My hypothesis:
CFS/ME is a manifestation of increased cerebral lactate, impaired glucose metabolism and reduced cerebral antioxidant activity as a result of postural reductions in blood flow to the brain. These reductions may manifest as POTS or NMH but may also manifest as abnormal cerebral autoregulation with synchronicity between blood pressure and cerebral perfusion. The result is CNS excitation.
These abnormalities are in my opinion primarily autoimmune in many cases, with autoantibodies to beta 2 adrenoreceptors and a3 ganglionic musc. receptors implicated and the possibility of beta 1 receptor stimulating autoantibodies or antibodies against peripheral norepinephrine transporter. The result is abnormal postural hemodynamics, altered sympathetic/parasympathetic balance, impaired vasomotor function, parasympathetic withdrawal and reduced cerebral blood flow.
CFS/ME is a manifestation of increased cerebral lactate, impaired glucose metabolism and reduced cerebral antioxidant activity as a result of postural reductions in blood flow to the brain. These reductions may manifest as POTS or NMH but may also manifest as abnormal cerebral autoregulation with synchronicity between blood pressure and cerebral perfusion. The result is CNS excitation.
These abnormalities are in my opinion primarily autoimmune in many cases, with autoantibodies to beta 2 adrenoreceptors and a3 ganglionic musc. receptors implicated and the possibility of beta 1 receptor stimulating autoantibodies or antibodies against peripheral norepinephrine transporter. The result is abnormal postural hemodynamics, altered sympathetic/parasympathetic balance, impaired vasomotor function, parasympathetic withdrawal and reduced cerebral blood flow.