350
  39. https://www.sciencedirect.com/science/article/abs/pii/S0165178116314184
  40. https://pmc.ncbi.nlm.nih.gov/articles/PMC9944009/
  41. https://www.cambridge.org/core/journals/acta-neuropsychiatrica/article/profiling-spontaneous-speech-decline-in-alzheimers-disease-a-longitudinal-study/A7E6279AC4D6272BA042B045681DC2AB
  42. https://pmc.ncbi.nlm.nih.gov/articles/PMC8772820/
  43. https://pmc.ncbi.nlm.nih.gov/articles/PMC6556563/
  44. https://pubmed.ncbi.nlm.nih.gov/9511946/
  45. https://www.sciencedirect.com/science/article/pii/0010440X94901643
  46. https://pmc.ncbi.nlm.nih.gov/articles/PMC4202542/
  47. https://pubmed.ncbi.nlm.nih.gov/9522104/
  48. https://pubmed.ncbi.nlm.nih.gov/7868850/
  49. https://www.cambridge.org/core/journals/the-british-journal-of-psychiatry/article/efficacy-of-antidepressants-in-treating-the-negative-symptoms-of-chronic-schizophrenia-metaanalysis/2AB14664EA1ACC94C4F3879096853DF5
  50. https://www.mdpi.com/2077-0383/13/18/5637
  51. https://pmc.ncbi.nlm.nih.gov/articles/PMC4466178/
  52. https://www.sciencedirect.com/science/article/abs/pii/S0924933809714208
  53. https://www.thelancet.com/journals/lanpsy/article/PIIS2215-0366(25)00001-X/fulltext
  54. https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0324685
  55. https://pmc.ncbi.nlm.nih.gov/articles/PMC8498814/
  56. https://pmc.ncbi.nlm.nih.gov/articles/PMC2632540/
  57. https://pmc.ncbi.nlm.nih.gov/articles/PMC4204509/
  58. https://www.sciencedirect.com/science/article/abs/pii/S0272735813000895
  59. https://pmc.ncbi.nlm.nih.gov/articles/PMC4092118/
Add your contribution
Related Hubs
User Avatar
No comments yet.