Jimmy Avari

A Patient With Bipolar Disorder and Antiphospholipid Syndrome

Antiphospholipidsyndrome (APS) is an autoimmune disorder which causes a hyper-coagulable state characterized by recurrent thrombosis. It has a diverse range of central nervous system manifestations. We describe a case of a 61 year old man with bipolar disorder and APS, and we compare this to a previously reported case. Additionally, we reviewed literature regarding APS-related markers and the relationship of APS to other psychiatric and neurologic illnesses. We discuss possible mechanisms for an association between APS and bipolar disorder. We encourage clinicians to be aware of this possible relationship and have proposed research strategies.

A Case of Arnold–Chiari Malformation Associated With Dementia

To the Editor: Arnold–Chiari malformation is a congenital brain anomaly that was first described by the Austrian pathologist Hans Chiari in the late 19th century. It is categorized into three types based on the degree of herniation. Type I malformation is characterized by downward displacement of the cerebellar tonsils through the foramen magnum; while in type II the cerebellar vermis and possibly the fourth ventricle and pons are involved. Type III malformation is the most severe and rarest form and consists of an encephalomeningocele that contains the brainstem and cerebellum. The malformation is known to produce variable clinical signs and symptoms of cerebellar, cervical and brainstem dysfunction. There is a paucity of literature pertaining to the neuropsychiatric illnesses associated with Arnold– Chiari malformation. To our knowledge, the only neuropsychiatric disorder reported in humans, in association with Arnold-Chiari malformation is anxiety. We now summarize a case of 53-year-old woman with Arnold–Chiari type I malformation who presented with dementia.

A case of primary progressive aphasia associated with depression

Primary progressive aphasia (PPA) is a neurodegenerative disease of gradual and progressive isolated loss of language (Mesulam, 2003). The age of onset peaks in the presenium (age 55–65 years) (Mesulam, 2001). It represents focal degeneration of the language network located in the left hemisphere of the brain and includes the perisylvian parts of the inferior frontal and temporoparietal regions (Mesulam, 2003). The major symptoms are confined to the area of language for the first few years. As the illness progresses, the neurodegenerative process extends to adjacent structures and affects other cognitive and behavioral domains (Mesulam, 2001). Diagnosing depression in PPA patients poses a clinical dilemma. There are no criteria that define depressive symptoms in PPA. The DSM‐IV diagnostic criteria for depression rely on symptoms reported by patients. There is a substantial overlap between symptoms of depression and those of PPA; symptoms such as social isolation and functional decline occur in both depressed and non‐depressed PPA patients. Differentiating between the two syndromes is clinically important to avoid underdiagnosis or overdiagnosis of depression and to provide appropriate treatment. We summarize a case of language impairment with characteristic symptoms of PPA who developed depression. We discuss the challenges in the diagnosis and our approach to meeting these challenges.

Late-onset folie à deux in monozygotic twins

Less than 500 cases of folie à deux have been reported worldwide making it a relatively rare psychiatric disorder (Lazarus, 1986). Lasègue and Falret initially defined the syndrome as a psychiatric disturbance that could be transferred from one individual to another under the following circumstances: if the individual that first exhibited the delusions (the “inducer”) was more intelligent and dominant than the secondary individual (the “induced”), if both patients were closely associated in social isolation, and if the delusions were non-bizarre and referred to shared anxieties or experiences (Arnone et al., 2006). The accepted treatment for this condition was separation of the inducer and the induced (Lazarus, 1986). In the DSM-5, shared psychotic disorder is noted as a sub-category in the section on other specified schizophrenic spectrum and other psychotic disorders rather than as a separate diagnostic entity in itself (Parker, 2014). Folie à deux is most often seen in first-degree relatives, which supports the conjecture that genetic vulnerability is a necessity rather than simply an association. Even when folie à deux is seen in unrelated individuals there is significant family psychiatric history in affected individuals (Kendler et al., 1986; Lazarus, 1985). On the other hand, the recorded resolution of symptoms upon separation from the dominant individual proves that environmental factors have significant influence on the pathogenesis and course of the disease (Lazarus, 1985). Our case of folie à deux in monozygotic twins aims to provide additional insight into the dynamics between nature and nurture.

White matter abnormalities predict residual negative self-referential thinking following treatment of late-life depression with escitalopram: A preliminary study

BACKGROUND Negative self-referential thinking is a common symptom of depression associated with poor treatment response. In late-life depression, white matter abnormalities may contribute to negative self-referential thoughts following antidepressant treatment. We investigated the association of fractional anisotropy (FA) in select regions of the negative valence system (NVS) with residual negative self-referential thoughts following treatment with escitalopram for late-life depression. METHODS The participants were older adults with major depression and psychiatrically normal controls. Depressed participants received 12 weeks of treatment with escitalopram. To assess self-referential thinking, participants completed a Trait Adjective Task at baseline and at week 12. Baseline MRI scans included a diffusion imaging sequence for FA analyses. RESULTS Participants with late-life depression differed from controls on all performance measures of the Trait Adjective Task at baseline and at 12 weeks. Depressed participants endorsed fewer negative personality traits and more positive personality traits at week 12 compared to baseline. Lower FA in the dorsal anterior cingulate and in the uncinate fasciculus in depressed participants was correlated with residual negative self-referential thinking (e.g., more endorsed negative adjectives, fewer rejected negative adjectives) at treatment end. LIMITATIONS The sample size is modest so the findings are preliminary. FA analyses were restricted to predetermined regions. CONCLUSIONS Negative self-referential thinking improved in depressed older adults following 12 weeks of treatment with escitalopram. Baseline FA in select white matter regions of the NVS was associated with residual negative self-referential thinking. These findings may help identify treatment targets for residual negative self-referential thoughts.

Neuroanatomy and Neuropathology

Common effects of aging on the brain include reduced brain volume and weight caused by neuronal atrophy and reduced synaptic density and increase in cerebrospinal fluid volume. The thalamus and hypothalamus are particularly vulnerable to effects of aging. Neuron number is relatively preserved in healthy aging. Patterns of atrophy and neuropathological changes differentiate normal from various types of pathologic aging. The anterior hippocampus shows marked atrophy in patients with Alzheimer’s disease compared with healthy aging.

Biochemistry and Neuropharmacology

Biochemical changes in the brain strongly contribute to age-related changes. In this chapter, theories of aging, including wear and tear, oxidative damage, DNA damage, and telomere shortening will be introduced. Also, the effects of aging on the neurotransmitters dopamine, serotonin, glutamate, gamma-aminobutyric acid, norepinephrine, and acetylcholine will be reviewed. These neurotransmitters are often the therapeutic targets of treatment interventions.

A Multi-tiered Model for Clinical Scholarship

The Accreditation Council for Graduate Medical Education (ACGME) stipulates that all psychiatric residents need familiarity with scholarship and research [1]. However, clinical scholarship in academic settings is under pressure, with demands of quick treatment and few resources. The tension between clinical demands and academic models grows as the necessary focus on outcome and cost swells. As National Institutes of Health (NIH) support shifts towards basic science research, clinical faculty struggle to function simultaneously as funded investigators. A mentorship and infrastructure deficit ensues for psychiatric residents, making the ACGME mandate harder to fulfill [2]. We propose a coordinated model for scholarship beginning withmedical students and offering programming for residents, early career, and senior faculty, to facilitate academic scholarship. A continuum model encourages idea sharing, creates accountability, and fosters community.