approach to neurologic illness in medical ICU
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The document summarizes evaluation and management of comatose patients in non-neurological intensive care units. It discusses clinical history taking, physical examination findings including vital signs, neurological examination, differential diagnosis of various causes of coma including metabolic, structural, medical conditions and those related to specific ICU settings. It also covers prognosis evaluation and management of conditions like brain death.
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This document discusses coma in non-neurological intensive care units. It covers various clinical assessments and differential diagnoses for comatose patients in ICUs. Key points include evaluating a patient's vital signs, neurological exam findings, potential precipitating medical conditions and distinguishing between metabolic/structural causes of coma. Common primary and secondary central nervous system processes that can lead to coma in medical and surgical ICUs are also outlined.
Management of hemiplegia
for downloading go to
http://medicalpresentation.blogspot.in/2012/09/clinical-approach-to-hemiplegia.html
Approach to a_patient_presenting_with_hemiplegia
1) A 60-year-old man presented with sudden onset right-sided hemiplegia upon waking.
2) On examination, he had right-sided weakness and sensory loss consistent with involvement of the left middle cerebral artery territory.
3) Brain imaging revealed an acute ischemic stroke in the left middle cerebral artery distribution, likely due to thrombotic occlusion of that vessel.
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Approach to hemiplegia
1. Hemiplegia is defined as weakness or paralysis of one side of the body caused by an upper motor neuron lesion above C5 in the pyramidal motor pathway.
2. Common causes of hemiplegia include vascular (85% ischemic, 15% hemorrhagic), tumors, head injuries, demyelinating diseases like multiple sclerosis, and metabolic disorders.
3. The clinical presentation depends on the cause and location of the lesion. Lesions in the internal capsule typically cause contralateral hemiplegia and hemisensory loss with facial and hypoglossal weakness on the same side.
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Haemorrhagic blood diseases: purpura, haemophilia.
Anticoagulants.
Trauma to the head: commonest of subdural haematoma.
II. Infective: ;
Encephalitis
Meningitis – Brain abscess.
III. Neoplastic: e.g. Meningioma.
IV. Demyelination: multiple sclerosis may present with hemiplegia.
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VI. Hysterical: patient suffering from paralysis in the absence of organic lesion.
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neurological illness in ICU
This document discusses coma in non-neurological intensive care units. It covers various clinical assessments and differential diagnoses for comatose patients in ICUs. Key points include evaluating a patient's vital signs, neurological exam findings, potential precipitating medical conditions and distinguishing between metabolic/structural causes of coma. Common primary and secondary central nervous system processes that can lead to coma in medical and surgical ICUs are also outlined.
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for downloading go to
http://medicalpresentation.blogspot.in/2012/09/clinical-approach-to-hemiplegia.html
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1) A 60-year-old man presented with sudden onset right-sided hemiplegia upon waking.
2) On examination, he had right-sided weakness and sensory loss consistent with involvement of the left middle cerebral artery territory.
3) Brain imaging revealed an acute ischemic stroke in the left middle cerebral artery distribution, likely due to thrombotic occlusion of that vessel.
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Approach to hemiplegia
1. Hemiplegia is defined as weakness or paralysis of one side of the body caused by an upper motor neuron lesion above C5 in the pyramidal motor pathway.
2. Common causes of hemiplegia include vascular (85% ischemic, 15% hemorrhagic), tumors, head injuries, demyelinating diseases like multiple sclerosis, and metabolic disorders.
3. The clinical presentation depends on the cause and location of the lesion. Lesions in the internal capsule typically cause contralateral hemiplegia and hemisensory loss with facial and hypoglossal weakness on the same side.
Hemiplegia
Hemiparesis is unilateral paresis, that is, weakness of the entire left or right side of the body (hemi- means "half"). Hemiplegia is, in its most severe form, complete paralysis of half of the body. Hemiparesis and hemiplegia can be caused by different medical conditions, including congenital causes, trauma, tumors, or stroke
Hypenension: Commonest cause of intracerebral haemorrhage.
Rupture of an intracranial aneurysm, angioma or A-V malformation: commonest cause of subarachnoid haemorrhage.
Haemorrhagic blood diseases: purpura, haemophilia.
Anticoagulants.
Trauma to the head: commonest of subdural haematoma.
II. Infective: ;
Encephalitis
Meningitis – Brain abscess.
III. Neoplastic: e.g. Meningioma.
IV. Demyelination: multiple sclerosis may present with hemiplegia.
V. Traumatic: e.g. Cerebral laceration and subdural haematoma.
VI. Hysterical: patient suffering from paralysis in the absence of organic lesion.
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Stroke is an emergency condition caused by a blocked artery or burst blood vessel in the brain. It can lead to serious disability or death if brain cells are not quickly treated. The main types of stroke are ischemic, caused by a blockage, and hemorrhagic, caused by a burst blood vessel. Timely treatment is critical to minimize brain cell death and damage. Management involves stabilizing vital functions, rapidly diagnosing the type of stroke, and administering appropriate treatments such as clot-busting drugs to reduce disability. A multidisciplinary approach is needed for long-term care and rehabilitation.
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This document discusses hemiplegia, which is total paralysis of one side of the body. Common causes include stroke, brain injury, and neurological conditions. Clinically, it presents with weakness, spasms, gait difficulties, and problems with activities of daily living. The pathogenesis involves damage to motor pathways in the brain that control the opposite side of the body. Diagnosis involves imaging and blood tests. Treatment includes medications, surgery, and long-term physical therapy focusing on range of motion, strengthening, mobility, and functional activities. The goals are to restore abilities, prevent complications, and improve quality of life.
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The document discusses stroke, including its definition, causes, risk factors, symptoms, assessment, recovery stages, and complications. Key points include:
- Stroke is defined as sudden neurological dysfunction due to abnormal cerebral circulation lasting over 24 hours.
- Common causes include atherosclerosis, cerebral thrombus, embolism from the heart.
- Risk factors include hypertension, diabetes, heart disease, smoking, obesity.
- Symptoms can include weakness, numbness, vision issues, speech problems.
- Recovery is assessed based on severity, duration, and affected brain region. Complications can include contractures, seizures, DVT.
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This document discusses various causes and presentations of pediatric stroke. Some key points:
- Arterial ischemic stroke and cerebral venous thrombosis have incidences of 5/100,000/yr and 1 in 2000 newborns respectively. Neonates have a higher risk than older children.
- Common causes of pediatric stroke include cardioembolism from congenital heart defects, arteriopathies like moyamoya disease, hematologic disorders like sickle cell anemia, and various genetic/metabolic conditions.
- Presentations depend on age but can include seizures, motor deficits, headaches, and decreased consciousness. Diagnosis involves imaging like MRI/MRA while treatment depends on the underlying cause but may include
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1) Pediatric strokes account for less than 5% of all strokes and affect 2-3 in 100,000 newborns and 12 in 100,000 children under 18 years of age. The annual incidence of pediatric strokes is reported to be between 2.5-2.7 per 100,000 children.
2) Risk factors for pediatric strokes include congenital heart defects, sickle cell anemia, coagulation disorders, and other conditions.
3) Prognosis after a pediatric stroke varies depending on the underlying cause, with 80% of children surviving 10 years after an ischemic stroke though most have residual hemiparesis. Hemorrhagic strokes carry a higher mortality risk than ischemic strokes.
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This document provides guidance on evaluating and managing comatose patients. It outlines the following key steps:
1. Ensure airway, breathing and circulation are stabilized. Treat any rapidly reversible causes of coma like hypoglycemia.
2. Use the Glasgow Coma Scale to assess the level of consciousness. Common causes of coma include head injuries, strokes, infections, tumors, and metabolic derangements.
3. Perform a full neurological exam including pupil size and response, motor function, and posture. Request diagnostic tests like bloodwork and CT or MRI as indicated.
4. Manage increased intracranial pressure with osmotic diuretics if present. Treat any identifiable structural or metabolic causes. Monitor
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The document provides an overview of the approach to evaluating and managing patients presenting with coma. It discusses the components of consciousness, relevant anatomy, disorders of consciousness, and a general clinical approach involving taking a history, performing a general and neurological examination to assess level of arousal, brainstem reflexes, and Glasgow Coma Scale. The examination aims to determine the cause of coma and guide immediate management of airway, breathing, and circulation issues.
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Stroke is caused by interrupted blood flow to the brain and can be ischemic (blockage of blood flow) or hemorrhagic (bleeding in the brain). The main symptoms include sudden weakness or numbness, trouble speaking or understanding, vision changes, and severe headache. Risk factors include high blood pressure, smoking, diabetes, obesity, high cholesterol, and atrial fibrillation. Diagnosis involves CT or MRI imaging of the brain along with medical history and exam. Treatment depends on the type of stroke but may include managing blood pressure, anticoagulants, surgery to repair burst blood vessels, and rehabilitation therapy.
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This document discusses systemic diseases that can cause central and peripheral nervous system disorders. It provides details on the nervous system anatomy and describes various types of neuropathies. Common causes of neuropathies discussed include diabetes, renal failure, electrolyte imbalances, connective tissue diseases, vitamin deficiencies, infections, and malignancies. The effects of these conditions and recommended diagnostic tests and treatments are summarized.
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Primary central nervous system vasculitis (PACNS) is a rare disorder characterized by inflammation of blood vessels within the brain and spinal cord. It can be classified as granulomatous or atypical based on biopsy findings. Common symptoms include headache, seizures, strokes, and cognitive or neurological deficits. Diagnosis involves neuroimaging showing vessel inflammation or infarction, and ruling out other causes. Treatment is typically high-dose corticosteroids. Other CNS vasculitides can be secondary to infections like varicella zoster virus or systemic conditions like giant cell arteritis that affect larger vessels. Reversible cerebral vasoconstriction syndrome is a related disorder of reversible cerebral artery constriction causing similar symptoms.
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The document discusses cerebrovascular diseases, focusing on ischemic and hemorrhagic stroke. It defines stroke, outlines the pathophysiology of ischemic stroke including necrotic and apoptotic pathways, and describes approaches to diagnosis and treatment. Treatment options for ischemic stroke include medical support to optimize cerebral perfusion, IV thrombolysis with rtPA within 3-4.5 hours, and endovascular techniques to restore blood flow and save ischemic penumbra.
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This document discusses hemiplegia, which is total paralysis of one side of the body. Common causes include stroke, brain injury, and neurological conditions. Clinically, it presents with weakness, spasms, gait difficulties, and problems with activities of daily living. The pathogenesis involves damage to motor pathways in the brain that control the opposite side of the body. Diagnosis involves imaging and blood tests. Treatment includes medications, surgery, and long-term physical therapy focusing on range of motion, strengthening, mobility, and functional activities. The goals are to restore abilities, prevent complications, and improve quality of life.
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Hemiplegia is the total paralysis of one side of the body that can be caused by stroke, head trauma, brain tumors, or other neurological conditions. It is characterized by an inability to voluntarily move the arm, leg, and trunk on the same side of the body. Symptoms vary but can include difficulties with walking, balance, grasping objects, muscle stiffness, spasms, and speech or swallowing. Treatment involves rehabilitation to help regain motor function through exercises and may include pharmacological interventions or surgery depending on the underlying cause.
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A cerebrovascular accident (CVA), also known as a stroke, occurs when blood flow to an area of the brain is interrupted, depriving brain tissue of oxygen and nutrients. This can be caused by a blood clot blocking an artery (thrombosis), bleeding within the brain (hemorrhage), or a blood clot traveling from another part of the body and lodging in the brain (embolism). Symptoms depend on the area of brain affected but may include weakness, numbness, vision issues, difficulty speaking, and more. Recovery depends on the severity and location of damage, with potential outcomes including permanent disability or recurrent strokes.
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A cerebrovascular accident (CVA), also known as a stroke, is caused by the loss of blood flow to an area of the brain resulting in cell death. It is a leading cause of death and disability. The majority of strokes are ischemic and caused by blockage of an artery by a clot or debris. Hemorrhagic strokes occur when a blood vessel ruptures, causing bleeding into or around the brain. Treatment focuses on prevention through risk factor control as well as acute interventions like clot-busting drugs. Rehabilitation aims to maximize recovery of function and independence.
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The document discusses stroke, including its definition, causes, risk factors, symptoms, assessment, recovery stages, and complications. Key points include:
- Stroke is defined as sudden neurological dysfunction due to abnormal cerebral circulation lasting over 24 hours.
- Common causes include atherosclerosis, cerebral thrombus, embolism from the heart.
- Risk factors include hypertension, diabetes, heart disease, smoking, obesity.
- Symptoms can include weakness, numbness, vision issues, speech problems.
- Recovery is assessed based on severity, duration, and affected brain region. Complications can include contractures, seizures, DVT.
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This presentation looks at some of the common conditions that can present with hemiplegia. Stroke is the commonest, however, there are several other causes that need to be considered in a patient presenting with hemiplegia.
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This document discusses paediatric stroke, including its causes, presentation, diagnosis, and management. The main types of paediatric stroke are arterial ischemic stroke, cerebral sinovenous thrombosis, and hemorrhagic stroke. Common causes include arteriopathy, cardiac issues, hematologic disorders, and perinatal factors. Clinical presentation depends on the age of onset. Diagnosis involves neuroimaging such as MRI. Management is often supportive but may include anticoagulation, revascularization procedures, or transfusions depending on the underlying condition. Prognosis depends on factors like age of onset and severity of neurological deficits.
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This document summarizes cerebrovascular disease and stroke. Stroke is the third leading cause of death and a common cause of disability. Imaging such as CT and MRI are used to distinguish between ischemic and hemorrhagic stroke and identify underlying vascular abnormalities. Risk factors include age, hypertension, cardiac sources of embolism, and other conditions. Treatment aims to reverse pathology, prevent complications, and reduce risk of further strokes.
stroke in pediatric population
This document discusses various causes and presentations of pediatric stroke. Some key points:
- Arterial ischemic stroke and cerebral venous thrombosis have incidences of 5/100,000/yr and 1 in 2000 newborns respectively. Neonates have a higher risk than older children.
- Common causes of pediatric stroke include cardioembolism from congenital heart defects, arteriopathies like moyamoya disease, hematologic disorders like sickle cell anemia, and various genetic/metabolic conditions.
- Presentations depend on age but can include seizures, motor deficits, headaches, and decreased consciousness. Diagnosis involves imaging like MRI/MRA while treatment depends on the underlying cause but may include
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1) Pediatric strokes account for less than 5% of all strokes and affect 2-3 in 100,000 newborns and 12 in 100,000 children under 18 years of age. The annual incidence of pediatric strokes is reported to be between 2.5-2.7 per 100,000 children.
2) Risk factors for pediatric strokes include congenital heart defects, sickle cell anemia, coagulation disorders, and other conditions.
3) Prognosis after a pediatric stroke varies depending on the underlying cause, with 80% of children surviving 10 years after an ischemic stroke though most have residual hemiparesis. Hemorrhagic strokes carry a higher mortality risk than ischemic strokes.
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The document provides an overview of the approach to evaluating and managing patients presenting with coma. It discusses the components of consciousness, relevant anatomy, disorders of consciousness, and a general clinical approach involving taking a history, performing a general and neurological examination to assess level of arousal, brainstem reflexes, and Glasgow Coma Scale. The examination aims to determine the cause of coma and guide immediate management of airway, breathing, and circulation issues.
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This document discusses altered mental status and coma. It describes different levels of consciousness including light coma and deep coma. The Glasgow Coma Scale is introduced as a tool to assess a patient's level of consciousness based on their eye, verbal, and motor responses. Common causes of altered mental status are summarized using the AEIOU TIPS mnemonic, covering factors like alcohol, electrolyte imbalances, infections, and trauma. Clinical presentations and emergency treatments including airway management, glucose administration, and antidotes for overdoses are outlined.
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The document provides guidance on approaching and managing a comatose patient. It outlines that the primary objectives are to stabilize, evaluate, and treat the patient by taking an organized sequential approach that prioritizes the airway, breathing, circulation, treating metabolic causes of coma like hypoglycemia, and evaluating for increased intracranial pressure or mass lesions. Secondary objectives include understanding the signs and symptoms of different causes of coma and developing a differential diagnosis. The document then provides detailed information on assessing different aspects of the comatose patient including their level of consciousness, neurological exam findings, breathing patterns, eye movements, motor response, and appropriate investigations.
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Similar to approach to neurologic illness in medical ICU
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3) Emergency treatment may include supplemental oxygen, IV thiamine, glucose, and antibiotics depending on suspected causes identified from history and examination.
Evaluating unconciousness in icu
This document discusses consciousness and disorders of consciousness. It begins by explaining that normal consciousness depends on interaction between the cerebral hemispheres and rostral reticular activating system in the brainstem. Disorders that disrupt these areas can cause altered consciousness states like unconsciousness, confusion, delirium, and coma. Coma is defined as an unarousable, unresponsive state. The causes, assessments, and management of disorders of consciousness like coma are then outlined.
Anesthetic management in Pediatric Neuromuscular disorders
This document summarizes the anesthetic management considerations for pediatric patients with various neuromuscular disorders. It discusses cerebral palsy, muscular dystrophies like Duchenne and Becker's, myotonias, mitochondrial myopathies, channelopathies, and malignant hyperthermia. Key points include increased sensitivity to medications, difficult airways, respiratory and cardiac issues, hypothermia risks, and triggering agents for malignant hyperthermia like succinylcholine and inhalational anesthetics. Close monitoring is important due to potential complications in the postoperative period.
Unconcious Paediatric Patient.pptx
This document discusses the management of unconscious patients. It begins with an introduction that defines consciousness and the causes of unconsciousness. It then describes the primary and secondary survey in managing unconscious patients, which involves assessing the airway, breathing, circulation, disability and exposing the patient. Specific treatments depend on the underlying cause, such as giving glucose for hypoglycemia or antibiotics for meningitis. Prognosis depends on factors like the cause, depth and duration of impaired consciousness. The document emphasizes that treatment should precede diagnosis in unconscious patients.
Coma
This document discusses coma, including its definition, causes, and approach to assessment and management. Coma is the deepest state of impaired consciousness where a patient cannot be aroused. Causes include structural brain injuries, infections, metabolic derangements, and drugs. Evaluation of a comatose patient involves assessing vital signs, neurological exam including pupil response and eye movements, investigations like blood tests and imaging, and treatment of reversible causes. Brain death is the complete and irreversible loss of brain function while cardiac and respiratory functions may be maintained artificially.
Acute confusion state & coma
1. Coma is defined as a deep sleep-like state from which the patient cannot be aroused. It can be caused by lesions that damage the reticular activating system in the upper midbrain or its projections, or destruction of a large portion of the cerebral hemisphere.
2. The causes of coma include cerebral mass lesions, metabolic disorders, toxic or drug-induced states, and widespread damage to the cerebral hemispheres.
3. Evaluation of a comatose patient involves assessing their history, performing a neurological examination including assessment of eye movements and motor responses, and ordering investigations such as CT/MRI, EEG, and CSF examination.
Wernicke encephalopathy
Wernicke encephalopathy is caused by thiamine (vitamin B1) deficiency. Thiamine plays a key role in brain energy metabolism. Lack of thiamine can damage brain tissue, especially in regions with high metabolic demand. Common causes include chronic alcoholism, prolonged starvation, pregnancy-related vomiting, and bariatric surgery. Symptoms include confusion, ataxic gait, and eye movement abnormalities. Treatment involves high dose parenteral thiamine supplementation.
Wernickeencephalopathy
Wernicke encephalopathy is caused by thiamine (vitamin B1) deficiency. Thiamine plays a key role in brain energy metabolism. Lack of thiamine can damage brain tissue, especially in regions with high metabolic demand. Common causes include chronic alcoholism, prolonged starvation, pregnancy-related vomiting, and bariatric surgery. Symptoms include confusion, ataxic gait, and eye movement abnormalities. Diagnosis involves clinical assessment and testing for thiamine deficiency. Treatment involves high-dose parenteral thiamine supplementation, which can improve symptoms if administered early.
APPROACH
This document provides an overview of coma, including definitions, terminology, causes, assessment approach, management, and prognosis. It defines coma as a state of unarousable unresponsiveness and discusses related altered states of consciousness like stupor, delirium, and vegetative state. Common causes of coma are categorized as those with focal signs, without focal signs but without meningeal irritation, and without focal signs but with meningeal irritation. The rapid assessment approach is outlined, including stabilization, history, neurological exam, investigations like CT/MRI, and management of identified issues. Prognosis depends on etiology, depth and duration of impaired consciousness, with infectious causes generally having better outcomes than hypoxic-
Hypoxic ischemic encephalopathy: Lecture on HIE
Clinically, more term babies suffered from hypoxic ischemic encephalopathy (HIE) than premature babies. However, pathologically, more premature babies suffered from HIE than term babies. The main clinical manifestations of HIE are symptoms of consciousness, including excitation symptoms like hyperalertness, irritability, and seizures, or depressing symptoms like coma and hypotonia. Management of HIE focuses on monitoring, controlling seizures, general supportive care, and recent advances like therapeutic hypothermia. The prognosis depends on the severity of brain damage and treatment, with mild or moderate cases often recovering completely but severe cases having a high risk of mortality or long-term complications.
Emergency in neurology
1. This document provides guidance on the evaluation and management of patients presenting with coma, transient ischemic attack (TIA), and ischemic stroke.
2. For patients presenting with coma, the assessment involves a detailed history, physical and neurological examination to localize the lesion. Coma etiologies are categorized based on presence of focal signs or meningism.
3. For TIA patients, risk stratification using the ABCD2 score helps determine short term risk of stroke. Acute ischemic stroke is managed with thrombolytic therapy if within 4.5 hours of onset, following strict inclusion/exclusion criteria.
4. Secondary stroke prevention focuses on antiplatelet/anticoagulant drugs based
Diagnostic methods
The document discusses various topics related to neurology including:
1. Common neurological disorders such as headache, low back pain, and stroke.
2. Components of a neurological examination including signs, reflexes, and tests of sensory and motor function.
3. Diagnostic tools used in neurology such as CT, MRI, angiography, EEG, lumbar puncture, and PET.
4. Types of disturbances of consciousness including those caused by brainstem or cortical damage.
5. Criteria for determining brain death.
Management of coma and altered sensorium 19.4.01
This document discusses the management of patients presenting with coma or altered sensorium. Key points include evaluating vital signs and providing emergency treatment to maintain ventilation, circulation, control seizures, and manage intracranial pressure. Further tests such as bloodwork and imaging studies can help identify potential metabolic, structural or toxic causes. Ongoing care focuses on preventing complications through careful monitoring and stimulation techniques.
NEUROLOGICAL MANIFESTION OF RENAL DISEASE
This document summarizes various neurological complications that can occur in patients with renal disease. It discusses central nervous system complications such as encephalopathy, dementia, and cerebrovascular disease. It describes the pathophysiology and treatment of various types of encephalopathy including uremic encephalopathy, Wernicke's encephalopathy, and dialysis encephalopathy. It also discusses peripheral nervous system complications including mononeuropathy, polyneuropathy, and myopathy.
Pathology of Stroke-CVA
The document describes a 62-year-old man named Robert who fell from a ladder while picking mangoes and was found unconscious. He was brought to the emergency department conscious but confused, complaining of left arm pain. His medical history includes hypertension. A physical exam found signs of head injury including a hematoma and neurological deficits on the right side of his body. The summary provides key details about the patient's condition and situation.
MGT. OF A COMATOSE PATIENT.pptx
The document defines coma as a state of unarousable unconsciousness caused by disruption of structures involved in arousal and awareness like the ascending reticular activating system, cortex and thalamus. Coma can result from structural brain damage or diffuse systemic issues. Differentials include intoxication, metabolic disturbances, infections, shock and neurological conditions. Initial assessment focuses on stabilization, identifying reversible causes, monitoring and preventing secondary brain damage. Further assessment involves detailed history, examination and investigations to determine the cause to guide management.
Genetic disorders
This document summarizes several genetic disorders including Down syndrome, Klinefelter's syndrome, Turner syndrome, Marfan syndrome, Ehlers-Danlos syndrome, cystic fibrosis, phenylketonuria, neurofibromatosis, tuberous sclerosis, and Friedreich's ataxia. It describes the genetic causes, characteristic physical features, complications, methods of diagnosis, and treatment options for each condition where relevant. The purpose is to provide an overview of common genetic disorders encountered in clinical practice.
APPROACH TO A PATIENT PRESENTING WITH LIMB WEAKNESS
This document provides an overview of how to approach a patient presenting with limb weakness. It discusses classifying the type of weakness, determining the etiology and risk factors, distinguishing features of upper motor neuron, lower motor neuron, neuromuscular junction, and myopathic weaknesses. It also covers the distribution of weakness, clinical examination, relevant investigations, and management considerations. The case presented involves a 39-year-old man with acute hemorrhagic stroke and hypertensive crisis presenting with right-sided hemiparesis.
Uremic Encephalopathy
Uremic encephalopathy occurs when toxins that are normally cleared by the kidneys build up in the bloodstream due to kidney failure. It causes a range of neurological symptoms from mild issues like fatigue to severe problems like seizures and coma. The condition develops when kidney function declines to the point that creatinine clearance levels fall below 15 mL/min. While the exact cause is unknown, it involves the accumulation of various toxins in the brain that disrupts cell metabolism and function. Prompt treatment with dialysis or kidney transplantation can reverse the neurological symptoms.
Birth asphyxia
This document defines birth asphyxia and discusses its epidemiology, causes, clinical presentation, investigations, management, and prognosis. Birth asphyxia is the inability to initiate breathing at birth and requires resuscitation. It can result from interrupted umbilical circulation, impaired maternal oxygenation, or failure of the neonate to transition to breathing after birth. Clinical presentation may include seizures, abnormal posturing, or hypoxic ischemic encephalopathy. Management involves immediate resuscitation and treatment of seizures and organ dysfunction. Outcomes range from full recovery to death, with prognosis worse with longer neurological symptoms, multi-organ involvement, or advanced hypoxic ischemic encephalopathy.
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Anesthetic management in Pediatric Neuromuscular disorders
Anesthetic management in Pediatric Neuromuscular disorders
APPROACH TO A PATIENT PRESENTING WITH LIMB WEAKNESS
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Repetitive nerve stimulation (RNS) involves electrically stimulating a nerve multiple times and measuring the response of the muscle. It is useful for diagnosing neuromuscular junction disorders. There are two main types - slow RNS at 3-5 Hz and rapid RNS at 20-50 Hz. The test evaluates changes in the compound muscle action potential (CMAP) amplitude between stimuli and with activation maneuvers. Specific patterns of response on RNS can help localize defects as pre-synaptic or post-synaptic. RNS, along with single fiber EMG, are key tests for diagnosing myasthenia gravis and other neuromuscular transmission disorders.
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3. Other conditions like Sjogren's syndrome, systemic lupus erythematosus, Behcet's disease and sarcoidosis can also present with LETM and involve both autoimmune and inflammatory mechanisms. Accur
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Lithium delays progression of amyotrophic lateral sclerosis in mice and humans. In mice, lithium treatment extended survival time, delayed onset of paralysis, and preserved motor neurons and mitochondria. A clinical trial of 44 ALS patients found that those receiving lithium and riluzole (n=16) survived over 15 months compared to 30% mortality in the riluzole-only group (n=38). Lithium also slowed symptom progression as measured by ALS rating scales and preserved lung function compared to riluzole alone. This study suggests lithium can delay disease progression in ALS patients.
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1) Plasma exchange (PE) significantly improves outcomes for patients with Guillain-Barré syndrome compared to supportive care alone based on data from multiple randomized controlled trials. PE results in greater improvement in disability and faster recovery.
2) Intravenous immunoglobulin (IVIg) is as effective as PE based on trials comparing the two treatments, with no significant differences in outcomes.
3) Combining PE and IVIg does not provide additional benefit over either treatment alone.
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Gbs hyperreflexia
This study investigated hyperreflexia in Guillain-Barré syndrome (GBS) and its relation to acute motor axonal neuropathy (AMAN) and anti-GM1 antibodies. The study found that some GBS patients with the AMAN pattern, anti-GM1 antibodies, and milder weakness developed hyperreflexia. Specifically, 33% of AMAN patients showed hyperreflexia compared to 12% of acute inflammatory demyelinating polyneuropathy patients. Hyperreflexia was associated with increased motor neuron excitability. The mechanism is unknown but may involve dysfunction of spinal inhibitory interneurons or upper motor neurons due to anti-GM1 antibodies. Hyperreflexia indicates less severe motor ax
Differential diagnosis of suspected multiple sclerosis
This document presents a consensus approach for the differential diagnosis of suspected multiple sclerosis (MS) developed by an international panel of MS experts. The panel sought to 1) define clinical and paraclinical "red flags" that suggest alternative diagnoses to MS, 2) more precisely define clinically isolated syndromes often the first presentation of MS, 3) provide diagnostic algorithms for common clinically isolated syndromes, and 4) propose consensus criteria for differentiating MS from other inflammatory demyelinating disorders. The panel conducted a literature review and developed consensus recommendations to aid in excluding alternative diagnoses and distinguishing MS from non-MS conditions.
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Artifacts in eeg final
This document discusses different types of artifacts that can appear on an EEG, including how to identify and eliminate them. It separates artifacts into physiological artifacts originating from the patient's body (e.g. eye movements, muscle activity), and extraphysiological artifacts from external sources (e.g. electrodes, equipment, environment). Specific artifact types like blinks, lateral eye movements, muscle activity are described. Guidelines provided on how to reduce artifacts include closing the eyes, relaxing muscles, ensuring good electrode contact, and shielding from environmental interference.
IIcranial nerve
This document provides detailed information about the anatomy and physiology of the visual system, including:
- The major structures of the retina and optic nerve pathway from the retina to the lateral geniculate nucleus.
- The roles of rods and cones in vision and their distribution in the retina.
- Blood supply to the retina and optic nerve structures.
- Projections from the lateral geniculate nucleus to the primary visual cortex and connections to extrastriate visual areas.
- Divisions of the visual fields and how lesions in different parts of the visual pathway present with specific visual field defects.
V isual evoked potentials
The document summarizes visual evoked potentials (VEPs), including:
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- International standards exist for stimulus parameters, recording procedures, and normal values.
- Pattern-reversal VEPs eliciting the P100 wave are most commonly used clinically. Factors like check size, contrast and age affect P100 latency and amplitude.
- Abnormalities suggest defects along the visual pathway from eye to cortex. Multi-channel recordings localize defects pre- or post-chiasm.
Multiple sclerosis and rituximab
This randomized, double-blind, placebo-controlled study evaluated the efficacy and safety of rituximab for relapsing-remitting multiple sclerosis. 104 patients were randomized to receive either rituximab or placebo intravenous infusions. The primary outcome was the number of gadolinium-enhancing lesions on MRI scans from weeks 12-24. Patients receiving rituximab had significantly fewer lesions compared to placebo, indicating rituximab reduces disease activity in multiple sclerosis. Rituximab also decreased relapse rates and reduced lesion volumes on MRI. The most common adverse events were mild to moderate infusion reactions. This study provides evidence that B cell depletion with rituximab is effective and relatively safe for rel
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This document summarizes the pathophysiology and treatment of Parkinson's disease (PD). It notes that PD involves loss of dopaminergic neurons as well as other neurotransmitter systems. Current treatment focuses on dopamine replacement therapy, though neuroprotective strategies are also discussed. A variety of medications are outlined for treating PD at different stages, including levodopa, dopamine agonists, COMT inhibitors, MAO inhibitors, and others. Treatment strategies seek to maximize functioning while minimizing motor complications. Advancing disease often requires more complex medication regimens to manage fluctuations and dyskinesias. Non-motor symptoms and future therapeutic directions are also briefly mentioned.
neurologic presentations of systemic vasculitis
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- Left untreated, TA can cause permanent vision loss. Treatment involves high-dose corticosteroids to suppress inflammation. Prednisone is gradually tapered over months or years to prevent relapses.
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oral drugs in multiple sclerosis
This document summarizes key findings from several clinical trials investigating new oral treatments for multiple sclerosis (MS). The FREEDOMS trial found that fingolimod was more effective than placebo at reducing relapses in MS patients over 24 months. The CLARITY trial showed that short-term treatment with cladribine tablets for 8-20 days per year provided benefits for relapsing-remitting MS. The TRANSFORMS trial found that fingolimod was more effective than weekly intramuscular interferon beta-1a injections at reducing MS symptoms over 12 months. Both new oral therapies showed efficacy advantages compared to existing injectable treatments, but require ongoing monitoring for potential long-term adverse effects.
multiple system atrophy-newer developments
This document summarizes recent insights into multiple system atrophy (MSA). MSA is a neurodegenerative disorder characterized by parkinsonism or cerebellar ataxia along with autonomic failure. Key points include: MSA is caused by the accumulation of alpha-synuclein protein aggregates in oligodendrogltes. Diagnostic criteria have been updated and neuroimaging may help with diagnosis. Prognosis is poor with mean survival of 7-9 years. Current treatments are only symptomatic and no disease-modifying therapies exist yet, though research into targets like alpha-synuclein aggregation are promising avenues.
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- 10. Neuro muscular blockers in ICU renal 137+ 80-100 pipecuronium renal 100+ 90-120 doxacurium renal 240 80-120 tubocurarine hepatic renal 110-140 120-180 pancuronium renal 80-100 30-67 rocuronium hepatic renal 60-130 20-60 vecuronium renal 20 30-40 atracuronium renal 2 12-18 mivacurium hepatic - 60-120 12-17 rapacurium renal -t1/2 5-10min succinylcholine
- 11. Sedatives in ICU Cbf,icp 2-14 ketamine Cbf,icp,cpp 40-50 propofol Cbf, cpp, icp 10-19 haloperidol 48-144 phenobarbitone Cbf,icp,cpp 2-4 thiopental 10 fentanyl Cbf,icp 4-11 morphine 7-10 midazolam 3-7 lorazepam Icp, cbf, 50-120 diazepam
- 15. Abnormal pupillary responses in coma Metabolic encephalopathy, B/l thalamic, pontine lesions, hydrocephalus,narcotics,OP,barbiturates Midbrain damage or compression Seizure Thalamus, sympathetic efferents from posterior hypothalamus, tegmentum, descending to the cervical cord Bilateral small ,reactive b/l dilated and unreactive b/l dilation&reactive Unilateral miosis
- 16. Pupillary responses and coma Compression of ipsilateral III nerve -Fascicular lesion -Nuclear lesion -Extracranial defect T1-T2 to carotid bifurcation -Between hypothalamus and spinal cord -ICA vs cavernous sinus vs SOF vs orbit Unilateral, unreactive & enlarged -unilateral ptosis -bilateral ptosis Unilateral,small,reactive, ipsilateral ptosis -with face anhydrosis -anhydrosis entire side of body -without anhydrosis
- 19. Cerebral herniation :clinical syndromes Decrease consciousness, small & reactive pupils, normal eye movements. Fixed pupils, cheyne stroke respiration, opthalmoplegia, decorticate posturing Initial obstruction hydrocephalus, thalamus, hypothalamus displacement Supra tentorial diffuse brain edema, haemorrage, midline tumors Central herniation Dilated ipsilateral pupil with preserved or sluggish reaction to light. CnIII,ophthalmoplegia,ipsilateral hemipareis Ipsilateral III compression Hemispheric/lateral middle fossa Uncal herniation
- 20. Cerebral herniation clincal syndromes All brainstem reflexes are lost, flaccid paralysis, ataxic respiration, then ceasing Medulla-lower pons, cerebellar tonsils Infra tentorial lesions Foramen magnum herniation Decerebrate posturing, midposition pupils, sometimes irregular and loss of pupillary, oculocephalic and oculo vestibular reflexes Midbrain and upper pons Advanced stage of central herniation, upward infra tentorial lesions Midbrain compression