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G Ramsaransing Department of
Neurology, Academisch Ziekenhuis Groningen, Hanzeplein 1, 9700 RB
Groningen, Netherlands
Correspondence to: J De Keyser
j.h.a.de.keyser{at}neuro.azg.nl
Carbamazepine is widely used to treat paroxysmal
neurological symptoms and pain. We report on five patients with
multiple sclerosis in whom disability was seriously enhanced by
treatment with carbamazepine at comparatively low dosages. It is
possible to misinterpret worsening of symptoms as an exacerbation of
multiple sclerosis.
Case 1
Case 2
A 48 year old man had had symptoms of multiple sclerosis for three
years, at first intermittent but eventually progressive, with mainly
ataxia and spastic weakness of the legs. He also had disabling
oscillopsia due to a multidirectional nystagmus. Two days after
starting carbamazepine (100 mg three times daily) he was unable to walk
because of increased weakness, but two days after stopping it he could
walk unassisted. Carbamazepine (50 mg three times daily) was restarted
one week later without any change in symptoms. When the dose was
increased to 100 mg three times daily he developed a profound weakness
of the legs, which disappeared two days after stopping treatment.
A 67 year old woman with secondary progressive multiple sclerosis
had a recurrence of right sided trigeminal neuralgia. Although she was
severely disabled (ataxia of all limbs and spastic weakness of her
legs), she could walk with a frame. Carbamazepine 100 mg three times
daily was started. Two days later she could not stand owing to weakness
of her legs. The sudden worsening was interpreted as an exacerbation,
and she was treated with intravenous methylprednisolone 500 mg daily
for five days, without benefit. Two weeks after discharge she was seen
at the clinic. Carbamazepine was stopped, and two days later she could walk with a frame. She recalled a less severe effect from carbamazepine during the previous episode of trigeminal neuralgia.
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Footnotes |
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Funding: GR was supported by Multiple Sclerosis International.
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References |
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| 1. | Sedgwick EM. Pathophysiology of the demyelinated nerve fibre. In Raine CS, McFarland HF, Tourtellotte WW, eds. In: Multiple sclerosis. Clinical and pathogenetic basis. London: Chapman and Hall, 1997:195-204. |
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