Cases reported "Sensation Disorders"

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1/62. Chronic axonal sensory and autonomic polyneuropathy without motor involvement: a new 'chronic inflammatory neuropathy?'.

    We report the case of a woman with axonal sensory and autonomic neuropathy lasting several months who improved in association with steroid administration. During the course of her disease and in the follow-up, the patient underwent repeated cerebrospinal fluid (CSF) examinations, neurophysiological somatic, autonomic nervous system studies and sural nerve biopsy. Clinical and laboratory assessments demonstrated the occurrence of a monophasic, chronic sensory and autonomic neuropathy. A sural nerve biopsy suggested an axonopathy. After a progressive worsening of symptoms lasting about 6 months, steroid treatment was started and within 6 months a complete recovery, with normalization of the CSF findings, was observed. Although the 'chronic inflammatory neuropathies' are still debated entities, the features of this chronic, exclusively sensory and autonomic neuropathy are new, and the occurrence of a high protein level in the CSF, together with the favorable outcome associated with steroid treatment, suggests that our case might be another variant in this debated area.
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2/62. cauda equina syndrome after spinal anaesthesia with hyperbaric 5% lignocaine: a review of six cases of cauda equina syndrome reported to the Swedish Pharmaceutical insurance 1993-1997.

    Six cases of cauda equina syndrome with varying severity were reported to the Swedish Pharmaceutical insurance during the period 1993-1997. All were associated with spinal anaesthesia using hyperbaric 5% lignocaine. Five cases had single-shot spinal anaesthesia and one had a repeat spinal anaesthetic due to inadequate block. The dose of hyperbaric 5% lignocaine administered ranged from 60 to 120 mg. Three of the cases were most likely caused by direct neurotoxicity of hyperbaric 5% lignocaine. In the other 3 cases, direct neurotoxicity was also probable, but unfortunately radiological investigations were not done to definitely exclude a compressive aetiology. All cases sustained permanent neurological deficits. We recommend that hyperbaric lignocaine should be administered in concentrations not greater than 2% and at a total dose preferably not exceeding 60 mg.
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3/62. Spinal dural arteriovenous fistulae draining to the anterior spinal vein: angiographic diagnosis.

    OBJECTIVE: To describe and present atypical spinal dural arteriovenous fistulae (SDAVFs) that drain into the anterior spinal vein (ASV) and thus cause some degree of difficulty in differentiating the anterior spinal artery from the ASV. methods: A retrospective review of 80 selective spinal angiography procedures (with or without endovascular treatment) performed on SDAVFs since 1980 identified three cases in which the venous drainage was into a dilated ASV via a radicular vein. The patients included two men and one woman, ranging in age from 55 to 82 years (mean age, 71 yr), all of whom presented with mild to severe progressive paraparesis and sensory disturbance. RESULTS: The appearance of the venous drainage mimicked that of the usual hairpin configuration of the radiculomedullary artery and therefore caused diagnostic difficulty. There are no characteristic clinical features that differentiate this form of SDAVF from the usual type of SDAVF. The angiographic criteria for identification of the ASV draining an SDAVF include the demonstration of the branching of the ASV and its drainage into the epidural vein, opacification of other medullary veins connected with the ASV, recognition of distortion of the hairpin shape, and the identification of the anterior spinal artery at the segment where the ASV is opacified. Two patients were treated with embolization and one with surgery. All patients improved after the treatment. CONCLUSION: Before performing endovascular treatment, thorough spinal angiography with an appropriate field of view must be performed to identify this unusual type of SDAVF.
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4/62. MRI of the spinal cord in myelopathy complicating vitamin B12 deficiency: two additional cases and a review of the literature.

    Focal spinal cord lesions have been present in all previously reported cases of MRI appearances in myelopathy complicating vitamin B12 deficiency. We describe two further cases showing mild atrophy only and review the salient features of the previous 11 publications. MRI findings reflect quite closely the known pathological changes in this condition.
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5/62. Neurological deficit following spinal anaesthesia: MRI and CT evidence of spinal cord gas embolism.

    A 62-year-old diabetic woman developed permanent neurological deficits in the legs following spinal anaesthesia. MRI showed oedema in the spinal cord and a small intramedullary focus of signal void at the T10 level, with negative density at CT. Intramedullary gas bubbles have not been reported previously among the possible neurological complications of spinal anaesthesia; a combined ischaemic/embolic mechanism is hypothesised.
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6/62. electrodiagnosis in spinal cord injured persons with new weakness or sensory loss: central and peripheral etiologies.

    OBJECTIVE: To assess the prevalence and causes of late neurologic decline of persons with spinal cord injury (SCI). DESIGN: Retrospective review of persons with SCI over a 9-year period. Those with complaints of new weakness or sensory loss were grouped into three categories based on clinical examination, electrodiagnosis, and imaging: (1) central pathology (ie, brain, spinal cord, or nerve root); (2) peripheral pathology (plexus or peripheral nerve); or (3) no identifiable etiology. The specific diagnoses of late neurologic decline were identified. SETTING: Regional veterans Affairs spinal cord Injury Service. patients: Five hundred two inpatient and outpatient adults with SCI. RESULTS: Nineteen percent of the study population complained of new weakness and/or sensory loss. Neurologic abnormalities were noted in 13.5%, 7.2% with central and 6.4% with peripheral causes. The most common pathologies were posttraumatic syringomyelia (2.4%) and cervical (1.6%) and lumbosacral (1.2%) myelopathy/radiculopathy. A specific etiology was not determined in 6 cases (1.6%). Peripheral involvement was mostly from ulnar nerve entrapment (3.4%) and carpal tunnel syndrome (3.0%). CONCLUSIONS: Late-onset neurologic decline is common after SCI and can result from central or peripheral pathology. Regular neurologic monitoring of SCI patients is recommended, since many with neurologic decline respond favorably if diagnosed and treated early.
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7/62. Acute axonal polyneuropathy in chronic alcoholism and malnutrition.

    In contrast to the classic, slowly progressive polyneuropathy in alcoholic patients, acute forms, clinically mimicking guillain-barre syndrome, are rare. We present a patient who developed motor weakness and sensory loss in all four limbs within four days. Laboratory data were consistent with long-term alcohol abuse and documented thiamine deficiency. Repeated cerebrospinal fluid examinations were normal. Electrophysiological studies showed an acute sensorimotor polyneuropathy with predominantly axonal involvement. We conclude that acute alcoholic neuropathy has to be distinguished from guillain-barre syndrome and other forms of acute polyneuropathy by using clinical, laboratory, and electrophysiological data. Both ethanol toxicity and vitamin deficiency could play a role in the pathogenesis.
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8/62. cauda equina syndrome due to lumbosacral arachnoid cysts in children.

    We describe the clinical, neuroradiological and surgical aspects of two children in whom symptoms attributable to cauda equina compression were caused by spinal arachnoid cysts. The first patient presented with recurrent urinary tract infections due to neurogenic bladder dysfunction, absent deep tendon reflexes and sensory deficit in the lower limbs. The second child presented with unstable gait as a result of weakness and diminished sensation in the lower extremities. Spinal magnetic resonance imaging revealed a lumbosacral arachnoid cyst in both patients. During surgery the cysts were identified and excised. Two years after surgery, the sensory deficits of the first patient have disappeared and patellar and ankle reflexes can be elicited, but there is no improvement in bladder function. Neurological examination of the second patient was normal. We conclude that the diagnosis of cauda equina syndrome should prompt a vigorous search for its aetiology. Lumbosacral arachnoid cysts are a rare cause of cauda equina syndrome in children.
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9/62. Sensory guillain-barre syndrome.

    OBJECTIVE: To report eight cases of sensory guillain-barre syndrome (GBS). BACKGROUND: The concept of sensory equivalent to ascending paralysis of GBS was raised in 1958, and the diagnostic criteria for a sensory loss and areflexia variant of GBS were proposed in 1981. However, clinical cases meeting these criteria have been relatively scarce. methods: During a 13-year period between 1986 and 1999, the authors collected eight cases of an acute sensory demyelinating neuropathy that met most of the proposed diagnostic criteria of a sensory variant of GBS. RESULTS: In all patients, sensory neuropathy was sudden at onset and peaked to maximal deficit within 4 weeks. In five (63%) cases, there was an antecedent viral illness. All patients had objective sensory loss and diminished or absent reflexes. None showed any muscle weakness. In all four patients in whom the spinal fluid was examined during the first 4 weeks, there was albuminocytologic dissociation. All of the patients had electrophysiologic evidence of demyelination in at least two nerves. Demyelination was demonstrated in motor nerve conduction in seven patients and in sensory nerve conduction in one, indicating that motor nerve conduction studies were the key for the diagnosis of demyelinating neuropathy. All patients had sensory nerve conduction abnormalities in at least one nerve. Three patients responded to immunotherapies. All had a favorable outcome, with a monophasic course of disease and no sign of relapse. CONCLUSION: The current study confirms the existence of sensory GBS.
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10/62. Acute posttraumatic spinal cord herniation. Case report and review of the literature.

    Transdural herniations of the spinal cord are rare, and those occurring acutely after a spinal cord injury (SCI) are particularly unusual. In this report, the authors present the case of acute posttraumatic spinal cord herniation in a patient who sustained severe polytraumatic injuries. The clinical manifestations were acute flaccid paralysis of the right leg and rapidly progressive sensorimotor deficits of the contralateral leg. The herniation was surgically reduced. Postoperatively left leg paralysis was completely resolved. The authors review the pertinent literature, and suggest that, with regard to another underlying pathophysiological mechanism, cases of acute posttraumatic spinal cord herniation should be differentiated from those "posttraumatic" cases in which herniation of the spinal cord occurs years or even decades after the traumatic event. To the best of the authors' knowledge, only one similar case has been previously reported. They conclude that acute posttraumatic spinal cord herniation should be included in the differential diagnosis of acute neurological deterioration after SCI.
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