William W. McDaniel

Ketamine appears associated with better word recall than etomidate after a course of 6 electroconvulsive therapies.

Abstract: Ten patients treated with electroconvulsive therapy (ECT) for depressive illness received anesthesia with either etomidate or ketamine. Three patients received both etomidate and ketamine anesthesia for ECT during separate episodes of depression. Patients anesthetized with ketamine for ECT had significantly less impairment of short-term memory function than did patients who received ECT with etomidate anesthesia. All patients who received both anesthetics for ECT during 2 different episodes had less memory loss during ECT with ketamine than with etomidate. These results show the importance of studying the effects of all anesthetic agents used during ECT on cognitive functions. The results imply that the effect of ECT on memory may be largely caused by effects mediated by glutamate at N-methyl-d-aspartate receptors and suggest that N-methyl-d-aspartate antagonists may offer protection from memory dysfunction during ECT.

Serotonin Syndrome: Early Management with Cyproheptadine

OBJECTIVE: T o report a psychiatric patient who developed serotonin syndrome after a medication overdose and whose marked mydriasis was quickly reversed by administration of cyproheptadine. This phenomenon was confirmed when other cases of serotonin syndrome were studied. METHOD: In the index patient as well as in three subsequent cases of serotonin syndrome, pupil diameter, muscle tone, mental status, and vital signs were monitored before and after a test dose of cyproheptadine as medications were discontinued and antiserotonergic therapy begun. RESULTS: In each patient, cyproheptadine produced rapid reversal of mydriasis within one hour of the initial dose. Other signs of serotonin syndrome remitted more slowly. As the signs and symptoms of serotonin syndrome remitted and pupils returned to normal size and reactiveness, cyproheptadine therapy seemed to produce mydriasis after each dose. Cessation of therapy after this point did not result in recurrence of symptoms. One patient developed serotonin syndrome twice. Two patients developed serotonin syndrome during treatment with medications that are partial serotonin antagonists (mirtazapine and nefazodone). CONCLUSIONS: Rapid reversal of mydriasis in serotonin syndrome by cyproheptadine may serve as a specific suppressive test for the condition, and possibly may add to our understanding of the syndrome. Treatment with cyproheptadine is not thought to abbreviate the illness, but provides symptomatic relief while symptoms persist.

Electroconvulsive therapy in complex regional pain syndromes

Three cases are presented in which electroconvulsive therapy (ECT) for depression led to the relief of comorbid complex regional pain syndrome as well as depression. In one of the cases, concomitant fibromyalgia was not relieved during 2 separate series of ECT. The literature regarding the role of ECT in the management of chronic pain is reviewed and discussed in light of recent findings about ECT and changes in neurotransmission associated with seizures.

Ketamine associated with improved memory function after ECT.

apraxia and, at the first EEGmeasurement 5 days after the latest ECT, she was slowcerebrated. EEG was without spikes and sharp waves, and our interpretation of the entire situation was that there might be a nonconvulsive status epilepticus, admittedly on weaker grounds. Such prolonged confusional states make the patient’s relatives, and also the nursing staff, highly uncomfortable. We were ourselves concerned enough to interrupt ECT and make the EEG measurements. To do otherwise might well have brought ECT into discredit even in a University Department like ours, where an average of about 800 ECT sessions are given yearly. The 3 reported cases should be considered rare, and they are the first of their kind observed for the 26 years that one of us (T.G.B.) has been in charge of the ECT unit in the department. Regardless of our observations being in contrast with the anticonvulsant theory of ECT, we find they should be reported in a journal dedicated to clinical and basic studies of ECT.

Madness of bipolar driver safety assessments

Madness of bipolar driver safety assessments William McDaniel, Hasan Memon, Elionora Katz, Stephanie Cristofano & James Catesby Ware To cite this article: William McDaniel, Hasan Memon, Elionora Katz, Stephanie Cristofano & James Catesby Ware (2016): Madness of bipolar driver safety assessments, Traffic Injury Prevention, DOI: 10.1080/15389588.2015.1054988 To link to this article: http://dx.doi.org/10.1080/15389588.2015.1054988

Catatonia Due to a General Medical Condition (Organic Catatonia)

While much has been written about catatonia, there are only a few scholarly reviews focused on catatonia due to a general medical condition, also referred to as organic catatonia. There has been a long list of causative conditions that account for the development of organic catatonia which are informative but not clinically helpful. We performed a literature search using the term ‘catatonia’ covering the last ten years. We found 31 titles of catatonia due to drugs and 76 titles of catatonia due to a general medical condition. Of these, 9 were catatonia due to NMDA antibody associated encephalitis. In order to update this body of knowledge, we have revisited the differential diagnosis of catatonia and attempted to delineate catatonia due to a general medical condition from phenomenologically similar but etiologically disparate conditions. We also focused on catatonia due to systemic lupus erythematosis. We also present a case of catatonia due to hydrocephalus to illustrate treatment issues. In spite of the pharmacologic treatment for catatonia, this patient has not improved. We hope that this review and discussion will aid in the identification and treatment of catatonia due to a general medical condition. Medical causes must be addressed to ensure the best outcome.

Catatonia in diagnostic and statistical manual of mental disorders, fifth edition

As international scholars of catatonia, we are concerned that the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-V) proposes to delete the codes 295.2 (schizophrenia, catatonic type) and 293.89 (catatonia secondary to a medical condition) and to substitute a noncoded “catatonia specifier” as the principal identifier. We believe that these changes will badly serve clinical practice and research. We advocate a unique and broadly defined code for catatonia in DSM-V. Catatonia is common among hospitalized psychiatric patients, including adults, adolescents, and occasionally children. In the 10 principal prospective studies from sites around the world, catatonia syndrome was identified in a mean (SEM) percentage of 9.8% (1.4%) of adult admissions (Table 1). These patients have multiple signs of catatonia (commonly >5); 68% (6%) are mute, and 62% (3%) are negativistic or withdrawn. Some are unable to eat, requiring parenteral nutrition and/or medication. TABLE 1 Prospective Studies of the Incidence of Catatonia Once catatonia is recognized, first-line treatment with benzodiazepines usually brings prompt relief, although high doses may be needed. If catatonia persists, electroconvulsive therapy is often rapidly beneficial. Every prospective study confirms that catatonia syndrome exists, occasionally becomes malignant, and requires prompt treatment. Under the proposed new guidelines for DSM-V, patients with catatonia syndrome will lack an informative diagnosis. Mutism, negativism, and withdrawal prevent assessment for mood, cognitive, and psychotic symptoms and impede proper delineation of episodes of prior illness. Without findings for a specific diagnosis, it is rational to use a provisional diagnosis of the catatonia syndrome to allow tests and treatments to proceed. Lacking recognition and treatment, catatonia may persist or worsen with adverse or life-threatening results. On the other hand, when patients with catatonia are identified and treated, they become verbal and interactive, allowing interviews and more definitive diagnoses, regardless of the primary pathological findings. When patients cannot provide information, clinicians may conflate or misdiagnose catatonia with schizophrenia (as in the DSM-IV schema), impute a psychotic process, foster the unproven use of neuroleptics, and risk adverse effects, such as conversion to malignant catatonia or the neuroleptic malignant syndrome. Similarly, assignment of catatonia to “psychosis not otherwise specified” (298.9, DSM-IV and DSM-V) would be erroneous because these patients often either lack hallucinations and delusions or cannot be assessed for them. The proposed elimination of DSM-IV “catatonia due to a general medical condition” (293.89) renders the coding for catatonia arising from general medical conditions problematic. At clinical presentation, the medical/toxic factors are rarely known, as time is often needed to identify these etiologies. We also note that noncoded specifiers are not useful for research on nosology, treatment, and outcome. To address all these issues, we urge inclusion in DSM-V of a specific diagnostic code for catatonia. One simple option is to retain the 293.89 code but revise its formulation to broadly encompass the catatonia syndrome without imputing a link to either primary psychiatric or general medical conditions. A unique and broadly defined code would foster recognition of the catatonia syndrome and permit research on nosology, treatment, and outcome. These goals are not met with the DSM-V plan for noncoded modifiers.

Catatonia in Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition [Editorial]

As international scholars of catatonia, we are concerned that the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-V) proposes to delete the codes 295.2 (schizophrenia, catatonic type) and 293.89 (catatonia secondary to a medical condition) and to substitute a noncoded “catatonia specifier” as the principal identifier. We believe that these changes will badly serve clinical practice and research. We advocate a unique and broadly defined code for catatonia in DSM-V. Catatonia is common among hospitalized psychiatric patients, including adults, adolescents, and occasionally children. In the 10 principal prospective studies from sites around the world, catatonia syndrome was identified in a mean (SEM) percentage of 9.8% (1.4%) of adult admissions (Table 1). These patients have multiple signs of catatonia (commonly >5); 68% (6%) are mute, and 62% (3%) are negativistic or withdrawn. Some are unable to eat, requiring parenteral nutrition and/or medication. TABLE 1 Prospective Studies of the Incidence of Catatonia Once catatonia is recognized, first-line treatment with benzodiazepines usually brings prompt relief, although high doses may be needed. If catatonia persists, electroconvulsive therapy is often rapidly beneficial. Every prospective study confirms that catatonia syndrome exists, occasionally becomes malignant, and requires prompt treatment. Under the proposed new guidelines for DSM-V, patients with catatonia syndrome will lack an informative diagnosis. Mutism, negativism, and withdrawal prevent assessment for mood, cognitive, and psychotic symptoms and impede proper delineation of episodes of prior illness. Without findings for a specific diagnosis, it is rational to use a provisional diagnosis of the catatonia syndrome to allow tests and treatments to proceed. Lacking recognition and treatment, catatonia may persist or worsen with adverse or life-threatening results. On the other hand, when patients with catatonia are identified and treated, they become verbal and interactive, allowing interviews and more definitive diagnoses, regardless of the primary pathological findings. When patients cannot provide information, clinicians may conflate or misdiagnose catatonia with schizophrenia (as in the DSM-IV schema), impute a psychotic process, foster the unproven use of neuroleptics, and risk adverse effects, such as conversion to malignant catatonia or the neuroleptic malignant syndrome. Similarly, assignment of catatonia to “psychosis not otherwise specified” (298.9, DSM-IV and DSM-V) would be erroneous because these patients often either lack hallucinations and delusions or cannot be assessed for them. The proposed elimination of DSM-IV “catatonia due to a general medical condition” (293.89) renders the coding for catatonia arising from general medical conditions problematic. At clinical presentation, the medical/toxic factors are rarely known, as time is often needed to identify these etiologies. We also note that noncoded specifiers are not useful for research on nosology, treatment, and outcome. To address all these issues, we urge inclusion in DSM-V of a specific diagnostic code for catatonia. One simple option is to retain the 293.89 code but revise its formulation to broadly encompass the catatonia syndrome without imputing a link to either primary psychiatric or general medical conditions. A unique and broadly defined code would foster recognition of the catatonia syndrome and permit research on nosology, treatment, and outcome. These goals are not met with the DSM-V plan for noncoded modifiers.