User:Gastro guy/neurologic
Introduction[edit]
Infectious diseases can cause a variety of systemic symptoms. In some cases, these symptoms can effect the nervous system, and manifest themselves as neurological or even psychiatric diseases. Infectious organisms can cause neurological symptoms by destroying nerve tissue, by triggering an immune response in the host which destroys tissue, through secretory mechanisms, and through unknown mechanisms.
Action by Destruction of Nerve Cells[edit]
AIDS Dementia Complex[edit]
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AIDS dementia complex (ADC; also known as HIV dementia, HIV encephalopathy and HIV-associated dementia) has become a common neurological disorder associated with HIV infection and AIDS. It is a metabolic encephalopathy induced by HIV infection and fueled by immune activation of brain macrophages and microglia.[1] These cells are actively infected with HIV and secrete neurotoxins of both host and viral origin. The essential features of ADC are disabling cognitive impairment accompanied by motor dysfunction, speech problems and behavioral change. Cognitive impairment is characterised by mental slowness, trouble with memory and poor concentration. Motor symptoms include a loss of fine motor control leading to clumsiness, poor balance and tremors. Behavioral changes may include apathy, lethargy and diminished emotional responses and spontaneity. Histopathologically, it is identified by the infiltration of monocytes and macrophages into the central nervous system (CNS), gliosis, pallor of myelin sheaths, abnormalities of dendritic processes and neuronal apoptosis.[2][1]
ADC typically occurs after years of HIV infection and is associated with low CD4+ T cell levels and high plasma viral loads. It is sometimes seen as the first sign of the onset of AIDS. Prevalence is between 10-20% in Western countries[3] and has only been seen in 1-2% of India-based infections.[4][5] With the advent of highly active antiretroviral therapy (HAART), the frequency of ADC has declined in developed countries. HAART may not only prevent or delay the onset of ADC in people with HIV infection, it can also improve mental function in people who already have ADC.
Dementia only exists when neurocognitive impairment in the patient is severe enough to interfere markedly with day-to-day function. That is, the patient is typically unable to work and may not be able to take care of him or herself. Before this, the patient is said to have a mild neurocognitive disorder.
See Also: AIDS Dementia Complex
Neurosyphilus[edit]
Neurosyphilis refers to a site of infection involving the central nervous system (CNS). Neurosyphilis may occur at any stage of syphilis. Before the advent of antibiotics, it was typically seen in 25-35% of patients with syphilis. Neurosyphilis is now most common in patients with HIV infection. Reports of neurosyphilis in HIV-infected persons are similar to cases reported before the HIV pandemic. The precise extent and significance of neurologic involvement in HIV-infected patients with syphilis, reflected by either laboratory or clinical criteria, have not been well characterized. Furthermore, the alteration of host immunosuppression by antiretroviral therapy in recent years has further complicated such characterization.
Approximately 35% to 40% of persons with secondary syphilis have asymptomatic central nervous system (CNS) involvement, as demonstrated by any of these on cerebrospinal fluid (CSF) examination:
- An abnormal leukocyte cell count, protein level, or glucose level
- Demonstrated reactivity to Venereal Disease Research Laboratory (VDRL) antibody test
There are four clinical types of neurosyphilis:
- Asymptomatic neurosyphilis
- Meningovascular syphilis
- General paresis[6]
- Tabes dorsalis
The late forms of neurosyphilis (tabes dorsalis and general paresis) are seen much less frequently since the advent of antibiotics. The most common manifestations today are asymptomatic or symptomatic meningitis. Acute syphilitic meningitis usually occurs within the first year of infection; 10% of cases are diagnosed at the time of the secondary rash. Patients present with headache, meningeal irritation, and cranial nerve abnormalities, especially the optic nerve, facial nerve, and the vestibulocochlear nerve. Rarely, it affects the spine instead of the brain, causing focal muscle weakness or sensory loss.
Meningovascular syphilis occurs a few months to 10 years (average, 7 years) after the primary syphilis infection. Meningovascular syphilis can be associated with prodromal symptoms lasting weeks to months before focal deficits are identifiable. Prodromal symptoms include unilateral numbness, paresthesias, upper or lower extremity weakness, headache, vertigo, insomnia, and psychiatric abnormalities such as personality changes. The focal deficits initially are intermittent or progress slowly over a few days. However, it can also present as an infectious arteritis and cause an ischemic stroke, an outcome more commonly seen in younger patients. Angiography may be able to demonstrate areas of narrowing in the blood vessels or total occlusion.
General paresis, otherwise known as general paresis of the insane, is a severe manifestation of neurosyphilis. It is a chronic dementia which ultimately results in death in as little as 2-3 years. Patients generally have progressive personality changes, memory loss, and poor judgement. More rarely, they can have psychosis, depression, or mania. Imaging of the brain usually shows atrophy.
Tabes dorsalis is a rare syndrome seen late in neurosyphilis. It can take as few as 3 years to manifest but averages occurs after 20 years. The symptoms are due to disease in the posterior columns of the spinal cord which are responsible for carrying sensory information to the brain from the body. Symptoms include sudden severe stabbing pains, loss of sensation, loss of reflexes, and Argyll Robertson pupils. The Argyll Robertson pupils account for half of the cases of tabes dorsalis and are manifested by a small pupil that does not constrict in response to light but does contract with accommodation.
Action by Auto-Immune Mechanisms[edit]
Neurocysticercosis[edit]
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Cysticercosis, or neurocysticercosis, is the most common parasitic infection of the central nervous system worldwide. It is caused by larvae of the tapeworm, Taenia solium, normally found in pork. The larvae, called oncospheres, form cysts in the body. If these worms are found in the intestine, they cause a different disease that is called taeniasis, which is discussed in the Taenia solium and Taenia saginata articles.
Cysticercosis occurs when Taenia solium eggs enter the stomach. This can be from food or water contaminated with infected human fecal material. Also, people with adult tapeworms in their small intestine (taeniasis) can autoinfect themselves with cysticercosis by vomiting, which pushes eggs into the stomach. When the eggs return to the intestines, the worms hatch and migrate into the skeletal muscles, heart, eyes and even the brain and spinal cord. Once there, they form small encapsulated cysts containing the worm.
Symptoms[edit]
In muscles, cysts cause painless swelling or create nodules under the skin. If cysts form in the eye, they can impair vision by floating in the eye and can cause blindness by causing swelling and detachment of the retina. Heart lesions can lead to abnormal rhythms or heart failure (rare). The most dangerous symptoms are a result of encystment in the central nervous system.
According to a Centers for Disease Control and Prevention Division of Parasitic Diseases, in neurocysticercosis (cysticercosis of the brain), "seizures, and headaches are the most common symptoms. However, confusion, lack of attention to people and surroundings, difficulty with balance, hydrocephalus (compression of the brain tissue due to obstruction of cerebrospinal fluid flow) may also occur." Often, there are few symptoms until the parasite dies.[7] When the parasite dies, the host's immune system detects the worm's remains and attacks them, causing swelling and scarring. This is what causes most of the symptoms. Spinal cord lesions can lead to partial loss of motor control, weakness, and even paralysis.
When death occurs, it is most often due to involvement of the brain resulting in hydrocephalus, cerebral edema, cerebral compression, or epileptic seizures.[8]
Diagnosis[edit]
Neurocysticercosis is difficult to diagnose in its early stage and may be apparent only when the first neurological symptoms start, or when a CT scan, or an MRI of the brain is performed for other reasons. Antibody tests or a biopsy of the affected area may be necessary to complete the diagnosis.
Action by Secretory Mechanisms[edit]
Entamoeba histolytica[edit]
Unknown Action[edit]
Neurosis from Amebiasis
http://www.nzetc.org/tm/scholarly/tei-WH2Surg-pt2-c1-2.html
Amebic neurosis: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1501897
http://www.ajtmh.org/cgi/content/abstract/1/1/146
http://books.google.com/books?id=54UaAAAAMAAJ&q=histolytica+neurosis&dq=histolytica+neurosis&pgis=1
- ^ a b Gray, F., Adle-Biassette, H., Chrétien, F., Lorin de la Grandmaison, G., Force, G., Keohane, C. (2001). "Neuropathology and neurodegeneration in human immunodeficiency virus infection. Pathogenesis of HIV-induced lesions of the brain, correlations with HIV-associated disorders and modifications according to treatments". Clin. Neuropathol. 20 (4): 146–155. PMID 11495003.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - ^ Adle-Biassette, H., Lévy, Y., Colombel, M., Poron, F., Natchev, S., Keohane, C. and Gray, F. (1995). "Neuronal apoptosis in HIV infection in adults". Neuropathol. Appl. Neurobiol. 21 (3): 218–227. doi:10.1111/j.1365-2990.1995.tb01053.x. PMID 7477730. S2CID 19576463.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - ^ Grant, I., Sacktor, H., and McArthur, J. (2005). "HIV neurocognitive disorders" (PDF). In H. E. Gendelman, I. Grant, I. Everall, S. A. Lipton, and S. Swindells. (ed.) (ed.). The Neurology of AIDS (2nd ed.). London, UK: Oxford University Press. pp. 357–373. ISBN 0-19-852610-5.
{{cite book}}:|editor=has generic name (help)CS1 maint: multiple names: authors list (link) - ^ Satishchandra, P., Nalini, A., Gourie-Devi, M., Khanna, N., Santosh, V., Ravi, V., Desai, A., Chandramuki, A., Jayakumar, P. N., and Shankar, S. K. (2000). "Profile of neurologic disorders associated with HIV/AIDS from Bangalore, south India (1989-96)". Indian J. Med. Res. 11: 14–23. PMID 10793489.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - ^ Wadia, R. S., Pujari, S. N., Kothari, S., Udhar, M., Kulkarni, S., Bhagat, S., and Nanivadekar, A. (2001). "Neurological manifestations of HIV disease". J. Assoc. Physicians India. 49: 343–348. PMID 11291974.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - ^ Richard B. Jamess, MD, PhD (2002). "Syphilis- Sexually Transmitted Infections, 2006". Sexually Transmitted Diseases Treatment Guidelines.
{{cite journal}}: External link in|title= - ^ Centers for Disease Control and Prevention Division of Parasitic Diseases fact sheet
- ^ Sorvillo FJ, DeGiorgio C, Waterman SH (2007). "Deaths from cysticercosis, United States". Emerg Infect Dis. 13 (2): 230–5. doi:10.3201/eid1302.060527. PMC 2725874. PMID 17479884.
{{cite journal}}: CS1 maint: multiple names: authors list (link)