Asia
The main vector (A. aegypti) also occurs in tropical and subtropical regions of Asia, the Pacific, and Australia, but yellow fever has never occurred there, until jet travel introduced 11 cases from the 2016 Angola and DR Congo yellow fever outbreak in Africa. Proposed explanations include:
That the strains of the mosquito in the east are less able to transmit yellow fever virus. That immunity is present in the populations because of other diseases caused by related viruses (for example, dengue). That the disease was never introduced because the shipping trade was insufficient.But none is considered satisfactory. Another proposal is the absence of a slave trade to Asia on the scale of that to the Americas. The trans-Atlantic slave trade probably introduced yellow fever into the Western Hemisphere from Africa. History
Early history
The evolutionary origins of yellow fever most likely lie in Africa, with transmission of the disease from nonhuman primates to humans. The virus is thought to have originated in East or Central Africa and spread from there to West Africa. As it was endemic in Africa, local populations had developed some immunity to it. When an outbreak of yellow fever would occur in an African community where colonists resided, most Europeans died, while the indigenous Africans usually developed nonlethal symptoms resembling influenza. This phenomenon, in which certain populations develop immunity to yellow fever due to prolonged exposure in their childhood, is known as acquired immunity.
This type of seizure has a specific term called "focal to a bilateral tonic-clonic seizure. Other generalized tonic-clonic seizures are idiopathic, start in large networks involving both hemispheres, and have a presumed genetic cause. Precipitating factors include chemical and neurotransmitter imbalances and a genetically or situationally determined seizure threshold, both of which have been implicated. The seizure threshold can be altered by fatigue, malnutrition, lack of sleep or rest, hypertension, stress, diabetes, the presence of strobe-flashes or simple light/dark patterns, raised estrogen levels at ovulation, fluorescent lighting, rapid motion or flight, blood sugar imbalances, anxiety, antihistamines and other factors. Tonic–clonic seizures can also be induced deliberately with electroconvulsive therapy.In the case of symptomatic focal epilepsy, the cause is often determined by MRI or other neuroimaging techniques showing that there is some degree of damage to a large number of neurons. The lesions (i.e., scar tissue) caused by the loss of these neurons can result in groups of neurons forming a seizure "focus" area with episodic abnormal firing that can cause seizures if the focus is not abolished or suppressed via anticonvulsant drugs. Mechanism
Prodrome
Most generalized tonic–clonic seizures begin without warning and abruptly, but some epileptic patients describe a prodrome. The prodrome of a generalized tonic–clonic seizure is a sort of premonitory feeling hours before a seizure. This type of prodrome is distinct from stereotypic aura of focal seizures that become generalized seizures. Phases
A tonic–clonic seizure comprises three phases: the tonic phase, clonic phase and postictal phase. Tonic phaseThe tonic phase is usually the first phase.