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Updated: Oct 20, 2025

Comprehensive Autopsy Program for Individuals with Multiple Sclerosis
Published on: July 19, 2019
[Paroxysmal dysarthria and ataxia - unusual MS manifestation]
Chrysostomos Papastergios1, Amen Shaker2, Bianca-Luciana Schiopu-Mariean3
1överläkare, neurologi, medicin- och geriatrikkliniken, Värnamo sjukhus.
Abstract:
Multiple sclerosis is a common inflammatory demyelinating disease of the central nervous system. Although many patients present permanent symptoms, a number of them suffer of deficits of paroxysmal character. One unusual manifestation of paroxysmal nature is episodes of dysarthria and ataxia known as PDA (paroxysmal dysarthria and ataxia). The mechanism behind this phenomenon, although not well understood, is hypothesised to relate with ephaptic activation of the neuroaxons within the demyelination plaques. Just a few patients worldwide have been reported at present. These symptoms can be effectively treated with anti-seizure medicines. We present the case of a female 48-year-old patient who shortly after an MS diagnosis developed paroxysmal dysarthria and ataxia related to a midbrain lesion and was eventually treated with carbamazepine.
Insights
Paroxysmal dysarthria and ataxia (PDA) is a rare neurological symptom in multiple sclerosis (MS). This case study highlights effective carbamazepine treatment for PDA linked to a midbrain lesion in an MS patient.
Area of Science:
- Neurology
- Neuroimmunology
- Neuroscience
Background:
- Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system.
- While many MS patients experience permanent symptoms, some develop transient, paroxysmal deficits.
- Paroxysmal dysarthria and ataxia (PDA) is an uncommon paroxysmal manifestation in MS.
Observation:
- A 48-year-old female patient with a recent MS diagnosis presented with episodes of dysarthria and ataxia.
- The paroxysmal symptoms were associated with a lesion in the midbrain.
- The underlying mechanism is hypothesized to involve ephaptic neurotransmission within demyelination plaques.
Findings:
- The patient's paroxysmal dysarthria and ataxia were effectively managed with carbamazepine, an anti-seizure medication.
- This case adds to the limited reported instances of PDA in multiple sclerosis patients.
- The midbrain lesion's role in triggering PDA symptoms was identified.
Implications:
- Anti-seizure medications, such as carbamazepine, represent a viable treatment option for managing paroxysmal dysarthria and ataxia in MS.
- Further research into the mechanisms of ephaptic activation in demyelinating lesions is warranted.
- Recognition of PDA as a treatable symptom can improve the quality of life for affected MS patients.
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