Pseudodementia Associated with Use of Ibuprofen

2003 ◽  
Vol 37 (1) ◽  
pp. 80-82 ◽  
Author(s):  
Allan L Bernstein ◽  
Ann Werlin

OBJECTIVE To report a case of dementing syndrome resulting from ibuprofen use. CASE SUMMARY A 76-year-old white man with normal mental status became confused, was lost in familiar places, and showed short-term memory loss after beginning a therapeutic regimen of ibuprofen 600 mg 3 times daily for osteoarthritis in anticipation of embarking on a foreign trip. Symptoms of dementia began within 1 week after taking ibuprofen and resolved completely within 1 week after the ibuprofen regimen was stopped. This pattern was repeated 6 months later, when the patient again traveled abroad. Consistently before, during, and after these events, the patient took atenolol, clonidine, lisinopril, aspirin, vitamin C, lecithin, vitamin E, and multivitamins. DISCUSSION Using the Naranjo probability scale, we reasoned that the patient's dementia-like syndrome could be attributed to the use of ibuprofen because pseudodementia appeared after the suspected drug was administered, improved when the drug was discontinued, reappeared when the drug was readministered, had no apparent alternative cause, manifested similarly after each exposure to ibuprofen, and was confirmed by the family's observation after both episodes. Objective causality assessment revealed that the adverse drug reaction was probable. CONCLUSIONS Use of ibuprofen must be considered during clinical evaluation of any patient with new onset of dementing illness. The Naranjo probability scale may be clinically useful for evaluating other pharmaceutical agents that may be contributing to development of dementia-like conditions.

2006 ◽  
Vol 26 (8) ◽  
pp. 1190-1192 ◽  
Author(s):  
Laura Galatti ◽  
Giovanni Polimeni ◽  
Francesco Salvo ◽  
Marcello Romani ◽  
Aurelio Sessa ◽  
...  

2018 ◽  
Vol 33 (6) ◽  
pp. 1923-1934 ◽  
Author(s):  
Mohammed Nuru ◽  
Nino Muradashvili ◽  
Anuradha Kalani ◽  
David Lominadze ◽  
Neetu Tyagi

1997 ◽  
Vol 18 (4) ◽  
pp. 320
Author(s):  
P. Lass ◽  
J. R. Buscombe ◽  
A. Davenport ◽  
S. Gacinovic ◽  
D. S. Thakrar ◽  
...  

2012 ◽  
Vol 46 (10) ◽  
pp. 1439-1439 ◽  
Author(s):  
Rebeca Iglesias Barreira ◽  
Belén Bardán García ◽  
Mónica Granero López ◽  
Iria Rodríguez Legazpi ◽  
Hortensia Álvarez Díaz ◽  
...  

Objective TO report a paradoxical reaction of Raynaud phenomenon following the repeated administration of iloprost in a patient with diffuse cutaneous systemic sclerosis with vascular involvement. Case Summary In January 2006, a 40-year-old male was diagnosed with diffuse cutaneous systemic sclerosis with pulmonary, esophageal, cutaneous, and vascular involvement (Raynaud phenomenon, with digital ulcers on his hands). In December 2008, treatment with iloprost was started due to worsening disease. Nine cycles of iloprost were administered at a rate of 0.5–1 ng/kg/min (6 hours per day, for 5 days every 6–8 weeks); the patient tolerated this treatment well. However, on the fourth day of cycles 10 and 11, the patient developed paradoxical Raynaud phenomenon in the hand with perfusion when the infusion was increased to 1 ng/kg/min, requiring treatment to be stopped. Treatment was continued during cycles 12 and 13 at 0.5 ng/kg/min; the patient tolerated the treatment well, although paradoxical Raynaud phenomenon occurred when the rate of infusion was increased. Discussion Raynaud phenomenon is extremely common in patients with scleroderma, and often is severe. Iloprost has vasodilating, antiplatelet, cytoprotective, and immunomodulating properties, and has been found to be an efficacious alternative to nifedipine for the treatment of Raynaud phenomenon in patients with scleroderma. The Naranjo probability scale indicated that iloprost was the probable cause of the paradoxical Raynaud phenomenon in this patient. Conclusions This case demonstrates a probable relationship between the rate of infusion of iloprost and the paradoxical reaction of Raynaud phenomenon.


1971 ◽  
Vol 178 (1053) ◽  
pp. 455-464 ◽  

1. Memory in day-old-chickens during the first few hours after learning can be made to decline by the prior intracranial injection of two classes of drugs. 2. Sodium pump inhibitors in increasing doses cause increasingly rapid loss of memory. 3. Protein synthesis inhibitors in increasing doses attain a maximum potency in causing memory decline and the rate may not be further accelerated by higher doses. 4. Adding a sodium pump inhibitor to the inhibition of protein synthesis increases memory loss. 5. Adding a protein synthesis inhibitor to a sodium pump inhibitor causes no further loss. 6. Therefore within a few minutes of learning a short-term memory of limited time span but independent of protein synthesis becomes supplemented and eventually replaced by a long-term storage requiring protein synthesis. The amount of long-term store is set by the amount of short-term memory. 7. The short-term store could be directly dependent on post-activation enhancement of Na + extrusion from neurons. Some physiological mechanisms by which this could be achieved and how this might activate protein synthesis are discussed.


1988 ◽  
Vol 22 (2) ◽  
pp. 142-145 ◽  
Author(s):  
James M. Dunn ◽  
Paul E. Groth ◽  
Anne DeSimone

Tocainide is a primary analog of lidocaine with antiarrhythmic properties used to treat ventricular rhythm disorders. A 76-year-old man with benign paroxysmal premature ventricular contractions was treated with tocainide and developed a generalized maculopapular lupoid eruption, bleeding from the lips and gingivae, vertigo, gross tremors of the extremities, fever, and short-term memory loss, which required hospitalization. The patient recovered slowly over three months with no permanent sequelae after discontinuing the drug and receiving rigorous supportive care. His excellent physical status and absence of concomitant illness contributed to an uneventful recovery. Tocainide is a potent cardioactive drug with a long biological half-life and should be used with caution.


2018 ◽  
Vol 26 (6) ◽  
pp. 612-614 ◽  
Author(s):  
Dahai Wang ◽  
Qinjian Hao ◽  
Lan He ◽  
Qiang Wang

Objective: To describe a case of leucine-rich, glioma inactivated 1 antibody-encephalitis presenting with psychosis. Methods: Case report. Results: A young man with leucine-rich, glioma inactivated 1-antibody encephalitis initially presented with acute psychotic symptoms, short-term memory loss and faciobrachial dystonic seizures. Magnetic resonance imaging revealed hippocampal lesions. Electroencephalography revealed frontotemporal slowing of background activity. Conclusion: Increased awareness of leucine-rich, glioma inactivated 1-antibody encephalitis may promote early recognition and treatment.


1999 ◽  
Vol 5 (1) ◽  
pp. 85-86
Author(s):  
KONSTANTINE K. ZAKZANIS ◽  
LARRY LEACH ◽  
MORRIS MOSCOVITCH

Severely impaired memory deprives amnesics of a sense of personal continuity in their daily lives, yet there are no tests that accurately measure this impairment (see Lezak, 1995). Several neuropsychological tasks have been developed to document the severity of memory loss in terms of memory span, such as the Brown–Peterson Technique (Peterson & Peterson, 1959), but the ecological validity of such tasks as measures of personal or temporal continuity is not obvious (see Heinrichs, 1990). Instead they measure memory in terms of how much information could be held in working or short-term memory, not memory span in the sense of continuity. To develop a new measure of amnesia with greater relation to everyday function, we had to examine the integrity of memory function in terms of temporal continuity in a way that would engage the patient in everyday behavior, such as informal conversation, and still allow memory function to be quantifiable. Thus, we set out to create a bedside task that could measure the span in which the patient with amnesia experiences temporal continuity. We call this measure the “span of temporal continuity,” or “personal and present span of existence.”


Sign in / Sign up

Export Citation Format

Share Document