A verage parental age is increasing in most Western countries, refl ecting the changes in professional and social life. Literature shows that in England and Wales from 1993 to 2003, the rate of older paternal age (35 to 54 years) increased from 25% to 40% and the mean paternal age increased from 29.2 years to 32.1 years. 1 Advanced paternal age is associated with accumulated environmental insults over time and is strongly associated with reductions in fertility due to impaired spermatogenesis. It is well known that in males, germ-line mutations are high due to the increased frequency of cell division over the life course. 2

BackgroundChorea is defined as a hyperactive movement disorder associated with involuntary, quick, and unpredictable muscle contractions of the limbs, face, and trunk. The unpredictable nature of these movements includes variation in speed, timing, and direction of movement. A wide variety of medications, medical conditions and illicit drugs have been associated with movement disorders. Examples include a multitude of antipsychotic induced movement disorders and dyskinesia related to dopaminergic agents, like levodopa and metoclopramide. Dyskinesias have been associated with psycho-stimulant use, such as methylphenidate. However, most cases reported were associated with large doses or chronic use. Aside from dyskinesia, methylphenidate is known to be associated with tic disorder, tremor, and muscle spasm. However, this case reported is unlike any of the above described and involved the development of chorea after only 2 days of moderate doses of methylphenidate, in a patient on chronic methadone maintenance treatment, with successful arrest of symptoms following discontinuation of the methylphenidate.Case PresentationA 47-year-old female was admitted to our hospital after presenting to the emergency department with 1 week of violent flailing movements. The ballistic flailing movements started acutely after 2 days of initiating methylphenidate in addition to her chronic methadone treatment and 2-week period of initiation of paroxetine. Lab work showed normal CBC, CMP, CRP, CK, and TSH. Urine drug screen, CT angiography of the head, and Huntington’s disease testing were all unremarkable, suggesting a decreased likelihood of illicit drugs, traumatic brain injury, or Huntington’s disease etiologies. Confirmation of the diagnosis was made as the chorea symptoms abruptly resolved upon discontinuation of methylphenidate and administration of intravenous Benadryl. The patient has been on methadone alone for 11 months and methylphenidate alone 2 years back with no involuntary movements or any similar presentation that shows the possibility of drug interaction through cytochrome P450 metabolism between Methylphenidate and methadone.ConclusionWe are presenting a rare case report that adds on to the scarce literature on methylphenidate-induced chorea. It also challenges the consulting psychiatrists to broaden their differential diagnosis for acute onset of choreiform movement disorders. This unique case intrigues the thought process to consider the interaction of methylphenidate in the presence of cytochrome P450 2D6 and 3A4 inhibitors like methadone.

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ABSTRACT:The term Catatonia was coined by Kraepelin in 1893 and was categorized as a subtype of dementia praecox. Bleuler in 1906 redefined it as catatonic Schizophrenia. Over the period of time by accumulating evidence of various case reports and studies its apparent that catatonia is not only seen in Schizophrenia, Affective disorders but is also seen secondary to various medical problems. There is very limited literature describing catatonia in the presence of neurological problems like Encephalopathy. The pathophysiology of Catatonia remains unclear. Given the involvement of common substrates like GABA, Dopamine and glutamate that are altered in many neurological problems and catatonia the differentiation and treatment become complicated.METHOD:We present the case of a 32-year-old male with bipolar II disorder, who was initially went through elective cholecystectomy complicated by bowel perforation and septic shock. Patient had to be intubated and had complicated ICU stay. Various consultation services including Neurology, Infectious disease, psychiatry, Intensivist got involved to address the multiple medical comorbidities like sepsis, encephalopathy and apathy. In spite of improving EEG showing resolving encephalopathy patient remained mute, immobile, not following any instructions, with no oral intake. All imaging including CT scan and MRI repeated 3 times over the period of time were negative. Patient’s psychiatric medications that includes Wellbutrin was held to minimize the risk of seizures. Patient’s neuro exam had positive Babinski and pupils dilated. He also had autonomic dysfunction. There were no clear-cut symptoms to enable us differentiating hypoxic brain injury and Malignant catatonia. We considered the differential diagnosis of Catatonia and initiated Ativan IV challenge.RESULTS:The patient was reassessed one hour after administration of lorazepam. He displayed slight response to Ativan by moving his fingers in the first 24 hrs. We had to continue to titrate the Ativan to very high doses in the period of 3 weeks with a very slow but good response.CONCLUSION:This case reflects the intricacy in diagnosing Catatonia complicated by Encephalopathy and the challenges in its treatment. We want to add on to the current literature on Catatonia masked by multiple medical comorbidities and the challenges of treatment