@stomachbugs0:

My tummy 😣🍕
My tummy 😣🍕
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Monday 12 October 2026 20:23:58 GMT
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1. Glymphatic congestion and impaired perivascular clearance When glymphatic flow slows, metabolic by-products, cytokines and neurotoxic proteins accumulate in motor, sensory and limbic circuits. This creates transient signalling failures that mimic weakness, collapses, sensory loss and cognitive shutdown. 2. Astrocyte polarity disruption (AQP4 dysfunction) Astrocytes control water flow, neuronal excitability, neurovascular coupling and glymphatic drainage. Loss of AQP4 polarity alters ion gradients, delays action potential recovery, and destabilises motor and sensory pathways. This is not psychological. It is cellular. 3. Microglial priming and neuroimmune sensitivity Microglia become hyper-responsive after trauma, infection, chronic stress, injury or autoimmune activation. Primed microglia exaggerate responses to normal signals, shutting down motor pathways or triggering tremors, gait disturbance and cognitive blanks. 4. Neurovascular coupling impairment When blood flow does not match neural demand, the brain experiences transient “functional energy shortages”. This causes TIA-like episodes, sudden limb weakness, vision changes, dizziness and collapses without lesions. 5. Disrupted gut–brain–immune signalling Peripheral inflammation, gut dysbiosis, mast cell activation and increased cytokines alter brain excitability and energy metabolism, amplifying functional symptoms. 6. Autoimmune-low grade inflammatory influence on neural firing Even when antibodies are not diagnostic, subclinical inflammation changes synaptic transmission, autonomic output, and cortical inhibition. This makes the brain more vulnerable to FND after injury, pain or infections. 7. Breakdown in lymphatic–glymphatic integration Cervical lymphatic stagnation (infections, trauma, structural tension, poor drainage) increases intracranial inflammatory load. This is strongly linked to dizziness, autonomic instability, sensory misfiring, limb heaviness and episodic motor shutdown. 8. Mitochondrial stress and neurometabolic insufficiency Neurons cannot sustain stable firing without adequate ATP. Mitochondrial dysfunction produces intermittent motor failure, tremors, fatigue crashes, brain fog and functional walking issues. 9. Cervical mechanotransduction and vagal–brainstem signalling errors Whiplash, instability, muscle tension or fascial restriction around the upper cervical region disrupt afferent inputs to the brainstem. This causes dizziness, gait abnormalities, migraines, POTS-like symptoms and functional collapses. 10. Dysregulated autonomic–immune cross-talk The autonomic system controls immunity and inflammation minute by minute. When these networks miscommunicate, the result is: • heart rate surges • blood pressure instability • limb weakness • sensory disturbances • bladder and gut dysfunction • episodic shutdown All of which are seen in FND. . #fnd #fndawareness #functionalneurologicaldisorder #fndwarrior #fndhopeuk
1. Glymphatic congestion and impaired perivascular clearance When glymphatic flow slows, metabolic by-products, cytokines and neurotoxic proteins accumulate in motor, sensory and limbic circuits. This creates transient signalling failures that mimic weakness, collapses, sensory loss and cognitive shutdown. 2. Astrocyte polarity disruption (AQP4 dysfunction) Astrocytes control water flow, neuronal excitability, neurovascular coupling and glymphatic drainage. Loss of AQP4 polarity alters ion gradients, delays action potential recovery, and destabilises motor and sensory pathways. This is not psychological. It is cellular. 3. Microglial priming and neuroimmune sensitivity Microglia become hyper-responsive after trauma, infection, chronic stress, injury or autoimmune activation. Primed microglia exaggerate responses to normal signals, shutting down motor pathways or triggering tremors, gait disturbance and cognitive blanks. 4. Neurovascular coupling impairment When blood flow does not match neural demand, the brain experiences transient “functional energy shortages”. This causes TIA-like episodes, sudden limb weakness, vision changes, dizziness and collapses without lesions. 5. Disrupted gut–brain–immune signalling Peripheral inflammation, gut dysbiosis, mast cell activation and increased cytokines alter brain excitability and energy metabolism, amplifying functional symptoms. 6. Autoimmune-low grade inflammatory influence on neural firing Even when antibodies are not diagnostic, subclinical inflammation changes synaptic transmission, autonomic output, and cortical inhibition. This makes the brain more vulnerable to FND after injury, pain or infections. 7. Breakdown in lymphatic–glymphatic integration Cervical lymphatic stagnation (infections, trauma, structural tension, poor drainage) increases intracranial inflammatory load. This is strongly linked to dizziness, autonomic instability, sensory misfiring, limb heaviness and episodic motor shutdown. 8. Mitochondrial stress and neurometabolic insufficiency Neurons cannot sustain stable firing without adequate ATP. Mitochondrial dysfunction produces intermittent motor failure, tremors, fatigue crashes, brain fog and functional walking issues. 9. Cervical mechanotransduction and vagal–brainstem signalling errors Whiplash, instability, muscle tension or fascial restriction around the upper cervical region disrupt afferent inputs to the brainstem. This causes dizziness, gait abnormalities, migraines, POTS-like symptoms and functional collapses. 10. Dysregulated autonomic–immune cross-talk The autonomic system controls immunity and inflammation minute by minute. When these networks miscommunicate, the result is: • heart rate surges • blood pressure instability • limb weakness • sensory disturbances • bladder and gut dysfunction • episodic shutdown All of which are seen in FND. . #fnd #fndawareness #functionalneurologicaldisorder #fndwarrior #fndhopeuk

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