Cases reported "Lyme Disease"

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1/38. Diaphragmatic paralysis due to lyme disease.

    lyme disease is a tick-borne spirochaete infection which, in a proportion of patients, can lead to neuropathy. This article describes a case of diaphragmatic paralysis due to lyme disease. A 39-yr-old male presented to the hospital because of an acute left facial palsy. Six weeks prior to admission he had developed a circular rash on his left flank during a camping holiday. He also complained of shortness of breath and arthralgia for 1 week. His chest radiograph demonstrated a raised right hemi-diaphragm. Diaphragmatic paralysis was confirmed by fluoroscopy (a positive sniff test). serology revealed evidence of recent infection by borrelia burgdorferi. On the basis of the patient's clinical presentation, a recent history of erythema migrans, and positive Lyme serology, a diagnosis of neuroborreliosis was made. He received oral doxycycline therapy (200 mg x day(-1)) for three weeks. Facial and diaphragmatic palsies resolved within eight weeks. On the basis of this case, a diagnosis of lyme disease should be considered in patients from endemic regions with otherwise unexplained phrenic nerve palsy.
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2/38. central nervous system infection caused by borrelia burgdorferi. Clinico-pathological correlation of three post-mortem cases.

    The spirochete borrelia burgdorferi (B. burgdorferi) may cause severe meningoencephalomyelitis as the sole manifestation of Lyme borreliosis. We would like to present three such cases, where definite neuroborreliosis was clinically diagnosed in two cases and possible neuroborreliosis was recognized in one case. Alive spirochetes were isolated and cultured from blood and cerebrospinal fluid (CSF) in both definite cases. B. burgdorferi as the causative agent of the infection was confirmed in CSF by polymerase chain reaction (PCR) in one definite case. In the possible case spirochetes were cultured from blood and CSF. Alive spirochetes were not isolated, however anti-B. burgdorferi antibody value in serum was significantly elevated. On necropsy gross examination brain edema without focal changes was detected in two cases. Cerebral atrophy was seen in Case 3. Microscopically, lymphocytic infiltrates, microglial diffuse and nodular activation, spongiform changes, diffuse demyelination of the cerebral and cerebellar white matter, and diffuse astrocytosis, were characteristic pathological features in all presented cases. Multifocal, perivascular degenerative changes in the cerebral and cerebellar white matter were observed in the first case. Inflammatory changes in the nuclei and roots of cranial nerves were present in the third case.
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3/38. Isolated neuritis of the sciatic nerve in a case of lyme disease.

    lyme disease is an infectious disease caused by the spirochete borrelia burgdorferi. The course of the disease is divided into three stages, the second of which may include various types of peripheral nervous system disturbances. We report the case of a patient with persistent deficits caused by the prevalent involvement of the sciatic nerve, confirmed by electrophysiological and neuropathological findings. The most significant bioptic results were axonal degeneration and perivascular inflammation. Damage to a single peripheral nerve as the dominant clinical expression during the course of lyme disease is an unusual finding that has been rarely described in the literature.
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4/38. paraneoplastic polyneuropathy preceding the diagnosis of Hodgkin's disease and non-small cell lung cancer in a patient with concomitant borrelia burgdorferi infection.

    A patient with painful peripheral neuropathy is presented, whose symptoms were thought to result from an infection with borrelia burgdorferi sensu lato. Investigations of the cerebrospinal fluid for signs of inflammation and borrelial antibodies were negative, and the patient did not benefit from repeated antibiotic treatment. Electrophysiologic studies and sural nerve biopsy showed axonal neuropathy consistent with a paraneoplastic syndrome. Further workup revealed mediastinal Hodgkin's disease (HD; nodular sclerosing subtype) Ann Arbor stage II and non-small cell cancer of the lung (stage T1N0M0). Surgical resection of the lung cancer and combined chemo- and radiotherapy for HD resulted in complete remission of both malignancies. While the preexisting neurologic symptoms persisted during treatment, neurography showed some improvement of the distal nerves. During radiation therapy the patient developed transient left-sided brachial plexopathy. This case illustrates that the diagnosis of borreliosis in patients with isolated painful peripheral neuritis cannot be based solely upon positive IgG titers and supports the requirement for a thorough workup for an underlying--potentially curable--disease. In addition, singular pulmonary lesions in the setting of HD should be suspected to have a separate cause.
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5/38. Optic neuropathy in children with lyme disease.

    Involvement of the optic nerve, either because of inflammation or increased intracranial pressure, is a rare manifestation of lyme disease. Of the 4 children reported here with optic nerve abnormalities, 2 had decreased vision months after disease onset attributable to optic neuritis, and 1 had headache and diplopia early in the infection because of increased intracranial pressure associated with Lyme meningitis. In these 3 children, optic nerve involvement responded well to intravenous ceftriaxone therapy. The fourth child had headache and visual loss attributable to increased intracranial pressure and perhaps also to optic neuritis. Despite treatment with ceftriaxone and steroids, he had persistent increased intracranial pressure leading to permanent bilateral blindness. Clinicians should be aware that neuro-ophthalmologic involvement of lyme disease may have significant consequences. If increased intracranial pressure persists despite antibiotic therapy, measures must be taken quickly to reduce the pressure.
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6/38. Acute onset of facial nerve palsy associated with lyme disease in a 6 year-old child.

    Pediatric facial nerve palsy (FNP) can result from a variety of etiologies including lyme disease, varicella, primary gingivostomatitis, herpes zoster oticus (Ramsay Hunt syndrome), coxsackievirus, trauma, otitis media, hiv, diseases causing tumors or demyelinations, compressions, and possibly Epstein Barr virus. lyme disease has been implicated as the cause of over 50% of the FNPs in children. The paralysis of the facial nerve disturbs motor function to the muscles of facial expression and results in a flaccid appearance of the face (unilateral or bilateral). This case report derails undiagnosed lyme disease presenting as a facial palsy in a 6 year, 5 month-old white female. The palsy was recognized and consultation with the child's physician prompted definitive diagnosis and treatment. A review of the literature and the implications of facial nerve palsy are discussed.
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7/38. sciatica, disk herniation, and neuroborreliosis. A report of four cases.

    We report four cases of sciatica in patients with same-level disk herniation confirmed by computed tomography and a final diagnosis of acute radiculitis caused by borrelia burgdorferi, with a favorable response to ceftriaxone therapy. The neurological manifestations of lyme disease are protean, and a potential contribution of concomitant disk disease to sciatica can lead to diagnostic wanderings. Disk lesions and infectious conditions that can cause sciatica are discussed. Whether a favorable response to antibiotic therapy should be taken as proof of B. burgdorferi radiculitis deserves discussion. In practice, in a patient with clinical manifestations suggesting disk-related nerve root pain and residing or having traveled to an endemic area, B. burgdorferi infection should be looked for, as both etiologies can coexist.
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8/38. Cranial nerve involvement with Lyme borreliosis demonstrated by magnetic resonance imaging.

    We report a patient with cranial nerve and meningeal symptoms secondary to Lyme borreliosis. MRI using gadolinium contrast material demonstrated this inflammatory process. The patient did not have the parenchymal lesions described in previous reports of patients with CNS Lyme borreliosis.
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9/38. Cutaneous lymphoid hyperplasia and other lymphoid infiltrates of the breast nipple: a retrospective clinicopathologic study of fifty-six patients.

    This study characterizes the clinicopathological spectrum of lymphoproliferations involving the breast nipple and/or areola. Morphologic, immunohistochemical, molecular-genetic, and clinical features of 58 specimens from 56 patients were analyzed. They were re-diagnosed as cutaneous lymphoid hyperplasia (CLH, n = 44); other benign lymphoid infiltrates (OBLI, n = 8); peripheral T-cell lymphoma, not otherwise specified (n = 1); cases with overlapping features of CLH and B-cell lymphoma (n = 3), one of them composed of spindle cells. Cutaneous lymphoid hyperplasia infiltrates were dense, composed mainly of B cells forming follicles with germinal centers (GC). Cutaneous lymphoid hyperplasia frequently showed features suggesting a malignancy as coalescing follicles with non-polarized germinal centers lacking mantle zones, and smudged infiltrates of lymphoid cells spreading into collagen (often as "Indian files"), smooth muscle, vessel walls, and nerve sheaths. Only two cutaneous lymphoid hyperplasias recurred; otherwise all patients are without disease (mean follow-up 62 months). Monoclonal rearrangement of immunoglobulin heavy chain gene was detected in five, and of T-cell receptor gamma gene in two cutaneous lymphoid hyperplasias using polymerase chain reaction (PCR), but the patients fared well too. In 47% of cases borrelia burgdorferi was detected by polymerase chain reaction and/or serology, of which one was monoclonal. We conclude that cutaneous lymphoid hyperplasia is the most common lymphoproliferation of the breast nipple, rarely recognized clinically, and often overdiagnosed histologically as lymphoma.
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10/38. Vasculitic mononeuritis multiplex in patient with lyme disease.

    Lyme borreliosis is an infectious disease caused by the spirochete borrelia burgdorferi. Neurological complications are frequently reported but the pathogenesis remains largely unknown. We report on a patient with positive borrelia antibodies at ELISA and immunoblotting and with histological and immunofluorescence study of peripheral nerve biopsy consistent with vasculitic neuropathy.
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