Right Temporal Lobe Glioblastoma Presenting as Distortions of Speech Processing
1Resident Physician, Department of Emergency Medicine, MetroHealth Medical Center, Cleveland, OH
2Chair, Department of Emergency Medicine, MetroHealth Medical Center, Cleveland, OH
3Chair, Department of Neurology, MetroHealth Medical Center, Cleveland, OH
4Attending Physician, Department of Emergency Medicine, MetroHealth Medical Center, Cleveland, OH
Charbonnet CC, Emerman CL, Ardelt AA, Effron D. Right temporal lobe glioblastoma presenting as distortions of speech processing. Consultant. 2023;63(3):e5. doi:10.25270/con.2022.08.000006
Received November 10, 2021. Accepted December 1, 2021. Published online August 8, 2022.
The authors report no relevant financial relationships.
David Effron, MD, Department of Emergency Medicine, MetroHealth Medical Center, 2500 MetroHealth Drive, Cleveland, OH 44109 (email@example.com)
While bilateral temporal lobes receive the same input from lower auditory neurons, the processing of sound is traditionally considered to be dominated by the left hemisphere. However, patients with right temporal lobe epilepsy have described auditory auras in which existing sound is distorted. Additionally, recent cortical response mapping to speech stimuli has demonstrated increased neural activation in the speech envelop in the right hemisphere compared to the left. This laterality is amplified in adverse conditions in which background noise degrades higher frequency components of speech. This is a case report of a 66-year-old man who intermittently perceived speech as if abnormally sped up. He was diagnosed with a right temporal lobe glioblastoma multiforme that caused distortion of the primary auditory cortex, secondary auditory cortex, and the anterior portion of the auditory association cortex. That distortions of specifically speech stimuli in adverse conditions resulted from local mass effect in the right temporal lobe adds to the evidence that processing of speech stimuli involves bilateral cerebral hemispheres in ways not yet fully elucidated.
A 66-year-old, right-handed man presented to the emergency department (ED) reporting the perception of hearing speech “in fast forward.” The perception was intermittent; episodes lasted for a few minutes and occurred without clear triggers. The first episode occurred the night before presentation. The phenomenon related to real persons contemporaneously in the room with him as well as characters on television shows he was watching.
The only associated symptom, as determined later by neurology consultants, was tingling on the tip of the patient’s tongue. The patient denied all other neurologic and psychiatric symptoms, including headaches, changes in vision, vertiginous symptoms, tinnitus, seizure-like activity, weakness, ataxia, nausea, and other hallucinations. He specifically denied hearing voices from persons not in the room. His past medical history was noteworthy for class 3 obesity, hypertension, hyperlipidemia, stage 1 chronic kidney disease, type 2 diabetes mellitus, and osteoarthritis.
The patient denied personal or family history of neurologic and psychiatric conditions, including strokes, seizure disorders, and psychoses. His only home medication was amlodipine. He denied recent medication changes. He reported weekly alcohol consumption and occasional cannabis use.
In the ED, the patient continued to experience the perception of hearing voices sped up, although the phenomenon did not occur every time someone spoke. His triage vital signs were unremarkable. A complete neurologic exam was also normal. Because the ED team was concerned that this symptom was an atypical presentation of temporal lobe epilepsy, they proceeded with a workup for new-onset seizures.
Diagnostic testing. Computerized tomography of the brain revealed a mass in the right temporal pole with extension along the lateral cortex associated with subcortical vasogenic edema. Mild local mass effect on the right temporal lobe was noted, but there was no midline shift or hydrocephalus.
Magnetic resonance imaging (MRI) of the brain showed an irregularly, heterogeneously enhancing mass in the right temporal lobe measuring 3.7 × 2.7 × 2.8 cm with peripheral rim–restricted diffusion, thick rind, and nodular-like enhancement. The cortically based mass abutted the dural interface with areas of hemorrhage (Figure 1).
Figure 1. Fluid-attenuated inversion recovery sequence axial slices progressing caudally.
The patient was admitted to the neurosurgery service and given levetiracetam and dexamethasone. An electroencephalogram demonstrated intermittent slowing in the right frontotemporal region. The patient underwent a right craniotomy and mass resection; a repeat MRI showed no residual neoplasm. Pathology later confirmed that the mass was a glioblastoma multiforme (GBM). The patient reported resolution of symptoms following surgery. He was discharged with prescriptions for levetiracetam and dexamethasone. At an outpatient appointment, he declined to undergo concurrent chemoradiation and has since been lost to follow-up.
Discussion. Whereas “hallucinations” are classically defined as perceptions in the absence of corresponding external stimuli; the perception of hearing actual stimuli in an altered manner as described in this case warrants a distinct term. Delgado and colleagues1 described 2 patients: one who described that people’s voices sounded like “dinosaur shouts” and one who saw bizarre body distortions in people’s faces. This team suggested that such “fantastic, perceptive distortions” be called “distorteidolias.”
Both patients in this report had strokes limited to the thalamic dorsomedial nucleus, a region that modulates brainstem inputs en route to the auditory and visual cortices. Our patient had a GBM limited to the right temporal pole, which receives auditory signals relayed through the thalamus.
First-order neurons extend from the cochlear nerve into the cochlear nucleus, from which second-order nerve fibers cross and ascend to the inferior colliculus. From the inferior colliculus, projections reach the medial geniculate body, also known as the thalamic auditory relay. Fourth-order auditory nerves project into the primary auditory cortex (PAC) in the temporal lobe. Specifically, the PAC is located in Brodmann area (BA) 41 in the transverse temporal gyrus, which is found in the upper and middle parts of the superior temporal gyrus (STG) near the lateral cerebral fissure.2,3
Our patient’s GBM measured 3.7 × 2.7 × 2.8 cm and was located in the right temporal pole. While the lesion occupied space primarily in the middle and inferior temporal lobe gyri, there was marked distortion of the local anatomy (Figure 2) as well as asymmetry of the right superior temporal gyrus compared with the contralateral region in the coronal view (Figure 3). Deformity of the primary auditory cortex (BA 41), the secondary auditory cortex (BA 42), and the anterior portion of the auditory association cortex (BA 22) was seen. The patient’s distorteidolias likely arose from distortions of nerves in these areas. Additionally, the tongue paresthesias were likely caused by distortion of the corresponding portion of the homunculus located nearby in the inferior postcentral gyrus of the primary somatosensory cortex.
Figure 2. 3D T1-weighted turbo field echo sagittal image demonstrating local distortion.
Figure 3. 3D T1-weighted turbo field echo postexcitation coronal section comparing right and left STG.
Although both temporal lobes receive the same input from these lower auditory neurons, the processing of sound is traditionally considered to be dominated by the left hemisphere. Although our patient’s phenomenon has not been previously documented, similar auditory processing distortions have been localized to the right STG.
Patients with epileptic foci in the STG have reported auditory hallucinations such as buzzing or roaring sounds.4 Other patients with right temporal lobe epilepsy have described auditory auras in which existing sound is distorted. This symptom usually occurs with early involvement of the auditory association cortex in the lateral aspects of the STG.5 Although our patient's condition was ultimately diagnosed as a GBM, the presenting symptom may have been one such seizure.
Previously established hypotheses regarding coding of different frequencies have speculated that slower temporal acoustic signals lateralize to the right hemisphere. Such frequency-specific encoding was not thought to extend to speech processing. However, recent cortical response mapping to speech stimuli has demonstrated both increased magnitude of neural activation as well as greater precision of the contours of the speech envelope in the right hemisphere compared with the left hemisphere.6
Additionally, neuroimaging has implicated the right temporal lobe under so-called “adverse” or “real-world listening conditions” in which background noise degrades the higher-frequency components of speech.7 Some case reports describe patients who develop impaired perception of speech after undergoing right temporal lobe resections as treatment for intractable epilepsy.8
One group found that patients developed profoundly impaired speech recognition when listening to sounds that were filtered to less than 1000 Hz to simulate muffled speech.7 This phenomenon was particularly pronounced following resection of the right STG. Such nuances of this functional architecture may explain why our patient experienced distorteidolias less frequently in the quiet examination room in the ED than he did at home when surrounded by more ambient noise.
Conclusions. A patient presented to the ED with the perception that speech was abnormally sped up. He underwent resection of a right temporal lobe GBM with complete resolution of symptoms. Given that the phenomenon occurred only with actual stimuli, this symptom was not a hallucination and may more appropriately be called a distorteidolia. This case report provides additional evidence that the processing of speech under adverse listening conditions involves the right temporal lobe, especially the STG.
1. Delgado MG, Bogousslavsky J. ‘Distorteidolias’ - fantastic perceptive distortion. Eur Neurol. 2013;70(1-2):6-9. https://doi.org/10.1159/000348361
2. Chapter 10: Cerebral Hemispheres/Telencephalon. In: Waxman SG, ed. Clinical Neuroanatomy, 29e. McGraw Hill; 2020.
3. Amthor FR. Chapter 13: Auditory & Vestibular Systems. In: Amthor FR, Theibert AB, Standaert DG, Roberson ED, eds. Essentials of Modern Neuroscience. McGraw Hill; 2020.
4. Chapter 15: Epilepsy and Other Seizure Disorders. In: Ropper AH, Samuels MA, Klein JP, Prasad S, eds. Adams and Victor's Principles of Neurology, 11e. McGraw Hill; 2019.
5. Weisholtz D, Sarkis R, Baslet G. Chapter 29: Neuropsychiatry of Epilepsy. In: Silbersweig DA, Safar LT, Daffner KR, eds. Neuropsychiatry and Behavioral Neurology: Principles and Practice. McGraw Hill; 2021.
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7. Boatman DF, Lesser RP, Crone NE, Krauss G, Lenz FA, Miglioretti DL. Speech recognition impairments in patients with intractable right temporal lobe epilepsy. Epilepsia. 2006;47(8):1397-1401. doi:10.1111/j.1528-1167.2006.00562.x
8. Nagle S, Musiek FE, Kossoff EH, Jallo G, Boatman-Reich D. Auditory processing following consecutive right temporal lobe resections: a prospective case study. J Am Acad Audiol. 2013;24(7):535-543. doi:10.3766/jaaa.24.7.2