Traumatic Brain Injury (TBI) is the number one cause of death and chronic disability for those under the age of 45. Unfortunately there are few current treatments available and there has been a large failure to translate neuroprotective treatments from animal models. One potential reason is that metabolic dysfunction, a key part of TBI pathophysiology is not addressed. Ketogenic diets and exogenous ketones have been shown to have neuroprotective effects through multiple mechanisms in animal models of TBI, including the reversal of metabolic dysfunction. I will discuss the current evidence for the KD in the treatment of TBI. I will also briefly discuss other nutritional and lifestyle factors in the treatment of TBI.
This document discusses drugs used in airway management during intubation. It covers:
1) Premedication drugs like opioids, lidocaine, and muscle relaxants given before intubation to reduce stress responses. Fentanyl is mentioned as a commonly used opioid.
2) Induction agents for intubation including midazolam, propofol, etomidate, and ketamine. Pros and cons of each are provided.
3) Muscular blockade drugs like succinylcholine and rocuronium for intubation, including dosages and side effects.
4) Post intubation sedation options like midazolam and fentanyl infusions to prevent injury and stress responses
The document discusses the anaesthetic management of diabetes mellitus, including the types and diagnosis of diabetes, physiology of insulin, perioperative response to surgery and anesthesia, complications, and considerations for management related to cardiovascular disease, renal dysfunction, neuropathies, and different types of surgery. It provides guidance on pre-operative, intra-operative, and post-operative glucose monitoring and management through intravenous fluids, insulin administration, and glycemic control targets. Surgical procedures for both insulin-dependent and non-insulin dependent diabetes are outlined.
This document provides an overview of chronic obstructive pulmonary disease (COPD), including its definition, pathology, risk factors, diagnosis, assessment, management, monitoring and treatment. COPD is characterized by persistent respiratory symptoms and airflow limitation caused by exposure to noxious particles or gases. Key aspects of management include smoking cessation, pharmacotherapy including bronchodilators and inhaled corticosteroids, pulmonary rehabilitation, oxygen therapy and treating exacerbations and comorbidities. The goals are to prevent and reduce symptoms, exacerbations and disease progression and improve quality of life.
The document provides an overview of metabolic equivalents (METs), including:
- Definitions of METs and how they are used to quantify the intensity of physical activities.
- Clinical importance of METs in describing functional capacity and prescribing exercise intensities.
- Classification of activity intensities based on MET thresholds.
- How METs are calculated and converted and how they relate to functional capacity.
- Use of METs in cardiac rehabilitation to progress patients through levels of activity intensity.
- Limitations of MET measures including assumptions about energy expenditure.
Oral ketamine can be used as an adjuvant analgesic in palliative care patients to help manage refractory pain. Low dose oral ketamine has been shown to reduce opioid consumption and improve pain relief when used together with opioids like morphine. While studies have not found oral ketamine to provide statistically significant pain relief on its own, it appears to have an opioid-sparing effect. Based on the evidence, an initial oral dose of 0.25-0.5 mg/kg of ketamine is recommended when used adjunctively with opioids in palliative care patients. Close monitoring is needed due to potential side effects like hallucinations.
Phantom Limb Pain is a condition where an amputee feels pain in a limb that is no longer there. It originates in the brain and spinal cord due to changes in the neurological connections previously associated with the amputated limb. Treatment involves pharmacological approaches like opioids, antidepressants, and anticonvulsants as well as nonpharmacological methods such as mirror therapy, TENS, and prosthetics. In severe cases, surgical interventions may provide relief but pain often returns. An integrated treatment plan tailored to the individual is most effective in managing Phantom Limb Pain.
This document discusses brain death, including its historical definition, current diagnostic criteria, pathophysiology, and management of organ donors. Key points include:
- Brain death is defined as irreversible cessation of all functions of the entire brain, including the brain stem.
- Diagnosis requires two examinations at least 6 hours apart showing coma, absence of brainstem reflexes, and apnea during a standardized test. Ancillary tests like EEG can be used if clinical criteria are inconclusive.
- After brain death, pathophysiological changes occur like hypotension, diabetes insipidus, and coagulopathies due to loss of autonomic and endocrine functions regulated by the brain.
This document discusses drugs used in airway management during intubation. It covers:
1) Premedication drugs like opioids, lidocaine, and muscle relaxants given before intubation to reduce stress responses. Fentanyl is mentioned as a commonly used opioid.
2) Induction agents for intubation including midazolam, propofol, etomidate, and ketamine. Pros and cons of each are provided.
3) Muscular blockade drugs like succinylcholine and rocuronium for intubation, including dosages and side effects.
4) Post intubation sedation options like midazolam and fentanyl infusions to prevent injury and stress responses
The document discusses the anaesthetic management of diabetes mellitus, including the types and diagnosis of diabetes, physiology of insulin, perioperative response to surgery and anesthesia, complications, and considerations for management related to cardiovascular disease, renal dysfunction, neuropathies, and different types of surgery. It provides guidance on pre-operative, intra-operative, and post-operative glucose monitoring and management through intravenous fluids, insulin administration, and glycemic control targets. Surgical procedures for both insulin-dependent and non-insulin dependent diabetes are outlined.
This document provides an overview of chronic obstructive pulmonary disease (COPD), including its definition, pathology, risk factors, diagnosis, assessment, management, monitoring and treatment. COPD is characterized by persistent respiratory symptoms and airflow limitation caused by exposure to noxious particles or gases. Key aspects of management include smoking cessation, pharmacotherapy including bronchodilators and inhaled corticosteroids, pulmonary rehabilitation, oxygen therapy and treating exacerbations and comorbidities. The goals are to prevent and reduce symptoms, exacerbations and disease progression and improve quality of life.
The document provides an overview of metabolic equivalents (METs), including:
- Definitions of METs and how they are used to quantify the intensity of physical activities.
- Clinical importance of METs in describing functional capacity and prescribing exercise intensities.
- Classification of activity intensities based on MET thresholds.
- How METs are calculated and converted and how they relate to functional capacity.
- Use of METs in cardiac rehabilitation to progress patients through levels of activity intensity.
- Limitations of MET measures including assumptions about energy expenditure.
Oral ketamine can be used as an adjuvant analgesic in palliative care patients to help manage refractory pain. Low dose oral ketamine has been shown to reduce opioid consumption and improve pain relief when used together with opioids like morphine. While studies have not found oral ketamine to provide statistically significant pain relief on its own, it appears to have an opioid-sparing effect. Based on the evidence, an initial oral dose of 0.25-0.5 mg/kg of ketamine is recommended when used adjunctively with opioids in palliative care patients. Close monitoring is needed due to potential side effects like hallucinations.
Phantom Limb Pain is a condition where an amputee feels pain in a limb that is no longer there. It originates in the brain and spinal cord due to changes in the neurological connections previously associated with the amputated limb. Treatment involves pharmacological approaches like opioids, antidepressants, and anticonvulsants as well as nonpharmacological methods such as mirror therapy, TENS, and prosthetics. In severe cases, surgical interventions may provide relief but pain often returns. An integrated treatment plan tailored to the individual is most effective in managing Phantom Limb Pain.
This document discusses brain death, including its historical definition, current diagnostic criteria, pathophysiology, and management of organ donors. Key points include:
- Brain death is defined as irreversible cessation of all functions of the entire brain, including the brain stem.
- Diagnosis requires two examinations at least 6 hours apart showing coma, absence of brainstem reflexes, and apnea during a standardized test. Ancillary tests like EEG can be used if clinical criteria are inconclusive.
- After brain death, pathophysiological changes occur like hypotension, diabetes insipidus, and coagulopathies due to loss of autonomic and endocrine functions regulated by the brain.
Phantom limb syndrome (PLS) involves feeling that an amputated limb is still present, while phantom limb pain (PLP) describes painful sensations like throbbing or electric shocks in the missing limb. Around 78% of amputees experience PLP. Theories for its causes include cortical remapping in the brain, enlarged representations in the thalamus, and aberrant signaling from injured nerves. While the exact mechanisms are unclear, a better understanding may lead to new treatments to reduce amputees' suffering from PLP.
The KDIGO 2022 Clinical Practice Guideline on Diabetes Management in CKD provides recommendations and guidance to help clinicians manage patients with both diabetes and chronic kidney disease. The guideline was developed by an international work group using the GRADE approach. It addresses topics such as comprehensive care, glycemic monitoring and targets, lifestyle interventions, glucose-lowering therapies, and approaches to management. The guideline aims to reduce risks of kidney disease progression and cardiovascular disease for these high-risk patients.
The document provides guidelines for treating hip fractures in the elderly. It notes that hip fractures are increasing with the ageing population and cost the NHS £2 billion annually, with 10% of patients dying within a month of the fracture. The guidelines discuss factors that must be considered including timing of surgery, analgesia, anaesthesia, surgical procedures, post-op mobilization, and informing patients and carers. Early surgery is recommended to treat co-morbidities and internal fixation, hemiarthroplasty or total arthroplasty may be used depending on the fracture type. Early mobilization starting the day after surgery and regular physiotherapy is also advised.
Thomas Test (or as it called Hugh Owen Thomas well leg raising test) is used to measure the flexibility of the hip flexor muscles. It’s used to test for hip flexion contracture and psoas syndrome, which is more common in runners, dancers, and gymnasts with symptoms of hip “stiffness” and “clicking” feeling when flexing at the waist.
For more, See:
https://www.orthofixar.com/special-test/thomas-test/
Diabetic neuropathy is a common complication of diabetes that affects up to 50% of patients with diabetes for over 25 years. It is caused by damage to peripheral nerves due to metabolic and vascular factors related to high blood glucose. Symptoms range from numbness to severe pain and loss of sensation. Treatment focuses on managing blood sugar levels to prevent neuropathy, as well as symptomatic relief through medications. Proper foot care is also important to prevent ulcers and other complications.
Brain death is a clinical diagnosis based on the absence of neurologic function and irreversible coma. A complete neurologic examination is required to determine brain death, which must show no brainstem reflexes, no response to stimuli, apnea on testing, and flaccid muscle tone. Ancillary tests like EEG or angiography can assist in diagnosis but are not required. Special considerations are needed for diagnosing brain death in newborns and preterm infants due to the potential for reversible conditions and lack of brain development. Death is declared after two examinations show no changes confirming an irreversible condition.
A thoracotomy is a surgical procedure where an incision is made through the chest wall to access the organs within the chest cavity like the lungs and heart. It is performed by a thoracic surgeon or emergency physician in a hospital operating room or emergency department. Reasons for thoracotomy include diagnosing and treating conditions like lung cancer or injuries from the chest. Risks include bleeding, infection and pain during a long recovery period.
Stroke rehabilitation aims to help stroke survivors achieve their highest level of function and independence. It involves both neurological and functional recovery processes. The majority of neurological recovery occurs within the first 3 months post-stroke, while functional recovery may continue for longer with rehabilitation therapies. An interdisciplinary team provides comprehensive rehabilitation addressing impairments in areas like mobility, self-care, communication and cognition. Early mobilization and prevention of complications are important. Outcome measures assess different domains of recovery. Rehabilitation goals must be specific, measurable, achievable and timely.
This document provides an overview of stroke rehabilitation. It discusses the objectives and goals of rehabilitation, which include achieving functional independence, facilitating recovery, and reintegrating the patient back into their home and community. It then covers various aspects of rehabilitation including management in the acute phase, prevention of secondary strokes, and rehabilitation approaches for specific impairments like the upper limb, walking, swallowing, and more. A variety of therapeutic techniques and treatments are described for each impairment.
Cauda Equina Syndrome is a condition involving the bundle of nerves originating from the lower end of the spinal cord. It can result from central disc herniations, spinal tumors, trauma, or other causes. Patients may experience LMN signs, saddle anesthesia, gait ataxia, and sexual/bladder/bowel dysfunction. MRI is used for diagnosis. Treatment requires immediate neurosurgical consultation and decompression, as delays can lead to permanent deficits.
acute stroke for rehab physician - dr trilochan shrivastavamrinal joshi
1. The document discusses acute management and rehabilitation of stroke, providing information on types of strokes, risk factors, signs and symptoms, investigations, treatments, and rehabilitation approaches.
2. It covers diagnostic testing including imaging, medications, and interventional procedures for ischemic and hemorrhagic strokes.
3. Rehabilitation services are described including physical, occupational and speech therapy in various settings from inpatient to home-based care with the goal of improving functional abilities and outcomes for stroke patients.
Anticoagulation expanding steadily over the past few decades.
In addition to Heparins and vitamin K antagonist, other anticoagulants that directly target the enzymatic activity of thrombin and factor Xa have been developed.
Post Natal Exercises after Caesarean Section.pptxMayuri Zanwar
Physiotherapy management in Post natal care focuses on addressing potential structural and functional impairments following childbirth like pelvic floor dysfunction, incontinence, and prolapse. Exercises are important for improving circulation, strengthening muscles like the pelvic floor and abdomen, and preventing issues like backaches. Specific exercises addressed include breathing exercises to improve lung function, scar mobilization and friction massage to enhance healing and prevent adhesions, and pelvic floor exercises to prevent dysfunction. References are provided on techniques like TENS and exercises to address issues like diastasis recti.
Nurses as the primary care providers would be the immediate health care professional to assess the patient's response and to determine whether he is improving or deteriorating. Signs of brain death can be identified and reported early by a nurse with adequate knowledge.
This document discusses neurogenic bowel dysfunction, which occurs when the bowel's normal functioning is disrupted by neurological damage or disease. It can cause constipation, diarrhea, or fecal incontinence. Common causes include spinal cord injury, stroke, or Parkinson's disease. Management involves regular bowel regimens to prevent accidents and complications like impaction. Approaches include diet, exercise, suppositories, manual evacuation, enemas, and oral laxatives. The goal is to establish a routine that empties the bowel and maintains quality of life.
Dysautonomia refers to a malfunction of the autonomic nervous system that controls involuntary body functions like heart rate, blood pressure, digestion, and sweating. The document discusses the anatomy and functions of the autonomic nervous system and its divisions. It then defines dysautonomia and lists various causes like diabetes, multiple sclerosis, and injuries. Common symptoms involve fatigue, dizziness, digestive issues, urinary problems, and temperature regulation difficulties. Tests of autonomic function are described that measure responses like heart rate and blood pressure during maneuvers to identify autonomic dysfunction.
The DCCT trial showed that intensive diabetes management reduced the risk of eye, kidney, and nerve complications compared to standard management. Intensive therapy aimed for blood glucose levels between 70-120 mg/dl, while standard therapy aimed to avoid symptoms of high or low blood glucose. The risks of intensive therapy were increased hypoglycemia and weight gain. The follow up EDIC study found metabolic memory effects, with long term benefits of early intensive control.
Dr Awaneesh Katiyar-Brain Trauma Foundation 4 - copyAwaneesh Katiyar
This document summarizes the key guidelines from the 4th edition of the Brain Trauma Foundation guidelines for severe traumatic brain injury. Some of the major topics and recommendations included:
- Early prophylactic hypothermia within 2.5 hours of injury is not recommended to improve outcomes for diffuse brain injury.
- While hyperosmolar therapy may lower intracranial pressure, there is insufficient evidence on effects on clinical outcomes to recommend a specific agent.
- For elevated intracranial pressure refractory to other treatments, continuous drainage of cerebrospinal fluid with an external ventricular drain or high-dose barbiturates may be considered.
This document presents a systematic review and meta-analyses of neuroprotective agents used for traumatic brain injury. It summarizes 18 randomized controlled trials evaluating the efficacy of various agents, including erythropoietin, citicoline, progesterone, oxygen, corticosteroids, monoaminergic agents, magnesium, cerebrolysin, and cyclosporine A. The primary objectives were to determine what new evidence exists since prior reviews in 2015 and evaluate the agents' effects on outcomes like mortality, functional recovery, and side effects. Most agents showed limited or no evidence of benefit, though erythropoietin, progesterone, and oxygen demonstrated some promising results requiring further large randomized trials.
This document discusses the evaluation of stroke. It begins by classifying the pathophysiologic processes that can cause stroke into four categories: those intrinsic to the vessel, those originating remotely as an embolism, those resulting from inadequate cerebral blood flow, and those from rupture of vessels in the brain. It then describes transient ischemic attacks, intracerebral hemorrhage, subarachnoid hemorrhage, and the three main subtypes of brain ischemia. The document outlines the initial assessment, history, physical exam, tests to confirm diagnosis including vascular studies, cardiac evaluation, and blood tests. It provides details on the appropriate cardiac and hypercoagulable testing based on a patient's history and symptoms.
Phantom limb syndrome (PLS) involves feeling that an amputated limb is still present, while phantom limb pain (PLP) describes painful sensations like throbbing or electric shocks in the missing limb. Around 78% of amputees experience PLP. Theories for its causes include cortical remapping in the brain, enlarged representations in the thalamus, and aberrant signaling from injured nerves. While the exact mechanisms are unclear, a better understanding may lead to new treatments to reduce amputees' suffering from PLP.
The KDIGO 2022 Clinical Practice Guideline on Diabetes Management in CKD provides recommendations and guidance to help clinicians manage patients with both diabetes and chronic kidney disease. The guideline was developed by an international work group using the GRADE approach. It addresses topics such as comprehensive care, glycemic monitoring and targets, lifestyle interventions, glucose-lowering therapies, and approaches to management. The guideline aims to reduce risks of kidney disease progression and cardiovascular disease for these high-risk patients.
The document provides guidelines for treating hip fractures in the elderly. It notes that hip fractures are increasing with the ageing population and cost the NHS £2 billion annually, with 10% of patients dying within a month of the fracture. The guidelines discuss factors that must be considered including timing of surgery, analgesia, anaesthesia, surgical procedures, post-op mobilization, and informing patients and carers. Early surgery is recommended to treat co-morbidities and internal fixation, hemiarthroplasty or total arthroplasty may be used depending on the fracture type. Early mobilization starting the day after surgery and regular physiotherapy is also advised.
Thomas Test (or as it called Hugh Owen Thomas well leg raising test) is used to measure the flexibility of the hip flexor muscles. It’s used to test for hip flexion contracture and psoas syndrome, which is more common in runners, dancers, and gymnasts with symptoms of hip “stiffness” and “clicking” feeling when flexing at the waist.
For more, See:
https://www.orthofixar.com/special-test/thomas-test/
Diabetic neuropathy is a common complication of diabetes that affects up to 50% of patients with diabetes for over 25 years. It is caused by damage to peripheral nerves due to metabolic and vascular factors related to high blood glucose. Symptoms range from numbness to severe pain and loss of sensation. Treatment focuses on managing blood sugar levels to prevent neuropathy, as well as symptomatic relief through medications. Proper foot care is also important to prevent ulcers and other complications.
Brain death is a clinical diagnosis based on the absence of neurologic function and irreversible coma. A complete neurologic examination is required to determine brain death, which must show no brainstem reflexes, no response to stimuli, apnea on testing, and flaccid muscle tone. Ancillary tests like EEG or angiography can assist in diagnosis but are not required. Special considerations are needed for diagnosing brain death in newborns and preterm infants due to the potential for reversible conditions and lack of brain development. Death is declared after two examinations show no changes confirming an irreversible condition.
A thoracotomy is a surgical procedure where an incision is made through the chest wall to access the organs within the chest cavity like the lungs and heart. It is performed by a thoracic surgeon or emergency physician in a hospital operating room or emergency department. Reasons for thoracotomy include diagnosing and treating conditions like lung cancer or injuries from the chest. Risks include bleeding, infection and pain during a long recovery period.
Stroke rehabilitation aims to help stroke survivors achieve their highest level of function and independence. It involves both neurological and functional recovery processes. The majority of neurological recovery occurs within the first 3 months post-stroke, while functional recovery may continue for longer with rehabilitation therapies. An interdisciplinary team provides comprehensive rehabilitation addressing impairments in areas like mobility, self-care, communication and cognition. Early mobilization and prevention of complications are important. Outcome measures assess different domains of recovery. Rehabilitation goals must be specific, measurable, achievable and timely.
This document provides an overview of stroke rehabilitation. It discusses the objectives and goals of rehabilitation, which include achieving functional independence, facilitating recovery, and reintegrating the patient back into their home and community. It then covers various aspects of rehabilitation including management in the acute phase, prevention of secondary strokes, and rehabilitation approaches for specific impairments like the upper limb, walking, swallowing, and more. A variety of therapeutic techniques and treatments are described for each impairment.
Cauda Equina Syndrome is a condition involving the bundle of nerves originating from the lower end of the spinal cord. It can result from central disc herniations, spinal tumors, trauma, or other causes. Patients may experience LMN signs, saddle anesthesia, gait ataxia, and sexual/bladder/bowel dysfunction. MRI is used for diagnosis. Treatment requires immediate neurosurgical consultation and decompression, as delays can lead to permanent deficits.
acute stroke for rehab physician - dr trilochan shrivastavamrinal joshi
1. The document discusses acute management and rehabilitation of stroke, providing information on types of strokes, risk factors, signs and symptoms, investigations, treatments, and rehabilitation approaches.
2. It covers diagnostic testing including imaging, medications, and interventional procedures for ischemic and hemorrhagic strokes.
3. Rehabilitation services are described including physical, occupational and speech therapy in various settings from inpatient to home-based care with the goal of improving functional abilities and outcomes for stroke patients.
Anticoagulation expanding steadily over the past few decades.
In addition to Heparins and vitamin K antagonist, other anticoagulants that directly target the enzymatic activity of thrombin and factor Xa have been developed.
Post Natal Exercises after Caesarean Section.pptxMayuri Zanwar
Physiotherapy management in Post natal care focuses on addressing potential structural and functional impairments following childbirth like pelvic floor dysfunction, incontinence, and prolapse. Exercises are important for improving circulation, strengthening muscles like the pelvic floor and abdomen, and preventing issues like backaches. Specific exercises addressed include breathing exercises to improve lung function, scar mobilization and friction massage to enhance healing and prevent adhesions, and pelvic floor exercises to prevent dysfunction. References are provided on techniques like TENS and exercises to address issues like diastasis recti.
Nurses as the primary care providers would be the immediate health care professional to assess the patient's response and to determine whether he is improving or deteriorating. Signs of brain death can be identified and reported early by a nurse with adequate knowledge.
This document discusses neurogenic bowel dysfunction, which occurs when the bowel's normal functioning is disrupted by neurological damage or disease. It can cause constipation, diarrhea, or fecal incontinence. Common causes include spinal cord injury, stroke, or Parkinson's disease. Management involves regular bowel regimens to prevent accidents and complications like impaction. Approaches include diet, exercise, suppositories, manual evacuation, enemas, and oral laxatives. The goal is to establish a routine that empties the bowel and maintains quality of life.
Dysautonomia refers to a malfunction of the autonomic nervous system that controls involuntary body functions like heart rate, blood pressure, digestion, and sweating. The document discusses the anatomy and functions of the autonomic nervous system and its divisions. It then defines dysautonomia and lists various causes like diabetes, multiple sclerosis, and injuries. Common symptoms involve fatigue, dizziness, digestive issues, urinary problems, and temperature regulation difficulties. Tests of autonomic function are described that measure responses like heart rate and blood pressure during maneuvers to identify autonomic dysfunction.
The DCCT trial showed that intensive diabetes management reduced the risk of eye, kidney, and nerve complications compared to standard management. Intensive therapy aimed for blood glucose levels between 70-120 mg/dl, while standard therapy aimed to avoid symptoms of high or low blood glucose. The risks of intensive therapy were increased hypoglycemia and weight gain. The follow up EDIC study found metabolic memory effects, with long term benefits of early intensive control.
Dr Awaneesh Katiyar-Brain Trauma Foundation 4 - copyAwaneesh Katiyar
This document summarizes the key guidelines from the 4th edition of the Brain Trauma Foundation guidelines for severe traumatic brain injury. Some of the major topics and recommendations included:
- Early prophylactic hypothermia within 2.5 hours of injury is not recommended to improve outcomes for diffuse brain injury.
- While hyperosmolar therapy may lower intracranial pressure, there is insufficient evidence on effects on clinical outcomes to recommend a specific agent.
- For elevated intracranial pressure refractory to other treatments, continuous drainage of cerebrospinal fluid with an external ventricular drain or high-dose barbiturates may be considered.
This document presents a systematic review and meta-analyses of neuroprotective agents used for traumatic brain injury. It summarizes 18 randomized controlled trials evaluating the efficacy of various agents, including erythropoietin, citicoline, progesterone, oxygen, corticosteroids, monoaminergic agents, magnesium, cerebrolysin, and cyclosporine A. The primary objectives were to determine what new evidence exists since prior reviews in 2015 and evaluate the agents' effects on outcomes like mortality, functional recovery, and side effects. Most agents showed limited or no evidence of benefit, though erythropoietin, progesterone, and oxygen demonstrated some promising results requiring further large randomized trials.
This document discusses the evaluation of stroke. It begins by classifying the pathophysiologic processes that can cause stroke into four categories: those intrinsic to the vessel, those originating remotely as an embolism, those resulting from inadequate cerebral blood flow, and those from rupture of vessels in the brain. It then describes transient ischemic attacks, intracerebral hemorrhage, subarachnoid hemorrhage, and the three main subtypes of brain ischemia. The document outlines the initial assessment, history, physical exam, tests to confirm diagnosis including vascular studies, cardiac evaluation, and blood tests. It provides details on the appropriate cardiac and hypercoagulable testing based on a patient's history and symptoms.
1) Intracerebral hemorrhage is now understood as a dynamic process that evolves over days rather than a single event. Recent studies have provided insights into hematoma expansion, edema formation, and optimal blood pressure control.
2) Ongoing clinical trials are exploring intensive blood pressure control, induced hypothermia, hypertonic saline use, and other therapies to reduce hematoma growth and edema, with the goal of improving outcomes.
3) For anticoagulant-related hemorrhages, rapidly reversing coagulopathy through agents like prothrombin complex concentrates or recombinant factor VIIa may help limit expansion and improve prognosis over traditional fresh frozen plasma therapy alone.
1. Thrombolytic therapy through pharmacological agents like rTPA, urokinase, and streptokinase is one of the most effective ways to treat acute ischemic stroke through revascularization.
2. A study of 36 patients who received thrombolytic therapy found that outcomes were best for anterior circulation minor strokes and posterior circulation strokes, and when intravenous thrombolysis was administered within 3 hours of onset of symptoms.
3. Complications from thrombolytic therapy like hemorrhaging were found to be dose-related, with normal CT scans before treatment not guaranteeing outcomes but abnormal CT scans relating to poorer prognosis.
Unanswered questions in thrombolytic therapy for acute ischemic stroke. 2013Javier Pacheco Paternina
This document discusses unanswered questions regarding thrombolytic therapy for acute ischemic stroke. It begins by providing background on stroke incidence and efforts to treat patients promptly. The introduction outlines key unanswered questions such as the optimal time window for tissue plasminogen activator treatment and whether other agents or endovascular therapies could further extend the time window. The document then reviews landmark studies on intravenous thrombolysis and the established 3-hour time window as well as efforts to extend the window. It also discusses other pharmacologic and mechanical treatment options and their respective time windows.
Health Policy - Use of IV tPA for Acute Ischemic StrokesZach Jarou
Stroke is a leading cause of death and disability in the US. Treatment with the drug tPA within 3 hours of stroke onset can reverse deficits, but it is underutilized due to its risk of hemorrhage and narrow treatment window. The document argues that public education on stroke symptoms and increasing the treatment window to 4.5 hours based on evidence from trials could increase tPA use and reduce disability, but its risks still require careful patient selection.
Medicinal Cannabis in the Treatment of Parkinson'sJames Van Geelen
An overview of the MMJ program in CT, cannabis' benefits in the treatment of parkinson's disease and an introduction to the world of medicinal cannabis.
Neuroprotective Agents To Reduce Neuronal Loss Following SciAnnabel De Coster
The document summarizes research into investigating the neuroprotective effects of the peptide PRARIY in models of spinal cord injury in vitro. The research aimed to characterize neuronal cell death induced by excitotoxic and inflammatory stimuli in cell culture models, study the uptake and localization of fluorescently-labelled PRARIY peptide in neurons, and determine if PRARIY provides neuroprotection compared to a scrambled control peptide. Preliminary results found PRARIY entered neurons and reduced cell death induced by glutamate, though results were inconclusive due to variability between experiments. Future work proposed improving the cell death model and further investigating PRARIY's effects and localization.
Relative Contraindications for Thrombolysis in Acute Ischemic StrokeSudhir Kumar
Thrombolysis with rt-PA (Actilyse) is approved for the treatment of acute ischemic stroke since 1996. However, only 10-15% people receive this very effective treatment. One of the factors for low rates of thrombolysis is a large number of relative contraindications. This talk discusses, how we can include several of the patients with relative contraindications for thrombolytic treatment.
The document outlines guidelines for lifestyle interventions and drug therapy based on LDL cholesterol levels and cardiovascular risk categories. It recommends initiating lifestyle changes and considering drug therapy for high risk patients when LDL is over 100 mg/dL, moderately high risk patients when over 130 mg/dL, moderate risk patients when over 160 mg/dL, and low risk patients when over 190 mg/dL.
Edaravone is a novel antioxidant that scavenges reactive oxygen species (ROS) and inhibits pro-inflammatory responses after brain ischemia. It has emerged as an ideal neuroprotective agent for acute ischemic stroke. Edaravone minimizes ischemic damage by trapping free radicals, preventing oxidative injury to brain cells, and limiting the downstream consequences of excitotoxicity such as mitochondrial disruption and DNA damage. Its neuroprotective effects help preserve viable brain cells in the ischemic penumbra.
CHA2DS2-VASc, Score CHADS2 score, and Hasbled scoreDJ CrissCross
The CHADS2 scoring system is a clinical prediction rule used to assess the risk of stroke in patients with non-rheumatic atrial fibrillation. It assigns points based on various risk factors, with a higher total score indicating greater risk of stroke. It is used to determine if anticoagulation therapy is required. The HAS-BLED scoring system evaluates bleeding risk for patients on oral anticoagulants for atrial fibrillation by assigning points for different risk factors, with a score of 3 or more indicating increased risk of major bleeding within one year.
This document provides information on managing patients with stroke. It discusses the objectives of reviewing stroke etiology, identifying stroke type based on exam, and acute management of ischemic and hemorrhagic strokes. It then covers the three main types of strokes - ischemic, intracerebral hemorrhage, and subarachnoid hemorrhage. Key aspects of acute stroke management are outlined, including the ABCs, use of the NIH Stroke Scale to determine severity, thrombolysis guidelines, complications to watch for, and supportive therapies. The importance of blood pressure control, glucose management, and avoiding fever are emphasized for optimizing patient outcomes.
Emergency treatment of stroke involves several steps:
1. Rapid diagnosis through imaging such as CT or MRI to determine if the stroke is ischemic or hemorrhagic.
2. For ischemic strokes within 3 hours, treatment with rTPA (recombinant tissue plasminogen activator) can dissolve clots and reduce long-term disability if eligibility criteria are met.
3. Intensive monitoring is required after rTPA to control blood pressure and watch for bleeding complications.
4. Surgery may be considered for large hemorrhagic strokes or subarachnoid hemorrhage from aneurysms to relieve pressure on the brain.
Stroke is a leading cause of death and disability worldwide. In India, stroke incidence and mortality rates are higher than in developed countries. The major risk factors for stroke include hypertension, smoking, diabetes, heart disease, and atrial fibrillation. Stroke occurs when blood flow to the brain is interrupted, causing cell death. Treatments aim to rapidly restore blood flow and protect brain cells. Thrombolysis can help dissolve clots but must be given within 3 hours, limiting its use. Neuroprotection seeks to protect brain cells and expand the time window for treatment.
Neuroprotective drugs aim to protect neurons from damage in conditions like stroke. Currently, there are no approved neuroprotective treatments for stroke. Various targets of neuroprotection have been investigated including inflammation, oxidative stress, excitotoxicity, and apoptosis. Many agents have shown promise in animal models but failed in clinical trials. Edaravone is the only drug approved in Japan for acute ischemic stroke. Ongoing research continues to explore new targets and combinations of therapies to develop effective neuroprotective treatments for stroke.
NEURODEGENERATION & NEUROPROTECTION-AN AYURVEDIC PERSPECTIVE.
WHAT AYURVEDA CAN OFFER BOTH IN PREVENTION & TREATMENT.FAMOUS PEOPLE SUFFERING FROM NEURODEGENERATION.MANDUKPARNI,SHANKHAPUSPI,POMGRENATE,ASWAGANDHA.BUDDHIBHRANSHA.NILANJAN DATTA.ROGNIDAN.PARKINSON,MULTIPLE SCLEROSIS,HUNTINGTONS CHOREA,ALZHEIMERS IN AYURVEDA TREATMENT.THANK YOU.ACKNOWLEDGEMENTS.DR.B.C.JANA.BHU.IPGAER AT SVSP,KOLKATA.BHU.
The document discusses the benefits of exercise for mental health. Regular physical activity can help reduce anxiety and depression and improve mood and cognitive function. Exercise causes chemical changes in the brain that may help protect against mental illness and improve symptoms.
Impacto de las tic en los destinos turisticos. Destinos turísticos inteligentesPedro Anton
Impacto de la TIC en un Destino Turístico.
Evento: Presentación del Plan estratégico de Turismo de la Mancomunidad de Vigo
Fecha: 11 de Enero de 2011
Lugar: Vigo
This document summarizes key points from a presentation on mechanisms of concussion. It defines traumatic brain injury as an injury caused by biomechanical forces that results in cellular dysfunction and death in some areas but an energy crisis in surviving cells. It notes that every traumatic brain injury starts as a concussion and discusses the neurometabolic cascade that occurs, including potassium and glutamate flux, hyperglycolysis, mitochondrial dysfunction, axonal injury, and cell damage/death. It reviews clinical studies showing acute hyperglycolysis and chronic metabolic depression after injury as seen on PET, MRS, and fMRI scans. The presentation emphasizes that traumatic brain injury should be viewed as a metabolic disorder.
IMPROVING RECOVERY AFTER A STROKE: EVIDENCES FOR CONTEMPORARY APPROACHESAdemola Adeyemo
This document outlines an MSc presentation on improving recovery after stroke through contemporary rehabilitation approaches. It discusses the epidemiology of stroke and common disabilities caused by stroke. Key principles for recovery like neuroplasticity are explained. Contemporary task-specific training approaches and motor learning paradigms are described in detail, including constraint-induced movement therapy, functional electrical stimulation, bodyweight supported treadmill training, robotics therapy, and virtual reality therapy. Evidence for how these approaches can enhance recovery through cortical reorganization is provided.
Cognitive impairment after mild and moderate tbithangneuro
Cognitive impairment was present in 41-61.9% of patients 3 months after mild or moderate traumatic brain injury (TBI). The study assessed 63 patients admitted to the hospital with mild or moderate TBI as determined by the Glasgow Coma Scale and CT scans. Cognitive impairment was measured using the Montreal Cognitive Assessment and was related to older age, lower education levels, and presence of brain lesions on CT scans. Brain regions involving attention, abstraction, and executive function were most commonly impaired.
A Multimodal Regenerative Approach JPNI November 2019Megan Hughes
Dr. Hughes discusses the TBI Therapy mutlimodal approach to treating traumatic brain injury including hyperbaric oxygen therapy (HBOT), IV nutrition, intransal PRP, insulin, and adult stem cells, cranial osteopathy, and the ketogenic diet at the JPNI conference in Broomfield.
Dr. Hughes discusses the TBI Therapy mutlimodal approach to treating traumatic brain injury including hyperbaric oxygen therapy (HBOT), IV nutrition, intransal PRP, insulin, and adult stem cells, cranial osteopathy, and the ketogenic diet at the OMED conference in Baltimore.
024 treating depression and depression-like behavior with physical activityGiliano Campos
This article reviews studies examining the neuroimmunomodulatory effects of physical activity on the brain in depression and depression-like behaviors. The review finds that physical activity enhances beneficial and reduces detrimental effects on the neuroimmune system. Specifically, physical activity appears to increase anti-inflammatory cytokines and factors while decreasing pro-inflammatory cytokines and factors. The effects are thought to occur both centrally in the brain and peripherally. Investigation of the neuroimmune effects of physical activity is a rapidly developing area that may help understand the biological mechanisms of physical activity's effects and inform new therapeutic approaches for depression.
This document presents a systematic review and meta-analysis of neuroprotective agents used for traumatic brain injury. It describes traumatic brain injury and various neuroprotective interventions that have been studied, including oxygen, corticosteroids, progesterone, monoaminergic agents, erythropoietin, magnesium, cerebrolysin, and citicoline. For each intervention, the document summarizes the relevant randomized controlled trials, findings on outcomes like mortality, and recommendations for further research. The overall goal is to evaluate the evidence on various neuroprotective agents and identify priorities for future clinical trials.
This document discusses long-term issues after traumatic brain injury (TBI) and how aging affects recovery and outcomes. It notes that the aging brain has a decreasing ability to repair itself. Older age at injury is associated with poorer outcomes, as deficits become more pronounced with age. Studies found significant cognitive, functional, and social deficits years post-injury. Moderate to severe TBI doubles the risk of Alzheimer's and other dementias. The document recommends maintaining physical, cognitive, and social function through exercise, cognitive strategies, and social engagement to support successful aging after TBI.
1 The Outcomes of Neural Stem Cell Transplantation and .docxhoney725342
1
The Outcomes of Neural Stem Cell Transplantation and Localized Drug Therapy on Patients
Suffering from Traumatic Brain Injury
John Doe
Panther ID: 12121212
Assignment #1
Florida International University
2
Introduction
TBI Trend and Growth
Traumatic Brain Injury (TBI) affects a wide variety of people nationwide. One constant
does remain; the human condition suffers, both internally and externally. Studies confirm that
caregivers of those who suffer from TBI may experience feelings of burden, distress, anxiety,
anger, and recurring depression (Brain Injury Association of America [BIAUSA], 2015). More
detrimental is the alarming number of deaths and disabilities caused by TBI, which contribute to
roughly 30% of ALL injury related deaths in the U.S. (Centers for Disease Control and
Prevention [CDCP], 2014). The effects of TBI can include impaired thinking or memory,
movement, sensation, or emotional function (CDCP, 2014). The ferocity and utter devastation of
those afflicted with this condition are severely hindered in life and in turn the negative prognosis
can have an enduring effect on relatives and even on a community as a whole. The proposed
study will review current literature and collective research models and data based on neural stem
cell transplantation on injured brains and their positive outcomes; as well as, the facilitation of
newly implemented procedures for localized drug therapy on their respective injury sites. Studies
are primarily collected in controlled laboratory setting and modeled on mice for efficacy of
desired treatment protocol. Study goals will also encompass current newly invested research at
the University of Miami Miller School of Medicine and the University of Michigan Medical
School so as to further support the indicated research listed above.
Background: Origins of TBI and Impact
TBI is primarily found in patients who suffer from penetrating head injuries that disrupt
the normal function of the brain. It is important to note that not all blows and bumps necessarily
result in TBI formation, but, is based on how serious head trauma is and can range from mild
3
(i.e. brief change in mental status) to severe (i.e. an extended period of unconsciousness or major
loss of cognitive and motor function) (CDCP, 2014). According to the CDCP (2014), most cases
of TBI result in mild symptoms, like concussions, but if left unchecked can result in serious
injury or even death in some cases. TBI has a very unpredictable form of recovery and many
factors can contribute to the ultimate outcome, such as, pre-morbid personality and oriented goal
direction of healthcare team and patient alike, length of coma, specific area of the brain or brain
stem damaged, family support, age the injury occurs, and care of specialized rehabilitation
services (BIAUSA, 2015).
General Problem Statement
The general problem is represented with the ...
The metabolic response to traumatic brain injury (TBI) involves undesirable alterations including disrupted metabolism and a hypercatabolic state. Several key pathways are affected by TBI, including glycolysis, gluconeogenesis, glycogenolysis, and proteolysis. In the brain, inflammation causes increased energy demands, resulting in hyperglycolysis and increased lactate uptake. Peripheral stores such as glycogen are mobilized via lactate and gluconeogenesis to support brain glucose needs. Throughout the body, TBI induces a hypermetabolic state characterized by increased protein breakdown and whole-body catabolism. This leads to severe malnutrition if not addressed through specialized nutrition protocols tailored for TBI patients' high protein and calorie requirements.
This document provides a literature review on the metabolic syndrome and the effects of resistance training on risk factors for the metabolic syndrome. It begins with definitions and descriptions of the metabolic syndrome, its components, diagnosis, prevalence, and pathophysiology. It then discusses resistance training and its effects on strength, muscle mass, and disease prevention in the elderly population. The literature review examines the effects of resistance training on insulin resistance, abdominal obesity, blood pressure, lipid profile, and potential mechanisms of effect. It notes inconsistencies in findings and questions about clinical significance. The aim of the study is to investigate the effects of a short-term, high-repetition resistance training protocol on metabolic syndrome risk factors in elderly adults.
Citicoline is a compound that occurs naturally in the human body and is involved in phospholipid synthesis. It has been proposed as a treatment for traumatic brain injury (TBI) due to its various biochemical and pharmacological properties. TBI can cause neurological and cognitive deficits and even death in severe cases. Citicoline may accelerate cerebral edema reabsorption and recovery in moderate to severe TBI patients, resulting in shorter hospital stays and improved outcomes with higher independence rates. While citicoline showed benefits when standards of TBI care were less advanced, its effect was diluted over time with improved care. The available data indicates citicoline can accelerate recovery from TBI through various mechanisms related to injury development.
The IOSR Journal of Pharmacy (IOSRPHR) is an open access online & offline peer reviewed international journal, which publishes innovative research papers, reviews, mini-reviews, short communications and notes dealing with Pharmaceutical Sciences( Pharmaceutical Technology, Pharmaceutics, Biopharmaceutics, Pharmacokinetics, Pharmaceutical/Medicinal Chemistry, Computational Chemistry and Molecular Drug Design, Pharmacognosy & Phytochemistry, Pharmacology, Pharmaceutical Analysis, Pharmacy Practice, Clinical and Hospital Pharmacy, Cell Biology, Genomics and Proteomics, Pharmacogenomics, Bioinformatics and Biotechnology of Pharmaceutical Interest........more details on Aim & Scope).
All manuscripts are subject to rapid peer review. Those of high quality (not previously published and not under consideration for publication in another journal) will be published without delay.
This study evaluated the effects of combining environmental enrichment (EE) and administration of the serotonin receptor agonist 8-OH-DPAT on behavioral recovery and histopathology following experimental traumatic brain injury (TBI) in rats. The study found that both EE and 8-OH-DPAT independently attenuated cell loss and improved motor and cognitive recovery after TBI. Combining the two therapies did not provide additional benefits beyond the individual treatments alone, except for reducing loss of cholinergic neurons more than EE alone. This suggests that combining therapies after TBI may not always yield greater recovery than single treatments.
The document provides information on traumatic brain injury (TBI) and medical nutrition therapy. It begins with an outline and overview of TBI, describing it as a disruption of normal brain function caused by external forces. It then discusses leading causes of TBI like falls and motor vehicle accidents. The document details the pathophysiology of primary and secondary brain damage following TBI. It also outlines the hypermetabolic consequences of TBI and current evidenced-based nutrition recommendations, including early enteral nutrition. Finally, it introduces a 94-year-old female patient admitted with a right-sided subdural hematoma following a ground level fall and provides her medical history, physical exam findings, labs, and vital signs.
The document summarizes guidelines from the Brain Trauma Foundation (BTF) for the management of severe traumatic brain injury (TBI). The BTF released the 4th edition of these guidelines in 2016 to provide evidence-based recommendations for treating severe TBIs. The guidelines provide recommendations on various treatment strategies, such as decompressive craniectomy, hypothermia, hyperosmolar therapy, cerebrospinal fluid drainage, ventilation, anesthetics/sedatives, and monitoring thresholds. Each recommendation is assigned a level depending on the quality of evidence.
This document summarizes recent research on treatments for acute spinal cord injuries. It discusses approaches such as neuroprotection, regeneration, transplantation, and rehabilitation that have been areas of focus. For neuroprotection, it reviews studies on methylprednisolone and other anti-inflammatory strategies. For regeneration, it discusses inhibiting glial scar formation and replacing damaged cells through transplantation of Schwann cells, olfactory ensheathing cells, and neural stem cells. However, it notes that while animal studies show promise for many of these approaches, there remain limitations and no proven therapies currently exist for acute spinal cord injuries.
This document discusses traumatic brain injury (TBI), including definitions, classifications, symptoms, diagnostic criteria, rating scales, pathology, causes, risk factors, guidelines for management, prognostic factors, complications, rehabilitation programs, and prevention. It defines TBI as an injury to the brain caused by external forces and classifies TBIs as mild, moderate, severe or persistent vegetative state based on factors like loss of consciousness and Glasgow Coma Scale scores. Rating scales discussed include Glasgow Coma Scale, Glasgow Outcome Scale, and Rancho Los Amigos levels. Causes include falls, road traffic accidents, violence and other injuries. Risk factors include age, gender, socioeconomic status and child abuse. Guidelines are provided for management and rehabilitation
Epidemiology and outcome of mild TBI / concussion – Indian and international ...Amit Agrawal
1) Traumatic brain injury (TBI) is a global health problem, with mild TBI (mTBI) accounting for 70-90% of cases. mTBI is associated with a variety of cognitive, somatic, and emotional symptoms.
2) While most patients resume normal function within weeks of an mTBI, about 15% have persistent symptoms at one year. Non-injury factors like depression or litigation are associated with poorer outcomes.
3) Defining and diagnosing mTBI poses challenges due to a lack of baseline data, objective measures, and the multitude of non-injury influences. Further research is needed on predictors of recovery timelines and outcomes after mTBI
8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
ABDOMINAL TRAUMA in pediatrics part one.drhasanrajab
Abdominal trauma in pediatrics refers to injuries or damage to the abdominal organs in children. It can occur due to various causes such as falls, motor vehicle accidents, sports-related injuries, and physical abuse. Children are more vulnerable to abdominal trauma due to their unique anatomical and physiological characteristics. Signs and symptoms include abdominal pain, tenderness, distension, vomiting, and signs of shock. Diagnosis involves physical examination, imaging studies, and laboratory tests. Management depends on the severity and may involve conservative treatment or surgical intervention. Prevention is crucial in reducing the incidence of abdominal trauma in children.
Here is the updated list of Top Best Ayurvedic medicine for Gas and Indigestion and those are Gas-O-Go Syp for Dyspepsia | Lavizyme Syrup for Acidity | Yumzyme Hepatoprotective Capsules etc
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by...Donc Test
TEST BANK For Community Health Nursing A Canadian Perspective, 5th Edition by Stamler, Verified Chapters 1 - 33, Complete Newest Version Community Health Nursing A Canadian Perspective, 5th Edition by Stamler, Verified Chapters 1 - 33, Complete Newest Version Community Health Nursing A Canadian Perspective, 5th Edition by Stamler Community Health Nursing A Canadian Perspective, 5th Edition TEST BANK by Stamler Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Pdf Chapters Download Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Pdf Download Stuvia Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Study Guide Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Ebook Download Stuvia Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Questions and Answers Quizlet Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Studocu Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Quizlet Test Bank For Community Health Nursing A Canadian Perspective, 5th Edition Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Pdf Chapters Download Community Health Nursing A Canadian Perspective, 5th Edition Pdf Download Course Hero Community Health Nursing A Canadian Perspective, 5th Edition Answers Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Ebook Download Course hero Community Health Nursing A Canadian Perspective, 5th Edition Questions and Answers Community Health Nursing A Canadian Perspective, 5th Edition Studocu Community Health Nursing A Canadian Perspective, 5th Edition Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Pdf Chapters Download Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Pdf Download Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Study Guide Questions and Answers Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Ebook Download Stuvia Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Questions Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Studocu Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Quizlet Community Health Nursing A Canadian Perspective, 5th Edition Test Bank Stuvia
Muktapishti is a traditional Ayurvedic preparation made from Shoditha Mukta (Purified Pearl), is believed to help regulate thyroid function and reduce symptoms of hyperthyroidism due to its cooling and balancing properties. Clinical evidence on its efficacy remains limited, necessitating further research to validate its therapeutic benefits.
share - Lions, tigers, AI and health misinformation, oh my!.pptxTina Purnat
• Pitfalls and pivots needed to use AI effectively in public health
• Evidence-based strategies to address health misinformation effectively
• Building trust with communities online and offline
• Equipping health professionals to address questions, concerns and health misinformation
• Assessing risk and mitigating harm from adverse health narratives in communities, health workforce and health system
2. Outline
● What is TBI?
● Epidemiology
● Pathophysiology
● Current Treatments and Focus
● Ketogenic Diets and Ketones
● TBI Studies using KD
● Other Fuel Sources
● Other Nutritional and Lifestyle Considerations
● Taking it to the Clinic and Potential Problems
3. What is TBI?
● Traumatic Brain Injury (TBI) is defined as an impact, penetration, or rapid
movement of the brain within the skull that results in an altered mental state
(Prins et al 2013)
● TBI is a very heterogenous disease (Kabadi and Faden 2014)
○ Every injury results from a unique set of circumstances (Meaney et al. 2014)
○ This leads to differences in severity and type of injury
○ Pre-injury conditions affect pathophysiology and outcome (UpToDate)
4. What is TBI?
● Generally TBI is classified by severity and injury type(UpToDate)
○ Mild (13-15), Moderate (9-12), and Severe (<8) by Glasgow Coma Scale
○ Concussion is often used synonymously with mild TBI (mTBI) but probably describes a subset of
milder brain injury
○ Diffuse or local, impact or nonimpact, closed or penetrating, blast related
5. What is TBI?
● Symptoms
○ mTBI is characterized by confusion and amnesia +/- preceding L.O.C.
○ Early: headache, dizziness, lack of awareness of surroundings, and nausea and vomiting
○ Late: mood and cognitive disturbances, sensitivity to light and noise, and sleep disturbances
(Post concussion syndrome)
○ Moderate and Severe TBI- persistent headache, focal neurologic symptoms, coma, problems
with speech and language, vision and other sensory perception, movement and balance
(Barkhoudarian et al. 2011)
6. What is TBI?
● Mild TBI usually has full recovery
● Moderate and Severe TBI are associated with permanent neurologic and
functional impairments
● Chronic disability due to TBI is common with a prevalence of 3.2-5.3 million
● TBI survivors can suffer from cognitive, behavioral, emotional,
endocrinological, and physical deficits
● Only 25% of survivors of severe TBI achieve long-term functional
independence
(UpToDate)
7. Epidemiology
● 1.74 million people
sustain a TBI in the
US every year
● The majority are of
TBIs are mild (75-
95%)
● Most prevalent cause
of death for those
under 45 and most
common cause of
long term disability
(CDC.GOV)
(UpToDate)
8. Epidemiology
● TBI caused by sports and military service are gaining attention more recently
due to:
○ TBI being considered the signature wound from Afghanistan and Iraq
conflicts
○ The link between sports related concussions and CTE
(Kabadi and Faden 2014, Hiebert et al. 2015)
9. Epidemiology
● The annual incidence of sports related concussions in the US is 1.6 to 3.8
million (Barkhoudarian et al. 2011)
● These numbers are likely underestimated as many cases go unreported
(Meaney et al. 2014)
● The likelihood of an athlete sustaining a concussion is as high as 20% per
season (UpToDate)
● There exists an opportunity for a second insult
10. Epidemiology
● From a survey of returning Iraq War vets, 5% reported injuries with loss of
consciousness and 10% with altered consciousness (UpToDate)
● The severity of combat related TBI tends to be higher compared to civilian
(Meaney et al. 2014)
● 67% of TBI injuries requiring hospitalization in US military operations in Iraq
and Afghanistan were from explosions (Meaney et al. 2014)
11. Pathophysiology of TBI
● Primary injury consists of the mechanical damage that happens at the time of
impact (or transfer of force)
● These forces tend to occur within 100 ms
● Shearing, stretching or compaction of axons and disruption of cell membranes
● Vascular injury which can cause intracerebral bleeding and hematoma
formation
● Focal: Vascular injury, Contusions, Lacerations
● Diffuse: Diffuse Axonal Injury (DAI)
(Mustafa and Al-Shboul 2013)
12.
13.
14.
15. TBI
Pathophysiology
● Mechanoporation and opening
of K+
channels leads to K+
efflux
and depolarization
● Release of excitatory amino
acids, especially glutamate
● Activation of receptors,
particularly NMDARs which
allow Ca2+
influx as well as K+
efflux (feedback loop)
● Spreading depression
(neurologic deficits)
● Ca2+
is sequestered by
mitochondria which induces
oxidative stress and causes
mitochondrial dysfunction
(Barkhoudarian et al. 2011)
16. TBI
Pathophysiology
● Ca2+
also activates many
enzymes that increase oxidative
free radical production and
impair cytoskeletal integrity
● Increased ATP demand to
restore ionic homeostasis,
period of hyperglycolysis
● Decreased ATP production due
to defects in glycolysis and
mitochondrial dysfunction
● Leads to energy crisis and if
severe ultimately apoptosis
(Barkhoudarian et al. 2011)
17. TBI
Pathophysiology
● Hypometabolic state caused by:
○ Decreased glucose
uptake
○ Decreased glycolytic
processing (decreased
hexokinase, GAPDH, and
PDH activity)
○ Shunting to reparative
pentose phosphate
pathway
○ Decrease in ATP
production due to
damage of ETC
complexes
○ Increase in oxidative
damage
(Prins and Matsumoto 2014)
18. TBI
Pathophysiology
● Initial hypermetabolic
period followed by
prolonged metabolic
depression
● Prolonged increase in Ca2+
● Prolonged reduction in
blood flow
● Metabolic recovery time
correlates with severity of
injury and age
● Moderate and severe TBI
may take 2 weeks to
several months
(MacFarlane and Glenn 2015)
19. Current Treatments and Pipeline
● There are very few treatments for TBI
● The current focus is on:
○ Controlling CBF by reducing ICP
○ Preventing hypotension or hypoxia
○ Managing temperature and blood glucose
○ Preventing infection and seizures
● Surgical interventions exist for hematomas, penetrating injuries and depressed
skull fracture
● Neuroprotection is a huge field of study but clinical translation has been poor
(Algattas and Huang 2014, Kabadi and Faden 2014, Stocchetti et al 2015)
○ HBOT and Hypothermia- animal studies were positive but clinical trials are weak and mixed
○ Other failures include EPO, Magnesium, Progesterone, Citicoline
21. What Should We Target Instead?
● Multitargeted approach will likely translate better (Kabadi and Faden 2014)
● Consensus is that neuroinflammation, free radical formation and metabolic
dysfunction are key determinants of outcome (Gajavelli et al. 2014)
● Mitochondria have been shown to be a key participant in TBI pathophysiology
(Gajavelli et al. 2014, Yokobori et al. 2014, Hiebert et al. 2015)
● Even when hypoxia, hypotension, and low CBF are “corrected” there is still
substantial damage from other mechanisms (Bouzat et al. 2013, Jalloh et al. 2015)
● Decreased cerebral metabolism is a consistent finding after TBI and associated
with poor outcomes (Bouzat et al. 2013)
● Markers of mitochondrial dysfunction through microdialysis (lactate, pyruvate,
and glucose) and MRS (NAA) correlate with severity and outcome (Gajavelli et al. 2014,
Yokobori et al. 2014)
23. Ketogenic diets and Ketone bodies
● Ketones are byproducts of fat metabolism produced during times of fasting or
starvation
● They are also produced when carbohydrates in the diet are severely restricted,
these are called ketogenic diets (KD)
● There are 3 main ketone bodies Beta-Hydroxybutyrate, Acetoacetate, and
Acetone.
● Ketone bodies enter the TCA cycle through conversion to Acetyl-CoA to
produce ATP
● Ketones can supply significant amount of brain’s energy demand
(Gano et al. 2014)
26. Established Mechanisms of KD in Neurologic Disease
● Shown to be neuroprotective in models of epilepsy and other neurologic
disease
● Ketones provide an alternative energy substrate
● Reverse mitochondrial dysfunction, stimulate mitochondrial biogenesis and
mitophagy
● KD and ketone bodies have been shown to reduce oxidative stress
● Decrease apoptosis
● Anti-inflammatory
● Increases CBF
● Reduces seizure threshold and changes balance of neurotransmitters
(Maalouf et al. 2009, Gano et al. 2014)
28. KD in TBI: Animal Studies
● These findings are from studies that have been done with multiple injury model
types and ages of rat
● Behaviorally KDs increase motor function and cognitive function after TBI
● KDs reduce lesion volume and edema
● Decrease number of apoptotic cells
● Decrease pro-apoptotic proteins such as BAX and Cytochrome C release
● Increase levels of ATP, creatinine, phosphocreatinine and normalizes NAA and
lactate
● Increase activity of ETC complex 2-3, bypass defects in complex 1
(White and Venkatesh 2011, Prins and Matsumoto 2014)
29. KD in TBI: Animal Studies
● Decrease markers of oxidative stress
● Increase levels of endogenous antioxidants
● Increase latency to seizure
● Protect against a second insult
● However one recent study showed that BHB did not prevent the BBB damage
after TBI (Orhan et al. 2016)
(White and Venkatesh 2011, Prins and Matsumoto 2014)
30. KD in TBI: Animal Studies
● However many of these findings are age dependent
● The neuroprotective effects are not seen as robustly in adult animals
● TBI physiology itself changes with age, the metabolic changes last longer
● KDs take longer to produce ketones in adults
● Older animals take longer to produces MCTs which transport ketone into the
brain
(Prins and Matsumoto 2014, Prins and Matsumoto 2014b)
31. KD in TBI: Human Studies
● There is only one published study in humans
● Ritter et al. placed 20 head injury patients on a carbohydrate free diet (KD) (Ritter
et al. 1996)
● Patients on the KD had stable blood sugar, lower blood lactate, and better
nitrogen balance
● However clinical outcomes were not reported on
● There is an ongoing clinical trial in pediatric TBI patients run by Matsumoto
○ ClinicalTrials.gov Identifier: NCT02174016
○ Estimated Primary Completion Date: December 2016
(White and Venkatesh 2011, Prins and Matsumoto 2014)
32.
33. Other Fuels: Lactate, Pyruvate, Glucose
● New data indicates that lactate, directly and indirectly, is the primary fuel after
brain injury
● Lactate-animal and human studies have been positive, multiple pleiotropic
effects similar to ketones
● Pyruvate- animal studies have been positive but safety is questionable, is also
converted to lactate
● Glucose- post TBI hyperglycemia is beneficial, neutral or harmful depending on
the study
● However no adverse effects with exogenous glucose in animal or human
studies
(Prins et al 2013, Brooks and Martin 2015, Glenn et al 2015, Glenn et al 2015b)
34. Other Nutritional Aspects
● Adequate calories-recommendation is full feeding within 7 days, TBI leads to a
catabolic state (UpToDate, Brooks and Martin 2015)
● Omega 3s- contribute to the fluidity of function of neural and synaptic
membranes
● Have demonstrated benefit in animal studies of TBI
● May reduce inflammation, increase neurotrophic factors, improve
mitochondrial function
● Improved learning and cognition on animal models of TBI
● No human trials, but 2 are currently recruiting for pediatric mTBI
(Pillsbury et al 2011, Prins and Matsumoto 2014)
35. Other Nutritional Aspects
● Acetyl-L-Carnitine-improved behavioral outcome and decreased lesion volume
in animal model of TBI (Scafidi et al., 2010)
● Zinc-Patients with TBI are at higher risk for developing zinc deficiency.
However zinc supplementation studies haven’t been positive
● Choline
● Creatine
● Vitamin D
● Antioxidants-Vit C, Vit E, CoQ10
● Phytochemicals-Resveratrol, Curcumin
(Pillsbury et al 2011)
36. Other Lifestyle Factors: Exercise and Fasting
● Preconditioning with exercise may provide protection against ischemic injury
(Yokobori et al. 2013)
● Delayed exercise has been shown to improve outcomes in animal studies (Kabadi
and Faden 2014, Hiebert et al. 2015)
● Similarly intermittent fasting and caloric restriction are known to be
neuroprotective in many models of neurologic disease including TBI (Maalouf et al
2009, Pani 2015)
37. Bench to Bedside: Taking This to the Clinic
● KD is already established for epilepsy so it would be easier to implement
● Ketone salts are available and esters are in the pipeline
● The problem is how and when to initiate it, hard to translate from animal data
● Will it work in adults as well? can we improve it with fasting or using ketone
salts and esters
● Combine with lactate?
● How much evidence do we need? Is what we already have actionable?
● Pretreatment for athletes and military?
(White and Venkatesh 2011, Prins and Matsumoto 2014)
38. Potential Problems with KD
● In human trials high doses of ketone esters caused serious GI side effects,
headache, and dizziness
● Ketone salt solutions are alkalizing and a large sodium load
● Exogenous ketones may stimulate insulin release and inhibit hepatic
ketogenesis
● KD have the potential for hypoglycemia, excessive acidosis, GERD,
nephrolithiasis, increased in uric acid and hypercholesterolemia
● Prolonged use had been associated with growth retardations, obesity, nutrient
deficiency, decreased bone density, hepatic failure, and immune dysfunction
● Reports of dilated cardiomyopathy on KD
(White and Venkatesh 2011, Prins and Matsumoto 2014)
39. Summary
● TBI is the number one cause of death and chronic disability in those under 45
● There are few current treatment options and a failure to translate animal
research
● Metabolic dysfunction is a key part of TBI pathophysiology currently not
addressed
● Ketogenic diets and ketones have been shown to be neuroprotective because
they address metabolic dysfunction, and so much more
● The animal data for KD in TBI is very promising but is age dependent
● Human trials are desperately needed
41. References
Abdul-Muneer, P. M., Namas Chandra, and James Haorah.
2015. “Interactions of Oxidative Stress and Neurovascular
Inflammation in the Pathogenesis of Traumatic Brain Injury.”
Molecular Neurobiology 51 (3). Springer: 966–79.
Algattas, Hanna, and Jason H. Huang. 2014. “Traumatic
Brain Injury Pathophysiology and Treatments: Early,
Intermediate, and Late Phases Post-Injury.” International
Journal of Molecular Sciences 15 (1): 309–41.
Appelberg, K. Sofia, David A. Hovda, and Mayumi L. Prins.
2009. “The Effects of a Ketogenic Diet on Behavioral
Outcome after Controlled Cortical Impact Injury in the
Juvenile and Adult Rat.” Journal of Neurotrauma 26 (4): 497–
506.
Barkhoudarian, Garni, David A. Hovda, and Christopher C.
Giza. 2011. “The Molecular Pathophysiology of Concussive
Brain Injury.” Clinics in Sports Medicine 30 (1). Elsevier: 33–
48, vii – iii.
Biros, M. H., and R. Nordness. 1996. “Effects of Chemical
Pretreatment on Posttraumatic Cortical Edema in the Rat.”
The American Journal of Emergency Medicine 14 (1).
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