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The optic nerve contains the nerve fibers of the retinal ganglion cells and transmits visual information from the eye to the brain. Damage to the optic nerve leads to pathological failures in the visual field. As part of the central nervous system, regeneration of nerve fibers in the optic nerve does not usually occur. Many diseases can cause damage to the optic nerve, i.e., glaucoma, diabetic retinopathy, optic nerve inflammation, tumors, accidents, or vascular occlusion. If the injury affects the complete cross-section of the optic nerve, the patient will suffer from total blindness in the corresponding eye. The leading causes of fiber damage in the optic nerve are glaucoma and diabetic retinopathy.

Glaucoma includes several eye diseases leading to the degeneration of optic nerve fibers. Affected patients suffer from visual field loss and blindness. The cause of the symptoms is elevated intraocular pressure or a poor relationship between intraocular pressure and blood flow to the optic nerve, leading to the injury of nerve fibers. Glaucoma is the leading cause of irreversible blindness worldwide, and risk factors include diabetes mellitus and low or strong fluctuations in blood pressure. Also, a very strong short- or long-sightedness can play a role. Diagnosis of glaucoma often happens relatively late, as patients only notice the damage when more significant areas of the retina are affected. The treatment focuses on lowering intraocular pressure or restoring physiological conditions (intraocular pressure/blood pressure). The goal is the prevention of disease progression, as already-induced damage cannot yet be repaired

The spinal cord resides inside the vertebra and builds the connection between the brain and limbs. The lower motoneurons lie in the ventral spinal cord and innervate the skeletal muscles. They are responsible for the execution of movements. The axons of the motoneurons exit the vertebral canal at the corresponding spinal nerve and innervate their target muscles. The lower motoneurons receive input from the so-called upper motor neurons in the brain motor cortex. The upper motoneurons are responsible for the initiation of intentional movements. The sensory neurons enter the spinal cord at the spinal nerve to transmit their signals via the spinal cord into different brain regions where the sensory information is processed.

Their cell bodies reside outside the spinal cord in the dorsal root ganglia. After processing the sensory input, the brain can initiate an appropriate reaction, for example, the activation of motoneurons to execute a movement. Damage from a traumatic spinal cord injury prevents the sensory information from reaching the brain and vice versa, the signal transduction from the motoneurons to the muscles. This results in neurological deficits and paralysis, although the peripheral nerve, including the sensory and motor fibers, may still be intact. Also, neurodegenerative diseases (e.g., amyotrophic lateral sclerosis), infections, or compression can lead to neuronal cell death in the spinal cord and an associated loss of function.

Traumatic brain injury (TBI) occurs when the head experiences extreme forces, during an accident, for example. The lightest form of TBI is a concussion, which is mostly harmless. However, cerebral hemorrhaging and other complications of TBI can be life-threatening. The leading causes of TBI are accidents and certain contact sports, such as ice hockey or American football. The Glasgow coma scale divides TBI into mild, moderate, and severe levels. Another distinction is whether the injury has resulted in a perforation of the scalp, the skull, and the dura mater. The symptoms caused by mild TBI depend on the damage's severity, including impaired consciousness, retrograde amnesia, nausea/vomiting, rarely anterograde amnesia, apathy, headaches, and dizziness. More substantial injuries lead to unconsciousness (greater than 60 min is classified as severe TBI) caused by entrapment of the brain, development of edema, or cerebral hemorrhages.

The damage to the brain after TBI occurs in two phases:

The first phase involves the direct damage triggered by an accident. This damage is hard to treat, as damaged neurons in the brain cannot regenerate.

In the second phase, secondary damage occurs due to pathophysiological processes inside the brain. These processes lead to the further destruction of neurons. In principle, these processes are treatable with pharmaceuticals.

The treatment of TBI depends on the severity of the damage. The primary goal is maintaining the brain's blood- and oxygen supply to protect neurons from secondary damage. The treatment of increased intracranial pressure (e.g., caused by edema) and brain hemorrhaging need particular attention.

Neurodegenerative diseases include a variety of disorders characterized by a gradual loss of CNS neurons. The most common neurodegenerative diseases are Alzheimer's disease, Parkinson's disease, and Huntington's disease. The cause of the disease may be genetic or sporadic, but this is often unknown. However, some cellular mechanisms contributing to cell damage have been identified in most conditions. These include disrupting the protein synuclein in Parkinson's disease and huntingtin in Huntington's disease). Also, mutations in heat shock proteins and chaperones increase oxidative stress, damage mitochondria or intracellular transport, and inflammatory reactions frequently occur in neurodegenerative diseases. Often certain brain regions are affected first, for example, the hippocampus in Alzheimer's or the dopaminergic neurons of the substantia nigra in Parkinson's disease. The symptoms vary depending on the condition and the affected brain region and include memory disorders, motor disturbances, orientation problems, personality changes, and changes in behavior. Currently, no cure or disease-modifying treatment exists, and only the symptoms can be relieved to a certain extent.

A stroke is a sudden disruption of blood flow in the brain and thus disturbs the oxygen and nutrient supply to brain tissue, causing local brain damage and a loss of neurons. The cause of stroke may be ischemia caused by the blockage of a blood vessel by a thrombus or vascular constriction. Furthermore, a brain hemorrhage can be responsible for critical undersupply to certain brain parts.

The typical symptoms are impaired consciousness, numbness, paralysis, weakness, speech problems, dizziness, gait disturbances, and headaches. Often, certain symptoms occur only on one body side because only one brain hemisphere or part of one hemisphere is affected. The goal of therapeutic intervention is to restore proper blood circulation as soon as possible to prevent neural damage.

If a vascular thrombus causes a stroke, lysis therapy is performed to dissolve the thrombus and thus the blockage of the vessel. If a brain hemorrhage causes a stroke, brain surgery is usually performed to stop the bleeding. Certain risk factors increase the likelihood of experiencing a stroke, including high blood pressure, diabetes, smoking, obesity, and high cholesterol levels. Because the neurons in the brain cannot regenerate, the damage to the affected cells is irreversible. However, physiotherapy and occupational therapy can help other brain areas take over lost functions, at least partially.

Multiple sclerosis (MS) is a chronic inflammatory autoimmune disorder and the most common neurological disease in young adults besides epilepsy. So far, the particular causes of the disease have not been resolved. However, it is scientifically accepted that the body's immune system attacks and destroys the myelin sheath in the white matter of the brain and spinal cord, resulting in inflammatory plaques.

The myelin sheath is the insulating layer surrounding the axons of nerve cells and is formed by oligodendrocytes in the CNS. The destruction of the myelin sheath results in disturbed signal transmission along the axons and, ultimately, the symptoms of MS. Initially, patients often suffer from relapsing-remitting forms of MS, meaning that phases without symptoms and less inflammation follow periods of inflammation and the related symptoms. Symptoms disappear during the remission phase because of an intrinsic repair mechanism called remyelination. During remyelination, oligodendrocyte precursor cells differentiate and form new myelin, restoring axonal function.

However, as the disease progresses, this repair mechanism ultimately fails, and the remaining axons die. The patient then develops a secondary, progressive form of MS where clinical symptoms no longer improve. In principle, inflammatory lesions may occur in each area of the brain. Therefore, symptoms are diverse. At the beginning of the disease, the optic nerve is commonly affected, resulting in vision problems. The standard treatments of MS aim to modulate the immune system, prevent relapses and delay axonal damage as long as possible.