This allows the bacteria to survive and eventually spread throughout the body.Days to weeks following the tick bite, the spirochetes spread via the bloodstream to joints, heart, nervous system, and distant skin sites, where their presence gives rise to the variety of symptoms of the disseminated disease. The spread of B. burgdorferi is aided by the attachment of the host protease plasmin to the surface of the spirochete.If untreated, the bacteria may persist in the body for months or even years, despite the production of B. burgdorferi antibodies by the immune system. The spirochetes may avoid the immune response by decreasing expression of surface proteins that are targeted by antibodies, antigenic variation of the VlsE surface protein, inactivating key immune components such as complement, and hiding in the extracellular matrix, which may interfere with the function of immune factors.In the brain, B. burgdorferi may induce astrocytes to undergo astrogliosis (proliferation followed by apoptosis), which may contribute to neurodysfunction. The spirochetes may also induce host cells to secrete quinolinic acid, which stimulates the NMDA receptor on nerve cells, which may account for the fatigue and malaise observed with Lyme encephalopathy. In addition, diffuse white matter pathology during Lyme encephalopathy may disrupt gray matter connections, and could account for deficits in attention, memory, visuospatial ability, complex cognition, and emotional status. White matter disease may have a greater potential for recovery than gray matter disease, perhaps because neuronal loss is less common.
This can occur more frequently when a person has CVI. Hence, a person with CVI can look at an optical illusion or abstract picture and perceive something that is significantly different from what a person without CVI will perceive.The presence of CVI does not necessarily mean that the persons brain is damaged in any other way, but it can often be accompanied by other neurological problems, the most common being epilepsy. Diagnosis
Diagnosing CVI is difficult. A diagnosis is usually made when visual performance is poor but it is not possible to explain this from an eye examination. Before CVI was widely known among professionals, some would conclude that the patient was faking their problems or had for some reason engaged in self-deception. However, there are now testing techniques that do not depend on the patients words and actions, such as fMRI scanning, or the use of electrodes to detect responses to stimuli in both the retina and the brain. These can be used to verify that the problem is indeed due to a malfunction of the visual cortex and/or the posterior visual pathway. See also
Cortical blindness

References
Further reading
Tallent, Aubri & Tallent, Andrei (2012). Little Bear Sees: How Children with Cortical Visual Impairment Can Learn to See. Little Bear Sees Publishing, of Wyatt-MacKenzie. p. 156. ISBN 978-1936214822. OCLC 1936214822. Roman-Lantzy, Christine (2019). Cortical Visual Impairment: Advanced Principles. New York: AFB Press. ISBN 978-1616480073. OCLC 1055566701. Roman-Lantzy, Christine (2017). Cortical Visual Impairment: An Approach to Assessment and Intervention 2nd Ed. New York: AFB Press. ISBN 978-0891286882.