Cases reported "Paralysis"

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1/74. A rare local anesthetic misadventure. Case report and anatomic considerations.

    When the mouth is fully opened, the depth to which the needle is inserted need not be great in order to pass through the submandibular gland capsule, and insertion of the needle behind the second molar tooth would result in passage behind the posterior border of the my-ohyoid muscle. The discussion indicates the relative ease with which fluid may penetrate the parapharyngeal space, particularly if pressure is used in injecting. Fluid diffusing into the region of the carotid triangle may have been responsible for the various symptoms, and anesthesia of the hypoglossal nerve, nerve, thyrohyoid nerve, internal and external laryngeal nerves, and carotid body possibly occurred. anesthesia of the vagus is a remote possibility.
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2/74. Uncompacted myelin in hereditary neuropathy with liability to pressure palsies with the 17 p11.2 deletion.

    A 16-year-old girl with a typical features of hereditary neuropathy with liability to pressure palsies (HNPP) and deletion on chromosome 17p11.2 was described. In the mother who was asymptomatic the same genetic defect was found. In a sural nerve biopsy obtained from the girl myelin thickenings characteristic for this disease and de- and remyelination in nerve fibers were found. Special attention was paid to the occurrence of uncompacted myelin, which was present in diffuse and focal forms. It is concluded that high amount of uncompacted myelin is characteristic for HNPP and it is probably related to the under-expression of peripheral myelin protein 22.
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3/74. Fulminant case of hereditary neuropathy with liability to pressure palsy.

    Hereditary neuropathy with liability to pressure palsy (HNPP) is typified as isolated nerve palsies caused by trivial compression or trauma. It rarely presents in two extremities and even more infrequently affects all four limbs simultaneously. We present a patient who concurrently experienced right shoulder, left hand, and bilateral foot weakness mimicking several multifocal conditions. electromyography suggested HNPP and subsequent nerve biopsy and genetic testing were confirmatory. The case demonstrates that HNPP can present in a fulminant manner and should be included in the differential diagnosis of acute multiple mononeuropathies. The possible causes for such a rapid clinical course in our patient are discussed.
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4/74. Hereditary neuropathy with liability to pressure palsies: a case report.

    Hereditary neuropathy with liability to pressure palsy is a rare autosomal dominant disorder characterized by multiple episodes of focal demyelinating neuropathies after minor trauma to peripheral nerves. It usually appears in early adulthood with recurrent attacks of pain, numbness, and muscular weakness along the distribution of the clinically affected nerve. Segmental demyelination and thickenings of the myelin sheath are the pathologic findings. Electrophysiologic studies show a nonuniform mild demyelinating neuropathy with prolonged distal latencies. Genetic tests are available to aid in diagnosis as molecular analysis has identified a deletion in the chromosome 17p11.2 in the majority of these patients. There is a paucity of information in the orthopaedic literature regarding hereditary neuropathy with liability to pressure palsy. A case report is presented of a patient with this disorder to promote awareness and recognition that this entity should be considered in patients with multiple nerve palsies.
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5/74. A novel 3'-splice site mutation in peripheral myelin protein 22 causing hereditary neuropathy with liability to pressure palsies.

    Hereditary neuropathy with liability to pressure palsies (HNPP) is an autosomal dominant, demyelinating peripheral neuropathy. Clinical hallmarks are recurrent painless focal neuropathies mostly preceded by minor trauma or compression at entrapment sites of peripheral nerves. In the majority of the patients, HNPP is caused by a 1.5 Mb deletion on chromosome 17p11.2-p12 containing the peripheral myelin protein 22 (PMP22) gene. Point mutations within this gene are reported in only a few families. We report a novel mutation in the PMP22 gene in a Spanish family with HNPP. The mutation is a 3' splice-site mutation, preceding coding exon 3 (c.179-1 G>C), causing a mild HNPP phenotype.
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6/74. Serratus anterior paralysis as an occupational injury in scaffolders: two case reports.

    BACKGROUND: shoulder complaints in scaffolders are very common and may result in permanent disability. methods: We present two case reports of patients who developed acute shoulder complaints. After lifting weights up to 50 kg both patients suffered an isolated lesion of the long thoracic nerve resulting in serratus anterior paralysis. RESULTS: Physical signs are unilateral winging of the scapula and loss of strength in the arm. A combined effect of pressure and stretching of the nerve resulted in an occupational injury with a different prognosis of reversibility in both patients. CONCLUSION: shoulder pads in the overall and limiting the weight to carry may prevent future injuries.
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7/74. The effect of focal twitching on the intracranial pressure during paralysis and mechanical ventilation.

    Three patients with head injuries developed minor facial twitching while their intracranial, intrathoracic and systemic arterial pressures were being monitored and they were on mechanical ventilation. These twitches were disclosed by the coincided great and damaging increases in the intracranial pressure, while the intrathoracic and arterial pressures were virtually unchanged. The intracranial hypertension was attributed to cerebral vasodilatation which was presumed to be due to the accumulation of cerebral metabolites since other causative factors such as systemic hypertension and hypoxia were under control. Cerebral elastance modulated the rise in intracranial pressure.
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8/74. Subdural spinal granuloma resulting from candida albicans without immunosufficiency: case report.

    STUDY DESIGN: This was a case of spinal subdural granuloma of candida albicans. A high cerebrospinal fluid protein level without pleocytosis (albuminocytologic dissociation) was observed. This case proved difficult to diagnose and treat. OBJECTIVES: To clarify the important issues in regard to the diagnosis and treatment of possible spinal subdural granuloma resulting from C. albicans. SUMMARY OF BACKGROUND DATA: Reports on subdural infection of C. albicans are very rare. Moreover, there are no reports of cases in which patients have survived this type of infection. methods: A 66-year-old man developed paralysis in the lower limbs, as well as vesicorectal disorder (anuresis). There were no obvious causes. Signs of meningeal irritation later appeared. A high cerebrospinal fluid protein level without pleocytosis was observed through a laboratory test. The cause of these disorders was unclear, and a final diagnosis could not be made on the basis of the test results and angiograph. Possible diagnoses included tumor, infection, and others such as guillain-barre syndrome. The authors therefore carried out surgery to reduce the pressure on the spinal cord and ultimately make a definitive diagnosis. RESULTS: The final diagnosis was spinal subdural granuloma of C. albicans. granuloma was widespread (T3-T10). Surgery, various drug treatments, and hyperbaric oxygen therapy all contributed to saving the patient's life. CONCLUSION: This was a very rare case of spinal subdural granuloma resulting from C. albicans, and the authors had difficulty diagnosing and treating the patient. A distinctive gadolinium-enhanced MRI was obtained. The effect of treatment by drugs alone was limited. An intraoperative ultrasonography proved useful. The authors concluded that a combination of early surgery and hyperbaric oxygen therapy was effective.
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9/74. Hereditary neuropathy with liability to pressure palsies with a small deletion interrupting the PMP22 gene.

    Hereditary neuropathy with liability to pressure palsies is associated with a deficiency in the Peripheral Myelin Protein 22 (PMP22). Most hereditary neuropathy with liability to pressure palsies cases are caused by a deletion of a 1.5 Mb region on chromosome 17p11.2-12 encompassing the PMP22 gene. We describe a hereditary neuropathy with liability to pressure palsies family that lacks the common deletion, but carries a small deletion spanning the 3' region of the PMP22 gene, causing only a partial deletion of one copy of the gene.
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10/74. Handlebar palsy--a compression syndrome of the deep terminal (motor) branch of the ulnar nerve in biking.

    We describe 3 patients who developed a severe palsy of the intrinsic ulnar supplied hand muscles after bicycle riding. Clinically and electrophysiologically all showed an isolated lesion of the deep terminal motor branch of the ulnar nerve leaving the hypothenar muscle and the distal sensory branch intact. This type of lesion at the canal of Guyon is quite unusual, caused in the majority of cases by chronic external pressure over the ulnar palm. In earlier reports describing this lesion in bicycle riders, most patients experienced this lesion after a long distance ride. Due to the change of riding position and shape of handlebars (horn handle) in recent years, however, even a single bicycle ride may be sufficient to cause a lesion of this ulnar branch. Especially in downhill riding, a large part of the body weight is supported by the hand on the corner of the handlebar leading to a high load at Guyon's canal. As no sensory fibres are affected, the patients are not aware of the ongoing nerve compression until a severe lesion develops. Individual adaptation of the handlebar and riding position seems to be crucial for prevention of this type of nerve lesion.
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