BRAIN STEM AUDITORY AGNOSIA: AUDITORY CORTEX ACTIVATED TDCS

✓ Auditory hallucinations were produced by electrical stimulation of the human upper brain stem during stereotaxic operations. The responses were confined to stimulation of the inferior colliculus, brachium of the inferior colliculus, medial geniculate body, and auditory radiations. Anatomical confirmation of an auditory site was obtained in one patient. The hallucination produced was a low-pitched nonspecific auditory “paresthesia” independent of the structure stimulated, the conditions of stimulation, or sonotopic factors. The effect was identical to that reported from stimulating the primary auditory cortex, and virtually all responses were contralateral. These observations have led to the following generalizations concerning electrical stimulation of the somesthetic, auditory, vestibular, and visual pathways within the human brain stem: the hallucination induced in each is the response to comparable conditions of stimulation, is nonspecific, independent of stimulation site, confined to the primary pathway concerned, chiefly contralateral, and identical to that induced by stimulating the corresponding primary auditory cortex. No sensory responses are found in the brain stem corresponding to those from the sensory association cortex.

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Effects of unilateral lesions of auditory cortex on brain stem thresholds for electrical stimulation

Experimental Neurology ◽

10.1016/0014-4886(79)90038-4 ◽

1979 ◽

Vol 65 (3) ◽

pp. 489-497

Author(s):

George M. Gerken

Keyword(s):

Electrical Stimulation ◽

Auditory Cortex ◽

Brain Stem

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Neuromodulation of Right Auditory Cortex Selectively Increases Activation in Speech-Related Brain Areas in Brainstem Auditory Agnosia

Cognitive and Behavioral Neurology ◽

10.1097/wnn.0000000000000162 ◽

2018 ◽

Vol 31 (3) ◽

pp. 151-155 ◽

Cited By ~ 2

Author(s):

Patricia E.G. Bestelmeyer ◽

Nick J. Davis ◽

Oren Poliva ◽

Robert D. Rafal

Keyword(s):

Auditory Cortex ◽

Brain Areas ◽

Auditory Agnosia

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The projection of the auditory cortex upon the diencephalon and brain stem in the cat

Brain Research ◽

10.1016/0006-8993(69)90160-7 ◽

1969 ◽

Vol 15 (2) ◽

pp. 305-340 ◽

Cited By ~ 252

Author(s):

I.T. Diamond ◽

E.G. Jones ◽

T.P.S. Powell

Keyword(s):

Auditory Cortex ◽

Brain Stem

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Simultaneous auditory agnosia: Systematic description of a new type of auditory segregation deficit following a right hemisphere lesion

10.1101/2020.02.27.968107 ◽

2020 ◽

Author(s):

Emma Holmes ◽

Nattawan Utoomprurkporn ◽

Chandrashekar Hoskote ◽

Jason D. Warren ◽

Doris-Eva Bamiou ◽

...

Keyword(s):

Auditory Cortex ◽

Young Patient ◽

Right Hemisphere ◽

Causal Explanation ◽

Primary Auditory Cortex ◽

List Type ◽

Cochlear Function ◽

Speech In Noise ◽

Auditory Agnosia ◽

Music Streaming

AbstractWe investigated auditory processing in a young patient who experienced a single embolus causing an infarct in the right middle cerebral artery territory. This lead to damage to auditory cortex including planum temporale that spared medial Heschl’s gyrus, and included damage to the posterior insula and inferior parietal lobule. She first reported difficulty hearing all sounds, which fully recovered within days, but she subsequently reported chronic difficulties with segregating speech from noise and segregating elements of music. Clinical tests showed no evidence for abnormal cochlear function. Follow-up tests confirmed difficulties with auditory segregation in her left ear that spanned multiple domains, including speech-in-noise and music streaming. Testing with a stochastic figure-ground task—a way of estimating generic acoustic foreground and background segregation—demonstrated that this was also abnormal. This is the first demonstration of an acquired deficit in the segregation of complex acoustic patterns due to cortical damage, which we argue is a causal explanation for the symptomatic deficits in the segregation of speech and music. These symptoms are analogous to the visual symptom of simultaneous agnosia. Consistent with functional imaging studies on normal listeners, the work implicates non-primary auditory cortex. Further, the work demonstrates a (partial) lateralisation of the necessary anatomical substrate for segregation that has not been previously highlighted.HighlightsRare case of auditory agnosia in a young patient with a right-hemisphere infarctDamage affecting non-primary auditory cortex, but sparing primary auditory cortexGeneralised auditory segregation deficit, revealed by auditory figure-ground taskThis explains segregation deficits for speech-in-noise and music streamingThe deficit affects stimuli presented on the left

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Permeability of the microcirculation in area postrema of rat

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100103802 ◽

1988 ◽

Vol 46 ◽

pp. 348-349

Author(s):

Shams M. Ghoneim ◽

Frank M. Faraci ◽

Gary L. Baumbach

Keyword(s):

Brain Stem ◽

Area Postrema ◽

Upper Body ◽

Sprague Dawley ◽

Sodium Cacodylate ◽

Acute Hypertension ◽

Sprague Dawley Rats ◽

Ultrastructural Characteristics ◽

The Brain ◽

Adjacent Brain

The area postrema is a circumventricular organ in the brain stem and is one of the regions in the brain that lacks a fully functional blood-brain barrier. Recently, we found that disruption of the microcirculation during acute hypertension is greater in area postrema than in the adjacent brain stem. In contrast, hyperosmolar disruption of the microcirculation is greater in brain stem. The objective of this study was to compare ultrastructural characteristics of the microcirculation in area postrema and adjacent brain stem.We studied 5 Sprague-Dawley rats. Horseradish peroxidase was injected intravenously and allowed to circulate for 1, 5 or 15 minutes. Following perfusion of the upper body with 2.25% glutaraldehyde in 0.1 M sodium cacodylate, the brain stem was removed, embedded in agar, and chopped into 50-70 μm sections with a TC-Sorvall tissue chopper. Sections of brain stem were incubated for 1 hour in a solution of 3,3' diaminobenzidine tetrahydrochloride (0.05%) in 0.05M Tris buffer with 1% H2O2.

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