Cases reported "Quadriplegia"

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1/108. Control of FES thumb force using slip information obtained from the cutaneous electroneurogram in quadriplegic man.

    A tetraplegic volunteer was implanted with percutaneous intramuscular electrodes in hand and forearm muscles. Furthermore, a sensory nerve cuff electrode was implanted on the volar digital nerve to the radial side of the index finger branching off the median nerve. In laboratory experiments a stimulation system was used to produce a lateral grasp (key grip) while the neural activity was recorded with the cuff electrode. The nerve signal contained information that could be used to detect the occurrence of slips and further to increase stimulation intensity to the thumb flexor/adductor muscles to stop the slip. Thereby the system provided a grasp that could catch an object if it started to slip due to, e.g., decreasing muscle force or changes in load forces tangential to the surface of the object. This method enabled an automatic adjustment of the stimulation intensity to the lowest possible level without loosing the grip and without any prior knowledge about the strength of the muscles and the weight and surface texture of the object.
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2/108. Acute quadriplegic myopathy unrelated to steroids or paralyzing agents: quantitative EMG studies.

    BACKGROUND: Quadriplegic myopathy (QM) and its variants generally are described in critically ill patients who are exposed to steroids and nondepolarizing muscle blocking agents (NDMBAs). methods: A patient with sepsis who was not exposed to steroids or an NDMBA infusion developed QM and was studied using serial quantitative electromyography. RESULTS: Clinical and electrophysiological studies identified evidence of a severe myopathy and muscle biopsy showed necrosis, calcifications and selective loss of myosin filaments in non-necrotic fibers. Her clinical recovery paralleled rises in motor unit action potential (MUAP) amplitudes studied by serial automatic decomposition electromyography (ADEMG). CONCLUSIONS: QM can develop with sepsis and without significant exposure to steroids and NDMBAs. ADEMG can be a useful tool in electrophysiological evaluation of critically ill patients with weakness.
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3/108. Tracheocarotid artery fistula infected with methicillin-resistant staphylococcus aureus.

    Massive life-threatening haemorrhage from a fistula between the trachea and a major blood vessel of the neck is a rare complication of the tracheostomy procedure, well-recognized by anaesthetists and otolaryngologists. Although the lesion is likely to be encountered at autopsy, it is not described in histopathological literature. The possible causes are discussed together with the macroscopic and microscopic appearances of the lesion. Suitable procedures for its identification and for obtaining appropriate histopathological blocks are suggested. Presence of methicillin-resistant staphylococcus aureus (MRSA) has not been documented before and might have contributed to the genesis of the fistula in this case.
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4/108. Acute quadriplegic myopathy in a 17-month-old boy.

    Acute quadriplegic myopathy is a rare condition associated with the use of nondepolarizing muscle-blocking agents and corticosteroids in the course of severe systemic illness. A 17-month-old boy underwent liver transplantation for fulminant hepatitis. He was intubated for 24 days and treated with vecuronium bromide and high-dose methylprednisolone. The child was weaned from the ventilator and presented extreme weakness in the upper limbs and total paralysis of the lower limbs. serum creatine kinase level was normal and electromyography showed myopathic abnormalities. Muscle biopsy showed severe type-1 fiber atrophy and selective loss of myosin thick filaments was seen on electron microscopy. Scattered regenerating fetal myosin-positive fibers were present, mu calpain was absent, while m calpain was diffusely expressed. Physical therapy was immediately started and the child recovered even though corticosteroids were not discontinued. The pathogenesis of acute quadriplegic myopathy is still unknown. We suggest that it could be due to abnormal protein turnover in the muscle. Several independent factors, such as corticosteroid treatment, immobilization, or cytokines, could take part in a cascade of events that leads to an excessive yet selective degradation of proteins involving myosin thick filaments and possibly components of sarcolemma, causing muscle inexcitability.
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5/108. Transient absence of F-waves in acute myelopathy: a potential source of diagnostic error.

    BACKGROUND: The frequent absence of F-waves in lesions of the nerve roots and proximal nerve is well known, with absence of F-waves occasionally the only electrophysiologic manifestation of early guillain-barre syndrome. It is less well known that acute central nervous system lesions can cause disappearance of F-waves. CASE DESCRIPTION: A 25 year old woman presented with quadriparesis and sensory loss progressive over several days. Hyporeflexia and hypotonia were present. Imaging studies were initially negative. Electrophysiologic testing was normal apart from the diffuse absence of F-waves. This led to strong consideration of the diagnosis of guillain-barre syndrome, and treatment for this diagnosis. However, imaging studies ultimately revealed the diagnosis to be transverse myelitis. F responses normalized 6 weeks after the initial study. CONCLUSIONS: F responses are significantly modulated by central nervous system factors. The relevant experimental and clinical literature is reviewed. The relevance of this to the diagnosis of guillain-barre syndrome has not been previously emphasized, but our experience confirms that the absence of F-waves in a patient with acute weakness accompanied by hyporeflexia and hypotonia does not distinguish between peripheral nerve and central nervous system lesions.
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6/108. spinal cord infarction and tetraplegia--rare complications of meningococcal meningitis.

    A previously healthy 25-yr-old female developed flaccid areflexic tetraplegia, with intact cranial nerve function, 36 h after the diagnosis of bacterial meningitis. polymerase chain reaction studies of cerebrospinal fluid and blood were positive for neisseria meningitidis, serogroup b. Magnetic resonance of the cervicothoracic spine revealed increased signal intensity and expansion in the lower medulla, upper cervical cord and cerebellar tonsils. Neurosurgical consultation recommended hyperventilation, dexamethasone and regular mannitol therapy rather than decompressive intervention. The clinical course over the following 12 days was complicated by the development of progressive central nervous and multisystem organ failure with disseminated intravascular coagulopathy. autopsy revealed cerebral oedema with cystic infarction extending from the medulla to the upper cervical cord and cerebellar tonsils. Flaccid areflexic tetraplegia with spinal cord infarction has not been reported following bacterial infection in an adult. The clinical implications would suggest complete central nervous system evaluation of patients recovering from meningococcal meningitis, since spinal cord lesions, although uncommon, do occur. In those very rare situations where a patient develops significant peripheral neurological deficits, urgent magnetic resonance imaging is warranted, to rule out an infective focus or an underlying anatomical anomaly.
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7/108. Event-related potentials in patients with total locked-in state due to fulminant guillain-barre syndrome.

    A series of electrophysiological investigations were performed over a 6-month period in two patients affected by fulminant Guillain-Barre polyradiculoneuropathy, who developed an ascending paralysis leading, within 72 h, to flaccid quadriplegia, internal and external ophthalmoplegia, absence of all brainstem reflexes and no respiratory effort: the clinical state resembled brain death. brain CTs were normal and spinal fluid examination revealed albuminocytological dissociation. All motor nerves tested were unexcitable, whereas sensory responses were markedly abnormal but present. Sequential EEG recordings revealed normal, partially reactive alpha rhythm in both patients. In one patient, normal auditory event-related potentials (ERPs: peak N1, P2, N2, P3, evoked in an 'oddball' paradigm) and CNV-like potentials could be recorded not earlier than the 20th day into the illness. In earlier recordings, N1 and P2 peaks as well as mismatch negativity (MMN) were present over the frontal and central scalp electrodes. This patient has now partially recovered motor functions and no cognitive defects are present, but he has little recollection of the events occurring in the first 2 weeks spent in the ICU, when he was completely paralyzed. The other patient generated normal N1 and P2 ERP peaks, but no N2, P3 and MMN were detected in a series of recordings. He died without having ever regained appropriate behavioral responses. The ERP abnormalities observed raise the matter of the origin of cognitive dysfunction in patients with severe and prolonged de-efferentation/de-afferentation. ERPs allow monitoring the level of alertness and attention and appear more specific than EEG in identifying a state of awareness in patients in which communication is severely impaired as a consequence of neurological disorders.
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8/108. Progressive infantile axonal polyneuropathy.

    polyneuropathies are relatively uncommon in early infancy and the majority of affected children are found to have hypomyelinating neuropathies. Axonal sensorimotor neuropathies have been described in childhood but the majority of affected children present at or after 6 months of age, have nonprogressive courses, and achieve the ability to walk, albeit late. Here we present three infants with infantile progressive axonal polyneuropathy from two families with nonconsanguineous parents. Each child presented shortly after the neonatal period and with rapid progression to quadriplegia. Involvement of the lower cranial nerves, phrenic nerves, or both was present in each child. electrophysiology was diagnostic in each child. While the diagnosis of spinal muscular atrophy was considered in each case, clinical presentation, biopsies, and genetic testing were inconsistent with this diagnosis. Recognition of this early form of progressive axonal neuropathy is important as respiratory compromise occurred early and the condition showed familial inheritance in two of our patients.
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9/108. Apoptotic features accompany acute quadriplegic myopathy.

    OBJECTIVE: To investigate the role of apoptosis in acute quadriplegic myopathy. BACKGROUND: Acute quadriplegic myopathy is a muscular disease characterized by diffuse flaccid weakness occurring in patients with severe systemic illness and exposure to corticosteroids or neuroblocking agents. Myofiber atrophy and thick filament loss are the distinguishing pathologic features on muscle biopsy. Increased calpains expression and lysosomal and nonlysosomal proteolytic pathways have been claimed as possible pathogenic factors. Nevertheless, the mechanisms leading to myofiber atrophy and thick filament loss need further investigation. patients AND methods: The expression of ubiquitin and proapoptotic proteases as well as dna fragmentation in muscle biopsies from three patients with acute quadriplegic myopathy were studied. RESULTS: All patients exhibited an important overexpression of caspases, calpain, cathepsin b, and ubiquitin, and the presence of numerous apoptotic nuclei in over 70% of myofibers. CONCLUSIONS: These data suggest that apoptosis mediated by proteolytic proteases may play a role in the pathogenesis of acute quadriplegic myopathy.
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10/108. Xanthogranulomatous funiculitis and epididymo-orchitis in a tetraplegic patient.

    STUDY DESIGN: A case report of xanthogranulomatous funiculitis and epididymo-orchitis. Xanthogranulomatous inflammation is an uncommon, non-neoplastic process characterised by destruction of tissue, which is replaced by a striking cellular infiltrate of lipid-laden macrophages. CASE REPORT: A 21-year male sustained complete tetraplegia at C-6 level, after a fall in 1998. The neuropathic bladder was managed with an indwelling urethral catheter. He had many unsuccessful trials of micturition. Sixteen months after the cervical injury, he noticed swelling of the left side of the scrotum following removal of a blocked catheter. He was prescribed antibacterial therapy. Four weeks later, physical examination revealed a hard and irregular swelling encompassing the testis, epididymis and spermatic cord. The clinical diagnosis was epididymo-orchitis progressing to pyocele. Through a scrotal incision, the swollen testis, epididymis and diseased segment of the spermatic cord were removed en masse. Histopathology showed extensive areas of necrosis, with xanthogranulomatous inflammation in the spermatic cord and to a lesser extent in the testis/epididymis. CONCLUSION: Repeated episodes of high-pressure urinary reflux along the vas deferens during dyssynergic voiding, and subsequent interstitial extravasation of urine together with chronic, low-grade, suppurative infection possibly led to development of xanthogranulomatous inflammation in the testis and the epididymis. Since tissue destruction is a feature of xanthogranulomatous inflammation, the definite and curative treatment is either complete (or, where applicable, partial) excision of the affected organ in most of the cases.
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