and axonal debris from inside the tubes causes them to eventu-They preferentially interact with proteins of the extracellular ally collapse. Proliferating Schwann cells organize themselves matrix such as fibronectin and laminin found within the into cellular bands resembling longitudinal columns called external lamina of the Schwann cell. Thus, if a sprout associates bands of Bungner. Cellular bands guide the growth of new itself with a band of Bungner, it regenerates between the layers nerve processes (neurites or sprouts) of regenerating axons. of external lamina of the Schwann cell. This sprout will grow Once the bands are in place, large numbers of sprouts begin to along the band at a rate of about 3 mm per day. Although many grow from the proximal stump (see Fig. 12.33c). A growth new sprouts do not make a contact with cellular bands and decone develops in the distal portion of each sprout that consists generate, their large number increases the probability of of filopodia rich in actin filaments. The tips of the filopodia reestablishing sensory and motor connections. After crossing establish a direction for the advancement of the growth cone. the site of injury, sprouts enter the surviving cellular bands in  FOLDER 12.3 Clinical Correlation: Reactive Gliosis: Scar Formation in the CNS
When a region of the CNS is injured, astrocytes near the leasion become activated. They divide and undergo marked hypertrophy with a visible increase in the number of their cytoplasmic processes. In time, the processes be-come densly packed with GFAP intermediate fla-ments. Eventually, scar tissue is formed. This process is referred to as reactive gliosis, while the resulting per-manent scar is most often called a plaque. Reactive glio-sis varies widely in duration, degree of hyperplasia, and time course of expression of GFAP immunostaining. Se-veal biological mechanisms for induction and mainte-nance of reactive gliosis have been proposed. The type of glial cell that responds during reactive gliosis depends on the brain structure that is damagd. In addition, activation of microglial cell population occurs almost immedietaly after any kind of injury to the CNS. These reactive mi-croglial cells migrate toward the site of injury and exhibit marked phagocitic activity. However, their phagocitic ac-tivity and ability to remove myelin debris is much less than that of monocyte-derived macrophages. Gliosis is a prominent feature of many diseases of the CNS, includ-ing stroke, neurotoxic damage, genetic diseases, inflam-matory demyelination, and neurodegenerative disorders such as multiple sclerosis. Much of the research in CNS regeneration is focused on preventing or inhibiting glial scar formation.
the distal stump. These bands then guide the neurites to their destination as well as provide a suitable microenvironment for continued growth (Fig. 12.33d). Axonal regeneration leads to Schwann cell redifferentiation, which occurs in a proximal-todistal direction. Redifferentiated Schwann cells upregulate genes for myelin-specific proteins and downregulate c-jun.
If physical contact is reestablished between a motor neuron and its muscle, function is usually reestablished.
Microsurgical techniques that rapidly reestablish intimate apposition of severed nerve and vessel ends have made reat tachment of severed limbs and digits, with subsequent reestablishment of function, a relatively common procedure. If the axonal sprouts do not reestablish contact with the appropriate Schwann cells, then the sprouts grow in a disorganized manner, resulting in the mass of tangled axonal processes known as traumatic neuroma or amputation neuroma. Clinically, traumatic neuroma usually appears as a freely movable nodule at the site of nerve injury and is characterized by pain, particularly on palpation. Traumatic neuroma of the injured motor nerve prevents reinnervation of the affected muscle.