Mood Disorders Flashcards
Neuroanatomy of mood disorders
Disturbances of the limbic system (e.g., increased activity in CC and amygdala & atrophy of hippocampus) - lead to emotional and autonomic symptoms
Atrophy –> amygdala, hippocampus, prefrontal cortex, stratum, nucleus accumbent, and cerebellum.
neurochemical changes - norepinephrine, serotonin, glutamate, and dopamine
Serotonergic neurons arise from which area of the brain?
raphe nuclei in the brainstem and project throughout the forebrain.
Gender differences in depression symptoms
Women - more cognitive symptoms (feelings of
sadness, worthlessness, and excessive guilt)
Men - more behavioral symptoms (become more frustrated, discouraged, irritable, social withdrawal, and angry)
Differences in depression symptoms between children and adolescents
Young children
- irritability and sadness remain the most sensitive predictors of depression. Also tend to report physical illness, avoid school and other activities, become overly attached to a parent, or express worry that a parent or family member may die.
Older children and adolescents tend to sulk, develop behavioral problems at school, hypersomnia, become more negative and irritable, and feel misunderstood or unappreciated.
Neuroanatomy of anxiety disorders
Limbic structures are generally involved:
Amygdala - senses and identifies fear and anxiety-laden stimuli and initiates the emotional response
Hypothalamus, pituitary, and adrenal gland (HPA axis) - respond to heighten sympathetic responses to the stressful stimuli
Cingulate and orbitofrontal cortex are responsible for feelings associated with the anxiety
Interconnected frontal cortex is responsible for control of the reactions to anxiety-producing stimuli
Neuroanatomy of OCD
increased activity in the:
caudate nucleus
anterior cingulate gyrus
orbitofrontal cortex
Neuroanatomy of PTSD
prefrontal cortex, amygdala (hyperarousal), and hippocampus
Decreased activation of Broca’s area has been associated with the difficulty patients have in labeling their experiences
Is GABA inhibitory or excitatory?
Inhibitory - playing a role in helping to induce relaxation and sleep, and in preventing overexcitation
(think gabapentin to reduce/inhibit seizure or nerve pain)
Is norepinephrine inhibitory or excitatory?
Excitatory (it’s a stress hormone) - maintains alertness and preparation to respond to external threats, such as the “fight or flight” response.
Average age of onset in children
10 years
Neuropsychological expectations in mood disorders
attention, working memory, executive functions, and retrieval-based memory (with sparing of recognition memory).
Greater impairments seen in visuospatial functioning and visuomemory (RCFT) in bipolar illness and OCD - Unipolar depression and other anxiety disorders do not demonstrate this pattern of performance.
Difficulties with immediate memory and limited benefit from repetition. Delayed recall is marked by deficits in retrieval (spontaneous recall), with relative sparing in recognition memory. Memory deficits are not as apparent when information is presented in a structured/story format.
What mood disorders is considered lifelong?
Bipolar Disorder
What specific area of the brain has been implicated in Tourette’s, OCD, and PANDAS?
The caudate nucleus - It is thought that poor functioning of the caudate results in an inability to properly regulate the transmission of information regarding worrying events or ideas between the thalamus and the orbitofrontal cortex.
Disruption of white matter connectivity within brain networks that modulate emotional behavior in early development leads to decreased connectivity among ventral prefrontal networks and limbic brain regions, especially amygdala, contributing to the onset of what disorder?
Bipolar Disorder - This was hypothesized to cause developmental failure in healthy ventral prefrontal- limbic modulation resulting in the onset of mania and ultimately, with progressive changes throughout these networks over time and with affective episodes, a bipolar course of illness.
Individuals with insomnia are 2 times more likely to develop ? and 10 times more likely to develop ?
GAD, MDD
What has the best outcomes for treating depression?
Medication or combination therapy (medication and psychotherapy)? Combination therapy
What are the neurobiological substrates of mania and Bipolar disorder?
Most consistent findings – reduction in volume and blood flow in the dorsal medial and dorsal lateral prefrontal cortices.
Ventral prefrontal cortices with reduced engagement and atypical connectivity with ACC, medial temporal structures, amygdala, and hippocampal gyrus.
White matter connectivity
Clinical recognized mood disorders and specifiers
Two major theories exist about Serotonin and Depression
- a deficit in serotonin activity may DIRECTLY cause depression.
- Serotonin deficit serves as a risk factor for depression, but is not direct cause.
What is the role of Dopamine in Depression?
Areas needs more research.
flat affect and avolition/apathy Negative symptoms, originally referred to as “negative” to signify a loss or decrease of normal function in contrast to positive symptoms, is a term that was first applied to the “five A’s,” affective flattening, alogia, anhedonia, avolition-apathy and attentional impairment. Alogia and attentional impairment, however, may better be considered part of the disorganization syndrome.
Signs & Symptoms of Depression
Signs and Symptoms of Mania
Clinically Recognized Anxiety Disorders in the DSM-5
Clinically Recognized Obsessive-Compulsive Disorders in the DSM-5
Clinically Recognized Trauma- and Stressor-Related Disorders in the DSM-5
