Background: Medication-induced tremor (MIT) is common in clinical practice and there are many medications/drugs that can cause or exacerbate tremors. MIT typically occurs by enhancement of physiological tremor (EPT), but not all drugs cause tremor in this way. In this manuscript, we review how some common examples of MIT have informed us about the pathophysiology of tremor. Methods: We performed a PubMed literature search for published articles dealing with MIT and attempted to identify articles that especially dealt with the medication's mechanism of inducing tremor. Results: There is a paucity of literature that deals with the mechanisms of MIT, with most manuscripts only describing the frequency and clinical settings where MIT is observed. That being said, MIT emanates from multiple mechanisms depending on the drug and it often takes an individualized approach to manage MIT in a given patient. Discussion: MIT has provided some insight into the mechanisms of tremors we see in clinical practice. The exact mechanism of MIT is unknown for most medications that cause tremor, but it is assumed that in most cases physiological tremor is influenced by these medications. Some medications (epinephrine) that cause EPT likely lead to tremor by peripheral mechanisms in the muscle (b-adrenergic agonists), but others may influence the central component (amitriptyline). Other drugs can cause tremor, presumably by blockade of dopamine receptors in the basal ganglia (dopamine-blocking agents), by secondary effects such as causing hyperthyroidism (amiodarone), or by other mechanisms. We will attempt to discuss what is known and unknown about the pathophysiology of the most common MITs.
Delusional infestation (DI), a form of psychosis, has rarely been reported in patients with Parkinson disease (PD). The clinical presentation and successful treatment of DI is illustrated through 5 cases. Each patient developed DI during treatment for moderate to advanced Parkinson's disease, and only 2 had cognitive impairment. Two patients were on monotherapy: 1 on a dopamine agonist and the other on trihexyphenidyl. Three patients were receiving complex combination therapy with 2 to 5 different antiParkinsonian medications at the onset of their delusion. Selective discontinuation or reduction of these medications was key to the resolution of DI in each patient. Although the medication adjustments differed, the changes resulted in the reduction of anticholinergic effects or extracellular striatal dopamine levels. This series emphasizes the clinical features and management strategies for this disruptive form of psychosis in patients with PD.Psychosis occurs in 15% to 30% of patients with Parkinson's disease (PD). 1 Although psychosis occurs more commonly in PD patients with dementia, it occurs in up to 20% of those without dementia. 1 Delusional infestation (DI) as manifestation of psychosis in PD has rarely been reported. [2][3][4][5] Patients with DI have an unshakeable false belief (delusion) of infestation with parasites, insects, or even inanimate objects like fibers. 2 Often, the delusion is triggered by a misinterpretation of a normal sensation and then is held as truth despite all evidence to the contrary.Karl Ekbom described DI as "real perceptions" (tactile illusions) interpreted in a delusional way in 1938, earning the eponym Ekbom's syndrome. 6 In 2002, DI with fibers and threads ("Morgellons phenomenon") "spread" via misinformation on the Internet. 6 Recently, infestation with "string" has been described in PD. 5 Here, we report a series of 5 patients with PD who developed DI and discuss clinical approaches to the treatment of DI in PD. Cases Patient 1A woman aged 82 years who had akinetic-rigid PD for 7 years was admitted to a psychiatry unit for DI of her nose with pungent bugs. She was on amantadine 100 mg twice daily and pergolide 4.5 mg once daily. Previous physicians treated her PD with high-dose pergolide, avoiding carbidopa/levodopa (L-dopa) because of her history of melanoma, although she had no recurrence for many years. Her motor symptoms were poorly controlled, and she had gait instability and falls. Carbidopa/L-dopa 25/100 mg was initiated and titrated to 4 times/day. Pergolide was tapered over 1 month then discontinued. Two weeks later, her DI resolved. She was followed until her death at age 84 years, and she never had a recurrence of melanoma or DI (Table 1). Patient 2A woman aged 66 years who had PD for 7 years developed dry mouth and a "parasitic film coating her teeth." This prompted an extensive oral hygiene regimen of brushing, flossing, use of a dental pick, and antiseptic mouthwash. She had normal insight and judgment in other matters. The anti-Parkinsonian medicati...
A 52-year-old woman with Parkinson disease (PD) since age 42 on carbidopa/levodopa 25/ 250 5 times/d developed "offs" characterized by left foot dystonia. After adding rasagiline 1 mg/ d, multihour episodes of gaze deviation, anxiety, retrocollis, and dyskinesias ensued (video, links.lww.com/WNL/A30). Symptoms, marginally improved with diphenhydramine, resolved when levodopa was held temporarily. They did not recur after discontinuation of rasagiline.Typical oculogyric crisis lasting hours with accompanying psychiatric features is rare in PD.1,2 It is more commonly associated with dopamine blockers, postencephalitic parkinsonism, and disorders of dopamine metabolism.1 Levodopa-induced brief suppressible gaze deviation, toward the side most affected in advanced PD, is more prevalent.
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