CASO 5
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This document describes a 61-year-old male presenting with progressive lower extremity weakness and spasticity. Imaging showed possible diagnoses of infarct, transverse myelitis, multiple sclerosis, or arteriovenous malformation (AVM). Further review found a dural AVM supplied by dural branches from intercostal, lumbar or sacral arteries, drained by perimedullary veins, with the nidus located in the dura covering a proximal nerve root. Dural AVMs typically cause Foix-Alajouanine syndrome, a slowly progressive ascending myelopathy due to cord edema. Treatment involves occlusion of draining veins by endovascular or surgical means.
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Kaposi sarcoma
This document reports on three cases of Kaposi's sarcoma (KS) in renal transplant recipients that developed concurrently with cytomegalovirus (CMV) infection within the first year after transplantation. The first case involved a 50-year-old man who developed KS lesions on the skin and gastrointestinal tract 3 months after being diagnosed with CMV infection. The second case was a 53-year-old man who developed KS skin lesions 5 months after transplantation accompanied by CMV infection. The third case was a 45-year-old woman who was diagnosed with KS skin lesions 8 months after transplantation during treatment for suspected CMV infection. All three patients presented with KS shortly after being diagnosed and treated for CMV infection, suggesting C
Angiosarcoma Review
This document summarizes the key differences between primary and secondary angiosarcoma (AS) of the breast. Primary AS typically affects younger women (median age 40) and presents as masses within the breast parenchyma, while secondary AS affects older women (median age 67-71) and develops in irradiated breast skin and subcutaneous tissue 7-10 years after radiation therapy. Both forms have a poor prognosis. Surgical management often involves mastectomy but optimal margins are unclear. Adjuvant chemotherapy and radiation have shown mixed results, and larger randomized trials are needed to determine their effectiveness for AS of the breast.
Infecciones necrotizantes tejidos blandos
Necrotizing infections of soft tissues (NSSTIs) are severe infections resulting in life-threatening soft tissue destruction. They are caused by toxin-secreting bacteria and are characterized by rapid, widespread progression of infection and necrosis along soft tissue planes. NSSTIs have an incidence of 500-1500 cases per year in the US and a mortality rate of 13.7%. Risk factors include diabetes, obesity, alcohol abuse, and malnutrition. NSSTIs can be caused by single agents like clostridia or streptococci (Type I) or be polymicrobial (Type II). Prompt surgical debridement and broad-spectrum antibiotics are key to managing these infections and preventing high morbidity and mortality.
Angiosarcoma
Angiosarcomas are rare and represent less than 2 percent of all sarcomas. The most frequently involved primary sites are heart, liver and breast with over 100 cases of each reported. Angiosarcomas of the lungs are usually metastasis. Differential diagnosis of vascular neoplasm metastatic to the lungs includes Kaposi sarcoma, epithelioid hemangioendothelioma, and angiosarcoma.
Primary angiosarcoma of the lung is extremely rare and is usually diagnosed quite late due to low index of suspicion.
Reported chest radiograph findings have ranged from normal to multiple nodular densities with or without pleural effusions to diffuse alveolar infiltrates compatible with pulmonary haemorrhage. Metastatic angiosarcoma lung lesions are commonly multiple. There have been reported as solid nodular or thin-walled cysts, with haemorrhagic change.
The HPE was consistent with an epithelioid angiosarcoma and this was also supported by positive reaction for factor VIII-related antigen, CD34 and CD31, which are specific markers for tumours derived from the endothelium.
Predisposing factors for angiosarcomas include polyvinyl chloride and thorium dioxide exposure, postmastectomy and postirradiation states (cutaneous angiosarcoma) and chronic empyema for pleural space angiosarcomas.
Kaposi's Sarcoma
El sarcoma de Kaposi es una enfermedad por la que se forman tumores malignos (cancerosos) en la piel, las membranas mucosas, los ganglios linfáticos y otros órganos.
Para detectar (encontrar) y diagnosticar el sarcoma de Kaposi se utilizan pruebas que examinan la piel, los pulmones y el tubo digestivo.
Después de que se diagnostica un sarcoma de Kaposi, se realizan prueban para determinar si las células cancerosas se diseminaron a otras partes del cuerpo.
Ciertos factores afectan el pronóstico (probabilidad de recuperación) y las opciones de tratamiento.
Dermatology(kaposis sarcoma)
Moritz Kaposi was a Hungarian physician who discovered the skin tumor that bears his name, Kaposi's sarcoma. The disease was later identified as an AIDS-defining illness caused by the human herpesvirus 8. Kaposi's sarcoma causes purplish skin lesions and can affect the lymph nodes and internal organs. It is typically treated with antiretroviral drugs and antiviral medications that target the herpesvirus.
Kaposi sarcoma
Kaposi sarcoma is a multifocal tumor caused by human herpesvirus 8. It has four clinical variants: classic, endemic, iatrogenic, and HIV/AIDS related. Classic Kaposi sarcoma occurs in elderly men and has a slow progression. African endemic Kaposi sarcoma has various patterns and a poor prognosis. Iatrogenic Kaposi sarcoma is rare and seen in transplant patients on immunosuppression. HIV/AIDS related Kaposi sarcoma is common in homosexual men and has a rapid progression. Kaposi sarcoma lesions are treated with radiation, chemotherapy, surgery, or intralesional cytotoxic therapy depending on severity and location.
Kaposi sarcoma
Kaposi Sarcoma is an intermediate grade tumor that is rare in the general population but commonly seen in AIDS patients. There are four types of Kaposi Sarcoma: chronic, lymphadenopathic, transplant-associated, and AIDS-associated. Kaposi Sarcoma is caused by infection of endothelial cells by the KSHV virus, which causes lytic and latent infection and leads to abnormal cell proliferation through cytokine production and disruption of normal cell growth regulation, resulting in the clinical manifestations of Kaposi Sarcoma such as macules, patches, and violaceous plaques and nodules. Treatment options include surgery, radiation, chemotherapy, antiretroviral drugs, IFN-A, and angiogenesis inhibitors.
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This document reports on three cases of Kaposi's sarcoma (KS) in renal transplant recipients that developed concurrently with cytomegalovirus (CMV) infection within the first year after transplantation. The first case involved a 50-year-old man who developed KS lesions on the skin and gastrointestinal tract 3 months after being diagnosed with CMV infection. The second case was a 53-year-old man who developed KS skin lesions 5 months after transplantation accompanied by CMV infection. The third case was a 45-year-old woman who was diagnosed with KS skin lesions 8 months after transplantation during treatment for suspected CMV infection. All three patients presented with KS shortly after being diagnosed and treated for CMV infection, suggesting C
Angiosarcoma Review
This document summarizes the key differences between primary and secondary angiosarcoma (AS) of the breast. Primary AS typically affects younger women (median age 40) and presents as masses within the breast parenchyma, while secondary AS affects older women (median age 67-71) and develops in irradiated breast skin and subcutaneous tissue 7-10 years after radiation therapy. Both forms have a poor prognosis. Surgical management often involves mastectomy but optimal margins are unclear. Adjuvant chemotherapy and radiation have shown mixed results, and larger randomized trials are needed to determine their effectiveness for AS of the breast.
Infecciones necrotizantes tejidos blandos
Necrotizing infections of soft tissues (NSSTIs) are severe infections resulting in life-threatening soft tissue destruction. They are caused by toxin-secreting bacteria and are characterized by rapid, widespread progression of infection and necrosis along soft tissue planes. NSSTIs have an incidence of 500-1500 cases per year in the US and a mortality rate of 13.7%. Risk factors include diabetes, obesity, alcohol abuse, and malnutrition. NSSTIs can be caused by single agents like clostridia or streptococci (Type I) or be polymicrobial (Type II). Prompt surgical debridement and broad-spectrum antibiotics are key to managing these infections and preventing high morbidity and mortality.
Angiosarcoma
Angiosarcomas are rare and represent less than 2 percent of all sarcomas. The most frequently involved primary sites are heart, liver and breast with over 100 cases of each reported. Angiosarcomas of the lungs are usually metastasis. Differential diagnosis of vascular neoplasm metastatic to the lungs includes Kaposi sarcoma, epithelioid hemangioendothelioma, and angiosarcoma.
Primary angiosarcoma of the lung is extremely rare and is usually diagnosed quite late due to low index of suspicion.
Reported chest radiograph findings have ranged from normal to multiple nodular densities with or without pleural effusions to diffuse alveolar infiltrates compatible with pulmonary haemorrhage. Metastatic angiosarcoma lung lesions are commonly multiple. There have been reported as solid nodular or thin-walled cysts, with haemorrhagic change.
The HPE was consistent with an epithelioid angiosarcoma and this was also supported by positive reaction for factor VIII-related antigen, CD34 and CD31, which are specific markers for tumours derived from the endothelium.
Predisposing factors for angiosarcomas include polyvinyl chloride and thorium dioxide exposure, postmastectomy and postirradiation states (cutaneous angiosarcoma) and chronic empyema for pleural space angiosarcomas.
Kaposi's Sarcoma
El sarcoma de Kaposi es una enfermedad por la que se forman tumores malignos (cancerosos) en la piel, las membranas mucosas, los ganglios linfáticos y otros órganos.
Para detectar (encontrar) y diagnosticar el sarcoma de Kaposi se utilizan pruebas que examinan la piel, los pulmones y el tubo digestivo.
Después de que se diagnostica un sarcoma de Kaposi, se realizan prueban para determinar si las células cancerosas se diseminaron a otras partes del cuerpo.
Ciertos factores afectan el pronóstico (probabilidad de recuperación) y las opciones de tratamiento.
Dermatology(kaposis sarcoma)
Moritz Kaposi was a Hungarian physician who discovered the skin tumor that bears his name, Kaposi's sarcoma. The disease was later identified as an AIDS-defining illness caused by the human herpesvirus 8. Kaposi's sarcoma causes purplish skin lesions and can affect the lymph nodes and internal organs. It is typically treated with antiretroviral drugs and antiviral medications that target the herpesvirus.
Kaposi sarcoma
Kaposi sarcoma is a multifocal tumor caused by human herpesvirus 8. It has four clinical variants: classic, endemic, iatrogenic, and HIV/AIDS related. Classic Kaposi sarcoma occurs in elderly men and has a slow progression. African endemic Kaposi sarcoma has various patterns and a poor prognosis. Iatrogenic Kaposi sarcoma is rare and seen in transplant patients on immunosuppression. HIV/AIDS related Kaposi sarcoma is common in homosexual men and has a rapid progression. Kaposi sarcoma lesions are treated with radiation, chemotherapy, surgery, or intralesional cytotoxic therapy depending on severity and location.
Kaposi sarcoma
Kaposi Sarcoma is an intermediate grade tumor that is rare in the general population but commonly seen in AIDS patients. There are four types of Kaposi Sarcoma: chronic, lymphadenopathic, transplant-associated, and AIDS-associated. Kaposi Sarcoma is caused by infection of endothelial cells by the KSHV virus, which causes lytic and latent infection and leads to abnormal cell proliferation through cytokine production and disruption of normal cell growth regulation, resulting in the clinical manifestations of Kaposi Sarcoma such as macules, patches, and violaceous plaques and nodules. Treatment options include surgery, radiation, chemotherapy, antiretroviral drugs, IFN-A, and angiogenesis inhibitors.
Locked in syndrome secondary a multiform glioblastoma in brain stem. ARTURO A...
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This document describes a rare case of a 48-year-old male who presented with progressive neurological symptoms and was eventually diagnosed with a locked-in syndrome secondary to a multiform glioblastoma tumor located in his lower pons, medulla, and cervical spinal cord. Locked-in syndrome is typically caused by a stroke, but can also be caused by demyelinating diseases or tumors. MRI imaging showed an irregular, enhancing tumor in these areas. A biopsy was performed and pathology found a high-grade astrocytoma. The patient's condition deteriorated and he died one week later, making this a unique case of a brainstem glioblastoma in an adult presenting as locked-in syndrome.Final clickable pps for vp s ymposium aha 2001
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Silvestrini Mauro. Cefalea e dissecazione arteriosa. ASMaD 2011
1) The document discusses the relationship between headaches and cervical artery dissection, noting that headaches are a common presenting symptom of dissections.
2) It reports that studies have found migraine is more common in patients who experience spontaneous cervical artery dissections compared to other stroke patients.
3) The mechanism by which migraine may increase the risk of dissection is unknown but possibly involves changes to the extracellular matrix and carotid artery distensibility.
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This document provides an overview of vasculitis, including classification, pathophysiology, clinical manifestations, investigations, and management approaches. It discusses several specific large vessel vasculitides - giant cell arteritis, Takayasu arteritis, and polyarteritis nodosa. Giant cell arteritis commonly involves temporal arteries and causes headaches. Takayasu arteritis primarily affects the aorta and its branches. Polyarteritis nodosa preferentially involves the skin, nerves, gastrointestinal tract and kidneys. Diagnosis relies on tissue biopsy and imaging. Treatment focuses on glucocorticoids, with additional immunosuppressants for severe or refractory disease.
Pediatric vasculitides
Vasculitis refers to inflammation of blood vessels. It is classified based on vessel size and pathology. The most common pediatric vasculitides are Henoch-Schonlein purpura and Kawasaki disease. Diagnosis involves evaluating symptoms, radiology like angiograms, histopathology of biopsied tissues, and serology tests like ANCA. Treatment depends on type and severity of vasculitis. Prognosis varies, with most children recovering fully from HSP or KD, while other types like AAV carry higher risks of organ damage and mortality if not properly treated.
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This document describes the case of a 48-year-old man with HIV/AIDS who presented with worsening dysphagia. He has a history of Kaposi sarcoma, pneumocystis pneumonia, and oral thrush. On examination, he has violaceous skin lesions and perianal ulcers. The leading diagnoses for his dysphagia are opportunistic infections such as candida esophagitis or herpes. He is being treated with antiretrovirals and antibiotics but his condition deteriorates and he passes away.
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2. It provides an overview of vasculitis, defining it as vessel wall inflammation and describing its various clinical features and etiologies, which can be infectious or non-infectious such as immune complex deposition or antineutrophil cytoplasmic antibodies.
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1) Achalasia is caused by degeneration of ganglion cells in the esophageal myenteric plexus, resulting in loss of peristalsis and incomplete LES relaxation. The cause is unclear but may be autoimmune, viral, or neurodegenerative.
2) It has an incidence of 1 in 100,000 annually and prevalence of 10 in 100,000. Symptoms include dysphagia, chest pain, regurgitation, and weight loss. Diagnosis involves b
THE VASCULITIS SYNDROME
Vasculitis is inflammation of blood vessels that can affect single or multiple organ systems. It is classified based on the size of vessels involved - large, medium, or small. Common large vessel vasculitis includes giant cell arteritis and Takayasu arteritis. Pathogenesis involves immune complex formation, ANCA, and T lymphocyte responses. Clinical manifestations are variable and depend on organ systems involved. Diagnosis involves criteria based on symptoms, labs like ESR, and biopsy when possible. Treatment focuses on reducing inflammation and preventing complications.
Calcifilaxiaiv 100615192457-phpapp02
This document summarizes an article about calciphylaxis, a calcification syndrome associated with cutaneous necrosis. It is most commonly seen in patients with renal disease and secondary hyperparathyroidism. The summary is as follows:
1) Calciphylaxis is a life-threatening vasculopathy that usually affects patients with renal disease. It causes ischemic cutaneous necrosis and has a high mortality rate.
2) Clinically, it presents with violaceous, reticulate skin lesions and areas of cutaneous necrosis. Risk factors include elevated calcium, phosphorus, and parathyroid hormone levels.
3) Diagnosis involves clinical findings as well as evidence of vessel calcification on imaging and hist
Calcifilaxiaiv 100615192457-phpapp02 (1)
This document summarizes an article about calciphylaxis, a calcification syndrome associated with cutaneous necrosis. It is most commonly seen in patients with renal disease and secondary hyperparathyroidism. The summary is:
1) Calciphylaxis is a life-threatening vasculopathy usually seen in patients with renal disease that can cause cutaneous necrosis.
2) It has a high mortality rate of 60-80% due to wound infection, sepsis, and organ failure.
3) Risk factors include elevated calcium, phosphorus, and parathyroid hormone levels. Diagnosis involves clinical findings as well as evidence of vessel calcification on imaging and histology.
Late onset jugular foramen syndrome following head trauma
Recklinghausen's disease. Neurological examination revealed spastic quadriparesis, prominent in the left extremities. Posterior column sensations were lost in all four limbs. Deep tendon reflexes were exaggerated in all four limbs. A positive Hoffman s and Babinsky signs and sign were present bilaterally. Gait was broad-based due to spasticity. Difficulty in urination was present .MRI of cervical spine was done at some other institute revealed a large well defined homogenously enhancing intradural extramedullary mass at C1-2 level on left side markedly compressing the cord, there was associated cord edema at adjacent cervical levels(fig.1&2). A provisional diagnosis of schwannoma or neurofibroma was kept since there was no dural tail or broad based attachment of tumor to dura.
Patient was advised surgical removal of tumour . Tumor was approached via midline incision in neck and C-1 to C-3 laminectomy was done. Dura was opened under microscope and tumor was found on left side and whole of the tumor was intra arachnoidal. To our surprise though tumor was mainly extra medullary on left side ,it had an intra-medullary extension. Extramedullary component was completely removed followed by intatumoral decompression of intra medullary part.Capsule of intramedullary component was densely adherent to spinal cord and small amount of tumor tissue had to be left behind to avoid post operative neurological deficit(fig.4). Duraplasty was done. In the postoperative period the power of the patient improved gradually and by the end of the first week she could walk without support and at the end of one month power in all four limbs was 5/5 , though spasticity remained in all four limbs. Her gait remain broad based and there is clumsiness while walking.
DISCUSSION
Intramedullary schwannomas are rare tumors . The first surgical description of a spinal tumor was made in 1888 by Sir Victor Horsley(3). In 1907 Von Eiselberg published the successful resection of an intramedullary neurofibrosarcoma. First intramedullary schwannoma was reported by Kernohanin1952 though Penfield had already described an intramedullary lesion with schwannoma characteristics in 1932(4).
We found 52 cases in the literature, in addition to our case. Of these cases only three have been reported as having both intramedullary and extramedullary component . Gorman etal., have reported the extramedullary component to be an exophytic extension of the intramedullary tumor from the enlarged spinal cord(5).
Mean age at presentation of these lesions is 40-years . They are usually single lesions affecting the cervical spinal cord (63%), the thoracic spinal cord (26%) and the lumbar spinal cord (11%). They have a slow growth pattern and because of this the average interval between first symptoms and diagnosis is 28.2 months (from six months to 20 years)(6). The most described clinical manifestation is the pyramidal syndrome followed by sensitivity complaints and sphincter dysfunctio
GBM--multicentric (1)
A 48-year-old female presented with headache and vomiting over 10 days. Imaging showed lesions in both hemispheres. She underwent resection of the lesions, one in the right frontal lobe and one in the left frontal lobe. Pathology found both lesions were glioblastoma grade IV. While multifocal glioblastoma is uncommon, there are several proposed mechanisms for its pathogenesis including spread through CSF or white matter tracts. Currently no clear guidelines exist for optimal management of multifocal glioblastoma.
CASO 1
A 35-year-old male presented with progressive loss of motor neuron strength. His symptoms included upper and lower motor neuron signs as well as bulbar signs. He was diagnosed with amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease, which is a progressive neurodegenerative disease that results in the death of motor neurons and leads to weakness, atrophy, and fasciculations. ALS usually causes death within 2 to 6 years due to respiratory complications.
CASO 3
Caudal Regression Syndrome is characterized by malformed genitals, anal atresia, and kidney abnormalities due to absent sacral vertebrae. It occurs in approximately 1 in 7,500 births and 16% of cases involve children of diabetic mothers. Imaging shows conus abnormalities in 95% of symptomatic patients, such as a truncated or high-lying spinal cord tip with a sparse cauda equina nerve bundle. There are two types - one with a truncated and high cord, and another with a truncated cord that is inferiorly located and tethered.
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This document describes a rare case of a 48-year-old male who presented with progressive neurological symptoms and was eventually diagnosed with a locked-in syndrome secondary to a multiform glioblastoma tumor located in his lower pons, medulla, and cervical spinal cord. Locked-in syndrome is typically caused by a stroke, but can also be caused by demyelinating diseases or tumors. MRI imaging showed an irregular, enhancing tumor in these areas. A biopsy was performed and pathology found a high-grade astrocytoma. The patient's condition deteriorated and he died one week later, making this a unique case of a brainstem glioblastoma in an adult presenting as locked-in syndrome.Final clickable pps for vp s ymposium aha 2001
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This document provides an overview of vasculitis, including classification, pathophysiology, clinical manifestations, investigations, and management approaches. It discusses several specific large vessel vasculitides - giant cell arteritis, Takayasu arteritis, and polyarteritis nodosa. Giant cell arteritis commonly involves temporal arteries and causes headaches. Takayasu arteritis primarily affects the aorta and its branches. Polyarteritis nodosa preferentially involves the skin, nerves, gastrointestinal tract and kidneys. Diagnosis relies on tissue biopsy and imaging. Treatment focuses on glucocorticoids, with additional immunosuppressants for severe or refractory disease.
Pediatric vasculitides
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Morbidity & mortality/GI Kaposi Sarcoma
This document describes the case of a 48-year-old man with HIV/AIDS who presented with worsening dysphagia. He has a history of Kaposi sarcoma, pneumocystis pneumonia, and oral thrush. On examination, he has violaceous skin lesions and perianal ulcers. The leading diagnoses for his dysphagia are opportunistic infections such as candida esophagitis or herpes. He is being treated with antiretrovirals and antibiotics but his condition deteriorates and he passes away.
Medical Comorbidities and their impacto on wound healing
This document discusses how medical comorbidities can impact wound healing. It emphasizes that treating the wound is only part of the story - managing the patient's underlying medical problems is also critical for healing. Several common comorbidities that can impair healing are described in detail, including diabetes, rheumatoid disease, nutritional deficiencies, medications, chemotherapy/radiation, and smoking. A thorough history and physical exam is important for identifying potential impediments to healing from comorbidities.
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1. The document discusses a case scenario of a 9-year-old boy, Yassin, who developed fatigue, palpitations, rash, and leg swelling after his family recovered from COVID-19.
2. It provides an overview of vasculitis, defining it as vessel wall inflammation and describing its various clinical features and etiologies, which can be infectious or non-infectious such as immune complex deposition or antineutrophil cytoplasmic antibodies.
3. The main immunological mechanisms that can initiate non-infectious vasculitis are discussed as immune complex deposition, antineutrophil cytoplasmic antibodies, anti–endothelial cell antibodies, and autoreactive
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Vasculitis refers to inflammation of blood vessels. It can present with a variety of clinical manifestations depending on the size of vessels involved. The Chapel Hill Consensus Conference created a classification system for major types of vasculitis including Wegener's granulomatosis, Churg-Strauss syndrome, and microscopic polyangiitis. Henoch-Schönlein purpura is the most common vasculitis in children, characterized by a vasculitis involving small vessels of the skin, GI tract, kidneys, joints, and rarely lungs and CNS, with IgA deposits in vessel walls. Granulomatosis with polyangiitis is a multisystem disease involving vasculitis of small to medium
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Acalasia
This document summarizes achalasia, an esophageal motility disorder. It discusses the epidemiology, pathophysiology, clinical presentation, diagnosis, and treatment of achalasia. The key points are:
1) Achalasia is caused by degeneration of ganglion cells in the esophageal myenteric plexus, resulting in loss of peristalsis and incomplete LES relaxation. The cause is unclear but may be autoimmune, viral, or neurodegenerative.
2) It has an incidence of 1 in 100,000 annually and prevalence of 10 in 100,000. Symptoms include dysphagia, chest pain, regurgitation, and weight loss. Diagnosis involves b
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Calcifilaxiaiv 100615192457-phpapp02
This document summarizes an article about calciphylaxis, a calcification syndrome associated with cutaneous necrosis. It is most commonly seen in patients with renal disease and secondary hyperparathyroidism. The summary is as follows:
1) Calciphylaxis is a life-threatening vasculopathy that usually affects patients with renal disease. It causes ischemic cutaneous necrosis and has a high mortality rate.
2) Clinically, it presents with violaceous, reticulate skin lesions and areas of cutaneous necrosis. Risk factors include elevated calcium, phosphorus, and parathyroid hormone levels.
3) Diagnosis involves clinical findings as well as evidence of vessel calcification on imaging and hist
Calcifilaxiaiv 100615192457-phpapp02 (1)
This document summarizes an article about calciphylaxis, a calcification syndrome associated with cutaneous necrosis. It is most commonly seen in patients with renal disease and secondary hyperparathyroidism. The summary is:
1) Calciphylaxis is a life-threatening vasculopathy usually seen in patients with renal disease that can cause cutaneous necrosis.
2) It has a high mortality rate of 60-80% due to wound infection, sepsis, and organ failure.
3) Risk factors include elevated calcium, phosphorus, and parathyroid hormone levels. Diagnosis involves clinical findings as well as evidence of vessel calcification on imaging and histology.
Late onset jugular foramen syndrome following head trauma
Recklinghausen's disease. Neurological examination revealed spastic quadriparesis, prominent in the left extremities. Posterior column sensations were lost in all four limbs. Deep tendon reflexes were exaggerated in all four limbs. A positive Hoffman s and Babinsky signs and sign were present bilaterally. Gait was broad-based due to spasticity. Difficulty in urination was present .MRI of cervical spine was done at some other institute revealed a large well defined homogenously enhancing intradural extramedullary mass at C1-2 level on left side markedly compressing the cord, there was associated cord edema at adjacent cervical levels(fig.1&2). A provisional diagnosis of schwannoma or neurofibroma was kept since there was no dural tail or broad based attachment of tumor to dura.
Patient was advised surgical removal of tumour . Tumor was approached via midline incision in neck and C-1 to C-3 laminectomy was done. Dura was opened under microscope and tumor was found on left side and whole of the tumor was intra arachnoidal. To our surprise though tumor was mainly extra medullary on left side ,it had an intra-medullary extension. Extramedullary component was completely removed followed by intatumoral decompression of intra medullary part.Capsule of intramedullary component was densely adherent to spinal cord and small amount of tumor tissue had to be left behind to avoid post operative neurological deficit(fig.4). Duraplasty was done. In the postoperative period the power of the patient improved gradually and by the end of the first week she could walk without support and at the end of one month power in all four limbs was 5/5 , though spasticity remained in all four limbs. Her gait remain broad based and there is clumsiness while walking.
DISCUSSION
Intramedullary schwannomas are rare tumors . The first surgical description of a spinal tumor was made in 1888 by Sir Victor Horsley(3). In 1907 Von Eiselberg published the successful resection of an intramedullary neurofibrosarcoma. First intramedullary schwannoma was reported by Kernohanin1952 though Penfield had already described an intramedullary lesion with schwannoma characteristics in 1932(4).
We found 52 cases in the literature, in addition to our case. Of these cases only three have been reported as having both intramedullary and extramedullary component . Gorman etal., have reported the extramedullary component to be an exophytic extension of the intramedullary tumor from the enlarged spinal cord(5).
Mean age at presentation of these lesions is 40-years . They are usually single lesions affecting the cervical spinal cord (63%), the thoracic spinal cord (26%) and the lumbar spinal cord (11%). They have a slow growth pattern and because of this the average interval between first symptoms and diagnosis is 28.2 months (from six months to 20 years)(6). The most described clinical manifestation is the pyramidal syndrome followed by sensitivity complaints and sphincter dysfunctio
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CASO 5
- 1. Case 4 2007
- 2. Clinical history 61-year-old male with progressive lower extremity weakness and spasticity.
- 3. Imaging A
- 4. Diagnosis ?
- 5. C CONGENITAL DISEASES, MALDEVELOPMENT, MIGRATIONAL DISORDERS, VARIANTS I BACTERIA, RICKETTSIA, FUNGUS,VIRUS, PARASITES, PRION M METABOLIC, IMMUNE, GLIOSIS, SCLEROSIS, DEGENERATION T CONTUSION, HEMATOMAS SUBDURAL, EPIDURAL, TRAUMA COMPLICATIONS, RADIOTERHAPY, CHEMOTHERAPHY V VASCULAR MALFORMATIONS ( AVM, VENOUS ANOMALY, CAPILLARY, CAVERNOUS ), ANEURYSMS,ANGIOPATHY, INTRACEREBRAL HEMORRHAGE, INFARCT, THROMBOSIS DISSECTION N PRIMARY SECONDARY
- 6. Diagnosis ? a.Infarct b.Transverse myelitis c.Multiple sclerosis d.AVM
- 7. C CONGENITAL DISEASES, MALDEVELOPMENT, MIGRATIONAL DISORDERS, VARIANTS I BACTERIA, RICKETTSIA, FUNGUS,VIRUS, PARASITES, PRION M METABOLIC, IMMUNE, GLIOSIS, SCLEROSIS, DEGENERATION T CONTUSION, HEMATOMAS SUBDURAL, EPIDURAL, TRAUMA COMPLICATIONS, RADIOTERHAPY, CHEMOTHERAPHY V VASCULAR MALFORMATIONS ( AVM, VENOUS ANOMALY, CAPILLARY, CAVERNOUS ), ANEURYSMS,ANGIOPATHY, INTRACEREBRAL HEMORRHAGE, INFARCT, THROMBOSIS DISSECTION N PRIMARY SECONDARY
- 9. Dural AVM , small arteriovenous communication supplied by dural branches arising from intercostal, lumbar or sacral arteries and drained by perimedullary veins (ascending or descending) Nidus is in dura covering proximal nerve root. Most (98-99%) are single lesions; double lesions in 1-2% of patients. Clinically: middle-aged or elderly men, slowly progressive and ascending myelopathy due to cord edema (sometimes called: Foix Alajouanine syndrome) Contrast enhancement in cord is common. Treatment: occlusion of draining veins by endovascular or surgical means
- 11. Foix–Alajouanine syndrome Is a spinal cord disorder caused by an arteriovenous malformation of the spinal cord.[ The patients present with symptoms indicating spinal cord involvement (paralysis of arms and legs, numbness and loss of sensation and sphincter dysfunction), Pathological examination reveals disseminated nerve cell death in the spinal cord and abnormally dilated and tortuous vessels situated on the surface of the spinal cord. Treatment : Surgical intervention ( removal of the nidus) Endovascular occlusion of the nidus Steroids for the myelopathy