Chronic Facial Pain in a 24-Year-Old University Student


9

Chronic Facial Pain in a 24-Year-Old University Student


Touch-Based Therapy Accessed via Auditory Pathways



G. Lorimer Moseley, Mark A. Jones



Interview


Tina was a 24-year-old right-handed female university student who presented along with her father. Tina reported a 9-year history of unilateral face pain, triggered by being hit on the side of the face with a softball. She presented for treatment of her face pain because it was greatly limiting her quality of life. She lived with her parents and a younger brother, who together provided substantial physical and emotional support. Her parents were both medical practitioners. Her mother worked full time as a rheumatologist, and her father worked as a general practitioner (GP), having reduced his hours in order to provide Tina with the help she needed. Tina was undertaking an architecture degree on a 0.25 normal load, such that she was currently in the second year of her degree, although she had been enrolled for 5 years.


Tina was about 160 cm tall and of slight build. The left side of her face was red and scattered with approximately 35 small vesicles.



Current Symptoms


Tina’s pain covered much of the left side of her face, sparing her lips (Fig. 9.1). It was clearly delineated along the midline of her face, with the right side of her face being completely pain-free. She described the pain as ‘burning’, ‘tender’, ‘sensitive’ and ‘stinging’. She described pain at rest that was present all the time, although it varied from tolerable to unbearable. She described no pain on the inside of her mouth, ear, jaw, teeth, temporomandibular joint or neck. On further questioning, Tina reported no headaches but occasional migraines (approximately once a year) that seemed random and without a trigger and which would ‘run their course’ – head pain with aura and photosensitivity for a few hours, sleep for 12–15 hours and ‘groggy’ the next day. She reported no neck stiffness, no episodes of dizziness and no visual disturbances, with the exception of a watery left eye. She reported no noticeable symptoms elsewhere. On further questioning, she reported occasional pins and needles in a glove distribution around her thumb and on the pad of her index finger. She did not notice a pattern in this that related to her face symptoms.


image

Fig. 9.1 Tina’s body chart. TMJ, temporomandibular joint.

Tina reported that touching her face was unbearable, wearing glasses was unbearable and having anything go near her face was almost unbearable. She reported that nothing eased her pain except sleeping. She had devised a method to ensure she slept on her right side. She slept 7–8 hours per night and woke without an alarm. Her pain tended to get slowly worse over the course of the day. She had not noticed any other cyclical pattern in her pain (weekly, menstrual cycle, seasonal).


On further questioning, Tina reported the following:




History


All history was conveyed by Tina or her father. As a 15-year-old, Tina was waiting for her turn to bat in a softball game. She remembers that she was very anxious at the time, but she was reluctant to describe why. The injury day was a warm day in spring, and she reported suffering from some significant hay fever at the time. She was hit in the side of the face with a softball that had been hit out of the field of play. She remembered experiencing immediate stinging pain, and she sustained a small cut on the side of her face. The small scar was visible on her cheekbone about 2 cm anterior to her left ear. Over the next few days, the pain remained constant and confined to her left cheek. A bruise emerged, and Tina’s father remembered it spreading across much of the side of her face.


Tina did not use any analgesics but did take a few days off school and ‘took it easy’. About 4 days after the incident, she was scratched by her cat at the wound site, and the wound was reopened. She remembers immediate pain across the left side of her face at that time. The wound became infected, and Tina was placed on broad-range oral antibiotics prescribed by her father. The pain increased noticeably over the week after the cat scratch and did not resolve in line with the resolution of the infection.


The pain remained reasonably constant from that time until now. The following responses outline the consistency of her pain over the previous 9 years:




Previous Assessments


Tina had been cleared of the following: trigeminal neuralgia (neurological assessment), psoriasis, psoriatic arthritis (rheumatological assessment), Bell’s palsy (neurological assessment) and temporomandibular joint injury or dysfunction (magnetic resonance imaging [MRI]; specialist physiotherapy assessment). Tina had undergone upper limb nerve conduction studies, x-ray, computed tomography (CT) scan, MRI scan and bone scan, each with no abnormalities detected.



Previous Treatments


Tina had undergone pharmacological interventions (opioids, gabapentin [nerve membrane stabilizer often called an ‘antiepileptic’ and often prescribed for peripheral neuropathic pain], non-steroidal anti-inflammatory drugs [NSAIDs], steroids), psychological interventions (hypnosis, meditation, cognitive-behavioural therapy, psychotherapy), a multidisciplinary pain management program, physiotherapy (temporomandibular joint manual therapy, biofeedback training, cervical spine manual therapy, cervical spine specific muscle training), acupuncture, homeopathy and craniosacral therapy. Reports from all physiotherapists who had seen her and her treating GP (not her father) were available. She described some pain relief with opioids and gabapentin, but both were intolerable because of side effects. She described no response to NSAIDs and an initial reduction in pain in response to steroids. That pain relief lasted about 3 months. She described no response to subsequent courses of steroids.


She described some help from learning to meditate and perform self-hypnosis and that she still used those techniques about once a day. She described no help from the multidisciplinary pain management program and that she found the program ‘insulting’ because they thought she was ‘making it up’. She felt that she was worsened by the physiotherapy, particularly the muscle training (which she also found confusing because she did not have neck pain) and jaw mobilizations (which she indicated were painful because of the physiotherapist’s hands on her face), and craniosacral therapy. She had been offered surgical intervention, but her mother had excluded that approach on the grounds that there was no evidence of nerve conduction compromise. This view was based on the lack of paraesthesia. No nerve conduction studies or electromyography of the face had been undertaken.



Impact of Pain on Her Life


Tina reported that her pain had had a huge impact on her life. She reported that it prevented her from attending most of her classes at school, and she attributed a low school-leaving mark to this (although note that she gained entry to a very competitive university degree). She reported that her pain prevented her from socializing because she could not bear having people or noise on her left.


She reported that her pain prevented her from wearing glasses, which made going out in the sun unpleasant. She could not wear a hat. Her left eye was often ‘scratchy’, sometimes watery, and she tended to squint. She reported being very self-conscious of the appearance of her face. Her pain did not prevent her from talking or eating or performing the requirements of daily living, as long as she could do them ‘at her own pace’.


She described herself as being ‘a bit depressed’ and ‘quite anxious’. She reported that previous formal assessments of both using standardized questionnaires (results not available to me) suggested that she had ‘moderate depression’ and ‘mild anxiety’. She reported that her depression was completely due to her face pain and that it has probably made her more anxious as well.


On further questioning, Tina reported that she found noises on her left to be bothersome and difficult to listen to. Her father reported that the family had learnt to talk to Tina from her right side because she found it difficult when they talked to her from her left.


When asked, ‘What do you think is causing this?’, Tina stated that she did not know but that something had ruined the blood and nerve supply to her face and that, presumably, the softball and wound problem damaged these nerves. When asked, ‘How do you think this will progress from here?’ she reported that she was not at all confident. I asked her father the same questions, and his responses were nearly identical.



General Health


Tina reported that her general health was good. She walked at a moderate pace for 30 minutes a day. GP reports indicated no health comorbidities and no medications over time other than those listed by Tina. All screening questions regarding ‘red flags’ or potential indicators of more serious or sinister pathology (e.g. night pain, weight loss, constitutional symptoms, etc.) were negative.



Reasoning Question:



  1. 1. Based on the information obtained through your interview, what were your hypotheses regarding the dominant ‘pain type’ (i.e. nociceptive, peripheral neuropathic, nociplastic)?

Answer to Reasoning Question:


My hypothesis was that Tina’s pain was being driven largely by a combination of enhanced efficacy of cortical networks that subserved her face pain and a loss of normal intracortical inhibitory drive. Of the choices you have given, my hypothesized mechanism most closely resembled nociplastic pain. That auditory stimuli seemed to modulate her symptoms offered corroboratory evidence of sensitivity and discriminative problems upstream of the somatosensory pathways. That said, I also thought that there might be primary nociceptive contributions but that it might be endogenously driven.


Reasoning Question:



  1. 2. If a nociceptive component were present, what potential ‘sources of symptoms’ (nociception) did you consider may be involved?

Answer to Reasoning Question:


I thought that the appearance of her face was consistent with peptidergic inflammation – vasodilation and vesicles not unlike those one sees in association with shingles. Peptidergic inflammation refers to inflammation at the terminals of nociceptors that is driven by the release of peptides from those nociceptors. This release can occur when the nociceptor is activated distally (action potentials propagate to other branches of the nociceptor) or proximally (action potentials propagate from the dorsal horn or dorsal root ganglion). In both cases, the action potentials cause the release of peptides at the terminals, and these peptides cause inflammation. My hypothesis was that this was most likely to be driven by descending facilitation because other potential drivers had been excluded by tests or had been unresponsive to therapies that I would expect to successfully modulate a primary nociceptive driver.


Reasoning Question:



  1. 3. Please discuss any potential ‘contributing factors’ (intrinsic or extrinsic) you hypothesized may have either predisposed to the onset of Tina’s persistent pain or contributed to its maintenance.

Answer to Reasoning Question:


It is difficult to identify clear contributing factors, but the following candidate mechanisms emerged from the history:



  1. 1. Pro-inflammatory state: Tina reported being an asthmatic and suffering from hay fever. She describes a highly inflammatory response to the initial injuries. She reports 3 months of reduced pain after the first course of steroids. The pattern of spread and presenting condition appeared highly consistent with peptidergic inflammation and loss of intracortical inhibition, itself most probably associated with intracortical inflammatory mechanisms (although this is still open to conjecture). That she reported symptoms in a non-dermatomal distribution on her ipsilateral thumb and index finger implicates primary sensory cortex involvement. All of these hypotheses are to some extent speculative.
  2. 2. Mood contributors: She reported being highly anxious at the time of the injury but did not expand on the reasons for that. I would hypothesize that this would put her in a ‘high-threat state’, itself more likely to be associated with inflammatory load and heightened activation of other protective systems. I would hypothesize that these contributors put her at elevated risk of a ‘hyper-protective response’. She also reported being depressed and anxious at presentation. Both are likely to be associated with a more pro-inflammatory and hyper-protective state.
  3. 3. Cognitive contributors: Tina reported that she believed that the nerves and blood supply to her face were ‘ruined’. She reported that the initial injury damaged her facial nerves. She reported attributing the several unmet expectations (e.g. a good school-leaving mark) to ‘the injury’. She reported attributing several disadvantages in life (e.g. going out in the sun) to ‘the injury’.

Clinical Reasoning Commentary:


As discussed in Chapters 1 and 2, ‘pain type’ and the neurobiological mechanisms underpinning Tina’s symptoms cannot be directly measured clinically (although they can be inferred) and therefore need to be hypothesized. Clinically, such hypotheses should be linked to features in the patient’s presentation, for example, as offered here, that Tina’s symptoms were modulated by auditory stimuli. The presence of primary nociceptive contributions is not dismissed but, if present, is hypothesized to be centrally driven.


Although the three broad categories of ‘pain type’ referred to in the Reasoning Question seem to have clinical utility (although unproven) with respect to implications to other hypothesis categories, including ‘precautions and contraindications to physical examination and treatment’, ‘management and treatment’ and ‘prognosis’, it must be acknowledged that this categorization is a simplistic characterization of more complex neurobiological mechanisms (see Chapter 2). However, as discussed in Chapter 1, the proposed hypothesis categories should not be taken as fixed constructs; rather, they simply reflect contemporary categories of clinical judgements to consider that can assist musculoskeletal clinicians to think about their reasoning. They have evolved considerably since their inception and must continue to evolve with the evolution of our understandings, with the overall aim of assisting recognition of relevant aspects to patients’ clinical presentations that are used to guide safe and effective management.


A range of potential contributing factors should be considered, including systemic factors (e.g. asthmatic and suffering from hay fever), emotional factors (e.g. anxiety) and numerous manifestations of cognitive factors (e.g. beliefs regarding nerve injury and ruined blood supply to face, negative self-concept, negative attribution that school-leaving mark is linked to injury and negative perceptions of participation restrictions, such as going out in the sun). As discussed in Chapters 1 and 4, it can be useful when listening for and explicitly screening for potential contributing factors to conceptualize them as intrinsic (physical, psychological, behavioural and hereditary) or extrinsic (environmental, social, cultural, etc.). As highlighted in this Clinical Reasoning Answer, it is often difficult to know with certainty whether or not potential contributing factors identified in the patient’s story (and later, the physical examination) are in fact relevant to the patient’s development and/or maintenance of the patient’s symptoms and disability. Nevertheless, it is important to hypothesize about potential contributing factors that inform other areas of reasoning, particularly ‘prognosis’ and ‘management’. The number of factors contributing to the onset and/or maintenance of symptoms and disability, the length of time they have been present and whether they can be modified combine to influence prognosis. Management almost always needs to target contributing factors for the broader aim of minimizing recurrence and future disability.



Examination


As we spoke, Tina held her head in left rotation. If I moved to Tina’s left, she too would move further, as though always ‘shielding’ the left side of her face from me or attempting to listen with her right ear. Her left eye would squint a little when she described the initial injury and subsequent infection or when she described aggravating activities and the nature of her pain. She did not seem to have a ptosis or any demonstrable palsy.


Tina would not allow me to touch her face. On closing her eyes, she reported an increase in warmth and pain when she placed her hand near her face, and the same thing happened whether it was her own hand or mine.


Movements of the mouth (opening, clenching, lateral deviations) or head and neck (flexion, extension, rotation, lateral flexion) did not modulate her pain, with the exception of a slight aggravation when she raised her eyebrows as high as she could and a clear aggravation in full right-side flexion that caused a puckering of the skin around some sores.


She had noticeably poor fine motor control of the left hand when her hand was situated near her face. On questioning at this time, she reported that she was a ‘touch-typer’ but had not noticed any problems with accuracy typing with either hand.


On sitting at a computer mimicking university work, she would hold her head in approximately 35 degrees left rotation. She did not think this was the case (i.e. she felt like she was facing the midline) until her true posture was revealed via a webcam. She was able to immediately correct her posture but returned to the default 35-degree posture as soon as I asked her another question or distracted her from the task in any way.



Further Assessments


Questionnaires



  • Patient-specific functional scale (PSFS) (Chatman et al., 1997). The patient selects four tasks or activities she can’t do now because of pain but would like to (i.e. is closely tied to short- and long-term goals). The patient then rates her ability to perform those tasks on a scale of 0–10. Final score = average of four measures. Tina selected the following tasks: computer-based university work; going out with friends; lying on her left side; wearing sunglasses. She scored 0.7 on the PSFS, indicating that she was not able to perform her desired activities.
  • Pain Catastrophising Scale (PCS) (Sullivan et al., 1995). This is a 13-item questionnaire. The scoring range is 0–42, with 42 indicating very catastrophic thoughts and beliefs related to pain. Tina scored 7, which is reasonably consistent with the wider pain-free population.
  • Pain Knowledge Questionnaire (PKQ) (Moseley, 2003b). This is a 19-item questionnaire that aims to quantify someone’s understanding of the biological mechanisms that underpin pain. The scoring range is 0–19, with 19 indicating high knowledge. A revised version with fewer items is recommended for test–retest applications (Catley et al., 2013a). Tina scored 6, which is consistent with an untrained chronic pain population.


Other Tests


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Apr 2, 2020 | Posted by in SPORT MEDICINE | Comments Off on Chronic Facial Pain in a 24-Year-Old University Student

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