Systemic infections may increase the risk of stroke through several mechanisms. Bacterial infections like infective endocarditis and meningitis have been linked to strokes, often due to inflammation and endothelial injury. Viruses such as HSV, VZV, HCV and HIV can cause vasculitis and coagulopathies leading to hemorrhagic or ischemic strokes. Fungi sometimes form cerebral abscesses or invade arteries, predisposing to aneurysms and thrombosis. Parasitic infections including Chagas disease are also associated with cardioembolic strokes. Overall, infections may exacerbate traditional stroke risk factors or directly cause strokes through inflammatory and thrombotic pathways.
Cerebral amyloid angiopathy (CAA) is characterized by cerebrovascular amyloid deposition and is a cause of cerebral hemorrhage in older individuals. It has a close association with Alzheimer's disease, with a prevalence of around 80-90% in AD patients. CAA becomes more common with age, affecting around half of elderly individuals. While there are no definitive treatments, hematoma evacuation appears relatively safe for younger patients with CAA-related hemorrhages.
Presurgical Evaluation Of Intractable EpilepsyNeurologyKota
The document discusses the presurgical evaluation of patients with intractable epilepsy. It describes how the goal is to localize the epileptogenic zone and assess risk to functions. Various tests are used to define zones like the ictal onset zone and irritative zone. Imaging like MRI, PET, SPECT and other tests help localize the epileptogenic lesion and functional deficits. Comprehensive presurgical evaluation including neuropsychological testing is needed to determine surgical candidacy and plan appropriate treatment.
This case report describes a 72-year old man who presented with two seizures. He had a history of stroke 9 months prior that caused left hemiplegia. MRI and CT scans confirmed an old right middle cerebral artery infarct. He was diagnosed with post-stroke epilepsy. Anti-epileptic medication was started and he was discharged seizure-free after 2 days. Stroke is a common cause of epilepsy in older adults, with seizures occurring in about 9% of post-stroke patients. Newer anti-epileptic drugs like lamotrigine are preferred for post-stroke epilepsy due to fewer side effects and interactions compared to older drugs.
This document discusses various aspects of evaluating and surgically treating epilepsy. It begins by outlining when epilepsy surgery should be considered, such as when seizures persist despite adequate medication. The aim of presurgical evaluation is to accurately map the epileptogenic zone and completely resect or disconnect the area responsible for seizures. Noninvasive and invasive testing methods are described to localize the seizure focus. Common surgical approaches like temporal lobectomy and extra-temporal lobectomy are explained. Outcomes of different procedures and factors influencing prognosis are also summarized.
Techiniques of clipping in aneurysm & endovascular optiondrajay02
This document discusses various techniques for clipping aneurysms, including:
- The history of aneurysm clipping and different clip designs.
- Types of clips such as temporary, permanent, fenestrated, and clip grafts.
- Techniques for clipping aneurysms including simple, fenestrated, multiple, and reconstruction clipping.
- Endovascular options for treating aneurysms such as historical developments, embolization coils, and stents.
This document discusses stroke, including its definition, types, symptoms, risk factors, evaluations, management, complications, and surgical treatments. Stroke is defined as a clinical syndrome caused by disrupted blood flow to the brain lasting over 24 hours. There are two main types - ischemic (80%) caused by blockage and hemorrhagic (20%) caused by bleeding. Evaluations include imaging like CT scans and MRIs to determine the specific location and cause of injury. Management focuses on airway/ventilation, blood pressure/volume control, temperature regulation, and glycemic control to prevent further brain damage. Surgical interventions may be needed for certain types of hemorrhagic stroke or complications.
This document provides an overview of the management of hypertensive intracerebral bleed (ICH). Key points include:
1) Uncontrolled hypertension is the leading risk factor for ICH. Early diagnosis with non-contrast CT is important for appropriate care and outcomes.
2) Acute management focuses on preventing hematoma expansion through aggressive blood pressure control to SBP 140 mmHg, reversing anticoagulants, and considering platelet transfusion.
3) Other priorities are treating increased intracranial pressure through measures like head elevation, osmotic therapies, and CSF drainage if hydrocephalus is present. Salvage therapies like induced coma and neuromuscular blockade are reserved for refract
Cerebral amyloid angiopathy (CAA) is characterized by cerebrovascular amyloid deposition and is a cause of cerebral hemorrhage in older individuals. It has a close association with Alzheimer's disease, with a prevalence of around 80-90% in AD patients. CAA becomes more common with age, affecting around half of elderly individuals. While there are no definitive treatments, hematoma evacuation appears relatively safe for younger patients with CAA-related hemorrhages.
Presurgical Evaluation Of Intractable EpilepsyNeurologyKota
The document discusses the presurgical evaluation of patients with intractable epilepsy. It describes how the goal is to localize the epileptogenic zone and assess risk to functions. Various tests are used to define zones like the ictal onset zone and irritative zone. Imaging like MRI, PET, SPECT and other tests help localize the epileptogenic lesion and functional deficits. Comprehensive presurgical evaluation including neuropsychological testing is needed to determine surgical candidacy and plan appropriate treatment.
This case report describes a 72-year old man who presented with two seizures. He had a history of stroke 9 months prior that caused left hemiplegia. MRI and CT scans confirmed an old right middle cerebral artery infarct. He was diagnosed with post-stroke epilepsy. Anti-epileptic medication was started and he was discharged seizure-free after 2 days. Stroke is a common cause of epilepsy in older adults, with seizures occurring in about 9% of post-stroke patients. Newer anti-epileptic drugs like lamotrigine are preferred for post-stroke epilepsy due to fewer side effects and interactions compared to older drugs.
This document discusses various aspects of evaluating and surgically treating epilepsy. It begins by outlining when epilepsy surgery should be considered, such as when seizures persist despite adequate medication. The aim of presurgical evaluation is to accurately map the epileptogenic zone and completely resect or disconnect the area responsible for seizures. Noninvasive and invasive testing methods are described to localize the seizure focus. Common surgical approaches like temporal lobectomy and extra-temporal lobectomy are explained. Outcomes of different procedures and factors influencing prognosis are also summarized.
Techiniques of clipping in aneurysm & endovascular optiondrajay02
This document discusses various techniques for clipping aneurysms, including:
- The history of aneurysm clipping and different clip designs.
- Types of clips such as temporary, permanent, fenestrated, and clip grafts.
- Techniques for clipping aneurysms including simple, fenestrated, multiple, and reconstruction clipping.
- Endovascular options for treating aneurysms such as historical developments, embolization coils, and stents.
This document discusses stroke, including its definition, types, symptoms, risk factors, evaluations, management, complications, and surgical treatments. Stroke is defined as a clinical syndrome caused by disrupted blood flow to the brain lasting over 24 hours. There are two main types - ischemic (80%) caused by blockage and hemorrhagic (20%) caused by bleeding. Evaluations include imaging like CT scans and MRIs to determine the specific location and cause of injury. Management focuses on airway/ventilation, blood pressure/volume control, temperature regulation, and glycemic control to prevent further brain damage. Surgical interventions may be needed for certain types of hemorrhagic stroke or complications.
This document provides an overview of the management of hypertensive intracerebral bleed (ICH). Key points include:
1) Uncontrolled hypertension is the leading risk factor for ICH. Early diagnosis with non-contrast CT is important for appropriate care and outcomes.
2) Acute management focuses on preventing hematoma expansion through aggressive blood pressure control to SBP 140 mmHg, reversing anticoagulants, and considering platelet transfusion.
3) Other priorities are treating increased intracranial pressure through measures like head elevation, osmotic therapies, and CSF drainage if hydrocephalus is present. Salvage therapies like induced coma and neuromuscular blockade are reserved for refract
Cerebral herniation occurs when brain tissue shifts from its normal position inside the skull due to swelling. This is usually caused by head injury, stroke, bleeding or tumors. There are several types of herniation including subfalcine, transtentorial, uncal, and cerebellar tonsillar herniation. Management involves reducing intracranial pressure through surgical removal of mass lesions, ventricular drainage, medical therapies like hyperventilation, hyperosmotic agents, induced hypertension, barbiturate coma or hypothermia, and in severe cases decompressive craniectomy. The condition progresses through stages as herniation worsens and involves specific neurological exam findings at each stage.
This document discusses several normal EEG patterns seen in sleep, including:
1) Positive occipital sharp transients of sleep (POSTs), which appear as sharp waves over the occipital regions during light sleep and stage 2 sleep in most healthy adults and children over 3 years old.
2) Posterior slow-wave transients associated with eye movements, seen as slow waves over the occipital regions following eye blinks or movements in children aged 6 months to 10 years.
3) Occipital slow transients or "cone waves", seen as high amplitude slow waves over the occipital regions during transitions from light to deep sleep in infants and children up to age 5.
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.
Temporal lobe epilepsy is one of the most common forms of epilepsy. It can be caused by hippocampal sclerosis or lesions in the temporal lobe. Hippocampal sclerosis involves neuronal loss and gliosis in the hippocampus and is the most common pathological finding in temporal lobe epilepsy patients. Interictal EEG findings like temporal intermittent rhythmic delta activity and temporal sharp waves help lateralize the seizure focus. Video EEG monitoring helps capture seizures and interictal discharges. Treatment involves antiepileptic drugs and potentially resective surgery for drug-resistant cases.
Comatose nonconvulsive status epilepticus (NCSE) is a condition characterized by a coma state accompanied by continuous or periodic epileptiform brain activity, as seen on EEG. The diagnosis requires both clinical assessment showing a comatose state as well as EEG confirmation of epileptiform discharges. Treatment involves administering anti-epileptic drugs (AEDs) and continuing the treatment if it leads to improvements in both the EEG findings and clinical condition. However, AEDs should not be continued if EEG abnormalities improve without accompanying clinical recovery, as clearing of EEG patterns alone may not indicate resolution of the underlying condition.
1) Neurological injury is a leading cause of death for patients who experience cardiac arrest and are successfully resuscitated. Only 30% of eligible patients receive post-arrest targeted temperature management (TTM), formerly known as therapeutic hypothermia.
2) TTM involves lowering a patient's body temperature to 32-34°C for 24 hours after resuscitation to reduce neurological injury from global hypoxic insult during cardiac arrest. Proper sedation, electrolyte monitoring, and a slow rewarming period are important aspects of TTM.
3) While TTM is the standard of care, additional neuroprotective strategies are being studied, including pharmacological approaches targeting cell death pathways and modulation of oxygen free radicals
Endovascular neurosurgery uses minimally invasive techniques guided by imaging to treat cerebral aneurysms, arteriovenous malformations, tumors, and vasospasm. Clinical trials show benefits to intra-arterial thrombolysis up to 6 hours and mechanical revascularization up to 8 hours after stroke. Endovascular techniques are also used to treat unruptured and ruptured aneurysms using coils, stents and flow diverters to occlude the aneurysm and prevent rebleeding. While effective, complications can include hemorrhage in up to 10% of mechanical thrombectomy cases.
This document discusses central nervous system vasculitis, including its classification, diagnosis, and treatment. It covers primary angiitis of the CNS and secondary causes. Diagnosis is challenging due to non-specific symptoms and lack of sensitive tests. Evaluation involves clinical assessment, CSF analysis, neuroimaging, and cerebral angiography. Treatment depends on the specific type but often involves immunosuppressants like cyclophosphamide with glucocorticoids. Pathology evaluation can help in difficult cases but has low sensitivity.
Intra operative neurophysiological monitoringKode Sashanka
This document discusses intra-operative neurophysiological monitoring during surgeries. It provides an overview of the need for monitoring, the types of monitoring used, and how they work. Monitoring includes EEG, somatosensory evoked potentials, motor evoked potentials, and more. These techniques provide real-time feedback on the functional status of the nervous system during surgery to help reduce risks. Anesthetic management and different monitoring systems are also reviewed.
The glymphatic system, a recently-discovered immune system of the central nervous system that offers opportunities for the development of techniques to modulate immune response. An opportunity for osteopathic manipulation research.
This document discusses various types of autoimmune encephalitis. It begins by providing clues that can suggest an autoimmune cause over infectious, including a subacute onset and fluctuating course. It then covers several specific autoimmune encephalitis subtypes defined by the neuronal surface antigens involved, such as anti-NMDA receptor and anti-LGI1 encephalitis. For each subtype, it discusses clinical features, investigations, and treatment approaches. The document aims to help clinicians differentiate between autoimmune and infectious causes of encephalitis.
Hirayama disease is a rare condition first described in 1959 that mainly affects teenage boys and young men. It causes progressive but non-fatal weakness and wasting of muscles in the forearm and hand, typically on one side only. Diagnosis involves MRI of the neck in full flexion showing a crescent-shaped lesion compressing the spinal cord. Treatment focuses on preventing neck flexion using a cervical collar, as the condition often resolves spontaneously within 6 years.
This document describes several benign EEG variants that can have an epileptiform appearance but are not epileptogenic. It discusses characteristics of alpha variants, mu rhythm, lambda waves, rhythmic mid-temporal theta discharges, wicket spikes, subclinical rhythmic electroencephalographic discharges of adults, phantom spike-wave discharges, and small sharp spikes. These benign variants can occur during drowsiness and light sleep and are seen in specific electrode sites, with features like attenuation with eye opening or movement in the case of mu rhythm. Accurate identification requires training to distinguish them from true epileptiform discharges.
The document discusses the goals and techniques used in the presurgical evaluation of patients with epilepsy. The main goals are to accurately map the brain region responsible for generating seizures (epileptogenic zone) while avoiding functional areas. Key techniques discussed include high-resolution MRI to identify lesions, scalp EEG monitoring to localize seizures, fMRI to map language and motor functions, and MRS to identify metabolic abnormalities. A multidisciplinary team evaluates all test results to localize the seizure focus and plan the safest surgery.
This document discusses various syndromes that can result from strokes in different areas of the brainstem. It begins with an overview of brainstem anatomy and blood supply. It then describes in detail the clinical presentations of medial and lateral midbrain syndromes, various pontine syndromes including medial and lateral inferior pontine syndromes, and medial and lateral medullary syndromes. Case examples are provided to illustrate the different neurological deficits that can occur based on the location of the brainstem stroke.
Calibration of an EEG machine involves checking various parameters to ensure accurate measurements. It is important as it allows correct interpretation of recordings and comparison to previous studies. Parameters checked include paper speed, pen alignment, centering and damping, time constant, high frequency filter, sensitivity, amplitude linearity, gain, noise level and more. Verifying these helps identify any issues needing adjustment and confirms the machine is functioning properly.
This presentation looks at generalised periodic epileptiform discharges and the various disorders like Creutzfeldt Jacob disease (CJD), SSPE and metabolic encephalopathies in which it is seen. SIRPID is also discussed. Triphasic waves are described. Radermacker complexes in SSPE are described.
The document summarizes the process of presurgical evaluation for epilepsy patients. It discusses how modern imaging techniques like video EEG monitoring, high-resolution MRI, fMRI, PET and SPECT are used to localize the epileptogenic zone noninvasively in most patients. When noninvasive methods are insufficient, invasive EEG monitoring using subdural or depth electrodes may be used. The goal is to precisely identify the brain area responsible for seizure generation to allow its surgical resection, while avoiding damage to critical functions. A classical example where surgery is often curative is mesial temporal lobe epilepsy.
05.31.13 Non-Convulsive Status Epilepticus (NCSE) - Bittel.pptFrankyQ2
This document summarizes the experience of a tertiary care center with non-convulsive status epilepticus (NCSE). It provides background information on NCSE including epidemiology, clinical features, EEG criteria for diagnosis, and treatment challenges. It then presents data from a review of NCSE cases at the institution from 2009-2013. The majority of cases were classified as complex partial status epilepticus and most patients presented with confusion or lethargy. Treatment often involved multiple anti-epileptic drugs and anesthesia in refractory cases. Outcomes depended on underlying etiology but NCSE was associated with prolonged ICU and hospital stays.
This document discusses electrodiagnostic criteria for Guillain-Barré syndrome (GBS) subtypes acute inflammatory demyelinating polyneuropathy (AIDP) and acute motor axonal neuropathy (AMAN). It reviews the evolution of criteria sets over time, including those proposed by Asbury, Albers, Cornblath, Ho, Hadden, and others. Key findings include that early electrodiagnosis can be difficult, with reversible conduction failure in AMAN sometimes mimicking AIDP. Serial nerve conduction studies are important for distinguishing subtypes and determining prognosis, as features may change over time. The document also discusses pathological mechanisms and involvement of sensory fibers.
Pediatric stroke can be caused by a variety of conditions including sickle cell disease, infections like varicella, cardiac diseases, moyamoya disease, cerebral venous sinus thrombosis, and vascular malformations. Diagnostic techniques like MRI, MRA, CT, and angiography are used to identify abnormalities and characterize the nature of the stroke. Common findings include lesions in the brain parenchyma that may involve gray or white matter or cross vascular territories, stenosis or occlusion of arteries, moyamoya vessels, and venous sinus thrombosis. Pediatric stroke requires identifying its underlying cause to provide appropriate treatment and management.
This document summarizes imaging findings related to subarachnoid hemorrhage (SAH). It describes that SAH appears as hyperdense linear structures on CT and hyperintense on FLAIR MRI. The location of blood can localize the source of bleeding such as anterior communicating artery aneurysms presenting with blood in the interhemispheric fissure. Complications include vasospasm, hydrocephalus, and superficial siderosis. Reversible cerebral vasoconstriction syndrome is also discussed, appearing as multifocal "string of beads" narrowing on angiography that resolves within 12 weeks.
Cerebral herniation occurs when brain tissue shifts from its normal position inside the skull due to swelling. This is usually caused by head injury, stroke, bleeding or tumors. There are several types of herniation including subfalcine, transtentorial, uncal, and cerebellar tonsillar herniation. Management involves reducing intracranial pressure through surgical removal of mass lesions, ventricular drainage, medical therapies like hyperventilation, hyperosmotic agents, induced hypertension, barbiturate coma or hypothermia, and in severe cases decompressive craniectomy. The condition progresses through stages as herniation worsens and involves specific neurological exam findings at each stage.
This document discusses several normal EEG patterns seen in sleep, including:
1) Positive occipital sharp transients of sleep (POSTs), which appear as sharp waves over the occipital regions during light sleep and stage 2 sleep in most healthy adults and children over 3 years old.
2) Posterior slow-wave transients associated with eye movements, seen as slow waves over the occipital regions following eye blinks or movements in children aged 6 months to 10 years.
3) Occipital slow transients or "cone waves", seen as high amplitude slow waves over the occipital regions during transitions from light to deep sleep in infants and children up to age 5.
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.
Temporal lobe epilepsy is one of the most common forms of epilepsy. It can be caused by hippocampal sclerosis or lesions in the temporal lobe. Hippocampal sclerosis involves neuronal loss and gliosis in the hippocampus and is the most common pathological finding in temporal lobe epilepsy patients. Interictal EEG findings like temporal intermittent rhythmic delta activity and temporal sharp waves help lateralize the seizure focus. Video EEG monitoring helps capture seizures and interictal discharges. Treatment involves antiepileptic drugs and potentially resective surgery for drug-resistant cases.
Comatose nonconvulsive status epilepticus (NCSE) is a condition characterized by a coma state accompanied by continuous or periodic epileptiform brain activity, as seen on EEG. The diagnosis requires both clinical assessment showing a comatose state as well as EEG confirmation of epileptiform discharges. Treatment involves administering anti-epileptic drugs (AEDs) and continuing the treatment if it leads to improvements in both the EEG findings and clinical condition. However, AEDs should not be continued if EEG abnormalities improve without accompanying clinical recovery, as clearing of EEG patterns alone may not indicate resolution of the underlying condition.
1) Neurological injury is a leading cause of death for patients who experience cardiac arrest and are successfully resuscitated. Only 30% of eligible patients receive post-arrest targeted temperature management (TTM), formerly known as therapeutic hypothermia.
2) TTM involves lowering a patient's body temperature to 32-34°C for 24 hours after resuscitation to reduce neurological injury from global hypoxic insult during cardiac arrest. Proper sedation, electrolyte monitoring, and a slow rewarming period are important aspects of TTM.
3) While TTM is the standard of care, additional neuroprotective strategies are being studied, including pharmacological approaches targeting cell death pathways and modulation of oxygen free radicals
Endovascular neurosurgery uses minimally invasive techniques guided by imaging to treat cerebral aneurysms, arteriovenous malformations, tumors, and vasospasm. Clinical trials show benefits to intra-arterial thrombolysis up to 6 hours and mechanical revascularization up to 8 hours after stroke. Endovascular techniques are also used to treat unruptured and ruptured aneurysms using coils, stents and flow diverters to occlude the aneurysm and prevent rebleeding. While effective, complications can include hemorrhage in up to 10% of mechanical thrombectomy cases.
This document discusses central nervous system vasculitis, including its classification, diagnosis, and treatment. It covers primary angiitis of the CNS and secondary causes. Diagnosis is challenging due to non-specific symptoms and lack of sensitive tests. Evaluation involves clinical assessment, CSF analysis, neuroimaging, and cerebral angiography. Treatment depends on the specific type but often involves immunosuppressants like cyclophosphamide with glucocorticoids. Pathology evaluation can help in difficult cases but has low sensitivity.
Intra operative neurophysiological monitoringKode Sashanka
This document discusses intra-operative neurophysiological monitoring during surgeries. It provides an overview of the need for monitoring, the types of monitoring used, and how they work. Monitoring includes EEG, somatosensory evoked potentials, motor evoked potentials, and more. These techniques provide real-time feedback on the functional status of the nervous system during surgery to help reduce risks. Anesthetic management and different monitoring systems are also reviewed.
The glymphatic system, a recently-discovered immune system of the central nervous system that offers opportunities for the development of techniques to modulate immune response. An opportunity for osteopathic manipulation research.
This document discusses various types of autoimmune encephalitis. It begins by providing clues that can suggest an autoimmune cause over infectious, including a subacute onset and fluctuating course. It then covers several specific autoimmune encephalitis subtypes defined by the neuronal surface antigens involved, such as anti-NMDA receptor and anti-LGI1 encephalitis. For each subtype, it discusses clinical features, investigations, and treatment approaches. The document aims to help clinicians differentiate between autoimmune and infectious causes of encephalitis.
Hirayama disease is a rare condition first described in 1959 that mainly affects teenage boys and young men. It causes progressive but non-fatal weakness and wasting of muscles in the forearm and hand, typically on one side only. Diagnosis involves MRI of the neck in full flexion showing a crescent-shaped lesion compressing the spinal cord. Treatment focuses on preventing neck flexion using a cervical collar, as the condition often resolves spontaneously within 6 years.
This document describes several benign EEG variants that can have an epileptiform appearance but are not epileptogenic. It discusses characteristics of alpha variants, mu rhythm, lambda waves, rhythmic mid-temporal theta discharges, wicket spikes, subclinical rhythmic electroencephalographic discharges of adults, phantom spike-wave discharges, and small sharp spikes. These benign variants can occur during drowsiness and light sleep and are seen in specific electrode sites, with features like attenuation with eye opening or movement in the case of mu rhythm. Accurate identification requires training to distinguish them from true epileptiform discharges.
The document discusses the goals and techniques used in the presurgical evaluation of patients with epilepsy. The main goals are to accurately map the brain region responsible for generating seizures (epileptogenic zone) while avoiding functional areas. Key techniques discussed include high-resolution MRI to identify lesions, scalp EEG monitoring to localize seizures, fMRI to map language and motor functions, and MRS to identify metabolic abnormalities. A multidisciplinary team evaluates all test results to localize the seizure focus and plan the safest surgery.
This document discusses various syndromes that can result from strokes in different areas of the brainstem. It begins with an overview of brainstem anatomy and blood supply. It then describes in detail the clinical presentations of medial and lateral midbrain syndromes, various pontine syndromes including medial and lateral inferior pontine syndromes, and medial and lateral medullary syndromes. Case examples are provided to illustrate the different neurological deficits that can occur based on the location of the brainstem stroke.
Calibration of an EEG machine involves checking various parameters to ensure accurate measurements. It is important as it allows correct interpretation of recordings and comparison to previous studies. Parameters checked include paper speed, pen alignment, centering and damping, time constant, high frequency filter, sensitivity, amplitude linearity, gain, noise level and more. Verifying these helps identify any issues needing adjustment and confirms the machine is functioning properly.
This presentation looks at generalised periodic epileptiform discharges and the various disorders like Creutzfeldt Jacob disease (CJD), SSPE and metabolic encephalopathies in which it is seen. SIRPID is also discussed. Triphasic waves are described. Radermacker complexes in SSPE are described.
The document summarizes the process of presurgical evaluation for epilepsy patients. It discusses how modern imaging techniques like video EEG monitoring, high-resolution MRI, fMRI, PET and SPECT are used to localize the epileptogenic zone noninvasively in most patients. When noninvasive methods are insufficient, invasive EEG monitoring using subdural or depth electrodes may be used. The goal is to precisely identify the brain area responsible for seizure generation to allow its surgical resection, while avoiding damage to critical functions. A classical example where surgery is often curative is mesial temporal lobe epilepsy.
05.31.13 Non-Convulsive Status Epilepticus (NCSE) - Bittel.pptFrankyQ2
This document summarizes the experience of a tertiary care center with non-convulsive status epilepticus (NCSE). It provides background information on NCSE including epidemiology, clinical features, EEG criteria for diagnosis, and treatment challenges. It then presents data from a review of NCSE cases at the institution from 2009-2013. The majority of cases were classified as complex partial status epilepticus and most patients presented with confusion or lethargy. Treatment often involved multiple anti-epileptic drugs and anesthesia in refractory cases. Outcomes depended on underlying etiology but NCSE was associated with prolonged ICU and hospital stays.
This document discusses electrodiagnostic criteria for Guillain-Barré syndrome (GBS) subtypes acute inflammatory demyelinating polyneuropathy (AIDP) and acute motor axonal neuropathy (AMAN). It reviews the evolution of criteria sets over time, including those proposed by Asbury, Albers, Cornblath, Ho, Hadden, and others. Key findings include that early electrodiagnosis can be difficult, with reversible conduction failure in AMAN sometimes mimicking AIDP. Serial nerve conduction studies are important for distinguishing subtypes and determining prognosis, as features may change over time. The document also discusses pathological mechanisms and involvement of sensory fibers.
Pediatric stroke can be caused by a variety of conditions including sickle cell disease, infections like varicella, cardiac diseases, moyamoya disease, cerebral venous sinus thrombosis, and vascular malformations. Diagnostic techniques like MRI, MRA, CT, and angiography are used to identify abnormalities and characterize the nature of the stroke. Common findings include lesions in the brain parenchyma that may involve gray or white matter or cross vascular territories, stenosis or occlusion of arteries, moyamoya vessels, and venous sinus thrombosis. Pediatric stroke requires identifying its underlying cause to provide appropriate treatment and management.
This document summarizes imaging findings related to subarachnoid hemorrhage (SAH). It describes that SAH appears as hyperdense linear structures on CT and hyperintense on FLAIR MRI. The location of blood can localize the source of bleeding such as anterior communicating artery aneurysms presenting with blood in the interhemispheric fissure. Complications include vasospasm, hydrocephalus, and superficial siderosis. Reversible cerebral vasoconstriction syndrome is also discussed, appearing as multifocal "string of beads" narrowing on angiography that resolves within 12 weeks.
Stroke is a major cause of death and disability globally. Diagnosis depends on clinical features and brain imaging to differentiate between ischemic stroke and intracerebral hemorrhage. Management of ischemic stroke has advanced with therapies like intravenous thrombolysis and endovascular thrombectomy shown to reduce disability if applied rapidly. Both hemorrhagic and ischemic strokes require identifying risk factors and mechanisms to target prevention interventions, while lifestyle changes are common to reducing risk for all stroke subtypes.
Opportunistic infections and diseases of the central nervous system are common in patients with HIV/AIDS. Post-mortem studies show that up to 70% of AIDS patients have CNS abnormalities. Common conditions include HIV encephalopathy, which causes cognitive and motor impairment; cerebral toxoplasmosis, the most common mass lesion; and primary cerebral lymphoma. Other opportunistic infections that can affect the brain include cryptococcosis, progressive multifocal leukoencephalopathy, tuberculosis, and herpes virus infections. Imaging findings may include cerebral atrophy, white matter lesions, enhancing mass lesions, meningeal enhancement, and hydrocephalus, depending on the specific condition.
Upper extremity arterial disease can be caused by large vessel occlusive diseases like atherosclerosis or embolism, or small vessel diseases like autoimmune disorders. Symptoms range from Raynaud's phenomenon to acute ischemia with pain and pallor. Evaluation involves vascular exams, imaging like ultrasound and angiography. Treatment depends on severity and includes medications for vasospasm, endovascular interventions for stenoses, or open surgery for severe occlusions.
This document discusses the differential diagnosis of acute and subacute non-traumatic paraplegia. Possible causes include vascular, inflammatory, and neoplastic disorders of the spinal cord. Vascular causes include ischemic myelopathy from conditions like atherosclerosis or vasculitis, as well as spinal hemorrhage or vascular malformations. Inflammatory disorders include transverse myelitis of various etiologies, as well as inflammatory lesions that compress the spinal cord. Diagnostic testing like MRI and lumbar puncture can help distinguish between these potential causes. Rapid diagnosis and treatment is important, as many cases can be prevented from becoming irreversible paraplegia if caught early, when symptoms are still developing.
This document discusses stroke and conditions that can mimic stroke. It begins by defining stroke as a sudden neurological deficit caused by arterial ischemia or hemorrhage. While ischemic stroke diagnosis is often straightforward, clinical diagnosis is inaccurate 10-30% of the time as other conditions like infections, seizures, or tumors can appear similar. The document then discusses using a pattern-based approach to differentiate arterial ischemic strokes from stroke mimics based on imaging appearance over time from acute to chronic stages. Specific vascular territories, imaging sequences, and distinguishing features of common mimics like seizures and tumors are reviewed.
Cerebral venous thrombosis (CVT) is an uncommon type of stroke caused by a blood clot in the brain's venous sinuses or veins. It has a significant morbidity. Common presentations include headache, seizures, and long-lasting neurological deficits. Diagnosis is made through imaging studies like MRI and MRV. Treatment involves management of increased intracranial pressure, seizures, and anticoagulation with heparin or thrombolytics to prevent extension of clots. Prognosis depends on factors like impaired consciousness, underlying cause and location of clots. Most patients recover without sequelae, but mortality can be high if left untreated.
This document provides an overview of Moyamoya disease. It defines Moyamoya disease as a progressive stenosis of the intracranial arteries, typically the internal carotid arteries and proximal middle and anterior cerebral arteries, accompanied by a compensatory network of collaterals at the brain's base. The cause is unknown but genetic factors are believed to play a role. Clinically, it can present with transient ischemic attacks, strokes, or hemorrhage. Diagnosis is based on neuroimaging findings on MRI, MRA, CTA or DSA showing the characteristic vascular changes. Treatment involves medical management as well as surgical revascularization procedures. Prognosis depends on the extent of vascular involvement and collateral formation.
Primary central nervous system vasculitis (PACNS) is a rare disorder characterized by inflammation of blood vessels in the brain and spinal cord. It presents with non-specific symptoms like headache, cognitive impairment, and focal neurological deficits. Diagnosis involves neuroimaging showing multifocal lesions, angiography revealing vessel narrowing and dilation, and brain biopsy detecting immune cell infiltration of vessel walls. While the cause is unknown, infectious agents may trigger PACNS. Treatment involves immunosuppression but prognosis depends on disease severity and response to treatment.
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.
This document discusses several topics related to central nervous system infections, including skull osteomyelitis, epidural abscess of the brain, subdural empyema, brain abscess, and spinal infection. It provides information on pathogens, pathogenesis, clinical features, diagnosis, and treatment for each condition. Key points include that skull osteomyelitis is usually caused by S. aureus or S. epidermidis and can result from direct inoculation or hematogenous spread. Brain abscesses often originate from a contiguous infectious source but can also be hematogenous, and treatment involves antibiotics, surgical drainage, or a combination. Spinal epidural abscess is most commonly located in the thoracic region and caused by S. aureus
Pediatric stroke can be caused by a variety of factors such as cardiac diseases, infections like varicella, sickle cell disease, moyamoy disease, cerebral sinus thrombosis, and genetic conditions like MELAS. The presentation of pediatric stroke depends on the location and size of the lesion in the brain. Diagnosis involves imaging techniques like CT, MRI, MRA and angiography. Early diagnosis and treatment is important to prevent long term neurological deficits in children.
This case involves a 2-year-old male child who presented with fever and seizures and was found to have meningeal irritation on examination. MRI showed bilateral symmetrical hyperintensities involving the cortical grey matter of the frontal, parietal, occipital and temporal lobes, as well as the insula and sylvian fissure, with restricted diffusion. There was also hyperintensity in the thalami and caudate heads without restriction. CSF analysis revealed lymphocytic pleocytosis. These findings are consistent with viral encephalitis.
Definition of stroke and cerebrovascular disorders and pathophysiology of cerebral infarct and CT imaging overview of acute-subacute and chronic infarcts and penumbra.
causes of cerebral edema , Radiological signs of acute infarct and hemorrhagic infarct and comparison of MRI and CT in the diagnosis of acute infarct
Role of diffusion weighted imaging (DWI) and diffusion perfusion mismatch
This document provides an overview of primary central nervous system vasculitis (PACNS), including:
1. PACNS is a rare inflammatory disease of blood vessels in the brain that causes varied neurological symptoms. The cause is unknown.
2. Diagnosis is challenging due to non-specific symptoms but may involve MRI, lumbar puncture, angiography, and brain biopsy. Brain biopsy provides the most definitive diagnosis but is not always possible.
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1. IN FECTI0N AS A RISK
FACTOR OF STROKE
Osama A. Ragab
Neurology, MD
2016
2. • Although established risk factors for stroke exist, some infectious
pathogens might confer additional risk either by aggravating
theses factors or having a direct causal role.
3. • Several findings suggest a possible association between systemic infection and
stroke.
• Some patients who had stroke lack traditional cerebrovascular risk factors.
• stroke incidence rises during cold months, which leads to speculation that
infections contribute to this seasonal fluctuation
4.
5. MECHANISM OF STROKE RELATED INFECTION
• Stimulation of the inflammatory response is thought to be the predominant
mechanism linking ischaemic stroke with infection .
• Inflammatory cascades promote atherosclerosis, plaque rupture, and
thrombosis, leading to ischaemic stroke.
• High-sensitivity C-reactive protein in the blood might be an independent
predictor of ischaemic stroke, but its precise association is unsettled.
• A systemic inflammatory response to infection can injure vascular endothelial
cells and predispose patients to intracranial haemorrhage.
8. INFECTIVE ENDOCARDITIS
• Stroke occurred in 17% of adult inpatients with infective endocarditis enrolled in a study done
in 25 countries.
• The risk of stroke was highest at presentation of infective endocarditis and declined within 1–
2 weeks after antibiotics were initiated.
9. • S aureus, β-haemolytic streptococci, and Streptococcus viridans are the most
frequently identified pathogens in infective endocarditis complicated by
intracranial haemorrhage.
• Degradation of the arterial wall by bacteria or septic embolisation causes
abnormal dilatations or mycotic aneurysms.
• These aneurysms can be numerous and occur at distal portions of the middle
cerebral artery, and their rupture is associated with a high mortality rate.
INFECTIVE ENDOCARDITIS
10. • Transesophageal echocardiogram at the level of the midesophagus demonstrating a large vegetation on the
left atrial side of the mitral valve (arrow). The patient reported no neurological symptoms, and a detailed
neurological examination was normal. Right, Axial MRI of the brain using a fluid-attenuation inversion
recovery sequence. The bright lesion in the left frontal cortex (arrow) represents ABE. LV indicates left
ventricle.
11. • T2* cerebral magnetic resonance imaging shows corticomeningeal small black dots related to
microhemorrhages (A). At the corresponding site of a left frontal microhemorrhage (white arrow),
axial and sagittal magnetic resonance angiography views (B and C) suggest the presence of a
fusiform mycotic aneurysm; arterial origin was confirmed by using cerebral angiography (D)
12. BACTERIAL MENINGITIS
• Brain infarction occurred in (25%) of patients with bacterial meningitis.
• venous infarction also complicates bacterial meningitis in 3–5% of patients.
• One prominent mechanism for arterial infarction is vasculitis, most commonly
associated with inflammation of large and medium cerebral blood vessels.
• Concentrations of interleukin-6 were notably elevated in the cerebrospinal fluid of
the patients.
• Reactive oxygen species and reactive nitrogen intermediates have been identified as
critical mediators of the pathogenesis of bacterial meningitis related stroke.
13.
14. • Bacterial meningitis may be complicated by intracranial haemorrhage in 1–3% of patients.
• Causative bacteria include S pneumoniae in 67% of patients, S aureus in 21% of patients, and
Pseudomonas aeruginosa or Listeria monocytogenes in a few patients .
• Intracranial haemorrhage might be evident at presentation, but in about two-thirds of cases,
the haemorrhage is diagnosed later in the clinical course.
• the most frequent types of cerebral haemorrhage are intraparenchymal (42%) and
subarachnoid (21%), followed by haemorrhagic transformation of infarction (17%) and
microhaemorrhages (13%).
BACTERIAL MENINGITIS
15. • D, Apparent diffusion coefficient maps showing an acute ischemic lesion involving the
complete MCA stroke territory.
• E ,MR angiography reveals a severe stenosis and reduced flow within the right distal internal
carotid artery and the proximal MCA (arrow) of the same patient.
• H, Ischemic infarct involving left posterior, inferior temporal, and occipital lobe. Additional
involvement of the splenium of the corpus callosum
16. • A 36 year old lady with meningitis showing A) normal cranial MRI but her B) MR venography
shows thrombosis of superior sagittal sinus (white arrow).
17. • Cerebral CT scan without contrast showing a hematoma in the basal ganglia in a patient with
meningitis due to S. pneumoniae.
18. TUBERCULOSIS
• In tuberculous meningitis, a necrotising meningoencephalitis develops with
leptomeningeal exudates that surround the brainstem and infiltrate the walls
of arteries and veins.
• The hypercoagulable state might be associated with low blood concentrations
of protein S and increased concentrations of factor VIII.
• The sites that are susceptible to cerebral infarction in patients with TB
meningitis are the basal ganglia, internal capsule, thalamus, cerebral cortex,
pons, and cerebellum
• Aneurysmal dilatation, ruptured mycotic aneurysm, and granulomatous septic
embolism have also been noted.
19. • Stroke occurs in 45% of patients with TBM both in early and later stage, mostly in basal
ganglia region, and predicts pooroutcome at 3 months.
• Stroke was significantly related to stage of meningitis, hydrocephalus, exudate, and
hypertension.
20. • Cranial MRI of patient with Tuberculosis meningitis (TBM) shows cortical and subcortical
infarcts in Diffusion weighted Imaging (DW1) (A) and T2 images (B).
23. HERPES SIMPLEX
• HSV-1, when causing meningoencephalitis, can lead to petechial cerebral haemorrhages and
intracranial haemorrhage in severe cases.
• Disruption of the blood–brain barrier, cerebral oedema, and necrosis, particularly involving
the temporal lobe, orbital gyrus, insula, and angular cortex are well described.
• The outcome of fulminant cerebral haemorrhage in the setting of HSV encephalitis is generally
poor, even with antiviral therapy .
• Areterial ischaemic stroke may occur but less frequent than haemorrhage.
24. An axial T2W MRI image shows an area of left medial temporal lobe encephalitis (left). On
the right, an axial CT image without contrast shows the presence of bleeding in the same
encephalitic area, with brainstem compression and obliteration of the lateral ventricle horn
25. • Brain MRI (T1 post-IV contrast) showing enhancement in the area of the ischemic
stroke.
26. VZV can spread to arteries in the central nervous system and
cause hemorrhagic or ischemic complications due to an
inflammatory vasculopathy.
VARICELLA ZOSTER VIRUS
27. Their findings provide evidence that HZ carries an increased risk of stroke or
TIA and that the effect of HZ on stroke decreases with increasing age.
28. • VaricStrokes related to VZV infection tend to affect the deep structures of the brain, including
the basal ganglia and internal capsules, as well as the cerebral cortex supplied by the
branches of the middle cerebral artery.
VARICELLA ZOSTER VIRUS
29. • Hepatitis C virus (HCV) could increase the long-term risk of stroke and stroke
death.
• This increase might occur either through cryoglobulinaemia, which leads to a
rise in deposition of immune complexes in the vessel wall or atherosclerosis
provoked by inflammation.
• It has been demonstrated that HCV lives and replicates within carotid plaque
and the virus enters and replicates inside human brain endothelial cells
• It is important to consider that a significant number of patients with HCV and
stroke did not show liver disease or had only a moderate disease.
HEPATITIS C VIRUS
30.
31. CNS vasculitis in a patient with HCV infection.
Brain MRI showed a left caudate nucleus and
lenticulocapuslar recent ischemic lesion in DWI
(a); an old infarction in, the right ACA territory,
and other white matter changes were visible in
FLAIR (b). Time of flight MR angiography
revealed multiple intracranial stenosis in the
proximal ACA, left ACP and basilar artery
segments (c). Conventional cerebral
angiography documented right ACA occlusion
(d), critical stenosis at the left A1/A2 segment
(e), and occlusion of the inferior 1/3 and of the
distal segment of right vertebral artery (f),
32. HIV
• HIV can directly invade the CNS as early as 8 days after systemic infection, producing
increased inflammatory markers in CSF and brain parenchymal inflammation.
• Thinning of the arterial media layer and fragmentation of internal elastic lamina occurs in
patients with chronic HIV .
• Several case series have reported aneurysmal and non-aneurysmal dilatation of arteries.
• Protein S deficiency is often identified in HIV,
• Other coagulopathies, namely antiphospholipid antibody syndrome, have been reported.
36. FUNGI
• Fungal meningitis typically cause vasculopathy of the large vessels traversing
the subarachnoid space,
• venous outflow obstruction, and endarteritis mechanistically account for
stroke.
• Fungi can also form focal brain parenchymal abscesses associated with
haemorrhage.
• The highly destructive organisms can invade the walls of major intracranial
arteries, including the basilar artery, predisposing to stroke and aneurysmal
rupture.
37. • Sagittal T2 and postcontrast sagittal and axial T2 images showing
heterogeneous T2 signal intensity lesion in the sphenoid sinus destroying the
posterior wall and with enhancing soft tissue extending into prepontine
cisterns encasing basilar artery and causing basilar artery thrombosis.
39. CHAGAS DISEASE
• Chagas disease, caused by the Trypanosoma cruzi, is the third most common parasitic
infection worldwide, with the largest infected population living in South America, Africa and
Iraq.
• Chagas disease is associated with cardioembolic stroke.
• Cerebral embolism most commonly occurs to the middle cerebral artery territory, affecting
70% of patients with Chagas cardiomyopathy.
40.
41. • Brain scans of patients with Chagas disease
• (A) MRI (fluid-attenuated inversion recovery sequence) showing several previous ischaemic strokes in
the territory of both middle cerebral arteries in a 37-year-old man. (B) MRI (T2 sequence) showing
cerebellar ischaemic infarction (in region of the posterior inferior cerebellar artery) in a 32-year-old
man.
42. NEUROCYSTICERCOSIS
• CNS infection with Taenia solium occurs when cysticerci lodge in the subarachnoid space,
brain parenchyma, or cerebral ventricles, causing local inflammation.
• Neurocysticerci can remain for years before undergoing degeneration, which stimulates an
inflammatory reaction with surrounding leptomeningeal deposition of exudative material.
This stage of infection is generally associated with seizure activity, increased intracranial
pressure, and ischaemic and haemorrhagic infarcts.
43. • (A) MRI fast imaging employing steady state
acquisition (FIESTA) axial image showing intra-
ventricular cystic lesions with ipsilateral
ventricular dilatation. (B) MRI T2W coronal
image displaying a left side temporo-parietal
infarction. (C) Computer tomography
angiography shows decrease blood flow
through LMCA (dotted arrow) and contralateral
ICA aneurism (white arrow). (D) Digital
substraction angiography confirmation of right
ICA aneurism (black arrow).
44.
45. SCHISTOSOMIASIS
• Cerebrovascular events can occur during any stage of schistosomiasis, but occur most often in
the subacute and chronic stages.
• Schistosomal ectopic eggs reach the CNS through retrograde flow through the venous plexus.
• Eosinophil-mediated toxicity may lead to vasculitis and small-vessel thrombosis in acute
schistosome vasculitis.
• Cerebral haemorrhage typically occurs in the setting of a meningitic granulomatous reaction
around schistosomal ova.
46.
47. MALARIA
• the mechanical theory claims that the obstruction of the capillaries and cerebral venules by
parasitized erythrocytes is caused by direct action of the parasite on the erythrocyte, distorting its
morphology.
• The results are thrombosis, anoxia, stroke, and tissue necrosis. In more serious cases, further
endothelial damage produces increase in capillary permeability and even hemorrhages.
• There is also a discoloration of the cortex due to hemozoine (malarial pigment).
Malaria digest haemoglobin and release high quantities of free heme, which is the non-protein
component of hemoglobin. Free heme is toxic to cells, so the parasites convert it into an insoluble
crystalline form called hemozoin.
Since the formation of hemozoin is essential to the survival of these parasites, it is an attractive target
for developing drugs .
Several currently used antimalarial drugs, such as chloroquine and mefloquine, are thought to kill
malaria parasites by inhibiting haemozoin biocrystallization.
48. • Cerebral malaria can cause cerebral edema, diffuse or focal compromise of the
subcortical white matter, and cortical, cerebellar and pontine infarctions .
49. • Brain vessels from four different cases of fatal falciparum malaria showing accumulations of
different parasite stages. A, late trophozoites, B, schizonts with abundant pigment; C, mid-stage
trophozoites; D; ring forms containing no intraerythrocytic pigment.
50. WHEN TO INVESTIGATE FOR INFECTIOUS
CAUSES
• Patients who have had strokes caused by infection might be misdiagnosed if lumbar puncture
is not done.
• However, lumbar puncture is not indicated when evaluating a typical patient (an elderly
person with atherosclerotic risk factors with sudden-onset focal neurological deficits).
• The clinical symptoms that might indicate infectious causes include a history of antecedent
fever, rash, and known prior infections.
• For immunocompromised patients, the suspicion should be higher and CSF should be obtained
in immunosuppressed patients.
• Meningeal enhancement or multifocal infarctions, particularly ones that do not respect
traditional arterial or venous territories, could raise the suspicion for infectious or
inflammatory pathologies.
51. TREATMENT
• Treatment of systemic infections that precede or accompany stroke requires prompt initiation
of effective antimicrobial therapy.
• The treatment of specific pathogens should generally follow established guidelines wherever
they exist.
• The role of oral or intravenous steroids alongside antibiotics with infections and new stroke is
also unclear.
• Infection is not an official contraindication for thrombolytic therapy; however, formal
recommendations for treatment cannot be made because of insufficient clinical data.
52. • No convincing evidence proves that anticoagulation prevents embolisation in either native or
prosthetic valve-related infectious endocarditis; in fact, the risk of intracranial haemorrhage
is probably increased with anticoagulation.
• Stable, unruptured, cerebral aneurysms are often sufficiently treated with antimicrobials
alone; however, surgery or endovascular therapy can be considered for ruptured aneurysms
or enlarging unruptured aneurysms.
TREATMENT