Cases reported "Neuritis"

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1/82. Surgical findings in idiopathic trigeminal neuropathy mimicking a trigeminal neurinoma.

    Idiopathic trigeminal neuropathy is a benign disorder where the main clinical feature is facial numbness limited to the territory of one or more divisions of the trigeminal nerve, persisting for a few weeks to several years and in which no underlying disease can be identified. The case of a 37-year-old man with a brief history of sensory and motor trigeminal symptoms who showed magnetic resonance imaging (MRI) findings consistent with a small trigeminal neurinoma is reported. The patient was operated on but no tumour could be found during surgery and a biopsy was taken from the portio major. Pathological diagnosis was chronic non granulomatous inflammatory reaction with areas of coagulation necrosis. Control MRI showed complete resolution of the trigeminal abnormalities. It is concluded that in patients with MRI findings suggestive of a small trigeminal schwannoma, benign idiopathic trigeminal neuropathy should also be considered in the differential diagnosis. A conservative approach with sequential MRI studies may avoid an unnecessary surgical exploration.
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2/82. Herpetic tracheitis and brachial plexus neuropathy in a child with burns.

    Herpetic tracheobronchitis is a well-recognized clinical entity that most commonly occurs in immunocompromised patients, including patients with burns. Although the diagnosis of herpetic tracheobronchitis is usually not made until postmortem examination, the presence of the condition can be established when histologic specimens of a patient with upper airway obstruction are studied. In this article, a case is described in which a child developed herpetic tracheitis after undergoing elective intubation after the grafting of burns of the face, neck, and upper extremity. The tracheitis resulted in severe upper airway obstruction that required tracheal dilatation and sequential bronchoscopic excisions of granulation tissue. The patient also developed a brachial plexus neuropathy that was most likely related to herpetic infection.
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3/82. Migrant sensory neuropathy: report of 5 cases and review of the literature.

    There are only a few case descriptions of migrant sensory neuropathy. We report the clinical, laboratory, and electrophysiological findings observed in 5 patients whose presentation conformed with Wartenberg's description of a chronic, disseminated migrant sensory mononeuritis. In one patient, intermittent cranial motor nerve involvement occurred as well. The sural nerve biopsy in this patient showed changes suggestive of focal ischemic nerve damage and electron microscopy confirmed a vasculopathy.
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4/82. "Pseudo-conduction block" in a patient with vasculitic neuropathy.

    A 63-year-old man presented with progressive asymmetric weakness and numbness in his hands of 2 weeks duration. Nerve conduction studies showed low amplitude motor evoked potentials of both median nerves. The right ulnar, left tibial and peroneal nerves had normal potentials on distal stimulation with markedly decreased amplitudes proximally, suggestive of "conduction block". Three weeks later, amplitudes were decreased throughout. The patient was diagnosed with vasculitis. The acute ischemic injury presumably resulted in axonal damage between the distal and proximal stimulation sites, with subsequent wallerian degeneration.
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5/82. gasoline sniffing multifocal neuropathy.

    The polyneuropathy caused by chronic gasoline inhalation is reported to be a gradually progressive, symmetric, sensorimotor polyneuropathy. We report unleaded gasoline sniffing by a female 14 years of age that precipitated peripheral neuropathy. In contrast with the previously reported presentation of peripheral neuropathy in gasoline inhalation, our patient developed multiple mononeuropathies superimposed on a background of sensorimotor polyneuropathy. The patient illustrates that gasoline sniffing neuropathy may present with acute multiple mononeuropathies resembling mononeuritis multiplex, possibly related to increased peripheral nerve susceptibility to pressure in the setting of neurotoxic components of gasoline. The presence of tetraethyl lead, which is no longer present in modern gasoline mixtures, is apparently not a necessary factor in the development of gasoline sniffer's neuropathy.
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6/82. Resection of the hook of the hamate. Its place in the treatment of median and ulnar nerve entrapment in the hand.

    Poor results can be anticipated with conventional surgical decompression of nerves entrapped within the hand in (1) those with underlying systemic disease causing primary neuropathy, (2) those with combined median and ulnar nerve palsies, and (3) those who have been previously operated upon for nerve entrapment within the hand. Eighteen patients belonging in these categories were surgically treated by resection of the hook of the hamate and (in some) by intraneural neurolysis. Using this technique, we have decreased our failure rate from 20 percent to less than one percent. We believe that failures can be eliminated if the patients destined to have poor results from the usual treatment are identified preoperatively and a more aggressive surgical decompression is used on this "at risk" group.
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7/82. Chronic granulomatous neuritis in idiopathic trigeminal sensory neuropathy. Report of two cases.

    Idiopathic trigeminal sensory neuropathy is a clinically benign disorder in which the main feature is facial numbness limited to the territory of one or more divisions of the trigeminal nerve; the disorder persists for a few weeks to several years. and no underlying disease can be identified. Magnetic resonance (MR) imaging findings are occasionally consistent with a small trigeminal neuroma of the left gasserian ganglion associated with idiopathic trigeminal sensory neuropathy. The authors report on two patients who were treated using a skull base approach in which the gasserian ganglion was exposed and the lesion was removed. The pathological diagnosis was chronic granulomatous neuritis. The authors conclude that, in patients with MR findings suggestive of a small trigeminal neuroma, benign idiopathic trigeminal sensory neuropathy should also be considered in the differential diagnosis. A conservative approach featuring sequential MR imaging studies may avoid an unnecessary surgical exploration.
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8/82. Subarachnoid block and enlargement of the spinal canal in hypertrophic neuritis.

    A case of Dejerine-Sottas hypertrophic neuritis is reported. The patient, a 45-year-old male, suffered from chronic hypertrophic polyneuropathy, abnormal pupils, fasciculations, tremor, back pain, impotence, sphincter disorders, cramps, and lightning pains in the lower extremities. Besides extensive subarachnoid block, there was X-ray evidence of enlargement of the bony spinal canal with scalloping of the lumbar vertebrae. Surgical exploration showed these abnormalities to be due to extreme hypertrophy of the cauda equina. Histologic findings in peripheral nerve and lumbar root biopsies were typical of hypertrophic neuropathy of the onion bulb type. Vertebral changes secondary to hypertrophied nerve roots appear not to have been described before in hypertrophic neuritis; however, knowledge of their possible occurrence may be of practical importance in the management of similar future cases. A simple way of visualizing enlarged peripheral nerves is briefly described.
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9/82. Neurogenic positional pedal neuritis. Common pedal manifestations of spinal stenosis.

    Neurogenic positional pedal neuritis is a presentation of neuritic symptoms in one or both feet usually affected by body position, specifically, the position of the spine. Its etiology is similar to that of neurogenic-induced claudication caused by spinal stenosis in that the symptoms are caused by compression or irritation of nerves of the lower lumbosacral spine, usually the fifth lumbar and first sacral nerve roots. Burning, stabbing, a cold feeling, aching, numbness, paresthesia, or a weak or tired feeling of the feet (during some part of the disease process) depend on spinal position and may occur during standing, walking, or even lying in bed. Symptoms may be severe and are often eliminated by lumbosacral spine flexion, such as by walking with wheeled support such as a grocery cart or walker; less frequently by negative-heel shoe modification, which can change the position of the lumbosacral spine in stance; or by alteration of sleeping position. This condition, which can include loss of protective sensation, is often misdiagnosed as neuropathy (especially in diabetic patients) or less frequently as biomechanical in origin. In diabetic patients, this condition is frequently the cause of failure of monochromatic infrared energy therapy for diabetic peripheral neuropathy. Treatment is aimed at reducing the spinal nerve or nerve root irritation. Clear definition of the pedal symptoms of spinal nerve compression within a single diagnostic category should facilitate identification and treatment.
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10/82. Inflammatory peripheral neuropathy following high dose chemotherapy and autologous bone marrow transplantation.

    A 40-year-old man with non-Hodgkin's lymphoma developed severe ascending sensorimotor neuropathy 10 days after treatment with high dose chemotherapy and autologous bone marrow rescue. The neuropathy had axonal plus demyelinating features on electrophysiological studies. sural nerve biopsy showed heavy infiltration of the epineurium and endoneurium with mononuclear cells. The patient had no other evidence of graft-versus-host disease. He failed to respond to plasmapheresis but responded to high dose steroids.
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