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At least 19 recordsLinked to original sources
PubMed1992

Lymphoma-induced polyradiculopathy in AIDS: two cases.

Progressive polyradiculopathy is a rare, well-documented complication of the acquired immunodeficiency syndrome in man. It has been commonly attributed to a cytomegalovirus (CMV) infection. We report two HIV-infected patients with clinical and electrophysiological features of a unique, subacute, progressive polyradiculopathy. Post-mortem examination in case 1 disclosed an infiltration of the leptomeninges, the lumbar spinal cord, and the anterior and posterior roots by a B-cell immunoblastic lymphoma. Immunochemistry for HIV1 and CMV was negative in the peripheral and the central nervous system. Case 2 showed bone-marrow involvement by a Burkitt type lymphoma. Specific chemotherapy was followed by both clinical improvement of the polyradiculopathy and complete remission on a second bone-marrow biopsy. These findings may indicate that a lymphoma must also be considered a possible cause of polyradiculopathy in AIDS.

Adult↗
PubMed1979

[Polyradiculopathy associated with bullous pemphigoid (author's transl)].

A sensorio-motor polyradiculopathy of subacute onset and a bullous pemphigoid form of herpetiform dermatitis (Dühring-Brocq disease) developed simultaneously in a 71-year-old man. Both conditions regressed under the influence of prednisone and azathioprine. The immediate cortico-dependence of the skin condition should be noted. Death occurred 9 months later, related to diffuse pulmonary aspergillosis. A paraneoplastic aetiology was sought unsuccessfully.

Aged↗
PubMed1992

[A case of sarcoid polyradiculopathy with nerve roots swelling demonstrated by myelography].

A 62-year-old woman was admitted to our hospital because of tingling numbness in the trunk and upper extremities. She was well until 18 days earlier, when she began to feel tingling numbness on the ulnar side of the left arm. During the next two weeks it spread gradually over the trunk and ulnar side of the bilateral arms. She had also progressive difficulty in taking hold of objects. On neurological examination she was alert and cooperative with normal articulation. The neck was supple. The cranial nerves were intact. Superficial sensation was bilaterally hypesthetic in the distribution from the 7th cervical through 12th thoracic segments. Mild weakness was distally noted in the upper extremities. Deep tendon reflexes were reduced or absent without laterality. Plantar responses were bilaterally flexor. Coordination and gait were normal. Routine laboratory examinations including blood counts, blood chemistries and urinalysis were unremarkable. Serum angiotensin converting enzyme (ACE) was slightly elevated. A lumbar puncture yielded clear, colorless cerebrospinal fluid (CSF) containing 22 white cells/mm3 and protein of 106 mg/dl. Conventional nerve conduction studies were normal. F-wave conduction studies revealed elevated F-ratios for the upper and lower extremities. Studies of short-latency somatosensory evoked potential showed mild prolongation of N13 recorded after stimulation of the right median nerve. An X-ray film of the spine was unremarkable except for mild narrowing of the C5-6 intervertebral disk space. Postcontrast magnetic resonance imaging of the spine with gadolinium-DTPA was unrevealing as well as a precontrast study. A myelogram disclosed enlarged lateral filling defects corresponding to cervical nerve roots from C6 through C8 bilaterally.(ABSTRACT TRUNCATED AT 250 WORDS)

Cervical Vertebrae↗
PubMed1992

Neurobrucellosis: clinical and therapeutic features.

Eighteen patients with neurobrucellosis are described. Eleven patients had meningitis alone or with papilledema, optic neuropathy, or radiculopathy. Four patients had meningovascular complications manifested by stroke or intracerebral hemorrhage from a presumed mycotic aneurysm. Two patients had parenchymatous dysfunction, including a child who had a cerebellar syndrome without evidence of direct infection of the central nervous system. One patient presented with polyradiculopathy. Twelve of 16 patients had pleocytosis; none had cell counts greater than 419 x 10(6)/L. Most patients had hypoglycorrhachia and elevated levels of protein in the cerebrospinal fluid (CSF). Results of an agglutination test for Brucella in serum were positive for all patients. Six of 16 patients had positive blood cultures, and four of 14 had positive CSF cultures. Antimicrobial treatment included concurrent administration of two or more of the following drugs: streptomycin, tetracycline (or doxycycline), rifampin, and trimethoprim-sulfamethoxazole. Eleven patients fully recovered. Five patients were left with residual neurological deficits. Four of these patients suffered permanent hearing loss, one of whom also had significant loss of vision in one eye. One elderly senile patient with meningovascular brucellosis remained in a vegetative state despite receiving antimicrobial therapy for 6 months. One patient died due to rupture of a mycotic aneurysm within 7 days of initiation of therapy. One other patient was treated after sustaining an intracerebral hemorrhage, but this patient's condition was diagnosed only after discharge.

Adolescent↗
PubMed1992

Diagnosis of human cytomegalovirus central nervous system disease in AIDS patients by DNA amplification from cerebrospinal fluid.

The utility of amplification of human cytomegalovirus (HCMV) DNA in cerebrospinal fluid (CSF) for the diagnosis of HCMV central nervous system (CNS) disease in AIDS patients was studied. CSF specimens from 30 patients with neurologic dysfunction were assayed by polymerase chain reaction (PCR), and the results were correlated with histopathologic findings, CSF culture, and clinical manifestations. PCR was positive in all 11 patients who had histopathologic evidence of HCMV CNS disease, including 4 who were CSF culture-negative. Three patients with HCMV polyradiculopathy had CSF positive by PCR. Nine patients negative for HCMV by neuropathologic study and an additional 7 patients with HCMV-unrelated clinical diagnosis were all CSF PCR-negative, despite concomitant systemic HCMV infection in 7. In addition, 24 asymptomatic human immunodeficiency virus-infected individuals were CSF PCR-negative. CSF PCR appears to be a sensitive and specific diagnostic method for detection of HCMV CNS disease in AIDS patients.

AIDS-Related Opportunistic Infections↗
PubMed1992

Clinical and electrophysiologic findings in chronic neuropathy of Lyme disease.

We evaluated 25 patients with Lyme disease and chronic peripheral neuropathy. All had immunologic evidence of exposure to Borrelia burgdorferi and no other identifiable cause of neuropathy. Neuropathic symptoms began a median of 8 months (range, 0 to 165) after erythema migrans and had been present for a median of 12 months (range, 2 to 168) prior to evaluation. Twelve patients (48%) had generally symmetric distal, nonpainful paresthesia, and another 12 (48%) had generally asymmetric radicular pain. One patient (4%) had asymptomatic neuropathy. The most common physical finding was multimodal sensory loss, which was observed in 13 patients (52%); weakness and hyporeflexia were less common. Motor or sensory nerve conduction was slightly slow in 16 patients (64%). The paresthesia group more often had abnormalities on physical examination and on nerve conduction testing than did the radicular group. In 75% to 80% of patients from both groups, however, needle examination showed denervation in paraspinal and limb muscles. Among 20 patients who underwent lumbar puncture, only one had a slight spinal fluid pleocytosis. Six months after treatment with intravenous ceftriaxone, 19 patients (76%) were clinically improved. We conclude that Lyme disease can be associated with a reversible, mild chronic axonal sensorimotor polyradiculoneuropathy or polyradiculopathy.

Adult↗
PubMed1992

Cytomegalovirus and the peripheral nervous system in AIDS.

Cytomegalovirus (CMV) has been associated with a spectrum of peripheral nerve syndromes in patients with AIDS. Lumbosacral polyradiculopathy, a rapidly progressive syndrome occurring in about 1% of AIDS patients, is characterized by low back pain, sphincter disturbance, progressive flaccid paraparesis, and neutrophil cerebrospinal fluid pleocytosis. CMV has been found consistently in the lumbosacral roots in association with inflammation, demyelination, and axonal loss. Anti-CMV therapy has been reported in open studies to prolong survival and may lead to improvement of the neurologic deficit. A few patients with mononeuritis multiplex have been found to have CMV inclusions associated with inflammation and axonal loss in the peripheral nerve. The diagnosis, dependent on finding CMV in a biopsy sample, has been made too infrequently to estimate the incidence and prognosis or response to treatment. Painful distal symmetrical peripheral neuropathy, the most frequent neuropathy in AIDS, is characterized by subacute onset of pain in the feet, with associated findings including mild sensory signs and fiber degeneration axonal atrophy on sural nerve biopsy. A prospective study found an association of this syndrome with CMV disease of other organs, and CMV has been found in the dorsal root ganglion in a single case. Anti-CMV therapy might be of benefit in these peripheral nerve syndromes; however, the effect of such treatment needs to be assessed in controlled studies.

Acquired Immunodeficiency Syndrome↗
PubMed1992

Peripheral neuropathies associated with human immunodeficiency virus infection.

In the 1990s, HIV has replaced syphilis as the "great masquerader." Virtually every level of the neuraxis may be affected in a patient with HIV infection. The superimposition of multiple levels of neuropathology further complicate the bedside neurologic diagnosis of an AIDS patient. This article has reviewed the variety of forms of peripheral neuropathy that may be associated with HIV infection and its treatment. Distal symmetrical polyneuropathy may be produced in patients with HIV infection by neurotoxic drugs (e.g., vincristine, INH, ddC, or ddI) or by vitamin B12 deficiency or may develop in the later stages of HIV infection without identifiable cause. GBS and CIDP occur with increased frequency in early HIV infection owing to presumed autoimmunity, and these IDPs respond to plasmapheresis or prednisone, similar to HIV-seronegative patients. A limited distribution of mononeuropathy simplex or multiplex occurs in patients with CD4 counts greater than 200; the neuropathy will usually spontaneously improve in these patients. Widespread mononeuropathy multiplex may occur in patients with AIDS and CD4 counts less than 50 and is then usually caused by CMV infections; those neuropathies are usually progressive unless antiviral treatment is given. Progressive polyradiculopathy usually occurs in patients with AIDS and low CD4 counts. If the cerebrospinal fluid has a polymorphonuclear pleocytosis, CMV infection is almost always present, and progression is expected unless ganciclovir therapy is promptly started. Finally, mild autonomic neuropathy is commonly present in HIV-infected patients. Protocols for the evaluation and therapy of cranial and peripheral neuropathies are presented (Figs. 6 and 7). It is unfortunate but likely that increasing numbers of "neuro-AIDS" patients will be encountered, not only in urban medical centers but also in general community practice. The pace at which research in the field of HIV research has proceeded is unprecedented. It is, therefore, important that neurologists stay at the forefront of investigation and clinical care of these complex disorders.

Autonomic Nervous System Diseases↗
PubMed1992

Other neurological diseases in HIV-1 infection: clinical aspects.

HIV-1-related neurological diseases, excluding opportunistic infections and HIV encephalitis, are considered here. Most occur in severely immunosuppressed patients, with CD4 counts of under 200 x 10(6) l-1. Primary brain lymphoma and metastases from systemic non-Hodgkin's lymphoma, the second commonest cause of cerebral mass lesions in AIDS, are usually aggressive B cell tumours. Their poor median survival after treatment, compared with that of lymphomas in non-AIDS patients, seems related to systemic complications, particularly opportunistic infections. Kaposi's sarcoma produces neurological symptoms exceptionally. Cerebral infarction is often unrecognized clinically but large vessel arteritic occlusions may occur. Intracranial haemorrhages occur mostly in thrombocytopenic patients. Seizures are frequently referred to the neurologist; investigation may lead to a diagnosis of AIDS. Nearly 50% of patients with seizures have cerebral toxoplasmosis or cryptococcal meningitis; HIV-1 encephalitis is presumed to be the cause in 30%. A subacute or chronic vacuolar myelopathy with pyramidal and posterior column signs is the commonest form of spinal cord involvement in AIDS; its cause remains unknown. Peripheral nerve syndromes occur at all stages of HIV-1 infection. Distal symmetrical peripheral neuropathies are the most frequent, particularly a painful form with axonal atrophy, associated with CMV infection, and seen during ARC or AIDS. Mononeuritis multiplex due to vasculitis, CMV, or lymphoma and a serious lumbosacral polyradiculopathy due to CMV are infrequent. The commonest myopathy is due to zidovudine (AZT); it usually responds to drug withdrawal. The nature, prognosis and optimal management of most other myopathies is yet to be determined.

AIDS Dementia Complex↗
PubMed1992

A pilot study of suramin in the treatment of progressive refractory follicular lymphomas.

Ten patients with progressive follicular lymphomas (seven with follicular mixed lymphomas, three with follicular, small cleaved cell lymphomas) with clinical indications for systemic therapy received parenteral suramin. Each had failed from one to six prior chemotherapeutic regimens and three had in addition received prior radiation therapy. All had measurable disease and nine of the ten had documented bone marrow involvement at the start of therapy. Suramin was administered at an initial infusion rate of 350 mg/m2/day, which was then modified on the basis of subsequent weekly plasma suramin concentrations in order to reach a final plasma concentrations of 250-350 micrograms/ml. Treatment cycles were repeated at eight week intervals. Nine of ten patients are evaluable for response. Five of nine evaluable patients achieved a partial remission as defined by a greater than 50% decrease in the sum of the product of all measurable lesions. Sites of response include: Peripheral (five patients) and central (four patients) adenopathy, disappearance of biopsy-proven skin involvement (one patient), malignant pleural effusions (one patient) and shrinkage of an enlarged spleen (two patients). Disappearance of B symptoms occurred in the one responder with these symptoms. Response duration varied from 3 to 9 months (mean 5.6 months) with time to subsequent systemic therapy varying from 5 to 12 months (mean 8 months). Drug related toxicity included the development of polyradiculopathy (one case), liver function abnormalities (three cases), thrombocytopenia (five cases), vortex keratopathy (two cases) and bacterial infection (two cases). We conclude that suramin has significant activity against follicular lymphomas refractory to standard chemotherapy and that its precise role in the treatment of lymphoproliferative neoplasms in general warrants further investigation.

Adult↗
PubMed1975

Cardiac monitoring and demand pacemaker in Guillain-Barré syndrome.

Life-threatening alterations of respiratory and cardiovascular functions may complicate the course of severe Guillain-Barre syndrome. Cardiac arrest, fore-warned by episodes of bradycardia or other arrhythmia, may occur despite adequately assisted respirations. A patient with Guillain-Barre syndrome required tracheostomy and ventilatory assistance. Continuous cardiac monitoring revealed that tracheal aspiration provoked an idioventricular rhythm of 40 beats per minute, which reverted to sinus rhythm after the procedure. To prevent cardiac arrest during the transition from idioventricular to sinus rhythm, a demand pacemaker was inserted into the right ventricle. Set to activate if the rate fell below 65 beats per minute, the pacemaker functioned both during and between tracheal aspiration procedures. Cardiac monitoring in severe cases of Guillain-Barre syndrome may detect potentially lethal arrhythmias that may then be avoided by a demand pacemaker.

Child↗