This document provides information on the differential diagnosis of vertigo from central nervous system causes. It discusses the pathophysiology, clinical presentation, evaluation, and treatment of various central causes of vertigo including migraine, vertebrobasilar insufficiency, cerebellar and brainstem infarction, cerebello-pontine angle tumors, and multiple sclerosis. The clinical history and physical exam aim to localize the lesion, while imaging, vestibular testing, and occasionally lumbar puncture aid diagnosis. Treatment involves managing the underlying condition, controlling risk factors, and using anti-vertigo medications.
Acute thiamine deficiency, also known as Wernicke's encephalopathy, is a neurological disorder most prevalent in males around age 50 with a history of alcoholism or malnutrition. It results from a lack of thiamine (Vitamin B1), which is important for brain cell function. Left untreated, it can lead to Wernicke-Korsakoff syndrome characterized by amnesia and confusion. Treatment involves emergency high dose parenteral thiamine supplementation.
Alcoholism and wernicke korsakoff syndrome treatmentkevinnsmiith
Wernicke-Korsakoff syndrome is a brain disorder caused by a thiamine (Vitamin B1) deficiency commonly found in alcoholics and those with malabsorption issues. It consists of two conditions - Wernicke encephalopathy causes damage to the lower brain, while Korsakoff syndrome causes memory issues. Symptoms include eye problems, confusion, muscle weakness, and inability to form new memories. Treatment involves high dose thiamine injections or supplements as well as detoxification and rehabilitation for alcoholics. Recovery rates vary, with about half recovering partially and a quarter not recovering at all.
Korsakoff's syndrome is a neurological disorder caused by thiamine (Vitamin B1) deficiency, most commonly seen in chronic alcoholics. It damages areas of the brain involved with memory formation. Symptoms include anterograde amnesia (inability to form new memories), retrograde amnesia (loss of existing memories), confabulation (recalling imaginary events), and confusion. Treatment focuses on thiamine supplementation through injections or orally, stopping alcohol use, and a nutritious diet to prevent further damage and support recovery.
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.
Wernicke-Korsakoff syndrome involves two phases - an acute Wernicke encephalopathy phase caused by thiamine (vitamin B1) deficiency, followed by a chronic Korsakoff syndrome phase involving memory impairment. It is commonly seen in alcoholics and involves symptoms like vision changes, unsteady gait, and memory problems. The syndrome results from damage to brain regions including the mammillary bodies and thalamus due to thiamine deficiency.
Demyelinating and Degenerative Disorders of the CNSGhie Santos
This document summarizes various demyelinating and degenerative disorders of the central nervous system (CNS). It discusses diseases that involve preferential damage to myelin such as multiple sclerosis and various leukodystrophies including metachromatic leukodystrophy and Krabbe disease. It also covers degenerative diseases such as Alzheimer's disease, Parkinson's disease, and Huntington's disease that are characterized by selective neuronal loss in specific brain regions. The morphology, pathogenesis, clinical features of each disease are described.
Alzheimer's disease is a progressive brain disorder that destroys memory and thinking skills. It is the most common cause of dementia among older adults. The main risk factor is increasing age, and it results from changes in the brain that affect memory, thinking, and behavior. Symptoms include memory loss and difficulties with problem-solving, planning, and language. It is caused by beta-amyloid plaques and tau tangles that interfere with communication between brain cells. There is no cure for Alzheimer's, but treatments can temporarily slow the worsening of dementia symptoms.
Acute thiamine deficiency, also known as Wernicke's encephalopathy, is a neurological disorder most prevalent in males around age 50 with a history of alcoholism or malnutrition. It results from a lack of thiamine (Vitamin B1), which is important for brain cell function. Left untreated, it can lead to Wernicke-Korsakoff syndrome characterized by amnesia and confusion. Treatment involves emergency high dose parenteral thiamine supplementation.
Alcoholism and wernicke korsakoff syndrome treatmentkevinnsmiith
Wernicke-Korsakoff syndrome is a brain disorder caused by a thiamine (Vitamin B1) deficiency commonly found in alcoholics and those with malabsorption issues. It consists of two conditions - Wernicke encephalopathy causes damage to the lower brain, while Korsakoff syndrome causes memory issues. Symptoms include eye problems, confusion, muscle weakness, and inability to form new memories. Treatment involves high dose thiamine injections or supplements as well as detoxification and rehabilitation for alcoholics. Recovery rates vary, with about half recovering partially and a quarter not recovering at all.
Korsakoff's syndrome is a neurological disorder caused by thiamine (Vitamin B1) deficiency, most commonly seen in chronic alcoholics. It damages areas of the brain involved with memory formation. Symptoms include anterograde amnesia (inability to form new memories), retrograde amnesia (loss of existing memories), confabulation (recalling imaginary events), and confusion. Treatment focuses on thiamine supplementation through injections or orally, stopping alcohol use, and a nutritious diet to prevent further damage and support recovery.
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.
Wernicke-Korsakoff syndrome involves two phases - an acute Wernicke encephalopathy phase caused by thiamine (vitamin B1) deficiency, followed by a chronic Korsakoff syndrome phase involving memory impairment. It is commonly seen in alcoholics and involves symptoms like vision changes, unsteady gait, and memory problems. The syndrome results from damage to brain regions including the mammillary bodies and thalamus due to thiamine deficiency.
Demyelinating and Degenerative Disorders of the CNSGhie Santos
This document summarizes various demyelinating and degenerative disorders of the central nervous system (CNS). It discusses diseases that involve preferential damage to myelin such as multiple sclerosis and various leukodystrophies including metachromatic leukodystrophy and Krabbe disease. It also covers degenerative diseases such as Alzheimer's disease, Parkinson's disease, and Huntington's disease that are characterized by selective neuronal loss in specific brain regions. The morphology, pathogenesis, clinical features of each disease are described.
Alzheimer's disease is a progressive brain disorder that destroys memory and thinking skills. It is the most common cause of dementia among older adults. The main risk factor is increasing age, and it results from changes in the brain that affect memory, thinking, and behavior. Symptoms include memory loss and difficulties with problem-solving, planning, and language. It is caused by beta-amyloid plaques and tau tangles that interfere with communication between brain cells. There is no cure for Alzheimer's, but treatments can temporarily slow the worsening of dementia symptoms.
Guillain-Barre Syndrome is an acute inflammatory disease of the peripheral nerves that commonly presents with muscle weakness following infections like herpes virus or Campylobacter jejuni. It causes ascending muscle weakness and paralysis that begins in the lower extremities and can affect breathing. Treatment involves close respiratory monitoring and may require intubation, as well as plasmapheresis or IVIG.
CNS Tutorial path.Acquired Metabolic Diseases of CNSimrana tanvir
Thiamine deficiency can cause Wernicke encephalopathy, characterized by brain hemorrhaging and necrosis, particularly in the mammillary bodies. Untreated Wernicke encephalopathy can lead to Korsakoff syndrome, marked by memory loss and confabulation. Vitamin B12 deficiency can cause anemia and spinal cord degeneration. Hypoglycemia selectively injures pyramidal neurons in the cortex and hippocampus. Hyperglycemia in uncontrolled diabetes can cause ketoacidosis or hyperosmolar coma, marked by dehydration, confusion and coma.
This document summarizes several demyelinating diseases of the central and peripheral nervous systems. It describes multiple sclerosis as the most common inflammatory demyelinating disease, affecting the brain and spinal cord, with classifications based on disease course. It also discusses central pontine myelinolysis, transverse myelitis, Guillain-Barre syndrome, and chronic inflammatory demyelinating polyneuropathy. For each, it provides details on characteristics, causes, clinical manifestations, diagnosis, and treatment.
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.
Kearns-sayre syndrome is a rare genetic disorder caused by abnormalities in the mitochondria's DNA. It affects people under age 20 and can cause paralysis of eye muscles, retinal degeneration, and weakness/damage of muscles, brain, heart and other organs over time. Doctors diagnose it through tests of protein/lactate levels or muscle biopsy to examine mitochondrial DNA. There is no cure currently, and symptoms worsen over time.
This document provides an overview of various neurological disorders and conditions. It begins by covering peripheral nerve disorders like neuropathy, myasthenia gravis, and muscular dystrophy. It then discusses specific neuropathies including diabetic neuropathy and nerve compression syndromes. Other sections address neurological diseases and disorders such as Guillain-Barre syndrome, multiple sclerosis, Parkinson's disease, stroke, epilepsy, headaches, and neurological infections. For each topic, it provides details on presentation, pathogenesis, clinical features, management, and treatment.
This document discusses various white matter diseases and disorders that can be seen on MRI. It provides details on the typical imaging appearance and characteristics of several leukodystrophies and other white matter conditions, including metachromatic leukodystrophy, adrenoleukodystrophy, Krabbe disease, vanishing white matter disease, maple syrup urine disease, megaloencephalic leukodystrophy, Pelizaeus-Merzbacher disease, mucopolysaccharidoses, Canavan disease, Alexander disease, Zellweger syndrome, and Leigh disease. Common findings discussed are T1 and T2 signal abnormalities, diffusion restriction, enhancement patterns, and metabolic abnormalities on MR spectroscopy.
This document provides a differential diagnosis for coma by classifying potential causes into those without focal signs or abnormal tests, those with meningeal irritation and abnormal CSF, and those with focal brain signs and abnormal imaging. Numerous intoxications, metabolic disturbances, infections, and other conditions are
FA is a very rare, genetic, recessive disease, affecting 1/50,000 people.
Originates from mutations in the “coding” of the mitochondria.
Discovered by Nicholaus Friedreich in the early 1860’s.
Both parents must have the dominant trait for a 25% chance of an offspring possessing the disease.
Not necessarily a disease that kills you, but eventually a wheelchair and regular assistance will be required.
Onset before age 20-25 year.
PRESENTATION IS COMPACT AND INFORMATIVE. HAS FLOWCHARTS AND DIAGRAMS. REFERENCE IS FROM LATEST ARTICLES AND STANDARD TEXTBOOKS. SERVES A GREAT DEAL TO BRUSH UP THE THEORETICAL KNOWLEDGE .
The document discusses the management of coma and related states of impaired consciousness. It begins with an outline of the presentation's objectives which are to define coma and similar conditions, describe causes and pathophysiology, clinical features, approach to comatose patients, and management. Coma is defined as unrousable unconsciousness without response to stimuli. Related states like minimally conscious state, vegetative state, and locked-in syndrome are differentiated from coma. Common causes of coma include structural brain injuries, metabolic disturbances, toxins and drugs. The Glasgow Coma Scale is used to assess level of consciousness. Initial management of comatose patients focuses on stabilizing vital functions before determining the underlying cause through history, exam
General approach and differential diagnosis of comaAn Chang
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
This document discusses the evaluation of a floppy infant. It begins by defining a floppy infant as one presenting with generalized hypotonia, often arising from an insult during the fetal or neonatal period. It describes the clinical examination of a floppy infant and differential diagnosis, which includes central nervous system causes, spinal cord disorders, peripheral nerve disorders, neuromuscular transmission defects, muscle diseases, and systemic disorders. Key examination findings that help localize the cause of hypotonia are discussed. Common etiologies like cerebral palsy, spinal muscular atrophy, and myasthenia gravis are also summarized.
This document discusses non-traumatic coma in children. It begins by providing incidence rates for non-traumatic coma (30 per 100,000 children per year) and traumatic brain injury (670 per 100,000). The rest of the document discusses the definition, causes, evaluation, management, and outcomes of non-traumatic coma in children. Infection is the most common cause. Mortality depends on the underlying etiology and can range from 3-84%. Overall mortality in studies is around 46%.
This case report describes a young female patient with a diagnosis of multiple sclerosis (MS). She initially presented at age 2 with ataxia. MRI of the brain showed widespread white matter lesions. She had two relapses over the next 8 months with new neurological symptoms and MRI lesions each time. Differential diagnoses considered included acute disseminated encephalomyelitis (ADEM) but she did not meet criteria. Her disease course and imaging supported a diagnosis of pediatric MS. She was treated with steroids during relapses with clinical improvement.
The document discusses diseases of white matter, focusing on primary demyelinating disorders. It describes how oligodendrocytes form myelin around axons, allowing for faster signal conduction. Primary demyelination can be caused by dysmyelinating disorders like leukodystrophies due to metabolic defects, or myelinoclastic disorders from immune attack on myelin. Specific leukodystrophies discussed include Krabbe disease, metachromatic leukodystrophy, and adrenoleukodystrophy. Multiple sclerosis is provided as a major example of an immune-mediated myelinoclastic disorder.
Approach to Macrocephaly / large head, Megalencephaly, Causes(Etiology), Work...Praveen Unki
1) Macrocephaly is defined as a head circumference (HC) more than two standard deviations above the mean for a patient's age and gender. HC is measured around the occiput and supraorbital ridges using a flexible tape.
2) Common causes of macrocephaly include hydrocephalus, megalencephaly, thickening of the skull, and brain edema from toxic or metabolic issues. Hydrocephalus is excess cerebrospinal fluid in the skull, while megalencephaly is enlargement of the brain.
3) Evaluation of macrocephaly involves obtaining a medical history, physical exam including head size and neurological assessment, and imaging tests such as MRI or CT of the brain
This document discusses different levels of consciousness ranging from conscious to comatose. Coma is defined as a state of unresponsiveness with no arousal to stimuli. Common causes of impaired consciousness and coma include hypoxia, shock, metabolic disturbances, drugs/alcohol, and central nervous system issues like stroke and head trauma. A coma is evaluated using factors like history, examination findings, Glasgow Coma Scale, and investigations. Management focuses on ABCs, treating the underlying cause, and prognosis depends on the cause and severity of coma. Related conditions like locked-in syndrome and persistent vegetative state are also outlined.
Adrenoleukodystrophy is a genetic disorder that results in the buildup of very long chain fatty acids in the body, mainly in the nervous system, testes, and adrenal glands. There are three main types that affect children and men. Symptoms include muscle loss, vision problems, seizures, cognitive and motor decline. It is diagnosed through blood and genetic tests and MRI. It is an X-linked hereditary disease caused by a mutation in the ABCD1 gene. While there is no cure, treatments aim to manage symptoms and prevent further progression of the disease.
The document outlines how to perform a neurologic examination, including:
1. Testing the 12 cranial nerves, beginning with smell (I), sight (II), eye movement (III, IV, VI), facial expression/sensation (V, VII), hearing/balance (VIII), and tongue/swallowing (IX, X, XII).
2. Evaluating motor skills like strength, tone, coordination and gait.
3. Checking reflexes, sensations of pain, temperature and touch.
4. Looking for signs of increased intracranial pressure or abnormal posturing.
The examination is organized to be thorough while also efficient and systematic.
Temporal lobe epilepsy (TLE) is characterized by recurrent seizures originating from the temporal lobe. Hippocampal sclerosis, involving cell loss in the hippocampus, is the most common pathological finding in TLE. Auras occur in about 80% of temporal lobe seizures and can involve somatosensory, special sensory, autonic, or psychic symptoms. Diagnostic workup involves brain imaging like MRI and PET, as well as EEG to identify abnormalities in the temporal lobe.
Guillain-Barre Syndrome is an acute inflammatory disease of the peripheral nerves that commonly presents with muscle weakness following infections like herpes virus or Campylobacter jejuni. It causes ascending muscle weakness and paralysis that begins in the lower extremities and can affect breathing. Treatment involves close respiratory monitoring and may require intubation, as well as plasmapheresis or IVIG.
CNS Tutorial path.Acquired Metabolic Diseases of CNSimrana tanvir
Thiamine deficiency can cause Wernicke encephalopathy, characterized by brain hemorrhaging and necrosis, particularly in the mammillary bodies. Untreated Wernicke encephalopathy can lead to Korsakoff syndrome, marked by memory loss and confabulation. Vitamin B12 deficiency can cause anemia and spinal cord degeneration. Hypoglycemia selectively injures pyramidal neurons in the cortex and hippocampus. Hyperglycemia in uncontrolled diabetes can cause ketoacidosis or hyperosmolar coma, marked by dehydration, confusion and coma.
This document summarizes several demyelinating diseases of the central and peripheral nervous systems. It describes multiple sclerosis as the most common inflammatory demyelinating disease, affecting the brain and spinal cord, with classifications based on disease course. It also discusses central pontine myelinolysis, transverse myelitis, Guillain-Barre syndrome, and chronic inflammatory demyelinating polyneuropathy. For each, it provides details on characteristics, causes, clinical manifestations, diagnosis, and treatment.
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.
Kearns-sayre syndrome is a rare genetic disorder caused by abnormalities in the mitochondria's DNA. It affects people under age 20 and can cause paralysis of eye muscles, retinal degeneration, and weakness/damage of muscles, brain, heart and other organs over time. Doctors diagnose it through tests of protein/lactate levels or muscle biopsy to examine mitochondrial DNA. There is no cure currently, and symptoms worsen over time.
This document provides an overview of various neurological disorders and conditions. It begins by covering peripheral nerve disorders like neuropathy, myasthenia gravis, and muscular dystrophy. It then discusses specific neuropathies including diabetic neuropathy and nerve compression syndromes. Other sections address neurological diseases and disorders such as Guillain-Barre syndrome, multiple sclerosis, Parkinson's disease, stroke, epilepsy, headaches, and neurological infections. For each topic, it provides details on presentation, pathogenesis, clinical features, management, and treatment.
This document discusses various white matter diseases and disorders that can be seen on MRI. It provides details on the typical imaging appearance and characteristics of several leukodystrophies and other white matter conditions, including metachromatic leukodystrophy, adrenoleukodystrophy, Krabbe disease, vanishing white matter disease, maple syrup urine disease, megaloencephalic leukodystrophy, Pelizaeus-Merzbacher disease, mucopolysaccharidoses, Canavan disease, Alexander disease, Zellweger syndrome, and Leigh disease. Common findings discussed are T1 and T2 signal abnormalities, diffusion restriction, enhancement patterns, and metabolic abnormalities on MR spectroscopy.
This document provides a differential diagnosis for coma by classifying potential causes into those without focal signs or abnormal tests, those with meningeal irritation and abnormal CSF, and those with focal brain signs and abnormal imaging. Numerous intoxications, metabolic disturbances, infections, and other conditions are
FA is a very rare, genetic, recessive disease, affecting 1/50,000 people.
Originates from mutations in the “coding” of the mitochondria.
Discovered by Nicholaus Friedreich in the early 1860’s.
Both parents must have the dominant trait for a 25% chance of an offspring possessing the disease.
Not necessarily a disease that kills you, but eventually a wheelchair and regular assistance will be required.
Onset before age 20-25 year.
PRESENTATION IS COMPACT AND INFORMATIVE. HAS FLOWCHARTS AND DIAGRAMS. REFERENCE IS FROM LATEST ARTICLES AND STANDARD TEXTBOOKS. SERVES A GREAT DEAL TO BRUSH UP THE THEORETICAL KNOWLEDGE .
The document discusses the management of coma and related states of impaired consciousness. It begins with an outline of the presentation's objectives which are to define coma and similar conditions, describe causes and pathophysiology, clinical features, approach to comatose patients, and management. Coma is defined as unrousable unconsciousness without response to stimuli. Related states like minimally conscious state, vegetative state, and locked-in syndrome are differentiated from coma. Common causes of coma include structural brain injuries, metabolic disturbances, toxins and drugs. The Glasgow Coma Scale is used to assess level of consciousness. Initial management of comatose patients focuses on stabilizing vital functions before determining the underlying cause through history, exam
General approach and differential diagnosis of comaAn Chang
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
This document discusses the evaluation of a floppy infant. It begins by defining a floppy infant as one presenting with generalized hypotonia, often arising from an insult during the fetal or neonatal period. It describes the clinical examination of a floppy infant and differential diagnosis, which includes central nervous system causes, spinal cord disorders, peripheral nerve disorders, neuromuscular transmission defects, muscle diseases, and systemic disorders. Key examination findings that help localize the cause of hypotonia are discussed. Common etiologies like cerebral palsy, spinal muscular atrophy, and myasthenia gravis are also summarized.
This document discusses non-traumatic coma in children. It begins by providing incidence rates for non-traumatic coma (30 per 100,000 children per year) and traumatic brain injury (670 per 100,000). The rest of the document discusses the definition, causes, evaluation, management, and outcomes of non-traumatic coma in children. Infection is the most common cause. Mortality depends on the underlying etiology and can range from 3-84%. Overall mortality in studies is around 46%.
This case report describes a young female patient with a diagnosis of multiple sclerosis (MS). She initially presented at age 2 with ataxia. MRI of the brain showed widespread white matter lesions. She had two relapses over the next 8 months with new neurological symptoms and MRI lesions each time. Differential diagnoses considered included acute disseminated encephalomyelitis (ADEM) but she did not meet criteria. Her disease course and imaging supported a diagnosis of pediatric MS. She was treated with steroids during relapses with clinical improvement.
The document discusses diseases of white matter, focusing on primary demyelinating disorders. It describes how oligodendrocytes form myelin around axons, allowing for faster signal conduction. Primary demyelination can be caused by dysmyelinating disorders like leukodystrophies due to metabolic defects, or myelinoclastic disorders from immune attack on myelin. Specific leukodystrophies discussed include Krabbe disease, metachromatic leukodystrophy, and adrenoleukodystrophy. Multiple sclerosis is provided as a major example of an immune-mediated myelinoclastic disorder.
Approach to Macrocephaly / large head, Megalencephaly, Causes(Etiology), Work...Praveen Unki
1) Macrocephaly is defined as a head circumference (HC) more than two standard deviations above the mean for a patient's age and gender. HC is measured around the occiput and supraorbital ridges using a flexible tape.
2) Common causes of macrocephaly include hydrocephalus, megalencephaly, thickening of the skull, and brain edema from toxic or metabolic issues. Hydrocephalus is excess cerebrospinal fluid in the skull, while megalencephaly is enlargement of the brain.
3) Evaluation of macrocephaly involves obtaining a medical history, physical exam including head size and neurological assessment, and imaging tests such as MRI or CT of the brain
This document discusses different levels of consciousness ranging from conscious to comatose. Coma is defined as a state of unresponsiveness with no arousal to stimuli. Common causes of impaired consciousness and coma include hypoxia, shock, metabolic disturbances, drugs/alcohol, and central nervous system issues like stroke and head trauma. A coma is evaluated using factors like history, examination findings, Glasgow Coma Scale, and investigations. Management focuses on ABCs, treating the underlying cause, and prognosis depends on the cause and severity of coma. Related conditions like locked-in syndrome and persistent vegetative state are also outlined.
Adrenoleukodystrophy is a genetic disorder that results in the buildup of very long chain fatty acids in the body, mainly in the nervous system, testes, and adrenal glands. There are three main types that affect children and men. Symptoms include muscle loss, vision problems, seizures, cognitive and motor decline. It is diagnosed through blood and genetic tests and MRI. It is an X-linked hereditary disease caused by a mutation in the ABCD1 gene. While there is no cure, treatments aim to manage symptoms and prevent further progression of the disease.
The document outlines how to perform a neurologic examination, including:
1. Testing the 12 cranial nerves, beginning with smell (I), sight (II), eye movement (III, IV, VI), facial expression/sensation (V, VII), hearing/balance (VIII), and tongue/swallowing (IX, X, XII).
2. Evaluating motor skills like strength, tone, coordination and gait.
3. Checking reflexes, sensations of pain, temperature and touch.
4. Looking for signs of increased intracranial pressure or abnormal posturing.
The examination is organized to be thorough while also efficient and systematic.
Temporal lobe epilepsy (TLE) is characterized by recurrent seizures originating from the temporal lobe. Hippocampal sclerosis, involving cell loss in the hippocampus, is the most common pathological finding in TLE. Auras occur in about 80% of temporal lobe seizures and can involve somatosensory, special sensory, autonic, or psychic symptoms. Diagnostic workup involves brain imaging like MRI and PET, as well as EEG to identify abnormalities in the temporal lobe.
A 27-year-old male patient presented with neurological symptoms including bilateral pyramidal signs, parkinsonian signs, and cerebellar signs. Tests found reduced serum ceruloplasmin and increased urinary copper. A liver biopsy showed increased copper concentration, leading to a diagnosis of Wilson's disease. MRI images showed symmetrical abnormalities in the basal ganglia and corticospinal tracts corresponding to edema, cysts, gliosis and demyelination. Slit lamp examination revealed Kayser-Fleischer rings around the cornea.
This document is a short case report from October 2009 edited by Professor Yasser Metwally of Ain Shams University. It describes the case of a 7-year-old female patient who presented with Lennox-Gastaut syndrome and was diagnosed with cortical dysplasia based on MRI findings. The MRI scans show lissencephaly, microgyria, pachygyria, and cystic white matter changes, as well as subependymal nodular heterotopia and brain atrophy. The case report is one in a series that is periodically updated on the editor's website.
This document provides an overview of psychosis in the elderly, including:
- Common causes are schizophrenia, affective disorders like depression, dementia, delirium, and Parkinson's disease.
- Biological factors underlie many psychotic symptoms. Antipsychotics are commonly used to treat psychosis but have risks.
- Psychosis is more prevalent in nursing home populations compared to community samples. As the population ages, cases of psychosis will rise significantly.
- Specific causes like Alzheimer's disease and depression are discussed in more detail, including their prevalence, clinical presentation, treatments and risks.
The document describes the case of a 7-year-old female patient presenting with Lennox-Gastaut syndrome and cortical dysplasia based on MRI findings. The MRI images show lissencephaly, microgyria, pachygyria, and heterotopic nodules, indicating abnormal brain development. The diagnosis is cortical dysplasia. The discussion section then provides an overview of normal brain development and segmentation, and describes disorders related to failures during these processes such as schizencephaly and holoprosencephaly.
This document describes a case of acute postinfectious cerebellitis in a 6-year-old male patient. The patient presented with cerebellar ataxia and headache 3 weeks after a viral infection. MRI imaging showed bilateral symmetrical lesions in the cerebellar white matter. Within a week of supportive treatment, the patient fully recovered and follow-up MRI was normal. The case is discussed as an example of a benign regressive postinfectious neurological disorder where an immune response causes reversible white matter edema seen on imaging.
A 60-year-old male presented with symptoms of cerebellopontine angle syndrome. Imaging showed a fusiform aneurysm affecting the vertebral arteries, which were asymmetrically dilated and encroaching on the cerebellopontine angle. A fusiform aneurysm is a diffuse, non-saccular dilatation of an artery. These aneurysms are often associated with hypertension and most commonly involve the vertebrobasilar system. They may cause neurological deficits through mass effect on surrounding structures, or by inducing ischemia through intraluminal thrombosis obstructing branch vessels.
This case discusses a 22-month-old female patient diagnosed with asymmetric dyskinetic cerebral palsy. MRI images show bilateral cystic necrosis of the lateral putamen and globus pallidus, likely due to perinatal hypoxia/ischemia. This resulted in an extrapyramidal form of cerebral palsy. Cerebral palsy is caused by nonprogressive brain defects or lesions early in development. Perinatal factors cause 70-80% of cases. Basal ganglia injury can result in dyskinetic cerebral palsy phenotypes.
This document discusses Behcet's disease and its neurological manifestations. It begins by introducing Behcet's disease and describing its characteristic symptoms. It then discusses the different types of central nervous system involvement, including:
1) A focal brain stem meningoencephalitis primarily affecting the midbrain and corticospinal tract, presenting with pyramidal signs.
2) Vascular involvement such as cerebral venous thrombosis, presenting with symptoms of increased intracranial pressure.
3) Rare cases of meningitis.
It provides details on lesion characteristics, differences between the primary parenchymal and vascular types, diagnostic criteria, and management approaches for the different neurological manifestations of Behcet's disease
A 30-year-old male presented with bilateral pyramidal tract signs, pseudobulbar palsy, and orogenital ulcers. MRI showed focal hypointense lesions in the pons, cerebral peduncle, and posterior internal capsule extending continuously and involving the corticospinal tract. The lesions enhanced with contrast, indicating vasogenic edema. This clinical and radiological picture is consistent with neuro-Behcet syndrome, a focal brainstem meningoencephalitis affecting the corticospinal tract bilaterally in a linear pattern from the midbrain downwards.
This document describes a case of septo-optic dysplasia with open lip schizencephaly in an 8-year-old male patient. Key findings included:
- Open lip or type II schizencephaly
- Deficient and hypoplastic septum pellucidum
- Hypoplastic optic nerves and optic chiasma
- Dysplastic cerebral cortex and hypoplastic corpus callosum
- Encephalocele
- Vacuolated pituitary gland
The diagnosis was determined to be septo-optic dysplasia with open lip schizencephaly based on the clinical and radiological findings.
This document is a short case publication from January 2010 edited by Professor Yasser Metwally of Ain Shams University. It describes a 9-year-old female patient who presented with Lennox-Gastaut syndrome and was diagnosed with cortical dysplasia based on postcontrast CT scans showing lissencephaly, pachygyria, and subependymal nodular heterotopia. The document provides references and information on accessing updated and longer versions of this case online.
This document discusses vertigo and disorders of equilibrium. It begins by defining equilibrium and its neural pathways. Vertigo is defined as an illusion of movement and is distinguished from non-vertiginous dizziness. A history, physical exam, and testing can help localize the cause as either peripheral or central. Peripheral causes like benign positional vertigo typically produce intermittent vertigo and nystagmus in one direction, while central causes may involve neurologic signs and multidirectional nystagmus. Specific peripheral disorders discussed in detail include benign positional vertigo and Meniere's disease.
This document discusses vertigo, which refers to a hallucinatory sensation of movement caused by a mismatch of sensory information from the vestibular, visual, and proprioceptive systems. Vertigo can be caused by lesions in the peripheral, intermediate, or central nervous system. Common causes of peripheral vertigo include BPPV, Meniere's disease, and labyrinthitis. Intermediate vertigo may be caused by vestibular neuronitis or acoustic neuroma. Central causes include stroke, MS, migraines, and brain tumors. Clinical tests like nystagmus patterns and the head thrust test can help differentiate peripheral from central vertigo. Treatment depends on the underlying cause but may include medications, exercises
Dizziness is a common complaint in older adults that increases in prevalence with age. It is a nonspecific term used to describe various sensations including vertigo, lightheadedness, and imbalance. Dizziness can be caused by disturbances in various body systems including the vestibular system, visual pathways, proprioceptive fibers, and brain. Common causes include benign positional vertigo, orthostatic hypotension, cerebrovascular disease, and medication side effects. A thorough history and physical exam is needed to evaluate dizziness due to its subjective nature and multiple potential causes.
Vertigo is a type of dizziness caused by dysfunction of the vestibular system in the inner ear that leads to a perception of motion, often spinning. It can cause nausea, vomiting, and difficulties with balance and walking. Vertigo is classified as either peripheral, arising from problems in the inner ear, or central, caused by issues in the brain. Common causes include benign paroxysmal positional vertigo, Ménière's disease, and vestibular neuritis. Treatment depends on the underlying cause but may include medications, repositioning maneuvers, injections, or surgery.
1) Dizziness and vertigo are common, with vertigo defined as a perception of movement and dizziness having various meanings.
2) Vertigo can be peripheral or central in origin, with peripheral vertigo arising from problems in the inner ear and central vertigo from problems in the brain or brainstem.
3) A thorough history, physical exam including tests like Dix-Hallpike, and sometimes ancillary testing can help differentiate between peripheral causes like benign paroxysmal positional vertigo or Ménière's disease versus central causes like vertebrobasilar insufficiency.
head ache dizziness and sphincter disturbance s.pptxSruthi Meenaxshi
This document discusses several topics related to sensory disturbances:
1) It describes the anatomy of the sensory system and how sensations are transmitted from receptors to the central nervous system.
2) It defines different types of sensory loss or disturbances like hypoesthesia, anesthesia, hypalgesia, and hyperpathia.
3) It outlines how to perform a sensory examination to localize lesions, including testing touch, proprioception, vibration, temperature, and pain. Higher cortical sensations can also be examined.
This document discusses various visual problems including field defects, diplopia, nystagmus, and vertigo. It defines these conditions and outlines their typical causes. Field defects can result from lesions anywhere along the visual pathway and present as scotomas, hemianopias or quadrantanopias. Diplopia can be binocular or monocular with various causes such as cranial nerve palsies or myasthenia gravis. Nystagmus includes jerk, pendular, and gaze-evoked types and may be congenital or acquired from vestibular or central nervous system lesions. Vertigo can be peripheral from issues like BPPV, Meniere's disease, or vestibular neur
Vertigo is a sensation of rotational or linear movement that is not actually occurring. It is caused by disturbances in the vestibular system of the inner ear. Benign paroxysmal positional vertigo (BPPV) and labyrinthitis are two common causes of peripheral vertigo. BPPV involves detached calcium crystals in the inner ear that cause vertigo with certain head movements and is treated with repositioning maneuvers. Labyrinthitis is an inner ear infection that causes both vertigo and hearing loss. It is usually viral in origin and causes sudden onset vertigo, nausea, and unilateral hearing loss.
The document discusses various causes of dizziness including vertigo, presyncope, disequilibrium, and non-specific dizziness. Vertigo is characterized by illusions of motion and is commonly caused by peripheral vestibular disorders. Positional vertigo can be distinguished from presyncope by provoking dizziness with changes in head position rather than lowering blood pressure. Disequilibrium causes an unsteady feeling when walking and may result from neurological or musculoskeletal disorders. Non-specific dizziness is difficult for patients to describe and has a broad differential diagnosis. Evaluation of dizziness involves distinguishing these subtypes and identifying potential causes based on associated symptoms, physical exam findings, and test results.
The document discusses the evaluation and management of dizziness and vertigo. It outlines the main categories of dizziness including otologic, central, medical, and unlocalized causes. Evaluation involves taking a thorough history, performing a physical exam including tests of nystagmus, and ordering investigations like an audiogram or MRI. Common diseases discussed in more detail include benign paroxysmal positional vertigo (BPPV), vestibular neuritis, Meniere's disease, and migraine-associated vertigo. Treatment focuses on treating the underlying cause, patient education, rehabilitation, and medications in some cases.
It contains description and salient points to diagnose various epileptic encephalopathies seen during infancy such as early myoclonic encephalopathies, Otahara syndrome, Dravet syndrome, West syndrome.
This document discusses various causes of falls, including syncope (transient loss of consciousness) and non-syncopal causes. It covers topics such as neurocardiogenic, cardiac, and neurological causes of syncope including seizures, progressive supranuclear palsy, third ventricular cysts, and more. Investigations discussed include Holter monitoring, loop recorders, tilt table testing, and imaging. Differential diagnosis and management are also covered.
Strange and abnormal movements are hallmarks of movement disorders, which are neurological diseases characterized by involuntary movements. The movements allow observers to suggest proper diagnoses and include tremors, chorea, athetosis, dystonia, hemiballismus, and more. EEG findings vary depending on the specific movement disorder and location of involvement in the central nervous system.
The document discusses various types of vertigo, dizziness, and imbalance that patients may experience and how medical personnel should evaluate and classify these symptoms. It covers peripheral causes like benign paroxysmal positional vertigo (BPPV), vestibular neuronitis, labyrinthitis, and Meniere's disease. It also discusses central/neurological causes and compares features of peripheral vs. central vestibular lesions. Evaluation involves taking a history, physical exam including nystagmus tests, and potentially imaging or other tests.
This document provides an overview of seizures and epilepsy, including:
1. It defines seizures and describes different seizure types such as partial seizures, absence seizures, tonic-clonic seizures, myoclonic seizures, and neonatal/infantile seizures.
2. Etiologies and classifications of epilepsy are discussed, including focal vs generalized and age-specific syndromes.
3. Details are given on symptoms, EEG findings, and treatment responses for different seizure types like partial motor/sensory seizures and complex partial seizures.
4. Causes of seizures including genetic, structural, metabolic and other factors are briefly outlined.
Ahd neuro-opthalmology - v. patel - nystagmus (1)Ram Gopal
This document defines and describes different types of nystagmus, including their neuroanatomical basis and localizing value. It discusses congenital and acquired nystagmus, differentiating between peripheral and central causes. Key points covered include the mechanisms underlying gaze holding and different forms of pathological nystagmus associated with lesions in various areas of the brainstem and cerebellum. The document emphasizes the importance of characterizing nystagmus to guide further neurological or medical evaluation and identifies potential treatment options.
This document provides guidance on evaluating and treating patients presenting with vertigo. It outlines key factors to determine such as whether the patient is experiencing true vertigo, orthostatic hypotension, or vague unsteadiness. Examination should include testing for nystagmus and evaluating the ears, cranial nerves, and cerebellar function. Based on findings, the etiology can be determined as central (involving the brainstem) or peripheral (involving the vestibular organs or eighth nerve). Treatment differs based on severity and includes anti-vertigo medications or hospitalization. Provocative maneuvers should only be used if not symptomatic, and anti-vertigo drugs avoided in elderly with dysequilibrium.
Ataxia and Vertigo can be caused by disorders of the peripheral or central nervous system. Peripheral causes include benign paroxysmal positional vertigo (BPPV), Meniere's disease, and vestibular neuronitis. BPPV is treated with particle repositioning maneuvers like the Epley maneuver. Meniere's disease causes episodes of vertigo, hearing loss, and tinnitus. Vestibular neuronitis causes sudden, intense vertigo that lasts for days. Central causes of ataxia and vertigo include lesions in the cerebellum or brainstem. Physical exams can help distinguish peripheral from central etiologies.
This document provides an overview of syncope (transient loss of consciousness). It discusses the pathophysiology, typical presentations, differential diagnoses, evaluation and treatment of different syncope types. The main causes discussed are neurally-mediated syncope (the most common), orthostatic hypotension, and cardiac syncope. For evaluation, the document recommends a thorough history, physical exam including orthostatic vital signs and carotid sinus massage in older patients, and tests like ECG, tilt table testing and cardiac monitoring. Treatment depends on the underlying cause, including fluid supplementation, compression stockings and pharmacotherapy for orthostatic hypotension, and pacing for cardiac syncope.
Similar to Neurological differential diagnosis...Vertigo (20)
The document discusses the benefits of exercise for mental health. It states that 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 alleviate symptoms of mental illness.
The document discusses the benefits of exercise for mental health. Regular physical activity can help reduce anxiety and depression and improve mood and cognitive functioning. Exercise causes chemical changes in the brain that may help protect against mental illness and improve symptoms.
The document discusses the benefits of exercise for mental health. Regular physical activity can help reduce anxiety and depression and improve mood and cognitive functioning. Exercise causes chemical changes in the brain that may help protect against mental illness and improve symptoms.
The document discusses the benefits of exercise for mental health. Regular physical activity can help reduce anxiety and depression and improve mood and cognitive functioning. Exercise causes chemical changes in the brain that may help protect against mental illness and improve symptoms.
The document discusses the benefits of exercise for mental health. Regular physical activity can help reduce anxiety and depression and improve mood and cognitive functioning. Exercise causes chemical changes in the brain that may help protect against mental illness and improve symptoms.
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.
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 for those who already suffer from conditions like depression and anxiety.
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.
This document discusses the radiological pathology of seizure disorders. It describes various developmental anomalies, neoplasms, infections, immune-mediated disorders, cerebrovascular diseases, and trauma that can cause seizures. Specific conditions mentioned include cortical dysplasia, tuberous sclerosis, Sturge-Weber syndrome, neuronal migration disorders, vascular malformations, infections, and immune-mediated Rasmussen's encephalitis. The document provides detailed descriptions of the histopathological findings and MRI/CT appearances of different lesions that can underlie seizure disorders.
This document discusses cerebral haemorrhage (ICH), which accounts for 10-15% of strokes. ICH can result from several mechanisms, including hypertension (47-66% of cases), cerebral amyloid angiopathy (CAA), and vascular malformations. CAA typically affects the elderly and causes lobar ICH that is often recurrent or involves multiple simultaneous haemorrhages. Vascular malformations like arteriovenous malformations (AVMs) and cavernous angiomas are a common cause of ICH in young, non-hypertensive patients. Imaging techniques like CT and MRI can identify vascular malformations and help determine the underlying cause of ICH.
Cerebral amyloid angiopathy (CAA) refers to the deposition of β-amyloid in the arteries of the cerebral cortex. It is commonly seen in Alzheimer's disease but can also occur in healthy elderly individuals. CAA can cause intracerebral hemorrhage, dementia, or transient neurological symptoms. The deposition damages blood vessels and increases the risk of hemorrhage. Imaging such as CT scans can detect hemorrhages characteristic of CAA, which are often lobar and cortical. Genetic factors like the ApoE genotype can influence the severity and presentation of CAA.
Cerebral microbleeds are small brain hemorrhages detected by MRI that are caused by leakage of blood from damaged small vessel walls. They are increasingly recognized in patients with cerebrovascular disease, Alzheimer's disease, vascular cognitive impairment, and normal elderly populations. Microbleeds in lobar regions may indicate cerebral amyloid angiopathy and link vascular and amyloid neuropathologies, while deep or infratentorial microbleeds often reflect hypertensive vasculopathy. Detection of microbleeds provides insight into cerebral small vessel disease and its relationship to cognitive impairment and dementia.
The document discusses the benefits of exercise for mental health. Regular physical activity can help reduce anxiety and depression and improve mood and cognitive functioning. Exercise causes chemical changes in the brain that may help protect against mental illness and improve symptoms.
A 57-year-old male patient presented with left lower limb weakness that had progressed over three months. MRI images showed bilateral, symmetrical lesions in the posterior parieto-occipital white matter, which had scalloped margins and did not enhance or cause mass effect. Based on the clinical presentation and MRI findings, the patient was diagnosed with progressive multifocal leukoencephalopathy (PML), a demyelinating disease caused by JC virus reactivation that predominantly affects immunocompromised individuals. PML lesions are typically multifocal and located in the white matter of the brain, most often in the parieto-occipital region.
Issues in radiological pathology: Radiological pathology of watershed infarct...Professor Yasser Metwally
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ISO/IEC 27001, ISO/IEC 42001, and GDPR: Best Practices for Implementation and...PECB
Denis is a dynamic and results-driven Chief Information Officer (CIO) with a distinguished career spanning information systems analysis and technical project management. With a proven track record of spearheading the design and delivery of cutting-edge Information Management solutions, he has consistently elevated business operations, streamlined reporting functions, and maximized process efficiency.
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Date: May 29, 2024
Tags: Information Security, ISO/IEC 27001, ISO/IEC 42001, Artificial Intelligence, GDPR
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This slide is special for master students (MIBS & MIFB) in UUM. Also useful for readers who are interested in the topic of contemporary Islamic banking.
Physiology and chemistry of skin and pigmentation, hairs, scalp, lips and nail, Cleansing cream, Lotions, Face powders, Face packs, Lipsticks, Bath products, soaps and baby product,
Preparation and standardization of the following : Tonic, Bleaches, Dentifrices and Mouth washes & Tooth Pastes, Cosmetics for Nails.
Assessment and Planning in Educational technology.pptxKavitha Krishnan
In an education system, it is understood that assessment is only for the students, but on the other hand, the Assessment of teachers is also an important aspect of the education system that ensures teachers are providing high-quality instruction to students. The assessment process can be used to provide feedback and support for professional development, to inform decisions about teacher retention or promotion, or to evaluate teacher effectiveness for accountability purposes.
How to Fix the Import Error in the Odoo 17Celine George
An import error occurs when a program fails to import a module or library, disrupting its execution. In languages like Python, this issue arises when the specified module cannot be found or accessed, hindering the program's functionality. Resolving import errors is crucial for maintaining smooth software operation and uninterrupted development processes.
Main Java[All of the Base Concepts}.docxadhitya5119
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Macroeconomics- Movie Location
This will be used as part of your Personal Professional Portfolio once graded.
Objective:
Prepare a presentation or a paper using research, basic comparative analysis, data organization and application of economic information. You will make an informed assessment of an economic climate outside of the United States to accomplish an entertainment industry objective.
A review of the growth of the Israel Genealogy Research Association Database Collection for the last 12 months. Our collection is now passed the 3 million mark and still growing. See which archives have contributed the most. See the different types of records we have, and which years have had records added. You can also see what we have for the future.
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Odoo 17 CRM allows us to track why we lose sales opportunities with "Lost Reasons." This helps analyze our sales process and identify areas for improvement. Here's how to configure lost reasons in Odoo 17 CRM
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Neurological differential diagnosis...Vertigo
1. DIFFERENTIAL DIAGNOSIS OF VERTIGO
Synonyms: dizziness, imbalance, disequilibrium
www.yassermetwally.com
INTRODUCTION
Background: Symptoms of vertigo are nonspecific. Vertigo occurs when there is an imbalance or disturbance
in vestibular function anywhere in the peripheral or central vestibular system (labyrinth, vestibular nerve,
brainstem, cerebellum, cortex). Etiology of vertigo includes familial, infectious, neoplastic, metabolic, toxic,
vascular, autoimmune, and traumatic causes. Distinguishing the site and cause of lesion resulting in vertigo is
important because some causes of central vertigo can be life threatening and require immediate attention.
Pathophysiology: Sensation of balance is the result of appropriate information from vestibular, ocular, and
proprioceptive sensory receptors that is properly integrated within the cerebellum and brainstem. Gait,
posture, and visual focus during head movement are all dependent on an intact sense of balance. Loss of
sensory information, central integration, or output control mechanisms all result in a sense of imbalance.
Central causes of vertigo result from a disruption of central integrators (brainstem, cerebellum) or a sensory
information mismatch (cortex). Lesions affecting the vestibular nerve or root entry zone (cerebello-pontine
angle lesions) result in imbalance by affecting primary vestibular sensory information.
Race: There is no racial predilection for CNS causes of vertigo.
Sex: Both men and women are equally affected.
Age: CNS causes of vertigo typically affect the older population groups because of the associated risk factors of
vascular causes of vertigo (hypertension, atherosclerosis, diabetes).
Younger age group is more commonly affected by migraine and multiple sclerosis.
Cerebellar tumors affect a bimodal population - children and adults.
Cerebello-pontine angle tumors typically affect people in the fifth to the eighth decade.
CLINICAL
History:
CNS causes of vertigo can present in a variety of ways. Vertigo can be sudden and severe in onset and
last for days or it may comprise recurrent attacks that last for minutes to hours. Less often central
vertigo presents as brief episodes of vertigo brought on by changes in head or body position.
Patient may describe an intense sensation of movement or tilting, or a severe sensation of imbalance;
sensation is aggravated by movement and improved by remaining stationary. It is important to
discriminate between vertigo (the sensation of movement or spinning) and lightheadedness.
Lightheadedness is often a symptom of a metabolic or cardiovascular abnormality.
Cause of vertigo often is revealed by history and physical examination.
In migraine-associated vertigo the patient gives a history of acute-onset vertigo that lasts either
minutes to a few hours or many hours to even days. Vertigo may precede, follow, or simultaneously
2. present with the headache (migraine without aura). Vestibular symptoms range in severity from
mild to severe. Vertigo may occur with other symptoms of aura (visual and somatosensory
paresthesias) before a headache (migraine with aura). Less commonly vertigo is a symptom of
basilar migraine. Basilar migraine is suspected when the vertigo is accompanied by binocular
visual deficits, diplopia, dysarthria, hearing loss, ataxia, or decreased consciousness.
Patients with presyncopal lightheadedness describe a sensation of wooziness, lightheadedness, or
unsteadiness. Sensations result from diffuse cerebral ischemia. Symptoms may occur
spontaneously if secondary to cardiac arrhythmia, or can be precipitated by activity (postural
hypotension, hyperventilation).
Vertebrobasilar artery (VBA) insufficiency - Vertigo is sudden in onset, lasts only minutes, is
associated with nausea and vomiting, and is accompanied by a range of neurological deficits
(extremity weakness, numbness, incoordination, dysarthria; diplopia, field defects; tinnitus,
hearing loss; loss of consciousness, drop attacks). Few or no residual signs or symptoms remain
after the TIA has resolved.
Symptoms and signs of posterior fossa cerebrovascular disease include vertigo, tinnitus, and ataxia.
Symptoms may be transient, permanent, recurrent, or isolated. Stroke syndromes involving the
posterior circulation are varied depending upon the involved territory. Wallenburg syndrome
(lateral medullary syndrome) presents with vertigo, nausea, vomiting, imbalance, ipsilateral facial
numbness and weakness, diplopia, dysphagia, and dysphonia. Infarction of the dorsolateral
pontomedullary region results in labyrinthine injury (severe vertigo, nausea, vomiting, hearing
loss) in addition to the signs and symptoms of Wallenburg syndrome. Cerebellar infarction also
presents with severe vertigo, nausea, vomiting, and ataxia. Basilar artery syndrome results from
infarction of the pons. Symptoms include vertigo, hearing loss, ataxia, ophthalmoplegia, blindness,
and regional sensory losses.
Cerebellar tumors may present with positional vertigo, imbalance while walking and standing, and
headaches. Specific features are dependent on tumor location (lateral, medial, ventricular), tumor
size, and growth rate. Primary cerebellar tumors typically occur in children. In adults, cerebellar
tumor usually results from metastasis.
Temporal lobe tumors may present as recurrent brief attacks of vertigo lasting minutes; it may be
followed by transient disorientation, amnesia, and dysphasia.
Brainstem lesions (neoplastic, vascular, posttraumatic) can have vertigo as a presenting symptom.
It may be brief or prolonged, depending on the extent of damage to the brainstem structures.
Cerebello-pontine angle (CPA) tumors typically result in disequilibrium or unsteadiness rather
than a sensation of vertigo. However, sudden change in tumor size with hemorrhage or disruption
of regional blood flow to the labyrinth may precipitate vertigo. Majority of tumors in the CPA are
vestibular schwannomas, followed by meningiomas, lipomas, cholesteatomas, and metastatic
tumors.
Vertigo is the initial presenting symptom in 5% cases of multiple sclerosis. The vertigo may last
several days to weeks; it may be positional in nature and is often associated with facial numbness
and weakness, and diplopia.
Posttraumatic vertigo may be peripheral in origin (benign paroxysmal positional vertigo,
perilymphatic fistula, labyrinthine concussion, labyrinthine fracture) or central (cerebral
concussion). Postconcussion syndrome usually follows a mild head injury. Symptoms are
characterized by vertigo, headaches, blurred vision, diplopia, fatigue, and personality changes.
3. Familial periodic ataxia syndromes represent a rare form of chronic recurring bouts of episodic
vertigo. There is a family history of recurrent spells of vertigo. Patients present with recurrent
vertigo, prominent nausea and vomiting, diplopia and dysarthria with the spells, and a progressive
truncal ataxia. Spells are precipitated by physical exertion or emotional stress. Acetazolamide is
effective in controlling episodic vertigo.
Rarely does central nervous system infection cause vertigo. Lyme neuroborreliosis can have vertigo
as a presenting feature of Lyme disease encephalopathy.
Psychogenic vertigo is a manifestation of panic or anxiety disorder. Patients will describe a
sensation of unsteadiness, vertigo, lightheadedness, and less often nausea and vomiting with the
symptoms.
Physical:
During asymptomatic periods, patients with migraine-associated vertigo have normal physical
examinations. During migraine, patients may exhibit motion-intolerance, diaphoresis, and vomiting.
Occasionally nystagmus is observed during an attack; rarely does the migraine include dysarthria,
aphasia, hemiparesis, or extremity ataxia.
When symptomatic, a cardiac examination may reveal arrhythmia as the cause of symptoms. If
hyperventilation is suspected, having the patient hyperventilate may precipitate the symptoms.
Orthostatic changes in pulse and blood pressure should be documented if accompanied by symptoms of
lightheadedness.
Direction changing, gaze-evoked nystagmus, and severe truncal ataxia with limb incoordination are
findings associated with cerebellar infarction. Lateral medullary infarction also will cause direction-
changing nystagmus, but there will be associated signs indicating brainstem damage such as decreased
gag reflex, facial numbness, Horner syndrome, and dysphonia. Saccadic eye movements are disrupted;
gait is ataxic. Lateral pontomedullary syndrome also presents with nystagmus, defective saccades, and
hearing loss.
CPA tumors that cause vertigo will also cause unilateral hearing loss and may present with nystagmus.
Nystagmus may be evident only in the dark or with Frenzel glasses, which remove visual fixation. Head
thrust test may reveal unilateral vestibular weakness. Large tumors may cause subtle facial weakness,
decreased corneal reflex, and facial dysesthesia.
Differentiation between central and peripheral causes of vertigo is facilitated by a precise oculomotor
examination. Spontaneous nystagmus that cannot be suppressed with visual fixation; nystagmus that
changes direction with gaze; purely vertical, horizontal, or torsional nystagmus; and saccade dysmetria
(overshoot and undershoot) are all signs of a potential central abnormality as the cause of vertigo.
Paroxysmal positional nystagmus that is of central origin usually does not fatigue with repeated
positioning maneuvers, has no latency of onset, lasts longer than 60 seconds, is often vertical in direction,
and may change direction with different head positions.
Vertigo of a panic attack can sometimes be elicited by having the patient hyperventilate. Most patients
with psychogenic vertigo do not have any pathological findings on otologic or neurologic examination.
Causes:
Central vertigo syndromes resulting from acute vascular events most commonly result from a
combination of hypertension and regional atherosclerosis.
4. Less commonly, arterial dissection secondary to neck extension, rotational injury, or osteoarthritic spurs
is the cause of disturbed posterior fossa blood flow.
Migraine and presyncopal lightheadedness are two forms of regional and global ischemia that may
present with vertigo or imbalance as the primary symptom.
WORKUP
Lab Studies:
Few laboratory studies facilitate the diagnosis of central causes of vertigo.
If vertigo is accompanied by prolonged nausea and vomiting, monitoring and replacing fluids and
electrolytes in the elderly would be prudent.
In the rare case of suspected neuroborreliosis, serology for Lyme disease with ELISA, Western blot, and
lymphocyte antigen stimulation assay would be indicated.
Cerebrospinal fluid should be obtained for Lyme antibody and polymerase chain reaction analysis
for Borrelia burgdorferi DNA.
Imaging Studies:
Imaging studies are indicated when there is a suspicion that the symptoms are the result of ischemia.
MRI and MR angiography are the most helpful studies in assessing posterior circulation disorders and
acute infarction.
Other Tests:
Formal evaluation with vestibular testing is indicated if the diagnosis is not apparent after obtaining a
history and performing a physical examination.
Caloric testing will reveal if there is a unilateral peripheral weakness.
Oculomotor testing can detect saccade, pursuit, and optokinetic disturbances.
Positional testing with infrared oculography can detect nystagmus and clearly define nystagmus
patterns.
Complete cardiac and peripheral vascular examination (ECG, Holter, echocardiogram, carotid and
vertebral doppler) should be performed if symptoms suggest hypoperfusion, embolic events, or
arrhythmia as the cause.
TREATMENT
Medical Care:
Medical treatment includes supportive care with fluid replacement and vestibular suppressants for
intractable vertigo with nausea and vomiting.
Treatment of migraine-associated vertigo includes analgesics and vestibular suppressants. Drugs useful
in the treatment of migraine include sumatriptan, propranolol, imipramine, amitriptyline, and
5. nortriptyline and vestibular suppressants diazepam and alprazolam. For further information on the
diagnosis and treatment of migraine headache please refer to the chapter Migraine Headache.
Control of hypertension, diabetes, and atherosclerosis is indicated for long-term prevention of further
complications. Cardiac arrhythmia should be controlled.
Drugs useful in the treatment of vertebrobasilar insufficiency include aspirin, ticlopidine, pentoxifylline,
heparin, and warfarin.
Acetazolamide is indicated for the treatment of familial ataxia syndrome.
Surgical Care:
Surgical treatment of central vertigo is limited to urgent posterior fossa decompression of cerebellar and
brainstem edema complicating the infarction.
Cerebello-pontine angle tumors are surgically removed on an elective basis. If there is a medical
contraindication, radiotherapy for tumor control is an option.
MEDICATION
The goal of pharmacotherapy is to reduce morbidity and prevent complications.
Drug Category: Antihistamines -- Prevent the histamine response in sensory nerve endings and blood
vessels. Are effective in treating vertigo.
Meclizine (Antivert, Antrizine, Meni-D) -- Decreases
excitability of middle ear labyrinth and blocks conduction in
Drug Name middle ear vestibular-cerebellar pathways. These effects are
associated with therapeutic effects in the relief of nausea
and vomiting.
Adult Dose 25 mg PO q4-6h
<12 years: Not established
Pediatric Dose
>12 years: Administer as in adults
Contraindications Documented hypersensitivity
May increase toxicity of CNS depressants, neuroleptics, and
Interactions
anticholinergics
Pregnancy B - Usually safe but benefits must outweigh the risks.
Caution in angle-closure glaucoma, prostatic hypertrophy,
Precautions pyloric or duodenal obstruction, and bladder neck
obstruction
Dimenhydrinate (Dimetabs, Dramamine) -- A 1:1 salt of 8
chlorotheophylline and diphenhydramine thought to be
useful in the treatment of vertigo.
Drug Name Diminishes vestibular stimulation and depresses
labyrinthine function through central anticholinergic effects.
However, prolonged treatment may decrease rate of
recovery of vestibular injuries.
Adult Dose 50 mg PO or IM q4-6h or 100 mg supp q8h
6. <2 years: Not established
2-5 years: Up to 12.5-25 mg PO q6-8h; not to exceed 75
mg/24h
6-12 years: 25-50 mg PO q6-8h; not to exceed 150 mg/24h
Pediatric Dose
>12 years: Administer as in adults
Alternatively, 1.25 mg/kg or 37.5 mg/m2 IM qid; not to
exceed 300 mg/d
Documented hypersensitivity; do not administer to
neonates; IV products may contain benzyl alcohol, which
Contraindications
has been associated with fatal quot;Gasping syndromequot; in
premature infants and low birth weight infants
Alcohol or other CNS depressants may have additive effect
Interactions on dimenhydrinate; may mask ototoxic symptoms, caused
by certain antibiotics and irreversible damage may result
Pregnancy B - Usually safe but benefits must outweigh the risks.
Do not treat severe emesis with antiemetic drugs alone; may
contain either sulfites or tartrazine, which may cause
allergic-type reactions in susceptible persons; may impede
Precautions
diagnosis of conditions, such as brain tumors, intestinal
obstruction and appendicitis; may obscure signs of toxicity
from overdosage of other drugs
Drug Category: Anticholinergics -- Work centrally by suppressing conduction in the vestibular cerebellar
pathways.
Scopolamine (Isopto) -- Blocks action of acetylcholine at
parasympathetic sites in smooth muscle, secretory glands
and the CNS. Antagonizes histamine and serotonin action.
Drug Name
Transdermal scopolamine may be the most effective agent
for motion sickness. Its use in vestibular neuronitis is
limited by its slow onset of action.
Adult Dose 0.6 mg PO q 4-6h or 0.5 mg transdermally q3d
6 mcg/kg/dose IM/SC/IV; not to exceed 0.3 mg/dose, or 0.2
Pediatric Dose
mg/m2 and repeat q6-8h
Documented hypersensitivity; primary glaucoma (including
initial stages), pyloric obstruction, toxic megacolon, hepatic
Contraindications
disease, paralytic ileus, severe ulcerative colitis, renal
disease, obstructive uropathy, and myasthenia gravis
Antipsychotic effectiveness of phenothiazines may be
decreased by coadministration with scopolamine;
anticholinergic side effects may be increased by concurrent
therapy and phenothiazine dosages should be adjusted as
Interactions necessary; coadministration with tricyclic antidepressants,
may increase anticholinergic side effects (eg, dry mouth,
constipation, urinary retention) due to additive effect
(tricyclic antidepressants with less anticholinergic activity
may be beneficial)
C - Safety for use during pregnancy has not been
Pregnancy
established.
Caution in the elderly because of increased incidence of
7. glaucoma; large doses may suppress intestinal motility and
precipitate or aggravate toxic megacolon; anticholinergics
may aggravate hiatal hernia associated with reflux
Precautions esophagitis; patients with prostatism can have dysuria and
may require catheterization; use cautiously in patients with
asthma or allergies; a reduction in bronchial secretions can
lead to inspissation and formation of bronchial plugs
Drug Category: Benzodiazepines -- By binding to specific receptor-sites these agents appear to potentiate
the effects of gamma-aminobutyrate (GABA) and facilitate inhibitory GABA neurotransmission and other
inhibitory transmitters. These effects may prevent vertigo and emesis.
Diazepam (Valium) -- Depresses all levels of CNS (eg,
limbic and reticular formation), possibly by increasing
Drug Name activity of GABA.
Individualize dosage and increase cautiously to avoid
adverse effects.
Adult Dose 5-10 mg PO/IV/IM q4-6h
<6 months: Not recommended
>6 months: 0.05-0.3 mg/kg/dose IM/IV over 2-3 min; repeat
Pediatric Dose in 2-4 h prn
Alternatively, 0.12-0.8 mg/kg/24h PO divided q6-8h; not to
exceed 10 mg/dose
Documented hypersensitivity; narrow-angle glaucoma;
Contraindications
children <3 mo
Increases toxicity of benzodiazepines in CNS with
Interactions coadministration of phenothiazines, barbiturates, alcohols,
and MAO inhibitors
Pregnancy D - Unsafe in pregnancy
Caution with other CNS depressants, low albumin levels, or
Precautions
hepatic disease (may increase toxicity)
Drug Category: Phenothiazines -- Effective in treating emesis possibly due to effects in dopaminergic
mesolimbic system.
Promethazine (Phenergan) -- For symptomatic treatment of
nausea in vestibular dysfunction.
Drug Name Antidopaminergic agent effective in treating emesis. Blocks
postsynaptic mesolimbic dopaminergic receptors in brain
and reduces stimuli to brainstem reticular system.
Adult Dose 25-50 mg PO/IM/PR q4-6h
<2 years: Not recommended
Pediatric Dose
>2 years: 0.25-1.0 mg/kg PO/IV/IM/PR 4-6 times/d prn
Contraindications Documented hypersensitivity
May have additive effects when used concurrently with
Interactions other CNS depressants or anticonvulsants; coadministration
with epinephrine, may cause hypotension
C - Safety for use during pregnancy has not been
Pregnancy
established.
Some of the adverse effects include CNS depression, dry
mouth, extrapyramidal symptoms, hypertension, and skin
rash Caution in cardiovascular or hepatic disease, seizures,
8. sleep apnea, and asthma; may enhance effects of other
Precautions medications that cause CNS depression including alcohol,
narcotics, sedatives, hypnotics, etc
Prochlorperazine (Compazine) -- May relieve nausea and
vomiting by blocking postsynaptic mesolimbic dopamine
Drug Name
receptors through anticholinergic effects and depressing
reticular activating system.
Adult Dose 5-10 mg PO/IM q6h 25 mg supp PR q12h
2.5 mg PO/PR q8h or 5 mg q12h, prn; not to exceed 15
mg/d
Pediatric Dose
0.1-0.15 mg/kg/dose IM; change to PO as soon as possible
IV dosing not recommended for children
Documented hypersensitivity; bone marrow suppression,
narrow angle glaucoma, severe liver or cardiac disease;
comatose patients or patients with large amounts of central
Contraindications
nervous system depressants in their system (eg, alcohol or
barbiturates); do not use in surgery in children <2 y or that
weigh <20 lb
Coadministration with other CNS depressants or
Interactions anticonvulsants may cause additive effects; with
epinephrine may cause hypotension
Pregnancy D - Unsafe in pregnancy
Side effects include CNS depression, blurred vision, and
hypotension; neuroleptic malignant syndrome and
extrapyramidal dystonic reactions may rarely occur
Drug-induced Parkinson’s syndrome or
Precautions
pseudoparkinsonism occurs quite frequently; akathisia is
most common extrapyramidal reaction in elderly; lowers
seizure threshold and should be used cautiously in patients
with a history of seizures
Drug Category: Monoaminergics -- May treat vertigo possibly through modulating the sympathetic
system.
Ephedrine (Pretz-D) -- Stimulates release of epinephrine
Drug Name
stores, producing alpha- and beta-adrenergic effects.
Adult Dose 25 mg PO q4-6h
< 2 years: Not recommended
Pediatric Dose 2-5 years: 3 mg q6-8h
>5 years: 6.25 mg PO/SC q6-8h
Documented hypersensitivity; angle-closure glaucoma, and
Contraindications
cardiac arrhythmias
Theophylline, atropine, or MAO inhibitors may increase
toxicity; alpha- and beta-blockers decrease vasopressor
Interactions
effects of ephedrine; cardiac glycosides and general
anesthetics increase cardiac stimulation of ephedrine
Pregnancy B - Usually safe but benefits must outweigh the risks.
Side effects include excitation, tremulousness, insomnia,
nervousness, palpitation, tachycardia, and symptoms
associated with sympathetic activation; bladder sphincter
9. spasm can occur and cause transient acute urinary retention;
caution in the elderly and patients with diabetes mellitus,
Precautions
hyperthyroidism, hypertension, cardiovascular disease,
prostatic hypertrophy, and cerebrovascular insufficiency
FOLLOW-UP
Further Outpatient Care:
After the underlying cause of vertigo has been identified and treated, supportive care with vestibular
suppressants and antiemetics are indicated for relief of vertigo.
BIBLIOGRAPHY
Asmundson GJ, Larsen DK, Stein MB: Panic disorder and vestibular disturbance: an overview of
empirical findings and clinical implications. J Psychosom Res 1998 Jan; 44(1): 107-20.
Curless RG, Schatz NJ, Bowen BC, et al: Lyme neuroborreliosis masquerading as a brainstem tumor in
a 15-year- old. Pediatr Neurol 1996 Oct; 15(3): 258-60.
Cutrer FM, Baloh RW: Migraine-associated dizziness. Headache 1992 Jun; 32(6): 300-4.
Davies RA, Luxon LM: Dizziness following head injury: a neuro-otological study. J Neurol 1995 Mar;
242(4): 222-30.
Stewart WF, Lipton RB, Celentano DD, Reed ML: Prevalence of migraine headache in the United States.
Relation to age, income, race, and other sociodemographic factors. JAMA 1992 Jan 1; 267(1): 64-9.
Welsh LW, Welsh JJ, Jaffe SC, Healy MP: Syndromal vertigo identified by magnetic resonance imaging
and angiography. Laryngoscope 1996 Sep; 106(9 Pt 1): 1144-51.
THE AUTHOR
Professor Yasser Metwally
Professor of neurology, Ain Shams University, Cairo, Egypt
http://yassermetwally.com