Written by Anthony Hardie
(91outcomes.blogspot.com) -- A new study suggest that the use of selective channel blockers improves fatigue in people with multiple sclerosis (MS), a condition thought to be more prevalent among veterans of the 1991 Gulf War than among people who did not have similar military service.
Additionally, the use of these blockers may also help prevent secondary axonal degeneration and the functional impairment that follows.
The study noted that among people with MS, “activity and heat typically serve to exacerbate symptoms of fatigue,” – a cause-and-effect reported among some veterans of the 1991 Gulf War suffering from Gulf War Syndrome (e.g. Gulf War Illness) who do not have MS.
Selective channel blockers like Famipridine – a Potassium channel blocker – are used to treat MS, because, according the manufacturer:
Patients with MS display a range of symptoms that arise from demyelination (loss of myelin sheath) in the central nervous system (CNS), which includes the brain, spinal cord and optic nerves.
While symptoms vary between patients, they commonly include blurred vision, slurred speech, numbness or tingling in the limbs and problems with balance and coordination, due to the loss of control over vital functions such as seeing, walking and talking.
Prominent inflammatory and autoimmune responses are also evident in patients with traumatic and compressive SCI, in whom there may also be demyelination.
Demyelination alters the structural and functional relationships of voltage-gated ion channels along the axonal membrane of the nerve cell.
Exposed channels cause potassium ions to leak, so causing the axon to 'short circuit'. By closing exposed potassium channels in these damaged nerve fibres, fampridine-SR enables the axon to transmit nerve impulses again.
The abstract (article) for the published study results is as follows:
Fatigue in multiple sclerosis: Mechanisms and management.
Multiple sclerosis [MS] is a chronic immune-mediated disorder of the central nervous system [CNS]. Fatigue may be a debilitating symptom in MS patients, adversely impacting on their quality of life. Clinically, fatigue may manifest as exhaustion, lack of energy, increased somnolence, or worsening of MS symptoms.
Activity and heat typically serve to exacerbate symptoms of fatigue.
There is now strong evidence to suggest that fatigue results from reduced voluntary activation of muscles by means of central mechanisms.
Given that axonal demyelination is a pathological hallmark of MS, activity-dependent conduction block [ADCB] has been proposed as a mechanism underlying fatigue in MS.
This ADCB results from axonal membrane hyperpolarization, mediated by the Na(+)/K(+) electrogenic pump, with conduction failure precipitated in demyelinated axons with a reduced safety factor of impulse transmission. In addition, Na(+)/K(+) pump dysfunction, as reported in MS, may induce a depolarizing conduction block associated with inactivation of Na(+) channels.
These processes may induce secondary effects including axonal degeneration triggered by raised levels of intracellular Ca(2+) through reverse operation of the Na(+)-Ca(2+) exchanger.
Restoration of normal conduction in demyelinated axons with selective channel blockers improves fatigue and may yet prove useful as a neuroprotective strategy, in preventing secondary axonal degeneration and consequent functional impairment.