1. 1
Mental Health Consultation
Patient Name: Tardive Dystonia Facility: XXXX
Date: 9-16-13
Additional history can be found elsewhere in this chart and will not be repeated here.
Reason for Referral: xx-year-old, white, xxxx, female… I was asked to see this “nearly catatonic”
mostly mute, resident newly admitted under PASSAR LevelII. Admitted from XXXX on 9-14-13.
Background Information: Excerpts from her complicated recent history follow:
“She was transferred to XXXX from XXXX on 5/22/13 for feverand altered mental status. She was taken
off of perphenazine aswellas herclomipramine.Shedeveloped rigidity,feverand hemodynamic instability.
There isa suspicion ofneurolepticmalignantsyndrome,however,creatine kinaselevels werenotelevated.
The patient seemed catatonic. All of her psychiatric medications were held. She improved but became
grandiose.”
“Transferred to Psychiatry here at XXXX on 6/5/13.Her medical status declined rapidly. She wassent
back to Medicine. She was delirious likely due to aspiration pneumonia and urinary tract infection.She
was not eating.She was psychotic as well.”
"Pt. has had 6 left temporal modified ECT with little essential change in behavior”.
“The differential diagnosis are serotonin syndrome, extrapyramidal symptoms, neuroleptic
malignant symptoms and cholinergic antagonistic symptoms. Upon review of the record, it seems the
patient was not on any selective serotonin reuptake inhibitor recently, the patient wasnot on any
medication that can cause serotonin syndrome during this hospital admission at XXXX. I amaware of the
administration of selective serotonin reuptake inhibitor during the hospital admission at XXXX, but
usually the symptoms of serotonin syndrome resolve after discontinuations of the selective serotonin
reuptake inhibitor. The patient was checked forcreatine kinase, which came back to be normal. The
patient doesnot have any spontaneous cIonus or inducible clonus on examination. So in spite of this
hyper rigidity and brisk reflex, I do not think the patient has serotonin syndrome. Though the patient was
consistently on antipsychotic medications, lack of severity of the symptoms and absence of
rhabdomyolysis, acute kidney injury,metabolic acidosis and mostly the lack of severity rules out the
neuroleptic malignant syndrome. Extrapyramidal symptomsare most likely”.
“She appearsto have a spinal disorder that could possibly include Guillain-Barre syndrome.”
“AXIS I; catatonic versus hypoactive delirium, schizophrenia by history”.
8/28/13- MRI of the Brain = “Chronic residual of old subarachnoid hemorrhage in the region of left
temporal lobe and cerebellar hemisphere…mild cortical atrophy with mild chronic periventricular
microvascular ischemic changes”
Current Medications: Ativan 0.5mg tid, Coumadin, Prilosec, Clonidine, Metoprolol, Prilosec, Norvasc,
Abilify 12mg qd. (Recent antipsychotics- Seroquel, Trilafon, Zyprexa)
Medical History: GERD, Dementia, Hyperlipidemia, Hypertension, Coronary Artery Disease,DVT,
Hypothyroidism, Bipolar Disorder, Schizophrenia, COPD, PVD, Bell’s Palsy, Benzodiazepine
dependence
2. 2
Mental Status Exam: She was alert. She stared at me without blinking and made occasional sounds as if
trying to communicate with me. Her facialexpression was apprehensive and frustrated. When I asked if
she understood me she seemed to try to indicate that she did. She could not move her arms, hands or eyes
on my command though I believe she tried.
Findings and Recommendations: This is a very difficult diagnostic puzzle. I think we should start by
ruling out one strong possibility.
Catatonic schizophrenia which was frequently mentioned as a possibility in her record is characterized
by stupor, negativism, rigidity, excitement, or posturing; sometimes there is rapid alteration between the
extremes of excitement and stupor. Associated features include stereotypic behavior, mannerisms, and
waxy flexibility; mutism is common. However,this is highly unlikely because this form of Schizophrenia
is very rare now and does not occur suddenly. It is a regressed form of end stage schizophrenia seen at the
end of a long progressive disease course. We generally do not see this now because treatment prevents
schizophrenics from regressing to this point. I have only seen three cases in 40 years.
Serotonin Syndrome which was also mentioned as a possibility includes the following S/S: agitation,
ataxia, diaphoresis, diarrhea, hyperreflexia, mental status changes, myoclonus, shivering, tremor, or
hyperthermia with these possible complications: seizures, aspiration pneumonia, Rhabdomyolysis, acute
renal failure, respiratory failure. However, this was ruled out because she had not recently taken SSRIs or
other serotonin agonist drugs.
Diagnosis of neuroleptic malignant syndrome is based on clinical features. Cardinal features are the
development of severe muscular rigidity, hyperthermia, autonomic instability, and changes in the level of
consciousness associated with the use of an antipsychotic medication. This was ruled out for a number of
reasons.
I think this may be Tardive Dystonia an uncommon complication of long-term treatment with
neuroleptic drugs. It is a variant of tardive dyskinesia and like tardive dyskinesia the signs emerge as the
neuroleptic medication is withdrawn and the risk of its development increases with advancing age.
Tardive Dystonia is a more severe and more incapacitating condition than tardive dyskinesia. Patients
with tardive dystonia show sustained postures of the face,neck,arms and/or trunk. They may freeze up
and become immobile and mute. The dystonia may be focal, segmental or generalized. The dystonic
contractures are often exacerbated by emotion and distress and may appear only during certain motor acts.
After long term treatment, she was abruptly taken off perphenazine a highly antidopaminergic first
generation antipsychotic then all of her problems began. Her problems could be a reflection of tardive
dystonia. In any case,it is worth immediately trying the following: restart perphenazine 8mg bid and
reduce Abilify to 6mg qd; find out her previous maintenance dose of perphenazine and increase to that
dose then DC Abilify. Abilify is very low in antidopaminergic properties. Observe for any change in
motor symptoms. Please keep me informed.
___________________________
Drew Chenelly, Psy.D.
Clinical Neuropsychologist
3. 3
Follow-up/ Mental Health Progress Note
Patient Name: Tardive Dystonia Facility: XXXX
Date(s): 10-21-13 Last seen: 9-16-13 Room: 145 W
Objective: I am seeing her again for follow-up. On 9-24-13 she was started on perphenazine
8mg bid. More recently, her Abilify was reduced to 2mg qd. By all accounts she has improved
some. According to the nurses “She is more alert with more movement…even talks in the
morning”. The nurses will try to obtain XXXX past perphenazine maintenance dose from the
family. The nurses will ask family to bring in a medication vial from home.
I again reviewed her chart for the perphenazine maintenance dose but that information was not
there. The history did show that she was abruptly taken off perphenazine and started on Seroquel
a total of 500mg qd in May of 2013. In July reports she was noted to have “significant rigidity of
the extremities…extended contractures…cog wheeling” and she was described as “obtunded”.
On interview: Her face was expressive. She was blinking. The staff told me that she was
speaking earlier. She even smiled and winked at me. Was able to move her neck and her trunk.
Assessment: The more I learn the more I am convinced that the problem is Tardive Dystonia
caused by the abrupt DC of her perphenazine in May. How much this can be reversed is a major
question and how to treat it without worsening it is a real dilemma. Clearly restarting her
perphenazine at a low dose has loosened her up some. Neither Abilify nor Seroquel could replace
perphenazine and keep the tardive disorder from emerging because they are both low in anti-
dopaminergic properties. Increasing the perphenazine will probably reduce the overt Tardive
Dystonia symptoms but will also likely worsen the underlying disorder. A total of 500mg of
Seroquel qd is about equivalent to 40mg of perphenazine qd. She is currently taking a total of
16mg of perphenazine a day.
I have done some research on this issues and found the most effective medications for tardive
dystonia are antidopaminergic drugs, either dopamine depletors (reserpine) or DRBAs
(risperdal). As with classical tardive dyskinesia, increasing doses of DRBAs might temporarily
help tardive dystonia, but continuing exposure may cause worse movements over time. In tardive
dystonia, anticholinergics (benztropine or trihexyphenidyl) are almost as effective as
antidopaminergic drugs. The atypical antipsychotic, clozapine, has been helpful in some patients.
For medically intractable tardive dystonia, bilateral globus pallidus stimulation using implantable
electrodes has been tried with some success.
Recommendations/Plan: For now would continue to try and ID her past perphenazine
maintenance dose. If we cannot get that info, would increase the perphenazine and DC the
Abilify then consider the above for a long term strategy.
DrewChenelly, Psy.D.
ClinicalNeuropsychologist
