SIADH as the first symptom of Guillain-Barré syndrome.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to E Schielke.
Explore the source record for details and available documents.
Human cytomegalovirus (HCMV) encephalitis in adult nonimmunosuppressed patients has rarely been reported. We have diagnosed HCMV encephalitis in an anti-HCMV immunoglobulin G-negative, nonimmunosuppressed young woman by HCMV DNA PCR and virus isolation from cerebrospinal fluid (CSF). At the same time, HCMV antigen and HCMV DNA could be demonstrated in peripheral blood leukocytes, and the virus was isolated in fibroblast cultures. After 22 days of acute illness, the virus disappeared from the CSF. Remarkably, the patient did not generate detectable anti-HCMV antibodies within 5 months after the beginning of illness. To investigate the significance of HCMV DNA detection in CSF, samples of CSF, blood cells, and serum from 35 nonimmunosuppressed patients with various neurological disorders (but no herpes simplex virus central nervous system [CNS] disease) were tested for HCMV DNA, antigen, and antibodies. Eleven of these patients were found to be positive for virus DNA and/or antigen in peripheral blood leukocytes. Additionally, HCMV DNA was detected in the CSF of two patients with noninflammatory CNS diseases. A causative role of HCMV in the CNS diseases of these two patients was not evident. In summary, HCMV DNA amplification from CSF samples is a very suitable method to verify HCMV-associated encephalitis, but it should be taken into consideration that there are few cases of positive PCR with DNA from CSF without any known clinical correlative.
The most common symptom of brain abscesses are headache, nausea, fever, disturbance of consciousness, focal signs and seizures. CT is the most useful investigation, showing ring-enhancing lesions with perifocal edema. Systemic inflammatory signs, cerebrospinal fluid changes and cerebral enhancement on leukocyte scintigraphy are of limited diagnostic value. In 10-20% of cases, diagnosis can only be established by biopsy. The most frequent organisms are aerobic streptococci, anaerobes, gram-negative bacilli and staphylococci. Metronidazole in combination with a third-generation cephalosporin and--in certain cases--an antistaphylococcal antibiotic should be given for at least 4 weeks. Conservative treatment can give satisfactory results in abscesses less than 2-3 cm in diameter. Medium-sized and deep-seated abscesses are treated by CT-guided stereotactic aspiration. In very large abscesses with the risk of herniation craniotomy and excision are necessary. Mortality is nowadays 5-15% and does not depend on treatment modalities. Prognosis is mainly determined by the patient's level of consciousness on admission.
Using polymerase chain reaction (PCR), 34 cerebrospinal fluid (CSF) samples from 28 patients with progressive multifocal leukoencephalopathy (PML) were analyzed. As controls, 116 samples were evaluated from 82 human immunodeficiency virus type 1 (HIV-1)-infected patients and 1 HIV-1-negative patient. Of the HIV-1-positive patients, 23 had cerebral toxoplasmosis, 10 had HIV leukoencephalopathy, and 49 had other neurologic complications. Detection of JC virus (JCV) DNA in CSF was increased 10-fold by the addition of carrier DNA before phenol-chloroform-isoamyl alcohol extraction. The primer pair JC 26/29, from the VP1/large T region, had a limit of detection of 10(5) JCV DNA molecules/100 microL. The primer pair JC 36/39, located in the large T gene region, had a 100-fold lower limit of detection. With JC 26/29, the sensitivity was 43% (12/28) and specificity was 100%. Using JC 36/39, sensitivity increased to 82% (23/28), and false-positive results were not observed. Diagnosis of PML is greatly aided by PCR analysis of CSF.
Bacterial abscesses involving the spinal canal are associated with a high morbidity and mortality. Most frequently, these lesions are found in the epidural, rarely in the subdural space. In this report, our clinical material consists of a series of 16 patients treated during the last seven years. The clinical presentation included local neurological signs (back pain, para-/tetraparesis, bladder dysfunction), disturbances of consciousness (ranging from drowsiness to deep coma) and general inflammatory signs (meningism, fever). All patients presented with risk factors (septic foci, chronic diseases, and iatrogenic causes). Laboratory investigations revealed typically pathological blood sedimentation rate, leucocytosis and CSF-pleocytosis. Radiologically, the diagnosis was confirmed by myelography, CT and preferably MRI. The abscesses were located epidurally in 14 and subdurally in 2 cases. The surgical treatment included laminectomy, or multiple flavectomies in extensive lesions. Drainage systems (either simple silicon outflow drains or suction-/irrigation systems) were installed in all cases, as well as antibiotic treatment. Results of treatment: Following an observation period of 0.5-6 years, we found complete recovery in six (38%) cases, six (38%) others were mildly disabled and four (25%) patients died. Focussing on the results of the two different drainage systems, we found a statistically significant superiority of the inflow-/outflow system. Complications included mandatory re-exploration, post-inflammatory hydrocephalus, syringomyelia, spinal instability, surgical treatment of peripheral septic foci and therapy resistant septicaemia. In conclusion, we propose that spinal epi- or subdural abscesses require surgical evacuation, using a suction-/irrigation drainage system, as well as antibiotic and intensive care treatment.
OBJECTIVE: The pathogenesis of neurologic and neuropsychologic dysfunction in HIV-1 infection is unclear. The purpose of the study was to determine an association between cerebral perfusion and HIV-1-related ocular microangiopathic syndrome. METHODS: We studied 28 HIV-1-infected patients, seven of whom presented with asymptomatic HIV infection, nine with lymphadenopathy syndrome or AIDS-related complex, and 12 with AIDS. Cerebral perfusion was semi-quantitatively measured by single photon emission computed tomography of the brain using technetium-99 hexamethyl-propylenamine oxime (HMPAO-SPECT). The conjunctival manifestation of HIV-1-related microangiopathic syndrome was measured by a rating scale determining blood-flow sludging and, retinal cotton-wool spots were counted. CD4 count, neopterin, beta 2-microglobulin (beta 2M), haemoglobin, and age were determined as putative confounding variables. RESULTS: Mean conjunctival sludge in patients with normal HMPAO-SPECT findings was 1.3 +/- 0.5 (mean +/- s.e.m.); no cotton-wool spots were present. In patients with slightly impaired HMPAO-SPECT, it was 2.1 +/- 0.6 and mean cotton-wool spot count was 1.1 +/- 0.4. In patients with severely impaired HMPAO-SPECT, mean conjunctival sludge was 4.5 +/- 0.3 and mean cotton-wool spot count was 4.9 +/- 1.1 HMPAO-SPECT findings were closely associated with conjunctival sludge (r = 0.72; P < 0.001) and number of cotton-wool spots (r = 0.78; P < 0.001), whereas only a slight association with staging of HIV disease was found (P = 0.052). Analysis of covariance controlling for CD4 count neopterin, beta 2M, age, and haemoglobin demonstrated a significant difference between the three HMPAO-SPECT groups for both the number of cotton-wool spots (P < 0.001) and the conjunctival sludge rating (P < 0.001). CONCLUSION: There was a close association between severity of HIV-1-related ocular microangiopathic syndrome and severity of cerebral hypoperfusion. Microvascular alterations might contribute to the pathogenesis of neurological and neuropsychological symptoms in patients with HIV-1 disease. Furthermore, the conjunctival sludge rating and the number of cotton-wool spots might be appropriate indicators for severity of microvascular changes of the central nervous system [corrected].
HIV encephalopathy, which is probably primarily caused by human immunodeficiency virus, is the most common neurological disorder in HIV-infected patients and is more frequent than opportunistic diseases of the central nervous system. It is characterized most often by slowly progressing cognitive impairment, psychomotoric slowing and increasing apathy. The syndrome is found almost exclusively in the late stages of HIV infection; its frequency in patients with full-blown AIDS is estimated as being between 40 and 70%. Although numerous studies have demonstrated alterations in the electrophysiological parameters, cerebral perfusion and cerebrospinal fluid in many asymptomatic patients, there are no reliable parameters that can predict the risk of developing HIV encephalopathy. Also, there is no sufficient correlation between the extent of the frequent but mostly subtle neuropathological changes and the clinical degree of the severity of the encephalopathy. The mechanisms causing cerebral injury are poorly understood. Recent studies indicate that the indirect effects of HIV infection of the brain are the most important pathogenetic factors. In particular, certain viral proteins and cytokines produced by infected macrophages or activated microglia seem to induce neuronal dysfunction and finally loss of nerve cells.
Explore the source record for details and available documents.
We have recorded postural performance in 50 HIV-infected patients in different stages of the disease (Walter Reed (WR) stages I-VI) by means of a force measuring platform. The results were compared with 50 age-matched controls. A significant instability was particularly evident when standing on an unstable foot support. In patients standing with "eyes closed", postural sway was significantly higher in every patient group (WR I-II: P less than 0.02, WR III-V: P less than 0.001, WR VI: P less than 0.001). Patients in stage WR I-II showed no relevant neurological abnormalities. In agreement with other neurophysiological data in the literature we suggest that postural imbalance could be an early sign of central nervous system penetration of HIV. No correlation with electromyographic or cerebrospinal fluid findings could be found.
In this prospective, randomized, open trial, 33 patients with Lyme neuroborreliosis were assigned to a 10-day treatment with either ceftriaxone, 2 g intravenously (iv) every 24 h (n = 17), or cefotaxime, 2 g iv every 8 h (n = 16). Of the 33 patients, 30 were eligible for analysis of therapeutic efficacy. Neurologic symptoms improved or even subsided in 14 patients of the cefotaxime group and in 12 patients of the ceftriaxone group during the treatment period. At follow-up examinations after a mean of 8.1 months, 17 of 27 patients examined were clinically asymptomatic. In one patient Borrelia burgdorferi was isolated from the cerebrospinal fluid (CSF) 7.5 months after ceftriaxone therapy. CSF antibiotic concentrations were above the MIC 90 level for B. burgdorferi in nearly all patients examined. Patients with Lyme neuroborreliosis may benefit from a 10-day treatment with ceftriaxone or cefotaxime. However, as 10 patients were symptomatic at follow-up and borreliae persisted in the CSF of one patient, a prolongation of therapy may be necessary.
In order to determine if brain perfusion abnormalities, which are known in patients with acquiredimmunodeficiency syndrome dementia, occur in early stages of human immunodeficiency virus infection, technetium 99m hexamethyl-propyleneamine oxime-single-photon emission computed tomography studies were performed in 20 patients infected with human immunodeficiency virus who belonged to Walter Reed stages I through IV. None of these patients demonstrated signs of dementia or severe neurological dysfunction. Pathological patterns of hexamethyl-propyleneamine oxime uptake were seen in 14 patients, seven of whom had normal results during neurological examination. Only four patients had signs of cerebral atrophy on cranial computed tomographic scan. These data suggest that subtle changes in cerebral perfusion seem to arise early in the course of human immunodeficiency virus infection and may indicate human immunodeficiency virus encephalopathy before neurological symptoms or noticeable structural damage occurs.
In forty patients at early and advanced stages of HIV infection (Walter Reed stages I-IV) regional cerebral blood flow was determined by 99mTc-HMPAO SPECT, comparing the results with CT and MRI findings. All patients with HIV encephalopathy (AIDS dementia complex) had pathologic SPECT results (multilocular, patchy uptake defects), but also in earlier and even earliest stages of HIV infection positive SPECT findings were observed. Compared to functional SPECT imaging, morphologically orientated methods (CT, MRI) were insensitive in detecting HIV-induced foci: more than 50% of the patients with pathologic SPECT findings had negative CT or MRI scans. Most patients in advanced Walter Reed stages had neurological abnormalities accompanied by positive SPECT. Subtle alterations of HMPAO uptake were observed even in a few cases of early HIV infection without neurological CNS symptoms. The data presented suggest that HMPAO SPECT is highly sensitive in the detection of altered brain perfusion not only in advanced but also early stages of HIV infection. Changes in regional cerebral blood flow are present before noticeable structural defects may be observed. Thus, it is suggested to use HMPAO SPECT in the evaluation and monitoring of patients with, and particularly at risk for, HIV encephalopathy.
Explore the source record for details and available documents.
The major pathological abnormalities of HIV encephalopathy are infiltrates of macrophages, multinucleated giant cells, microglial nodules and demyelination. Elevated myelin basic protein (MBP) levels in the cerebrospinal fluid (CSF) provide a marker for central nervous system demyelination. The purpose of this study was to investigate the possible role of CSF MBP as a useful and early marker for HIV encephalopathy. The CSF of 40 consecutive patients with HIV infection of various clinical stages was investigated, including 13 patients with clinical signs of HIV encephalopathy. CSF MBP was elevated in 2 patients (5.0 and 5.3 ng/ml), both of whom had moderate to severe HIV encephalopathy. The course of the disease was rapid in both patients. In the remaining 38 patients, CSF MBP levels were marginally elevated (n = 12) or normal (n = 26). Our results suggest that CSF MBP is not a sensitive marker for the diagnosis and evaluation of HIV encephalopathy, but may be an indicator of prognosis for the course of the disease. There were only few findings of elevated CSF MBP levels in patients with HIV encephalopathy in the current study, and this may be because the disorder progressed slowly in most patients. It is possible that CSF MBP levels in HIV encephalopathy may only be elevated with acute clinical deterioration but are normal in slowly progressive forms of demyelination, as seen in multiple sclerosis.