thought_disorder

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Thought Disorder

Thought disorder refers to a disturbance in the form (structure) or content of thinking, leading to impaired communication or abnormal beliefs. It is most often associated with schizophrenia-spectrum disorders but also occurs in mood disorders, neurodegenerative diseases, and structural brain lesions.

Involves abnormalities in the *form* or *process* of thinking, typically assessed by observing speech patterns.

Symptom Description
Derailment (loose associations) Shifting from one idea to another with little logical connection.
Tangentiality Answers diverge from the topic and never reach the point.
Incoherence (word salad) Speech becomes incomprehensible due to disorganized grammar and logic.
Neologisms Creation of new, idiosyncratic words.
Clang associations Linking words by sound rather than meaning.
Perseveration Repeating the same idea or phrase despite topic change.

Reflect distorted or false beliefs.

Type Example
Delusions Fixed false beliefs (e.g., persecutory, grandiose).
Paranoia Belief that others intend harm.
Magical thinking Belief that thoughts influence reality in supernatural ways.

Though classically psychiatric, thought disorders can arise in neurological conditions such as:

  • Frontal lobe lesions – executive dysfunction and disorganized thought.
  • Temporal lobe epilepsy – may include paranoia or hyperreligiosity.
  • Cerebellar dysfunction – part of the *Cerebellar Cognitive Affective Syndrome* (CCAS), also called “dysmetria of thought”.
Thought disorder is a disruption in the normal pattern of thinking, often observed as disorganized, illogical, or incoherent speech. It reflects abnormalities in how ideas are generated, connected, and communicated, and may signal underlying psychiatric or neurological disease.

In a editorial commentary Annie I. Drapeau, and Anthony M. Kaufmann, from the University of Manitoba, Winnipeg published in the Journal of Neurosurgery to critically reflect on the burgeoning hypothesis that Chiari malformation type I (CM-I) may contribute to cognitive and affective dysfunction and that posterior fossa decompression (PFD) might yield therapeutic benefits beyond relief of pressure-related symptoms. The authors caution against the premature endorsement of PFD for neuropsychiatric complaints in CM-I patients without classic decompression indications. They underscore the need for rigorous control of confounding variables, the inclusion of control groups, and standardized methodologies in future research. There is skepticism about the interpretation of postoperative cognitive and affective improvements due to potential placebo effects, resolution of pain, and medication cessation, rather than direct pathophysiological relief 1)

This editorial is a necessary tempering of enthusiasm following Henry et al.'s exploratory prospective study on cognitive and affective changes post-PFD in CM-I. The authors provide a methodologically grounded critique, emphasizing the dangers of misattributing causality to associative findings, especially in the absence of a control group or rigorous baseline psychiatric profiling 2)

The editorial's strength lies in its careful parsing of psychometric data, awareness of selection bias, and cautious evaluation of the surgical implications. It deftly illustrates how incidental radiological findings (like CM-I) might spur unwarranted interventions without solid mechanistic links. The comparison to microvascular decompression outcomes in cranial nerve disorders is apt and effective in conveying the cautionary message.

Its limitations are those of the editorial format—it does not provide new data but rather serves to contextualize existing results. However, as a scholarly commentary, it is exemplary in tone, scope, and scientific restraint.

Final Verdict: An intellectually rigorous and judicious editorial that should guide neurosurgeons and researchers in critically appraising speculative surgical indications. A must-read for those exploring neuropsychiatric extensions of CM-I pathology.

Takeaway for Neurosurgeons: Posterior fossa decompression should not be pursued for cognitive or affective complaints in CM-I absent traditional surgical indications. Await stronger evidence.

Bottom Line: The cerebellum’s cognitive role is intriguing, but current evidence does not justify PFD in asymptomatic CM-I patients with only psychiatric symptoms.

Rating: 8.5/10

Title: Considering Chiari Malformation Type I Decompression for Disorders of Thought

Citation: Drapeau AI, Kaufmann AM. Considering Chiari malformation type I decompression for disorders of thought. J Neurosurg. 2025 Jul;143(1):1–3. doi:10.3171/2024.10.JNS242051.

Publication Date: February 21, 2025

Corresponding Author: annie.drapeau@umanitoba.ca

Categories: Editorials, Chiari Malformation, Cerebellar Neuroscience

Tags: Chiari malformation type I, posterior fossa decompression, cognitive dysfunction, affective disorders, cerebellar function, neurosurgical indications, editorial, neuropsychology, depression, anxiety


1)
Drapeau AI, Kaufmann AM. Editorial. Considering Chiari malformation type I decompression for disorders of thought. J Neurosurg. 2025 Feb 21;143(1):1-3. doi: 10.3171/2024.10.JNS242051. PMID: 39983123.
2)
Henry LC, McDowell MM, Stephenson TL, Crittenden JB, Byrd AL, Fernández-de Thomas RJ, Chang YF, Nowicki KW, Mantena R, Strick PL, Friedlander RM. Predecompression and postdecompression cognitive and affective changes in Chiari malformation type I. J Neurosurg. 2025 Feb 21;143(1):4-12. doi: 10.3171/2024.8.JNS241363. PMID: 39983117.
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