This presentation provides information on Guillain-Barre syndrome (GBS) and chronic inflammatory demyelinating polyneuropathy (CIDP). It discusses their etiology, clinical presentation, diagnosis, and physiotherapy management. Both GBS and CIDP result from an autoimmune attack on peripheral nerves causing demyelination. While GBS is acute, CIDP is chronic with progressive symptoms over time. Clinical features include weakness, numbness, and sensory loss. Physiotherapy focuses on maintaining function, mobility, and recovery through various exercises depending on the patient's stage of illness. Prognosis is generally good, with around 65% of GBS patients achieving near complete recovery within a year.
A 20-year-old male presented with headaches, double vision, difficulty swallowing and nasal regurgitation over the past 1-3 weeks. On examination, he had neck stiffness and multiple cranial nerve palsies. Imaging showed diffuse pachymeningeal enhancement and bilateral papilledema. Cerebrospinal fluid analysis was consistent with basal meningitis. He was started on antitubercular treatment but developed severe anemia and splenomegaly, and was ultimately diagnosed with acute lymphocytic leukemia involving the central nervous system.
Novel approach to diagnosis of mycobacterial and bacterialNeurologyKota
This document discusses the diagnosis of mycobacterial and bacterial infections of the central nervous system. It provides clinical features of tuberculous meningitis, patterns of tuberculosis in the CNS, and challenges in diagnosing tuberculous meningitis. Various diagnostic techniques and scoring systems are summarized, including the Thwaites diagnostic score, Lancet consensus score, and advances in molecular diagnosis using next generation sequencing, multiplex PCR panels, and nanotechnology-based approaches. Imaging characteristics of tuberculous granulomas on MRI are also outlined.
This document provides diagnostic criteria for chronic inflammatory demyelinating polyneuropathy (CIDP), including:
1) Clinical criteria for typical and atypical CIDP with inclusion/exclusion factors.
2) Definite, probable, and possible electrophysiological criteria involving compound muscle action potential tests.
3) Supportive diagnostic criteria including cerebrospinal fluid analysis, MRI findings, nerve conduction studies, and nerve biopsy results.
It also outlines inclusion/exclusion criteria and supportive criteria specifically for diagnosing pure sensory CIDP without motor involvement.
CIDP is a chronic acquired demyelinating neuropathy. It has two patterns - a continuous progressive course over months to years or a relapsing course with partial recovery between episodes. Diagnosis requires documentation of demyelination through electrodiagnostic testing, CSF analysis and sometimes nerve biopsy. Treatment includes corticosteroids, IVIG and plasmapheresis, which are effective in around 50-70% of patients. Corticosteroids are usually the first line treatment, starting with high dose prednisone and slowly tapering as response occurs.
All u want to knew about epidemiology, pathology, pathogenesis, clinical picture, investigation, differential diagnosis, different treatment modalities.
MRI is the gold standard for diagnosing multiple sclerosis (MS). It can detect focal demyelinating lesions appearing as hyperintense areas on T2-weighted MRI. Different MRI sequences like T1, T2, FLAIR, and gadolinium contrast help identify lesions at various stages. MS lesions typically occur in periventricular white matter, corpus callosum, brainstem, and spinal cord. Advanced MRI techniques like MTR, DTI, and MRS provide additional insights into MS pathology by detecting subtle tissue damage. MRI plays a key role in the diagnostic criteria for MS by demonstrating dissemination of lesions in space and time. It is also used as an outcome measure in clinical trials to monitor
This presentation provides information on Guillain-Barre syndrome (GBS) and chronic inflammatory demyelinating polyneuropathy (CIDP). It discusses their etiology, clinical presentation, diagnosis, and physiotherapy management. Both GBS and CIDP result from an autoimmune attack on peripheral nerves causing demyelination. While GBS is acute, CIDP is chronic with progressive symptoms over time. Clinical features include weakness, numbness, and sensory loss. Physiotherapy focuses on maintaining function, mobility, and recovery through various exercises depending on the patient's stage of illness. Prognosis is generally good, with around 65% of GBS patients achieving near complete recovery within a year.
A 20-year-old male presented with headaches, double vision, difficulty swallowing and nasal regurgitation over the past 1-3 weeks. On examination, he had neck stiffness and multiple cranial nerve palsies. Imaging showed diffuse pachymeningeal enhancement and bilateral papilledema. Cerebrospinal fluid analysis was consistent with basal meningitis. He was started on antitubercular treatment but developed severe anemia and splenomegaly, and was ultimately diagnosed with acute lymphocytic leukemia involving the central nervous system.
Novel approach to diagnosis of mycobacterial and bacterialNeurologyKota
This document discusses the diagnosis of mycobacterial and bacterial infections of the central nervous system. It provides clinical features of tuberculous meningitis, patterns of tuberculosis in the CNS, and challenges in diagnosing tuberculous meningitis. Various diagnostic techniques and scoring systems are summarized, including the Thwaites diagnostic score, Lancet consensus score, and advances in molecular diagnosis using next generation sequencing, multiplex PCR panels, and nanotechnology-based approaches. Imaging characteristics of tuberculous granulomas on MRI are also outlined.
This document provides diagnostic criteria for chronic inflammatory demyelinating polyneuropathy (CIDP), including:
1) Clinical criteria for typical and atypical CIDP with inclusion/exclusion factors.
2) Definite, probable, and possible electrophysiological criteria involving compound muscle action potential tests.
3) Supportive diagnostic criteria including cerebrospinal fluid analysis, MRI findings, nerve conduction studies, and nerve biopsy results.
It also outlines inclusion/exclusion criteria and supportive criteria specifically for diagnosing pure sensory CIDP without motor involvement.
CIDP is a chronic acquired demyelinating neuropathy. It has two patterns - a continuous progressive course over months to years or a relapsing course with partial recovery between episodes. Diagnosis requires documentation of demyelination through electrodiagnostic testing, CSF analysis and sometimes nerve biopsy. Treatment includes corticosteroids, IVIG and plasmapheresis, which are effective in around 50-70% of patients. Corticosteroids are usually the first line treatment, starting with high dose prednisone and slowly tapering as response occurs.
All u want to knew about epidemiology, pathology, pathogenesis, clinical picture, investigation, differential diagnosis, different treatment modalities.
MRI is the gold standard for diagnosing multiple sclerosis (MS). It can detect focal demyelinating lesions appearing as hyperintense areas on T2-weighted MRI. Different MRI sequences like T1, T2, FLAIR, and gadolinium contrast help identify lesions at various stages. MS lesions typically occur in periventricular white matter, corpus callosum, brainstem, and spinal cord. Advanced MRI techniques like MTR, DTI, and MRS provide additional insights into MS pathology by detecting subtle tissue damage. MRI plays a key role in the diagnostic criteria for MS by demonstrating dissemination of lesions in space and time. It is also used as an outcome measure in clinical trials to monitor
A 49-year-old man presents with progressively worsening headaches, vomiting, and blurry vision over 3 months before having a seizure. Imaging shows a brain lesion. He undergoes surgical debulking followed by radiation and chemotherapy. The most likely diagnosis is glioblastoma multiforme based on the clinical presentation and management. Glioblastoma multiforme is an aggressive primary brain tumor that commonly causes seizures and neurological deficits. Prognosis is generally poor despite aggressive treatment.
1. This case presentation describes a 30-year-old female patient admitted with complaints of muscle pain for 2 months, general weakness for 1 month, and difficulty swallowing for 10 days.
2. On examination, the patient had reduced muscle strength and elevated CPK and LDH levels. EMG showed signs consistent with inflammatory myopathy.
3. The patient was diagnosed with polymyositis based on clinical signs, laboratory findings, and EMG results. She was started on high-dose steroids and other treatments.
This document discusses leptomeningeal metastasis (LM), also known as neoplastic meningitis. LM occurs when cancer spreads to the membranes surrounding the brain and spinal cord. The document covers the epidemiology, pathophysiology, clinical presentation, diagnosis, and treatment of LM. Key points include that LM most often originates from breast, lung, or skin cancers and presents with neurological deficits affecting the brain, cranial nerves, or spinal cord. Diagnosis involves MRI, lumbar puncture for cerebrospinal fluid analysis, and ruling out other causes. Prognosis is generally poor with median survival of only a few months.
Chronic Inflammatory Demyelinating Polyradiculoneuropathy (CIDP) is a rare neurological disorder characterized by progressive weakness and impaired sensory function caused by damage to the peripheral nervous system. It has an incidence rate of 1-2 per 100,000 people and predominantly affects males over 50 years old. CIDP is diagnosed based on progressive muscle weakness, reduced reflexes, nerve conduction studies showing demyelination, elevated CSF protein, and nerve biopsy with signs of demyelination. Treatment involves intravenous immunoglobulin, plasma exchange, steroids, or other immunosuppressants, with around 50% of patients experiencing improvement with therapy.
(1) This document presents a case of a 90-year-old male patient who has been chronically ventilated since 2004 due to chronic illness polyneuropathy.
(2) Chronic illness polyneuropathy is a common condition affecting up to 90% of critically ill patients that causes respiratory muscle weakness and difficulty weaning patients from ventilators.
(3) There is no definitive treatment for chronic illness polyneuropathy. Management focuses on prevention through controlling risk factors like sepsis, steroids, and hyperglycemia as well as supportive care and physical therapy to accelerate recovery.
Vitamin B12 deficiency is a common cause of nutritional myelopathy. It presents as slowly progressive myelopathy involving the posterior and lateral spinal cord. Peripheral neuropathy and neuropsychiatric manifestations may also occur. Diagnosis is based on low vitamin B12 levels and elevated methylmalonic acid and homocysteine levels. Treatment involves lifelong parenteral vitamin B12 replacement therapy. Neurological symptoms may improve over months following treatment. Nitrous oxide exposure can also cause vitamin B12 deficient myelopathy, especially in individuals with underlying B12 deficiency.
This document discusses resistant and relapsing polymyositis. It begins by defining resistant disease as when a patient does not respond to adequate doses of steroids plus another immunosuppressant for at least three months. It then discusses several treatment options for resistant disease, including rituximab, intravenous immunoglobulin, tacrolimus, and others. It also describes four scenarios for relapsing polymyositis and the recommended approaches for each scenario.
Membranous nephropathy is a common cause of nephrotic syndrome in adults. It has variable natural history, with about 1/3 of patients achieving spontaneous remission, 1/3 having persistent proteinuria but stable renal function, and 1/3 progressing to end-stage renal disease over 5-10 years. Several factors predict poorer prognosis, including older age, nephrotic syndrome, lower serum albumin and higher proteinuria levels. Studies show immunosuppressive therapy may alter the natural history for patients at high risk of progression, but risks of treatment must be weighed against the likelihood of spontaneous remission.
This document summarizes a presentation on the management of primary central nervous system lymphoma. It discusses the epidemiology, pathogenesis, clinical features, investigations including imaging and pathology, prognostic factors, treatment including chemotherapy protocols and radiation therapy techniques, and a review of literature on clinical trials. The review of literature summarizes 11 key studies comparing outcomes of different chemotherapy regimens, use of whole brain radiation therapy, and impact on survival and neurotoxicity.
Hodgkin's lymphoma accounts for about 30% of malignant lymphomas. It originates in the lymphatic system and was first described by Thomas Hodgkin in 1832. There are four main subtypes: nodular lymphocyte predominant, nodular sclerosing, mixed cellularity, and lymphocyte depleted. It typically presents as painless, enlarged lymph nodes and has a bimodal age distribution, most commonly affecting those aged 25-30 and over 55. Staging involves imaging such as CT and PET scans to determine the extent of disease. Treatment depends on the stage but commonly involves chemotherapy, radiation, or a combination. Prognosis is generally good even for advanced stages.
leptomeningeal metastases, leptomeningeal carcinomatosis, clinical features of leptomeningeal metastases, pathophysiology of leptomeningeal metastases, diagnosis of leptomeningeal metastases, CSF analysis, MRI findings in leptomeningeal metastases, treatment of leptomeningeal metastases,
This document discusses primary central nervous system lymphoma (PCNSL) through several sections. It begins with an introduction that defines PCNSL and classifications. It then covers the pathology of PCNSL through sections on cell origin and pathogenesis, epidemiology, macroscopic and microscopic features, immunohistochemistry, genetics, radiology, growth patterns and spread, grading/behavior, and prognosis. Further sections discuss the presentation, differential diagnosis, investigations, and management protocol for patients with PCNSL.
Enzyme replacement therapy in neurological disordersNeurologyKota
This document discusses enzyme replacement therapy (ERT) for lysosomal storage disorders. It provides details on ERT including its development, mechanisms, available products, dosing and costs. Challenges with ERT include limited blood-brain barrier penetration and immunogenicity. Alternative therapies discussed include substrate reduction therapy, pharmacological chaperones, and direct delivery of enzymes into the cerebrospinal fluid. ERT remains the standard treatment but has limitations for treating neurological manifestations of lysosomal storage disorders.
Primary CNS lymphoma (PCNSL) is a rare form of non-Hodgkin's lymphoma confined to the brain and spinal cord. It most commonly affects immunocompetent elderly patients and presents with neurological symptoms. Diagnosis requires biopsy and imaging shows contrast-enhancing lesions. Standard treatment is high-dose methotrexate-based chemotherapy with consolidation radiotherapy, though radiotherapy is being used less due to neurotoxicity risks, especially in older patients. The prognosis remains poor with median survival around 2 years despite treatment.
Non-Hodgkin's lymphoma can invade the brain and central nervous system, leading to primary central nervous system lymphoma (PCNSL). PCNSL resembles diffuse large B-cell lymphoma but the molecular mechanisms that cause PCNSL are uncertain. Survival has improved with methotrexate-based chemotherapy instead of radiation, but most patients eventually relapse. Advances in imaging and molecular markers have improved diagnosis but better tools are still needed to monitor treatment response and identify therapeutic targets.
This document discusses critical illness polyneuropathy and myopathy (ICU-acquired weakness). It begins by defining these conditions and noting their prevalence among critically ill patients. Risk factors include prolonged mechanical ventilation, sepsis, multi-organ failure, and high doses of corticosteroids or neuromuscular blocking agents. The pathophysiology involves systemic inflammation impairing nerve and muscle function through various mechanisms. Clinically, ICUAW presents as a generalized, symmetrical weakness developing after critical illness onset. Investigations can include nerve conduction studies, electromyography, and muscle/nerve biopsies to differentiate between polyneuropathy and myopathy. Management focuses on preventing ICUAW by minimizing risk factors like intensive insulin therapy and limiting neu
1) MRI is useful for diagnosing and monitoring multiple sclerosis (MS). Common MRI findings in MS include ovoid lesions perpendicular to ventricles that appear as high signal on T2-weighted and FLAIR images.
2) Different MS subtypes have distinct clinical patterns. Relapsing-remitting MS (RRMS) accounts for 58% of cases and is characterized by neurological symptoms lasting over 24 hours followed by complete or partial recovery with intervals of at least one month between relapses.
3) Optimal MRI protocols for evaluating MS include 3D FLAIR, DIR, and SWI sequences which can help detect cortical and subclinical lesions. Monitoring for contrast enhancing lesions on post-g
This patient presented with transverse myelitis involving the cervical spinal cord, with a history of previous transverse myelitis in the dorsal region and left optic neuritis. MRI showed longitudinally extensive lesions involving the cervical and dorsal spinal cord and left optic nerve enlargement. This clinical and radiological picture is consistent with neuromyelitis optica (NMO), also known as Devic's disease, an inflammatory disorder that predominantly involves the optic nerves and spinal cord. NMO can be difficult to distinguish from multiple sclerosis but tends to cause more severe episodes of optic neuritis and transverse myelitis.
Research section. Cervical spondylitic myelopathy, Clinico-radiological appro...Professor Yasser Metwally
Research section. Cervical spondylitic myelopathy, Clinico-radiological approach: Correlation with the Hemorheological parameters and vascular risk factors
http://yassermetwally.com
http://yassermetwally.net
A 49-year-old man presents with progressively worsening headaches, vomiting, and blurry vision over 3 months before having a seizure. Imaging shows a brain lesion. He undergoes surgical debulking followed by radiation and chemotherapy. The most likely diagnosis is glioblastoma multiforme based on the clinical presentation and management. Glioblastoma multiforme is an aggressive primary brain tumor that commonly causes seizures and neurological deficits. Prognosis is generally poor despite aggressive treatment.
1. This case presentation describes a 30-year-old female patient admitted with complaints of muscle pain for 2 months, general weakness for 1 month, and difficulty swallowing for 10 days.
2. On examination, the patient had reduced muscle strength and elevated CPK and LDH levels. EMG showed signs consistent with inflammatory myopathy.
3. The patient was diagnosed with polymyositis based on clinical signs, laboratory findings, and EMG results. She was started on high-dose steroids and other treatments.
This document discusses leptomeningeal metastasis (LM), also known as neoplastic meningitis. LM occurs when cancer spreads to the membranes surrounding the brain and spinal cord. The document covers the epidemiology, pathophysiology, clinical presentation, diagnosis, and treatment of LM. Key points include that LM most often originates from breast, lung, or skin cancers and presents with neurological deficits affecting the brain, cranial nerves, or spinal cord. Diagnosis involves MRI, lumbar puncture for cerebrospinal fluid analysis, and ruling out other causes. Prognosis is generally poor with median survival of only a few months.
Chronic Inflammatory Demyelinating Polyradiculoneuropathy (CIDP) is a rare neurological disorder characterized by progressive weakness and impaired sensory function caused by damage to the peripheral nervous system. It has an incidence rate of 1-2 per 100,000 people and predominantly affects males over 50 years old. CIDP is diagnosed based on progressive muscle weakness, reduced reflexes, nerve conduction studies showing demyelination, elevated CSF protein, and nerve biopsy with signs of demyelination. Treatment involves intravenous immunoglobulin, plasma exchange, steroids, or other immunosuppressants, with around 50% of patients experiencing improvement with therapy.
(1) This document presents a case of a 90-year-old male patient who has been chronically ventilated since 2004 due to chronic illness polyneuropathy.
(2) Chronic illness polyneuropathy is a common condition affecting up to 90% of critically ill patients that causes respiratory muscle weakness and difficulty weaning patients from ventilators.
(3) There is no definitive treatment for chronic illness polyneuropathy. Management focuses on prevention through controlling risk factors like sepsis, steroids, and hyperglycemia as well as supportive care and physical therapy to accelerate recovery.
Vitamin B12 deficiency is a common cause of nutritional myelopathy. It presents as slowly progressive myelopathy involving the posterior and lateral spinal cord. Peripheral neuropathy and neuropsychiatric manifestations may also occur. Diagnosis is based on low vitamin B12 levels and elevated methylmalonic acid and homocysteine levels. Treatment involves lifelong parenteral vitamin B12 replacement therapy. Neurological symptoms may improve over months following treatment. Nitrous oxide exposure can also cause vitamin B12 deficient myelopathy, especially in individuals with underlying B12 deficiency.
This document discusses resistant and relapsing polymyositis. It begins by defining resistant disease as when a patient does not respond to adequate doses of steroids plus another immunosuppressant for at least three months. It then discusses several treatment options for resistant disease, including rituximab, intravenous immunoglobulin, tacrolimus, and others. It also describes four scenarios for relapsing polymyositis and the recommended approaches for each scenario.
Membranous nephropathy is a common cause of nephrotic syndrome in adults. It has variable natural history, with about 1/3 of patients achieving spontaneous remission, 1/3 having persistent proteinuria but stable renal function, and 1/3 progressing to end-stage renal disease over 5-10 years. Several factors predict poorer prognosis, including older age, nephrotic syndrome, lower serum albumin and higher proteinuria levels. Studies show immunosuppressive therapy may alter the natural history for patients at high risk of progression, but risks of treatment must be weighed against the likelihood of spontaneous remission.
This document summarizes a presentation on the management of primary central nervous system lymphoma. It discusses the epidemiology, pathogenesis, clinical features, investigations including imaging and pathology, prognostic factors, treatment including chemotherapy protocols and radiation therapy techniques, and a review of literature on clinical trials. The review of literature summarizes 11 key studies comparing outcomes of different chemotherapy regimens, use of whole brain radiation therapy, and impact on survival and neurotoxicity.
Hodgkin's lymphoma accounts for about 30% of malignant lymphomas. It originates in the lymphatic system and was first described by Thomas Hodgkin in 1832. There are four main subtypes: nodular lymphocyte predominant, nodular sclerosing, mixed cellularity, and lymphocyte depleted. It typically presents as painless, enlarged lymph nodes and has a bimodal age distribution, most commonly affecting those aged 25-30 and over 55. Staging involves imaging such as CT and PET scans to determine the extent of disease. Treatment depends on the stage but commonly involves chemotherapy, radiation, or a combination. Prognosis is generally good even for advanced stages.
leptomeningeal metastases, leptomeningeal carcinomatosis, clinical features of leptomeningeal metastases, pathophysiology of leptomeningeal metastases, diagnosis of leptomeningeal metastases, CSF analysis, MRI findings in leptomeningeal metastases, treatment of leptomeningeal metastases,
This document discusses primary central nervous system lymphoma (PCNSL) through several sections. It begins with an introduction that defines PCNSL and classifications. It then covers the pathology of PCNSL through sections on cell origin and pathogenesis, epidemiology, macroscopic and microscopic features, immunohistochemistry, genetics, radiology, growth patterns and spread, grading/behavior, and prognosis. Further sections discuss the presentation, differential diagnosis, investigations, and management protocol for patients with PCNSL.
Enzyme replacement therapy in neurological disordersNeurologyKota
This document discusses enzyme replacement therapy (ERT) for lysosomal storage disorders. It provides details on ERT including its development, mechanisms, available products, dosing and costs. Challenges with ERT include limited blood-brain barrier penetration and immunogenicity. Alternative therapies discussed include substrate reduction therapy, pharmacological chaperones, and direct delivery of enzymes into the cerebrospinal fluid. ERT remains the standard treatment but has limitations for treating neurological manifestations of lysosomal storage disorders.
Primary CNS lymphoma (PCNSL) is a rare form of non-Hodgkin's lymphoma confined to the brain and spinal cord. It most commonly affects immunocompetent elderly patients and presents with neurological symptoms. Diagnosis requires biopsy and imaging shows contrast-enhancing lesions. Standard treatment is high-dose methotrexate-based chemotherapy with consolidation radiotherapy, though radiotherapy is being used less due to neurotoxicity risks, especially in older patients. The prognosis remains poor with median survival around 2 years despite treatment.
Non-Hodgkin's lymphoma can invade the brain and central nervous system, leading to primary central nervous system lymphoma (PCNSL). PCNSL resembles diffuse large B-cell lymphoma but the molecular mechanisms that cause PCNSL are uncertain. Survival has improved with methotrexate-based chemotherapy instead of radiation, but most patients eventually relapse. Advances in imaging and molecular markers have improved diagnosis but better tools are still needed to monitor treatment response and identify therapeutic targets.
This document discusses critical illness polyneuropathy and myopathy (ICU-acquired weakness). It begins by defining these conditions and noting their prevalence among critically ill patients. Risk factors include prolonged mechanical ventilation, sepsis, multi-organ failure, and high doses of corticosteroids or neuromuscular blocking agents. The pathophysiology involves systemic inflammation impairing nerve and muscle function through various mechanisms. Clinically, ICUAW presents as a generalized, symmetrical weakness developing after critical illness onset. Investigations can include nerve conduction studies, electromyography, and muscle/nerve biopsies to differentiate between polyneuropathy and myopathy. Management focuses on preventing ICUAW by minimizing risk factors like intensive insulin therapy and limiting neu
1) MRI is useful for diagnosing and monitoring multiple sclerosis (MS). Common MRI findings in MS include ovoid lesions perpendicular to ventricles that appear as high signal on T2-weighted and FLAIR images.
2) Different MS subtypes have distinct clinical patterns. Relapsing-remitting MS (RRMS) accounts for 58% of cases and is characterized by neurological symptoms lasting over 24 hours followed by complete or partial recovery with intervals of at least one month between relapses.
3) Optimal MRI protocols for evaluating MS include 3D FLAIR, DIR, and SWI sequences which can help detect cortical and subclinical lesions. Monitoring for contrast enhancing lesions on post-g
This patient presented with transverse myelitis involving the cervical spinal cord, with a history of previous transverse myelitis in the dorsal region and left optic neuritis. MRI showed longitudinally extensive lesions involving the cervical and dorsal spinal cord and left optic nerve enlargement. This clinical and radiological picture is consistent with neuromyelitis optica (NMO), also known as Devic's disease, an inflammatory disorder that predominantly involves the optic nerves and spinal cord. NMO can be difficult to distinguish from multiple sclerosis but tends to cause more severe episodes of optic neuritis and transverse myelitis.
Research section. Cervical spondylitic myelopathy, Clinico-radiological appro...Professor Yasser Metwally
Research section. Cervical spondylitic myelopathy, Clinico-radiological approach: Correlation with the Hemorheological parameters and vascular risk factors
http://yassermetwally.com
http://yassermetwally.net
This document summarizes a case study of an 11-year-old female patient presented with congenital left sided hemiaplasia and Lennox Gastaut syndrome. MRI images showed abnormalities including a large right-sided cyst, agenesis of the septum pellucidum, lissencephaly, hemimegalencephaly, and heterotopias. The patient was diagnosed with Aicardi syndrome associated with multiple cortical dysplasias. The author provides criteria for suggestive of Aicardi syndrome and information on accessing additional case studies and publications on the author's website.
This case discusses a 40-year-old male patient who presented with gradual paraplegia and sensory loss. MRI revealed an intramedullary ependymoma in the dorsal spinal cord that was cystic with bands, causing cord expansion. Ependymoma is the most common intramedullary spinal tumor in adults. The patient was diagnosed with a spinal ependymoma based on the radiological and clinical findings. Complete surgical resection of intramedullary ependymomas offers the best chance for reduced recurrence and improved prognosis.
A 30-year-old male patient presented with a history of grand mal seizures occasionally preceded by visual hallucinations. An MRI revealed a type II left occipital cavernoma, seen as a well-defined lobulated lesion with heterogeneous signal intensity due to thrombosis, fibrosis, calcification, and hemorrhage. The cavernoma has a characteristic "popcorn-like" appearance. The MRI findings are consistent with a diagnosis of intramedullary cavernoma.
A 40-year-old female patient presented with fever, seizures, impaired consciousness, and signs of meningeal irritation. She was diagnosed with herpes simplex encephalitis. The document includes 6 figures showing MRI images of the brain that demonstrate abnormalities in the temporal lobes consistent with herpes simplex encephalitis. An addendum provides information on accessing updated versions and related publications on the editor's website.
A 40-year-old female patient presented with headache, seizures, and altered consciousness. She was diagnosed with venous congestive encephalopathy secondary to venous sinus thrombosis based on MRI findings. The MRI showed dilation and enhancement of the dural sinuses and cortical veins, subcortical abnormalities, and a thrombosed superior sagittal sinus. The case publication was edited by Professor Yasser Metwally and provides MRI images illustrating the findings.
Case record...Vertebral hemangioma with multisegmental retromedullary lipomaProfessor Yasser Metwally
A 51-year-old female presented with paraplegia. Imaging showed a D4 vertebral hemangioma with epidural extension. This was causing compression of the spinal cord by a retromedullary lipoma rather than the hemangioma itself. The lipoma was likely reactive to the hemangioma. Surgical removal of the lipoma significantly improved the patient's symptoms. Vertebral hemangiomas typically appear dotted on imaging due to thickened vertical trabeculae. While usually asymptomatic, they can rarely cause symptoms by vertebral collapse, epidural extension, or bleeding.
This document presents the case of an 11-year-old female patient with Aicardi syndrome. Imaging shows a large cyst on the right side of the brain along with agenesis of the corpus callosum, cortical dysplasias including hemimegalencephaly, lissencephaly, and heterotopias. Aicardi syndrome is characterized by agenesis of the corpus callosum, infantile spasms, and chorioretinal lacunae. Modern imaging has revealed additional brain abnormalities including cortical migration defects, heterotopias, and cysts. The patient's presentation is consistent with Aicardi syndrome based on the imaging and clinical findings.
This document summarizes a case study of a 6-year-old male patient who presented with cerebellar ataxia and headache 3 weeks after a viral infection. Clinical exams revealed trunk and limb ataxia, nystagmus, and papilledema. Brain scans showed bilateral symmetrical lesions in the cerebellar white matter. The patient was diagnosed with acute postinfectious cerebellitis and fully recovered within a week of supportive treatment. The case study is intended to demonstrate the characteristic MRI findings of postinfectious cerebellitis.
This document discusses a case of spinal multiple sclerosis in a 40-year-old patient. MRI images show well-defined pencil-shaped lesions occupying 2-3 spinal segments that are hypointense on T1-weighted images and hyperintense on T2-weighted images. Diffuse abnormalities are also seen as poorly demarcated hyperintense regions on T2-weighted images. The diagnosis is spinal multiple sclerosis. The document then discusses features of spinal MS lesions seen on MRI such as focal lesions, diffuse abnormalities, and spinal cord atrophy, and compares features of MS to other conditions like neuromyelitis optica.
Cavernous carotid aneurysms are the most common type of extradural intracranial aneurysm. They are usually congenital and saccular in shape, arising from branches of the internal carotid artery within the cavernous sinus. About a quarter of cases are bilateral. Rupture can cause a carotid-cavernous fistula. Large unruptured aneurysms can compress nearby structures through mass effect as they expand upward and laterally within confined spaces of the skull. Cranial nerves are frequently compressed, which can impair eye movements or vision. On angiography, a thrombosed aneurysm may be difficult to detect due to surrounding tissue opacification.
This document provides a summary of age dependent epileptic syndromes and focuses on primary generalized epilepsy and benign Rolandic epilepsy. It discusses the key characteristics of each condition including typical age of onset, common seizure types and EEG patterns. The summary concludes that these conditions are age determined and often seen in childhood, with seizures typically remitting by late adolescence.
This document summarizes a case report published by Professor Yasser Metwally in January 2010. It describes a 50-year-old male patient who presented with limited horizontal eye movement for 4 years. Imaging showed a posterior pontine glioma. The patient declined treatment and later presented with worsening symptoms. MRI revealed a diffuse brain stem glioma involving the pons, midbrain and crus cerebri. The patient died 2 days after hospitalization. The case report is accompanied by 5 figures illustrating the imaging findings.
A 22-year-old male presented with increased intracranial pressure, meningeal irritation signs, and bilateral papilledema. MRI images showed enhancement of the leptomeninges and pachymeninges, ventricular dilation, and periventricular lesions. He was diagnosed with lymphomatous meningitis affecting both the leptomeninges and pachymeninges.
Topic of the month.... The role of gamma knife in the management of benign br...Professor Yasser Metwally
This document discusses the use of radiation therapy to treat benign intracranial tumors. It provides an overview of the different radiation therapy strategies including stereotactic radiosurgery (SRS), stereotactic radiotherapy (SRT), and fractionated radiation therapy. It describes the key factors in determining which strategy to use such as tumor location, needed dose, and tolerance of surrounding tissues. The document also reviews different radiation sources and delivery methods including 3D conformal radiation therapy and intensity-modulated radiation therapy (IMRT).
1) A 58-year old male developed central pontine myelinolysis (CPM) and extrapontine myelinolysis (EPM) four days after being discharged from the ICU following treatment for hyponatremia.
2) CPM was first described in 1959 as a demyelinating condition affecting the pons seen in alcoholic and malnourished patients. Subsequent studies found it can result from rapid correction of hyponatremia.
3) The pathogenesis of CPM/EPM involves rapid correction of hyponatremia causing an osmotic gradient that opens the blood-brain barrier, allowing blood factors to enter and cause demyelination. The specific
The document discusses two conditions: paroxysmal nocturnal hemoglobinuria (PNH) and atypical hemolytic uremic syndrome (aHUS). PNH is a complement-mediated hemolytic anemia treated with the drug eculizumab, a C5a inhibitor. aHUS is a complement-mediated thrombotic microangiopathy that can cause stroke, heart attack, and kidney failure, and is also treated with eculizumab. The document asks the reader to identify PNH, aHUS, and the mode of action of eculizumab.
Primary CNS Vasculitis - diagnostic and therapeutic challengesDiana Girnita
1. This 38-year-old male presented with severe frontal headache, speech difficulties, weakness, and confusion. Imaging showed multiple small white matter lesions that progressed significantly over 4 days.
2. Cerebrospinal fluid analysis showed elevated white blood cells and protein with positive oligoclonal bands. Infectious and autoimmune workups were negative.
3. Brain biopsy showed early acute ischemic changes and a microscopic focus of acute infarction without evidence of vasculitis, inflammation, or other pathologies. This is consistent with a diagnosis of primary central nervous system vasculitis.
A 67-year-old male presented with headache, facial weakness, and limb weakness. Imaging showed lesions in the left thalamus, midbrain, pons, and cerebellum enhancing on MRI. Biopsy of the thalamic lesion found diffuse large B-cell lymphoma. Further testing found lymphoma in peri-renal soft tissue as well. This represents either secondary CNS lymphoma with systemic involvement or synchronous primary lesions, unusual for primary CNS lymphoma.
leptomeningeal metastases, leptomeningeal carcinomatosis, clinical features of leptomeningeal metastases, pathophysiology of leptomeningeal metastases, diagnosis of leptomeningeal metastases, CSF analysis, MRI findings in leptomeningeal metastases, treatment of leptomeningeal metastases,
This medical record is for a 10-year-old male admitted with coma secondary to complicated pyogenic meningitis and clinical malaria. He presented with a 4-hour history of failure to communicate and had developed abnormal body movements, fever, and headache over the prior days. On examination he was comatose with normal vital signs. Laboratory tests showed normal CBC and imaging was not notable. He was diagnosed with coma secondary to complicated pyogenic meningitis and clinical malaria with moderate acute malnutrition. Treatment included antibiotics, antimalarials, anticonvulsants, and steroids to control seizures, eradicate infections, and decrease symptoms while monitoring for effectiveness and safety.
This document discusses hypertrophic cardiomyopathy (HCM) and provides several key points:
1. HCM has a prevalence of about 1 in 500 people in the general population. In Palermo, Italy where there are 1.2 million residents, it is estimated that at least 6,000 patients have HCM.
2. HCM is caused by mutations in genes encoding sarcomere proteins. The most common genes involved are beta myosin heavy chain, myosin binding protein C, and troponin T.
3. While most HCM patients have left ventricular hypertrophy, some mutation carriers may be "genotype positive/phenotype negative" without overt hypertrophy. These individuals
Primary Small Cell Neuroendocrine Carcinoma of the Petrous Apex: A Report of ...IJBNT Journal
Small cell neuroendocrine carcinomas (SCNEC) are extremely rare in the head and neck region, known to be highly aggressive with poor prognosis. We report the second case in the literature of a poorly differentiated SCNEC involving the petrous apex of the temporal bone, and we present its management.
This document discusses neurological problems that can arise in patients with hematological neoplasms. It covers direct neoplastic involvement of the nervous system such as primary central nervous system lymphoma and leptomeningeal metastasis. It also discusses indirect manifestations like paraneoplastic cerebellar degeneration. Treatment involves an interdisciplinary approach between oncologists, neurologists, and other specialists. Diagnosis involves imaging, spinal fluid analysis, biopsies, and consideration of both direct tumor involvement and indirect paraneoplastic mechanisms.
Progressive multifocal leukoencephalopathy (PML) is a fatal brain disease caused by JC virus in immunocompromised patients. This study examines two PML patients using diffusion-weighted MRI (DWI) and diffusion tensor imaging (DTI) to analyze lesion development. DWI showed abnormal diffusion within lesions, correlating with clinical progression speed. DTI revealed decreased anisotropy and increased diffusion in affected regions, detecting different disease stages not seen on standard MRI. DWI and DTI appear useful for monitoring PML disease activity and response to treatment.
This document presents the case of a 70-year-old man who presented with progressive left greater than right sensorineural hearing loss and gait instability over 3-4 months. His medical history includes diabetes, hypertension, COPD, prostate cancer, and a total colectomy. Physical exam revealed horizontal nystagmus to the left, decreased hearing on the left, and an inability to perform tandem gait. MRI showed diffuse hyperintense nodular lesions involving the cerebellum, brainstem, and spine. The differential diagnosis discussed includes neurosarcoidosis, metastatic disease, primary CNS tumors such as glioma, and leptomeningeal metastases.
This document provides an outline for a course on childhood acute lymphoblastic leukemia (ALL). It covers the definition and epidemiology of ALL, risk factors, clinical presentation, diagnosis, management including treatment phases, complications, prognosis, and prevention. ALL is the most common childhood cancer characterized by excessive lymphoblasts. It peaks between ages 2-3 and has a survival rate over 85% with current treatments over 2-3 years consisting of induction, intensification, and maintenance chemotherapy, along with intrathecal therapy targeting the central nervous system. Complications can include tumor lysis syndrome, infections, and secondary cancers. Prognosis depends on risk factors like age and white blood cell count. Prevention focuses on limiting environmental exposures like benz
This document presents a case study of a 12-year-old girl who presented with prolonged fever for over 20 days. Testing showed bi-cytopenia (anemia and leukopenia), hepatosplenomegaly, lymphadenopathy, and positive EBV and parvovirus serology. A bone marrow biopsy revealed hemophagocytosis. She was ultimately diagnosed with hemophagocytic lymphohistiocytosis (HLH), a life-threatening hyperinflammatory condition. Treatment for HLH involves prompt institution of therapies like steroids, chemotherapy, to prevent irreversible organ damage from the hyperactive immune response.
Primary Non-Hodgkin’s Lymphoma of The Bone (PLB) is rare entity [1,2,3]. Patients generaly present with localised bone pain, soft-tissue swelling or palpable mass. Pathological fracture of the proximal femur and humerus secondary to soft-tissue tumors is well documented in the literature. Lymphomas presenting primarly at these sites with pathological fracture is unusual. A review of the world literature shows that the incidence of the skeletal manifestations from NHL is less than 5%, and in all these cases, bony involvement was reported many years after presentation of the primary cancer. Histopathologically, PLB usually represents diffuse large B-cell lymphoma. We report 56-year-old female patient case report of Primary non-Hodgkin’s limphoma of proximal femur and proximal femur with pathological fracture and management. In January 2014. A 56-year-old woman was diagnosed with stage IV B primatry large-cell diffuse primary non-Hodgik’s lymphoma. After one year of initial diagnostic procedures and chemotherapy with rituximab together with cyclophosphamide, vincristine, procarbazine, and prednisolone she achieved a total response.
BACKGROUND: Sequential Epstein-Barr virus (EBV)–positive B cell lymphoma to the initial diagnosis of angioimmunoblastic T cell lymphoma (AITL) is very rare, the exact mechanism and standard therapy of which is still being explored. CASE: A 50-year-old man was admitted to our hospital in January 2014 with a three-week history of enlargement of multiple lymph nodes. His initial pathological evaluation indicated AILT. The reactivation of EBV was observed during the immunosuppression therapy for AITL, accompanied by onset of subcutaneous nodules proven to be EBV-positive diffuse large B cell lymphoma (DLBCL) based on the pathological findings of rebiopsy. The patient was successfully treated with chidamide, a histone deacetylase (HDAC) inhibitor, and rituximab.
Conclusion: The sufficient surveillance for serum EBV and repeat biopsy is necessary for patients with AITL, and this treatment modality may become an active option.
Keywords: angioimmunoblastic T cell lymphoma, Epstein-Barr virus, HDAC inhibitor, non-Hodgkin lymphoma, peripheral T cell lymphoma
This document discusses Superior Vena Cava Syndrome (SVCS), which occurs when the Superior Vena Cava (SVC) is compressed, reducing blood flow from the head and upper body. The document covers the case presentation of a patient with SVCS, including symptoms, imaging findings, and treatment. It then provides details on the anatomy, etiologies, clinical features, imaging and classification of SVCS. Treatment options for malignant causes of SVCS such as radiation therapy, chemotherapy and stenting are described. A grading system and treatment algorithm for SVCS are also presented.
A 30-year-old man presented with a right testicular mass and bilateral gynecomastia. Radical right orchiectomy showed a Leydig cell tumor on histopathology.
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Mrs. E.W., a 73-year-old woman, presented with dizziness, clumsiness in her left hand, and unsteadiness over one week. Her symptoms progressed to include speech problems, weakness on her left side, and balance issues. Testing revealed abnormalities in her cerebellum but no acute cause was found. Over several weeks her condition deteriorated further. Additional testing uncovered a small tumor in her right breast. She was ultimately diagnosed with paraneoplastic cerebellar degeneration caused by an underlying primary B-cell lymphoma of the breast.
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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.
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Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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Case record...Paraneoplastic leukoencephalopathy
1. CASE OF THE WEEK
PROFESSOR YASSER METWALLY
CLINICAL PICTURE
CLINICAL PICTURE:
A 48-year-old female patient was admitted to our hospital due to sudden gait disturbance. One month prior to the
admission, She suddenly began to experience difficulty performing simple calculations and dressing himself. This
patient visited a local hospital, where She was diagnosed with cerebral infarction and treated with anticoagulation
therapy; no relevant disease, medication, smoking, or alcohol history was noted. She had lost 8 kg in the 6 months
prior to this event, and She was easily fatigued and experienced night sweating and general weakness. Her cognitive
impairment worsened over the next several weeks. She visited our hospital in order to obtain a second opinion.
On admission, the patient was alert and Her orientation was intact. She was a right-handed. She was apathetic,
showed right/left disorientation, and had difficulty performing simple calculations and writing. Her reading and
comprehension were normal. Cognitive functioning was assessed using the Mini-Mental State Examination
(MMSE), on which She scored 18 points out of a possible 30; She lost 5 points on the calculation item, 3 points on
memory recall, 2 points on time orientation, 1 point on writing, and 1 point on the interlocking pentagons item. The
only abnormal finding on cranial nerve examination was mild dysarthria. Her motor power was symmetric and
preserved in all four extremities, but all muscles were moderately hypertonic. Her deep-tendon reflexes were
increased on both sides. She showed symmetric and intact responses to all sensory stimuli and Her cortical senses
were intact. Her neck was supple, and carotid bruit was not audible. She exhibited small, shuffling, and hesitant
steps on gait examination.
The patient's blood pressure was 107/75 mmHg, and Her heart rate was 90 beats/min. We performed brain
magnetic resonance imaging (MRI) and routine blood tests. Brain MRI showed multiple lesions with high signal
intensity in the white matter of the bilateral hemisphere on fluid-attenuated inversion recovery and diffusion-
weighted imaging (DWI), and magnetic resonance angiography showed normal intracerebral and carotid arteries
(Fig. 4A). Apparent diffusion coefficient (ADC) mapping and enhanced T1-weighted imaging were not included in
the MRI analyses. Blood test results showed increased liver enzymes, but serology findings were negative for
hepatitis B and C viruses, the Venereal Disease Research Laboratory Test, and human immunodeficiency virus. A
coagulation panel disclosed normal prothrombin and activated partial thrombin times, but the levels of C and S
proteins were markedly decreased, ranging from only 30% of the normal value. She was negative for serum
autoantibodies, including antinuclear antibody, lupus anticoagulant, and antineutrophil cytoplasmic antibody.
RADIOLOGICAL FINDINGS
RADIOLOGICAL FINDINGS:
2. Figure 1. Precontrast (A) and postcontrast (B) MRI T1 images showing scattered cerebellar, temporal lobes and
brain stem hypointense zones, with mild enlargement of the temporal horns bilaterally. Also noticed meningeal
enhancement completely ensheathing the pons.
Figure 2. MRI FLAIR (A,B) and MRI T2 images showing scattered hyperintese zones around the 4th ventricle and
withen the pons. The hyperinetse zones has no mass effect.
3. Figure 3. MRI FLAIR images showing bilateral hyperintense zones scattered in the cerebral white matter and the
immediate periventricular area, especially involving the genu of the corpus callosum. The hyperintense lesions
apparently have no mass effect. Notice the moderate hydrocephalic changes.
Figure 4. Brain MRI data. Brain MRI showing multifocal white-matter lesions with high signal intensity on fluid-
attenuated inversion recovery (FLAIR), MRI, and DWI, with an increased apparent diffusion coefficient value.
Compared to the initial image (A), the lesions
An abdominal computed tomography was performed to exclude a hepatic malignancy. This revealed multiple ill-
defined, low-attenuation lesions, and multifocal, patchy, arterial, high-attenuation lesions in both lobes of the liver,
with splenomegaly and bilateral adrenal gland enlargement, suggesting lymphoma. Brain MRI performed 4 weeks
after the initial MRI showed enlargement of multifocal confluent subcortical lesions, with increased signal on ADC
maps, suggesting an inflammatory lesion such as demyelinating disease, rather than an acute infarction (Fig. 4B).
4. The lesions were not associated with a mass effect and showed no definite enhancement. Whole-body 18F-
fluorodeoxyglucose (FDG) and positron-emission tomography (PET) revealed multiple hypermetabolic lesions in
the bilateral adrenal glands, liver, and lymph nodes, as shown in Fig. 5. However, there was no alteration of brain
metabolism.
Figure 5. Whole-body FDG PET. Fusion PET
with abdominal computed tomography (CT)
revealed multiple hypermetabolic lesions
involving the liver, lymph nodes, and both
adrenal glands (A, B: white arrows). Brain
PET did not show any significant alteration of
metabolism.
A lumbar puncture study was performed to exclude CNS infection or leptomeningeal involvement of lymphoma.
This showed normal opening pressure with a clear color, and two white blood cells were found, with markedly
increased levels of protein (191.2 mg/dL) and glucose (92 mg/dL; serum glucose, 136 mg/dL). Polymerase chain
reaction studies against viral genes, including human herpes virus types 1-6 and JC virus were all negative. There
was no evidence of tuberculosis, Lyme disease, or fungal infection in staining and culture studies of a lumbar
puncture specimen. Malignant cells were not found on repeated cytologic evaluation of lumbar puncture specimens.
No oligoclonal band or myelin basic protein was found. The presence of paraneoplastic autoantibodies was not
evaluated and a biopsy of the brain lesion was not undertaken. A liver mass biopsy disclosed diffuse large B-cell
lymphoma. The patient was diagnosed with paraneoplastic leukoencephalopathy due to diffuse large B-cell
lymphoma and was treated with systemic chemotherapy, including cyclophosphamide, doxorubicin, vincristine, and
prednisone. Her cognitive impairment and gait disturbance gradually improved over the next 2 months, She
regained the ability to calculate and write letters, Her MMSE score improved to 28, and She regained the ability to
walk and to articulate when speaking. The final brain MRI showed that the extent of the lesion had markedly
decreased (Fig. 4C).
A large proportion of patients with paraneoplastic disorders can be grouped into the clinicopathologic entity of
paraneoplastic encephalomyelitis (PEM). Small cell lung carcinoma is the tumor most commonly associated with
PEM, and some patients with a variety of other neoplasms. PEM is characterized clinically and pathologically by
patchy, multifocal involvement of any or all areas of the cerebral hemispheres, limbic system, cerebellum, brain
stem, spinal cord, dorsal root ganglia, and autonomic ganglia. Neuronal loss is accompanied by a variable degree of
perivascular and leptomeningeal infiltration of mononuclear cells, including T and B lymphocytes and plasma cells.
[13,14] Leptomeningeal infiltration might be responsible for the Leptomeningeal enhancement observed in this
case.
DIAGNOSIS:
DIAGNOSIS: STROKE MIMICKING PARANEOPLASTIC LEUKOENCEPHALOPATHY AS AN INITIAL
MANIFESTATIONS OF DIFFUSE LARGE B-CELL LYMPHOMA
DISCUSSION
DISCUSSION:
Systemic lymphoma can be difficult to recognize due to its diverse manifestations. Paraneoplastic
leukoencephalopathy has rarely been reported in the context of lymphoma.
5. We report a 45-year-old man with systemic lymphoma whose initial manifestation was sudden-onset
leukoencephalopathy, mimicking stroke. This patient, who was eventually diagnosed with diffuse large B-cell
lymphoma, initially presented with sudden cognitive impairment and gait disturbance. Radiological studies
suggested a paraneoplastic leukoencephalopathy. Chemotherapy for lymphoma resulted in clinical and radiological
improvement.
This case signifies the diversity of CNS manifestations, which include cerebral infarction, lymphoma invasion,
atypical infectious encephalitis, and paraneoplastic encephalopathy, [1,2,5,6] in a patient with systemic lymphoma.
The presenting sudden-onset focal neurologic deficit and high-signal-intensity lesion on DWI suggested an initial
diagnosis of cerebral infarction. The combined systemic symptoms, including progressive weight loss, night
sweating, and general weakness, were suggestive of systemic disease, but they were neglected. It is unlikely that a
patient with cerebral infarction would have a progressive clinical course after symptom onset and slow-growing
lesions on brain MRI. The newly expanded lesion had high signal values on both DWI and ADC mapping. It is
therefore highly unlikely that this lesion was the result of acute infarction given that the latter exhibits a high signal
value on DWI and a low ADC value during the acute stage as a result of isotropically restricted water diffusion by
cytotoxic edema. [7]
Brain lymphoma usually presents as a single or multiple enhancing lesions in immunocompetent patients. [8]
However, intravascular infiltration of large B-cell lymphoma shows different MRI findings, typically involving the
white matter, with minimal enhancement after contrast administration and little mass effect, and is typically
referred to as intravascular lymphomatosis. [5] It has been reported that the ADC values of CNS lymphomas are
lower than those of other intracerebral tumors and are close to those seen in acute infarction.9 Intravascular
infiltration of large B-cell lymphoma shows low ADC values due to combined ischemic brain injuries. [10] However,
this patient had a lesion with high signal values on ADC mapping. Additional studies were performed to exclude
CNS malignancy.
FDG PET allows the evaluation of metabolic activity and provides additional information that aids in the
differentiation between lymphoma and nonneoplastic conditions, including CNS lymphoma.[11] The brain lesion in
our patient did not show increased metabolism, suggesting that it was not neoplastic. Cytologic evaluation of
repeated lumbar puncture specimens did not show malignant cells, and the protein level was markedly increased,
suggesting an active inflammatory or demyelinating process. Lumbar puncture specimens were checked repeatedly
for the presence of viral genes, and the results were consistently negative against JC virus and other infectious
pathogens. The findings of brain MRI, FDG PET, and lumbar puncture studies strongly suggested that the brain
lesion in our patient did not involve direct lymphoma invasion or infectious disease, but rather resulted from an
active inflammatory disease such as demyelinating encephalopathy. Our patient showed a good response to systemic
chemotherapy, suggesting paraneoplastic leukoencephalopathy as the most probable diagnosis.
There have been a few reported cases of combined demyelinating CNS lesions in patients with systemic malignancy.
[3,4] There has been one report of diffuse encephaloradiculopathy involving the cerebrum, brainstem, cerebellum,
and peripheral nerves in a patient with silent hepatocellular carcinoma. [3] Tumor-associated immunological
interruption was suggested as a possible mechanism underlying diffuse demyelination of the nervous system. [3]
Another case report describes acute multifocal CNS demyelination as the initial presentation of lung
adenocarcinoma without CNS metastasis. [4] The pathomechanism may involve paraneoplastic autoantibodies or
immunomodulation by the malignancy itself and/or by treatment. Brainstem or temporal lobar involvement in
systemic malignancy is more commonly reported than cerebral white-matter involvement, a condition known as
limbic encephalitis, which is often associated with several autoantibodies, including the anti-Hu antibody. [4]
However, self-limiting, acute, disseminated encephalomyelitis cannot be excluded as a possible diagnosis in this
case. [12]
The findings of this case suggest that systemic lymphoma involves the CNS in the form of paraneoplastic
encephalopathy. It must be differentiated from cerebral infarction, direct lymphoma invasion, and atypical
infection in order to determine the therapeutic plan and accurately forecast the prognosis. This case also suggests
that systemic malignancy must be considered in the differential diagnosis of young patients with sudden-onset
neurological deficits due to brain lesions involving multifocal white matter.
SUMMARY
6. SUMMARY
The presented case indicates that diffuse large B-cell lymphoma may initially appear as a treatable
leukoencephalopathy. Lymphoma and leukemia are systemic diseases that affect many organs, including the central
nervous system (CNS). [1] These cancers may affect the CNS directly via the production of intraparenchymal or
extra-axial mass lesions, or meningeal infiltration, or indirectly by coagulopathy, metabolic disturbance, or
paraneoplastic antibody production. [1] Atypical infections, such as John Cunningham (JC) virus or toxoplasmosis,
can lead to the development of brain lesions in lymphoma patients. [2] Paraneoplastic leukoencephalopathy as an
initial manifestation of systemic malignancy is rare, but several reports have described its intriguing clinical course
and possible pathomechanism. [3,4] Although biopsy sampling is mandatory for a definitive diagnosis, it is often
impossible to perform due to the location or size of the lesion, or patient refusal. The recent considerable progress
in imaging technologies has provided a noninvasive modality for assessing intracranial lesions in lymphoma
patients.We present herein a case of a man with sudden gait disturbance and cognitive impairment who was
initially diagnosed with cerebral infarction, but was subsequently diagnosed with paraneoplastic encephalopathy
associated with systemic lymphoma.
Paraneoplastic encephalomyelitis (PEM) is a multifocal inflammatory disorder of the central nervous system (CNS)
associated with remote neoplasia. Frequently, the disorder is accompanied by subacute sensory neuronopathy
(SSN) due to involvement of the dorsal root ganglia. Anti-Hu antibodies may be detected in both of these conditions.
Although various malignancies have been reported in PEM, 80% of cases are associated with bronchial cancer,
typically small-cell lung carcinoma. Neurologic manifestations commonly precede the diagnosis of cancer, although
variable presentations have been reported. Symptoms usually progress over the course of weeks to months,
reaching a plateau of neurologic disability. Neurologic impairment may be more debilitating than the associated
cancer. No effective therapeutic approaches have been established, although immunosuppressive therapies are
employed commonly.
Neurologic dysfunction probably results from an autoimmune reaction directed against onconeural antigens in the
human nervous system. Polyclonal immunoglobulin G (IgG) anti-Hu antibodies or type 1 antineuronal nuclear
antibodies are most prevalent (~50%), although several other circulating autoantibodies have been identified. Some
patients have no identifiable paraneoplastic antibodies. These markers of paraneoplasia have an undetermined
pathogenic role. Cytotoxic T cell–mediated neuronal damage is suspected, although no animal models have been
developed to confirm this.
Almost all cases of PEM with anti-Hu antibodies are related to small-cell lung carcinoma. These antibodies react
with a group of 35- to 40-kilodalton neuronal RNA-binding proteins, including HuD, PLE21/HuC, and Hel-N1.
Nuclear and cytoplasmic staining of CNS neurons demonstrates the presence of these antibodies. A ubiquitous
protein, HuR, is also an antigenic target. The neuronal proteins are homologous to the embryonic lethal abnormal
visual (Elav) protein in Drosophila species. Anti-Hu antibodies may alter the production of these proteins, which
are essential for the development, maturation, and maintenance of the vertebrate nervous system. Intrathecal
synthesis of anti-Hu antibodies may represent an autoimmune cross-reaction with neurologic tissue, triggered by a
remote carcinoma.
Other PEM antibodies include anti-CV2, anti-Yo, anti-Ma1, anti-Ta or anti-Ma2, and several other atypical
antibodies. Recent reports have noted detection of the prion-related 14-3-3 protein and of herpes simplex virus by
polymerase chain reaction (PCR) in the cerebrospinal fluid (CSF) of patients with PEM. The significance of these
findings is unclear.
Addendum
A new version of this PDF file (with a new case) is uploaded in my web site every week (every Saturday and
remains available till Friday.)
To download the current version follow the link "http://pdf.yassermetwally.com/case.pdf".
You can also download the current version from my web site at "http://yassermetwally.com".
To download the software version of the publication (crow.exe) follow the link:
http://neurology.yassermetwally.com/crow.zip
The case is also presented as a short case in PDF format, to download the short case follow the link:
http://pdf.yassermetwally.com/short.pdf
At the end of each year, all the publications are compiled on a single CD-ROM, please contact the author to
7. know more details.
Screen resolution is better set at 1024*768 pixel screen area for optimum display.
For an archive of the previously reported cases go to www.yassermetwally.net, then under pages in the right
panel, scroll down and click on the text entry "downloadable case records in PDF format"
Also to view a list of the previously published case records follow the following link
(http://wordpress.com/tag/case-record/) or click on it if it appears as a link in your PDF reader
REFERENCES
References
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