Informal gold miners with mercury toxicity: Novel asymmetrical neurological presentations.

Mercury is a highly toxic heavy metal that may cause neurological, respiratory, gastrointestinal and dermatological illnesses. Previously described neurological manifestations of mercury toxicity are symmetrical, and include a pancerebellar syndrome, generalised seizures and encephalopathy. Mercury is used in the gold mining process, and in artisanal or illicit gold mining, often without necessary protection. Here we describe the cases of two artisanal gold miners from western Johannesburg, South Africa, who presented with atypical neurological manifestations of mercury toxicity. Patient 1 presented with focal seizures, an asymmetrical cerebellar syndrome and an acute encephalopathy. Patient 2 had unilateral cerebellar ataxia. Both patients had toxic mercury levels, with no other cause identified for their symptoms. Patient 1 responded well to chelation therapy, but patient 2 refused admission and further medical treatment. The neurological manifestations of mercury toxicity are typically symmetrical, whereas our two patients presented with markedly asymmetrical features. It is important to maintain a high index of suspicion for mercury poisoning, even in patients with atypical and unilateral or asymmetrical presentations. A prompt diagnosis and the commencement of early chelation therapy have the potential to produce good outcomes.

Non-traumatic myelopathy at the Chris Hani Baragwanath Hospital, South Africa--the influence of HIV.

BACKGROUND: Non-traumatic myelopathy from developing regions has been described widely. In these regions infections, mainly tuberculosis, followed by acute transverse myelitis and neoplasms, dominate. These are also regions of high HIV prevalence. In developed regions, the most prominent reported spinal cord disease in HIV/AIDS is vacuolar myelopathy (VM). Other myelopathy causes in HIV/AIDS include opportunistic infections, neoplasms, vascular lesions and metabolic disease. In developing regions, opportunistic infections are more commonly encountered with VM occurring less frequently. AIM: To determine the influence of HIV on the myelopathy spectrum in an HIV endemic region. DESIGN: Prospective case series. METHODS: Hundred unselected consecutive in-patients admitted with myelopathy were studied. Myelopathy aetiologies were established by collating information obtained from magnetic resonance imaging (MRI) scans, CSF and blood studies, CXR findings, non-neurological illness and response to treatment. Data were analysed in terms of two cohorts, HIV positive and HIV negative. RESULTS: Approximately 50% of the patients presenting and admitted to our hospital with non-traumatic myelopathy are HIV positive. The HIV positive myelopathy patients were younger (20-40 years) and had infectious aetiologies. Tuberculosis was the most frequently identified cause of myelopathy. The majority of HIV-positive patients had advanced HIV infection. Anti-retroviral treatment did not influence myelopathy aetiologies. The HIV-negative patients were older and had neoplasms, followed by degenerative spondylosis as the main myelopathy causes. CONCLUSION: HIV influences the non-traumatic myelopathy spectrum in regions with high HIV prevalence. Empiric treatment of HIV-myelopathy patients with anti-tuberculous medications where resources are severely limited has merit.

Human immunodeficiency virus associated intracranial aneurysms: report of three adult patients with an overview of the literature.

BACKGROUND AND PURPOSE: Aneurysms have been described in HIV infected patients. These involve predominantly extracranial blood vessels with specific histological and clinical features. Intracranial aneurysms are rare and have been identified mainly in children. METHODS: Case reports and literature review. RESULTS: Three black South African HIV positive adult patients with intracranial aneurysms were identified. The clinical, laboratory and radiological features are described. CONCLUSIONS: Intracranial aneurysms occur in both adults and children infected with HIV. More information is required on this association. The frequency in terms of numbers of cases indicates that it is an uncommon association or manifestation of HIV. The characteristics of the aneurysms suggest that they are distinctive and not a chance or coincidental co-occurrence of congenital or arteriosclerotic aneurysms.

Reduced risk of toxoplasma encephalitis in HIV-infected patients--a prospective study from Gauteng, South Africa.

Toxoplasma seroprevalence was determined in 307 consecutive HIV-infected medical inpatients at the Helen Joseph Hospital, Johannesburg, South Africa, using an enzyme linked immunosorbent assay to detect immunoglobulin G (IgG) and IgM antibodies. The mean age of patients was 36 years, with a female to male ratio of 1.3 to 1. The mean CD4 count was 109 cells/mL. Toxoplasma antibodies were detected in 25 patients (8%). Twenty-two of these patients were IgG positive and IgM negative, i.e. reactivation toxoplasmosis. Only two patients (0.65%) had clinical manifestations of toxoplasmosis (one toxoplasma encephalitis and one retinitis). The risk for toxoplasma encephalitis (TE) was 0.33%. These results indicate that the toxoplasma seroprevalence and the TE risk in this population is low. The implication from this study is that in HIV-infected populations where the toxoplasma seroprevalence is low, the TE risk will be low and empiric treatment of focal brain lesions with anti-toxoplasma therapy may be inappropriate.

Protein S deficiency in HIV associated ischaemic stroke: an epiphenomenon of HIV infection.

The purpose of the study was to determine the relevance of protein S deficiency in HIV infected patients with ischaemic stroke. In total, 33 HIV positive patients with ischaemic stroke, previously described by us, were prospectively compared with control groups for occurrence of protein S deficiency. The control groups comprised an equal number of consecutive matched HIV positive and negative patients without and with stroke respectively. Data were analysed in contingency tables using Fisher's exact test. Protein S deficiency occurred significantly more frequently in HIV positive compared with HIV negative stroke patients (p < 0.001). However, by including HIV positive patients without stroke as a control group and comparing this group with the HIV positive stroke group we found that protein S deficiency is statistically related to HIV infection and not stroke occurrence. Our data indicate that the presence of protein S deficiency in HIV positive patients with stroke is an epiphenomenon of HIV infection.

Management of HIV-associated focal brain lesions in developing countries.

BACKGROUND: HIV-associated focal brain lesions (HFBL) are caused by opportunistic infections, neoplasms, or cerebrovascular diseases. In developed countries, toxoplasma encephalitis (TE) is the most frequent cause, followed by primary CNS lymphoma (PCNSL). Guidelines based on these causes however are poorly suited to developing countries, where treatable infections predominate as causes of HFBL. AIM: To determine a practical approach to the management of HFBL in developing countries. DESIGN: Case series. METHODS: Patients (n = 32) were managed based on presumed aetiologies of the focal brain lesions, determined by collating information from CT scans, CSF and blood studies, concurrent non-neurological illness and response to treatment. RESULTS: The principal presumed cause of HFBL was tuberculosis (69%). The therapeutic response was good in 69% of patients. DISCUSSION: In developing countries, infections are the predominant cause of HFBL, the principal causes being infections that are endemic to the populations being studied. Empiric treatment based on limited investigations should be directed according to the nature of such infections. A modified algorithm is proposed.

Demyelinating disorder of the central nervous system occurring in black South Africans.

OBJECTIVES: To investigate the nature and cause in eight black South African patients of a recurrent (multiphasic), remitting, and relapsing demyelinating disease of the CNS. METHODS: The clinical and laboratory investigations and radiological manifestations of these patients were documented. RESULTS: Each patient had two or more acute attacks of demyelinating disease affecting the CNS. The clinical presentations of the patients were predominantly those of multiphasic neuromyelitis optica (NMO). Brain MRI in these patients showed features consistent with those described for acute disseminated encephalomyelitis (ADEM), as well as lesions that are described in multiple sclerosis. There was involvement of the corpus callosum in addition to typical ADEM lesions. Laboratory investigations excluded all other known causes of multiphasic CNS demyelination. Oligoclonal antibodies were not detected in these patients at any time. The patients were all from a population with a low risk for MS (black South Africans). CONCLUSION: The patients described here represent a new phenotypic expression of a recurrent (multiphasic), steroid sensitive, inflammatory demyelinating disorder of the CNS occurring in black South Africans. The disorder is either a distinct inflammatory demyelinating disorder of the CNS of as yet unknown aetiology, or a varied form of MS (ADEM/NMO) occurring in a population with a low risk (where the genetic trait and environmental risk factors for MS do not exist) for MS.