Myoclonus is an unusual phenomenon in patients with Parkinson’s disease (PD), especially non-demented patients. The development of myoclonus in the course of PD may herald alternative diagnoses such as corticobasal syndrome.1 However, since myoclonus may be due to other medical conditions, a diagnosis other than neurodegenerative disease should be considered. Herein, we describe a patient with PD who had hypothyroidism presenting as abrupt development of myoclonus.
A 59-year-old male patient previously diagnosed with PD at age 48 was admitted for encephalopathy, severe exacerbation of parkinsonism, and myoclonus. He had been treated with levodopa and had an excellent response for the first 5 or 6 years of the disease. He underwent bilateral subthalamic nucleus deep brain stimulation surgery (DBS) at age 54 years because of severe dyskinesia and motor fluctuation despite meticulous medication adjustment. Following DBS, his parkinsonism was alleviated, and he could engage in socially active work. One month before admission, he had a delusion that a spy was watching him and visual hallucinations developed. His caregiver reported that the patient slept for almost 20 hours a day. His articulation deteriorated to the point where his family could hardly understand his words. He became unable to walk without assistance. His caregiver continued to regularly administer the antiparkinsonian drugs to prevent further symptom aggravation. Although the patient continued taking his usual PD medication, his condition worsened. On admission, generalized bradykinesia and rigidity were severely aggravated. Remarkably, myoclonus was present in all four extremities. The myoclonus appeared while maintaining posture and during action and was more prominent in both distal upper extremities, involving the shoulders. The mainly positive myoclonus was not stimulus sensitive. Electrophysiologic studies were not conducted. The results of thyroid function testing included in the routine admission blood work-up revealed an undetectable free thyroxine level and an elevated thyroid-stimulating hormone level of 200.6 µIU/mL (normal: 0.4-4.1 µIU/mL). Further investigation into the patient’s medical history revealed that he underwent total thyroidectomy for papillary thyroid cancer at age 56 and had been treated with levothyroxine at another hospital. However, he had accidentally stopped taking levothyroxine for about 2 months before the current admission. Based on his medical history and laboratory test results, levothyroxine therapy was restarted immediately. After supplementation, his parkinsonism, psychosis, sleep-related problems, emotional lability, and myoclonus markedly improved. By hospital day 10, his general condition stabilized to his previous disease status.
Our patient showed rapid deterioration of psychotic, emotional, sleep-related, and motor symptoms over a few weeks, which is uncommon and may not be explained by exacerbation of PD itself. Myoclonus is also unusual in patients with PD. The prompt and dramatic improvement following levothyroxine administration further suggests hypothyroidism as the cause of this patient’s rapid, global deterioration.
There is limited information on patients with aggravated parkinsonism due to hypothyroidism2,3 or hyperthyroidism.4,5 The accompanied encephalopathy and myoclonus, which were reversed by levothyroxine therapy, have not yet been reported in patients with PD and hypothyroidism. This lack of literature may be partly due to a low level of suspicion because the symptoms aggravated by hypothyroidism can be masked by and misconstrued as deterioration of PD itself.
Based on this didactic case and as pointed out by other authors,2–4 thyroid function assessment should not be overlooked in patients with PD who experience rapid aggravation of parkinsonism, encephalopathy, and myoclonus. Since hypothyroidism can be managed with appropriate medication, it should be included in the list of differential diagnoses of unusual aggravation of parkinsonism and symptoms that are not typical for PD, especially when the patient has underlying thyroid disease.
1 Funding: None.
2 Financial Disclosures: None.
3 Conflicts of interest: The authors report no conflict of interest.
4 Ethics Statement: This study was reviewed by the authors’ institutional ethics committee and was considered exempted from further review.
Caviness, JN (2007). Myoclonus. Parkinsonism Relat Disord 13: S375–84. [PubMed]
Munhoz, RP Teive, HA Troiano, AR Hauck, PR Herdoiza Leiva, MH Graff, H et al. (2004). Parkinson's disease and thyroid dysfunction. Parkinsonism Relat Disord 10(6): 381–3. doi: 10.1016/j.parkreldis.2004.03.008. [PubMed]
Kim, HT, Edwards, MJ, Lakshmi Narsimhan, R and Bhatia, KP (2005). Hyperthyroidism exaggerating parkinsonian tremor: a clinical lesson. Parkinsonism Relat Disord 11(5): 331–2. doi: 10.1016/j.parkreldis.2005.01.009. [PubMed]
Prakash, KM and Kek, PC (2010). Hyperthyroidism “masked” the levodopa response in newly diagnosed Parkinson's disease patients. Parkinsonism Relat Disord 16(10): 691–2. [PubMed]