Wow interesting, can you send a video of him walking 10 steps toward the camera and 10 steps away.

If you can’t even bend his knees it’s probably an open S2 wedge subluxation sounding your fingers into S1/2 or do gentle prone drop into S2 or activator . Check also his acetabulum for possible hip clicking or CHD

Parkinson’s & Rigidity Chiropractic Clinical Summary Sheet summary from our modules. 🧠 Primary Neurological Drivers Core structures involved: - Substantia nigra↓ Dopamine production → impaired movement initiation - Basal ganglia↓ Coordination of tone, rhythm, and fluidity - Brainstem↑ Tone dysregulation → rigidity, postural change, autonomic load ⚠️ Clinical Expression - Rigidity (↑ global muscle tone) - Bradykinesia (slow movement initiation) - Tremor (resting) - Altered gait + reduced arm swing - Facial masking / jaw rigidity - Autonomic dysregulation 🧬 Functional Understanding (Your Framework) - Brain becomes “over-braked” - Loss of fluid neurological adaptability - Dominance of high-tone, protective patterns - Significant brainstem overwhelm + ganglionic irritation 🔧 Chiropractic Intervention Strategy Clinical Goal: 👉 Reduce rigidity by improving tone regulation, afferent input, and nervous system adaptability 1. Brainstem Decompression & Cranial Work Key areas: - Occiput - Temporal bones - Sphenoid Objective: - Down-regulate brainstem overwhelm - Improve CSF dynamics + cranial rhythm - Reduce global tone load 2. Upper Cervical Spine (C0–C2) Focus: - Precise adjustments to restore: Proprioceptive input Brainstem signalling clarity - Outcome: - Improved communication into basal ganglia loops - Reduced rigidity expression 3. TMJ & Mandibular Ganglia (Critical) Key structures: - TMJ joint - Ramus of mandible - Embedded ganglia Why it matters: - Major sensory driver into brainstem - Jaw rigidity = increased neurological noise Application: - Release TMJ - Work the ramus + ganglia - Sweep neural irritation Outcome: - ↓ Brainstem overload - ↓ facial + global rigidity - Improved head/neck freedom 4. Thoracic Sympathetic Chain (T1–T5)

Endo is intrinsically linked to insulin sensitivity. Here’s a clear, practitioner-facing summary you can use in teaching, seminars, or clinical communication: The Link Between Insulin Sensitivity & Endometriosis — A Practitioner Perspective Endometriosis is not just a local pelvic condition — it is a systemic neuro-immune-metabolic disorder. 1. Insulin Sensitivity as a Foundational Driver Reduced insulin sensitivity (hyperinsulinaemia) contributes to a physiological environment that supports endometriosis through: - Chronic low-grade inflammation → elevated cytokines and prostaglandins - Oxidative stress → tissue irritation and impaired cellular repair - Estrogen dysregulation → insulin influences aromatase activity and estrogen signalling - Abnormal tissue growth signalling → promotes lesion persistence and angiogenesis In essence, insulin resistance primes the terrain for lesion survival and symptom amplification. 2. The Nervous System: The Missing Regulator Endometriosis is also a condition of autonomic dysregulation and neuroinflammation. Common patterns include: - Sympathetic overdrive (fight/flight dominance) - Reduced vagal tone (impaired anti-inflammatory signalling) - Heightened pain perception due to central sensitisation Endometriotic lesions themselves are richly innervated, meaning the nervous system is not just reacting to the condition — it is actively participating in it. 3. Why Ganglia & Autonomic Regulation Matter The autonomic nervous system — via its ganglia — directly influences: - Pelvic organ function (uterus, ovaries, bowel, bladder) - Vascular tone and blood flow - Immune system modulation - Inflammatory signalling pathways - Hormonal feedback loops (HPA axis) When these ganglionic pathways are dysregulated: - Inflammation is amplified - Tissue sensitivity increases - Circulation and drainage are compromised - Pain becomes persistent and exaggerated 4. Clinical Implication: Regulation Changes the Terrain