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The Musculoskeletal Wrangler, Wonthaggi (2026)

22/08/2026

Cluster headache
Part 3: management
📍An updated literature review by Petersen et al. (2024) provide a contemporary review of CH, bringing together advances in its diagnosis, clinical management and understanding of underlying pathophysiology.
ACUTE TREATMENT:
🟢*High flow oxygen
🟢*Triptans – subcutaneous (eg: Sumatriptan) and/or intranasal
❌Simple analgesics and opioids and NOT recommended due to inefficacy
TRANSITIONAL TREATMENTS:
🟠Corticosteroids – oral prednisone
🟠Greater occipital nerve blocks – local anaesthetics and/or corticosteroids
LONG-TERM PREVENTATIVE TREATMENT:
🟢**Calcium channel blockers (eg: Verapamil)
🟠Mood stabilisers (eg: Lithium)
🟠Antiepileptics (eg: Topiramate)
EMERGING INTERVENTIONS:
⚠️Melatonin or high dose vitamin D3
⚠️CGRP-targeted therapy (Erenumab)
⚠️Neuromodulation: occipital nerve stimulation or sphenopalatine ganglion stimulation
⚠️Hallucinogens (serotonin agonists) – L*D and/or psilocybine
⚠️Ketamine
⚠️Gepants
⚠️Botulinum toxin A
*Substantial symptom relief in >75% attacks
**Up to >50% reduction in attack frequency
SUMMARY:
📚Management of cluster headache involves acute treatment with high-flow oxygen and/or subcutaneous or intranasal triptans, which rapidly abort individual attacks. Verapamil is the mainstay of preventive treatment, with corticosteroids often used as short-term transitional therapy; alternatives for refractory or chronic cluster headache include lithium, topiramate and emerging therapies such as CGRP-targeted treatments.
MW
Reference:
Petersen AS, Lund N, Goadsby PJ, Belin AC, Wang SJ, Fronczek R, et al. Recent advances in diagnosing, managing, and understanding the pathophysiology of cluster headache. Lancet Neurol. 2024;23(9):907-918.
Hoffmann J, May A. Diagnosis, pathophysiology, and management of cluster headache. Lancet Neurol. 2018;17(1):75-83.

22/08/2026

Cluster headache
Part 2: pathophysiology
📍Two literature reviews by Hoffman & May (2018) and Petersen et al. (2024) provide a contemporary overview of Cluster headache (CH), bringing together advances in its diagnosis, clinical management and understanding of underlying pathophysiology.
PATHOPHYSIOLOGY (see image):
🧑‍⚕️ CH is a complex neurobiological disorder involving interactions between the hypothalamus, trigeminal system and cranial autonomic pathways:
🔆The hypothalamus appears central to the circadian and circannual periodicity of CH. Its involvement may help explain the characteristic timing of attacks, including their tendency to occur during sleep and at particular times of day or year.
🔆Activation of the trigeminovascular system is thought to generate the intense unilateral pain of an attack. This involves activation of trigeminal afferents and release of neuropeptides, particularly calcitonin gene-related peptide (CGRP).
🔆Trigeminal activation engages the trigeminal autonomic reflex, producing parasympathetic activation and the characteristic ipsilateral cranial autonomic features, including lacrimation, conjunctival injection and nasal congestion
🔆CGRP appears to have an important role in CH pathophysiology. Evidence that CGRP-targeted therapies can reduce attack burden provides clinical support for its involvement, although CGRP is unlikely to represent the sole mechanism underlying CH.
SUMMARY:
📚This growing body of work represents an emerging model rather than a completely established mechanism; how these systems interact to produce the highly characteristic cycling of individual attacks and cluster bouts remains unresolved.
MW
References:
Hoffmann J, May A. Diagnosis, pathophysiology, and management of cluster headache. Lancet Neurol. 2018;17(1):75-83.
Petersen AS, Lund N, Goadsby PJ, Belin AC, Wang SJ, Fronczek R, et al. Recent advances in diagnosing, managing, and understanding the pathophysiology of cluster headache. Lancet Neurol. 2024;23(9):907-918.

22/08/2026

Cluster headache
Part 1: epidemiology, classification and diagnosis
BACKGROUND:
🔎Cluster headache (CH) is a primary headache disorder and the most common of the trigeminal autonomic cephalalgias (TACs).
📍An updated literature review by Petersen et al. (2024) provide a contemporary review of CH, bringing together advances in its diagnosis, clinical management and understanding of underlying pathophysiology. The authors emphasise that although CH has a distinctive clinical phenotype, it remains under-recognised and can be profoundly disabling because of the extreme intensity and recurrent nature of attacks.
EPIDEMIOLOGY:
📉Prevalence between 41 and 381 individuals per 100,000
📈Male predominance of between 3:1 and 9:1 ratio
CLASSIFICATION (see image):
🔆Episodic cluster headache (weeks to months with remission periods >3 months
🔆Chronic cluster headache (>1 year without remission, or with remission periods ❤ months
DIAGNOSTIC CRITERA:
🧑‍⚕️ Characterised by recurrent attacks of severe or very severe, strictly unilateral pain*, typically in the orbital, supraorbital and/or temporal regions, lasting 15–180 minutes* when untreated. Ipsilateral autonomic symptoms and marked restlessness/agitation*
*Helps distinguish from migraine which is not strictly unilateral, typically lasts 4-72hrs and is often aggravated by routine physical activity and relieved by resting quietly.
MW
Reference:
Petersen AS, Lund N, Goadsby PJ, Belin AC, Wang SJ, Fronczek R, et al. Recent advances in diagnosing, managing, and understanding the pathophysiology of cluster headache. Lancet Neurol. 2024;23(9):907-918.

22/08/2026

Migraine and aura
Part 3: clinical features and symptomatology
📍A detailed expert opinion by Kissoon & Cutrer (2017) provides an overview of the different neurologic manifestations associated with migraine, with particular attention to migraine aura.
CLINICAL FEATURES:
🔆Aura typically develops gradually over several minutes, evolves over approximately 5–60 minutes, and may occur before, during or after the headache phase or, less commonly, in the absence of headache.
PREVALENCE:
📈Aura is experienced by approximately 25–30% of people with migraine and is most commonly visual.
SYMPTOMATOLOGY:
👁️ Typical visual symptoms include scintillations, zig-zag lines, flashing lights and scotomas. Sensory symptoms may include mostly upper limb, unilateral tingling or numbness
🗣️ Language aura: can be difficult to categorize, namely characterised by impaired attentional performance, lack of concentration, mental “cloudiness” or “fuzziness”, and in severe cases, transient amnesia or aphasia.
💪 Motor aura: weakness described as mild clumsiness through to complete hemiplegia, “alien limb” phenomena or apraxia.
🧠 Brainstem aura manifestations present concerningly, and should likely be formally screened for serious pathology. Symptoms can be consistent with a CVA, incl. vertigo, dysarthria, tinnitus, diplopia, impaired consciousness and hypacusis etc.
MW
Reference:
Kissoon NR, Cutrer FM. Aura and other neurologic dysfunction in or with migraine. Headache Currents. 2017; 57(7): 1179-1194.

22/08/2026

Migraine and aura
Part 2: pathophysiology
📍.
A detailed expert opinion by Kissoon & Cutrer (2017) provides an overview of the different neurologic manifestations associated with migraine, with particular attention to migraine aura.
PATHOPHYSIOLOGY (see image):
📝 The prevailing explanation for typical migraine aura is cortical spreading depression (CSD): a wave of neuronal and glial depolarisation followed by a period of suppressed neuronal activity that propagates across the cerebral cortex.
🧑‍⚕️ CSD helps explain the characteristic temporal evolution and sequential nature of aura, while activation of trigeminovascular pathways provides a link between neurologic dysfunction and headache.
🧠 The diversity of migraine manifestations however, suggests that migraine involves distributed and interacting neural networks, rather than a single isolated cortical mechanism.
SUMMARY:
📖Aura represents a particularly important manifestation, characterised by reversible, usually gradually evolving focal neurologic symptoms, most commonly visual, sensory or language disturbances.
MW
Reference:
Kissoon NR, Cutrer FM. Aura and other neurologic dysfunction in or with migraine. Headache Currents. 2017; 57(7): 1179-1194.

22/08/2026

Migraine and aura
Part 1: classification
DEFINITION:
📝 Migraine aura is a transient neurological phenomenon that occurs in association with migraine and is characterised by reversible focal neurological symptoms, most commonly visual, sensory or language disturbances.
📍A detailed expert opinion by Kissoon & Cutrer (2017) provides an overview of the different neurologic manifestations associated with migraine, with particular attention to migraine aura.
CLASSIFICATIONS (see image):
🔆A key clinical issue is distinguishing migraine-associated neurologic symptoms from secondary neurologic pathology. Atypical, persistent, abrupt-onset or progressive neurologic deficits warrant consideration of alternative diagnoses.
SUMMARY:
📖Migraine with aura is classified according to the neurological features of the aura, most commonly visual, sensory and/or language symptoms (typical aura), but it can also include motor weakness (hemiplegic migraine), brainstem symptoms (migraine with brainstem aura), or rarely monocular visual disturbance (retinal migraine). Aura may occur with or without a subsequent headache, with the neurological symptoms typically being fully reversible and developing gradually over minutes.
MW
Reference:
Kissoon NR, Cutrer FM. Aura and other neurologic dysfunction in or with migraine. Headache Currents. 2017; 57(7): 1179-1194.

22/08/2026

Recognising a migraine attack
BACKGROUND:
🔎Acute migraine treatment, particularly triptans, may be more effective when taken early, while pain is still mild. It remained unclear whether people with a confirmed migraine diagnosis can reliably recognise a new headache as a migraine while in its early stages, before it reaches its peak intensity?
📍An early observational study by Ng-Mak et al. (2007) followed 182 migraine patients to the likelihood that they can recognise a new attack early enough to act on it. They found around 92% of migraine attacks were correctly identified (91 Sn and 97 Sp). Features such as photophobia, nausea, visual disturbance and increasing headache severity helped patients recognise an emerging migraine attack.
📍An earlier study similarly found that only 53% of 3,074 people meeting diagnostic criteria for migraine identified their headaches as migraine, meaning that almost half were unaware that their headaches represented migraine. Common alternative labels included “stress headache” and “sinus headache.” Such misattribution may contribute to delays in appropriate care, suboptimal treatment choices and less effective communication with healthcare professionals.
📍A later study by Viana et al. (2020) demonstrated in a large transcontinental cohort, that many people with migraine don't conceptualise their recurrent headaches as migraine in the first place. Many (64%) would frequently attribute their symptoms to a headache rather than a migraine, particularly when in the presence of comorbidities such as neck pain or sinusitis.
SUMMARY:
⚠️Although most people with established migraine can generally recognise individual attacks at onset, broader awareness and diagnostic recognition remains relatively narrow or poor. Patients commonly identify characteristic features such as photophobia, nausea, visual disturbance and increasing headache severity, yet in their absence, many fail to recognise their recurrent headaches as migraine.
📚The presence of comorbid symptoms or conditions, such as neck pain or sinusitis, may further confound symptom interpretation and contribute to diagnostic misattribution.
📖Limited diagnostic awareness and difficulty recognising the early features of an attack may therefore delay appropriate identification and treatment, potentially reducing the effectiveness of acute migraine management.
MW
References:
Ng-Mak DS, Cady R, Chen YT, Ma L, Bell CF, Hu XH. Can migraineurs accurately identify their headaches as “migraine” at attack onset? Headache. 2007;47(5):645-653.
Lipton RB, Stewart WF, Liberman JN. Self-awareness of migraine: interpreting the labels that headache sufferers apply to their headaches. Neurology. 2002;58(9 Suppl 6):S21-S26.
Viana M, Khaliq F, Zecca C, Figuerola MDL, Sances G, Di Piero V, et al. Poor patient awareness and frequent misdiagnosis of migraine: findings from a large transcontinental cohort. Eur J Neurol. 2020;27(3):536-541.

21/08/2026

Headache chronotype
DEFINITION:
📝 Headache chronotype refers to the characteristic temporal or circadian pattern of headache occurrence, including its typical timing in relation to the 24-hour sleep–wake cycle.
📍An older conceptual paper by Rothner (1995) provides a structured approach to the clinical evaluation of headache in children and adolescents. Rothner identifies the temporal pattern of headache as a key component of the clinical history, providing important diagnostic and risk information. This involves establishing how the headache begins, its frequency and recurrence, how it changes over time, and whether symptom-free intervals occur.
CHRONOTYPES & CLASSIFICATIONS *see image):
🟢Acute: a single, isolated episode with no previous history, requiring consideration for potential primary or secondary causes.
🟢Acute-recurrent: a common pattern of repeated headache episodes separated by symptom-free intervals
🟢Chronic non-progressive: Another common headache that is frequent or constant, without progressive worsening
🟠Mixed: Acute-recurrent headaches, usually migraine, occurring on a background of chronic-daily headache
🔴Chronic-progressive: the most concerning pattern of Headache with a gradual increase in frequency and/or severity
SUMMARY:
📖Despite the age of these concepts, Rothner’s key contribution remains the recognition that the temporal behaviour of headache is diagnostically meaningful.
📚Establishing the temporal profile helps clinicians characterise headaches as isolated, recurrent, persistent, progressive, or mixed, while also identifying patterns that may warrant further investigation.
MW
Reference:
Rothner AD. The evaluation of headaches in children and adolescents. Semin Pediatr Neurol. 1995;2(2):109-118.

16/08/2026

Pain threshold
Effect of group size and synchrony
BACKGROUND:
🔎Synchronised activity, such as rowing, dancing or singing, can increase pain thresholds, potentially reflecting activation of endogenous opioid mechanisms and/or enhanced social bonding. However, it remains unclear whether the magnitude of this effect differed according to the size of the group.
📍An experimental study by Lewis & Sullivan (2018) investigated among 33 healthy participants whether exercising in a larger group produces a greater increase in pain threshold than exercising with a partner during a 20min synchronised rowing session.
FINDINGS:
📈Exercising synchronously within a larger group produced a significantly higher pain threshold than the paired condition at 10 minutes post-exercise.
IMPLICATIONS:
🕺Synchrony may have hypoalgesic effects
👥Social connectedness and group interaction as potential contributors to endogenous pain modulation.
SUMMARY:
📖Pain modulation is not exclusively an individual physiological phenomenon. Social and interpersonal factors may influence the degree to which an individual experiences pain.
⚠️Importantly, the study provides evidence about experimental pain modulation, rather than demonstrating a clinical treatment effect for people with chronic pain.
MW
Reference:
Lewis Z, Sullivan PJ. The effect of group size and synchrony on pain threshold changes. Small Group Res. 2018;49(6):723-738.

16/08/2026

Low back pain (LBP):
Conceptual overlap of psychological constructs
BACKGROUND:
🔎Constructs such as pain-related distress, fear, pain-catastrophising, self-efficacy, and illness perceptions are frequently assessed separately in research and clinical practice, yet there is considerable overlap between them.
📍An observational study by Campbell et al. (2013) examined the extent to which commonly used psychological constructs in adults with LBP are conceptually distinct.
PAIN-RELATED DISTRESS:
🔆Encompasses interrelated emotional responses associated with experiencing LBP, including anxiety, depression, worry, and emotional distress.
📈Greater psychological distress is associated with greater pain intensity and self-reported disability. Individuals experiencing greater distress may also be more likely to report maladaptive cognitive and behavioural responses to their pain.
COGNITIVE COPING:
🔆Refers to how individuals think about and mentally respond to their pain.
⚠️Constructs such as catastrophising, coping, and psychological distress may share substantial underlying variance, potentially capturing a broader pattern of negative cognitive-emotional responses to pain rather than entirely independent psychological processes.
CAUSAL BELIEFS:
🔆Refer to an individual's perceptions about what has caused their LBP and why it is occurring.
⚠️These beliefs are not necessarily isolated from emotional distress or coping. Rather, they form part of the broader cognitive framework through which individuals interpret and make sense of their pain.
PERCEPTIONS OF THE FUTURE:
💡Reflect an individual's expectations about the likely course and consequences of their LBP, including beliefs about persistence, recovery, and future disability.
⚠️Such expectations are closely connected with how individuals interpret their pain and may influence their emotional and cognitive responses to the experience of LBP.
INFERENCE:
📚Importantly, the authors argued that strong correlations between psychological constructs do not necessarily mean that they are interchangeable. Rather, different measures may capture related dimensions of a broader psychological response to pain.
📚Consequently, psychological constructs should be interpreted within their broader conceptual context, rather than assuming that each represents a completely discrete psychological process.
SUMMARY:
📖What a person believes their pain means, how they emotionally respond to it, how they think about it, and what they expect will happen next are closely interconnected rather than independent psychological processes
MW
Reference:
Campbell P, Bishop A, Dunn KM, Main CJ, Thomas E, Foster NE. Conceptual overlap of psychological constructs in low back pain. Pain. 2013;154(8): 1783-1791.

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