Secondary Logo

Journal Logo

General Medical Conditions: Case Report

Intermittent Muscle Spasms in a Professional Baseball Player

Smith, Marissa M. MD1; Sethi, Nitin K. MD2; Kinderknecht, James MD1

Author Information
Current Sports Medicine Reports: 1/2 2017 - Volume 16 - Issue 1 - p 36-37
doi: 10.1249/JSR.0000000000000331


Intermittent muscle spasms are a common complaint of professional and amateur athletes. In the majority of cases the cause is innocuous and related to fatigue, overexertion, and dehydration. Paroxysmal exercise-induced dyskinesia (PED) is an uncommon but treatable cause of muscle spasm.

Case Report

A 17-yr-old male right-handed minor league baseball player for the New York Mets presented with complaint of intermittent muscle spasms. Patient reported episodes wherein he would abruptly feel tightness in the left side of his body predominantly the left leg. Sometimes, when throwing a baseball, his right shoulder would feel tight. These episodes would occur during high-intensity exercise, and in total, he reported 30 such episodes over a 4-yr period. He recalled that the episodes started at the age of 13 yr. He denied painful cramping during an episode. During a typical episode, he was able to speak and did not suffer loss of body tone or hand grip. Usual duration of the episode was reported to be 10 to 15 sec. These episodes were described by his athletic trainers as if he suddenly froze or became “paralyzed” while running between the bases. No accompanying seizure activity or alteration in his mental status was reported during the episodes. Patient was evaluated in the Dominican Republic where it was felt his symptoms were possibly related to low calcium and supplementation was advised. But as symptoms continued despite calcium supplementation, further evaluation in the United States was recommended. Video recorded on a cellular phone by an athletic trainer showed what appeared to be dystonic posturing of the left leg lasting about 3 sec occurring after finishing a run to first base (video 1, The patient reported that his brother had similar episodes and had controlled his symptoms by avoiding high-intensity sports. The remainder of his medical history, family and social history, and review of systems was unremarkable. Physical and neurological examinations were normal. Complete blood count and chemistry were normal with creatine phosphokinase (CPK) of 169 µg/L, LDH = 127 U/L, aldolase = 3.5 units per liter, thyroid stimulating hormone (TSH) = 2.05 mIU/L, parathormone (PTH) = 28 pg/mL, serum ammonia = 35 mcg/dL. Antinuclear antibody (ANA) and double stranded DNA (dsDNA) were both negative.

Lumbar puncture was declined by patient. During 24-h ambulatory EEG study, six typical events of limb tightness were reported with no surface EEG correlate. No interictal epileptiform features were noted. MRI of brain with and without contrast was normal. Metabolic disorders such as glycogen storage disease (example McArdle’s disease which is characterized by exercise intolerance, muscle pain, early fatigue, and painful cramps), mitochondrial disorders, muscle channelopathies, seizure disorder, conversion disorder, and malingering were all considered in the differential diagnoses, paroxysmal kinesigenic dyskinesia (PKD) was thought to be the most likely diagnosis. Low dose carbamazepine 100 mg twice daily was prescribed. The patient has since returned to compete at the elite level having suffered no further episodes of muscle spasms. Genetic testing could not be carried out as patient moved to Puerto Rico. Just over 25% of cases of PKD are inherited.


Paroxysmal diskinesias was first described in the literature in the 1940s, though an earlier similar description is cited from 1892 in Japan (3,4). Most recently, these have been classified into three subtypes. These include PKD, paroxysmal nonkinesigenic dyskinesia (PNKD), and PED. In this heterogeneous group of disorders, abnormal movements may include dystonia, chorea, athetosis, ballismus, or a combination of these. In between episodes of dyskinetic movements, the patient has normal movements and cognition. Recent research has identified genetic causes of many, though not all, of these heterogeneous disorders.

PKD is seen most frequently after brief episodes of exertion or when a person is startled. Muscles affected tend to be unilateral, and affecting the limbs preferentially, though can occur to any part of the body, with symptoms lasting for seconds to minutes (6–8). This is consistent with the presentation of our athlete, as symptoms tended to occur after a quick base-running period. As compared with epileptic attacks, during PKD attacks, patients typically retain consciousness during their attacks and are able to recall the attacks after they have ended as was in our reported athlete.

Though routine laboratory and imaging testing is usually noncontributory, a complete evaluation, including thyroid function, complete metabolic panel, muscle enzymes, and inflammatory markers, is necessary. Neuroimaging to rule out a structural cause of symptoms and an electroencephalogram (EEG) to evaluate for seizure disorder is necessary. Epileptic discharges on EEG should caution against a diagnosis of PKD.

Just over 25% of cases of PKD are inherited in an autosomal dominant pattern, with the majority being sporadic and the onset generally before the age of 40 yr, frequently beginning in childhood (9). Over the years, much work in the genetics of PKD has been done. It has been found that many of those suffering from PKD have mutations on chromosome 16. Genetic testing has improved and may be of benefit in some patients, though it is known that multiple abnormal loci exist and all are likely not identified at this time. Still, if a family history exists, or there is question of diagnosis, obtaining genetic testing may be of benefit.

Once a diagnosis has been made, treatment with carbamazepine is curative of symptoms in the majority of cases, with other anticonvulsants showing therapeutic effect as well (1,6,7). In some cases, diagnosis can be difficult and starting treatment and evaluating a beneficial effect may help make the diagnosis because other paroxysmal dyskinesias do not have such reliable outcomes with anticonvulsive treatments. PKD is seen most in younger populations, and many will grow out of their symptoms in their 20s and 30s, so reassessment of their need for treatment should be evaluated (6). The complete resolution of symptoms after starting carbamazepine makes the diagnosis of PKD more likely in our patient, despite not having genetic testing completed at the time of this writing.

The other paroxysmal dyskinesias include PNKD and PED. In PNKD, the dyskinesia is triggered by emotions, intake of alcohol or caffeine, or fatigue with symptoms generally lasting from minutes to hours. Treatment with medications is not as predictable as in PKD, though some may benefit from clonazepam. Avoidance of known triggers is likely most important. PED has the hallmark presentation of dystonic reactions lasting from 5 to 30 min after sustained physical exercise. The most difficult to treat, there is limited benefit from anticonvulsants or benzodiazepams. There is some growing evidence that a ketogenic diet may decrease the symptoms of PED, though avoidance of triggers may be the most effective treatment (1,5,8). The paroxysmal dyskinesias are a rare entity found in the medical literature, though there is growing information regarding them as genetic testing continues to improve. PKD frequently affects younger populations, triggered by quick movements and exertion, resulting in brief dyskinetic movements. As such, these could be seen in athletes and should be part of the differential of players presenting with dyskinetic movements. It is further important to understand that treatment works well in many of these patients, which may allow them to perform athletics at all levels of skill.

JK and MMS report no disclosures. NKS serves as associate editor, The Eastern Journal of Medicine.


1. Bhatia KP. Paroxysmal dyskinesias. Mov. Disord. 2011; 26:1157–65.
2. Bruno MK, Hallett M, Gwinn-Hardy K, et al. Clinical evaluation of idiopathic paroxysmal kinesigenic dyskinesia: new diagnostic criteria. Neurology. 2004; 63:2280–7.
    3. Kato N, Sadamatsu M, Kikuchi T, et al. Paroxysmal kinesigenic choreoathetosis: from first discovery in 1892 to genetic linkage with benign familial infantile convulsions. Epilepsy Res. 2006; 70(Suppl 1):S174–84.
    4. Mount LA, Reback S. Familial paroxysmal choreoathetosis: a preliminary report on a hitherto undescribed clinical syndrome. Arch. Neurol. Psychiatry. 1940: 841.
    5. Strzelczyk A, Burk K, Oertel WH. Treatment of paroxysmal dyskinesias. Expert Opin. Pharmacother. 2011; 12:63–72.
    6. Sun W, Li J, Zhu Y, et al. Clinical features of paroxysmal kinesigenic dyskinesia: report of 24 cases. Epilepsy Behav. 2012; 25:695–9.
    7. Unterberger I, Trinka E. Diagnosis and treatment of paroxysmal dyskinesias revisited. Ther. Adv. Neurol. Disord. 2008; 1:4–11.
    8. Waln O, Jankovic J. Paroxysmal movement disorders. Neurol. Clin. 2015; 33:137–52.
    9. Weber YG, Lerche H. Genetics of paroxysmal dyskinesias. Curr. Neurol. Neurosci. Rep. 2009; 9:206–11.

    Supplemental Digital Content

    Copyright © 2017 by the American College of Sports Medicine