Structural brain areas commonly affected in both subjective tinnitus and posttraumatic stress disorder are the amygdala, auditory cortex, cerebellum, dorsal cochlear nucleus, hippocampus, inferior colliculus, nucleus accumbens, prefrontal cortex, and the thalamus. This investigation compares and contrasts magnetic resonance imaging, positron emission tomography, and photon emission computed tomography findings in an attempt to discover similarities in structural brain changes for both subjective tinnitus and posttraumatic stress disorder that may lead to more effective management and therapeutic techniques for both afflictions. Speculations about ambiguous relationships between structural changes and specific symptomology are discussed along with recommendations for further research.
Tinnitus is broadly divided into either subjective or objective tinnitus. In subjective tinnitus, only the patient can hear sounds or noises, while objective tinnitus is usually due to some physical anomaly such as muscular spasms near the ear and can be heard by others. Subjective tinnitus is often experienced by individuals with posttraumatic stress disorder (PTSD), and for some sufferers the constant perception of sound is debilitating and thus far not effectively treatable (Fagelson, 2007; Mirz et al., 1999).
This paper will explore some current findings regarding subjective tinnitus in the absence of PTSD, and compare this information with similar MRI and PET imaging studies performed on individuals with PTSD in order to more fully understand structural brain changes associated with both PTSD and tinnitus.
Review of Subjective Tinnitus Symptoms
Subjective tinnitus is often referred to as a phantom sensation or auditory hallucination because sound is perceived in either one or both ears without any audible external input (Melcher et al., 2000; Mirz et al., 2000; Giraud et al., 1999; Lockwood et al., 1998). Many individuals experiencing tinnitus admit to hearing buzzing, hissing, chirping, whooshing, static as one might hear over the radio or television, or even a single tone (Giraud et al., 1999). These perceptions may be continuous or episodic, and result in varying degrees of psychological and emotional distress. About 35% of tinnitus sufferers experience significant hearing loss, and in a small percentage of individuals the affliction is severe enough to be permanently disabling (Mühlau et al., 2005; Lockwood et al., 1998).
Tinnitus may be caused by physical injury, hearing loss, disease processes, loud noises (Kaltenbach et al., 2005; Melcher et al., 2000), or as a result of ototoxicity as seen in salicylate poisoning (Guitton et al., 2003).
Review of PTSD Symptoms
PTSD is characterized by exposure to a traumatic stressor with the event(s) persistently re-experienced in some manner, psychological and emotional numbing or detachment, plus hypervigilance and exaggerated startle reflexes (American Psychiatric Association, 2000). Among the many symptoms of PTSD, the most frequently reported are depression and anxiety, suicidal ideation, feelings of unreality or detachment, and tinnitus. The occurrence of PTSD and tinnitus are remarkably similar, with each affecting nearly 10% of the American population (Fagelson, 2007).
Selected Brain Areas Involved in the Perception of Tinnitus or the Experience of PTSD
The amygdalae are ovoid-shaped bundles of neurons located on the anterior ends of the stria terminalis, somewhat underneath the thalamus and adjacent to the hippocampus in each of the temporal lobes (Diamond, 1985). They are involved primarily with maintaining protective alertness, emotional information processing, and fear conditioning (Davis&Whalen, 2001).
Several studies have confirmed increased activation of the amygdala in individuals with PTSD by using single photon emission computed tomography (SPECT), PET (positron emission tomography), and MRI (magnetic resonance imaging), while a novel experiment involving the injection of amobarbital into the anterior choroidal arteries also implicated the amygdala as a contributing factor in the perception of tinnitus (DeRidder et al., 2006; Shin et al., 2006).
The auditory cortices receive information from the cochleae and are located on the superior temporal gyrus, corresponding roughly to Brodmann’s areas 41 and 42 in each temporal lobe (Diamond et al., 1985). Cerebral blood flow studies have demonstrated increased perfusion in the auditory cortex region corresponding to BA 41 during induced episodes of tinnitus, indicating increased activity during tinnitus episodes (Mirz et al., 1999; Lockwood et al., 1998). In addition, MRI studies have revealed significant increases in the volume of auditory cortex grey matter with corresponding decreases in the white matter of children and adolescents suffering from PTSD (DeBellis et al., 2002).
Behind the pons, medulla, and midbrain of the brainstem are the two hemispheres of the cerebellum (Diamond, 1985). Among its many functions are determining the spatial origination and orientation of sound (Salmi et al., 2007). Using SPECT, PET, and MRI techniques, studies indicate an abnormal activation and increased total perfusion within the cerebellum of individuals with PTSD (Liberzon&Martis, 2006; Nutt&Malizia, 2004; Bonne et al., 2003), while tinnitus sufferers displayed abnormalities in circulatory perfusion within the cerebellum (Shulman&Strashun, 1999).
Dorsal cochlear nucleus
The dorsal cochlear nuclei (DCN) are situated on the dorsal lateral surfaces of the brainstem (Diamond, 1985) and are involved in the fine discrimination between similar sounds, particularly with regard to speech (Caspary et al., 2005). Although the dorsal cochlear nuclei have been thought of as the origin of tinnitus, Brozoski & Bauer (2005) demonstrated with rats that removal of the DCN does not diminish the perception of tinnitus, but may in fact lead to an increased perception of sound ipsilateral to the nucleus that was removed.
The hippocampi are two C-shaped structures underlying the thalamus on the terminal ends of the supracallosal gyrus in the medial temporal lobes (Diamond, 1985). They are involved with the conversion of short-term memory into long-term memory, application of stored memories to new situations, and keeping track of spatial relationships such as remembering where things are in space and time (Adams & Morrison, 2003; Dusek & Eichenbaum, 1997).
MRI studies have demonstrated significant hippocampal volume reductions with exposure to traumatic situations (Nutt & Malizia, 2004), but surprisingly the hippocampi are capable of neurogenesis with appropriate medication, such as paroxetine or phenytoin (Bremner, 2006; Eriksson et al., 1998). Investigations using PET have confirmed that tinnitus perception is in part a hippocampal phenomenon (Mirz et al., 2000; Lockwood et al., 1998). Additional studies have found that relief of both tinnitus and PTSD symptomology occurs with administration of selective serotonin reuptake inhibitors (SSRIs) like paroxetine (Fagelson, 2007).
The inferior colliculi (IC) occupy dorsal lateral positions on the midbrain just below the medial geniculate bodies of the thalamus (Diamond, 1985), and are involved with the auditory startle reflex (Wang et al., 2002), plus detection of pitch and modulation (Caspary et al., 2002).
MRI investigations with tinnitus sufferers have indicated that not only are the IC asymmetrically stimulated with the perception of sound, but that consistently the right IC receives more stimulus. The IC is also highly sensitive to salicylates and demonstrates increased activity in the presence of aspirin-containing substances (Mühlau et al., 2005; Melcher et al., 2000). Additionally, as the IC is intimately involved with auditory startle reflexes, this region may be in part responsible for some PTSD symptoms (Vinkers et al., 2007).
The accumbens nuclei are located near the caudate head and the anterior putamen on each side of the forebrain (Diamond, 1985). They secrete GABA, dopamine, and serotonin and are part of the mesolimbic dopamine reward system (Brundege & Williams, 2002). These structures are involved in the modulation, flow, and processing of auditory input, regulate emotions evoked while listening to music, and conditioned fear responses (Menon & Levitin, 2005; Schwienbacher et al., 2004).
Investigations using MRI with tinnitus patients have demonstrated a significant decrease in the amount of grey matter associated with the nucleus accumbens, indicating reduced sensory information output to the thalamus and prefrontal cortex (Mühlau et al., 2005). SPECT studies demonstrated a significant increase in blood flow to the nucleus accumbens in patients with PTSD (Liberzon et al., 1999).
The prefrontal cortices are the most anterior portions of the frontal lobes (Diamond, 1985). The regions are involved with higher executive functions such as planning, goal-setting, choice, discrimination of appropriate social behaviors, fear conditioning, and discriminatory response to auditory stimuli (Miller & Cohen, 2001).
MRI, PET, and SPECT investigations have revealed that in general, individuals with PTSD possess a smaller frontal cortex with diminished activity. However a few studies have indicated an increase in medial frontal cortex activity with highly symptomatic PTSD patients (Shin et al., 2006; Nutt & Malizia, 2005), while tinnitus sufferers appear to have an increase in right prefrontal cortex activity (Mirz et al., 2000).
The thalamus is located at the base of both cerebral hemispheres and form the greater portion of the diencephalon (Diamond, 1985). It processes and disseminates sensory input to the appropriate regions within the cerebral cortex, regulates sleep cycles (Lugaresi, 1992), arousal, awareness, and physical activity (Cain et al., 2002). Mühlau et al. (2005) found an increase in grey matter within the thalamus, possibly a result of extensive tonotopic reorganization in tinnitus sufferers (Saunders, 2007). In PTSD patients, the thalamus exhibits increased activity with MRI studies (Lanius et al., 2003).
Although there has been much research done to date concerning the causes and neural associations present in tinnitus, very little investigation has been performed regarding the etiology of tinnitus in individuals with PTSD. What little information regarding tinnitus and PTSD appears infrequently as anecdotal evidence on the Web, usually as single case descriptions or in online support group forums.
What this literature search has attempted to do is gather what unrelated research exists about tinnitus and PTSD and look for any similarities between findings. The results are intriguing, because similarities exist in virtually all of the brain structures examined. For instance, the activation of the amygdala has been directly implicated in both tinnitus and PTSD (DeRidder et al., 2006; Shin et al., 2006), while the increased perfusion of the auditory cortex evident in tinnitus (Mirz et al., 1999; Lockwood et al., 1998) may be a natural result of increased grey matter seen in PTSD (DeBellis et al., 2002). The thalamus demonstrates a similar situation, with increased grey matter in tinnitus and increased perfusion in PTSD (Saunders, 2007; Lanius et al., 2003). However, a decrease in grey matter is seen in the nucleus accumbens in tinnitus while perfusion of the structure increases with PTSD (Liberzon et al., 1999).
The cerebellum possibly reveals an analogous relationship between the abnormal perfusion evident in tinnitus (Shulman & Stashun, 1999), and hyperactivation plus increased perfusion associated with PTSD (Lieberzon & Martis, 2006; Nutt & Malizia, 2004). Additionally, studies by Bonne, et al. (2003) showed a positive correlation between the perceived severity of PTSD accompanied by depression, and demonstrable increases in cerebellar perfusion.
The hippocampus is intimately involved in the perception of tinnitus and the experience of PTSD symptoms, and reflects this relationship through significant decreases in overall volume and functionality (Nutt & Malizia, 2004; Mirz et al., 2000; Lockwood et al., 1998). Some relief for both afflictions is possible with the administration of appropriate SSRIs (Bremner, 2006; Eriksson et al., 1998).
Hypervigilance demonstrated by many individuals with PTSD may be explained in part by the inferior colliculus, although no evidence as yet exists as to the mechanism (Vinkers et al., 2007). However, an exaggerated startle reflex could be explained by the susceptibility of the IC to ototoxic substances as seen in salicylate-induced tinnitus (Mühlau et al., 2005; Melcher et al., 2000). Perhaps endogenous stress hormones present in PTSD are toxic over time, thereby
contributing to hypervigilance and increased startle reflexes.
The prefrontal and medial frontal cortices are also involved with both PTSD and tinnitus (Shin et al., 2006; Nutt & Malizia, 2005; Mirz et al., 2000), and the increase in medial and right prefrontal activity may reflect the necessity for both tinnitus and PTSD patients to exert greater focus and control over their actions and activities in order to compensate for distracting or debilitating symptoms.
Sufficient similarities appear to exist between the structural brain changes seen in both PTSD and tinnitus to warrant further investigation. In particular, the presence of stress hormones and their effects on the central nervous system need to be researched in depth. Discovering the relationships between increased grey matter, decreased functionality, and symptomology would also be of great importance as techniques to modulate functionality may result from such investigations.
Also, the possible function of the dorsal cochlear nucleus in PTSD requires investigation, as much attention has been given to this brain structure with regard to tinnitus. Brozoski & Bauer’s (2005) studies with rats and ablation of the DCN demonstrated an increase in ipsilateral tinnitus,and the same may be true of tinnitus comorbid with PTSD.
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