Postoperative speech impairment

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Postoperative speech impairment refers to a decline or alteration in a patient’s ability to speak after undergoing a surgical procedure. This condition can range from mild word-finding difficulties to complete loss of speech (aphasia), and may be temporary or permanent, depending on several factors.

Neurosurgical procedures:

Surgeries involving the dominant hemisphere (especially the left frontal or temporal lobes) can affect Broca’s or Wernicke’s areas.

Brain tumor resections, epilepsy surgery, or AVM clipping.

Stroke or ischemia during or after surgery.

Anesthesia-related complications:

Hypoxic events (low oxygen during surgery).

Prolonged intubation causes vocal cord injury.

Cranial nerve injury:

Injury to cranial nerves IX, X, or XII may affect articulation or phonation.

Edema or mass effect:

Postoperative swelling can temporarily impair speech centers or tracts.

Psychogenic causes:

Postoperative stress, delirium, or conversion disorders.

Neurological exam: Assess fluency, comprehension, repetition, naming, reading, and writing.

Imaging: MRI or CT to rule out new ischemic events, edema, or hemorrhage.

Laryngoscopy: If vocal cord dysfunction is suspected.

Neuropsychological testing: For subtle deficits or rehabilitation planning.

Dysarthria: Impaired articulation due to muscle weakness or incoordination.

Aphasia: Language dysfunction (e.g., expressive, receptive, global).

Apraxia of speech: Motor planning disorder, not due to weakness.

Speech and language therapy (SLT): Early and tailored intervention.

Medical treatment: Reduce cerebral edema (e.g., steroids), manage seizures.

Surgical revision: In rare cases, to relieve pressure or reposition structures.

Multidisciplinary care: Neurologists, neurosurgeons, ENT, rehabilitation teams.

A multicentre European study addresses a longstanding question in pediatric neurosurgery outcomes: is tumor volume associated with the risk of developing cerebellar mutism Syndrome (CMS), particularly its core feature—postoperative speech impairment (POSI)?

The study prospectively evaluated 360 children undergoing surgery for posterior fossa tumors, with speech status assessed within two weeks post-op and categorised into habitual speech, reduced speech, severely reduced speech, and mutism. Preoperative MRI was used to calculate tumour volume using BrainLab Elements SmartBrush™ ¹⁾.

Robust sample size from multiple European centres enhances generalisability.

Semi-automated volumetric analysis reduces measurement bias.

Stratified risk model for medulloblastoma offers actionable clinical value.

No association was found between tumor volume and POSI when considering all tumor types.

A significant correlation was discovered for medulloblastoma: every 1 cm³ increase in volume slightly elevated the risk of POSI (OR 1.04).

An optimal cut-off volume of 16.5 cm³ was identified. Children with medulloblastoma below this threshold had a 13% risk, while those above faced a 50% risk.

The finding applies only to medulloblastomas, limiting generalisability across posterior fossa pathologies.

Functional outcomes beyond speech (e.g., cognition, motor) were not assessed.

The predictive value of the model needs external validation in non-European cohorts.

This study presents a clear volumetric threshold for assessing POSI risk in children with medulloblastoma. It underscores the value of preoperative planning not just for technical feasibility but also for predicting neurological outcomes. The proposed cut-off can help guide shared decision-making and family counselling, as well as prompt early speech therapy referral in high-risk cases.

While the overall volume of posterior fossa tumours may not be a universal predictor of postoperative speech impairment, this paper sheds light on a valuable exception. The findings for medulloblastoma could be incorporated into future risk models and decision-support systems in paediatric neuro-oncology.