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We report the occurrence of symptoms of mania related to corticosteroid injection at the celiac plexus for chronic pancreatitis. Corticosteroids are associated with mental status changes, including mania, confusion, depression, hallucinations, and paranoia. The literature suggests that mania is second to psychosis as the most common corticosteroid-related mental status change. Although a relation to dose and daily exposure exists, we found no reports of mania related to a single regional steroid injection.
A yr-old woman with familial pancreatitis resulting in palliative distal pancreatectomy presented for chronic pain. She gave a history of mania resulting from two separate previous corticosteroid trials; a brief orally administered tapered course of dexamethasone and a single intraarticular injection of unknown corticosteroid for bursitis of the right shoulder.
In each case, manic symptoms were reported to have been profound but brief, marked by insomnia, agitation, racing thoughts, and grandiosity. She reported no intervening episodes of mania, other than these two corticosteroid-related episodes, no other formal psychiatric history, and was taking no other medications at the time.
We discussed with the patient the potential therapeutic options for providing comfort other than treatment at the celiac plexus and the possibility of mania after corticosteroid administration. Once all other appropriate options had been exhausted, we offered, and the patient accepted, corticosteroid injection with local anesthetic at the celiac plexus.
Because valproic acid is associated with hepatotoxicity, we chose to offer carbamazepine as the only other option for a preemptive mood stabilizer. Celiac plexus nerve blockade was performed by standard procedure, as described later. The procedure was tolerated without complication.
Approximately 10 min after the injections, the patient reported complete resolution of previously severe abdominal pain. After the procedure, the patient reported no difficulty and exhibited normal behavior until approximately 25 h after the procedure. At this time, she was observed in the hospital store dressed in bright red bedroom clothing and having spent several hundred dollars.
She was found to have a mental status change comprising expansive affect, racing, tangential and grandiose thoughts, pressured and loud speech, and poor insight and judgment. There was no difficulty with sleep until the night after onset of manic symptoms, which was marked by complete lack of sleep. Her manic symptoms resolved after 4 days of treatment with haloperidol and clonazepam. The doses of these medications were tapered and discontinued after 6 days without recurrence of manic symptoms.
A yr-old woman with chronic pancreatitis and ampullary stenosis of the pancreatic duct presented with chronic epigastric pain. She had previously undergone endoscopic retrograde cholangiopancreatography, sphincterotomy, and surgical sphincterotomy, with recurrence of symptoms. Stent placement also failed to relieve pain. She was taking no medications at the time of presentation.
Her medical history was significant for cytomegalovirus hepatitis and cholecystectomy for choledocholithiasis, appendectomy, and hysterectomy. Her epigastric pain persisted, despite previous aggressive medical management, and she was offered an analgesic celiac plexus block with a combination of local anesthetic and corticosteroid. On each occasion, treatment induced profound but brief symptoms of agitation and either euphoria or dysphoria associated with insomnia for several days, heightened energy, obsessive behaviors, racing thoughts, and verbosity.
She reported no intervening episodes of mania other than these two corticosteroid-related episodes, and she had no other psychiatric diagnosis. Despite the known possibility of recurrence of these symptoms, the patient chose to have the procedure. Her mental status was evaluated, before and after injection, by administering the Young Mania Rating Scale.
Immediately after the celiac plexus block, the patient reported decreased pain, which lasted h, after which her pain returned to its previous baseline intensity and did not subside. The patient signed out of the hospital, against medical advice, approximately 41 h after the corticosteroid injection. She reported no difficulty with sleep until 72 h after injection, at which time she experienced complete lack of sleep for 48 h postinjection nights 3 and 4.
She described this period of insomnia as euphoric, with prominent sexual aggressiveness. She noted that after sleeping for 6 h on the fifth postinjection night, she became irritable, with obsessive thoughts.
She refused treatment for agitation. Her Young Mania Rating Scale score after corticosteroid injection at the celiac plexus was 33, consistent with mania. Celiac plexus block was performed using bilateral posterior approach with C-arm fluoroscopic guidance, with the patient in prone position.
Under fluoroscopic guidance, the needle was advanced to a position approximately 1. Accurate placement was confirmed by bilateral injection of 5 ml of 1: After negative aspiration, a 3-ml test dose of 1. A mixture that contained 15 ml local anesthetic solution 1: Total dosage of triamcinolone was mg.
The addition of corticosteroid to a celiac plexus block provides pain relief in some, but not all, cases, and its mechanism is unknown. Since the introduction of corticosteroids into clinical practice, there have been countless reports of associated neuropsychiatric symptoms. The incidence of neuropsychiatric effects related to repeated corticosteroid use is reported to be substantial. Both patients reported on here had a previous history of brief mental status change with limited exposure to corticosteroid.
In each case, there was no psychiatric history other then when exposed to corticosteroid. Whether the manic symptoms seen here could have been "functional," induced by suggestion, or a placebo response can never be ruled out completely. However, the literature has never reported such cases.
The early literature does not support the commonly held suspicion that premorbid psychiatric illness predisposes to steroid-induced mental disturbance. There is only a single report of persistent psychiatric illness after an exposure to steroids, although, in this case, the authors acknowledge that it is difficult to determine whether psychiatric illness would have developed in this patient anyway.
Although neuropsychiatric manifestations from corticosteroids may be potentially dangerous in the short term, they are usually treatable, and there is little evidence to suggest that these acute side effects lead to long-term effects. It is not clear whether pretreatment with mood-stabilizing drugs before steroid administration is of value, but, theoretically, this may be an advantageous approach in the steroid-sensitive patient. Specific mechanisms to explain the CNS side effects of corticosteroids remain unclear.
Recent work in a variety of animal species, including humans, suggests that corticosteroids increase mesolimbic catecholamine concentrations, particularly dopamine. It would be of value to determine the incidence of corticosteroid-related adverse effects, and to correlate these adverse effects with either pharmacokinetic measures, such as peak plasma concentrations and elimination half-life, or with biological activity, such as hypothalamic-pituitary adrenal axis suppression.
Although the cause of such events may be the same, the underlying alterations in physiology may be different, and thereby explain variations in duration of effects. The prognosis for acute corticosteroid-related neuropsychiatric complications is usually excellent, because dosage reduction or discontinuation of therapy usually results in full recovery.
Therapy for CNS side effects of corticosteroids remains directed toward controlling symptoms, primarily with dopamine antagonists such as butyrophenones, benzodiazepines such as clonazepam, and mood stabilizers such as lithium or anticonvulsants.
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