[46] This relationship is further supported by the fact that mice lacking NMNAT2, which are normally not viable, are completely rescued by SARM1 deletion, placing NMNAT2 activity upstream of SARM1. Patients with more extensive WD had poorer grip strength, dexterity, and range of movement. Another feature that results eventually is Glial scar formation. While Alzheimer's disease (AD) is the most common neurodegenerative disease that causes it, more than 50 In addition, recovery of injury is highly dependent on the severity of injury. https://jneuroinflammation.biomedcentral.com/articles/10.1186/1742-2094-8-110, "An 85-kb tandem triplication in the slow Wallerian degeneration (Wlds) mouse", https://www.youtube.com/watch?v=kbzYML05Vac, https://www.https://www.youtube.com/watch?v=P02ea4jf50g&t=192s, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4315870/, https://www.physio-pedia.com/index.php?title=Wallerian_Degeneration&oldid=274325, Reduced or loss of function in associated structures to damaged nerves, Gradual onset of numbness, prickling or tingling in feet or hands, which can spread upward into legs and arms, Sharp, jabbing, throbbing, freezing, or burning pain. Sensory symptoms of VIPN start in the fingertips and toes and often persist after discontinuation of vincristine (Boyette-Davis et al., 2013). Peripheral nerve injury: principles for repair and regeneration. At the time the article was last revised Derek Smith had no recorded disclosures. MRI demonstrating promise in both diagnosing and monitoring injury, especially in the surgical setting. Fluorescent micrographs (100x) of Wallerian degeneration in cut and crushed peripheral nerves. [2] Usually, the rate of clearance is slower in the Central Nervous System(CNS) than in the Peripheral Nervous System (PNS) due to the clearance rate of myelin. Neuroradiology. Within a nerve, each axon is surrounded by a layer of connective tissue called theendoneurium. This condition has two main causes: 1) degenerative diseases affecting nerve cells, such as Friedreich's disease, and 2) traumatic injury to the peripheral nerves. 4.7-T diffusion tensor imaging of acute traumatic peripheral nerve injury. hb```aB =_rA However, their recruitment is slower in comparison to macrophage recruitment in PNS by approximately 3 days. Sunderland grade 2 is only axon damage; Sunderland grade 3 is axon and endoneurium damage; and, Sunderland grade 4 is axon, endoneurium, and perineurium damage. Imaging studies are not the standard of care for peripheral nerve injuries, but studies such as magnetic resonance imaging (MRI) and ultrasound (US) can be used to identify nerve derangement and rupture, and neuroma formation. The cell bodies of the motor nerves are located in the brainstem and ventral horn of the spinal cord while those of the sensory nerves are located outside of the spinal cord in the dorsal root ganglia (Fig 1)1. . As in axonotmesis, if there is any re-innervation by collaterals, EMG may reveal polyphasic MUAPs and/or satellite potentials, while the slower axonal re-growth will eventually result in larger amplitude, longer duration potentials. There is significant room for improvement in the development of more formal diagnostic tools, aiding prognostication for these difficult and sometimes severe injuries. [12] Thus the axon undergoes complete fragmentation. The most common symptoms of a pinched nerve include neck pain that travels down the arms and shoulders, difficulty lifting things, headache, and muscle weakness and numbness or tingling in fingers or hands. Motor symptoms, which include any changes related to movement, are frequently present with mononeuropathies. Wallerian degeneration. This is the American ICD-10-CM version of G31.9 - other international versions of ICD-10 G31.9 may differ. Oligodendrocytes fail to recruit macrophages for debris removal. Extensive axonotmesis cannot be differentiated initially from neurotmesis by either clinical or electrodiagnostic examination. Axons have been observed to regenerate in close association to these cells. G and H: 44 hours post crush. During injury, nerves become more hyperintense on T2 and, given the chronicity, muscle atrophy may be present and localized edema canbeseen. Currently GARD is able to provide the following information for Wallerian degeneration: Population Estimate: This section is currently in development. These. Please Note: You can also scroll through stacks with your mouse wheel or the keyboard arrow keys. Carpal tunnel and . . The time period of response is estimated to be prior to the onset of axonal degeneration. Waller experimented on frogs in 1850, by severing their glossopharyngeal and hypoglossal nerves. [1] A related process of dying back or retrograde degeneration known as 'Wallerian-like degeneration' occurs in many neurodegenerative diseases, especially those where axonal transport is impaired such as ALS and Alzheimer's disease. If soma/ cell body is damaged, a neuron cannot regenerate. European Journal of Neuroscience, 2: 408-413. glial cell line-derived neurotrophic factor, nicotinamide mononucleotide adenylyltransferase 1, Connective tissue in the peripheral nervous system, "Wallerian degeneration, wld(s), and nmnat", "Endogenous Nmnat2 is an essential survival factor for maintenance of healthy axons", "NMNAT: It's an NAD + Synthase It's a Chaperone It's a Neuroprotector", Current Opinion in Genetics & Development, "Experiments on the Section of the Glossopharyngeal and Hypoglossal Nerves of the Frog, and Observations of the Alterations Produced Thereby in the Structure of Their Primitive Fibres", "An 85-kb tandem triplication in the slow Wallerian degeneration (Wlds) mouse", "Nerve injury, axonal degeneration and neural regeneration: basic insights", "Endocytotic formation of vesicles and other membranous structures induced by Ca2+ and axolemmal injury", "Axon degeneration: molecular mechanisms of a self-destruction pathway", "Multiple forms of Ca-activated protease from rat brain and muscle", "Microanatomy of axon/glial signaling during Wallerian degeneration", "Complement depletion reduces macrophage infiltration and ctivation during Wallerian degeneration and axonal regeneration", "Degeneration of myelinated efferent fibers prompts mitosis in Remak Schwann cells of uninjured C-fiber afferents", "Delayed macrophage responses and myelin clearance during Wallerian degeneration in the central nervous system: the dorsal radiculotomy model", "Changes of nerve growth factor synthesis in nonneuronal cells in response to sciatic nerve transection", "Interleukin 1 increases stability and transcription of mRNA encoding nerve growth factor in cultured rat fibroblasts", "Ninjurin, a novel adhesion molecule, is induced by nerve injury and promotes axonal growth", https://doi.org/10.1111/j.1460-9568.1990.tb00433.x, "A gene affecting Wallerian nerve degeneration maps distally on mouse chromosome 4", "Non-nuclear Wld(S) determines its neuroprotective efficacy for axons and synapses in vivo", "A local mechanism mediates NAD-dependent protection of axon degeneration", "NAD(+) and axon degeneration revisited: Nmnat1 cannot substitute for Wld(S) to delay Wallerian degeneration", "Targeting NMNAT1 to axons and synapses transforms its neuroprotective potency in vivo", 10.1002/(SICI)1096-9861(19960729)371:3<469::AID-CNE9>3.0.CO;2-0, "dSarm/Sarm1 is required for activation of an injury-induced axon death pathway", "Sarm1-mediated axon degeneration requires both SAM and TIR interactions", "Resolving the topological enigma in Ca 2+ signaling by cyclic ADP-ribose and NAADP", "SARM1 activation triggers axon degeneration locally via NAD destruction", "+ Cleavage Activity that Promotes Pathological Axonal Degeneration", "S, Confers Lifelong Rescue in a Mouse Model of Severe Axonopathy", "Pathological axonal death through a MAPK cascade that triggers a local energy deficit", "MAPK signaling promotes axonal degeneration by speeding the turnover of the axonal maintenance factor NMNAT2", "Attenuated traumatic axonal injury and improved functional outcome after traumatic brain injury in mice lacking Sarm1", https://en.wikipedia.org/w/index.php?title=Wallerian_degeneration&oldid=1136392406. Axonal degeneration may be necessary pathophysiological process for serum CK elevation given that not just AMAN patients but also AIDP patients . Question: QUESTION 1 Carpal tunnel and tarsal tunnel syndrome cause nerve degeneration resulting in specific symptoms and changes in the nerves. 08/03/2017. Degeneration usually proceeds proximally up one to several nodes of Ranvier. Augustus Waller, in 1850, introduced the criteria for axonopathy in peripheral nerve from his sequential studies of experimental nerve crush injury. In the first weeks to months, re-innervation by collaterals may result in polyphasic MUAPs and/or satellite potentials, while the slower axonal re-growth will eventually result in larger amplitude, longer duration potentials. Marquez Neto OR, Leite MS, Freitas T, Mendelovitz P, Villela EA, Kessler IM. In PNS, the permeability increases throughout the distal stump, but the barrier disruption in CNS is limited to just the site of injury. An important gene associated with Wallerian Degeneration is SARM1 (Sterile Alpha And TIR Motif Containing 1), and among its related pathways/superpathways are Neuroscience and NAD metabolism. Myelin clearance is the next step in Wallerian degeneration following axonal degeneration. If any of your symptoms worsen or change after your physical exam, it is important to follow-up with your health care provider. It occurs between 7 to 21 days after the lesion occurs. It occurs between 7 to 21 days after the lesion occurs. Nerve Structure: https://commons.wikimedia.org/w/index.php?curid=1298429. 2005;26 (5): 1062-5. This occurs by the 7th day when macrophages are signaled by the Schwann cells to clean up axonal and myelin debris. Severity is classified by pathologic findings: neurapraxia, axonotmesis, and neurotmesis, also known as Seddon Classification. (2010) Polish journal of radiology. [16] !/$vhwf,cliHx$~gM])BP(Reu[BG4V`URV.//] L7o}%.^xP]-0n'^5w7U?YO}U[QtPog7fj(HY7q . Entry was based on first occurrence of an isolated neurologic syndrome . yet to be fully understood. Affected axons may . The distal nerve, particularly . Transient detection of early wallerian degeneration on diffusion-weighted MRI after an acute cerebrovascular accident. "Experiments on the section of the glossopharyngeal and hypoglossal nerves of the frog, and observations of the alterations produced thereby in the structure of their primitive fibres." 3-18-2018.Ref Type: Online Source. I give my consent to Physiopedia to be in touch with me via email using the information I have provided in this form for the purpose of news, updates and marketing. Another source of macrophage recruitment factors is serum. Get Top Tips Tuesday and The Latest Physiopedia updates, The content on or accessible through Physiopedia is for informational purposes only. 2001;13 (6 Pt 1): 1174-85. Chong Tae Kim, MD, Jung Sun Yoo, MD. In comparison to Schwann cells, oligodendrocytes require axon signals to survive. 1. Wallerian degeneration is a phenomenon that occurs when nerve fiber axons are damaged. Available from, The Young Orthopod. The axon then undergoes a degeneration process that can be anterograde or orthograde (Wallerian) [1] or retrograde. It is noteworthy that these TAD-like lesions do not come with classic Wallerian-type axonal degeneration and evolve through a dose limiting manner [12,13,14]. What will the . [26] Schwann cells upregulate the production of cell surface adhesion molecule ninjurin further promoting growth. T2-weighted images are more helpful than T1. Muscle fatigue, or the decline of performance during an exercise or task, after muscle reinnervation is one limiting factor in the rehabilitation process. However, Wallerian degeneration is thought of as a rare or a late finding in MS. Methods: Studies showing a classic Wallerian degeneration pattern in the corticospinal tract were selected from a review of MR studies from patients enrolled in a longitudinal treatment trial. Possible sources of proliferation signal are attributed to the ErbB2 receptors and the ErbB3 receptors. Muscle and tendon transfers can lead to adhesive scarring in the antagonist muscle and prevent proper tendon function. Axonal degeneration can be caused by at least four different mechanisms. AJNR Am J Neuroradiol. or clinical procedures, such as a hearing test. Injury and electrodiagnostic findings are time dependent and therefore, it is suggested to delay these studies for several weeks to better witness specific findings and delineate injury severity. [6] The process by which the axonal protection is achieved is poorly understood. About Wallerian degeneration. Furthermore, this microdamage alters only the static phase firing sensory component of the stretch reflex and leaves the dynamic sensory encoding basically unharmed . Becerra JL, Puckett WR, Hiester ED, Quencer RM, Marcillo AE, Post MJ, Bunge RP. Surgical repair criteria are based on open or closed injuries and nerve continuity. The effect of cooling on the rate of Wallerian degeneration. Nerve entrapment syndromes (meaning a common group of signs and symptoms), occurs in individuals as a result of swelling of the surrounding tissues, or anatomical abnormalities. Read more, Physiopedia 2023 | Physiopedia is a registered charity in the UK, no. In the three decades since the discovery of the Wallerian degeneration slow (WldS) mouse, research has generated . According to the FA AH/UH, patients were also classified into groups with minimal or extensive Wallerian degeneration (WD). Peripheral neurological recovery and regeneration. 3. Another key aspect is the change in permeability of the blood-tissue barrier in the two systems. The following code (s) above G31.9 contain annotation back-references that may be applicable to G31.9 : G00-G99. Perry, V. H., Lunn, E. R., Brown, M. C., Cahusac, S. and Gordon, S. (1990), Evidence that the Rate of Wallerian Degeneration is Controlled by a Single Autosomal Dominant Gene. . In the cord, Wallerian degeneration can occur both rostrally (involving the dorsal columns above the injury) and caudally (involving the lateral corticospinal tracts below the injury) 8. [32][33] The protection provided by the WldS protein is intrinsic to the neurons and not surrounding support cells, and is only locally protective of the axon, indicating an intracellular pathway is responsible for mediating Wallerian degeneration. CNS regeneration is much slower, and is almost absent in most vertebrate species. Following injury, distal axons undergo the process of Wallerian degeneration, and then cell debris is cleared to create a permissive environment for axon regeneration. Begins within hours of injury and takes months to years to complete. Various possibilities have been studied to improve/accelerate nerve repair/regeneration via neuronal-death reduction and axonal-growth enhancement. The activated macrophages clear myelin and axon debris efficiently, and produce factors that facilitate Schwann cell migration and axon . About the Disease ; Getting a Diagnosis ; . PERIPHERAL NEUROPATHIES Caused by injury to peripheral axons Classification: generalized symmetrical polyneuropathies, generalized neuropathies and focal or multifocal neuropathies Pathophysiology Wallerian generation - traumatic injury leading to severed nerve. The most commonly observed pattern is an injury to the precentral gyrus (such as may be seen in an MCA infarct) with resultant degeneration of the corticospinal tracts. With time, partial axonal loss may result in reduced amplitude and slowed conduction, while complete axonal injury results in loss of action potentials. 8-13 The cerebral peduncle is ideal for assessing postinfarction wallerian degeneration . Murinson et al. 4. Purves D, Augustine GJ, Fitzpatrick D, Hall WC, LaMantia AS, McNamara JO, White LE. Incidence. If neural regeneration is successful, the conduction velocity of the injury returns to 60% to 90% of pre-injury level (but this does not usually adversely affect clinical recovery). Requires an intact endoneurial tube to re-establish continuity between the cell body and the distal terminal nerve segment. A and B: 37 hours post cut. Gordon T, English AW. Axonal degeneration is followed by degradation of the myelin sheath and infiltration by macrophages. Paralysis and sensory loss develop acutely, but nerve conduction of the distal segment only remains intact until the distal segment is consumed by Wallerian degeneration. 75 (4): 38-43. After a short latency period, the transected membranes are sealed until degeneration which is marked by the formation of axonal sprouts. PDF | Background Elevated serum creatine kinase (CK) levels have been reported in patients with Guillain-Barr syndrome (GBS), more frequently in. Wallerian degeneration is the simplest and most thoroughly studied model of axonal degeneration. However recovery is hardly observed at all in the spinal cord. 2001; Rotshenker 2007)] could all be factors affecting the visual white matter depending on . It is seen as a contiguous tract of gliosis leading from a region of cortical or subcortical neuronal injury towards the deep cerebral structures, along the expected topographical course of the involved white matter tract. These factors together create a favorable environment for axonal growth and regeneration. The term "Wallerian degeneration" is best reserved to describe axonopathy in peripheral nerve; however, similar changes can be seen in spinal cord and brain. . . It may result following neuronal loss due to cerebral infarction, trauma, necrosis, focal demyelination, or haemorrhage . Injuries to the myelin are usually the least severe, while injuries to the axons and supporting structures are more severe (Fig 2). Diagram of Central and Peripheral Nervous System. Schwann cells emit growth factors that attract new axonal sprouts growing from the proximal stump after complete degeneration of the injured distal stump. 8. Treatment can involve observation, repair, tendon transfers or nerve grafting depending on the acuity, degree of injury, and mechanism of injury. The 3 major groups found in serum include complement, pentraxins, and antibodies. After injury, the axonal skeleton disintegrates, and the axonal membrane breaks apart. American journal of neuroradiology. NCS can demonstrate the resolution of conduction block or remyelination. MR neurography can identify nerve discontinuity of a nerve, but over 50% of high-grade nerve transections have minimal to no gap present. The activity of SARM1 helps to explain the protective nature of the survival factor NMNAT2, as NMNAT enzymes have been shown to prevent SARM1-mediated depletion of NAD+. [9] A brief latency phase occurs in the distal segment during which it remains electrically excitable and structurally intact. support neurons by forming myelin that encases nerves. 5. Peripheral nerve reconstruction after injury: a review of clinical and experimental therapies. Wallerian Degeneration "Wallerian Degeneration" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings). On the contrary, axonotmesis and neurotmesis take longer to recover and may not recover as well, or at all. Ultrasonography of traumatic injuries to limb peripheral nerves: technical aspects and spectrum of features. In addition, however, there is a diffuse inflammatory process in the "normal" white matter of MS patients, which by itself is associated with blood . In healthy nerves, nerve growth factor (NGF) is produced in very small amounts. The role of magnetic resonance imaging in the evaluation of peripheral nerves following traumatic lesion: where do we stand? These require further exploration and clinical trials: The current standards of care for peripheral nerve injury is based on serial examinations and/or electrodiagnostics. As axon sprouting and regeneration progress, abnormal spontaneous potentials decrease and MUAPs may appear variable. Additionally, high resolution MRI (1.5 and 3 Tesla) can further enhance injury detection. Peripheral neurological recovery and regeneration. The decreased permeability could further hinder macrophage infiltration to the site of injury. [44] This collapse in NAD+ levels was later shown to be due to SARM1's TIR domain having intrinsic NAD+ cleavage activity. Willand MP, Nguyen MA, Borschel GH, Gordon T. Electrical Stimulation to Promote Peripheral Nerve Regeneration. It is produced by Schwann cells in the PNS, and by oligodendrocytes in the CNS. Time: provider may be able to have study done sooner if a timely EMG isdifficultto obtain. Mice belonging to the strain C57BL/Wlds have delayed Wallerian degeneration,[28] and, thus, allow for the study of the roles of various cell types and the underlying cellular and molecular processes. Axon and myelin are both affected [11] These signaling molecules together cause an influx of macrophages, which peaks during the third week after injury. Reinnervated fibers have been shown to fatigue earlier compared to non-injured fibers, especially during isometric repetitive actions. The rate of degradation is dependent on the type of injury and is also slower in the CNS than in the PNS. Strategies to promote peripheral nerve regeneration: electrical stimulation and/or exercise. In neuropraxia (Sunderland grade 1) there is focal demyelination with impaired sensory and motor function distal to the lesion but preserved axonal continuity. Common Symptoms. sciatic nerve constriction was linked to intraneural edoema, localised ischemia, and wallerian degeneration. The macrophages, accompanied by Schwann cells, serve to clear the debris from the degeneration.[5][6]. This is referred to as Wallerian degeneration, and it can also occur due to local injury, like a deep cut through a nerve. %%EOF Wallerian degeneration is the process of antegrade degeneration of the axons and their accompanying myelin sheaths following proximal axonal or neuronal cell body lesions. [38], The provided axonal protection delays the onset of Wallerian degeneration. In cases of cerebral infarction, Wallerian degeneration appears in the chronic phase (>30 days). While Schwann cells mediate the initial stage of myelin debris clean up, macrophages come in to finish the job. The mutated region contains two associated genes: nicotinamide mononucleotide adenylyltransferase 1 (NMNAT1) and ubiquitination factor e4b (UBE4B). [6] The protective effect of the WldS protein has been shown to be due to the NMNAT1 region's NAD+ synthesizing active site. Medical & Exercise Physiology School.Wallerian degeneration/ regeneration process of nerve fiber/axon cut and progressive response. No associated clinical symptoms have been reported . [ 1, 2] The term brachial may be a misnomer, as electrodiagnostic and radiologic evidence often . [7] Within 4 days of the injury, the distal end of the portion of the nerve fiber proximal to the lesion sends out sprouts towards those tubes and these sprouts are attracted by growth factors produced by Schwann cells in the tubes. The prognosis, in general, is more favorable for a demyelinating lesion than for a lesion producing axonal loss. In most cases Physiopedia articles are a secondary source and so should not be used as references. NCS: In the first few days after the injury, there will be reduced conduction across the lesion but conduction may be normal above and below the lesion until Wallerian degeneration occurs. Macrophage entry in general into CNS site of injury is very slow. Common signs and symptoms of peripheral nerve injuries include: Fig 2. By using our website, you agree to our use of cookies. Descriptors are arranged in a hierarchical structure, which enables searching at various levels of specificity. 385 0 obj <> endobj 2. [48][49] One explanation for the protective effect of the WldS mutation is that the NMNAT1 region, which is normally localized to the soma, substitutes for the labile survival factor NMNAT2 to prevent SARM1 activation when the N-terminal Ube4 region of the WldS protein localizes it to the axon. Waller A. De simone T, Regna-gladin C, Carriero MR et-al. Wallerian degeneration of the pyramidal tract Wallerian degeneration of the pyramidal tract. The degenerating nerve also produce macrophage chemotactic molecules. . Reference article, Radiopaedia.org (Accessed on 04 Mar 2023) https://doi.org/10.53347/rID-18998, {"containerId":"expandableQuestionsContainer","displayRelatedArticles":true,"displayNextQuestion":true,"displaySkipQuestion":true,"articleId":18998,"questionManager":null,"mcqUrl":"https://radiopaedia.org/articles/wallerian-degeneration/questions/1308?lang=us"}, View Maxime St-Amant's current disclosures, see full revision history and disclosures, stage 1: degeneration of the axons and myelin sheaths with mild chemical changes (0-4 weeks), stage 2: rapid destruction of myelin protein fragments that were already degenerated, lipids remain intact (4-14 weeks), stage 4: atrophy of the white matter tracts (months to years), brainstem atrophy with or without hypointensity. Natural history of peripheral nerve injury, Table 2: Electrodiagnostic Findings at 1 Month following Peripheral Nerve Injury, Rehabilitation management of peripheral nerve injury, Surgical repair of peripheral nerve injury. The cleaning up of myelin debris is different for PNS and CNS. MAPK signaling has been shown to promote the loss of NMNAT2, thereby promoting SARM1 activation, although SARM1 activation also triggers the MAP kinase cascade, indicating some form of feedback loop exists. London 1850, 140:42329, 7. Mild to moderate autotomy, guarding, excessive licking, limping of the ipsilateral hind paw, and avoidance of placing weight on the injured side were noticed aer the procedure. In Wallerian degeneration, the SARM1 pathway is likely activated by the consequences of the . Patients treated with vincristine predictably develop neuropathic symptoms and signs, the most prominent of which are distal-extremity paresthesias, sensory loss, . Wallerian degeneration is the process of antegrade degeneration of the axons and their accompanying myelin sheaths following proximal axonal or neuronal cell body lesions. 0 Because peripheral neuropathy most frequently results from a specific disease or damage of the nerve, or as a consequence of generalized systemic illness, the most fundamental treatment involves prevention and control of the primary disease. [27] These lines of cell guide the axon regeneration in proper direction. [10] Degeneration follows with swelling of the axolemma, and eventually the formation of bead-like axonal spheroids. Panagopoulos GN, Megaloikonomos PD, Mavrogenis AF. These symptoms include muscle weakness or atrophy, the loss of muscle mass of the affected area. soft tissue. The dynamic signal intensity changes at magnetic resonance (MR) imaging in active and chronic wallerian degeneration in the corticospinal tract were evaluated. [21] Grafts may also be needed to allow for appropriate reinnervation. Schwann cell activation should therefore be delayed, as they would not detect axonal degradation signals from ErbB2 receptors. nerve injuries account for approximately 3% of injuries affecting the upper extremity and hand. Many rare diseases have limited information. Traumatic injury to peripheral nerves results in the loss of neural functions. This proliferation could further enhance the myelin cleaning rates and plays an essential role in regeneration of axons observed in PNS. If gliosis and Wallerian degeneration are present . Possible source for variations in clearance rates could include lack of opsonin activity around microglia, and the lack of increased permeability in the bloodbrain barrier. In neurotmesis (Sunderland grade 5), the axon and all surrounding connective tissue (endoneurium, perineurium, and epineurium) are damaged (i.e., transected nerve). Nerve fibroblasts and Schwann cells play an important role in increased expression of NGF mRNA. Diffusionweighted imaging (DWI) and corresponding apparent diffusion coefficient (ADC) map in a patient with a large parietooccipital lobar intracerebral hemorrhage, showing reduced diffusion (bright on DWI and dark on ADC) in the splenium of the corpus callosum from Wallerian degeneration.