The phenomenon is so common when DEC is used that this drug is the basis of a skin patch test used to confirm that diagnosis. The drug patch is placed on the skin, and if the patient is infected with O. volvulus microfilaria, localized pruritus and urticaria are seen at the application site. Nodding disease
This is an unusual form of epidemic epilepsy associated with onchocerciasis although definitive link has not been established. This syndrome was first described in Tanzania by Louise Jilek-Aall, a Norwegian psychiatric doctor in Tanzanian practice, during the 1960s. It occurs most commonly in Uganda and South Sudan. It manifests itself in previously healthy 5–15-year-old children, is often triggered by eating or low temperatures and is accompanied by cognitive impairment. Seizures occur frequently and may be difficult to control. The electroencephalogram is abnormal but cerebrospinal fluid (CSF) and magnetic resonance imaging (MRI) are normal or show non-specific changes. If there are abnormalities on the MRI they are usually present in the hippocampus. Polymerase chain reaction testing of the CSF does not show the presence of the parasite. Cause
The cause is Onchocerca volvulus. Life cycle
The life of the parasite can be traced through the black fly and the human hosts in the following steps:
A Simulium female black fly takes a blood meal on an infected human host, and ingests microfilaria. The microfilaria enter the gut and thoracic flight muscles of the black fly, progressing into the first larval stage (J1.). The larvae mature into the second larval stage (J2.
Braak stages I and II are used when NFT involvement is confined mainly to the transentorhinal region of the brain, stages III and IV when theres also involvement of limbic regions such as the hippocampus, and V and VI when theres extensive neocortical involvement. This should not be confused with the degree of senile plaque involvement, which progresses differently. Other diseases
Primary age-related tauopathy (PART) dementia, with NFTs similar to AD, but without amyloid plaques. Chronic traumatic encephalopathy (CTE)
Progressive supranuclear palsy (PSP)
Corticobasal degeneration (CBD)
Frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17)
Vacuolar tauopathy
Lytico-bodig disease (Parkinson-dementia complex of Guam)
Ganglioglioma and gangliocytoma
Meningioangiomatosis
Postencephalitic parkinsonism
Subacute sclerosing panencephalitis (SSPE)
As well as lead encephalopathy, tuberous sclerosis, Pantothenate kinase-associated neurodegeneration, and lipofuscinosisIn both Picks disease and corticobasal degeneration, tau proteins are deposited as inclusion bodies within swollen or "ballooned" neurons.Argyrophilic grain disease (AGD), another type of dementia, is marked by an abundance of argyrophilic grains and coiled bodies upon microscopic examination of brain tissue. Some consider it to be a type of Alzheimers disease. It may co-exist with other tauopathies such as progressive supranuclear palsy and corticobasal degeneration, and also Picks disease.Tauopathies are often overlapped with synucleinopathies, possibly due to interaction between the synuclein and tau proteins.The non-Alzheimers tauopathies are sometimes grouped together as "Picks complex" due to their association with frontotemporal dementia, or frontotemporal lobar degeneration. See also
Proteopathy

References


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