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Introduction Because areas of knowledge are fragmented, potentially useful information in one field may go unnoticed by researchers in other related, but non-communicating fields of study. This is especially true for medical knowledge. Swanson (1990) observed that such fields of study are noninteractive or mutually isolated. Undiscovered relationships between noninteractive bodies of literature, according to Swanson, can be exploited to generate new theories about etiology or treatment for different conditions. One of the ways in which complementary fields of literature may be linked is through the common causes of different conditions. There are many terms for hypersensitivity to sensory stimuli. Hyperesthesia (Head, 1929) and sensory defensiveness (Knickerbocker 1980) both refer to intolerance for sensory stimuli. People with hyperesthesia or sensory defensiveness may react negatively to normally benign light, sound, touch or temperature. Hyperacusis is a lowered threshold of discomfort for sounds. In photophobia, normal intensities of light are painful. This paper will describe different types of hypersensitivity to sensory stimuli. It will also describe a possible common underlying cause for some cases of this oversensitivity and investigate whether diagnostic or therapy techniques for sensory defensiveness, hyperesthesia, hyperacusis or photophobia, used with a variety of participant populations, may be useful for people with traumatic brain injury (TBI). 1 Early Descriptions of Hyperesthesia Hyperesthesia was observed by Henry Head (1929) in patients with spinal cord injuries and brain injuries. Initially, these patients showed elevated thresholds for tactile sensation. With the partial return of feeling some of these patients developed more vivid sensations of pressure, pinprick, heat and cold. Sensitivity to temperature and roughness affected eating. One participant, who suffered a stroke, said “food always seems rough and cold” on the affected side. In addition to touch and temperature, Head’s participants exhibited aversive responses to sound. Head believed that the thalamus was responsible for establishing the “feeling tone” of different sensations. Subcortical lesions disrupted connections between the thalamus and cortex. He attributed exaggerated responses to a loss of cortical control over sensory stimuli. Riddoch (1938) noted that pain from thalamic lesions was often exacerbated by loud noises and bright lights. Extremes of heat and cold also caused pain. For one of his patients cold water, applied to the affected side, produced a “shock, like electricity”. Even a drop of rain on the participant’s left hand provoked a violent reaction. Pain often radiated throughout the affected side of the patient’s body. Strong smells or tastes sometimes elicited pain, though not as often as other types of stimuli. 2 Sensory Defensiveness A. Jean Ayres (1972), citing Head’s (1929) description of hyperesthesia, used the term tactile defensiveness to describe a developmental disorder. Ayres, an occupational therapist, observed that people with congenital disorders, such as autism or mental retardation, were often tactilely defensive; they reacted negatively to light touch on their face, arms or legs. Hypersensitivity to hot or cold was also common. Because of these problems, people with tactile defensiveness avoided certain activities of daily living, such as showering, washing their face or cutting their nails (Fisher et al. 1991). Knickerbocker (1980) used the term sensory defensiveness to describe a condition in which other sensory modalities, such as audition, vision, olfaction or taste, not just touch elicited aversive reactions. Sensory defensiveness was reported among children with cerebral palsy and hemiplegia (O’Malley and Griffith, 1977) as well as people who were developmentally delayed or autistic (Barenek et al. 1997). Dunn (2001) pointed out that people who were sensitive to one type of sensory stimuli often reacted defensively to other types of input. She and other occupational therapists developed sensory integration rating scales (Dunn 2001, Brown et al. 2001). . Sensitivity to sensation was one dimension on that scale. People with autism, for example, were rated by others as having significantly different responses to touch, light sound, etc. than control participants. Dunn (2001) also advocated using her scale to study people with traumatic brain injury (TBI). 3 Miller et al (1999) measured electrodermal responses (EDR) to sensory stimuli in participants with Fragile X syndrome. EDR reflected reactions of the sympathetic nervous system (SDS) to threatening or startling stimuli. Participants with Fragile X syndrome showed significantly greater responses to olfactory, auditory, visual, tactile and vestibular stimuli than did control participants. Davies and Gavin (2007) used electroencephalography (EEG) and Event Related Potentials (ERPs) to compare the responses of children with impaired sensory processing, as classified by the Sensory Profile, motor skill assessments and clinical observations, with a control group of children who were developing typically. The authors measured participants’ responses to pairs of auditory clicks. These responses, resulting in a positive deflection on EEG 50 milliseconds post stimulus (P50), evaluated the ability of participants’ brains to filter repeated stimuli. Reduced amplitude to the second click of the P50 indicated intact sensory gating. The authors found that children with impaired sensory processing showed less sensory grating than the control group, although the differences were not statistically significant. Alexander (1987) noted that infants and children with cerebral palsy often had difficulty tolerating tactile sensation that was light, fast, and poorly graded. When applied to the face or mouth, such sensation led to defensive reactions, such as tonic bite reflex and tongue retraction. These defensive reactions hindered feeding and oral cares. Children who were hypersensitive to taste, 4 texture, smell or temperature might exhibit food or liquid selectivity (Bahr 2001), rejecting all but a few types of food. Photophobia Intolerance for light, or photophobia, may be caused by damage to the eye itself. Bacotti (2001) noted that ocular causes of photophobia included corneal scratches, cataract surgery, dry eye syndrome, glaucoma, macular degeneration and diabetes. Conditions such as migraines, tumors and intracranial hemorrhages were causes of non-ocular photophobia. Cummings et al. (1981) described a patient who exhibited intolerance to light after right occipital and thalamic infarctions. Three months after a right posterior artery occlusion, he demonstrated unusual sensitivity to bright lights. The authors described this condition as central dazzle rather than true photophobia because the patient found bright light to be merely disagreeable not painful. Hyperacusis Dubby, Sinks, and Pterein, (2000) found that people with hyperacusis perceived as painful sounds that were at a comfortable level of loudness for people with normal hearing. Marriage and Barnes (1995) differentiated between central and peripheral hyperacusis. Peripheral hyperacusis could be caused by the loss of the stapedial or acoustic reflex and was therefore associated with Bell’s palsy, Ramsey Hunt syndrome and myasthenia gravis. Sensory hearing loss with recruitment was also associated with peripheral hyperacusis. 5 Neurological conditions associated with central hyperacusis included migraine, depression, benzodiazepine dependence, pyridoxine deficiency, musicogenic epilepsy, Tay Sach’s disease, post-traumatic stress syndrome and chronic/post-viral fatigue syndrome. Tinnitus and photophobia frequently accompanied hyperacusis, further suggesting a central etiology. Similarly, Gopal et al. (2000) observed that a patient with hyperacusis also experienced hypersensitivity to touch and light. Marriage and Barnes (1995), noting that disturbed serotonin function was common to each of these neurological conditions, theorized that a serotonin deficiency was linked to hyperacusis. Hyperacusis was also found in individuals with William’s syndrome (Klein et al. 1990, Meyerson and Frank 1987, Nigam and Samuel 1994). In fact, 95% of people with Williams’s syndrome exhibited hyperacusis (Nigam and Samuel 1994). William’s syndrome is a genetic disorder characterized by infantile hypercalcemia, supralvular aortic stenosis, mental retardation and distinctive facial features (Meyerson and Frank 1987). Hypersensitivity and TBI There has been a limited amount of research concerning hypersensitivity to stimuli in persons with TBI. Bohen et al. (1991, 1992) noted that individuals who suffered post-concussive syndrome exhibited visual and acoustic hyperesthesia. Their participants reported discomfort at lower levels of luminance and sound intensity than people without brain injuries. Waddell and Gronwall (1982) also studied individuals with post-concussive syndrome. Their 6 participants were more sensitive than persons without brain injuries to light and sound. Only differences in tolerance for light, however, achieved statistical significance. Jackowski et al. (1996) described participants who complained of photophobia following TBI. Outdoor, fluorescent and bright light sources were listed as causes of discomfort. Participants also had difficulty reading due to reduced letter contrast sensitivity. Padula, Argyris and Ray (1994) listed photophobia as one of a cluster of symptoms that could affect vision after TBI. Arciniegas et al. (1999) used EEG to study P50 waveforms of evoked responses to paired auditory stimuli by three participants with TBI. All three showed reduced sensory gating for auditory stimuli. They also showed reduced concentration in noisy environments. The authors suggested that TBI, by reducing acetylcholine available to the hippocampus, might reduce sensory gating. This disruption in the ability to filter stimuli might contribute to impaired memory and attention. The Rivermead Post Concussion Symptoms Questionnaire (RPQ) included light and noise sensitivity among the symptoms measured by the scale (Potter et al. 2006). As with other post-concussive symptoms in Chan’s (2001) study, increased sensitivity to light and noise was also reported by participants without a history of brain injury. Based on his findings, Chan recommended that self-report checklists not be used exclusively to diagnose post-concussive syndrome. He advocated that self-reports of symptoms should be part of a broader assessment. 7 Fluharty and Glassman (2001) described a client with severe brain injury who reacted aversively to touch, loud noises and extremes of hot or cold. The client struck out at people who touched him unexpectedly or who made loud noises. He refused to participate in Activities of Daily Living (ADLs), such as showering or brushing his teeth, which subjected him to uncomfortable sensations. He frequently complained about the taste of foods and refused to eat many items on his tray. Gilmore et al. (2003) presented a case study of a man post severe traumatic brain injury who exhibited oral-facial hypersensitivity. The participant exhibited reduced oral movements due to abnormal tone. These problems limited oral movement and sensation. Defensive reactions to attempted oral hygiene included jaw clenching, reflex biting lip pursing and facial grimacing. Brown et al. (1992) also noted that individuals with closed head injuries (CHI) often exhibited hypersensitivity to oral and facial stimulation. They described a patient with a CHI who showed increased muscle tone when anything was placed in his mouth. He also exhibited severe dysphagia and a bite reflex. Complicating these problems was the fear and anxiety elicited by oral stimulation. The patient’s affective reaction further increased muscle tone. Not only was the client unable to eat, he could not even tolerate oral stimulation during speech therapy. 8 Habituation The descriptions of hyperesthesia, sensory defensiveness, central photophobia and hyperacusis exhibited similar features. There might be some undiscovered implicit, logical connection between the literatures and some shared condition. Habituation might provide such a connection. According to Kazdin (2000), habituation is “a decrement in response as a result of repeated stimulation”. People may be hypersensitive to sensory stimuli because they do not habituate to repeated stimuli. Since people who are hypersensitive to sensory stimuli are unable to filter the barrage of sensations from everyday life, the sensations overwhelm them. Impaired habituation has been posited as an underlying mechanism in sensory defensiveness (Reisman and Gross, 1992). Similarly, the nervous systems of people with central hyperacusis may fail to habituate to startle responses (Dubby, Sinks, and Peterein, 2000). Central hyperacusis may be linked to impaired serotonin metabolism (Phillips and Carr, 1998). According to this theory, neural systems may use serotonin to inhibit and modulate central nervous system responses to sensory input. Central auditory nuclei receive input from serotonergic systems. Implications Dunn (2001) pointed out that individuals who are sensitive to one type of sensory stimuli are often defensive toward other modalities. She developed sensory integration rating scales for both adults and children. Although 9 normative data has so far focused on the normal variation of unimpaired populations (i.e. college students and their relatives), Dunn plans to study special populations of adults, including those with traumatic brain injury. If hypersensitivity in one sensory modality increases the likelihood of hypersensitivity in other modalities, that fact would have clinical implications: professionals who see patients who are hypersensitive to one type of sensation (i.e. sound, vision, touch) might want to test or refer patients for testing and treatment for other sensory modulation problems. Audiologists studying or diagnosing people with hyperacusis might supplement tests of hyperacusis with questions about the participant’s ability to tolerate other sensory stimuli. Arani (1999) did this and found that hyperacusis was often accompanied by hypersensitivity to light, touch, balance, smell or taste. An ophthalmologist, who discovered that a patient with photophobia was also hypersensitive to sound, might refer that patient to an audiologist. Descriptive questionnaires, (Potter et al. 2006, Dunn 2001) might provide information to improve understanding of the condition or suggest compensatory techniques. Clinically, professionals who see patients hypersensitive in more than one sensory modality might want to refer the patients to others who could treat the condition affecting that modality. Neuropsychologists often must perform examinations, particularly in forensic cases, in which sensory hypersensitivities may confound test results and represent adverse co-morbid interactions that need to be understood separately and in relationship to cognitive and emotional factors. 10 Sensory hypersensitivity is cited as one among a number of physical factors including headache and other pain (especially when it becomes chronic), fatigue and sleep disturbance, sensory loss, and dizziness, related to the head but not the brain injury, which can directly or indirectly influence functional outcome (Kay et al, 1992). Even without symptoms of sensory hypersensitivity, patients frequently complain of distractibility and difficulty attending to more than one thing at a time. Treatment approaches that improve habituation for one type of disorder might improve habituation for other types of disorders. Improved habituation, in turn, might improve the ability of people with sensory disorders to integrate sensory information. Miller et al. (1999) noted higher EDR, which is increased sensitivity to sensation, among children with Fragile X syndrome in their study who were not taking medication. In this group of 25 children, 68% of the participants were receiving medications: 10 received selective serotonin reuptake inhibitors, 3 were given stimulants and 2 received anti-convulsants. The authors suggested that future research should investigate the effects of medication on responsiveness to sensory stimuli. Gopal et al. (2000) described the effects of selective serotonin reuptake inhibitors (SSRIs) on the habituation for sound of a participant with hyperacusis, depression, and hypersensitivity to touch, pressure and light. The participant, as well as her younger sister, had a history of hypersensitivity to sensory stimuli. The authors measured auditory responses, including pure-tone threshold testing, 11 uncomfortable loudness level testing and auditory brainstem responses (ABRs) in the participant. Treatment increased the participant’s ability to habituate to repeated auditory stimuli, as measured by her auditory brainstem responses (ABRs). Selective serotonin reuptake inhibitors raised the threshold for uncomfortable loudness levels, indicating greater tolerance for sound. Increased amplitudes of ABRs in the unmedicated condition may have indicated reduced habituation to sound. The participant also reported, with administration of SSRIs, increased tolerance of everyday sounds, bright lights, and touch. An earlier prescription of imipramine, a tricyclic anti-depressant had not alleviated her symptoms. In contrast, Carman (1973) found that the mood of individuals with both hyperacusis and depression improved following treatment with imipramine. This group showed greater improvement in affect than did the auditory-normal group of depressed patients. The author hypothesized that both hyperacusis and depression were symptoms of central serotoninergic hypoactivity in this subgroup of patients. He did not report whether hyperacusis improved with drug treatment. Cummings and Gittinger (1981) found that drug treatment with amitriptyline hydrochloride, a tricyclic antidepressant, and perphanazine, a tranquilizer, reduced their patient’s sensitivity to light. The patient had right occipital and thalamic infarctions. Sensitivity to light diminished with initial drug treatment but then returned when this treatment was discontinued due to acute urinary retention. Following transurethral prostatectomy for benign prostatic 12 hypertrophy, drug therapy was reinstituted and the patient’s sensitivity to light diminished again. Arciniegas et al. (1999) suggested that cholinergic medications might improve sensory gating for persons with TBI. In additions, such drugs might improve attention and memory. The authors point out that studies need to be conducted to determine whether drugs that augment cholinergic function, such as donepezil, improve sensory and cognitive function in TBI. They suggest that EEG studies might provide a marker of sensory gating for this population. Ayres (1972) recommended giving people with tactile defensiveness a diet of sensory stimulation. This diet was designed to stimulate participants’ higher cortical centers, thereby helping them integrate threatening tactile input with knowledge about the situation as well as other sensations. This integration, in turn, would let participants recognize the seemingly threatening input as harmless. Occupational therapists have observed beneficial effects with sensory integration treatment. Deep pressure, designed to facilitate habituation, increased participants’ tolerance for other types of stimuli. Studies of sensory integration techniques have reported generalized improvements in the sensory modulation abilities of an adult (Reisman and Gross 1992) and children (Miller, Coll, and Schoen, 2007, Stagnitti, Raison and Ryan, 1999). Alexander (1987) reported that deep pressure, applied to the sides and biting surfaces of the gums and teeth may reduce tonic biting reflex for children with cerebral palsy. Gilmore et al. (2003) described a desensitization program 13 for a client with oral-facial hypersensitivity following traumatic brain injury. Touch was first applied distally, on the participant’s hands and shoulders with the therapist’s hands. Desensitization then progressed to neck, forehead, head and the area around the mouth. As the client tolerated tactile input, the therapist moved proximally. Stimulation within the mouth, of the teeth, palate and tongue, was provided by an oral sponge, toothbrush or electric toothbrush. The authors found that a 2 week desensitization program reduced defensive reactions, including a bite reflex. These changes allowed the client to participate in oral hygiene and eat yogurt or thickened liquids. Brown et al. (1992) described a systematic desensitization program in which a psychologist helped a patient establish a hierarchy of potentially threatening types of oral stimulation. The patient began by imagining situations about which he was slightly fearful, such as a nurse bringing him food. While relaxed, he alternated between thinking about neutral situations and ones about which he was anxious. Using this procedure, he was able remain relaxed while imagining more extreme scenarios, such as a tongue blade touching the back of his mouth or a choking episode. This program, combined with oral stimulation by a speech-language pathologist, helped the patient tolerate oral feeding. Bahr (2001) presented a similar desensitization program for reducing oral hypersensitivity for children and adults with impaired sensory integration, including people with traumatic brain injury. She described an oral massage sequence that, like Gilmore’s (2003), proceeded from distal to proximal structures. Bahr (2001) suggested using oral massage (Nuk) brushes or oral 14 sponges to provide deep pressure to the oral structures. These structures included the lips, gums, teeth, hard palate and tongue as well as the inner portion of the cheeks. Bahr (2001) also described a protocol for increasing food tolerance for clients with food and liquid selectivity. Therapists would note which foods were accepted or rejected by clients. They would also note the temperature, taste, temperature and smell of foods which the client tolerated. This data would be used to generate lists of new foods to try. Starting with foods possessing qualities acceptable to the client, the therapist would gradually introduce the client to a greater variety of foods. Tinted lenses, prescribed by ophthalmologists, may help people with photophobia cope with hypersensitivity to light. Jackowski et al (1996) found that light filtering lenses improved by 39% the reading rate of participants with traumatic brain injury and photophobia. The reading rate of participants without brain injury was unaffected by the lenses. Another approach to ameliorating the effects of inability to tolerate sensations is to modify the environment to reduce the frequency and intensity of aversive stimuli. In Fluharty and Glassman’s (2001) case study of an adult with a traumatic brain injury, intolerance for touch and noise was minimized by changing his daily routines. Resistance to bathing, for example, was improved by having the client take baths instead of showers. The fact that taking a bath did not involve pinprick sensations with extremes of hot or cold temperature 15 made it less offensive to the client than showering. Providing distraction in the presence of loud noises made them less likely to elicit aggressive responses. Meyerson and Frank (1987) described a desensitization program for a client with William’s syndrome. Tape recording aversive sounds, then playing them back with gradually increasing loudness, increased a client’s ability to tolerate them. A similar approach could be used for clients with traumatic brain injury. Jastreboff and Jastreboff (2000) described a program, Tinnitus Retraining Therapy (TRT), to ameliorate hyperacusis and tinnitus. Their program included the use of sound generators to facilitate habituation. Sound levels were initially set near the threshold of hearing then gradually increased. The authors also emphasized the importance of avoiding the overuse of ear protection: reducing auditory input increased the hyper-sensitivity of the auditory system. In fact, gradually enriching the sound environment of individuals with hyperacusis helped them tolerate sound. One of the benefits of exploring complementary literatures is that it generates testable hypotheses. Among the theories for people with TBI generated by comparing literatures of sensation are the following: 1. Hypersensitivity to sensation, as measured by rating scales, will correlate with measures, such as, Galvanic Skin Response or Evoked Potentials. 16 2. Threshold of discomfort tests such as those employed by Bohnen et al. (1991) will also correlate with rating scales and with other instrumental measures. 3. Intolerance for one type of sensation, if caused by central nervous system damage, will increase the likelihood that hypersensitivity to other types of sensory stimuli will be present. 4. Treatments designed to increase habituation will ameliorate sensory hypersensitivity. These might include drug treatments, such as the use of SSRIs or cholinergic medications, or behavioral approaches. It should be emphasized that the above are hypothesis and await further experimental evidence. Much of the research regarding hypersensitivity to sensory stimuli has focused on populations with specific types of hypersensitivity among people with diverse etiologies. Additional research is needed on the incidence of hypersensitivity among people with TBI. It would also be helpful to study sensory disorders longitudinally to determine if they change as the severity of participants’ other deficits lessen. At the present time, client reports of photophobia or hyperacusis are frequently attributed to desire for compensation or pre-injury adjustment issues (Lishman, 1988). Instrumental or psychophysical measures might help resolve controversies surrounding forensic aspects of hypersensitivity. Data from instrumental tests might complement participants’ reports of symptoms. Different types of assessments, such as symptom questionnaires, behavioral observations, physiological and threshold of discomfort tests might provide 17 complementary windows into hyperesthesia. Using a variety of measures to assess sensation could result in a better understanding of hyperesthesia in traumatic brain injury. 18