Taral R. Sharma

What Is the Evidence to Support the Use of Therapeutic Gardens for the Elderly

Horticulture therapy employs plants and gardening activities in therapeutic and rehabilitation activities and could be utilized to improve the quality of life of the worldwide aging population, possibly reducing costs for long-term, assisted living and dementia unit residents. Preliminary studies have reported the benefits of horticultural therapy and garden settings in reduction of pain, improvement in attention, lessening of stress, modulation of agitation, lowering of as needed medications, antipsychotics and reduction of falls. This is especially relevant for both the United States and the Republic of Korea since aging is occurring at an unprecedented rate, with Korea experiencing some of the worlds greatest increases in elderly populations. In support of the role of nature as a therapeutic modality in geriatrics, most of the existing studies of garden settings have utilized views of nature or indoor plants with sparse studies employing therapeutic gardens and rehabilitation greenhouses. With few controlled clinical trials demonstrating the positive or negative effects of the use of garden settings for the rehabilitation of the aging populations, a more vigorous quantitative analysis of the benefits is long overdue. This literature review presents the data supporting future studies of the effects of natural settings for the long term care and rehabilitation of the elderly having the medical and mental health problems frequently occurring with aging.

Case Reports of Neuroleptic Malignant Syndrome in Context of Quetiapine Use

A retrospective analysis was followed on 20 case reports covering the possible correlation between the atypical antipsychotic, quetiapine, and neuroleptic malignant syndrome (NMS), determined by the study of 7 different NMS criteria guidelines. A great majority (19) of the case studies did not meet the requirements of all 7 guidelines, frequently due to unreported information. Nor was quetiapine proven to be the sole cause of the possible NMS in the two age groups investigated. Only one case was found to have no other medication or medical conditions confounding the relationship of quetiapine and NMS symptoms, and that case was in the context of a significant quetiapine overdose. The other 19 cases demonstrated the difficulty of identifying the cause of NMS when polypharmacy and other medical conditions are involved. The authors note the need for caution in deciding both the presence of NMS and the causal factors of the symptoms.

Coprophagia and Pica in Individuals with Mild to Moderate Dementia and Mixed (Iron Deficiency and Macrocytic) Anemia

brain magnetic resonance imaging to augment diagnostic accuracy. For the same reason, metaiodobenzylguanidine (MIBG) cardiac scintigraphy was performed in most participants. Individuals with a history of abdominal surgery, gastrointestinal diseases such as ulcerative colitis and cholecystolithiasis, diabetes mellitus, and other systemic diseases that might potentially cause IPO or volvulus were excluded. For the same reason, individuals patients taking trihexyphenidyl and other anticholinergic agents were excluded. Two-hundred fifty individuals with PD (132 men, 118 women; mean age 67 (range 46–84); mean disease duration 5.3 years (range 1–15 years)) were enrolled in the study. Of these, six (2.4%) had been admitted to the gastroenterology unit because of emergency IPO (five cases) or sigmoid colon volvulus (case 3 and at the second admission of case 6) (Table 1). All six patients had acute onset of abdominal bloating, pain, nausea, or vomiting. Abdominal X-ray and computed tomography showed dilation of the colon with or without the small intestine in all six individuals. Two cases with volvulus showed a double loop sign at the sigmoid colon, which required emergency endoscopic reposition. The clinical features of the six individuals were as follows: mean age 78.5 (range 69–82); three male, three female; ordinary Hoehn Yahr motor grade 3.2 (range 2–5); illness duration 5.3 years (range 2–9 years; taking a large levodopa dose 420 mg/d (in 5); constipation; regular bowel medication (e.g., magnesium oxide) (in 5); urinary dysfunction (in 5); mean hospital stay 44 days (range 1– 112 days); no recurrence after discharge for mean 1.3 years (range 1–4 years). One patient (case 2) died from aspiration pneumonia. Mechanisms of constipation in PD are prolonged colonic transit (autonomic) and disturbed defecation (somatic and autonomic), reflecting Lewy body pathology in the myenteric plexus. The incidence of IPO and volvulus in our cases (2.4%, 6/250) is almost in accordance with that found in the previous study (7.1%, 8/ 112). After hospitalization, patients were started on mosapride (selective 5HT-4 stimulating agent), domperidone (peripheral dopaminergic blocker), and Dai-Kenchu-Tou (an herbal medicine containing hydroxy-beta-sanshool with 5HT-3-stimulating properties), which seemed to prevent the recurrence of IPO. In conclusion, the incidence of emergency IPO in individuals with PD at a movement disorder and gastroenterology clinics was 2.4%; all were older adults. Although rare, emergency IPO requires hospitalization and may have a poor outcome. Therefore, preventative treatment of constipation with prokinetic drugs is necessary particularly in older adults with PD. The present study was approved by the ethics committee at Sakura Medical Center, Toho University, Japan.

Psychiatric comorbidities in patients with celiac disease: Is there any concrete biological association?

Celiac disease (CD) is a unique autoimmune disorder that occurs in genetically susceptible individuals after the ingestion of gluten, a protein found in wheat and some other cereals. The immunologically based inflammation induces atrophy of the villous structure of the jejunum, leading to malabsorption of variable severity. Subclinical and nonspecific forms of CD have been found to be increasingly common with a classic presentation of malabsorption syndrome (reference A). We present a case of OCD (obsessive compulsive disorder) in combination with depressive symptoms with the further complication of eating disorder not otherwise specified, in an adolescent male, for whom psychiatry was consulted because of treatment-refractory weight loss. We compare the elements of the case to other descriptions in the current, English language professional literature. Our literature review includes multiple search terms for the professional journals including, but not limited to, psychiatric comorbidities in celiac disease, behavioral disturbances of celiac disease, celiac disease in psychiatry, etc., to establish a possible association of psychiatric disorders, especially obsessive compulsive disorder and Celiac disease.

Bath salts-induced delirium and brief psychotic episode in an otherwise healthy young man.

To the Editor: Poison centers took 2,237 calls through mid-May 2011 regarding toxic products marketed as bath salts. Bath salts contain methylenedioxypyrovalerone (MDPV), a chemical that is not approved for medical use in the United States.1 We are reporting a case to document that delirium and a reversible brief psychotic episode can be induced by easily available bath salts, which are undetected on routine urine or blood drug screen and thus require special attention in public health and law enforcement. Case report. Mr A, a 28-year-old white man, was brought to the emergency department in 2011 for investigation of confusion and an altered level of consciousness after recreational ingestion of bath salts (“Lady Bubbles”). The previous night, he had ingested 750 mg of “Lady Bubbles.” The following day, Mr A was found in a confused and disoriented state with both hands soaked in blood. The patient reportedly cut his wrists with a glass, and a broken window was found near the scene. He was taken to the emergency department, where he displayed a fluctuating level of consciousness; disorientation to name, place, and time; marked loosening of associations; and bizarre, agitated, and disorganized behavior. The patient received 1 dose of ziprasidone 20 mg intramuscularly in the emergency department. Mr A’s vital signs were within normal limits; physical examination was unremarkable except for bilateral superficial lacerations with one 1.5-cm full-thickness laceration on his left forearm and one 3-cm full-thickness laceration on his right forearm. Results of extensive blood work, including complete blood count, electrolytes, and liver and renal function tests, were within normal limits. The urine toxicology screen was negative for cannabis, amphetamines, hallucinogens, benzodiazepines, cocaine, opiates, and 3,4-methylenedioxymethamphetamine. His blood alcohol level was < 0.01%. Computed tomography of the head revealed no abnormalities, and remaining workup of sudden onset of altered mental status showed no abnormal results. Initial psychiatric consultation obtained in the emergency department revealed him to be somnolent, difficult to rouse, uncooperative, and profoundly confused. A diagnosis of hallucinogenic (and possibly bath salts–induced) delirium (DSM-IV criteria) was made. Mr A had no psychiatric history and was physically healthy. There were no difficulties within the family. His biological father suffered from depression and committed suicide when the patient was 8 years old. The patient was unemployed and was living at his mother’s house. He had also ingested 250 mg of “Lady Bubbles” a couple of days prior to this episode that resulted in increased heart rate, elated mood, and increased socialization. He had experimented with cocaine and heroin on approximately 10 occasions in the past and reported subjective effects of euphoria and increased talkativeness lasting for a few hours, but no other sequelae. During the first 24 hours of hospitalization, Mr A’s level of consciousness improved; he became more alert and better oriented to time, place, person, and situation. He continued to endorse symptoms of delusional ideation involving misidentification and command auditory hallucinations asking him to “kill himself.” The patient and his psychiatrist agreed to a short-term trial of perphenazine 4 mg twice a day to target psychotic symptoms and then further evaluation after discontinuation of medication. By the third day of hospitalization, his thought disorder improved, his mood was euthymic, and he consistently denied any command auditory hallucinations or delusional ideation. At the time of discharge, the patient reported passing out after taking bath salts with no recollection of events resulting in hospitalization and during the first 24 hours of hospitalization. He was discharged home to the care of his mother; his physicians believed that his improvement had been significant enough that psychiatric admission was not warranted. Classes of designer drugs like bath salts are intended to have pharmacologic effects similar to those of controlled substances but to be chemically distinct from them, thus avoiding legal control. Bath salts for recreational use are sold at “head shops” and on the Internet with names such as “Zoom” and “White Rush.” These products also have been labeled as “plant food” and “pond water cleaner” and sold in ways to circumvent detection or enforcement. Some products are labeled as “novelty collector’s items,” despite additional, pharmaceutical-like labels that indicate dosage.1 The products are believed to contain MDPV, a chemical that is not approved for medical use in the United States, which is believed to lead to very severe paranoia.1 MDPV is a norepinephrine and dopamine reuptake inhibitor. Bath salts are no longer legal alternatives in the United States, as an at least 1-year-long ban by the Drug Enforcement Administration has gone into effect as of March 1, 2011. Some of the patients presenting to the emergency department with bath salt abuse were found to have mental illness.2 We present a case of reversible brief delirium and psychotic episode following ingestion of bath salts in an otherwise healthy young man. Our case shows dose-dependent effects of MDPV. At lower doses, it causes increased talkativeness and sociability, while at higher doses, it causes a psychotic reaction. Bath salts–related brief psychosis is reversible and can be treated with antipsychotics or benzodiazepines. In conclusion, physicians should be aware of the increasing availability of bath salts in “special” plant food or pond cleaner—an availability about which potential abusers may already know. Bath salt use should be included in the differential diagnosis of conditions with sudden onset of delirium and brief psychotic symptoms in younger individuals experimenting with illicit substances despite negative toxicology screen. An increased incidence of reversible brief psychotic episodes might be induced by easily available bath salts, which are undetected on routine urine or blood drug screen. This phenomenon requires attention from a public health and law enforcement perspective.

Citalopram-Induced Seizures in a Healthy Adult Taking an FDA-Approved Dosage: A Case Report

To the Editor: A retrospective review of published literature disclosed case reports of seizures following citalopram overdose.1 We present a case of citalopram-induced seizures in an otherwise healthy woman taking a US Food and Drug Administration (FDA)–approved dosage. Case report. Ms A, a 50-year-old African American woman, had a past psychiatric history significant for major depressive disorder, no comorbid medical history, and no previously documented seizure disorder. She presented to the emergency department in October 2010 after 2 witnessed generalized tonic-clonic seizures, lasting 2 minutes each, on 2 consecutive days. She was confused upon presentation to the emergency department. Citalopram 20 mg po daily had been started 4 days prior to the first seizure. She had taken sertraline 50 mg po daily for a year, but had stopped taking that drug several years previously after depression did not improve. At the time of presentation, she had been taking gabapentin 300 mg po daily for Mortons neuroma. Past medical and surgical histories were not significant for any major illness. Family history was negative for seizure disorder, stroke, or myocardial infarct. She was an employed single mother of 6 children. She smoked half a pack of cigarettes daily, but there was no history of alcohol or illegal drug use. Physical and neurologic examinations revealed no abnormalities. Ms A was admitted to the general medical floor for observation, which lasted for 4 days. Complete blood cell count, comprehensive metabolic panel findings, thyroid-stimulating hormone level, alcohol level, and urine drug screen findings were within normal limits. Findings of cranial computed tomography and magnetic resonance imaging, with and without contrast, were within normal limits. Electroencephalogram (EEG) also revealed no abnormalities, and no evidence of an epileptic focus was found. Upon Ms As admission to the medical unit, citalopram was stopped; there were no further seizures during her stay in the hospital or in 1 month of follow-up. To the best of our knowledge, there is no published case of seizures associated with short-term use of citalopram within the FDA-approved dosage range of 20 to 40 mg/d2 in healthy adults. We were unable to identify any other cause of the seizures. Prolonged previous uneventful use of sertraline ruled out a general reaction to the selective serotonin reuptake inhibitor (SSRI) class. Citalopram evokes spontaneous EEG spikes in normal rats, and reduces paired-pulse inhibition in both normal and epileptic rats.3 To the best of our knowledge, this is the first report to document that citalopram may induce seizures at low doses, even in a patient who had tolerated another SSRI in the past. If practitioners recognize this association, expensive investigations and extensive hospital stays may be prevented, although prudent practice would very likely still require the type of investigations undertaken with our patient.

“Holes in My Head”: A Case of Primary Delusional Parasitosis in a Patient With End-Stage Renal Disease

To the Editor: Delusional parasitosis is a somatic type delusional disorder in which sufferers maintain a fixed false belief that they are infested with parasites. Secondary forms of delusional parasitosis are addressed by treating the primary associated psychological or physical condition. We present a case of primary delusional parasitosis in a patient with end-stage renal disease. Case report. Mr A, a 63-year-old African American man, was admitted in 2010 to the medical floor from the dialysis unit after making some bizarre statements during a dialysis session. Psychiatry consult was requested by the medical team after the patient continued to endorse a fixed delusion that he had had 2 holes in his forehead for 2 months, which appeared intermittently and were reported by the patient to have closed before he was interviewed by the psychiatric consult team. Mr A also stated that he was not sure if any worms were crawling around in his head (pointing to his head) and was in the hospital to get the condition investigated. Upon further interview, the patient reported feeling that bugs were crawling on his skin, and he explained that insects were the reason for his severe pruritus and chronic skin condition. The patient also had a past history of increased confusion and making bizarre statements during dialysis sessions. His medical history was significant for diabetes mellitus with retinopathy, end-stage renal disease, anemia, glaucoma with partial blindness, and cutaneous lymphocytosis as well as chronic pruritus treated by glucocorticoid. Findings of head computed tomography without contrast were within normal limits, except for mild age-related generalized atrophy. Significant laboratory values included serum PO4 level of 6.2 mg/dL, serum magnesium level of 1.6 mg/dL, serum chloride level of 95 mg/dL, random blood glucose level of 375 mg/dL, blood urea nitrate level of 32 mg/dL, serum creatinine level of 5.5 mg/dL, and estimated glomerular filtration rate 13 mL/h. Differential diagnosis included chronic delirium due to dialysis and polypharmacy, delusional parasitosis, and cognitive disorder not other specified. Psychiatric consultants recommended optimization of medications and reduction of polypharmacy: Mr A was using clobetasol topical cream twice a day, fluocinonide topical twice a day, and terbinafine topical cream twice a day and taking triamcinolone 80 mg 4 times a day, finasteride 5 mg at night, clonidine 0.3 mg 3 times a day, furosemide 80 mg twice a day, hydralazine 20 mg 4 times a day, heparin 5,000 mg subcutaneously 3 times a day, labetalol 400 mg 3 times a day, isosorbide mononitrate 60 mg daily, ropinirole 1 mg at night, sliding scale insulin, pravastatin 20 mg at night, sodium bicarbonate 650 mg 3 times a day, diazepam 5 mg every 8 hours as needed, and zolpidem 12.5 mg at night. The patient was prescribed a number of sedating medications, including diazepam, zolpidem, clonidine, and hydroxyzine. Both ropinirole and hydralazine have been shown to cause psychotic symptoms.1,2 The patient’s diazepam was discontinued. His medical team was also advised to start a low dose of haloperidol, 1 mg twice a day, for delusions. The medical team was advised to premedicate with an antipsychotic, adjust the patient’s dialysis schedule, and consider changing dialysate to help reduce delirium; although dialysate was not changed, the other 2 changes were implemented as recommended. Confusion and delusions subsided after 4 days, at which time he was discharged from the hospital. Delusional parasitosis is usually diagnosed as a subtype of delusional disorder. The mean age at onset is 56.9 years, and the male-to-female ratio is 1:1.5.1 Patients describe a parasitic invasion on or inside the skin; they may bring in objects such as hair, lint, or skin—the “matchbox sign”—as proof of the infestation despite normal findings on examination.2 Patients rarely seek the help of a psychiatrist; rather, because of their belief in a somatic complaint, patients often see primary care physicians or dermatologists for treatment.1,2 Management initially involves ruling out a general medical condition and excluding the use of drugs, illicit or prescribed. Traditionally, treatment is pimozide, a dopamine antagonist, although some patients may respond to neuroleptics such as haloperidol or risperidone. Duration of treatment varies from 2 weeks to 3 months before use is tapered, but compliance can be challenging.1,3,4 Careful strategy is required to convince patients with delusional parasitosis of the importance of a psychiatric referral.

Dose dependent, new onset QTc prolongation in a patient with paranoid schizophrenia receiving Clozapine.

Mr. XYZ is a 56 year old African-American male with a past psychiatric history significant for chronic remitting schizophrenia, paranoid type; past medical history of open angle glaucoma, Vitamin B12 deficiency, hyperlipidemia, chronic dermatitis, thrombocytopenia, allergic rhinitis, and no history of reported cardiac disease and is a resident of a group home. Patient has been tried on multiple antipsychotics including quetiapine, aripiprazole, haloperidol, risperdal and ziprasidone with no success. Patient has also been tried on combined therapy of atypical and typical antipsychotics with multiple mood stabilizers including valproic acid, oxcarbazine, carbamazepine and lithium carbonate without much success. After obtaining drug-free baseline Electrocardiogram (EKG) showing QTc/QT of 411/ 416 ms, patient was given a trial of clozapine as an outpatient with 14-day monitoring of blood work, which was titrated to target patient’s psychiatric symptoms. QTC was measured automatically by a General Electric (GE) EKG machine. In an incidental finding patient had dose dependent QT and QTc changes on EKG as displayed in Fig. 1 and Table 1. Patient responded well with clozapine with baseline psychotic symptoms but patient’s QTc

Brief Reversible Psychosis and Altered Mental Status in a Patient With Folate Deficiency: A Case Report

To the Editor: Vitamin B12 and folate deficiencies can result from inadequate intake, impaired absorption, or increased requirement, or the cause can be multifactorial such as in the setting of chronic alcoholism.1 Hematologic manifestations can include a megaloblastic, macrocytic anemia.1 Many individuals with an underlying vitamin B12 deficiency are labeled with other psychiatric diagnoses including major depressive disorder, bipolar disorder, and panic disorder.1 A deficiency of vitamin B12 or folate leads to an increased level of homocysteine, a highly toxic metabolite to neural and vascular development. Homocysteine has even been linked to a higher risk of cognitive decline and Alzheimer’s disease and a 5-fold increase in the rate of brain atrophy.2 Our case presents a patient with severe cognitive decline in the setting of a folate deficiency. Case report. A 49-year-old white male patient of a psychiatric hospital was transferred to the emergency department for complaints of altered mental status. He was refusing to eat and did not sleep at night prior to his presentation to the emergency department. He demonstrated disorganized thoughts, disorganized behavior, and psychomotor retardation. His Montreal Cognitive Assessment (MoCA; English [Original] version, www.mocatest.org) score was 3/30 and he was giving 3- and 4-digit numbers as his phone number, which was a substantial change from his baseline. His past medical history was significant for hypertension and bipolar disorder, which were well maintained with metoprolol and risperidone, respectively. He has had 29 prior psychiatric hospitalizations, mainly related to his continuous substance abuse. At presentation to the emergency department, the patient’s vital signs were within normal limits except for a blood pressure of 167/106 mm Hg. Initially, he was noted to have a mild tremor on bilateral upper extremities and to be looking toward the ceiling as if he were seeing things; however, he was nonverbal. He was disoriented to person and time, but aware and oriented to place. No neurologic deficits were documented; however, the examining physician was unable to assess muscle strength, gait, or cerebellar testing because the patient did not cooperate with the physical examination. The full physical examination was otherwise unremarkable. Differential diagnosis included metabolic derangement, encephalopathy, or delirium, which could be secondary to his long-standing history of illicit substance abuse. Noncontrast computed tomography scan of the head and subsequent magnetic resonance imaging were performed and showed no acute changes. Significant laboratory results included minor macrocytosis (mean corpuscular volume of 100.1 μm3), thrombocytopenia (141 × 103/mL), and hypoalbuminemia (3.6 g/dL). Results of the thyroid panel and creatine kinase and ammonia levels were all within normal limits, and the urine drug screen was negative for substances of abuse. His B12 was found to be on the lower end of normal at 341 pg/mL, and he was folate-deficient at 6.8 ng/mL. The patient was admitted to the hospital and given one B12 intramuscular injection and started on a daily regimen of folic acid (1 mg), thiamine, and a multivitamin. He was hospitalized for 2 days, during which he resumed oral food intake and increased his daily activities and communication. At that time, he was discharged back to the psychiatric hospital with instruction to continue folic acid supplementation and to have monthly B12 injections. He was alert and oriented to time, place, person, and situation. Mental status examination showed that he was more organized, with no disorganized behavior or hallucinations. His score on the MoCA returned to his baseline of 18/30 prior to admission, and at a later assessment was 19/30, which was appropriate to his baseline for age and education. In our case, we were presented with a unique situation of severe cognitive decline in the setting of a folate deficiency. In our literature review, we were unable to identify any cases of acute dementia with an associated isolated folate deficiency. While the patient presented with both a vitamin B12 and a folate deficiency, the vitamin B12 deficiency appears to have been less severe than the folate deficiency. Supplementation with folic acid and B12 resolved our patient’s symptoms in addition to augmentation with antipsychotics. Prior literature3 has discussed the role of folate deficiency in psychiatric conditions by mentioning the masking effect of folate on a vitamin B12 deficiency and thereby delaying the presentation of macrocytic anemia. Other case reports4 of cobalamin-responsive psychosis cited normal folate levels. While previous studies5 have indicated the role of vitamin B12 deficiency in psychiatric manifestations, there have been no determinations of the time to irreversible myelin damage.

Scopolamine for Management of Extrapyramidal Side Effects as a Result of Antipsychotic Medication Use: A Case Report and Brief Review of the Literature

To the Editor: Clinicians prescribe antimuscarinic compounds to treat the extrapyramidal side effects of neuroleptic medications. However, scopolamine has not been used for the management of such side effects. To the best of our knowledge, this is the first case of using scopolamine transdermal patch for management of extrapyramidal side effects of antipsychotic medications.