rTMS in ADHD
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1) Repetitive Transcranial Magnetic Stimulation (rTMS) is a new tool that could provide a new therapy and hope for treating ADHD. It has been found effective in treating other neurological and psychiatric disorders. 2) rTMS may target the prefrontal-caudate-cerebellar pathways and dopamine abnormalities involved in ADHD by modulating neurotransmitters like dopamine through cortico-striatal projections. 3) Carefully conducted clinical trials are still needed, but initial evidence suggests rTMS may help treat ADHD symptoms and is a safe technique worth exploring further.
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Journal.pone.0051910
1) Methylphenidate (MPH) enhances NMDA receptor response in the medial prefrontal cortex of rats.
2) This effect occurs via sigma-1 receptors and requires PLC, PKC and IP3 receptor signaling pathways.
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NEURO PAPER
This document summarizes research on the potential adverse effects of the ADHD medication Adderall XR on neurocognitive brain health. It discusses that while Adderall is effective in treating ADHD symptoms, research is limited on long-term effects. The medication increases dopamine levels in the brain and can alter the autonomic nervous system. Some studies have found psychiatric issues and brain abnormalities in long-term Adderall users. However, more research is still needed to determine if Adderall causes permanent neurological damage or if symptoms are due to other factors like sleep deprivation. The document calls for more research using neurological imaging to properly diagnose ADHD and avoid inappropriate exposure to medications.
Transcranial magnetic stimulation.ppt
Transracial magnetic stimulation (TMS) is a non-invasive brain stimulation technique that uses magnetic fields to induce electric currents in brain tissue. TMS has applications as both a research tool and therapeutic treatment. As a research tool, TMS can map brain regions and disrupt function to study areas like motor control and language. Therapeutically, TMS shows promise for neurological disorders like Parkinson's and psychiatric conditions such as treatment-resistant depression. While TMS has fewer side effects than ECT, risks include seizures, headaches, and temporary cognitive changes. Ongoing research aims to optimize TMS treatment parameters and duration for greater therapeutic efficacy.
Transcranial magnetic stimulation power point[1].ppt
Transracial magnetic stimulation (TMS) is a non-invasive brain stimulation technique that uses magnetic fields to induce electric currents in brain tissue. TMS has applications as both a research tool and therapeutic intervention. As a research tool, TMS can map brain functions and create temporary lesions to study brain regions. Therapeutically, TMS shows promise for neurological disorders like Parkinson's and psychiatric conditions such as treatment-resistant depression. While TMS has fewer side effects than ECT, risks include seizures and headaches, and its efficacy is modest compared to sham treatments for some disorders. Ongoing research aims to optimize TMS parameters and techniques.
ADHD Treatments and Psychopharmacology
Neuropsychopharmacology and interventions for Attention/Hyperactivity-Deficit Disorder in both children and adults
Glutamate and schizophrenia
- Glutamate-based theories of schizophrenia focus on dysfunction of brain glutamate systems, particularly NMDA receptors. These theories originated over 20 years ago and have led to new conceptualizations of schizophrenia and potential assessment and treatment approaches.
- Dopamine dysfunction in schizophrenia may be caused by genetically determined abnormalities or by NMDA receptor dysfunction impairing dopamine system regulation. Disturbances in both glutamate and dopamine systems likely contribute to positive symptoms.
- Glutamate and NMDA receptors are widely distributed in the brain, suggesting schizophrenia involves dysfunction beyond prefrontal and limbic regions, including sensory cortices. Deficits in auditory and visual processing correlate with impaired functioning.
- While past drug trials targeting glut
Intro to Psychopharmacology
1) Prolonged stress can sensitize brain circuits, leaving them in a hyperactivated state even after the stressor is removed. This "presymptomatic" state increases risk for psychiatric symptoms but produces no observable symptoms.
2) Additional stressors can cause stress-sensitized circuits to break down, first producing subtle symptoms and later more severe symptoms as breakdown progresses.
3) Matching treatments to specific symptoms and the brain circuits involved in producing those symptoms provides a rational approach for selecting and combining medications.
PET Application In Psycology
PET scans use radioactive tracers to produce 3D images of functional brain processes. They have provided insights into mental disorders like depression and schizophrenia. Studies with depressed patients found abnormalities in prefrontal cortex activity and lower glucose metabolism, suggesting deficits in these brain regions. PET scans have also found less serotonin transporter binding in depressed individuals, indicating differences in the serotonin system between healthy and depressed people. For schizophrenia, PET scans have found greater dopamine receptor binding, revealing abnormalities in the dopamine system that may underlie the disorder.
SCHIZOPHRENIA JUST THE FACTS
MOST OF THE FINDINGS IN RESEARCH WERE DOCUMENTED IN THE ARTICLES OF RAJIV TANDON... THIS PRESENTATION HAS THE FACTS FROM THOSE ARTICLES
The Endocrinology of Aging.ppt
The document discusses aging and the endocrinology of aging. It notes that several hormone levels change with age: thyroid secretion decreases, the thymus gland involutes, cortisol levels decrease, and the pancreas decreases secretion of enzymes and hormones. Overall, some hormone levels like aldosterone, growth hormone, and estrogen decrease with age, while others like LH and FSH may increase, and still others like cortisol remain unchanged. These hormonal changes can lead to physical, sexual, and psychological symptoms in older individuals. The effects of declining testosterone and DHEA levels are also examined.
BIOMARKERS AND SCHIZOPHRENIA1233445677.ppt
Biomarkers are objective indicators of disease that can aid in diagnosis. For schizophrenia, potential biomarkers studied include neurochemical, genetic, imaging, and neurophysiological factors. Dopamine and glutamate dysfunction are implicated. Imaging shows reductions in prefrontal and temporal gray matter volume. Neurophysiological measures like P50 sensory gating and P300 amplitude are impaired. No single biomarker has been validated yet due to heterogeneity, but continued multimodal research integrating genetics, imaging, and other factors may help establish biomarkers to improve diagnosis and treatment of schizophrenia.
Brain Impairments in ADHD
This is a paper I wrote for school on brain impairments in attention deficit hyperactivity disorder, with a focus on neuroanatomical differences and connectivity patterns. I reviewed findings from various studies, considered their limitations, and proposed directions for future research.
Neurobiology of depression
(a) Several brain areas have been found to have abnormal activity or structure in patients with major depressive disorder (MDD) compared to healthy controls, including the prefrontal cortex, anterior cingulate cortex, hippocampus, amygdala, and orbitofrontal cortex.
(b) Imaging studies have found both hypoactivity and hyperactivity in different areas, and treatment has been shown to help normalize some of these abnormalities.
(c) The prefrontal cortex and limbic system including the hippocampus and amygdala appear to be particularly involved, and their structural and functional connections may contribute to MDD.
Parkinson s disease gene therapy success by design meets failure by efficacy ...
The document discusses 9 gene therapy clinical trials conducted over the past decade to treat Parkinson's disease. None of the trials have produced sufficiently robust clinical efficacy to enable approval, despite demonstrating safety. The trials collectively show gene therapy can safely generate biologically active proteins in the brain without risk or harm. However, improved clinical trial design, patient selection, outcome measures, and animal models are still needed to advance efficacy. The trials represent progress for the gene therapy field, but a renewed focus on efficacy is required to move programs forward.
Anti depression
This document provides an overview of anti-depression including definitions, epidemiology, etiology, hypotheses, symptoms, diagnosis, and antidepressants. It defines depression according to the WHO as a common mental disorder characterized by sadness and loss of interest. It notes the lifetime prevalence varies from 3-17% depending on country, and is higher in women. Several hypotheses for the etiology of depression are discussed related to neurotransmitters, receptors, and neuroendocrine factors. Common symptoms and diagnosis criteria from the DSM-V are outlined. Finally, it describes several classes of antidepressants including TCAs, MAOIs, SSRIs, and SNRIs and discusses their mechanisms of action, advantages/disadvantages, side
New Developments in the Treatment of Mood Disorders
Roger F Haskett MD
University of Pittsburgh School of Medicine Western Psychiatric Institute and Clinic
Medicine, Culture, and Spirituality Conference
September 9, 2011
Antiparkinson drugs
Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by tremors, muscle rigidity, slow movement, and impaired balance. It results from the loss of dopamine-producing neurons in the substantia nigra region of the brain. Current treatment focuses on replacing dopamine levels in the striatum through the use of levodopa and dopamine agonists, as well as reducing dopamine breakdown using MAO-B inhibitors. Levodopa is effective at reducing PD symptoms but its effects wear off over time. Combining it with carbidopa helps deliver more levodopa to the brain and reduce side effects. Dopamine agonists and MAO-B inhibitors such as selegiline and rasagiline are
Parkinson's disease
Parkinson's disease is a neurological disorder caused by loss of dopamine-producing neurons in the substantia nigra. Its main symptoms are tremors, rigidity, bradykinesia, and impaired balance and coordination. Diagnosis is based on medical history and clinical examination showing the characteristic motor symptoms. Treatment aims to control symptoms and preserve function, primarily using dopamine replacement therapy such as levodopa and dopamine agonists. Other options include deep brain stimulation surgery for advanced cases with motor fluctuations or dyskinesia.
Parkinson's disease
Parkinson's disease is a neurological disorder caused by loss of dopamine-producing neurons in the substantia nigra. Its main symptoms are tremors, rigidity, bradykinesia, and impaired balance and coordination. Diagnosis is based on medical history and clinical examination showing the characteristic motor symptoms. Treatment aims to control symptoms and preserve function, primarily using dopamine replacement therapy such as levodopa and dopamine agonists. Other options include deep brain stimulation surgery for advanced cases with motor fluctuations or dyskinesia.
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The Electrocardiogram - Physiologic Principles
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Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
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