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1/7. Subacute sensory neuropathy associated with Epstein-Barr virus.

    A 35-year-old man experienced severe sensory loss, pseudoathetosis, and areflexia during recovery from a severe viral illness. Sensory nerve action potentials were absent, motor conduction velocities were mildly slowed, and blink reflexes were normal. magnetic resonance imaging (MRI) revealed abnormal signal within the central and dorsal aspects of the thoracic cord. Acute and convalescent Epstein-Barr virus (EBV) titers suggested EBV as the etiology. Subacute sensory neuropathy, with peripheral and central nervous system involvement, is a rare complication of EBV infection.
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ranking = 1
keywords = central nervous system, nervous system
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2/7. gait rehabilitation in a patient affected with charcot-marie-tooth disease associated with pyramidal and cerebellar features and blindness.

    Charcot-Marie-Tooth (CMT) disease, an inherited neuropathy characterized by length-dependent degeneration of the motor and sensory nerve fibers with consequent distal muscle atrophy and sensory reduction, can be associated with symptoms and signs of involvement of the central nervous system and/or cranial nerves. We present a patient with relatively severe CMT, cerebellar ataxia, pyramidal involvement, and blindness due to Leber's hereditary optic neuropathy. The patient presented with poor standing and gait, with consequent severe disability. Factors responsible for the patient's functional impairment (plantarflexor failure, footdrop, foot rotation, knee flexor contracture, poor proprioception, cerebellar dysfunction, spastic paraparesis, blindness) were identified and addressed by a rehabilitation management, which included, as a main intervention, ankle stabilization by drop-foot boots instead of ankle-foot orthoses. Improved balance and independent ambulation resulted from rehabilitation.
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ranking = 1
keywords = central nervous system, nervous system
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3/7. Foot drop due to cranial gunshot wound.

    OBJECTIVE: We present a case of foot drop from hemorrhagic contusion after cranial gunshot, which has never been reported. methods: A 21-year-old man was admitted with inability of dorsiflexion 1 day after a tangential gunshot wound of the scalp. The scalp skin was cut by the rifle bullet. He had foot drop and his neurological examination was normal except for weakness at dorsiflexion of the right foot. Pathological reflexes and sensation failure were not detected. T1- and T2-weighted magnetic resonance images showed hyperintense contusion at the right superior frontal gyrus and mild subdural hemorrhage. peripheral nervous system examination was electrophysiologically normal. Motor-evoked potentials showed the location of the lesion at the motor cortex because no electrical record was obtained from the right anterior tibial and extensor digitorum brevis muscles, and there was a normal record on the left. Six months later, the patient's neurological examination was uneventful. CONCLUSION: When a cranial gunshot wound injury victim presents with foot drop, the central causes should be included in the differential diagnosis list.
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ranking = 0.2966335172973
keywords = nervous system
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4/7. central nervous system superficial siderosis following spinal surgery.

    Superficial siderosis of the central nervous system is a rare progressive disease associated with hemosiderin deposition on the leptomeninges of the neuraxis. In addition to tumors and vascular lesions, dural sleeve pseudomeningoceles caused by brachial plexus avulsion injury may be the bleeding source in this disease. The authors describe a patient who underwent anterior cervical spine surgery for spinal cord compression due to the ossification of posterior longitudinal ligament. The operation was complicated by a dural tear and subsequent psedomeningocele formation. Nine years later, this patient developed superficial siderosis. The possible mechanisms involved in the development of superficial siderosis in this patient will be discussed.
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ranking = 2.1865340691892
keywords = central nervous system, nervous system
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5/7. Acute exertional compartment syndrome in the setting of anabolic steroids: an unusual cause of bilateral footdrop.

    Acute exertional compartment syndrome is the result of muscle ischemia within a tight fascial compartment. We report a 22-year-old boxer, with recent intake of anabolic steroids, who developed acute exertional compartment syndrome of the lower legs following an assault from which he had to run away. He presented with bilateral footdrop. Nerve conduction studies (NCS) and electromyography (EMG) were consistent with bilateral deep and superficial peroneal neuropathies, but magnetic resonance imaging (MRI) demonstrated hemorrhagic necrosis of the pretibial muscles. This case illustrates that the differential diagnosis for footdrop includes not only central and peripheral nervous system and muscle causes, but also compartment syndromes.
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ranking = 0.2966335172973
keywords = nervous system
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6/7. A case of foot drop as an expression of brain metastases?

    Foot drop can be defined as a significant weakness in ankle and toe dorsiflexion. Injury to the dorsiflexors or to any point along the neural pathways that supply these muscles can result in a foot drop. Injury to the peroneal nerve is usually the major precipitant. Other causes vary from trauma to surgical nerve injury, as well as leg compartment syndromes or dorsiflexor injuries, peripheral nerve injuries, stroke, neuropathies, drug toxicities, spinal stenosis, L5 sciaticas, systemic diseases such as connective tissue diseases, vasculidities, or diabetes. This report focuses on a patient presenting with a foot drop as an unusual manifestation of brain metastasis. His minimal symptomatology seemed to point towards a local process. Therefore, early recognition and prompt treatment are essential. The central nervous system must be the target of investigations when the workup fails to disclose the proper etiology. Potential diagnostic delays may occur. Certain cases may require a more aggressive approach.
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ranking = 1
keywords = central nervous system, nervous system
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7/7. betamethasone and improvement of neurological symptoms in ataxia-telangiectasia.

    BACKGROUND: To our knowledge, there have been no reports on the control of central nervous system symptoms in patients with ataxia-telangiectasia. OBJECTIVE: To preliminarily determine the effectiveness of corticosteroid therapy on the central nervous system symptoms of a child with ataxia-telangiectasia in whom neurological signs improved when, occasionally, he was given betamethasone to treat asthmatic bronchitis attacks. DESIGN: Case report. SETTING: Tertiary care hospital.Patient A 3-year-old boy with the classic hallmarks and a proved molecular diagnosis of ataxia-telangiectasia. INTERVENTIONS: We used betamethasone, 0.1 mg/kg per 24 hours, divided every 12 hours, for 4 weeks to preliminarily determine its effectiveness on the child's central nervous system symptoms and its safety. methylprednisolone, 2 mg/kg per 24 hours, divided every 12 hours, was then given in an attempt to perform a long-term treatment. RESULTS: There were improvements in the child's neurological symptoms 2 or 3 days after the beginning of the drug treatment. After 2 weeks of treatment, the improvement was dramatic: the disturbance of stance and gait was clearly reduced, and the control of the head and neck had increased, as had control of skilled movements. At 4 weeks of treatment, adverse effects mainly included increased appetite and body weight and moon face. No beneficial effect was obtained when, after 4 weeks, betamethasone was replaced with methylprednisolone. Six months later, without therapy, the child continued to experience severe signs of central nervous system impairment. CONCLUSION: Controlled studies to better understand the most appropriate drug and therapeutic schedule are required.
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ranking = 4
keywords = central nervous system, nervous system
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