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Differentiating multiple sclerosis (MS) from alternative demyelinating diseases of the central nervous system and systemic medical conditions that mimic MS is challenging. A simple three-step approach is used in this text to guide readers through clinical cases to define MS and rule out competing causes. Case presentations are used to illustrate simple pearls and other clues that will aid clinicians in assessing and managing difficult clinical situations. The chapters are organized to reflect challenges regarding specific anatomical territories affected by MS and its mimickers, namely evaluation of impairment in the optic nerves, brain, brainstem, cerebellum, and spinal cord. Specific examples are used where the author or the treating physician was correct or incorrect in investigating or managing a particular question. The wisdom of hindsight thus generated becomes an invaluable and enduring lesson. The text is written in a coaching style, buttressed by the strong pedagogic wisdom of the author.
Fingolimod was first synthesized in the early 1990s as part of an extensive program of chemical derivatization of myriocin, with the goal of creating a novel immunosuppressant that would be more potent and less toxic in vivo. Fingolimod's mechanism of action in multiple sclerosis (MS) is not known with certainty. Fingolimod was initially developed to prevent allograt rejection after demonstration that it was effective in a variety of animal transplantation models, including kidney, heart, pancreatic islet cells and skin. Fingolimod was approved by the Food and Drug Administration (FDA) to reduce relapses and disability progression in relapsing forms of MS. Fingolimod's generally good safety profile and tolerability, including oral route of administration, make fingolimod an attractive treatment option for patients with relapsing forms of MS. Better delineation of the mechanisms leading to both the beneficial and adverse effects of fingolimod is necessary to develop more effective and better-tolerated compounds.
Gait apraxia is a gait disorder not attributable to motor, cerebellar, or sensory dysfunction. Gait impairment is common in Multiple Sclerosis (MS), but is mostly attributed to spasticity and ataxia. Impairment ratings scales are designed accordingly and do not separately evaluate apraxia.
To describe 15 patients with gait apraxia resulting from MS as their major functional impairment.
The Mayo Clinic database (1994-2007) was searched for the terms MS and gait apraxia. Inclusion criteria: Definite MS, significant gait apraxia. Exclusion criteria: alternative disorder causing apraxia, predominantly spastic/ataxic gait disorder.
9 (60%) of the patients were women, and 12 (80%) had a progressive MS course. Gait apraxia was evident at a median of 8 years (range 0-34) following MS onset. Median EDSS at recognition of gait apraxia was 6.5 (range 5-8). Cognitive dysfunction was present in 11 (73%) and neurogenic bladder dysfunction in 14 (93%). The commonest MRI findings were confluent periventricular T2 lesions, T1 hypointensity and generalized cerebral atrophy with symmetrical ex vacuo ventricular enlargement.
Gait apraxia can cause significant functional impairment in MS patients, and may be underrecognized. The natural course of the neurological deficit in such patients is unknown, and may differ from that of MS patients with other ambulatory disabilities.