Background: Primary writing tremor is a task-specific phenomenon that has been described as variants of essential tremor or dystonia.Phenomenology Shown: We describe the case of a 63-year-old female who initially had primary writing tremor, later developed Parkinson's disease, and once initiated on carbidopa/levodopa had improvement in her parkinsonism and her writing tremor.Educational Value: As neither essential tremor nor typical brachial dystonia respond to carbidopa/levodopa, our case documents that at least some cases of primary writing tremor are not variants of either dystonia or essential tremor.

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A 75-year-old man sustained an out-of-hospital asystolic arrest, with return of spontaneous circulation after 5 minutes of chest compressions, norepinephrine, and sodium bicarbonate. Several hours later, he developed generalized myoclonus, resolving after the administration of midazolam, propofol, and fosphenytoin. After holding these medications on hospital day 2, the myoclonus did not return. Computed tomography revealed a chronic right parietal infarct, and a 2-hour electroencephalogram was invariant with burst suppression. Examination on days 1, 2, and 3 revealed coma with only a cough reflex present, and he was breathing over the set rate of the ventilator. On day 4, he lost his cough reflex and developed short bursts of rapid respirations consistent with cluster breathing (Figure 1), resolving the next day and subsequently requiring the ventilator to initiate respirations. Ultimately, palliative care was pursued, and the patient was terminally extubated and died on hospital day 6.Cluster breathing is a classic but rarely reported phenomenon associated with lesions of the lower pons or upper medulla. 1 In our patient, the contemporaneous loss of cough reflex with the transient presence of cluster breathing may have reflected a rostrocaudal progression of cerebral edema after anoxic injury.

Chorea is a common hyperkinetic movement disorder that can have a large differential diagnosis. Causes can include genetic and sporadic etiologies, including metabolic abnormalities, autoimmune, structural, paraneoplastic, psychogenic, and iatrogenic causes. The workup can be challenging due to this large number of possible causes, and can include basic metabolic and specialized blood analysis such as genetic testing, in addition to imaging studies and cerebrospinal fluid analysis. Treatment of symptoms outside the realm of reversible causes can be challenging, and is a major focus of current research. This review covers sporadic causes, genetic causes, and management. Figures show a flowchart for evaluation of patients with chorea, a computed tomography scan of a Huntington disease patient showing caudate head atrophy, brain computed tomography scan showing calcification, and acanthocytosis. Videos show mild and moderate Huntington disease, Huntington disease-like 2,  and chorea-acanthocytosis. Tables list metabolic abnormalities that can manifest as chorea, paraneoplastic and nonparaneoplastic syndromes associated with chorea, and reported successful therapies for chorea.