By: Sean Lennox, Audiologist MSc.
Multiple Sclerosis (MS) is a disorder arising from the demyelination of the axons of the central nervous system (CNS), which leads to inefficient or distorted electrochemical neural transmission. The symptoms arise from slowed information transmission between neurons and the electrical current jumping from damaged nerve tracts to adjacent nerve tracts.
The slowed signal transmission resulting from the loss of the myelin sheath of axonsand dendrites leads to functional deficits including muscular weakness, slowing of locomotion, poor information processing and comprehension, and overall fatigue. The inadvertent jumping of electric charge between neural dendrite leads to faulty cross-talk causing symptoms of muscular tension, neuropathy causing pain, involuntary spasms, and poor gait and ataxia.
There are two subtypes of MS which correspond to the time course of the illness: relapsing/remitting and primary progressive. The relapsing/remitting patient has attacks of MS symptoms when inflammation of focal lesions worsens temporarily for days, weeks, or months followed by an incomplete recovery from symptoms known as the remitting phase which can last weeks to years. The primary progressive phase MS patient has neurologic symptoms that continue to worsen from the start of the disorder and they tend to have a worse prognosis (Compston and Coles, 2002).
The suspected etiology of MS has yet to be fully determined, however two primary hypotheses exist: genetic and geographic variances. Scientists believe that MS has some level of heritability; although it is most likely formed by polygenic anomalies. Therefore, given the correct pattern or collection of gene traits a person becomes more likely to have MS. In addition,
one theory predicts that MS could be the result of viral attack and that one’s genetic make-up could make a person more prone to contract MS over time.
The incidence of this disorder has been reported to be around 7 new cases per 100 000 every year in the USA (Compston and Coles, 2002). In 1992 the prevalence of MS was 350 000 for the USA (Anderson, Ellenberg, Leventhal, Reingold, Rodriguez, and Silberberg, 1992). Compston and Coles, (2002) report that the current prevalence of MS in the United States is 120 per 100 000, while in Canada the prevalence is 240 per 100 000 (MS Society of Canada, 2005). It is considered a younger person disorder as most MS patients are diagnosed at around 30-40 years of age. There appears also to be a geographic preponderance for MS as those who live in areas furthest from the equator tend to have a higher prevalence. Around 80% of MS patients have the relapsing /remitting form of the disease.
General symptomatology of MS patients is all extremely broad as the sclerotic lesions of the brainstem and CNS have such an over-arching effect on the functioning of the entire body. Some of the main symptoms that may be reported are fatigue, cognitive slowing, gait ataxia, poor balance, optic neuritis, tremor, vertigo, vision and oculomotor impairments, urinary and bowel incontinence, and depression (Frohman, Frohman, Zee, McColl, and Galetta, 2005; Compston and Coles, 2002).
An MRI is the primary tool for diagnosis as the size and number of plaques is observed. At least 2 distinct plaques need to be observed and the patient must have suffered at least two MS like attacks before the patient can be diagnosed. The balance assessment findings for MS patients are dependent largely on the location of the demyelination lesions. For example, if the lesion is primarily affecting the brainstem and specifically the oculomotor centres, the medial lateral flocculus (MLF), and vestibular nuclei of the brainstem there would be significant abnormality in the oculomotor assessment of the VNG. In addition, MS affecting the vestibulo spinal tract of the brainstem can lead to a longer vestibular evoked myogenic potential (VEMP) latency and lower
amplitudes than a control group of normal participants (Sartucci and Logi, 2002). During oculomotor testing of a MS patient, the Audiologist may observe a host of oculomotor abnormalities that are covered extensively in (Frohman et al, 2005). These abnormalities can include but are not limited to: pendular nystagmus, rebound nystagmus, poor tracking or pursuit, and disorganized and inaccurate saccades. Internuclear ophthalmoplegia a lesion of the MLF is common which leads to poor adduction of the contralateral medical rectus leading to abnormal oculomotor results for pursuit and saccadic testing.
Treatment for this disorder has included invasive surgical procedures as well as medical treatment and physical rehabilitation.
Medications include anti-inflammatory drugs such as beta-interferon and steroids when the MS symptoms are at the peak of the active phase attack (MS society of Canada, 2005; Compston and Coles, 2002). Medical treatments of the disorder have been effective at preventing attacks so that permanent damage occurs at a slower rate; however, medications and treatments have yet to be effective at reversing sclerotic damage once the axon and not just the myelin sheath has been compromised (Compston and Coles, 2002).
Patients with the primary active phase of MS tend to have worse outcomes than those who suffer from the relapsing remitting type of MS meaning deterioration of the CNS is swifter and more debilitating. These patients tend to see continuous neurologic degradation from onset without seeing periods where symptoms remit and partial healing can occur.
Anderson, D.W.,Ellenberg, J.H., Leventhal, C.M., Reingold, S.C., Rodriguez, M., Silberberg, D.H. (1992). Revised estimate of teh prevalence of multiple sclerosis in the United States. Annals of Neurology. 31: 333-336
Compston and Coles.(2002). Multiple Sclerosis. The Lancet. 359:1221-1231.
Frohman, EM., Frohman,TC., Zee, D., McColl, R., and Galetta, S. (2005) The neuro-ophthalmology of multiple sclerosis. Lancet Neurology.4:111-121.
Multiple Sclerosis Society of Canada. (2005). Study reports regional variation of MS rates
across Canada. Toronto, Ontario.