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Examination of the Migraine Patient
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Examination of the Migraine Patient

A Complete Clinical Workbook

Part I: The Neuro-Metabolic Examination of the Migraine Patient

1. Introduction: The Neuro-Metabolic Model of Migraine

1.1 The Paradigm Shift: Migraine is a complex neurological disorder, but a growing body of evidence re-frames it as a systemic condition with metabolic underpinnings. This evolving perspective moves beyond the traditional symptomatic approach to identify the root physiological dysregulation that lowers the brain's threshold for a migraine attack. For a functional medicine practitioner, this means the primary job is to act as a "medical detective" to uncover the underlying "why" of a patient's symptoms.

1.2 The Clinical Imperative: A Phased Approach: The framework presented here is designed to integrate a patient's history with targeted testing. This avoids unnecessary or random lab work and ensures every test serves a purpose. This phased strategy enables a precise, data-driven approach, transforming subjective patient complaints into objective, actionable findings.

2. Foundational Pillars of Metabolic Assessment

2.1. Insulin Resistance: Decoding the Hyperglycemic-Neurovascular Connection

A patient's clinical history is the starting point for investigating insulin resistance. Answers to questions about sugar cravings, dizziness between meals, and headaches after eating can be a powerful "bedside test".

2.1.1 Bedside Examination & Physical Indicators

Abdominal Obesity: Measure waist circumference for central obesity.

Acanthosis Nigricans: Inspect skin for dark, velvety patches.

Skin Tags (Acrochordons): Examine neck, armpits, or eyelids.

High Blood Pressure: Readings of 130/80 mmHg or higher.

Orthostatic Blood Pressure: A rapid drop upon standing can indicate autonomic dysfunction.

2.1.2 Validated Tests & Examinations

HOMA-IR: A validated surrogate marker for insulin resistance calculated from fasting glucose and insulin.

Oral Glucose Tolerance Test (OGTT): The gold standard for diagnosing glucose tolerance abnormalities.

Triglyceride-Glucose (TyG) Index: A reliable and low-cost surrogate for insulin resistance.

Bedside Clinical Questionnaire: A tool to uncover symptomatic patterns of insulin resistance.

2.2. Mitochondrial Function: The Energetic Nexus of Neuronal Excitability

A diminished energy supply can lower the brain's excitability threshold, making it more vulnerable to a migraine attack. This "neuroenergetic deficit" may explain exertion-triggered migraines or chronic fatigue.

2.2.1 Bedside Examination & Physical Indicators

Muscle Weakness & Fatigue: Test for weakness, particularly in the face, neck, arms, and legs.

Ptosis (Drooping Eyelids): Examine for drooping upper eyelids.

Ataxia: Conduct a physical examination for balance and coordination.

Brain Fog and Memory: Assess for self-reported difficulty with cognitive function.

2.2.2 Validated Tests & Examinations

Urinary Organic Acids Test (OAT): Evaluates byproducts of metabolic and mitochondrial function.

Homocysteine: High levels are associated with vascular damage and neuroinflammation.

Micronutrient Assessment (CoQ10 & Riboflavin): Essential cofactors in the mitochondrial electron transport chain.

2.3. Gut-Brain Axis: Assessing the Microbiome and Intestinal Integrity

An imbalance in the gut microbiome (dysbiosis) or a compromised intestinal lining ("leaky gut") can trigger a systemic inflammatory response that fuels neuroinflammation and lowers the migraine threshold.

2.3.1 Bedside Examination & Physical Indicators

Abdominal Palpation: Palpate for distension, tenderness, or masses.

Skin Rashes & Eczema: Inspect for signs of systemic inflammation or food sensitivities.

Malabsorption Signs: Assess for pale skin or brittle hair and nails.

2.3.2 Validated Tests & Examinations

GI-MAP® Comprehensive Stool Analysis: Provides a detailed profile of gut health.

SIBO Breath Test: A non-invasive tool for diagnosing Small Intestinal Bacterial Overgrowth.

Zonulin (Serum & Stool): A protein marker for "leaky gut".

IgG Food Sensitivity Testing: Measures the body's IgG antibody response to foods.

2.4. Autoimmunity & Inflammation: The Inflammatory Threshold for Pain

Chronic inflammation can lower the threshold for pain perception and is a common underlying factor in migraine. This can be driven by autoimmunity, where the immune system mistakenly attacks the body's own tissues, including neural structures.

2.4.1 Bedside Examination & Physical Indicators

Joint Examination: Check for swelling, redness, or tenderness in joints.

Lymph Node Palpation: Assess for swollen or tender lymph nodes.

Skin Inspection: Look for rashes like a malar (butterfly) rash, common in lupus.

2.4.2 Validated Tests & Examinations

C-Reactive Protein (CRP) & ESR: General markers of inflammation.

Antinuclear Antibody (ANA): A screening test for autoimmunity.

Thyroid Antibodies (TPO & TG): To screen for Hashimoto's thyroiditis.

Neural Zoomer Plus: Advanced testing for cross-reactive antibodies to neural tissues.

2.5. Hormone Function: The Endocrine Modulators of Migraine Pathophysiology

Fluctuations in hormones, especially estrogen, are well-known triggers for migraine. Investigating the entire endocrine system, including thyroid and adrenal hormones, is crucial.

2.5.1 Bedside Examination & Physical Indicators

Menstrual Cycle Tracking: Correlate headache frequency with the menstrual cycle.

Thyroid Palpation: Check for goiter or nodules.

Adrenal Assessment: Look for signs like unusual fatigue, salt cravings, or hyperpigmentation.

2.5.2 Validated Tests & Examinations

DUTCH Test: A comprehensive dried urine test for hormones and their metabolites.

Comprehensive Thyroid Panel: Includes TSH, free T4, free T3, reverse T3, and antibodies.

Sex Hormone Panel (Serum): Measures levels of estrogen, progesterone, and testosterone.

2.6. Stress & Cortisol: Evaluating HPA Axis Dysregulation and Adaptability

The Hypothalamic-Pituitary-Adrenal (HPA) axis governs the stress response. Chronic stress leads to dysregulation of cortisol, which can increase inflammation and excitability in the brain.

2.6.1 Bedside Examination & Physical Indicators

Perceived Stress Scale (PSS): A validated questionnaire to assess stress levels.

Pupillary Light Reflex: Slow constriction or dilation can indicate autonomic imbalance.

Sleep Quality Assessment: Evaluate patterns of insomnia or non-restorative sleep.

2.6.2 Validated Tests & Examinations

Salivary Cortisol Profile: Measures the diurnal rhythm of cortisol.

Heart Rate Variability (HRV): An objective measure of autonomic nervous system balance and resilience.

2.7. Serotonin Dysfunction: A Nuanced Look at Neurotransmitter Imbalance

While serotonin is implicated in migraine, its role is complex. A functional approach looks at the entire lifecycle of serotonin, from precursor availability to receptor sensitivity.

2.7.1 Bedside Examination & Physical Indicators

Mood Assessment: Screen for symptoms of depression or anxiety, which are often comorbid with low serotonin.

Digestive Complaints: Note issues like constipation, as 90% of serotonin is produced in the gut.

2.7.2 Validated Tests & Examinations

Urinary Neurotransmitter Testing: Measures levels of serotonin and other key neurotransmitters.

Amino Acid Profile: Assesses levels of precursors like tryptophan.

3. Integrative Analysis & Clinical Implementation

The metabolic pillars discussed are not isolated systems but are deeply interconnected. By using questionnaires and a phased testing approach, a clinician can piece together the patient's unique story. This manual provides the foundational framework necessary to translate these objective findings into a targeted, personalized neuro-metabolic care plan.

4. Comprehensive Summary of Clinical Tests

Metabolic Pillar Test 1 Test 2 Test 3 Test 4
Insulin Resistance HOMA-IR (< 1.0) Oral Glucose Tolerance Test (OGTT) (< 140 mg/dL) Triglyceride-Glucose (TyG) Index Clinical Questionnaire & Exam
Mitochondrial Function Urinary Organic Acids Test (OAT) (Mid-Range) Homocysteine (< 9 ÎĽmol/L) Blood Biomarkers (GDF-15, FGF-21) N-Acetyl-Aspartate (NAA) Blood Level
Gut Function GI-MAP® Stool Analysis SIBO Breath Test Zonulin (IgA/IgG Antibodies) (Low Levels) IgG Food Sensitivity Test
Autoimmunity & Inflammation hs-CRP (< 1.0 mg/L) ESR ANA Panel Mast Cell Activation Markers (Tryptase)
Hormone Function Serum Sex Hormone Panel DUTCH Plus CAR Test (Steep Diurnal Curve) Comprehensive Thyroid Panel (TSH 0.5–2.0 μIU/mL) Serum Prolactin Level
Stress & Cortisol DHEA-S and Cortisol Ratio (5:1 to 6:1) Salivary Cortisol Diurnal Rhythm (4-point) Cortisol Awakening Response (CAR) Bedside Heart Rate Variability (HRV)

Part II: The Neurological Examination of the Migraine Patient

1. Introduction: The Neuro-Metabolic Model of Migraine

1.1 The Paradigm Shift: Migraine is far from a simple headache; it is a complex neurological disorder rooted in neuronal hyperexcitability and a predisposition for the brain to lose control over sensory inputs. A functional neurological approach moves beyond symptom management to act as a "medical detective," using a systems-based examination to uncover the underlying dysfunctions that lower a patient's migraine threshold. This framework focuses on localizing these dysfunctions to specific areas of the central nervous system, providing a foundation for targeted, personalized neuro-rehabilitative and therapeutic strategies.

1.2 The Clinical Imperative: A Phased Approach: The examination framework is built on a phased approach that integrates patient history with a focused physical and neurological examination. This methodical process ensures that clinical findings are directly linked to objective markers of dysfunction. The approach follows three phases: Clinical Discovery (Bedside), Neurological Bedside Examination, and Integrative Analysis.

1.3 Differentiating Upper vs. Lower Motor Neuron Lesions: A fundamental principle of the neurological examination is the ability to differentiate between a lesion in the upper motor neuron (UMN) and the lower motor neuron (LMN). This distinction is critical for a functional neurologist because it helps to precisely localize the source of the neurological problem, informing whether the issue originates in the central nervous system (e.g., brainstem) or in the peripheral nervous system (e.g., cranial nerve).

1.4 Red Flags: When to Suspect Other Pathology: While the primary goal of the clinical examination is to confirm a migraine diagnosis and identify its underlying functional drivers, it is critically important to be vigilant for "red flag" symptoms and signs that may indicate a more serious or life-threatening condition. These findings warrant immediate medical referral and further investigation.

2. Initial Clinical Assessment: Vital Signs

2.1 Orthostatic Vital Signs: Procedure and Interpretation: Orthostatic hypotension, or a significant drop in blood pressure upon standing, is a key indicator of autonomic nervous system (ANS) dysfunction and should be a standard part of the bedside examination. The presence of ANS dysregulation is a common feature in migraine patients and can provide an important clue to the underlying pathophysiology.

3. The Neurological Examination: A Systems-Based Approach

3.1. Cerebellum and Vestibulocerebellum: The Balance and Coordination Hub

The cerebellum is crucial for balance, coordination, and sequencing body functions. Dysfunction can lead to vertigo, poor balance, and unsteady gait.

3.1.1 Bedside Examination & Physical Indicators

Postural Assessment: Observe for head forward posture, pelvic tilt, or excessive kyphosis/lordosis.

Gait Analysis: Look for an ataxic (unsteady) gait, abnormal arm swing, or sway during the Fukuda step test.

Balance Assessment: A positive Romberg's test or inability to maintain balance with eyes closed.

Coordination and Motor Control: Test for dysmetria (overshooting) on the Finger-to-Nose Test.

3.2. Trigeminal Cervical Nucleus (TCN): CN V, VII Pain Hub

The TCN is the brain's central pain relay for the head and neck. Dysfunction can lead to headaches and referred pain in the face and jaw.

3.2.1 Bedside Examination & Physical Indicators

Jaw Palpation: Check for jaw deviation, muscle spasm, or pain/clicking in the TMJ.

Cervical Spine Exam: Test for restricted range of motion or tenderness in upper cervical muscles.

Facial Sensation: Test for asymmetry in sensation in all three divisions of the trigeminal nerve.

Jaw Jerk Reflex: An exaggerated reflex indicates an upper motor neuron lesion.

3.3. Lower Medulla: CN IX, X, XI, XII & Autonomic Control

The lower medulla is a part of the brainstem that controls automatic functions such as swallowing, digestion, and cardiovascular reflexes. Dysfunction in this area can cause symptoms that are often comorbid with migraine, such as nausea, vomiting, dizziness, and heart rate changes upon standing.

3.3.1 Bedside Examination & Physical Indicators

Orthostatic Vital Signs: A drop in blood pressure or rise in heart rate upon standing indicates orthostatic intolerance.

Palate and Tongue Examination (CN IX, X, & XII): Look for symmetrical elevation of the soft palate and uvula; no signs of tongue wasting or fasciculation.

Pharyngeal Reflexes and Swallowing (CN IX & X): Check for a symmetric gag reflex and ability to swallow without difficulty.

Trapezius and SCM Examination (CN XI): Test for symmetrical strength in the trapezius and sternocleidomastoid muscles.

3.4. Pons: CN V, VI, VII, VIII & Horizontal Gaze

The pons is a critical part of the brainstem that integrates sensory input, controls facial movement, and houses nuclei for several key cranial nerves. Dysfunction here can cause laterality of symptoms, dizziness, hearing changes, and eye movement deficits.

3.4.1 Bedside Examination & Physical Indicators

General Observation: Note if symptoms are consistently more severe on one side.

Facial Motor Exam & Blink Reflex: Check for facial asymmetry and a quick, symmetrical blink reflex.

Extra-Ocular Movements (CN VI): Test the ability to abduct both eyes fully and smoothly.

3.5. Midbrain: Oculomotor, Arousal, and Pain Modulation

The midbrain is a small but critical area involved in pain modulation, emotional responses, and the "fight-or-flight" response. Dysfunction here can lead to a reduced pain tolerance, anxiety, depression, and sensitivity to light.

3.5.1 Bedside Examination & Physical Indicators

Pupillary Light Reflex: Assess for symmetrical, brisk, and consensual pupillary constriction.

Oculomotor Exam: Convergence and Divergence: Check the near point of convergence (NPC).

Glabella Tap Response and Blink Rate: Blinking should cease after the first few taps.

Behavioral Observation: Observe for mood changes, anxiety, or an exaggerated stress response.

3.6. Hypothalamus: The Master Regulator

The hypothalamus is the master control center that regulates hormones, sleep, appetite, and body temperature. Assessing this area is crucial for understanding the root cause of a patient's symptoms.

3.6.1 Bedside Examination & Physical Indicators

Vital Sign Assessment: Check for orthostatic hypotension or poor peripheral perfusion.

Physical Signs of Hormonal Dysfunction: Look for abdominal obesity, facial rounding, or dry skin/thinning hair.

Thermoregulation Assessment: Inquire about a history of feeling too hot or too cold.

Actigraphy and Sleep Diary: Assess for a reversed circadian rhythm or lack of restorative sleep.

3.7. Thalamocortical and Cortical Function: The Sensory Processor

This is the highest level of sensory processing, and dysfunction in this area can make patients hypersensitive to external stimuli like loud noises, bright lights, and strong smells.

3.7.1 Bedside Examination & Physical Indicators

Light and Sound Sensitivity: Note any withdrawal or aversion to normal room lighting or sound.

Two-Point Discrimination, Stereognosis, and Graphesthesia: Test the ability to perceive two points, recognize objects by touch, and recognize writing on the skin.

Speech and Language Assessment: Check for signs of aphasia, such as difficulty finding words.

Cognitive Examination: Assess memory, focus, and mental status.

4. Integrative Analysis & Clinical Implementation

The neurological pillars discussed are not isolated systems but are deeply interconnected. By using questionnaires and a phased testing approach, a clinician can piece together the patient's unique story. This manual provides the foundational framework necessary to translate these objective findings into a targeted, personalized neuro-metabolic care plan.

Part III: Wayne's Migraine Examination Sequence

This sequence synthesizes the neurological and metabolic examinations into a cohesive clinical flow, progressing from subjective data to objective testing and a personalized plan.

Phase 1: Clinical Discovery and Data Collection (The "Why")

1.1 MIDAS Score: Administer the questionnaire to establish a baseline measure of migraine-related disability.

1.2 Perceived Stress Scale (PSS): Quantify the patient’s stress load to assess HPA axis dysregulation.

1.3 Metabolic and Neurological Survey: Use structured questionnaires to localize potential functional deficits.

1.4 Evaluation of Existing Labs and Imaging: Review recent external labs and imaging to identify "red flags".

Phase 2: Objective In-Office Assessment (The "What")

2.1 History and Deep Dive: Review all data, focusing on clarifying "Red Flag" symptoms that require immediate referral.

2.2 Vital Signs: Measure Orthostatic Vital Signs to assess Autonomic Nervous System function.

2.3 Neurological & Physical Exam: Conduct targeted exams to localize dysfunction and establish laterality (left vs. right side deficits).

2.4 Physical Exam: Focused examination for key metabolic and inflammatory indicators.

Phase 3: Testing & Implementation (The "How")

3.1 Discuss Further Testing Options: Select a phased approach for lab testing based on clinical findings.

3.2 Initial Plan: Formulate a preliminary plan based on immediate objective findings.

3.3 Further Detailed Refinement of the Plan: Review results from targeted labs and adjust the plan to be highly specific.

Part IV: The Neuro-Rehabilitative Treatment Plan

1. The Role of the Sensory Therapist

The clinician's role is defined by a clear hierarchy of action: First, do no harm and rule out pathology. Then, resolve sensory pathology, restore function, optimize sensory input, and advise on lifestyle change for recovery.

2. Designing a Treatment Plan (Planning and Target Setting)

The design process must be systematic: Decide on the area of greatest concern, choose treatable areas, set realistic outcomes and timeframes, and accept that complete resolution may not be possible.

3. Central Fatigue and Therapeutic Threshold

Before implementing therapy, assess the patient's capacity to tolerate stimulation. The goal is to start with less therapy and avoid overstimulation, tailoring home care to increase metabolic threshold using a graded approach.

4. Road Map To Treatment (SCOPE: Strategy for Clinical Objective-based Execution)

The treatment strategy (SCOPE) is built on the laterality findings established in the neurological examination. Identify the area of the neuroaxis and physiology primarily involved. For the Cerebellum (CB), stimulus should favor the ipsilateral side. For the Cortex/Brainstem, stimulus should favor the contralateral side. Focus on motor control for CB and muscle activation for Cortex.

Unified Appendix

Appendix A: Metabolic Examination Appendix

1.1 Functional Laboratory Values and Optimal Ranges

Section Lab Test Sample Type Optimal / Functional Range
2.1. Insulin ResistanceFasting InsulinSerum< 5 ÎĽIU/mL (Target: 2-5)
2.1. Insulin ResistanceFasting GlucoseSerum75 – 90 mg/dL
2.1. Insulin ResistanceHbA1cBlood4.6% – 5.3%
2.1. Insulin ResistanceHOMA-IR (Calculated)Calculated< 1.0 (Target: 0.5 – 1.0)
2.2. Mitochondrial FunctionHomocysteine (Total)Serum/Plasma< 9 μmol/L (Target: 6 – 8)
2.2. Mitochondrial FunctionCoQ10Whole Blood> 1.0 μg/mL (Target: 1.5 – 2.5)
2.3. Gut-Brain AxisSecretory IgA (sIgA)StoolHigh End of Reference Range
2.3. Gut-Brain AxisZonulin/Lactulose:MannitolSerum/UrineLow/Intact Ratio
2.3. Gut-Brain AxisFecal CalprotectinStool< 50 ÎĽg/g
2.4. Autoimmunity & Inflammationhs-CRPSerum< 1.0 mg/L (Target: < 0.5)
2.5. Hormone FunctionFree T3Serum3.0 – 4.0 pg/mL
2.5. Hormone FunctionTSHSerum0.5 – 2.0 μIU/mL
2.6. Stress & Cortisol4-Point Salivary CortisolSalivaFollows a steep diurnal curve
2.6. Stress & CortisolDHEA-SSerum/SalivaMid-Range for Age

Appendix B: Neurological Examination Appendix

2.1 Clinical Grading Appendix and Referral Guidelines

Blood Pressure and Heart Rate: Normal is below 130/85 mmHg. High is 130/85 mmHg or higher. Immediate referral for a sudden, severe headache with a reading of 180/120 mmHg or higher.

Oxygen Saturation: Normal is 95% or higher. Abnormal is 90-94%. Immediate referral for a reading below 90%.

References

Part I References: Del Moro, L. et al. (2024), Del Moro, L. et al. (2022), Cavestro, C. et al. (2025), Ali, M. et al. (2022), Özcan, R.K. et al. (2019), Maghbooli, M. et al. (2021), Sacco, S. et al. (2014), Celikbilek, A. et al. (2015), Markley, H.G. (2012), Sun, W. et al. (2025), Sadeghvand, S. et al. (2023), Gaul, C. et al. (2015), Sazali, S. et al. (2021), Wang, Y. et al. (2023), Nematgorgani, S. et al. (2022), Yong, D. et al. (2023), Ülfer, G. et al. (2025), Alpay, K. et al. (2010), Mugo, C.W. et al. (2025), Mitchell, N. et al. (2011), Thuraiaiyah, J. et al. (2022), Ha, W.S. et al. (2024), Biscetti, L. et al. (2021), Park, C.G. et al. (2022), Li, R. et al. (2024), Gül, Z.B. et al. (2021), Nappi, R.E. et al. (2022), Sacco, S. et al. (2012), Starikova, N.L. et al. (2019), Gazerani, P. (2021), Tasnim, S. et al. (2023), Hu, Y.Y. et al. (2024), Sic, A. et al. (2025), Moon, H.J. et al. (2017), An, Y.C. et al. (2019), Hamel, E. (2007), Ferrari, M.D. et al. (1989), Körtési, T. et al. (2022), Gasparini, C.F. et al. (2017), D'Andrea, G. et al. (1989).

Part II References: Noseda, R. et al. (2022), Wang, M. et al. (2022), Kros, L. et al. (2018), Koppen, H. et al. (2017), Biscetti, L. et al. (2023), Salahi, M. et al. (2022), Messina, R. et al. (2023), Ashina, S. et al. (2021), Yamanaka, G. et al. (2023), Frimpong-Manson, K. et al. (2024).

Part III References: Stewart, W.F. et al. (2000), Zandifar, A. et al. (2014), Hans, A. et al. (2023), Lipton, R.B. et al. (2014).

Part IV References: Gonsalvez, I. et al. (2021), Liu, L. et al. (2020), Shin, J.H. et al. (2014), Song, Y. et al. (2024).