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1.
Article in English | MEDLINE | ID: mdl-33101763

ABSTRACT

Background: Ziconotide (ZCN), a nonopioid analgesic, is first-line intrathecal therapy for patients with severe chronic pain refractory to other management options. We describe three cases of ZCN-induced movement disorders. Cases: Case one is a 64-year-old woman who presented with oro-lingual (OL) dyskinesia with dysesthesias and bilateral upper extremity kinetic tremor. Case two is a 43-year-old man with a 20-month history of ZCN treatment who developed OL dyskinesia with dysesthesias, involuntary left hand and neck movements, hallucinations, dysesthesias on his feet, and gait imbalance. Case three is a 70-year-old man with a 4-month history of ZCN use who developed OL dyskinesia with dysesthesias. Conclusions: Intrathecal treatment of pain with ZCN may be complicated by a drug-induced movement disorder where OL dyskinesia is characteristic. The movement disorder is likely to be dose related and reversible with ZCN discontinuation, but a chronic movement disorder is also possible.


Subject(s)
Analgesics, Non-Narcotic/adverse effects , Chronic Pain/drug therapy , Dyskinesia, Drug-Induced/physiopathology , omega-Conotoxins/adverse effects , Adult , Aged , Analgesics, Non-Narcotic/administration & dosage , Female , Humans , Male , Middle Aged , omega-Conotoxins/administration & dosage
2.
J Neuropsychiatry Clin Neurosci ; 28(4): 292-298, 2016.
Article in English | MEDLINE | ID: mdl-27255855

ABSTRACT

Damage to the brain's mood regulation systems may contribute to poststroke depression. This study examines relationships between depression symptoms and psychosocial factors and then uses multivariate lesion-symptom mapping to localize depression symptoms in people with chronic left hemisphere stroke. Depression symptoms relate inversely to education and directly to physical disability. Damage in the left dorsolateral prefrontal cortex is associated with greater depression symptoms. These results demonstrate a neurological contribution to depression symptoms in chronic left hemisphere stroke and provide evidence of convergent biological mechanisms for poststroke depression symptoms and major depression with regard to left dorsolateral prefrontal cortex dysfunction.

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