We look at the differences and similarities between seizures and paroxysmal dyskinesias.
There is significant overlap in the clinical presentation for seizures and paraoxysmal dyskinesias. The term dyskinesia specifically means difficulty performing a voluntary movement. Often this is due to other involuntary movements of the body that prohibit the voluntary movement. Paroxysmal means episodic.
Despite their somewhat similar appearance, unlike seizures, dyskinesias do not appear to originate in the cerebral cortex. Instead, we believe they originate either in the basal nuclei or muscle membranes. The neurotransmitters thought to play a role in the etiology of dyskinesias include GABA, glutamate, acetylcholine, serotonin, and dopamine, as well as channelopathies and mutations in membrane transfer proteins.
Types of Movements Observed
Dyskinesias typically fall into either hyperkinetic (most commonly), or hypokinetic movements. Some of the terms used in human dyskinesias include dystonia (abnormal tonicity), chorea (irregular, dance-like movements), athetosis (slow, writhing movements), or ballism (flailing movements of a limb). These movements may occur in a single or multiple limbs. Key features that allow differentiation from seizures include bilateral limbs affected without loss of consciousness (effectively ruling out seizure), and lack of autonomic signs (e.g., no hypersalivation).
Much like the workup for idiopathic epilepsy, the first step in approaching such cases is to rule in/out any underlying disease processes using appropriate diagnostic testing (e.g., CBC, serum biochemical profiles, urine analysis, endocrine testing, serology for infectious diseases, cerebrospinal fluid analysis, advanced imaging). Most cases appear to be inherited/idiopathic.
Therapeutic goals are two-fold: 1) treat the underlying disease process, if identified; and/or 2) control clinical signs. Anti-epileptic drugs are typically not effective in treating dyskinesias. There can be significant variation in treatment response for dyskinesias. As such, if a treatment trial with one medication is not effective, it is worth trying a different medication.
Acetazolamide (5-10 mg/kg PO q 12 h) or, alternatively, clonazepam (0.5 mg/kg PO q 8-12 h) have been recommended. Acetazolamide has yielded good outcome in certain inherited dyskinesias, though it may cause hypokalemia and hyperpnea at therapeutic doses. Where acetazolamide is used, supplementation with potassium gluconate at 2-4 mEq/day (titrated higher or lower to maintain normal potassium) is co-administered. Due to acid/base effects, potassium gluconate is the preferred formulation of potassium supplementation.
We hope this brief guide has given you some insight into dealing with seizures and paroxysmal dyskinesias.