United States

Background: Moyamoya disease (MMD) is a progressive vascular disorder in which the carotid artery becomes narrowed, reducing blood flow to the brain. This most commonly presents as stroke in children and young adults and typically occurs between 5 and 10 years of age in children and between 30 and 50 years of age in adults. MMD survivors have the highest prevalence of mental disorders, including depression, anxiety, and post-traumatic stress disorder {PTSD}. This case aims to increase awareness of an unusual presentation of MMD as a psychiatric disorder. 

Case Presentation: A 16-year-old Dominican boy presented to the psychiatric ER due to mood dysregulation and aggression. He had a medical history of MMD, Sickle cell disease, Frontal lobe epilepsy, and a cerebrovascular accident in 2019. He was all right till 2019; then, he experienced a cerebrovascular accident/stroke, learned of his diagnosis, and underwent immediate neurosurgical intervention. His home medications include Aspirin, Valproate, and Hydroxyurea. He reported recent aggression and stated he started “beating his brother and would not stop.” He said he often had terrible headaches, and his attack worsened. The COVID-19 pandemic worsened his anxiety and depression. The patient was diagnosed with Mood disorder due to a medical condition. His treatment plan included continued outpatient monitoring with a psychiatrist and continuation of medication.

Discussion: Only psychiatric presentations of MMD are rare in literature. The clinical symptoms of MMD include ischemic stroke, TIA’s, hemorrhagic stroke, epilepsy, headache, and cognitive dysfunction, and they vary depending on age. In children, hyperactivity, impaired concentration, anxiety, mood lability, and poor academic performance have also been described. Identifying and treating psychiatric symptoms is essential to improve the quality of life in patients with MMD.


AMA Research Challenge 2022

Mental Distress and Medical Illness in Children and Adolescents with MoyaMoya Disease

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Charles Lopresto, DO

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poster

Background: Paragangliomas are rare extra-adrenal catecholamine-secreting tumors. Since sympathetic symptoms of anxiety and paragangliomas are similar, diagnosis and treatment can be complicated when these pathologies are simultaneously present.
Case Presentation: Mr. V is a 27-year-old Hispanic male with no past psychiatric history who presented to the psychiatric consult liaison service for concerns of anxiety in the setting of paroxysmal episodes of autonomic dysregulation related to a malignant, metastatic thoracic paraganglioma. The patient asked the nursing staff to check his blood pressure more often in the evening to be aware of an upcoming episode of chest palpitations, sweating, and feeling like he was “going to die,” prior to symptom onset. Psychiatry considered differential diagnoses of generalized anxiety disorder, specific phobia disorder, and anxiety secondary to a medical condition. Lorazepam 0.25 mg one tab at night reduced symptom frequency and severity.
Discussion: Paragangliomas, closely related to pheochromocytomas, are known to present as episodic hypertension, sweating, and tachycardia. Medical sources for this patient’s symptoms might not explain the clinical aspects of the case. The patient developed anxiety triggered by his anticipation of these episodic symptoms which further enhanced the patient's sympathetic stimulation, resulting in increased frequency of hypertensive episodes. Episodic hypertension due to a psychiatric diagnosis like anxiety or panic disorder, even when unaccompanied by a diagnosis of paraganglioma, can result in an undesirable feedback cycle of hypertension and anxiety. Patients with pheochromocytomas, for which current literature is more robust, are six times more likely to experience anxiety and depression compared to patients without pheochromocytomas. The symptoms these pathologies have in common, including hypertension and tachycardia, can be treated with medications that reduce sympathetic nervous system activity, specifically anxiolytic medications like Alprazolam. One case described a patient with concomitant pheochromocytoma and paraganglioma whose sympathetic symptoms were improved with Citalopram. In order to provide the best treatment and symptomatic relief for the patient, psychiatrists need to discuss the importance of identifying and separating the psychiatric symptoms of a medical condition from the medical diagnosis itself.

Paraganglioma and Anxiety, A Physiologic Feedback Cycle: Case Report and Review of Literature

Psychedelic hallucinogens such as psilocybin has seen a resurgence in popularity as a novel therapeutic in psychiatry. Parkinson Disease (PD) is a neurodegenerative disorder with both motor and non-motor symptoms, arising from loss of dopaminergic neurons in the substantia nigra. Given the limited efficacy of current treatment options especially for non-motor symptoms of PD, psilocybin may offer a promising solution. Here I present a case of a patient with symptomatic improvements in the motor symptoms of PD, depression, and suicidality following the ingestion of 10mg and 25mg of psilocybin on two separate occasions as part of a clinical trial. Psilocybin, a 5-HT1A and 5-HT2A receptor partial agonist, was able to exert therapeutic effects in the patient likely via the restoration of disrupted serotonin signaling in PD, which has been well-established in literature.

Psilocybin as a Potential Novel Therapeutic for Motor and Non-Motor Symptoms in Parkinson Disease

Case Presentation
A 68 year old male navy veteran with past medical history of bipolar I disorder, depression, posttraumatic stress disorder (PTSD), hypertension, and hyperlipidemia presented to the ED with a two hour history of right facial droop, right-sided weakness, and aphasia. NIH stroke scale at the time was 7. Stroke alert was called. CT head without contrast and CT angiogram of head and neck showed no acute abnormalities. His wife was informed of a possible cerebrovascular accident (CVA) event; she did not grant consent for Tissue Plasminogen Activator (TPA) as the
patient has had similar episodes in the past. Psychiatry diagnosed the patient with delirium secondary to bipolar I disorder and PTSD. Patient was admitted and the dosing of his Depakote, Zoloft, Seroquel, and PRN Ativan was adjusted. Neurology ruled out a vascular event and deemed the patient to have retarded catatonia, while recommending continuing his home medications atorvastatin and aspirin. Two weeks later, the patient was back to baseline functions with an NIH score of 0. He was stable enough to be discharged to an outpatient facility.

Discussion
Neuropsychiatry remained a largely unexplored realm until the past few decades. In this case, stroke-like symptoms in the setting of bipolar I disorder and PTSD alluded to retarded catatonia. However, unlike the majority of catatonic patients that show immediate improvement via benzodiazepine therapy, our patient did not respond to Ativan. His symptoms were resolved gradually with elapsed time and by titrating his psychiatric medications. Catatonia, although with unknown pathophysiology, is hypothesized to implicate the basal ganglia-cortex and basal ganglia-thalamus pathways and possess genetic predispositions as well as environmental influences.

Conclusions
The utmost importance of patient history in guiding management is highlighted in this case. Brain areas regulating mood, emotion, cognition, and perception can suffer from neurochemical imbalances and metabolic hyperactivity, which can lead to damages to specific brain regions, resulting in neurological manifestations. Improved characterization of this overlap will shed light on clarification of risk factors, better recognition of stroke-mimetics, efficient usage of diagnostic tests, and optimization of treatment in psychiatric patients, supplying necessary answers to psychiatric patients and lessening the burden on caregivers.

Psychiatric Illness Manifesting as Stroke-like Symptoms - Treading the Unknown Waters

Suicidality Induced by Hoarding Disorder: A Case Report and Review of Literature

Abstract Title: Transient Eosinophilic Colitis in Clozapine Use
Background
Two main pathways have been implicated in the etiology of eosinophilia including an increased cytokine-mediated differentiation of eosinophils evident in extrinsic eosinophilic disorders. A study following 66 patients who remained on clozapine for one year showed a cumulative incidence rate of 5.9% for eosinophilia. This case report illustrates a presentation of Eosinophilic Colitis and the clinical significance of absolute eosinophil thresholds in patients on Clozapine

Case Presentation
A 59-year-old male, with past psychiatric history of schizoaffective disorder, presented following a pretrial evaluation for criminal charges, with delusions and hallucinations. His records showed multiple psychiatric inpatient hospitalizations, 20 electroconvulsive treatments and successful management with Paliperidone. On admission, he voiced delusional statements. Mental status exam revealed delusions but no gross thought disorganization or hallucinations. He received a trial of Clozapine with baseline Complete Blood Count (CBC) with differential showing Absolute Neutrophil Count (ANC) 7,051cells/uL, Eosinophils 0 and Hemoglobin 12.0g/dL. Clozapine was titrated up to only 150mg given he developed explosive diarrhea. A repeat CBC with differential showed ANC 9,449 cells/uL, Eosinophils 12.0 x 109/L (High) with C-Reactive Protein (CRP) 5.3mg/L. Clozapine was immediately discontinued without any protocol for restarting clozapine following symptom resolution. Following the Risk Evaluation and Mitigation Strategies (REMS) protocol, subsequent monitoring of CBC with differentials, revealed ANC 10,377cells/uL, CRP 9.9mg/L, with eosinophils normalizing within a week. He was started on Aripiprazole for better control of mood and psychotic symptoms. 

Discussion
Eosinophilic colitis (EC) is a rare inflammatory condition with many factors including psychotropic drugs implicated in the pathogenesis of secondary EC. The pathophysiology of eosinophilia induced particularly by clozapine is still unknown, but given almost immediate resolution with continued treatment, the possibility of an acute allergic reaction has been suggested in literature. While EC lacks guidelines with regards to diagnostic criteria, particularly threshold values for eosinophilia, a review article implied that eosinophilia is not a potential ground for clozapine discontinuation. Given it is a diagnosis of exclusion with no standardized monitoring recommendations, exceedingly high values need to be evaluated for setting threshold values as one criterion for clozapine discontinuation.





Transient Eosinophilic Colitis in Clozapine Use

Uncommon Neuropsychiatric Manifestations in Thyrotoxicosis

Background
Parkinson’s Disease and its treatments have been associated with affective changes, psychosis, and sensorial abnormalities given this pathology’s roots in dopaminergic neural circuitry. These effects are more commonly observed with high-dose dopaminergic agent administration or sharp dopamine agonist tapers, but they are relatively unique with levodopa withdrawal.

Case Presentation
A 70s-aged female Parkinson’s Disease patient was admitted for encephalopathy, affective changes, and hallucinations. She was anxious, but intermittently alert and oriented. She stopped her carbidopa-levodopa 25-100 mg, three tablets, thrice daily, one week prior due to abdominal pain. She subsequently experienced weakness, tremors, and hallucinations of people around her stove, then called emergency services. Her son verified her recent medication non-adherence. She lived alone and was recently unsupported. The possibility of accidentally taking excess levodopa was firmly denied.

The patient started levodopa five years ago, periodically complaining of stomach pain. Geriatric psychiatry outpatient managed her controlled depression. She had mild shadow hallucinations and cognitive decline in the past year, but the current episode was markedly worse. During inpatient neurology, confusion and agitation worsened. Infectious workup and head CT were unremarkable. Levodopa-carbidopa was restarted at home dose. Several drugs were added: Quetiapine 100 mg nightly plus a 25 and 75 mg tablet throughout the day, pimavanserin 34 mg daily, and a rivastigmine 4.6 mg daily patch. Psychiatry adjusted home lorazepam to 0.25 mg four times daily, continuing mirtazapine 15 mg nightly and desvenlafaxine 100 mg daily. Her mental status overall improved to an outpatient-manageable state over six weeks.

Discussion
Common high-dose side effects of dopaminergic agents include psychosis and hallucinations. Sharp medication tapers can also cause problems: E.g., Dopamine Agonist Withdrawal Syndrome with medications like pramipexole involves dysphoria and panic attacks. Exacerbated altered mental state and hallucinations from levodopa withdrawal is more unique; it has been observed, but mainly in rare, older reports. More common levodopa withdrawal complications include stiffness, rigidity, tremor, and thrombosis risk, versus hallucinations. Moreover, visual hallucinations, in general, have an inconsistent literature association with dopaminergic agents. This case presents an unusual levodopa withdrawal manifestation for clinical consideration when generating differential diagnoses and deciding treatment options.

Visual Hallucinations and Altered Mental Status Exacerbation Associated with Acute Levodopa Withdrawal

Background

Actinomyces species are gram-positive, anaerobic microorganisms found in the oral cavity and are often associated with dental abscesses or other oral-cervicofacial disease. Pulmonary actinomycosis is rare and its presentation may be confused with pulmonary tuberculosis or malignancy.

Case Presentation

A 66-year-old male with a PMH of psoriasis and tobacco use presented to the office with a several-week history of a productive cough with yellow sputum and malaise. He denied fevers, SOB, recent travel, weight loss and only drank alcohol socially. He was recently seen in an emergency department for similar symptoms, diagnosed with pneumonia, and completed an antibiotic course without clinical improvement. On physical examination, vital signs were within normal limits and lung auscultation
revealed scattered rhonchi bilaterally with bibasilar rales. HEENT exam revealed poor dentition. Laboratory studies were unremarkable. CT chest revealed a right lower lobe endobronchial soft tissue density with complete opacification of the basilar bronchi, along with scattered sub-centimeter nodules. He was referred for hospitalization where broad-spectrum antibiotics were initiated. A bronchoscopy
revealed a foreign body in the RLL, which was later confirmed to be a peanut; the patient subsequently reported eating peanuts in bulk. Cultures of endobronchial washings were positive for Actinomyces and Enterobacter. The remainder of his hospitalization was unremarkable; he was transitioned to Augmentin for a three-month course and discharged with outpatient follow-up. Repeat CT chest after completion of antibiotics revealed significant improvement in the RLL infiltrate.

Discussion

Pulmonary actinomycosis is a relatively rare disease; the exact incidence rate is unknown. Risk factors associated with the disease include underlying respiratory disorders, alcoholism, poor dental hygiene, and facial/dental trauma. Although it can occur at any age, it is usually seen in patients between 20-50 years of age. Symptoms can be nonspecific; patients may present with fever, SOB, productive cough, hemoptysis, chest pain, or malaise. Diagnostic imaging, such as chest x-ray and CT scan, may be helpful but definitive diagnosis requires cultures positive for Actinomyces species; this is often obtained via bronchoscopy. The treatment involves an extended course of antibiotics, usually a penicillin. The prognosis is excellent in patients with early detection and appropriate treatment.

A Nutty Finding: A Rare Case of Pulmonary Actinomycosis due to Peanut Aspiration

Introduction 
Propofol infusion syndrome (PRIS) is a rare and fatal complication of high dose administration of propofol. We introduce a case report of a critically-ill patient who received high-dose intravenous (IV) pushes of propofol that resulted in rhabdomyolysis, metabolic acidosis, shock, multi-organ failure, and death. 

Patient Course 
A 48-year-old male diagnosed with acute respiratory distress syndrome (ARDS) due to COVID-19 pneumonia was intubated and sedated with propofol and fentanyl. He initially improved on the ventilator, but began to suffer emesis. Ileus was suspected. Imaging was not consistent with aspiration. Patient began to require large propofol boluses for adequate sedation and ventilation, greater than 4mg/kg/hr for several hours. The patient declined with progressive renal failure and increasing creatine kinase (CK). Due to elevation of CK and concern for PRIS, sedative medication was changed to midazolam. Patient soon required continuous renal replacement therapy (CRRT) due to oliguria/hyperkalemia. Evidence of shock liver became apparent. Patient required progressive amounts of vasopressors. Family decided to pursue comfort measures due to poor prognosis. 

Discussion 
PRIS is related to impaired free fatty acid metabolism and mitochondrial activity disruption causing an imbalance between energy production and utilization leading to peripheral and cardiac muscle necrosis. Typically, doses greater than 4-5mg/kg/hr are used in PRIS cases. Other hallmarks of PRIS include metabolic acidosis, kidney and cardiac failure, and hypertriglyceridemia. Treatment is generally supportive. Immediate withdrawal of propofol is recommended on suspicion. Other risk factors for PRIS include mitochondrial disease, exogenous catecholamine or glucocorticoid administration, inadequate carbohydrate intake, or critical illness. 

Our patient’s history fits with PRIS, due to his treatment with steroids and vasopressors, along with large doses of propofol. Carbohydrate rich diet may slow the progression of PRIS. Our patient worsened after cessation of tube feeds, potentially contributing to this patient’s syndrome. After our presented patient’s clinical picture became more evident for PRIS, sedation was transitioned to a non-propofol regimen, utilizing midazolam. In retrospect, a cardiac workup may have benefited diagnosis, as the literature seems to demonstrate that cardiac involvement is common. Triglyceride surveillance may aid in detection of impending complications of propofol, due to correlation with iatrogenic pancreatitis. 

Conclusion 
PRIS is a rare, lethal syndrome that has the best prognosis with early detection; our case demonstrates need for high index of suspicion for PRIS, and utilization of early interventions such as recognition of laboratory excursions, withdrawal of propofol, utilization of fluids, and a carbohydrate rich diet.

A Rare Case of Propofol Related Infusion Syndrome

Background
Nontuberculous mycobacteria (NTM) are found ubiquitously in water supplies, dust and soil. Rarely they can cause pulmonary infections, although the true incidence is difficult to establish due to limitations in diagnosing the disease. Newer estimates project a higher incidence than previously thought, likely due to increased awareness of the pathogen and increased numbers of immunocompromised patients. NTM are difficult to diagnose because they do not grow in standard bacterial culture media. We present a case of a patient who required several encounters with the healthcare system before a pulmonary NTM could be established. 

Case Presentation
A patient with a history of COPD on home oxygen presented with acute hypoxic respiratory failure and unintentional 20% loss of body weight over 6 months. A cavitary lung lesion was discovered 6 months prior to this presentation. Biopsies at that time were inconclusive. The patient underwent sputum testing on this admission due to her failure to thrive and history of cavitary lesion. She had two positive acid fast bacilli sputum cultures, which further speciated to non-tuberculosis mycobacteria, Mycobacteria chimaera and Mycobacteria peregrinum. Susceptibilities were obtained and the patient was started on a multidrug regimen with good maintenance of her functional status. 

Discussion
NTM exist naturally in the environment and can be found anywhere from home shower heads to hospital dialysis machines. Diagnosis should not be considered until other causes have been ruled out. There are stringent guidelines for diagnosis, which pose an additional barrier to identifying and treating these patients. 
Guidelines for NTM pulmonary disease have the following criteria: both pulmonary and systemic symptoms must be present, there must be radiologic findings, and there must be appropriate exclusion of other diagnoses. There are microbiological criteria as well which requires at least two separate cultures. This further strains limited resources and jeopardizes the chance of making an appropriate diagnosis. NTM are difficult to diagnose because they do not grow in standard bacterial culture; few labs are capable of culturing these evasive bacteria. Despite this, clinicians should consider NTM in any patient who presents with signs of lung disease without a known cause.

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Mental Distress and Medical Illness in Children and Adolescents with MoyaMoya Disease

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