Please read this.
A Case of Mutism Subsequent to Cocaine Abuse
Gianluca La Monaca MD, Anthony Donatelli MD and Jack L. Katz MD (1999)
The patient was a 35-year-old unemployed married Black woman living with her husband and two children. She had a 12-year history of crack-cocaine abuse. She was brought to the hospital emergency room (ER) by her husband due to progressive mental status and behavioral changes over a number of weeks, culminating in mutism, choreiform activity, chewing movements, excessive showering, and inappropriate affect, ranging from irrational laughter to irritability. There was no history of alcohol abuse or head trauma. She was not on any medications and had not used any substances since the change in her mental status. Medical history was positive for small bowel resection 7 years prior, for questionable Crohn's disease. The husband stated that, after the birth of their children, the patient began leaving the house for as many as 3 days with several hundred dollars to buy crack-cocaine. At times, she would use up to $400 on cocaine and would ask for more money from her fellow users. He said that this behavior had gone on for 12 years, during which time his wife was away from home about 40% of the time on cocaine binges. Occasionally, she would also use marijuana.
The patient's final crack-cocaine binge cost $2,000 and lasted 3 days. She was brought home by her fellow abusers and awoke partially mute, staring, and acting inappropriately. She would wander off, hide food, and speak garbled words, usually repeating the same sentence numerous times.
In the ER, she was uncooperative, displayed psychomotor restlessness, and would periodically dance in the evaluating room. She was mute except for occasionally murmuring, “Right?” She had multiple repetitive movements (tongue biting and abdominal thrusting). She was able to follow simple commands. Her affect was labile and inappropriate. Full mental status examination could not be performed because of her uncooperativeness and mutism. Brain CT revealed diffuse atrophy, but was otherwise negative. Neurological consultation was obtained. There were no focal findings. She was admitted to psychiatry. Comprehensive medical work-up, including Veneral Disease Research Laboratories (VDRL), human immunodeficiency virus (HIV), rheumatoid factor (RF), antinuclear antibody (ANA), antiDNA, angiotensin converting enzyme (ACE), purified protein derivative (PPD), thyroid function tests (TFTs), drug screen, vitamin B12, folate, complete blood count (CBC), SMAC, urinalysis, chest x-ray, heavy metal screen, and EEG, was within normal limits. Brain MRI was also negative, except for some diffuse atrophy. The working diagnosis was psychosis NOS, rule out catatonic schizophrenia.
The patient received a 4-week trial of haloperidol. After 2 weeks she had stopped speaking altogether. Bizarre, disorganized behavior continued. She would take off her clothes inappropriately. She hoarded food, held food in her mouth, wandered into other patients' rooms, and defecated on the floor.
Carbamazepine was added to the haloperidol, but, due to the patient's drooling and extrapyramidal symptoms, haloperidol and carbamazepine were tapered off. The patient was started on risperidone, the dose gradually being raised to 3 mg twice daily. There was no improvement and, after 2 weeks on this regimen, she was taken off risperidone and administered an amytal interview. The patient received an intravenous solution of 5% amobarbital sodium at a rate of 1 cc per minute. She was given a total of 6 cc (300 mg), causing drowsiness and nystagmus. She did not speak at any point in the interview. The negative response to the amytal interview and the lack of any response to two neuroleptics and one mood stabilizer led us to rethink our diagnosis. We, therefore, obtained a brain SPECT scan. The scan was clearly abnormal, showing decreased perfusion in the anterior aspect of the left temporal lobe and, to a lesser extent, in both frontal lobes (left greater than right). As the patient was right-handed it was concluded that the neural associative areas related to speech were affected.
Based on these various tests and the patient's clinical course, we concluded that her mutism and clinical presentation were probably due to organic lesions secondary to heavy chronic crack-cocaine abuse. She was discharged on no medications after a 3-month stay, slightly improved (less psychomotor agitation) but still mute, to be followed by neurology as an outpatient. The patient's family declined any recommended rehabilitative services and chose to care for her at home. Follow-ups at 3 and 6 months found her unchanged.
In our patient, there was no known previous psychiatric history except for the substance abuse. The catatonic state did not improve with the discontinuation of cocaine, even after more than 3 months of hospitalization. The patient's condition did not respond to conventional treatment with neuroleptics and other psychotropic medications.
The patient's mental status changes appeared to be permanent, presumably secondary to the massive and prolonged use of crack. Its effects on brain perfusion provoked a permanent change in brain physiology responsible for the patients mutism. A follow-up of the patient at 3 and 6 months after discharge showed no change in her mental status.
![:\](https://bluelight.org/xf/BL_Images/Orig_Emoji/wrygrin.gif "wry grin :\")
), leaves me with a slight limp and pain, which sucks BAD as I live in the upstairs floor of a house- doing that trek with a few pinholes in my leg and groceries in my arms = ouch! 
