In an effort to aid the clinician in the differential diagnosis of catatonic states, we assessed the nature of electroencephalography (EEG) findings in both medical and psychiatric forms of catatonia. An exhaustive review of the literature on catatonia due to a general medical condition (CDGMC) was performed in addition to a prospective review of catatonic patients at The Ohio State University Neuwpsychiatric Facility.

A total of 105 patients had documented, specific clinical and EEG information, with neurologic conditions accounting for 82.8% of case reports. Results from the case series of 31 episodes of catatonia indicate that there is an increased likelihood of diffuse slowing in patients with CDGMC versus psychiatric catatonia. Given the observed rate of abnormalities, EEG is an important but underutilized tool in the differential diagnosis of catatonic disorders.

Opioid use disorder (OUD) is a disorder that can lead to several negative outcomes, including overdose and death. A variety of opioids can be abused by individuals including both prescribed and non-prescribed opioids. Continued opioid use can be driven by negative affective states associated with opioid withdrawal. Several treatments exist in the field including medication assisted treatments such as methadone, buprenorphine, and naltrexone. Treatments such as clonidine and lofexidine can also be used to assist with decreasing withdrawal symptoms. Increasing adherence to treatment can further improve patient outcomes and promote continuation with treatment. A variety of methods to reduce relapse can also be utilized such as opioid agonists and maintenance therapy. According to the Centers for Disease Control, opioid overdoses contributed to 67.8% of overdose deaths in 2017.

Excellent treatment for Alzheimer's disease remains an unmet medical need. Although current therapies improve patients' abilities compared to placebo and temporarily maintain performance above baseline on a number of outcome measures, additional therapies are needed to augment the benefits over baseline and to prolong these improvements.

Autism and related disorders occur in as many as one in 500 children. Recognizing the need for uniform recommendations to help guide the initial diagnostic evaluation and referrals in this area, an initial working group of the Cure Autism Now Foundation promulgated the following consensus guidelines for autism screening and diagnostic referral. Although these recommendations were formulated using the best information currently available, they are likely to be modified as the results of additional studies become available; however, they provide a useful tool for clinicians involved in the management of children with autism and related developmental abnormalities.

In this paper we will review recent neuroimaging research in schizophrenia, with an aim to critically evaluate several recent proposals concerning the nature and the timing of the neuroanatomic abnormalities underlying the disorder. Specifically, enlargement of cerebrospinal fluid spaces, deficits in cortical gray matter, and reduced volume of mesiotemporal structures have all been reported in patients in the first episode of schizophrenia, their first-degree relatives, and individuals with schizotypal personality disorder, supporting the possibility that these abnormalities reflect a genetically mediated neurodevelopmental disorder. These findings from the empirical literature will be synthesized from the perspective of dual cytoarchitectonic trends theory of neurodevelopment, as well as in relation to current conceptions of the schizophrenia prodrome. We believe that the evidence shows that sufficient groundwork has been laid to begin longitudinal neuroimaging studies of adolescents at clinical risk for schizophrenia, in order to more definitively determine the pathophysiology of the disorder. Such information could have significant implications in terms of understanding the prediction, treatment, and ultimately the prevention of schizophrenia.

Neuropsychological (NP) test batteries have evolved as an amalgam of intelligence tests, various individual measures of “biological” cognition, and sensory and motor testing. The early emphasis of NP testing was to identify “organicity” and central nervous system lesion localization. More recent approaches have emphasized the profiling of performance across individual neurocognitive domains (eg, attention, memory, and language) to facilitate diagnosis and treatment planning. However, the field is still hampered by the use of many tests that are antiquated, excessively long, or of dubious psychometric quality. Some of these problems may have contributed to the current under-utilization of NP testing in diagnostic workups of neuropsychiatric disorders. This paper reviews some of the recent changes in the field that hold promise for substantially shortening assessments, improving diagnostic reliability, and making NP testing more cost-effective and practical.

Patients living with human immunodeficiency virus represent a growing population, and an increased number of central nervous system presentations can be expected over the next decade. Emerging data suggests that both HIV-seropositive patients and cocaine-abusing patients may be at special risk of seizure phenomena. This case report discusses the risks of new-onset seizure activity when these two risk factors converge, which is a common occurrence in this population. Data from the fields of neuroanatomy and neurovirology are presented to explain the heightened risk of this patient population and provide the practitioner with an improved understanding of the central nervous system complexities in HIV.

Tourette syndrome (TS) is a complex neurobehavioral disorder principally characterized by motor and vocal tics. However, features of obsessive-compulsive and attention-deficit/hyperactivity disorders are often present. The basal ganglia and associated brain structures have been implicated in the pathophysiology of TS, as well as in these related conditions. Specifically, it is believed that the neuroanatomically and functionally defined basal ganglia thalamocortical loops are involved in TS. These loops are composed of a sequence of connections originating in the cortex and passing in series through the striatum (caudate and putamen), globus pallidus, and thalamus before returning to the cortical areas of origin. This review concentrates on the neuroimaging findings in Ts, particularly as they relate to alterations in components of the basal ganglia thalamocortical circuits. These neuroimaging data suggest that the major abnormalities in TS involve striatal or cortical dysfunction, as well as dysfunction of dopaminergic systems that regulate basas ganglia neurotransmission.

Autistic disorder and catatonia are neuropsychiatric syndromes defined by impairments in social interaction, communication, and restricted, stereotypical motor routines. Assessments of children with these disorders are typically restricted in scope by the patients' limited ability to comprehend directions. The authors performed systematic assessments of dyskinesias on six prepubertal boys with autistic disorder and mental retardation and on one adolescent male with catatonia to determine if this type of information could be routinely obtained. The boys with autistic disorder had more stereotypies and tics, a greater degree of akathisia and hyperactivity, and more compulsions than the adolescent with catatonia. Catatonia was associated with catalepsy and dystonic postures. The authors conclude that the diagnostic accuracy and specificity of neuropsychiatric syndromes may be enhanced by the systematic assessment of the dyskinesias associated with each condition.

The term limbic encephalitis has been used with an oncological precedent for over 50 years and, since then, has been applied in relation to multiple antibodies found in its etiological process. Over the last decade, the psychiatric community has brought paraneoplastic autoimmune limbic encephalitis (PALE) to a new light, scattering the once known relationships between said screened antibodies responsible for causing limbic encephalitis. Due to the fact that some individuals with this condition have a psychiatric syndrome as an initial manifestation, the aim of this updated scoping review is to reestablish a causal relationship between the onconeuronal autoantibodies, both intracellular and extracellular, possible underlying malignancies and subsequent neuropsychiatric syndrome. In pair with it, there is the idea of sketching a cleaner thorough picture of what poses as psychiatric symptoms as well as possible therapeutics. Even though the always evolving epistemology of the neurosciences achieved a significant unveiling of what includes PALE in its relevant pathological subgroups, the amount of gray literature still is much superior, appealing to a further research with more randomized controlled trials, with larger populations, so that the results corroborate the small amount of data that already exist and posteriorly be applied in the general population.

Peripheral neuropathy associated with human immunodeficiency virus type 1 (HIV-1) infection is a major cause of morbidity in this patient population. Due to the associated chronic pain, its management has come within the purview of neuropsychiatrists. This paper will focus on the primary pathogenic aspects of HIV-1–associated peripheral neuropathies. The specific syndromes of greatest concern are distal sensory polyneuropathy, toxic neuropathy, inflammatory demyelinating polyradiculoneuropathy, and cytomegalovirus-related progressive polyradiculoneuropathy. The treatments available for these conditions and their efficacy are discussed.

Patients with schizophrenia have increased mortality due to higher rates of suicide. However, natural causes of death, such as cardiovascular disease, also contribute greatly to excess mortality. Significant sources of cardiovascular risk in this patient population include high smoking prevalence, inactive lifestyles, poor dietary habits, and the metabolic effects of atypical antipsychotics. These sources of risk interact with underrecognition of common medical conditions by mental health providers, limited access to primary care services, and undertreatment of health conditions in the general medical setting. For many patient with severe mental illness, the mental health setting represents the sole source of medical care, making the psychiatrist the de facto primary care provider for these individuals. With the recent focus on medical consequences of antipsychotic treatment, psychiatrist have an obligation to minimize these adverse effects by choosing antipsychotics with lower risk for metabolic side effects, and becoming familiar with the screening and management of common medical conditions.

Patients with seizure of frontal lobe origin can present with bizarre behavior. At times, this bizarre behavior can be unrecognized or confused with seizure of other origin with nonepileptic events or with psychiatric disorder.

I recently saw a patient who began to experience events that were characterized by terrible fear which was followed by irritability. It was as if she could not stand in place where she was at and felt like running away. She was referred to a psychiatrist who diagnosed her to have panic disorder. She was subsequently treated for panic disorder. Her symptoms did not improve; therefore, she came to see me for a second opinion. Upon asking, the patient reported that the episodes were always the same and that they lasted approximately seconds to minutes. Due to the stereotypicity of the event and a normal routine electroencephalography (EEG), we requested that she would undergo a 24-hour video-monitoring EEG. Stereotypicity can help the physician in the differential diagnosis of psychiatric disorder versus a seizure disorder. During 24-hour video-monitoring EEG, she experienced several of these events. Also, a computer tomography scan was performed, which showed a small meningioma in the orbital frontal region.

Depressed subjects have deficits in facialemotion recognition that resemble the deficits found in persons with focal right hemisphere brain damage. To locate the brain regions responsible for this problem, the authors imaged regional cerebral blood flow (rCBF) with H2O15 positron emission tomography in 10 mood-disordered patients, as well as in 10 age- and sex-matched healthy comparison subjects, while the subjects matched photographs for facial emotion or, as a control, facial identity. While matching faces for emotion, mood-disordered subjects had decreased rCBF activation bilaterally in their temporal lobes, as well as in the right insula, compared with healthy comparison subjects. Abnormal function of limbic and paraiimbic regions may partially explain the facial emotion-recognition deficits previously noted in depressed subjects.