Crohn disease neurologic manifestations …

Jasvinder Chawla MD MBA

General Neurology

Updated 08.04.2023
Released 02.05.2007
Expires For CME 08.04.2026

Crohn disease: neurologic manifestations

Author: Jasvinder Chawla MD MBA

See Contributor Disclosures

Editor: Amy A Pruitt MD

Crohn disease: neurologic manifestations

In This Article

Quick Link

Introduction

Overview

Crohn disease is an inflammatory bowel disease that predominantly involves the terminal ileum and colon. However, a wide range of extraintestinal complications may also compose a portion of the clinical picture. Extraintestinal manifestations may precede the onset of gastrointestinal symptoms by several years. Neurologic disorders associated with inflammatory bowel disease are reported in 3% of patients, but they often represent an important cause of morbidity as well as a diagnostic challenge. Besides the disease itself, the increasing use of immunosuppressant and other therapies may also play a crucial role in the development of neurologic disorders of different types and pathogenesis. Virtually all components of the nervous system, both central and peripheral, may become involved. Vigilance in recognizing neurologic dysfunction in the setting of Crohn disease, with prompt institution of appropriate treatment, can be important in avoiding irreversible consequences.

Key points

	• Crohn disease is one of the inflammatory diseases that predominantly involve the gastrointestinal system, especially the terminal ileum and colon.
	• A wide range of extraintestinal complications may compose a portion of the clinical picture. Neurologic dysfunction is an infrequent but potentially devastating extraintestinal manifestation of Crohn disease. Virtually all components of the nervous system, both central and peripheral, may become involved.
	• Vigilance in recognizing neurologic dysfunction in the setting of Crohn disease, with prompt institution of appropriate treatment, can be important in avoiding irreversible consequences.

Historical note and terminology

Crohn, Ginzburg, and Oppenheimer pooled their experiences and described a condition they termed “terminal ileitis” (23). Colonic involvement was later recognized, prompting a renaming of the process as “regional enteritis” or “granulomatous enterocolitis.” However, it has become customary to use the eponymous designation, “Crohn disease.”

Earlier descriptions of what probably was Crohn disease can be found. Ulcerative colitis and Crohn disease are the most widely recognized members of a group of conditions collectively labeled inflammatory bowel disease. Despite many similarities, the clinical features and pathological profiles of the 2 conditions also demonstrate decided differences (Table 1). Neurologic dysfunction has been described in both. However, the focus in this article will be specifically on Crohn disease and its neurologic complications.

Table 1. Gastrointestinal Features of Inflammatory Bowel Disease

Ulcerative colitis

• Exacerbations and remissions typical
• Urgent, bloody diarrhea
• Nausea and anorexia
• Weight loss
• Abdominal pain usually not prominent

Crohn disease

• Exacerbations and remissions typical
• Non-bloody, less urgent diarrhea
• Weight loss
• Abdominal pain prominent
• Anal and perianal lesions and fistulas
• Intestinal stricture formation

Clinical manifestations

Presentation and course

Clinical features are primarily gastrointestinal and consist of abdominal pain and non-bloody diarrhea. In addition, weight loss is common. Scarring and stricture formation can lead to partial intestinal obstruction, and fistula formation is also frequent. The clinical course of Crohn disease often entails exacerbations and remissions. Although Crohn disease may involve virtually all levels of the gastrointestinal tract, it demonstrates a distinct predilection for the distal small intestine and proximal colon. In contrast to ulcerative colitis, involvement in Crohn disease is patchy or segmental and extends deeply, often transmurally. Non-caseating granulomas may form, but are not invariably present.

Extraintestinal manifestations of Crohn disease are surprisingly common, with reported frequencies ranging from approximately 25% to over 50% of individuals (44; 80; 116; 17; 89). Some of the extraintestinal manifestations, such as involvement of joints, skin, mouth, and eyes, seem to correlate with the presence of active colonic inflammation. Karmody and colleagues reviewed sensorineural hearing loss as an extraintestinal association of inflammatory bowel disease (56). As inflammatory bowel disease is considered to be a local or systemic immunopathy, the associated sensorineural hearing loss might also be an expression of systemic immune dysfunction. Other clinical processes, such as gallstones and renal calculi, correlate more directly with small intestinal involvement (44).

Neurologic manifestations in inflammatory bowel disease patients are more common than previously estimated and may follow a different pattern of involvement in Crohn disease and ulcerative colitis (119). Even though the prevalence is not clear, the neurologic dysfunction in Crohn disease has multifactorial etiology with both peripheral as well as central nervous system involvement (78). In comparison with many of the systemic manifestations of inflammatory bowel disease, neurologic involvement occurs less frequently in Crohn disease. Lossos and colleagues reported the presence of neurologic involvement in 3% of 638 persons they studied with either Crohn disease or ulcerative colitis (67). In their comprehensive review, they described 4 categories of neurologic involvement: peripheral neuropathy, myopathy or myoneural junction dysfunction, cerebrovascular disease, and myelopathy. Other groups of investigators have also documented demyelinating processes, seizures, and encephalopathy in patients with inflammatory bowel disease. Although neurologic impairment often becomes evident during periods of disease activity, it can also emerge when the disease process is in the dormant phase.

Localization and etiologies of neurologic dysfunction in Crohn disease

(Contributed by Dr. Jasvinder Chawla.)

Peripheral nervous system involvement. The peripheral nervous system is the dominant site of neurologic dysfunction in ulcerative colitis and Crohn disease, accounting for 31.5% of neurologically affected patients (67). A rather extensive array of peripheral neuropathic processes has received recognition. Acute inflammatory demyelinating neuropathy (Guillain-Barré syndrome), axonal sensorimotor neuropathy, mononeuropathy, brachial plexopathy, mononeuritis multiplex, multiple compressive neuropathies, and cranial neuropathies have all been described in the setting of inflammatory bowel disease (67; 24; 77; 19).

Nerve and nerve root disease. Gondim and colleagues performed a retrospective study of 18 patients with Crohn disease and 15 with ulcerative colitis who had developed peripheral neuropathy with no other identifiable etiology (41). The neuropathy was demyelinating in nature in 5 of the 18 (28%) individuals with Crohn disease. In 2 of the 5 (11%), it demonstrated characteristics of multifocal motor neuropathy, whereas in the other 3 (17%) it met criteria for chronic inflammatory demyelinating neuropathy. Eleven patients (61%) had large-fiber axonal neuropathy (4 sensory, 7 sensorimotor), and 2 (11%) were diagnosed with small-fiber neuropathy. Small- and large-fiber axonal sensory neuropathies were more frequently present in younger individuals, whereas patients with large fiber sensorimotor axonal neuropathy tended to be older. Although both axonal and demyelinating neuropathies often responded to immunotherapy, the response was more consistent and robust in patients with demyelinating neuropathy. Among individuals with demyelinating neuropathy who underwent immunomodulatory therapy, 80% experienced moderate (20%) or major (60%) improvement, whereas 60% in the non-demyelinating group derived moderate benefit. Its phenotype is diverse (most commonly small to predominantly axonal sensory large-fiber neuropathy), but usually more severe in Crohn disease (42).

The actual pathologic process inciting the peripheral neuropathy in individuals with Crohn disease is uncertain. In some instances, nutritional factors (folate or vitamin B12 deficiency) have been responsible (22; 66), whereas in others the peripheral neuropathy has been attributed to medications used in treatment, such as metronidazole (28; 106). In other cases, the explanation is not so clear (79). Response to immunosuppressive therapy or plasmapheresis has suggested an autoimmune basis, at least in some instances, and vasculitis with circulating immune complexes has been identified by some investigators (54). However, not all cases have been immunoresponsive. Infection with Campylobacter jejuni has been linked to both acute inflammatory demyelinating neuropathy and exacerbations of inflammatory bowel disease, but the organism has not been identified in any individual experiencing the combination of the 2 processes. As for nerve root involvement, this is rare and has been described in context with lumbar spinal infection secondary to colonic diverticular disease in 1 of the case reports (52). In addition, Smith and Kavar reported a patient with Crohn disease who developed an extensive spinal epidural abscess communicating with an intra-abdominal collection (105).

A distinctive and unusual type of cranial nerve involvement may also become evident in individuals with Crohn disease. Melkersson-Rosenthal syndrome is characterized by the clinical constellation of recurrent facial nerve palsy, intermittent orofacial swelling, and fissuring of the tongue (lingua plicata). Not only has this syndrome been noted in the presence of Crohn disease, its pathologic hallmark, noncaseating granuloma formation, also is seen in Crohn disease. This has led some to suggest that Crohn disease and Melkersson-Rosenthal syndrome are actually part of the same pathologic spectrum (64). Laryngeal involvement in Crohn disease is very rare, and almost 10 cases have been reported with difficulty in breathing due to edema and ulceration from the larynx to the hypopharynx. Hasegawa and colleagues described the first case in which limited ulceration occurred on the vocal fold without airway involvement (47). Caramoy and colleagues made the diagnosis of chronic recurrent retinopathy centralis serosa due to many years of corticosteroid intake for bronchial asthma and Crohn disease (14). Photodynamic therapy was carried out on the right eye and the corticosteroids were discontinued.

Muscle and myoneural junction disease. Muscle involvement may develop in the setting of both ulcerative colitis and Crohn disease, but occurs more frequently in the latter. It accounted for 16% of the cases of neurologic dysfunction in the series compiled by Lossos and colleagues (67). A variety of myopathic processes has been noted in the presence of Crohn disease. Shimoyama and colleagues revealed that myositis in Crohn disease is immune-mediated based on similar CD68-positive macrophages from the resected colon as well as the muscle (101).

Rhabdomyolysis may develop in individuals with Crohn disease (16). Although rhabdomyolysis may be secondary to electrolyte depletion, it may also occur without obvious provocation. The rhabdomyolysis may be subclinical, producing no noticeable symptoms of muscle involvement.

Inflammatory myopathic processes are another potential extraintestinal manifestation of Crohn disease. Dermatomyositis, polymyositis, rimmed vacuole myopathy, and granulomatous myositis have all been noted in this setting. Approximately 50% of the time the appearance of myositic symptoms correlates with disease activity in the bowel. However, the symptoms of myositis may even precede the appearance of gastrointestinal dysfunction in some patients (03). Myositis may also be completely asymptomatic, with only elevation of serum creatine phosphokinase as a clue (48). As with peripheral nerve involvement, an autoimmune basis generally is presumed to be present. Vasculitis involving muscle has also been described in the setting of Crohn disease (39). Focal myositis may also occur. In fact, myositis involving the gastrocnemius muscle has been christened the “gastrocnemius myalgia syndrome” (18). Orbital myositis, sometimes recurrent, has also been reported in Crohn disease (29).

Dysfunction at the myoneural junction may on rare occasions occur in the context of Crohn disease. Myasthenia gravis has been reported (73; 32), although descriptions of this association are sparse. It is of interest that in at least 1 individual with Crohn disease and myasthenia, improvement in gastrointestinal problems (perineal and perianal abscesses and fistulas) occurred following thymectomy (32).

Psoas abscess formation is an important, well-recognized complication of Crohn disease (12; 62; 102; 117) that carries with it the potential for significant morbidity and even mortality (114; 07). Abscess formation is a consequence of a fistulous extension into the psoas muscle, and is characterized clinically by flank, pelvic, or abdominal pain, fever, leukocytosis, flexion contracture of the hip, and gait impairment. Psoas abscess may be the presenting clinical feature of Crohn disease (88). Diagnosis is confirmed by ultrasound or abdominal CT. Abscesses in other muscles, such as the obturator and hamstring, may also develop in the setting of Crohn disease (25; 59). Crohn disease and ulcerative colitis patients are more prone to neuromuscular diseases than patients with gastritis and dyspepsia (43).

Central nervous system involvement. A variety of causes may attribute to central nervous system involvement, including demyelination, cerebrovascular disease, seizures, sleep disturbance, encephalopathy, and spinal cord dysfunction.

Demyelinating disease. An association between inflammatory bowel disease and multiple sclerosis has been suggested (58; 45; 108). Although the association may be stronger for ulcerative colitis than it is for Crohn disease (87; 82), cases of concomitant Crohn disease and multiple sclerosis have also surfaced (86; 11). In several instances, a temporal correlation between the onset of the demyelinating process and the institution of anti-tumor necrosis alpha factor therapy with infliximab was evident (113; 33). Barabino and colleagues described the first report of optic neuritis in a pediatric patient with Crohn disease (06). This could be part of an autoimmune disorder such as a recurrent isolated optic neuritis, the first manifestation of multiple sclerosis, or perhaps another developing demyelinating disease. A study done by Kunchok and colleagues revealed that exposure to TNF inhibitors in patients with autoimmune diseases appeared to be associated with increased risk for inflammatory CNS events; however, this needs to be further researched (60).

Spinal cord dysfunction. Chronic, slowly progressive myelopathy is yet another neurologic manifestation of inflammatory bowel disease, accounting for 26% of the patients with neurologic involvement in the series of Lossos and colleagues (67). Most, though not all, of these individuals were suffering from Crohn disease rather than ulcerative colitis. An inflammatory basis was suspected and oligoclonal banding was noted in 1 patient. Subacute combined degeneration of the spinal cord, secondary to vitamin B12 deficiency following resection of the terminal ileum, may also be responsible for the development of myelopathy in persons with Crohn disease (10; 04). Epidural or subdural spinal empyema, secondary to fistulous extension from the rectum, is a rare complication of Crohn disease, and may present with back and leg pain and progressive leg weakness (92; 51; 49; 37).

Cerebrovascular disease. Vascular complications are well documented though relatively infrequent extraintestinal manifestations of inflammatory bowel disease. In a massive undertaking, Talbot and colleagues reviewed the records of 7199 patients with either Crohn disease or ulcerative colitis and noted the presence of vascular complications in 1.3% (112). Deep venous thrombosis and pulmonary embolus were the most common sites of involvement, whereas individuals with cerebrovascular events accounted for only 9.8% of the total vascular complications (9 of 92 patients). For reasons that are uncertain, vascular complications occur more frequently in ulcerative colitis than in Crohn disease (26). Cerebrovascular events in inflammatory bowel disease may appear both during active exacerbations and during periods of disease quiescence.

Cerebrovascular complications in Crohn disease may emerge in a variety of forms. Large artery disease, such as carotid artery stenosis, with consequent cerebral infarction has been reported in individuals with Crohn disease (118). Multiple strokes may occur and may precede the appearance of bowel symptoms (72). Spinal cord ischemia has also been described (104). Venous sinus thrombosis, especially involving the superior sagittal sinus, is another potential cerebrovascular complication of Crohn disease (103; 35; 76; 69; 94) and may also be the presenting feature (94). Cerebral vasculitis, with multiple lesions in the brain and involvement of multiple vessels on neuroimaging, is yet another potential cerebrovascular manifestation of Crohn disease (40; 96; 36).

Inflammatory bowel disease carries an increased risk of venous and arterial thrombosis. The pathogenic mechanisms of this predisposition are unclear; however, a possible role of inherited risk factors for thrombosis in determining this predisposition has been suggested. Hyperhomocysteinemia may impart an increased risk for thromboembolic events in individuals with Crohn disease (71; 81), and strokes related to either vitamin B12 (84) or vitamin B6 (118) deficiency have been reported. Hypercoagulability due to a variety of factors, including elevations of factors V, VIII, platelets, and fibrinogen, along with decreased antithrombin III, has also been described in the context of Crohn disease (97; 13; 09). Ischemic stroke in Crohn disease has been reported in the setting of antiphospholipid syndrome, with the presence of both anticardiolipin and lupus anticoagulant antibodies (75). However, other investigators have documented that anticardiolipin antibodies, although elevated in patients with Crohn disease, do not correlate with the presence of thromboembolic disease (02).

In fact, no single or specific abnormality has been identified as the sole hypercoagulable culprit in persons with Crohn disease and no consistent abnormality of any of the routinely recognized coagulopathy susceptibility factors has been discovered (55). Furthermore, responses to both immunosuppressive therapy and anticoagulation have been reported in patients who have suffered vascular events, suggesting that a single explanation is improbable and that both hypercoagulable and autoimmune processes may be playing roles in different individuals (40; 96).

Seizures are an infrequently reported neurologic complication of inflammatory bowel disease (31). They may occur as a complication of the surgical management of these diseases, presumably precipitated by factors such as fluid overload, electrolyte imbalance, hypoxia, and steroid administration or withdrawal (99). Seizures have also been reported as a complication of cyclosporine treatment in individuals with Crohn disease (05; 90). Preliminary human studies have shown that patients with inflammatory bowel disease are at increased risk for altered sleep patterns (109). Changing circadian rhythm significantly worsens the development of colitis in animal models. Further research is recommended to clarify the role of disturbances in inflammatory bowel disease (83).

Diffuse encephalopathy with altered consciousness may also develop in individuals with Crohn disease. Both Wernicke encephalopathy and possible selenium-induced encephalopathy have been described in individuals receiving total parenteral nutrition (57; 46). Wernicke encephalopathy has also been reported in an individual with clinically inactive Crohn disease (30). Acute encephalopathy may also be precipitated by agents used to treat Crohn disease, such as sulfasalazine (98). Derrey and colleagues described a first case of an intracerebral inflammatory pseudotumor in the literature associated with an inflammatory bowel disease (27). No clear association has been found, but the intracranial lesion could be the result of the immunosuppressive therapy for Crohn disease, or part of a systemic disimmune process.

As far as sleep disorders are concerned, in a study done by Takahara and colleagues in a Japanese population, they revealed that restless legs syndrome should be considered as one of the causes of sleep disturbance; however, it does not impact the quality of life in patients with Crohn disease (111).

Prognosis and complications

The prognosis of any neurologic event occurring in the setting of Crohn disease depends on the specific clinical situation and etiology of the process in question.

Clinical vignette

A 31-year-old man presented with intractable pelvic pain and intermittent diarrhea. His past medical history was unremarkable except for off-and-on diarrhea and abdominal pain for at least the previous 10 years. The patient had been diagnosed with irritable bowel syndrome, but his symptoms persisted despite symptomatic treatment. He continued to have progressive weight loss of almost 50 pounds and had recently developed pain in the pelvis and anterior and posterior right thigh, leading him to visit the emergency department. The patient was found to have a high-grade fever and leucocytosis. He underwent testing, including colonoscopy, and was diagnosed with Crohn disease. An abdominal CT revealed psoas abscess as a consequence of a fistulous extension into the psoas muscle. A combination of low-dose prednisone, azathioprine, and intermittent infliximab was prescribed for the management of this patient.

Biological basis

Etiology and pathogenesis

An autoimmune etiology, characterized by a dysregulated mucosal immune response to antigens normally present within the intestinal lumen, is suspected by most investigators to underlie the development of Crohn disease (01; 63). However, persistent speculation has also focused on the theory that the organism, Mycobacterium avium subspecies paratuberculosis, which incites a very similar granulomatous bowel disease in cattle (Johne disease), might be the actual cause of Crohn disease and that the immune response is, therefore, an appropriate or exaggerated response to the foreign stimulus (50; 100; 15). Genetic factors also appear to play a role in the generation of the immune response in Crohn disease in that the NOD2/CARD15 gene, which is involved in the immune detection of bacterial products, has been identified as a susceptibility gene for Crohn disease (74; 85). Huff and colleagues have shown that association results and expression data support IRF1 as a strong candidate for Crohn disease causation (53). These data indicate that the 503F variant has hitchhiked to relatively high frequency, thus, forming the IBD5 risk haplotype.

The etiology of the various neurologic complications of Crohn disease is diverse and is discussed in the paragraphs describing the specific neurologic complications in the Clinical Manifestations section.

The gastrointestinal pathological changes in Crohn disease consist of areas of focal intestinal inflammation that may begin with surface ulcers but can ultimately extend transmurally with potential formation of sinus tracts and fistulas. Fibrosis, with thickening of the bowel wall, may also develop and lead to stricture formation. Steiner and colleagues evaluated whole body protein metabolism during corticosteroid therapy in children with newly diagnosed Crohn disease (107). Previous studies demonstrated decreased protein breakdown following either corticosteroid or anti-TNF-α therapy. There were no significant differences in protein breakdown or loss between Crohn disease patients at diagnosis and controls. Whole body protein breakdown and loss increased significantly following 2 weeks of corticosteroid therapy in children with newly diagnosed Crohn disease, which may have profound effects on body composition.

Neurovascular complications of both venous and arterial kinds can be seen in patients with inflammatory bowel disease. The pathogenic mechanisms are complex and postulated to have low serum folate, pyridoxine, and cyanocobalamin levels in association with elevated homocysteine levels as well as increased activation of platelets and microvascular endothelial dysfunction (21). The pathogenesis of peripheral nervous system damage in inflammatory bowel disease also remains unclear. However, multiple mechanisms have been proposed, including immune, iatrogenic related to several drugs, and micronutrient deficiencies secondary to malabsorption-related disorders (34).

Diagnostic workup

The diagnostic workup of any neurologic complication of Crohn disease depends on the type of neurologic process present and must be tailored to fit the specific situation.

Localization and etiologies of neurologic dysfunction in Crohn disease

(Contributed by Dr. Jasvinder Chawla.)

In each instance, the goal is to confirm the presence of the specific problem and to exclude other processes that might be occurring simultaneously with, but independently from, the Crohn disease itself. Some general guidelines for evaluation follow.

If peripheral nerve involvement is suspected, electromyography and nerve conduction velocity studies should be performed and additional laboratory studies obtained, as would be done for any routine peripheral neuropathy evaluation. It is particularly important to remember the potential for vitamin B12 deficiency in patients with Crohn disease as a consequence of terminal ileum involvement. Gemignani and colleagues described the utility of corneal confocal microscopy as a useful tool in patients with Crohn disease and non-length-dependent small-fiber neuropathy (38). Although vitamin D deficiency has been associated with neuromuscular dysfunction, there were no differences in serum vitamin D levels between the Crohn disease and healthy controls to explain the decreased muscle strength (93). Cerebrospinal fluid examination should be obtained if the clinical or electromyography and nerve conduction velocity features suggest a demyelinating process. In a study looking into the role of vitamin D and inflammatory bowel disease, the authors found no difference in mean serum 25(OH)D concentration between children and adolescents (115). In addition, patients with inflammatory bowel disease and increased erythrocyte sedimentation rate have significantly lower 25(OH)D than controls. The authors have recommended that inflammatory bowel disease patients with elevated erythrocyte sedimentation rate should be observed for vitamin D deficiency.

If the clinical presentation suggests muscle or myoneural junction involvement, electromyography and nerve conduction velocity should be obtained. Additional laboratory studies such as muscle enzymes and erythrocyte sedimentation rate are also useful. Muscle biopsy may be needed in some situations. If psoas abscess is suspected, ultrasound or CT of the abdomen and pelvis should be obtained. MRI may also be diagnostic.

MRI of the brain or spinal cord, as dictated by exam findings, is the primary means to identify potential demyelinating processes. CSF examination is also important. Evoked potentials, including visual, somatosensory, and brainstem, may also provide useful information.

The presence of myelopathy in an individual with Crohn disease should prompt neuroimaging of the spine with MRI. Once again, the possibility of vitamin B12 deficiency with consequent subacute combined degeneration should always be kept in mind and excluded with appropriate laboratory studies.

The diagnostic evaluation of an individual with Crohn disease who presents with symptoms or signs of cerebrovascular dysfunction should be undertaken expeditiously, as with any patient presenting with a cerebrovascular event. An emergent CT scan should be obtained to exclude intracranial bleeding. Subsequent studies may include MRI, MR angiography, MR venography, or conventional angiography, depending on the clinical situation. Cardiac evaluation with echocardiography may be considered and, in most instances, an extensive evaluation looking for evidence of a hypercoagulable state will be indicated.

In the patient presenting with a seizure or a diffuse encephalopathy, a structural lesion should be excluded with appropriate neuroimaging, typically with an MRI. An electroencephalogram should also be obtained. Metabolic and nutritional (particularly thiamine and vitamin B12 deficiency) derangements must be vigorously sought with appropriate laboratory studies. Of course, if the clinical picture suggests the possibility of meningitis, CSF examination becomes necessary. Biochemical concentrations of neurotransmitters or metabolites may change in corresponding brain regions in patients with Crohn disease, and Lv and colleagues have discussed the combined role of fMRI with magnetic resonance spectroscopy to detect these brain changes (68).

References

01: Ahmad T, Tamboli CP, Jewell D, Colombel JF. Clinical relevance of advances in genetics and pharmacogenetics of IBD. Gastroenterology 2004;126:1533-49. PMID 15168365
02: Aichbichler BW, Petritsch W, Reicht GA, et al. Anti-cardiolipin antibodies in patients with inflammatory bowel disease. Dig Dis Sci 1999;44:852-6. PMID 10219848
03: Al-Kawas FH. Myositis associated with Crohn’s colitis. Am J Gastroenterol 1986;81:583-5. PMID 2872796
04: Baker SM, Bogoch A. Subacute combined degeneration of the spinal cord after ileal resection and folic acid administration in Crohn’s disease. Neurology 1973;23:40-1. PMID 4734499
05: Barabino A, Castellano E, Gandullia P, Biscaldi E. A girl with severe fistulizing Crohn’s disease. Dig Liver Dis 2000;32:792-4. PMID 11215560
06: Barabino AV, Gandullia P, Calvi A, Vignola S, Arrigo S, Marco RD. Sudden blindness in a child with Crohn's disease. World J Gastroenterol 2011;17(38):4344-6. PMID 22090792
07: Bartolo DC, Ebbs SR, Cooper MJ. Psoas abscess in Bristol: a 10-year review. Int J Colorectal Dis 1987;2:72-6. PMID 3625011
08: Benavente L, Moris G. Neurologic disorders associated with inflammatory bowel disease. Eur J Neurol 2011;18(1):138-43. PMID 20500801
09: Benjilali L, Aidi S, El Mansouri H, Benabdejlil M, Jiddane M, El Alaoui Faris M. Cerebral thrombosis complicating Crohn's disease: two cases. J Stroke Cerebrovasc Dis 2011;20(6):565-9. PMID 22078296
10: Best CN. Subacute combined degeneration of spinal cord after extensive resection of ileum in Crohn’s disease: report of a case. Br J Med 1959;5156:862-4. PMID 13800127
11: Buccino GP, Corrente G, Visintini D. Crohn’s disease and multiple sclerosis: a single case report. Ital J Neurol Sci 1994;15:303-6. PMID 7843946
12: Burul CJ, Ritchie JK, Hawley PR, Todd IP. Psoas abscess: a complication of Crohn’s disease. Br J Surg 1980;67:355-6. PMID 7388331
13: Calderon R, Cruz-Correa MR, Torres EA. Cerebral thrombosis associated with active crohn’s disease. P R Health Sci J 1998;17:293-5. PMID 9883477
14: Caramoy A, Lappas A, Fauser S, Kirchhof B. [Central scotoma and blurred vision in a patient with Crohn's disease]. [Article in German] Ophthalmologe 2009;106(9):836-8. PMID 19440721
15: Chamberlin WM, Naser SA. Integrating theories of the etiology of Crohn’s disease. On the etiology of Crohn’s disease: questioning the hypotheses. Med Sci Monit 2006;12:RA27-33. PMID 16449960
16: Chiba M, Igarashi K, Ohta H, Ohtaka M, Arakawa H, Masamune O. Rhabdomyolysis associated with Crohn’s disease. Jpn J Med 1987;26:255-60. PMID 3626167
17: Christodoulou DK, Katsanos KH, Kitsanou M, Stergiopoulou C, Hatzis J, Tsianos EV. Frequency of extraintestinal manifestations in patients with inflammatory bowel disease in Northwest Greece and review of the literature. Dig Liver Dis 2002;34:781-6. PMID 12546513
18: Christopoulos C, Savva S, Pylarinou S, Diakakis A, Papavassiliou E, Economopoulos P. Localised gastrocnemius myositis in Crohn’s disease. Clin Rheumatol 2003;22:143-5. PMID 12740681
19: Coert JH, Dellon AL. Neuropathy related to Crohn’s disease treated by peripheral nerve decompression. Scand J Plast Reconstr Surg Hand Surg 2003;37:243-4. PMID 14582760
20: Cognat E, Crassard I, Denier C, Vahedi K, Bousser MG. Cerebral venous thrombosis in inflammatory bowel diseases: eight cases and literature review. Int J Stroke 2011;6(6):487-92. PMID 22017824
21: Cojocaru IM, Cojocaru M, Sapira V, Ionescu A, Tacu N. Cerebrovascular complications in patients with inflammatory bowel disease. Rom J Intern Med 2014;52(1):39-44. PMID 25000677
22: Contamin F, Ollat H, Levy VG, Thierman-Duffaud D. Involvement of the peripheral and pyramidal nervous system in Crohn disease. Determining the role of folic acid deficiency. Sem Hop 1983;59:1381-5. PMID 6306822
23: Crohn BB, Ginzburg K, Oppenheimer GD. Regional ileitis: a pathological and clinical entity. JAMA 1932;99:1323-8. PMID 6361290
24: Demarquay JF, Caroli-Bose FX, Buckley M, et al. Right-sided sciatalgia complicating Crohn’s disease. Am J Gastroenterol 1998;93:2296-8. PMID 9820424
25: Denton ER, Jamieson CP, Rankin SC. Case report: abscess of the adductor muscles of the thigh–an unusual complication of Crohn’s disease. Br J Radiol 1996;69:865-6. PMID 8983593
26: Derdeyn CP, Powers WJ. Isolated cortical venous thrombosis and ulcerative colitis. AJNR Am J Neuroradiol 1998;19:488-90. PMID 9541304
27: Derrey S, Charpentier C, Gérardin E, et al. Inflammatory pseudotumor of the cerebellum in a patient with Crohn's disease. World Neurosurg 2012;77(1):201.e13-6. PMID 22405397
28: Duffy LF, Daum F, Fisher SE, et al. Peripheral neuropathy in Crohn’s disease patients treated with metronidazole. Gastroenterology 1985;88:681-4. PMID 2981752
29: Durno CA, Ehrlich R, Taylor R, Buncic JR, Hughes P, Griffiths AM. Keeping an eye on Crohn’s disease: orbital myositis as the presenting symptom. Can J Gastroenterol 1997;11:497-500. PMID 9347163
30: Eggspuhler AW, Bauerfeind P, Dorn T, Siegel AM. Wernicke encephalopathy – a severe neurological complication in a clinically inactive Crohn’s disease. Eur Neurol 2003;50:184-5. PMID 14530629
31: Elsehety A, Bertorini T. Neurologic and neuropsychiatric complications of Crohn’s disease. South Med J 1997;90:606-10. PMID 9191736
32: Finnie IA, Shields R, Sutton R, Donnelly R, Morris AI. Crohn’s disease and myasthenia gravis: a possible role for thymectomy. Gut 1994;35:278-9. PMID 8307484
33: Freeman HJ, Flak B. Demyelination-like syndrome in Crohn’s disease after infliximab therapy. Can J Gastroenterol 2005;19:313-6. PMID 15915246
34: García-Cabo C, Morís G. Peripheral neuropathy: an underreported neurologic manifestation of inflammatory bowel disease. Eur J Intern Med 2015;26(7):468-75. PMID 26211733
35: Garcia-Monco JC, Gomez Beldarrain M. Superior sagittal sinus thrombosis complicating Crohn’s disease. Neurology 1991;41:1324-5. PMID 1824551
36: Gekka M, Sugiyama T, Nomura M, Kato Y, Nishihara H, Asaoka K. Histologically confirmed case of cerebral vasculitis associated with Crohn's disease--a case report. BMC Neurol 2015;15:169. PMID 26390922
37: Gelfenbeyn M, Goodkin R, Kliot M. Sterile recurrent spinal epidural abscess in a patient with Crohn’s disease: a case report. Surg Neurol 2006;65:178-84. PMID 16427419
38: Gemignani F, Ferrari G, Vitetta F, Giovanelli M, Macaluso C, Marbini A. Non-length-dependent small fibre neuropathy. Confocal microscopy study of the corneal innervation. J Neurol Neurosurg Psychiatry 2010;81(7):731-3. PMID 20581138
39: Gilliam JH 3rd, Challa VR, Agudelo CA, Albertson DA, Huntley CC. Vasculitis involving muscle associated with Crohn’s colitis. Gastroenterology 1981;81:787-90. PMID 7262523
40: Gobbele R, Reith W, Block F. Cerebral vasculitis as a concomitant neurological illness in Crohn’s disease. Nervenarzt 2000;71:299-304. PMID 10795098
41: Gondim FA, Brannagan TH 3rd, Sander HW, Chin RL, Latov N. Peripheral neuropathy in patients with inflammatory bowel disease. Brain 2005;128:867-79. PMID 15705608
42: Gondim Fde A, de Oliveira GR, Teles BC, et al. Clinical and electrodiagnostic findings in patients with peripheral neuropathy and inflammatory bowel disease. Inflamm Bowel Dis 2015a;21(9):2123-9. PMID 25993692
43: Gondim Fde A, Oliveira GR, Teles BC, Souza MH, Braga LL, Messias EL. A case-control study of the prevalence of neurological diseases in inflammatory bowel disease (IBD). Arq Neuropsiquiatr 2015b;73(2):119-24. PMID 25742581
44: Greenstein AJ, Janowitz HD, Sachar DB. The extra-intestinal complications of Crohn’s disease and ulcerative colitis: a study of 700 patients. Medicine 1976;55:401-2. PMID 957999
45: Gupta G, Gelfand JM, Lewis JD. Increased risk for demyelinating diseases in patients with inflammatory bowel disease. Gastroenterology 2005;129:819-26. PMID 16143121
46: Hahn JS, Berquist W, Alcorn DM, Chamberlain L, Bass D. Wernicke encephalopathy and beriberi during total parenteral nutrition attributable to multivitamin infusion shortage. Pediatrics 1998;101:10-4. PMID 9417174
47: Hasegawa N, Ishimoto S, Takazoe M, et al. Recurrent hoarseness due to inflammatory vocal fold lesions in a patient with Crohn's disease. Ann Otol Rhinol Laryngol 2009;118(7):532-5. PMID 19708494
48: Hayashi K, Kurisu Y, Ohshiba S, et al. Report of a case of Crohn’s disease associated with hyper-creatine phosphokinase-emia. Jpn J Med 1991;30:441-5. PMID 1803046
49: Heidemann J, Spinelli KS, Otterson MF, Binion DG. Case report: magnetic resonance imaging in the diagnosis of epidural abscess complicating perirectal fistulizing Crohn’s disease. Inflamm Bowel Dis 2003;9:122-4. PMID 12769446
50: Hermon-Taylor J, Bull T. Crohn’s disease caused by Mycobacterium avium subspecies paratuberculosis: a public health tragedy whose resolution is long overdue. J Med Microbiol 2002;51:3-6. PMID 11800469
51: Hershkowitz S, Link R, Ravden M, Lipow K. Spinal empyema in Crohn’s disease. J Clin Gastroenterol 1990;12:67-9. PMID 1968073
52: Hopton B, Barron D, Ambrose S, Millner P. The flatulent spine: lumbar spinal infection secondary to colonic diverticular abscess: a case report and review of the literature. J Spinal Disord Tech 2008;21(7):527-30. PMID 18836367
53: Huff CD, Witherspoon D, Zhang Y, et al. Crohn's disease and genetic hitchhiking at IBD5. Mol Biol Evol 2012;29(1):101-11. PMID 21816865
54: Humbert P, Monnier G, Billerey C, Birgen C, Dupond JL. Polyneuropathy: an unusual extraintestinal manifestation of Crohn’s disease. Acta Neurol Scand 1989;80:301-6. PMID 2554634
55: Jackson LM, O’Gorman PJ, O’Connell J, Cronin CC, Cotter KP, Shanahan F. Thrombosis in inflammatory bowel disease: clinical setting, procoagulant profile and Factor V Leiden. QJM 1997;90:183-8. PMID 9093595
56: Karmody CS, Valdez TA, Desai U, Blevins NH. Sensorineural hearing loss in patients with inflammatory bowel disease. Am J Otolaryngol 2009;30(3):166-70. PMID 19410121
57: Kawakubo K, Iida M, Matsumoto T, et al. Progressive encephalopathy in a Crohn’s disease patient on long-term total parenteral nutrition: possible relationship to selenium deficiency. Postgrad Med J 1994;70:215-9. PMID 8183758
58: Kimura K, Hunter SF, Thollander MS, et al. Concurrence of inflammatory bowel disease and multiple sclerosis. Mayo Clin Proc 2000;75:802-6. PMID 10943233
59: Koudela K, Treska V, Koudelova J, Koudela K. Primary obturator pyomyositis. Zentralbl Chir 2005;130:80-3. PMID 15717246
60: Kunchok A, Aksamit AJ Jr, Davis JM 3rd, et al. Association between tumor necrosis factor inhibitor exposure and inflammatory central nervous system events. JAMA Neurol 2020;77(8):937-46. PMID 32421186
61: Kurata JH, Kantor-Fish S, Frankl H, Godby P, Vadheim CM. Crohn’s disease among ethnic groups in a large health maintenance organization. Gastroenterology 1992;102:1940-8. PMID 1587413
62: Leu SY, Leonard MB, Beart RW Jr, Dozois RR. Psoas abscess: changing patterns of diagnosis and etiology. Dis Colon Rectum 1986;29:694-8. PMID 3769683
63: Lim WC, Hanauer SB. Emerging biologic therapies in inflammatory bowel disease. Rev Gastroenterol Disord 2004;4:66-85. PMID 15184826
64: Lloyd DA, Payton KB, Guenther L, Frydman W. Melkersson-Rosenthal syndrome and Crohn’s disease: one disease or two? Report of a case and discussion of the literature. J Clin Gastroenterol 1994;18:213-7. PMID 8034917
65: Loftus EV Jr. Clinical epidemiology of inflammatory bowel disease: incidence, prevalence, and environmental influences. Gastroenterology 2004;126:1504-17. PMID 15168363
66: Lossos A, Argov Z, Ackerman Z, Abramsky O. Peripheral neuropathy and folate deficiency as the first sign of Crohn’s disease. J Clin Gastroenterol 1991;13:442-4. PMID 1655863
67: Lossos A, River Y, Eliakim A, Steiner I. Neurologic aspects of inflammatory bowel disease. Neurology 1995;45:416-21. PMID 7898687
68: Lv K, Fan YH, Xu L, Xu MS. Brain changes detected by functional magnetic resonance imaging and spectroscopy in patients with Crohn's disease. World J Gastroenterol 2017;23(20):3607-14. PMID 28611513
69: Maag J, Prayson RA. Intracranial sinus thrombosis in a patient with Crohn disease and factor V Leiden mutation. Arch Pathol Lab Med 2003;127:1037-9. PMID 12873183
70: Mack DE, Wilson PM, Gilmore JC, Gunnell KE. Leisure-Time Physical Activity in Canadians Living With Crohn Disease and Ulcerative Colitis: Population-Based Estimates. Gastroenterol Nurs 2011;34(4):288-294. PMID 21814062
71: Mahmood A, Needham J, Prosser J, et al. Prevalence of hyperhomocysteinaemia, activated protein C resistance and prothrombin gene mutation in inflammatory bowel disease. Eur J Gastroenterol Hepatol 2005;17:739-44. PMID 15947551
72: Manzino M, Tomasina C. Multiple cerebral infarctions in Crohn’s disease. Report of a case. Minerva Med 1996;87:253-5. PMID 8700352
73: Martin RW, Shah A. Myasthenia gravis coexistent with Crohn’s disease. J Clin Gastroenterol 1991;13:112-3. PMID 2007731
74: Mathew CG, Lewis CM. Genetics of inflammatory bowel disease: progress and prospects. Hum Mol Genet 2004;13:161-8. PMID 14764625
75: Mevorach D, Goldberg Y, Gomori JM, Rachmilewitz D. Antiphospholipid syndrome manifested by ischemic stroke in a patient with Crohn’s disease. J Clin Gastroenterol 1996;22:141-3. PMID 8742656
76: Milandre L, Monges D, Dor V, Juhan-Vague I, Khalil R. Cerebral phlebitis and Crohn disease. Rev Neurol (Paris) 1992;148:139-44. PMID 1604124
77: Moormann B, Herath H, Mann O, Ferbert A. Involvement of the peripheral nervous system in Crohn disease. Nervenarzt 1999;70:1107-11. PMID 10637818
78: Nemati R, Mehdizadeh S, Salimipour H, et al. Neurological manifestations related to Crohn's disease: a boon for the workforce. Gastroenterol Rep (Oxf) 2019;7(4):291-7. PMID 31413837
79: Nemni R, Fazio R, Corbo M, Sessa M, Comi G, Canal N. Peripheral neuropathy associated with Crohn’s disease. Neurology 1987;37:1414-7. PMID 3039409
80: Novotny DA, Rubin RJ, Slezak FA, Porter JA. Arterial thromboembolic complications of inflammatory bowel disease. Report of three cases. Dis Colon Rectum 1992;35:193-6. PMID 1735324
81: Oldenburg B, Van Tuyl BA, van der Griend R, Fijnheer R, van Berge Henegouwen GP. Risk factors for thromboembolic complications in inflammatory bowel disease: the role of hyperhomocysteinaemia. Dig Dis Sci 2005;50:235-40. PMID 15745078
82: Pandian JD, Pawar G, Singh GS, Abraham R. Multiple sclerosis in a patient with chronic ulcerative colitis. Neurol India 2004;52:282-3. PMID 15269508
83: Parekh PJ, Oldfield Iv EC, Challapallisri V, Ware JC, Johnson DA. Sleep disorders and inflammatory disease activity: chicken or the egg? Am J Gastroenterol 2015;110(4):484-8. PMID 25155226
84: Penix LP. Ischemic strokes secondary to vitamin B12 deficiency-induced hyperhomocystinemia. Neurology 1998;51:622-4. PMID 9710054
85: Philpott DJ, Viala J. Towards an understanding of the role of NOD2/CARD15 in the pathogenesis of Crohn’s disease. Best Pract Res Clin Gastroenterol 2004;18:555-68. PMID 15157827
86: Purrmann J, Arendt G, Cleveland S, et al. Association of Crohn’s disease and multiple sclerosis. Is there a common background. J Clin Gastroenterol 1992;14:43-6. PMID 1556407
87: Rang EH, Brooke BN, Hermon-Taylor J. Association of ulcerative colitis with multiple sclerosis. Lancet 1982;2:555. PMID 6125706
88: Ricci MA, Meyer KK. Psoas abscess complicating Crohn’s disease. Am J Gastroenterol 1985;80:970-97. PMID 2933953
89: Rogler G, Scholmerich J. Extraintestinal manifestations of inflammatory bowel disease. Med Klin (Munich) 2004;99:123-30. PMID 15024484
90: Rosencrantz R, Moon A, Raynes H, Spivak W. Cyclosporine-induced neurotoxicity during treatment of Crohn’s disease: lack of correlation with previously reported risk factors. Am J Gastroenterol 2001;96:2778-82. PMID 11569712
91: Rubin DT, Panaccione R, Chao J, Robinson AM. A practical, evidence-based guide to the use of adalimumab in Crohn's disease. Curr Med Res Opin 2011;27(9):1803-13. PMID 21809894
92: Sacher M, Gopfrich H, Hochberger O. Crohn’s disease penetrating into the spinal cord. Acta Pediatr Scand 1989;78:647-9. PMID 2782087
93: Salacinski AJ, Regueiro MD, Broeder CE, McCrory JL. Decreased neuromuscular function in Crohn's disease patients is not associated with low serum vitamin D levels. Dig Dis Sci 2013;58(2):526-33. PMID 22949179
94: Samal SC, Patra S, Reddy DC, Sharma UP. Cerebral venous sinus thrombosis as a presenting feature of Crohn’s disease. Indian J Gastroenterol 2004;23:148-9. PMID 15333975
95: Sands BE. Crohn’s disease. In: Feldman M, Friedman LS, Sleisenger M, editors. Sleisenger’s and Fordtran’s gastrointestinal and liver disease. 7th ed. Philadelphia: Saunders, 2002:2005-38.
96: Schluter A, Krasnianski M, Krivokuca M, Spielmann RP, Neudecker S, Hirsch W. Magnetic resonance angiography in a patient with Crohn’s disease associated cerebral vasculitis. Clin Neurol Neurosurg 2004;106:110-3. PMID 15003300
97: Schneiderman JH, Sharpe JA, Sutton DM. Cerebral and retinal vascular complications of inflammatory bowel disease. Ann Neurol 1979;5:331-7. PMID 443768
98: Schoonjans R, Mast A, Van Den Abeele G, et al. Sulfasalazine-associated encephalopathy in a patient with Crohn’s disease. Am J Gastroenterol 1993;88:1416-20. PMID 8105680
99: Schulak JA, Moossa R, Block GE, Kirsner JB. Convulsions complicating colectomy in inflammatory bowel disease. JAMA 1977;237:1456-8. PMID 403303
100: Shanahan F, O’Mahony J. The mycobacteria story in Crohn’s disease. Am J Gastroenterol 2005;100:1537-8. PMID 15984977
101: Shimoyama T, Tamura Y, Sakamoto T, Inoue K. Immune-mediated myositis in Crohn's disease. Muscle Nerve 2009;39(1):101-5. PMID 19086077
102: Shokouh-Amiri MH, Palnaes Hansen C, Moesgaard F, Bulow S. Psoas abscess complicating Crohn’s disease. Acta Chir Scand 1989;155:409-12. PMID 2688345
103: Sigsbee B, Rottenberg DA. Sagittal sinus thrombosis as a complication of regional enteritis. Ann Neurol 1978;3:450-2. PMID 727725
104: Slot WB, van Kasteel V, Coerkamp EG, Seelen PJ, van der Werf SD. Severe thrombotic complications in a postpartum patient with active Crohn’s disease resulting in ischemic spinal cord injury. Dig Dis Sci 1995;40:1395-9. PMID 7781467
105: Smith C, Kavar B. Extensive spinal epidural abscess as a complication of Crohn's disease. J Clin Neurosci 2010;17(1):144-6. PMID 19914072
106: Stahlberg D, Barany F, Einarsson K, Ursing B, Elmqvist D, Persson A. Neurophysiologic studies of patients with Crohn’s disease on long-term treatment with metronidazole. Scand J Gastroenterol 1991;26:219-24. PMID 1849313
107: Steiner SJ, Noe JD, Denne SC. Corticosteroids Increase Protein Breakdown and Loss In Newly Diagnosed Pediatric Crohn Disease. Pediatr Res 2011;70(5):484-8. PMID 21814156
108: Stovicek J, Liskova P, Lisy J, Hlava S, Keil R. Crohn's disease: is there a place for neurological screening? Scand J Gastroenterol 2014;49(2):173-6. PMID 24299027
109: Swanson GR, Burgess HJ, Keshavarzian A. Sleep disturbances and inflammatory bowel disease: a potential trigger for disease flare. Expert Rev Clin Immunol 2011;7(1):29-36. PMID 21162647
110: Kafil TS, Nguyen TM, MacDonald JK, Chande N. Cannabis for the treatment of Crohn's disease and ulcerative colitis: evidence from Cochrane reviews. Inflamm Bowel Dis 2020;26(4):502-9. PMID 31613959
111: Takahara I, Takeshima F, Ichikawa T, et al. Prevalence of restless legs syndrome in patients with inflammatory bowel disease. Dig Dis Sci 2017;62(3):761-7. PMID 28035549
112: Talbot RW, Heppell J, Dozois RR, Beart RW Jr. Vascular complications of inflammatory bowel disease. Mayo Clin Proc 1986;61:140-5. PMID 3080643
113: Thomas CW Jr, Weinshenker BG, Sandborn WJ. Demyelination during anti-tumor necrosis factor alpha therapy with infliximab for Crohn’s disease. Inflamm Bowel Dis 2004;10:28-31. PMID 15058523
114: Van Dongen LM, Lubbers EJ. Psoas abscess in Crohn’s disease. Br J Surg 1982;69:589-90. PMID 7127038
115: Veit LE, Maranda L, Fong J, Nwosu BU. The vitamin d status in inflammatory bowel disease. PLoS One 2014;9(7):e101583. PMID 24992465
116: Veloso FT, Carvalho J, Magro F. Immune-related systemic manifestations of inflammatory bowel disease. A prospective study of 792 patients. J Clin Gastroenterol 1996;23:29-34. PMID 8835896
117: Veroux M, Angriman I, Ruffolo C, et al. Psoas abscess: a rare complication of Crohn’s disease. Acta Chir Belg 2004;104:187-90. PMID 15154577
118: Younes-Mhenni S, Derex L, Berruyer M, et al. Large-artery stroke in a young patient with Crohn’s disease. Role of vitamin B6 deficiency-induced hyperhomocysteinemia. J Neurol Sci 2004;221:113-5. PMID 15178225
119: Zois CD, Katsanos KH, Kosmidou M, Tsianos EV. Neurologic manifestations in inflammatory bowel diseases: current knowledge and novel insights. J Crohns Colitis 2010;4(2):115-24. PMID 21122494

Contributors

All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.

Author

Jasvinder Chawla MD MBA

Dr. Chawla of Loyola University Medical Center has no relevant financial relationships to disclose.
See Profile

Editor

Amy A Pruitt MD

Dr. Pruitt of the University of Pennsylvania School of Medicine has no relevant financial relationships to disclose.
See Profile

Former Authors

Ronald F Pfeiffer MD (original author)

Patient Profile

Age range of presentation: 6 to 65+ years
Sex preponderance: female>male, >1:1
Heredity: heredity may be a factor
Population groups selectively affected: none selectively affected
Occupation groups selectively affected: none selectively affected

ICD & OMIM codes

ICD-9: Regional enteritis: 555
ICD-10: Crohn’s disease [regional enteritis]: K50
OMIM: Inflammatory bowel disease1; IBD1: #266600

This is an article preview.
Start a Free Account
to access the full version.

Nearly 3,000 illustrations, including video clips of neurologic disorders.
Every article is reviewed by our esteemed Editorial Board for accuracy and currency.
Full spectrum of neurology in 1,200 comprehensive articles.
Listen to MedLink on the go with Audio versions of each article.

Questions or Comment?

MedLink®, LLC

3525 Del Mar Heights Rd, Ste 304
San Diego, CA 92130-2122

Toll Free (U.S. + Canada): 800-452-2400

US Number: +1-619-640-4660

Support: service@medlink.com

Editor: editor@medlink.com

ISSN: 2831-9125

Crohn disease: neurologic manifestations

Associated Disorders

Inflammatory bowel disease
Melkersson-Rosenthal syndrome
Multiple sclerosis
Myelopathy
Peripheral neuropathy

Differential Diagnosis

ulcerative colitis

Also Relevant

Acute inflammatory demyelinating polyradiculoneuropathy
Melkersson-Rosenthal syndrome
Multiple sclerosis
Myasthenia gravis
Small fiber neuropathies
- Vitamin B12 deficiency

Clinical Categories

General Neurology

Crohn disease: neurologic manifestations

Introduction

Overview

Key points

Historical note and terminology

Table 1. Gastrointestinal Features of Inflammatory Bowel Disease

Ulcerative colitis

Crohn disease

Clinical manifestations

Presentation and course

Prognosis and complications

Clinical vignette

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Differential diagnosis

Diagnostic workup

Management

Special considerations

Anesthesia

Media

References

Contributors

Author

Editor

Former Authors

Patient Profile

ICD & OMIM codes

This is an article preview. Start a Free Account to access the full version.

Questions or Comment?

Also in This Category

Neurogenetics and genetic and genomic testing

Acute traumatic spinal cord injury

Tumors of the skull base

Toxic and nutritional deficiency optic neuropathies

Nystagmus

Third nerve palsy

Brain death/death by neurologic criteria

Outpatient rehabilitation of chronic neurologic conditions

This is an article preview.
Start a Free Account
to access the full version.