Samenvatting Cervicothoracale Regio.docx

# Screening and clinical reasoning for neck pain This topic explores the crucial role of screening and clinical reasoning in managing neck pain, focusing on differentiating normal from abnormal presentations and developing effective treatment plans. ## 1. Screening and clinical reasoning for neck pain ### 1.1 The importance of screening for neck pain Screening for neck pain is essential to determine whether a presentation is within the normal spectrum of symptoms or if it indicates an abnormality requiring further investigation or specific management. Given the high prevalence of neck pain, understanding normal versus abnormal presentations is a core clinical skill. This process helps guide decision-making regarding further examination, referral, and the appropriate scope of practice for the clinician. > **Tip:** A significant portion of individuals presenting with neck pain can be managed effectively after initial screening, with a portion requiring no further intervention beyond that. ### 1.2 Clinical reasoning in neck pain management Clinical reasoning involves a structured approach to patient care, encompassing several key elements: * **Clinical examination:** Gathering subjective and objective information. * **Evaluation of findings:** Interpreting the collected data. * **Diagnosis:** Determining the underlying cause or nature of the problem. * **Prognosis:** Predicting the likely course of the condition. * **Treatment planning:** Developing a strategy for intervention. This process is followed by the implementation of interventions and ongoing reassessment. ### 1.3 Prevalence and incidence of neck pain Neck pain is highly prevalent, with significant annual incidence rates. Recovery rates can be moderate, but recurrence is common. * **General population prevalence:** Approximately 23.1% mean prevalence, with a mean one-year prevalence of 25.8%. * **Incidence:** 10.4% to 21.3% one-year incidence. * **Recovery:** 33% to 65% recover within one year. ### 1.4 Causes of neck pain The majority of neck pain is musculoskeletal in origin, though non-musculoskeletal causes can also contribute. Factors involved include pain perception, sensorimotor control, dizziness, posture, and balance. ### 1.5 Classifications of neck pain Several classification systems exist to categorize neck pain based on its origin, pathology, and temporal aspects. #### 1.5.1 Classification by origin * **Mechanical/idiopathic:** Pain arising spontaneously without a clear external cause. * **Traumatic:** Pain resulting from an injury. * **Degenerative:** Pain associated with age-related changes in tissues. #### 1.5.2 Classification by time course * **Acute:** Recent onset. * **Subacute:** Symptoms persisting beyond the acute phase. * **Chronic:** Long-standing symptoms. #### 1.5.3 Classification by underlying mechanism This involves understanding the nature of the pain, such as nociceptive, inflammatory, neuropathic pain, or central sensitization. #### 1.5.4 Classification based on treatment goals Subgrouping patients based on their response to specific interventions or their treatment objectives. ### 1.6 Anamnestical screening Anamnesis (history taking) is a critical first step in screening for neck pain. It involves collecting data and comparing it against incidence and prevalence figures, identifying relevant red flags, and assessing the patient's history of other conditions (tractusanamnese). Key aspects include: * **Nature of pain:** Is it related to posture or movement? * **Course of symptoms:** How has the pain evolved? * **Patient's primary complaint:** A brief inventory of their concerns. #### 1.6.1 Red flags in neck pain screening Red flags are signs and symptoms that suggest a serious underlying pathology. These can be generic or region-specific. ##### 1.6.1.1 Generic red flags * Unexplained signs or symptoms after recent trauma. * Persistent and unexplained fever. * Unexplained significant weight loss (over 5 kilograms per month). * Long-term corticosteroid use. * Constant pain that does not diminish with rest or position change. * History of malignancy. * Nocturnal pain not influenced by posture or movement. * Extensive neurological signs and symptoms. > **Tip:** If red flags indicate an abnormal course of symptoms, the patient should be referred back. If the course is normal despite the presence of a red flag, treatment can proceed cautiously. ##### 1.6.1.2 Red flags for cervical trauma (Canadian C-Spine Rule and NEXUS) These rules are specifically for post-traumatic neck pain, particularly following motor vehicle collisions (MVCs). * **Canadian C-Spine Rule:** Identifies patients who require cervical spine imaging based on factors like mid-cervical tenderness, distracting injuries, neurological deficits, altered level of consciousness, and intoxication. * **NEXUS Criteria:** Aims to identify patients for whom cervical spine radiography is not indicated if all five criteria are met: absence of posterior midline cervical tenderness, no signs of intoxication, normal level of alertness, no focal neurological deficit, and no painful distracting injury. #### 1.6.2 Non-musculoskeletal causes It is crucial to differentiate mechanical neck pain from non-musculoskeletal causes. While movement-related pain is common, conclusions should not be drawn too quickly. Short-duration pain (1-2 days) may resolve naturally without intervention. #### 1.6.3 Referred pain The source of symptoms may not always be the affected structure. Referred pain should be considered, and the relevant referral zones must be known. ### 1.7 Classification by time course and irritability Different classification systems categorize neck pain based on its temporal aspects and the degree of irritability of the tissues. * **APTA classification:** * **Acute phase:** High irritability. * **Subacute phase:** Moderate irritability. * **Chronic condition:** Low degree of irritability, with pain worsening in end-range positions or under pressure. * **KNGF (Dutch Association of Physiotherapists) guidelines:** Emphasize psychosocial factors and the symptom course. ### 1.8 Clinical reasoning concepts and influencing factors Regardless of the specific clinical reasoning model used, the focus is on identifying the source and nature of symptoms, as well as influencing factors. * **Influencing factors:** * **Environmental factors:** Including social support. * **Behavioral, emotional, and psychosocial factors:** Such as coping strategies and stress. * **Pathological/systemic factors:** Indicating serious underlying disease. * **Musculoskeletal factors:** Related to the physical condition of the tissues. The assessment also considers precautions or contraindications for examination or treatment, management strategies, and prognosis. ### 1.9 Prognosis and natural course of neck pain The natural course of neck pain is highly variable. * **Idiopathic neck pain:** Most significant changes occur within the first 6 to 12 weeks. Pain can decrease substantially within the first 6 weeks. * **Influencing factors for prognosis:** * **Age:** Older age is often associated with poorer prognosis. * **Previous episodes:** A history of neck pain is a significant predictor. * **Anamnestic information:** Detailed history can provide prognostic clues. * **Prognostic factors in the working population:** * **Unfavorable:** Older age (45-59 years), previous neck complaints, type of work (blue-collar vs. white-collar), low job control, and work situation. * **Favorable:** Changes in workload during work and general physical training. * **Prognostic factors in the general population:** * **Unfavorable:** Older age, passive coping mechanisms. Degenerative changes are *not* necessarily unfavorable. * **Favorable:** Younger age, good social support, good mental well-being. The KNGF guidelines propose treatment profiles (A, B, C, D) that consider the severity of the condition and the presence of psychosocial factors. ### 1.10 Neuromuscular control and motor dysfunction in neck pain Neck pain can be associated with disorders in the neuromuscular system, impacting muscle function, range of motion (ROM), and movement fluidity. #### 1.10.1 Manifestations of neuromuscular dysfunction * **Muscle guarding:** Superficial muscles like the sternocleidomastoid (SCM), trapezius, and levator scapulae may become overactive as a protective mechanism. * **Increased muscle co-activation:** Synergistic muscles (e.g., flexors and extensors) may co-contract, which is not functionally efficient. * **Reduced muscle strength.** * **Decreased ROM and less fluid movement.** * **Gestrored proprioception.** #### 1.10.2 Structural muscular changes These can include atrophy, fatty infiltration (especially in Whiplash Associated Disorders - WAD), altered contractile properties, and changes in muscle fiber type. Deep cervical flexors (DCF) are often less active in individuals with neck pain compared to control groups. #### 1.10.3 Motor system dysfunction following whiplash In post-traumatic neck pain (whiplash), there can be an increased reliance on superficial muscles relative to deep muscles, and this can manifest within a month of the trauma. #### 1.10.4 Delayed onset of muscle activation * **External activation (balance perturbation):** Patients with neck pain may exhibit a delayed activation of neck muscles in response to balance disturbances. * **Internal activation (visual stimulus):** Similarly, there can be a delayed onset of deep cervical flexor (DCF) activity before an intended arm movement. This indicates a deficit in automatic feedforward control. #### 1.10.5 Muscle activation during functional activities Muscles in patients with WAD are often more active during a task and remain active for longer after the task is completed compared to those with idiopathic neck pain. #### 1.10.6 Selective muscle activation The SCM, for instance, may remain active throughout a movement where it should only be engaged during specific ranges, indicating inefficient activation patterns. #### 1.10.7 Joint position error (JPE) Patients with moderate to severe neck pain, particularly WAD, often demonstrate larger JPEs, indicating impaired proprioception. This deficit can develop rapidly. #### 1.10.8 Structural changes: Fiber types and fat infiltration * **Muscle fiber transformation:** A shift from slow-twitch oxidative type-I fibers towards fast-twitch glycolytic type-IIB fibers can occur, particularly in ventral muscles. * **Fat infiltration:** This is more common in WAD and can increase over time, possibly due to inflammation and reduced muscle maintenance. #### 1.10.9 Therapeutic implications of neuromuscular changes * **Rapid assessment and intervention:** Neuromuscular changes can occur quickly, necessitating early evaluation and intervention. * **Standard active examination:** Can provide valuable insights into coordination and muscle activation. * **Targeted exercises:** Focusing on low-load exercises, coordination, endurance, correct movement patterns, and co-contractions. * **Functional exercises:** Incorporating functional tasks and postural training. > **Example:** When assessing neck flexion, observe the timing of SCM contraction and the eccentric action of the extensors. Note the location of movement (high or low cervical). #### 1.10.10 Specific exercise principles * **Task division:** Breaking down complex movements into simpler components. * **Gradual progression:** Starting with simple exercises and building up. * **Feedback:** Providing both verbal and tactile feedback. * **Specificity:** Targeting specific muscle groups, such as the deep neck flexors (longus colli, longus capitis). #### 1.10.11 Deep neck flexor (DNF) training Proper positioning during DNF exercises is crucial. Overlordosis in the cervical spine can hinder effective DNF activation. * **Pressure pain threshold (PPT):** Active exercises for DNFs can improve PPT and reduce pain intensity more effectively than passive mobilization. * **Pain intensity reduction:** Active exercise groups show greater reductions in pain intensity compared to passive groups. * **Muscle activation:** DNFs become more active, and superficial muscles become less active after successful interventions. #### 1.10.12 Deep extensor muscles While less researched than flexors, deep neck extensors like the semispinalis cervicis are important for stability and proprioception. Suboccipital muscles, situated deepest, are crucial for proprioception and maintaining head alignment on C1. Superficial muscles are primarily responsible for movement. #### 1.10.13 Effectiveness of interventions Specific training, particularly early intervention for deep neck flexors, can be effective. Studies suggest that combining manual therapy with exercise, dry needling, or other techniques can yield positive short-term results for reducing headache intensity and frequency. However, the evidence for definitive recommendations is often of low certainty. ### 1.11 Neck pain with radiating pain Differentiating between referred pain and radiating pain (neurological deficit) is important. Progressive muscle weakness (e.g., drop hand) is a red flag for a Grade 3 condition. * **Grade 2:** Referred pain in the upper extremity. * **Grade 3:** Radiating pain. #### 1.11.1 Cervical radicular syndrome This involves irritation of a nerve root, often caused by disc herniation, facet joint osteophytes, or foraminal stenosis. Prolonged pressure on a nerve can lead to ischemia, edema, inflammation, and fibrosis. #### 1.11.2 Diagnosis of cervical radicular syndrome Diagnosis relies on a combination of: * **Anamnesis:** Character of pain (shooting, tingling, burning), arm pain exceeding neck pain, and potential local pain around irritated joints. * **Physical examination:** Including a cluster of tests such as Spurling's test, Upper Limb Tension Tests (ULTTs), and neurological assessments (sensation, strength, reflexes). * **Imaging:** May be used for confirmation or to rule out other pathologies, but is not always necessary. #### 1.11.3 Somatic referred pain Pain originating from somatic structures like joints, ligaments, or trigger points can be perceived in different areas, including the scapular region. ### 1.12 Cervicogenic headache (CEH) Cervicogenic headache is a type of headache that arises from dysfunction in the cervical spine. * **Neuroanatomical basis:** The trigeminocervical nucleus, where fibers from the trigeminal nerve and upper cervical segments converge, is implicated. Irritation in the upper cervical spine can be misinterpreted as a trigeminal stimulus. * **Prevalence:** While debated, cervicogenic headache is considered a milder form of headache, but it can be overdiagnosed. Migraine and tension-type headaches are more common. * **Diagnostic criteria:** Include neck involvement, mechanical provocation (movement, pressure), decreased range of motion, ipsilateral shoulder or arm pain, and confirmation by anesthetic block. The pain is typically unilateral and not characterized by pulsating or lancinating qualities. * **Pathophysiology:** Primarily involves referred pain, often from the upper cervical segments, and can be influenced by trigger points. * **Clinical assessment:** Involves history taking, specific clinical tests focusing on the upper cervical segments, and palpation of joints and muscles. * **Treatment:** May include manual therapy (mobilizations, manipulations), exercise therapy (e.g., DNF training, postural advice), and education about referred pain. > **Tip:** Be cautious not to overdiagnose cervicogenic headache simply because a patient experiences both neck pain and headache. #### 1.12.1 Medication overuse headache This is a secondary headache that can develop in individuals who frequently take headache medication. It is characterized by frequent headaches and sustained medication use, often transforming from episodic to continuous pain. Management involves withdrawal of the offending medication. #### 1.12.2 Red flags for headaches New headaches presenting after age 40 or 50, atypical auras, temporal pain in those over 50, sudden onset headaches, fever, and persistent headaches warrant further investigation. ### 1.13 Whiplash Associated Disorders (WAD) WAD refers to a spectrum of clinical complaints that result from an acceleration-deceleration mechanism of injury, typically following a motor vehicle collision. * **Definition:** An indirect trauma where energy is transferred to the neck, potentially causing injury to soft tissues. * **Symptoms:** Can include neck pain, headache, dizziness, sleep disturbances, and concentration problems. * **WAD grading:** Similar to general neck pain classifications, with grades ranging from 0 (no complaints) to 4 (structural pathologies like fractures requiring surgery). WAD 2A, 2B, and 2C describe varying degrees of pain, ROM limitations, and the presence of psychological components like kinesiophobia, hyperalgesia, and post-traumatic stress. * **Pathophysiological mechanisms:** While the exact mechanisms are debated, injury to soft tissues, facet joints, ligaments, and muscles is suspected. Low-intensity impacts can still cause injury. * **Assessment:** May include imaging to rule out fractures (Grade 4), but should consider pre-existing degenerative changes. * **Prognosis:** While many individuals recover within three months, a significant percentage experience chronic neck pain or disability. * **Influencing factors for chronicity:** Higher initial Neck Disability Index (NDI) scores, older age, hyperarousal symptoms (from Post-Traumatic Stress Diagnostic Scale), pain processing mechanisms (lowered pain thresholds, reduced inhibition), and psychological factors like kinesiophobia and negative expectations. > **Example:** When assessing a patient with potential WAD, consider using the NDI to gauge their disability level and predict their prognosis. * **Management:** Involves a multidisciplinary approach, including exercises (motor control, strength, endurance), education, advice, mobilization, and potentially medication. Imaging is generally reserved for suspected Grade 4 injuries. > **Tip:** For WAD Grade 1 and 2, focusing on active recovery and minimal intervention in the initial phase is often recommended, unless specific red flags are present. ### 1.14 Comparison of APTA and KNGF guidelines * **KNGF:** Places greater emphasis on the biopsychosocial model and the symptom course. * **APTA:** Differentiates between acute, subacute, and chronic presentations based on tissue irritability, with a specific focus on headache management. ### 1.15 Case studies and examination preparation Understanding comparable case studies and practicing specific assessment techniques (e.g., ULTT, Spurling's test, joint palpation) is vital for exam preparation. Specificity in describing treatment goals, progression of exercises, and rationale for interventions is key. --- # Motor control and neuromuscular dysfunction in neck pain This topic delves into the neuromuscular adaptations associated with neck pain, exploring muscle guarding, altered muscle activation patterns, reduced strength, proprioceptive deficits, and structural muscle changes, and their implications for rehabilitation. ### 2.1 Overview of neuromuscular dysfunction in neck pain Neck pain is a highly prevalent condition, with a significant lifetime prevalence and a tendency for recurrence. Beyond pain, individuals often report stiffness, a feeling of being "locked," cracking sensations, and difficulties with activities like looking up or driving. These symptoms are frequently linked to impairments within the neuromuscular system. While acute episodes of neck pain may resolve relatively quickly, maintaining function and preventing recurrence is often more challenging, largely due to these underlying neuromuscular deficits. ### 2.2 Types of neuromuscular dysfunction #### 2.2.1 Muscle guarding and co-activation In response to pain or injury, superficial neck muscles may engage in "muscle guarding," a protective mechanism leading to increased tension and stiffness. This is often observed in muscles such as the sternocleidomastoid (SCM), trapezius, and levator scapulae. Additionally, there can be an increase in muscle co-activation, where antagonistic muscles (e.g., flexors and extensors) contract simultaneously. This non-functional co-contraction can lead to inefficient movement and increased muscle fatigue. #### 2.2.2 Reduced muscle strength and range of motion Neck pain is frequently associated with a decrease in muscle strength and a reduction in the range of motion (ROM). Movements may become less fluid, and there can be a less specific recruitment of muscles during functional tasks. #### 2.2.3 Altered proprioception Proprioception, the sense of the relative position of one's own parts of the body and strength of effort being employed in movement, is often impaired in individuals with neck pain. This can manifest as a greater joint position error (JPE), meaning a reduced ability to accurately sense and reposition the head and neck. Patients with moderate to severe neck pain often exhibit larger repositioning errors, and these deficits can develop relatively quickly, sometimes within a month of injury. This proprioceptive deficit is particularly noted in conditions like whiplash-associated disorders (WAD) and can be correlated with symptoms like dizziness. #### 2.2.4 Structural muscle changes Long-term or significant neck dysfunction can lead to structural changes within the muscles themselves. These include: * **Atrophy:** A decrease in muscle size. * **Fat infiltration:** An increase in fat within the muscle tissue, often measured as muscle fat infiltration (MFI). This is particularly noted in conditions like WAD and chronic low back pain, impacting muscle function and potentially contributing to reduced activity and maintenance of muscle quality. * **Changes in contractile properties:** Alterations in how muscle fibers generate force and respond to activation. * **Muscle fiber type transformation:** A shift in the proportion of muscle fiber types, potentially from slow-twitch oxidative type I fibers (endurance-focused) to fast-twitch glycolytic type IIB fibers (power-focused). This transformation can occur more rapidly in ventral muscles compared to dorsal muscles. #### 2.2.5 Delayed onset of muscle activation A significant neuromuscular dysfunction observed in neck pain patients, particularly after whiplash, is a delayed onset of muscle activation. This can occur in response to both external perturbations (e.g., balance disturbances) and internal cues (e.g., anticipating an arm movement). * **External activation (balance perturbation):** When the body experiences a sudden shift in balance, neck muscles need to activate rapidly to stabilize the head. Studies show that individuals with neck pain take longer to initiate this protective muscle response compared to healthy controls. This delay can leave the cervical spine vulnerable to reactive forces. * **Internal activation (feedforward control):** In anticipation of a voluntary movement, such as reaching with an arm, the neck muscles should pre-activate to stabilize the cervical spine. In neck pain patients, particularly with whiplash, there is a delay in the activation of deep cervical flexors (DCF), indicating a deficit in this automatic feedforward control system. This delay suggests that the deep cervical muscles, crucial for maintaining cervical lordosis and joint stability, are not adequately prepared for the forces generated by arm movements. #### 2.2.6 Over-activation of superficial muscles In many cases of neck pain, there is an increased reliance on superficial muscles (e.g., SCM, anterior scalenes) for tasks that should primarily engage deeper, more stabilizing muscles. This over-activation of superficial muscles can lead to increased fatigue and a feeling of tightness. This pattern is observed even in seemingly simple tasks and can be indicative of underlying motor control deficits. ### 2.3 Motor control dysfunction following whiplash injury Whiplash-associated disorders (WAD) are often characterized by significant motor control and sensorimotor dysfunction. These dysfunctions can manifest early, sometimes within a month of the trauma, and have implications for prognosis. The deficits include: * **Increased use of superficial muscles:** Patients with moderate to severe WAD tend to use superficial muscles more in relation to deep muscles. * **Delayed activation:** As mentioned above, there is a delayed onset of muscle activity in response to perturbations and anticipated movements. * **Proprioceptive deficits:** Higher joint position errors are common, particularly with rotational movements and in patients experiencing dizziness. * **Altered muscle activation during functional tasks:** Muscles may remain active for longer periods after a task is completed, contributing to fatigue. ### 2.4 Therapeutic implications The rapid onset of neuromuscular changes underscores the importance of early assessment and intervention. Even during standard active examinations, therapists can identify issues with muscle coordination, activation patterns, and fluidity of movement. #### 2.4.1 Early assessment and intervention Identifying these neuromuscular deficits early is crucial. Therapists can begin to address them from the first session. * **Observation during active movement:** Assessing the coordination of muscle activation during flexion, extension, and rotation of the neck can reveal issues like improper muscle recruitment or excessive co-contraction. * **Palpation:** Palpating superficial muscles like the SCM can indicate whether they are inappropriately engaged during specific movements. #### 2.4.2 Exercise-based interventions Rehabilitation strategies should focus on retraining motor control and restoring neuromuscular function. Key principles include: * **Low-load exercises:** Starting with exercises that do not provoke pain. * **Coordination training:** Focusing on improving the timing and sequencing of muscle activation. * **Endurance training:** Building the capacity of muscles to sustain activity. * **Correct movement patterns:** Practicing smooth, controlled movements, often with immediate feedback. * **Co-contraction exercises:** Training antagonistic muscles to work together appropriately. * **Functional exercises:** Integrating motor control retraining into activities that mimic daily life. * **Task breakdown:** Decomposing complex tasks into simpler components to facilitate learning. * **Feedback:** Providing both verbal and tactile cues to guide movement and muscle activation. #### 2.4.3 Specific exercise targets * **Deep cervical flexors (DCF):** Exercises like cranio-cervical flexion (CCF) are vital for retraining these deep stabilizers. The correct execution of CCF has been shown to increase pressure pain thresholds (PPT) and reduce pain intensity more effectively than passive mobilization. It also leads to reduced activity in superficial muscles, which is a desired outcome. * **Deep neck extensors:** While less studied than flexors, deep neck extensors also play a crucial role in stability and proprioception. * **Suboccipital muscles:** These deep muscles are critical for fine-tuning head position and proprioception. #### 2.4.4 Therapeutic modalities * **Manual therapy:** Mobilizations and manipulations of the thoracic and (high) cervical spine can be beneficial in conjunction with exercise. * **Dry needling:** Combined with other interventions, dry needling has shown promise in reducing short-term headache intensity and frequency. * **Education:** Explaining concepts like referred pain and the role of neuromuscular control is essential for patient engagement and self-management. > **Tip:** When assessing deep neck flexors, ensure the patient's position on the treatment table does not create excessive cervical lordosis, which can hinder the engagement of these deep muscles. A towel roll may be necessary to achieve a more neutral alignment. > **Tip:** For patients with neck pain, encouraging them to perform short bouts of exercises (e.g., 2-3 minutes) throughout the day can act as a form of self-administered pain relief by engaging muscles appropriately and reducing over-reliance on superficial muscles. #### 2.4.5 Differentiating between grades of neck pain and WAD It is important to differentiate between various grades of neck pain and WAD, as this guides treatment. For instance, progressive muscle weakness (a neurological deficit) would be considered a red flag (Grade 3), requiring specific attention. Clinical prediction rules, such as those assessing NDI scores and hyperarousal symptoms, can help identify individuals at higher risk of developing chronic disability, allowing for tailored early interventions. #### 2.4.6 The role of pain processing and psychological factors Disturbances in pain processing, such as heightened sensitivity to mechanical or thermal stimuli (e.g., cold hyperalgesia), are common in chronic neck pain and WAD. Catastrophizing and negative expectations can also influence outcomes. A comprehensive approach that addresses motor function, pain mechanisms, and psychosocial factors is essential for effective management. #### 2.4.7 Timing of intervention The evidence suggests that specific motor control exercises should be initiated as early as possible, even in the acute stages, to counter the rapid development of neuromuscular deficits. > **Example:** In assessing a patient with potential cervicogenic headache, clinicians should evaluate mobility in the upper cervical segments (C0-C3) and palpate for joint tenderness. The Flexion-Rotation Test (FRT) with a cut-off of 30°-34° can be a useful diagnostic tool. Combining manual therapy with specific exercises targeting deep neck flexors and improving postural control is a key element of management. --- # Cervicogenic headaches and radicular syndromes This section details headaches originating from the cervical spine and radicular syndromes, covering their pathophysiology, diagnostic criteria, clinical assessment, and treatment. ### 3.1 Cervicogenic headache (CEH) Cervicogenic headache is a type of headache caused by dysfunction in the cervical spine. While its exact classification is debated in neurology, it is a recognized entity characterized by neck involvement and mechanical provocation. #### 3.1.1 Pathophysiology of CEH The primary pathophysiological mechanism for cervicogenic headache is referred pain. Irritation of structures in the upper cervical spine, particularly segments C0-C2, can lead to pain perceived in the trigeminal nerve distribution. The trigeminocervical nucleus, where fibers from the trigeminal nerve and upper cervical roots converge, plays a crucial role in this referred pain phenomenon. Specifically, fibers from the ophthalmic division of the trigeminal nerve project to the lower branches of this nucleus, facilitating the misinterpretation of upper cervical irritation as trigeminal nerve pain. This interaction works in both directions, meaning trigeminal irritation can also cause neck pain, complicating diagnosis. #### 3.1.2 Diagnostic criteria for CEH The diagnosis of cervicogenic headache relies on a combination of history taking and clinical assessment, adhering to specific criteria: * **Major Criteria:** * Evidence of neck involvement. * Mechanical provocation: Pain is induced or exacerbated by specific neck movements, sustained postures, or palpation of the neck. * Reduced range of motion (ROM) in the neck. * Ipsilateral shoulder or arm pain may be present. * Confirmation by an anesthetic block of a relevant cervical structure. * Head pain characteristics: * Moderately intense, not typically pulsating or lancinating. * Rather continuous, similar to neck pain. * Often starts in the occipital region. * Unilateral pain, without side-shifting during attacks (unlike migraine which can shift sides). * **Associated Symptoms:** These are generally rare in CEH. * **Patient Response:** Marginal effect of specific migraine medications like indomethacin, ergots, or triptans. #### 3.1.3 Clinical assessment of CEH The clinical assessment for CEH involves a thorough history and specific physical examinations: * **History Taking:** * **Location and Characteristics of Headache:** Where is the pain? Is it frequent? Is there an evolving pattern? Intensity? Type of pain (throbbing, shooting, stabbing)? * **Time Aspects:** Course of attacks, duration, and frequency. * **Age of Onset:** Patients often present after a prolonged period of suffering. * **Associated Signs and Symptoms:** Presence of other symptoms. * **Patient Response to Treatment:** How do they respond to medications? * **Medication Overuse Headache:** Screen for frequent headache (more than 15 days/month) and regular medication use (3 months or more), particularly with ergotamines/triptans (≥ 10 days/month) or simple analgesics (≥ 15 days/month). Manual therapies are ineffective for medication overuse headaches. * **Red Flags:** * First headache after age 40. * New headache after age 50. * Atypical aura, or aura without headache. * Temporal pain in patients over 50 years old, with hardened and tender temporal arteries. * Sudden or sentinel headaches. * Headaches associated with fever, meningitis, or neurological deficits. * **Clinical Tests:** * **Anteroposition:** Assessment of forward head posture. * **Mobility Assessment:** * **General Mobility:** Assessing the overall ROM of the cervical spine. * **Segmental Mobility:** Focusing on specific upper cervical segments (C0-C1, C0-C2). * **Flexion-Rotation Test (FRT):** Developed specifically for CEH, a cutoff of 30-34 degrees is considered indicative. * **Deep Neck Flexor (DNF) Activation:** Assessing the ability to activate the deep neck flexor muscles. * **Joint Palpation:** Palpating C0-C3 for tenderness. * **Provocation Tests:** * **Spurling's Test:** (High specificity) May indicate radicular involvement but can also provoke pain from facet joints. * **Traction Test:** Applying traction to the cervical spine. * **Valsalva Maneuver:** Can increase intrathecal pressure. * **Upper Limb Tension Tests (ULTTs):** (High sensitivity for radiculopathy) Used to assess neural tension. * **CROM (Cervical Range of Motion):** Measuring ROM in all planes. * **Trigger Point Palpation:** While often associated with tension headaches, trigger points can contribute to referred pain. #### 3.1.4 Treatment of CEH Treatment for cervicogenic headache typically involves a multimodal approach, tailored to the chronicity of the condition: * **Education:** Explaining referred pain mechanisms and the rationale for treatment is crucial, especially for chronic pain. * **Postural Advice:** Encouraging regular changes in posture, such as sitting upright for 15 seconds every quarter hour. * **Deep Neck Flexor (DNF) Training:** Exercises to strengthen and improve the endurance of the deep neck flexor muscles to support posture. * **Manual Therapy:** * **Mobilizations and Manipulations:** Targeting thoracic and upper cervical joints to restore mobility. * **Spinal Joint Manipulation combined with Dry Needling:** Found to be highly effective for reducing short-term headache intensity and frequency. * Other effective combinations include muscle-energy technique + exercise, soft tissue techniques + exercise, and dry needling + exercise. * **Exercise Therapy:** * **Low-load exercises, coordination, and endurance training.** * **Practicing correct movement patterns.** * **Co-contraction exercises.** * **Functional exercises:** Incorporating functional tasks, breaking them down into simpler steps, and providing feedback. * **Self-sustained natural apophyseal glide (SNAG) techniques** for C1-C2 segments. * **Addressing Underlying Pathophysiology:** Considering the interplay between motor control, pain mechanisms, and psychosocial factors. ### 3.2 Radicular syndromes Radicular syndromes involve irritation or compression of a nerve root as it exits the spinal canal, leading to pain, numbness, or weakness along the distribution of that nerve. #### 3.2.1 Pathophysiology of Radicular Syndromes The core mechanism is pressure or irritation on a nerve root, which can stem from several causes: * **Herniation with Radicular Conflict:** A herniated intervertebral disc can press directly on the exiting nerve root. * **Osteophytosis:** Bone spurs from facet joints or uncovertebral joints can narrow the intervertebral foramen, compressing the nerve. * **Stenotic Foramen:** Narrowing of the neural foramen due to degenerative changes. * **Entrapment Neuropathies:** Other forms of nerve entrapment. * **Fibrosis:** Scar tissue formation around the nerve root. * **Demyelination:** Damage to the myelin sheath surrounding the nerve. * **Axon Degeneration:** Damage to the nerve fibers themselves. * **Neuro-inflammation:** Inflammation of the nerve. The duration of nerve compression is critical. Prolonged ischemia (lack of oxygen) due to vascular compromise can lead to edema, inflammation, fibrosis, and the generation of ectopic impulses (spontaneous firing of the nerve). #### 3.2.2 Clinical presentation of Radicular Syndromes * **Pain:** Typically described as radiating, shooting, tingling, or burning pain, often more severe in the arm than in the neck. * **Neurological Deficits:** * **Sensory changes:** Numbness or altered sensation along the dermatome of the affected nerve root. * **Motor deficits:** Weakness in specific muscles innervated by the nerve root (e.g., a "drop hand"). This progressive muscle weakness is a red flag, indicating Grade 3 involvement. * **Reflex changes:** Diminished or absent deep tendon reflexes. * **Referred Pain:** Local nociception around the irritated nerve root or associated structures can refer pain to other areas, such as the scapular region. * **Associated Symptoms:** Patients may experience symptoms consistent with cervical radicular syndrome, including localized pain around joints and ligaments. #### 3.2.3 Diagnostic criteria for Radicular Syndromes Diagnosis relies on a comprehensive approach combining history and physical examination: * **Anamnesis:** Detailed questioning about the nature, location, and radiation of pain, as well as associated neurological symptoms. * **Physical Examination:** * **Neurological Examination:** Assessment of sensation, motor strength (key muscles), and reflexes. * **Cluster of Tests:** (e.g., Rubinstein-Wainner criteria) * Positive Spurling's Test (high specificity): Suggests nerve root compression. * Positive Upper Limb Tension Test (ULTT) (high sensitivity): Indicates neural tension. * Cervical ROM < 60 degrees of rotation. * Positive traction test. * Positive Valsalva maneuver. * **Cervical Spine MRI:** May be indicated to visualize nerve root compression from disc herniation, osteophytes, or foraminal stenosis. #### 3.2.4 Treatment of Radicular Syndromes Treatment strategies aim to reduce nerve root irritation and improve function: * **Conservative Management:** * **Non-Steroidal Anti-Inflammatory Drugs (NSAIDs):** Often effective for acute radicular pain, particularly in patients with Grade 2 involvement (referred pain). * **Manual Therapy:** Mobilizations and soft tissue techniques. * **Therapeutic Exercise:** * **Low-load exercises, coordination, and endurance training.** * **Correct movement patterns.** * **Functional exercises.** * **Traction** can be beneficial. * **Education:** Informing the patient about the condition and management plan. * **Interventional Procedures:** In severe or persistent cases, interventions like epidural steroid injections may be considered. * **Surgical Intervention:** Reserved for cases with significant neurological deficits, progressive weakness, or intractable pain unresponsive to conservative treatment. ### 3.3 Cervicogenic headache vs. Radicular Syndromes While both conditions involve the cervical spine, they are distinct: * **Cervicogenic Headache (CEH):** Primarily a headache originating from cervical dysfunction, characterized by neck pain and mechanical provocation leading to head pain. The pain is typically unilateral and occipital. * **Radicular Syndrome:** Involves direct irritation or compression of a nerve root, leading to symptoms along the nerve's distribution (e.g., radiating arm pain, weakness, numbness). While neck pain can be present, the hallmark is the radiating neurological symptoms. It is crucial for clinicians to differentiate between these conditions, as treatment approaches may vary. A comprehensive assessment, including specialized tests and potentially imaging, is essential for accurate diagnosis and effective management. --- > **Tip:** When assessing patients with headache, always consider medication overuse as a potential contributing factor. A detailed medication history is crucial. > > **Tip:** For radicular syndromes, differentiating between somatic referred pain and true radicular pain is key. The presence of neurological deficits (weakness, numbness) strongly suggests radiculopathy. > > **Tip:** Be aware that symptoms from the scalene muscles can mimic cervical radicular pain. Careful palpation and provocative testing are necessary to distinguish these. --- # Whiplash Associated Disorders (WAD) This topic explores Whiplash Associated Disorders (WAD), a spectrum of injuries resulting from indirect trauma to the neck, often from motor vehicle collisions, characterized by varied symptoms and influenced by multiple factors. ### 5.1 Definition and mechanism of injury Whiplash Associated Disorders (WAD) are typically the result of an indirect, post-traumatic acceleration-deceleration mechanism. The head, weighing approximately 4 kilograms, is subjected to significant energy transfer during such events. For instance, in a rear-end collision, the torso moves forward, propelling the head against the headrest, then the head is catapulted forward. This can lead to soft tissue injuries and a wide range of clinical symptoms beyond neck pain. ### 5.2 WAD grading and classification A grading system, similar to general neck pain classifications, is used to categorize WAD: * **WAD 0:** No complaints. * **WAD 1:** Subclinical; minimal complaints. Management involves observing the natural course without significant intervention. * **WAD 2A:** Local hyperalgesia, muscle pain, and reduced range of motion without a psychological component. This is comparable to typical neck pain symptoms. * **WAD 2B:** Includes a psychological component, such as kinesiophobia (fear of movement due to fear of causing further damage), as identified by the TAMPA scale. * **WAD 2C:** Involves a disturbed pain system (hypersensitivity) and post-traumatic stress, which is a significant predictor of outcomes. * **WAD 3:** Characterized by neurological signs. * **WAD 4:** Indicates structural pathologies such as fractures, requiring surgical intervention. A newer classification model also exists: * **WAD 0:** No complaints. * **WAD 1:** Subclinical, minimal complaints. * **WAD 2A:** No psychological component, comparable to typical neck pain with local hyperalgesia, muscle pain, and reduced ROM. * **WAD 2B:** Presence of a psychological component like kinesiophobia. * **WAD 2C:** Disturbed pain system (hypersensitivity) and post-traumatic stress. * **WAD 4:** Structural pathologies, fractures. The severity of symptoms often correlates with the complexity of the WAD grade. ### 5.3 Symptoms of WAD WAD can present with a broad spectrum of symptoms, including: * Neck pain * Headaches * Dizziness * Sleep disturbances * Concentration problems * Fatigue * Feeling of stiffness or tightness * Clicking or cracking sensations * Difficulty looking upwards or driving * Prolonged computer use discomfort ### 5.4 Pathophysiology and injury mechanisms The exact pathophysiological mechanism of WAD is not fully understood, but it is suspected to involve damage to soft tissues. Even low-intensity impacts, comparable to bumper cars at an amusement park, can cause injury. The forces involved during a whiplash event include retraction, extension, protraction, and flexion. Headrests can limit extension, potentially reducing injury risk at lower loads. **Potential sites of injury include:** * Joint capsules of the facet joints. * Annuli fibrosi. * Ligamentous ruptures. * Fractures. Post-mortem studies and animal experiments have provided some evidence of damage to joint capsules, ligaments, and facet joints. Muscle damage can be indicated by elevated serum creatine kinase levels. Imaging such as X-rays, CT, and MRI can be used, but it's important to note that degenerative changes may be present in individuals, especially older adults, and pre-exist the injury. X-rays are primarily used to rule out fractures and can be lengthy. ### 5.5 Natural course and prognosis of WAD The natural course of WAD generally shows a good chance of recovery within 3 months. However, a significant proportion of individuals may experience persistent neck pain (up to 50% after 1 year), with 30% reporting moderate to severe pain or functional limitations. This leads to substantial personal and economic costs. **Factors influencing prognosis and recovery include:** * **Natural Course:** Initial recovery is often spontaneous, and intervention should be considered when the course deviates from normal. * **Early Assessment:** Swift assessment and intervention are crucial as neuromuscular changes can occur rapidly (within a month). * **Neck Disability Index (NDI):** A higher initial NDI score in post-traumatic patients can indicate a greater likelihood of a worse outcome. * **Psychological Factors:** * **Post-Traumatic Stress Disorder (PTSD):** Affects 10-25% of individuals and is a significant predictor of chronic disability. Specific subscales like hyperarousal within the PDS are important to assess. * **Kinesiophobia:** Fear of movement. * **Negative Expectations:** Can influence pain perception and recovery. * **Catastrophizing:** Exaggerating the threat value of pain. * **Pain Processing:** * **Cold Hyperalgesia:** Reduced tolerance to cold stimuli. * **Pressure Pain Thresholds:** Decreased ability to tolerate pressure, potentially extending beyond the neck region. * **Altered Pain Modulation:** Reduced inhibitory mechanisms can make individuals more susceptible to pain from various stimuli. * **Age:** While evidence can be inconsistent, older age generally has a negative impact on recovery. * **Motor Function:** * **Motor and Sensorimotor Control Deficits:** These can manifest early, often within a month, and impact prognosis. * **Delayed Onset of Muscle Activation:** Both external (e.g., balance disturbance) and internal (e.g., visual cue for arm movement) stimuli may elicit delayed muscle responses in individuals with WAD. * **Increased Superficial Muscle Activation:** Muscles like SCM, trapezius, and levator scapulae may become overactive, while deep cervical flexors (DCF) might be less active. * **Proprioceptive Impairment:** Difficulty with joint position sense, particularly in moderate to severe cases. * **Structural Muscular Changes:** Muscle atrophy, fatty infiltration, altered contractile properties, and changes in muscle fiber type (e.g., shift from Type I to Type II fibers). * **Other Factors:** * Previous episodes of neck pain. * Work-related factors (e.g., high job demands, low control over workload). * Smoking. * Lack of social support. A clinical prediction rule can help identify individuals with an increased probability of developing chronic moderate to severe disability, considering older age, initially higher NDI levels, and hyperarousal symptoms. ### 5.6 Management of WAD The management of WAD involves a multi-faceted approach, considering the underlying pathophysiological model and influencing factors: * **Education and Advice:** Crucial, especially for chronic pain, involving explanations of referred pain and reassurance about the natural course. * **Exercises and Staying Active:** * **Low-load exercises:** Gentle movements. * **Coordination and Endurance training:** To improve neuromuscular control. * **Correct movement patterns:** Practicing fluid and controlled movements. * **Motor Control Exercises:** Focusing on specific muscle activation, especially deep cervical flexors (e.g., longus colli, longus capitis) and extensors. These exercises aim to improve recruitment patterns, reduce co-contractions, and enhance proprioception. Immediate feedback (verbal and tactile) is vital. * **Functional Exercises:** Incorporating daily activities into training. * **Task Breakdown:** Starting with simple movements and progressing gradually. * **Mobilizations and Manipulations:** Applied to thoracic and high-cervical regions to address joint dysfunction. * **Pain Management:** * **Pharmacological:** NSAIDs can be useful for acute radicular symptoms. Medication overuse headache needs careful attention. * **Interventions:** Techniques like dry needling may be considered. * **Interdisciplinary Therapy:** A multidisciplinary approach is often necessary, especially when psychological factors are prominent. * **Imaging:** Only used to rule out structural pathologies like fractures (WAD grade 4). The Canadian C-Spine Rule or NEXUS criteria can guide the need for imaging in trauma patients. **Therapeutic principles include:** * **Early Intervention:** Addressing neuromuscular changes as soon as possible. * **Specific Exercise:** Targeting deep neck flexors and extensors. * **Feedback:** Providing immediate and consistent feedback on movement and muscle activation. * **Reciprocal Inhibition:** Activating agonists can help inhibit antagonists. * **Self-Management:** Educating patients to manage their pain through exercises at home. The combination of manual therapy (e.g., spinal joint manipulation, dry needling) and exercise therapy has shown promising results in reducing headache intensity and frequency in cervicogenic headaches, which can be associated with WAD. While evidence quality varies, motor control exercises, strength training, and stretching are generally recommended, tailored to the individual patient and therapist expertise. --- ## Common mistakes to avoid - Review all topics thoroughly before exams - Pay attention to formulas and key definitions - Practice with examples provided in each section - Don't memorize without understanding the underlying concepts

| Term | Definition | |------|------------| | Cervicothoracic region | The area of the spine encompassing the cervical (neck) and thoracic (upper back) vertebrae. | | Neck pain | Pain experienced in the neck region, which can be a symptom of various conditions and may present with a wide spectrum of symptoms including pain, weakness, fatigue, perceived disability, dizziness, concentration problems, and headache. | | Clinical reasoning | A systematic process used by clinicians to analyze patient information, evaluate findings, establish a diagnosis, determine a prognosis, and develop an appropriate treatment plan. | | Aspecific neck complaints | Neck complaints where a precise underlying cause cannot be identified through examination. | | Prevalence | The proportion of a population that has a specific condition or characteristic at a given point in time or over a specific period. | | Incidence | The rate at which new cases of a disease or condition occur in a population over a specified period. | | Musculoskeletal causes | Conditions related to the muscles, bones, joints, ligaments, and tendons. | | Sensorimotor | Pertaining to both sensory and motor functions, often referring to the interplay between the nervous system and the musculoskeletal system in controlling movement. | | Quebec Neck Pain Task Force | A classification system for neck pain, categorizing it based on factors like onset, mechanism, and temporal aspects. | | Idiopathic | Of unknown cause. | | Traumatic | Relating to or caused by physical injury. | | Degenerative | Characterized by a gradual deterioration of structure or function. | | Acute | Having a sudden onset, sharp rise, and short course. | | Subacute | Intermediate in duration or severity between acute and chronic. | | Chronic | Persisting for a long time or constantly recurring. | | Nociception | The sensory nervous system process that initiates, processes, and modulates the perception of pain. | | Inflammation | A localized physical condition in which part of the body becomes reddened, swollen, hot, and often painful, especially as a reaction to injury or infection. | | Neuropathic pain | Pain caused by damage or disease affecting the somatosensory nervous system. | | Sensitization | An increase in the responsiveness of the nervous system to stimuli, often leading to increased pain perception. | | Somatosensory | Relating to the sensory impulses originating from the body, typically from the skin, muscles, and joints. | | Prognostic indicators | Factors that help predict the likely outcome of a disease or condition. | | Clinical Prediction Rules (CPRs) | Tools that combine a patient's clinical information to estimate the probability of a particular outcome. | | Screening | A process to identify individuals at risk for a specific condition, often followed by further investigation if indicated. | | Red flag | A sign or symptom that suggests the possibility of a serious underlying medical condition requiring urgent investigation. | | Anamnestisch | Relating to information gathered from a patient's medical history. | | Tractusanamnese | A systematic inquiry into the patient's symptoms and medical history. | | Motor Vehicle Collision (MVC) | An accident involving at least one vehicle on a road. | | Canadian C-Spine Rule | A clinical decision rule used to determine the need for imaging of the cervical spine after trauma. | | Midline c-spine tenderness | Tenderness elicited upon palpation of the spinous processes in the midline of the cervical spine. | | NEXUS criteria | A set of criteria used to determine whether cervical spine radiography is indicated after trauma. | | Non-musculoskeletal causes | Conditions that do not originate from the muscles, bones, or joints. | | Gerefereerde pijn (Referred pain) | Pain perceived at a location other than the site of the painful stimulus. | | Motor control | The process by which the central nervous system organizes and executes movement. | | Neuromuscular system | The system comprising nerves and muscles, responsible for movement and other bodily functions. | | Muscle guarding | Involuntary contraction of muscles to protect an injured area. | | SCM (Sternocleidomastoid) | A large superficial neck muscle that acts to flex the head and neck. | | Trapezius | A large paired trapezoid-shaped muscle that is responsible for moving, rotating, and retracting the scapula and extending the head at the neck. | | Levator scapulae | A muscle in the neck that elevates the scapula. | | Muscle co-activation | The simultaneous contraction of agonist and antagonist muscles, which can be functional for stabilization or dysfunctional if excessive. | | Proprioception | The sense of the relative position of one's own parts of the body and strength of effort being employed in movement. | | Atrophy | The wasting away or decrease in size of an organ or tissue. | | Fat infiltration | The accumulation of fat within muscle tissue. | | Deep Cervical Flexors (DCF) | Muscles located in the deep anterior neck responsible for flexing the cervical spine. | | Global movers | Larger, superficial muscles that produce gross movements. | | Local stabilizers | Smaller, deeper muscles that provide stability to a joint. | | Whiplash Associated Disorder (WAD) | A neck injury caused by a sudden, forceful hyperextension and hyperflexion of the neck, typically from a rear-end automobile collision. | | External activation | Muscle activation triggered by external stimuli, such as a balance perturbation. | | Internal activation | Muscle activation triggered by internal stimuli, such as a planned motor task. | | Feedforward control | A predictive mechanism that anticipates the sensory consequences of a motor command and adjusts muscle activity accordingly. | | Joint Position Error (JPE) | A measure of the inaccuracy in the perceived position of a joint. | | Muscle Fat Infiltration (MFI) | A measure of the amount of fat within a muscle. | | Low load exercises | Exercises performed with minimal resistance or effort. | | Coordination | The ability to use different parts of the body together smoothly and efficiently. | | Endurance | The ability to sustain prolonged physical or mental effort. | | Deep neck flexors | Muscles such as Longus Colli and Longus Capitis, crucial for stabilizing the cervical spine. | | Craniocervical flexion (CCF) | A movement involving flexion at the joints between the skull (cranium) and the first two cervical vertebrae (C0-C1 and C1-C2). | | Pressure Pain Threshold (PPT) | The point at which a pressure stimulus becomes painful. | | Reciprocal inhibition | The relaxation of one muscle in response to the contraction of its antagonist. | | Suboccipital muscles | A group of small muscles located at the base of the skull that are primarily involved in proprioception and fine head movements. | | Myofascial pain | Pain originating from the muscles and their surrounding connective tissue (fascia). | | Interventions | Therapeutic strategies or actions taken to address a health condition. | | Radiculair syndroom | A condition caused by compression or irritation of a spinal nerve root. | | Herniation | The displacement of tissue from its normal position. | | Radicular conflict | Compression or irritation of a nerve root. | | Osteophytosis | The formation of bone spurs (osteophytes). | | Foramen | A natural opening or passage in the body, such as a nerve root opening in the spine. | | Stenosis | The narrowing of a passage or cavity. | | Ischemia | Insufficient blood supply to an organ or tissue. | | Edema | Swelling caused by excess fluid trapped in the body's tissues. | | Fibrosis | The thickening and scarring of connective tissue. | | Demyelination | The loss of the myelin sheath that surrounds nerve fibers. | | Neuro-inflammation | Inflammation of the nervous system. | | Entrapment neuropathies | Nerve damage caused by compression. | | Spurling's test | A provocative test used to assess for cervical radiculopathy. | | ULTT (Upper Limb Tension Test) | A test used to assess the mobility and sensitivity of nerves in the upper limb. | | Neural tension | The stretching or compression of nerves. | | Somatic referred pain | Pain perceived in a somatic (body) region different from the source of the stimulus. | | Trigger points | Hypersensitive spots in muscles that can cause referred pain. | | Scaleni | A group of three muscles in the neck that can contribute to neck pain and mimic radicular symptoms. | | Cervicogenic headache (CEH) | Headache that originates from dysfunction in the cervical spine. | | Trigeminocervical nucleus | A part of the brainstem where sensory input from the trigeminal nerve and upper cervical nerves converges, potentially leading to referred pain. | | N. trigeminus (Trigeminal nerve) | A cranial nerve that provides sensation to the face and motor control to the muscles of mastication. | | Ipsilateral | On the same side of the body. | | CROM (Cranio-cervical range of motion) | The extent of movement possible at the joints between the skull and the cervical spine. | | SNAG (Sustained Natural Apophyseal Glide) | A manual therapy technique used to improve joint mobility. | | Manual therapy | Hands-on techniques used to diagnose and treat musculoskeletal conditions. | | Dry needling | A technique that involves inserting thin needles into trigger points or tight muscles to relieve pain and improve function. | | Biopsychosocial model | A framework that considers the biological, psychological, and social factors that influence health and illness. | | Kinesiophobia | Fear of movement, often associated with chronic pain conditions. | | Posttraumatic Stress Disorder (PTSD) | A mental health condition triggered by experiencing or witnessing a terrifying event. | | Hyperarousal | A state of increased physiological and psychological alertness, often a symptom of PTSD. | | NDI (Neck Disability Index) | A questionnaire used to assess the impact of neck pain on a patient's daily function. | | PDS (Posttraumatic Stress Diagnostic Scale) | A scale used to assess for symptoms of PTSD. | | Muscle spindle | A sensory receptor within muscles that detects changes in muscle length and rate of change, contributing to proprioception. | | Global movers | Larger, superficial muscles that produce gross movements. | | Local stabilizers | Smaller, deeper muscles that provide stability to a joint. | | Proprioception | The sense of the relative position of one's own parts of the body and strength of effort being employed in movement. | | Suboccipital muscles | A group of small muscles located at the base of the skull that are primarily involved in proprioception and fine head movements. | | Myofascial pain | Pain originating from the muscles and their surrounding connective tissue (fascia). | | Interventions | Therapeutic strategies or actions taken to address a health condition. | | Radiculair syndroom | A condition caused by compression or irritation of a spinal nerve root. | | Herniation | The displacement of tissue from its normal position. | | Radicular conflict | Compression or irritation of a nerve root. | | Osteophytosis | The formation of bone spurs (osteophytes). | | Foramen | A natural opening or passage in the body, such as a nerve root opening in the spine. | | Stenosis | The narrowing of a passage or cavity. | | Ischemia | Insufficient blood supply to an organ or tissue. | | Edema | Swelling caused by excess fluid trapped in the body's tissues. | | Fibrosis | The thickening and scarring of connective tissue. | | Demyelination | The loss of the myelin sheath that surrounds nerve fibers. | | Neuro-inflammation | Inflammation of the nervous system. | | Entrapment neuropathies | Nerve damage caused by compression. | | Spurling's test | A provocative test used to assess for cervical radiculopathy. | | ULTT (Upper Limb Tension Test) | A test used to assess the mobility and sensitivity of nerves in the upper limb. | | Neural tension | The stretching or compression of nerves. | | Somatic referred pain | Pain perceived in a somatic (body) region different from the source of the stimulus. | | Trigger points | Hypersensitive spots in muscles that can cause referred pain. | | Scaleni | A group of three muscles in the neck that can contribute to neck pain and mimic radicular symptoms. | | Cervicogenic headache (CEH) | Headache that originates from dysfunction in the cervical spine. | | Trigeminocervical nucleus | A part of the brainstem where sensory input from the trigeminal nerve and upper cervical nerves converges, potentially leading to referred pain. | | N. trigeminus (Trigeminal nerve) | A cranial nerve that provides sensation to the face and motor control to the muscles of mastication. | | Ipsilateral | On the same side of the body. | | CROM (Cranio-cervical range of motion) | The extent of movement possible at the joints between the skull and the cervical spine. | | SNAG (Sustained Natural Apophyseal Glide) | A manual therapy technique used to improve joint mobility. | | Manual therapy | Hands-on techniques used to diagnose and treat musculoskeletal conditions. | | Dry needling | A technique that involves inserting thin needles into trigger points or tight muscles to relieve pain and improve function. | | Biopsychosocial model | A framework that considers the biological, psychological, and social factors that influence health and illness. | | Kinesiophobia | Fear of movement, often associated with chronic pain conditions. | | Posttraumatic Stress Disorder (PTSD) | A mental health condition triggered by experiencing or witnessing a terrifying event. | | Hyperarousal | A state of increased physiological and psychological alertness, often a symptom of PTSD. | | NDI (Neck Disability Index) | A questionnaire used to assess the impact of neck pain on a patient's daily function. | | PDS (Posttraumatic Stress Diagnostic Scale) | A scale used to assess for symptoms of PTSD. | | Muscle spindle | A sensory receptor within muscles that detects changes in muscle length and rate of change, contributing to proprioception. |