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Table of Contents    
Year : 2018  |  Volume : 66  |  Issue : 6  |  Page : 1815-1817

Thalamic hypophonia and the neural control of phonation

Department of Neurological Sciences, Christian Medical College, Vellore, Tamil Nadu, India

Date of Web Publication28-Nov-2018

Correspondence Address:
Dr. Appaswamy T Prabhakar
Department of Neurological Sciences, Christian Medical College, Vellore - 632 004, Tamil Nadu
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.246247

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How to cite this article:
Prabhakar AT, Shaikh AI, Vijayaraghavan A, Rynjah G. Thalamic hypophonia and the neural control of phonation. Neurol India 2018;66:1815-7

How to cite this URL:
Prabhakar AT, Shaikh AI, Vijayaraghavan A, Rynjah G. Thalamic hypophonia and the neural control of phonation. Neurol India [serial online] 2018 [cited 2022 May 26];66:1815-7. Available from: https://www.neurologyindia.com/text.asp?2018/66/6/1815/246247


Hypophonia is the reduction in speech volume and is an uncommon finding in stroke. We report a 55-year old man who presented with hypophonia following a left thalamic hemorrhage. Ventral thalamus is an important node in the neural control of phonation, and lesions in this location can result in hypophonia.

Hypophonia is the reduction in speech volume and is commonly seen in Parkinson's disease and in local pathologies that affect the recurrent laryngeal nerve or vocal cord.[1] It has also been rarely described in vascular lesions of the thalamus.[2],[3] We describe a case of hypophonia secondary to a left thalamic hemorrhage and review the neural control of phonation.

A 55-year old, right-handed man, with a history of hypertension, a past history of right hemiparesis and occasional alcohol use, presented with altered behavior and right hemiparesis. His relatives had found him difficult to awaken one morning and hence took him to a local hospital. In the hospital, he was found to have right hemiparesis and the computed tomographic (CT) scan of the brain done on Day 1 showed a left anterior thalamic hemorrhage. He was found to be excessively drowsy over the next few days, until the time of discharge 1 week later. His right hemiparesis improved over 1 month and he became fully awake and alert. Following this, he had speaking difficulty and memory problems. Although he was able to understand spoken speech and write normally, his voice had become soft. It was as if he was whispering all the time. He was managed with supportive treatment and blood pressure control. On a follow-up visit after 10 months, he was found to have persistence of his soft voice and whispering speech with occasional memory problems. His neurological examination at this point revealed the patient to be conscious and cooperative. He was oriented to time, place, and person. His forward digit span was normal; he was able to recall two of three words at 5 and 10 min, respectively. On assessing his speech and language, he was found to have a hypophonic speech, which was hardly audible and was associated with loss of prosody. His language comprehension and repetition were normal. His fluency was normal despite his soft voice. He scored normal in the category and phonemic fluency tests. There were no paraphasias or stuttering noted. Though his handwriting had changed from before, he was able to write without errors and had no difficulty in reading. His cranial nerve examination was normal except for a supranuclear type of up-gaze restriction and left mimetic facial palsy. Motor and sensory examinations were normal. He had no cerebellar signs. His gait was normal. MRI revealed features of an old ventral thalamic hemorrhage. Otorhinolaryngologic examination ruled out a recurrent laryngeal nerve and vocal cord pathology. Hypophonia following the left thalamic lesion was considered and the patient was initiated on speech therapy. He had mild symptomatic improvement on the follow-up visit after 2 months.

Phonation or vocalization is a critical component in the process of human speech production. Phonation requires a stream of air from the lungs to be forced through the closed glottis causing oscillation of the vocal cords. The sound waves thus produced by the oscillation of the vocal cords travel up through the larynx, pharynx, nasal cavity, and mouth where they undergo further modulation.[4] All vowels and most consonants require phonation to be spoken.[4] Vocalization is a highly specialized function both in humans and animals and it is known to provide an evolutionary advantage for demonstrating dominance and in making mate choices.[5] There are two hierarchically organized networks that are known to control vocalization [Figure 1].[6] One is the sensorimotor cortical system that supports the production of learned vocalizations such as speech, and the other is the limbic motor system that controls innate vocalizations.[6]
Figure 1: Schematic illustration of the networks involved in phonation. The boxes in blue connected by the blue solid line represent the sensorimotor cortical pathway with its two feedback loops which is responsible for learnt vocalisations. The red boxes connected by the red dotted lines represent the limbic pathway which controls innate vocalizations. The green boxes are the secondary association areas involved in phonation. The yellow boxes represent the common pathway where the sensory-motor and the limbic pathways converge

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The sensorimotor cortical pathway runs from the motor cortex via the reticular formation to the phonatory motor neurons. This circuit includes two feedback loops. One of the feedback loops projects from the motor cortex to the ventral thalamus via the putamen and then back to the motor cortex.[6] The second feedback loop projects to the pontine nuclei, the cerebellum, and via the ventral thalamus back to the cortex.[6] Based on human functional (f)-MRI studies, the cortical areas identified in the voice network are the larynx motor cortex, associated premotor cortex, supplementary motor area (SMA), the primary auditory area, and the auditory association cortex of the posterior superior temporal gyrus (STG).[7]

The limbic pathway for innate vocalization projects from the anterior cingulate cortex to the periaqueductal gray (PAG) and via the pontine and medullary reticular formation to the phonatory motoneurons.[6] Animal studies have demonstrated that stimulation of lateral and ventrolateral columns in the PAG results in complex vocalizations, and lesions of PAG can results in mutism.[8] PAG is also known to integrate the expiratory and laryngeal activity required for the generation of vocalization.[8] Even though there are two separate networks that control phonation, there is interaction between the two as there is convergence of both these networks at the level of the reticular formation.[6]

In our patient, we postulate that the hypophonia was likely due to the disruption of the feedback loops of the voice network at the level of ventral thalamus. Hypophonia has been previously described in vascular lesions of the thalamus, including infarcts, hemorrhage, and cerebral deep venous occlusion.[3],[9],[10],[11] Disruption of the thalamo-cortical loops due to the degeneration of nigro-striatal projections to the ventral thalamus may be the reason why patients with Parkinson's disease have hypophonia as a common feature.[1],[12],[13]

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  References Top

Liotti M, Ramig LO, Vogel D, New P, Cook CI, Ingham RJ, et al. Hypophonia in Parkinson's disease: Neural correlates of voice treatment revealed by PET. Neurology 2003;60:432-40.  Back to cited text no. 1
Kumral E, Kocaer T, Ertübey NO, Kumral K. Thalamic hemorrhage. A prospective study of 100 patients. Stroke 1995;26:964-70.  Back to cited text no. 2
Blacker DJ. Softly spoken strokes: Two patients with marked hypophonia as a feature of strokes involving the anterior thalamus. J Clin Neurosci 2003;10:243-5.  Back to cited text no. 3
Pisanski K, Cartei V, McGettigan C, Raine J, Reby D. Voice modulation: A window into the origins of human vocal control? Trends Cogn Sci 2016;20:304-18.  Back to cited text no. 4
Puts DA, Jones BC, DeBruine LM. Sexual selection on human faces and voices. J Sex Res 2012;49:227-43.  Back to cited text no. 5
Jürgens U. The neural control of vocalization in mammals: A review. J Voice 2009;23:1-10.  Back to cited text no. 6
Brown S, Laird AR, Pfordresher PQ, Thelen SM, Turkeltaub P, Liotti M. The somatotopy of speech: Phonation and articulation in the human motor cortex. Brain Cogn 2009;70:31-41.  Back to cited text no. 7
Benarroch EE. Periaqueductal gray: An interface for behavioral control. Neurology 2012;78:210-7.  Back to cited text no. 8
Koutsouraki E, Xiromerisiou G, Costa V, Baloyannis S. Acute bilateral thalamic infarction as a cause of acute dementia and hypophonia after occlusion of the artery of Percheron. J Neurol Sci 2009;283:175-7.  Back to cited text no. 9
Murray BJ, Llinas R, Caplan LR, Scammell T, Pascual-Leone A. Cerebral deep venous thrombosis presenting as acute micrographia and hypophonia. Neurology 2000;54:751-3.  Back to cited text no. 10
Rodríguez-López C, Ayuso García B, Moreno García S. Hypophonia as a sign of thalamus lesion: A case report. Int J Neurosci 2017;128:100-1.  Back to cited text no. 11
Moretti R, Caruso P, Crisman E, Gazzin S. Thalamus and Language: What do we know from vascular and degenerative pathologies. Neurol India 2018;66:772-8.  Back to cited text no. 12
[PUBMED]  [Full text]  
New AB, Robin DA, Parkinson AL, Eickhoff CR, Reetz K, Hoffstaedter F, et al. The intrinsic resting state voice network in Parkinson's disease. Hum Brain Mapp 2015;36:1951-62.  Back to cited text no. 13


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This article has been cited by
1 Subcortical Aphasia
Marcia Radanovic, Victor N Almeida
Current Neurology and Neuroscience Reports. 2021; 21(12)
[Pubmed] | [DOI]


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