{"title":"Psychodynamic counselling after stroke: a pilot service development project and evaluation","authors":"Alys Mikolajczyk, A. Bateman","doi":"10.47795/knif1633","DOIUrl":"https://doi.org/10.47795/knif1633","url":null,"abstract":"","PeriodicalId":34274,"journal":{"name":"Advances in Clinical Neuroscience Rehabilitation","volume":"63 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2012-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80500827","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
I n the original description, this clinical syndrome consisted of the development of external and internal ophthalmoplegia, cerebellar ataxia in the arms and legs and absence of the tendon reflexes, over a period of four or five days. The rather acute onset of such ocular signs associated with cerebellar ataxia was apt to be alarming to a neurologist in 1955, the year the principal case was studied. The patient developed severe ataxia of gait and diplopia in 24 hours. After four days there was complete external and internal ophthalmoplegia, ataxia that precluded feeding himself and made it impossible to stand or walk unaided. On examination, along with other findings, the tendon reflexes were absent. The patient’s mind was clear. The several diagnoses that came to mind included vertebral-basilar thrombosis with a stroke, Wernicke’s disease, botulism, multiple sclerosis and the Guillain-Barré syndrome. The cerebrospinal fluid (CSF) contained a few lymphocytes and a normal protein. Dr David Cogan, a world figure in neuro-ophthalmology, was asked to see the patient in consultation and strongly recommended vertebral-basilar angiography. This became the focus of debate among several consultants. At that time, the procedure was carried out by means of a direct ‘stick’ with a needle that passed through the common carotid artery in the neck to reach the vertebral artery. I knew of several instances in which serious complications had occurred, including death. Our patient was not generally ill and subjecting him to angiography seemed too risky. Also I vaguely recalled seeing or hearing of a somewhat similar case in Montreal in the past few years, that had recovered. The discussion was continuing when on hospital day 5, spontaneous recovery began without special therapy. In ten days improvement was remarkable. The CSF was re-examined on the 30th day and contained 348mg protein per 100ml. This swung the final diagnosis toward acute polyneuritis of the Guillain-Barré type. It has been my custom since the days of neurological residency to keep a list of every patient examined. The cases are then sorted out according to broad categories of diagnosis – stroke, multiple sclerosis, tumour, parkinsonism etc and the largest group by far, undiagnosed. As soon as convenient I travelled to Montreal with the undiagnosed list. In short order two cases were found, both examined in 1953. The first was examined in consultation during the acute stage of the neurological illness that had followed acute pneumonia. In a period of three days the patient developed an internal and external ophthalmoplegia absent tendon reflexes and a wide-based ataxic gait. He had pins and needles in the tips of the fingers but sensation was normal in the fingers and toes. The CSF protein was 35mg per 100ml in the acute stage of the illness and was unchanged after six weeks. The second test had been performed when investigating the possibility of Guillain-Barré polyneuropathy. Neurological recove
{"title":"The Origin of Miller Fisher Syndrome","authors":"","doi":"10.47795/zjkf6411","DOIUrl":"https://doi.org/10.47795/zjkf6411","url":null,"abstract":"I n the original description, this clinical syndrome consisted of the development of external and internal ophthalmoplegia, cerebellar ataxia in the arms and legs and absence of the tendon reflexes, over a period of four or five days. The rather acute onset of such ocular signs associated with cerebellar ataxia was apt to be alarming to a neurologist in 1955, the year the principal case was studied. The patient developed severe ataxia of gait and diplopia in 24 hours. After four days there was complete external and internal ophthalmoplegia, ataxia that precluded feeding himself and made it impossible to stand or walk unaided. On examination, along with other findings, the tendon reflexes were absent. The patient’s mind was clear. The several diagnoses that came to mind included vertebral-basilar thrombosis with a stroke, Wernicke’s disease, botulism, multiple sclerosis and the Guillain-Barré syndrome. The cerebrospinal fluid (CSF) contained a few lymphocytes and a normal protein. Dr David Cogan, a world figure in neuro-ophthalmology, was asked to see the patient in consultation and strongly recommended vertebral-basilar angiography. This became the focus of debate among several consultants. At that time, the procedure was carried out by means of a direct ‘stick’ with a needle that passed through the common carotid artery in the neck to reach the vertebral artery. I knew of several instances in which serious complications had occurred, including death. Our patient was not generally ill and subjecting him to angiography seemed too risky. Also I vaguely recalled seeing or hearing of a somewhat similar case in Montreal in the past few years, that had recovered. The discussion was continuing when on hospital day 5, spontaneous recovery began without special therapy. In ten days improvement was remarkable. The CSF was re-examined on the 30th day and contained 348mg protein per 100ml. This swung the final diagnosis toward acute polyneuritis of the Guillain-Barré type. It has been my custom since the days of neurological residency to keep a list of every patient examined. The cases are then sorted out according to broad categories of diagnosis – stroke, multiple sclerosis, tumour, parkinsonism etc and the largest group by far, undiagnosed. As soon as convenient I travelled to Montreal with the undiagnosed list. In short order two cases were found, both examined in 1953. The first was examined in consultation during the acute stage of the neurological illness that had followed acute pneumonia. In a period of three days the patient developed an internal and external ophthalmoplegia absent tendon reflexes and a wide-based ataxic gait. He had pins and needles in the tips of the fingers but sensation was normal in the fingers and toes. The CSF protein was 35mg per 100ml in the acute stage of the illness and was unchanged after six weeks. The second test had been performed when investigating the possibility of Guillain-Barré polyneuropathy. Neurological recove","PeriodicalId":34274,"journal":{"name":"Advances in Clinical Neuroscience Rehabilitation","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2005-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89453402","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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