SCIENTIFIC
Catatonia Associated with Buprenorphine-Induced Toxic Leukoencephalopathy
AUTHORS : Danielle DeCicco , MD , PhD 1 , 2
Jessica Thayer , MD 1 , 2 Ziad Dimachkie , MD 1 , 2 , 3
1
School of Medicine , West Virginia University
2
Department of Medicine , J . W . Ruby Memorial Hospital
3
Section of Hospital Medicine , Department of Medicine , J . W . Ruby Memorial Hospital
CASE REPORT
Emergency medical services transported a 28-year-old unresponsive female soiled with urine , found without clothes , and unable to speak . History was primarily obtained by first responders from male friends present at the scene . Five hours prior she had ingested buprenorphine . Electronic medical records ( EMR ) indicated that two weeks prior , she delivered a baby with no prenatal care . She had buprenorphine positivity on a urine drug screen at that time . She was prescribed buprenorphine in the past , but she was not currently taking a prescription version . Medical , surgical , and family history per EMRs with collateral information from her mother was non-contributory . Social history included opiate use disorder , past benzodiazepine use disorder , and tobacco use disorder .
On examination , her vitals were within normal ranges and remained stable throughout the entire course of hospitalization . Notable examination findings included mutism , waxy flexibility , catalepsy , stupor , rigidity , diaphoresis , and negativism . She had a persistent leftward gaze with occasional extremity movements . She exhibited rigidity and resistance to movement in her bilateral upper extremities . Her Glasgow Coma Score was as follows : eyes – 4 , verbal – 1 , and motor – 5 . She never required intubation . She exhibited bilateral upper extremity rigidity noted at the shoulder and elbow and 5 / 5 resistance and rigidity in her biceps bilaterally .
ABSTRACT
It is well-known that West Virginia ( WV ) is one of the states most affected by the opioid epidemic . Recently , WV has implemented a program to expand buprenorphine use as part of a multi-prong approach to treat opioid use disorder accompanied by positive outcomes . However , buprenorphine can be diverted and obtained outside of a medical provider ’ s guidance . Given the prevalence of buprenorphine use in
Her strength was grossly rated at 3 / 5 . No tremors were present . Biceps , patellar , and Achilles reflexes were 2 + bilaterally . Plantar reflex was down going bilaterally , and a Hoffman ’ s sign was not present bilaterally .
The initial work-up included negative screening tests for hepatitis C , human immunodeficiency virus , syphilis , gonorrhea , and chlamydia . Complete blood count showed no elevation in white blood cells or neutrophils . C-reactive protein levels were within normal limits . Serum lipase and ammonia were within normal limits . Troponin was negative . Blood and urine cultures showed no growth . Her serum contained no acetaminophen or alcohol , and a hepatic function test panel was normal . A thyroid stimulating hormone test was unremarkable , and no electrolyte or acid-base disturbances were present . A urine drug screen was delayed due to concern for sexual assault but was positive for buprenorphine and benzodiazepines with likely contamination with diazepam given in-house on admission before being able to obtain the urine specimen . A comprehensive blood-based drug panel was positive for diazepam metabolites but negative for other benzodiazepines or synthetic cannabinoids , indicating that the only other drug for which she was positive was diazepam . A send-out blood laboratory study for cathinone use failed to rule out ingestion given inappropriate sample parameters , though she had no history of using these substances .
WV , we aim to present original clinical data prompting clinicians to recognize buprenorphine as a potential cause of toxic leukoencephalopathy . We describe the case of a 28-year-old female who presented with catatonia believed to be secondary to buprenorphine , and we discuss the diagnostic challenges and therapeutic management of buprenorphine-induced toxic leukoencephalopathy .
Imaging studies included an unremarkable computed tomography scan of the chest , abdomen , pelvis , neck , and brain without contrast . Psychiatry and neurology services were consulted . An electroencephalogram was remarkable for high amplitude , sharply contoured theta slowing ; however , it did not show underlying diffuse or multifocal dysfunction or seizure-like or epileptic discharges . A brain magnetic resonance imaging ( MRI ) revealed multiple foci of symmetric white matter cytotoxic edema involving bilateral centrum semiovale and the splenium of the corpus callosum thought to represent a toxic leukoencephalopathy ( TL ) ( Figure 1 ).
Her characteristic physical examination and imaging findings were concerning for catatonia related to TL . Per the psychiatry team ’ s recommendation , a lorazepam challenge was attempted . Two milligrams of IV lorazepam were given followed by monitoring for a response for 30 minutes . A typical response would be seen within 30 minutes , but she exhibited no response . 1 Three hours later , there was still no response . Given the MRI findings in conjunction with the clinical assessment and drug screen results , acute buprenorphine induced TL was determined to be the cause of her catatonic state . Electrical convulsant therapy ( ECT ) was being discussed for her next step in care , but her encephalopathy improved with conservative therapy , which entailed treating her substance withdrawal symptoms with clonidine , loperamide , and ondansetron . She did require nasogastric
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