The tremor can then be classified by which position most accentuates the tremor:

Treatment
There is no cure for most tremors. The appropriate treatment depends on accurate diagnosis of the cause. Some tremors respond to treatment of the underlying condition. For example, in some cases of psychogenic tremor, treating the patients underlying psychological problem may cause the tremor to disappear. A few medications can help relieve symptoms temporarily. Medications
Medications remain the basis of therapy in many cases. Symptomatic drug therapy is available for several forms of tremor:
Parkinsonian tremor drug treatment involves L-DOPA or dopamine-like drugs such as pergolide, bromocriptine and ropinirole; They can be dangerous, however, as they may cause symptoms such as tardive dyskinesia, akathisia, clonus, and in rare instances tardive (late developing) psychosis. Other drugs used to lessen parkinsonian tremor include amantadine and anticholinergic drugs like benztropine
Essential tremor may be treated with beta blockers (such as propranolol and nadolol) or  primidone, an anticonvulsant
Cerebellar tremor symptoms may decrease with the application of alcohol (ethanol) or benzodiazepine medications, both of which carry some risk of dependence or addiction
Rubral tremor patients may receive some relief using L-DOPA or anticholinergic drugs. Surgery may be helpful
Dystonic tremor may respond to diazepam, anticholinergic drugs, and intramuscular injections of botulinum toxin. Botulinum toxin is also prescribed to treat voice and head tremors and several movement disorders
Primary orthostatic tremor sometimes is treated with a combination of diazepam and primidone. Gabapentin provides relief in some cases
Enhanced physiological tremor is usually reversible once the cause is corrected.
Of 722 randomized patients, 552 had cytogenetic results; 137 (25%) had high-risk cytogenetic abnormalities and 172 (32%) had 1q21 amplification alone. PFS was improved with IRd versus placebo in both high-risk and standard-risk cytogenetics subgroups: in high-risk patients, with median PFS of 21.4 versus 9.7 months; in standard-risk patients, with median PFS of 20.6 versus 15.6 months. This PFS benefit was consistent across subgroups with individual high-risk cytogenetic abnormalities, including patients with del(17p). PFS was also longer with IRd versus placebo- in patients with 1q21 amplification, and in the "expanded high-risk" group, defined as those with high-risk cytogenetic abnormalities and/or 1q21 amplification. IRd demonstrated substantial benefit compared with placebo in relapsed/refractory multiple myeloma patients with high-risk and standard-risk cytogenetics, and improves the poor PFS associated with high-risk cytogenetic abnormalities. Pregnancy and breastfeeding
Ixazomib and lenalidomide are teratogenic in animal studies. The latter is contraindicated in pregnant women, making this therapy regimen unsuitable for this group. It is not known whether ixazomib or its metabolites pass into the breast milk. Side effects
Common side effects of the ixazomib+lenalidomide+dexamethasone study therapy included diarrhoea (42% versus 36% under placebo+lenalidomide+dexamethasone), constipation (34% versus 25%), thrombocytopenia (low platelet count; 28% versus 14%), peripheral neuropathy (28% versus 21%), nausea (26% versus 21%), peripheral oedema (swelling; 25% versus 18%), vomiting (22% versus 11%), and back pain (21% versus 16%). Serious diarrhoea or thrombocytopenia occurred in 2% of patients, respectively.Side effects of ixazomib alone were only assessed in a small number of people.