Three patients with intestinal pseudo-obstruction secondary to multiple sclerosis are reported. This is a serious complication with significant morbidity and mortality, which is infrequently recognized in clinical practice and rarely reported in the medical literature

Berne

Feldman

Graves

Gupta

Hinds

Lynch

McDougall

Murr

Pender

Read

Schuffler

Shutter

Williams

Crossref

Intestinal pseudo-obstruction complicating multiple sclerosis

Lane, S. W.

Pender, M. P.

University of Queensland eSpace

Internal Medicine Journal, (2005) 35(3) 191-192. 
http://dx.doi.org/10.1111/j.1445-5994.2004.00753.x   
   
Brief Communication  
 
Intestinal Pseudo-Obstruction Complicating Multiple 
Sclerosis  
S. W. Lane and M. P. Pender  
  
Abstract 
 
Three patients with intestinal pseudo-obstruction secondary to multiple sclerosis are 
reported. This is a serious complication with significant morbidity and mortality, which is 
infrequently recognized in clinical practice and rarely reported in the medical literature.  
 
  
Keywords 
bowel obstruction; gastroparesis; intestinal pseudo-obstruction; multiple sclerosis 
 
 
Intestinal pseudo-obstruction is a rarely reported, but serious complication of multiple 
sclerosis that may lead to significant morbidity and mortality. It is likely to be due to 
interruption of neural pathways in the brainstem and spinal cord by primary demyelination 
and axonal loss. 
  Case 1: A 49-year-old man had a history of multiple sclerosis of the primary 
progressive type for 18 years. His disease had caused severe disability with persistent 
diplopia, atonic bladder, requiring intermittent self-catheterization, and limitation of walking 
distance to 10 m with the aid of a walking frame. His comorbidities included obesity, 
hypercholesterolaemia, obstructive sleep apnoea (requiring continuous positive airways 
pressure support at night), and type 2 diabetes mellitus diagnosed 1 year previously. His 
current medications were: atorvastatin 20 mg daily, celecoxib 200 mg daily, amitriptyline 50 
mg daily, baclofen 25 mg t.d.s and omeprazole 20 mg b.d. Three and a half years previously, 
he had developed severe abdominal pain and distension and was diagnosed with large bowel 
obstruction. At laparotomy, no mechanical obstruction was found and a defunctioning 
colostomy was made. Over the next 3 years, he had two further revisions to the stoma 
because of parastomal herniation. On the current admission, he underwent total colectomy. 
The histopathology showed greatly reduced colonic folds with colonic thickness of 2 mm and 
smooth muscle hypertrophy. There were three polyps ranging from 5 to 15 mm in diameter. 
There was no malignancy or diverticular disease. The findings were consistent with colonic 
pseudo-obstruction. 
  Case 2: A 49-year-old woman had a history of multiple sclerosis for 12 years. This 
had caused severe disability. At the time of the current admission, she was unable to walk 
and, owing to gastroparesis and oesophageal dysmotility, was fed through a jejunostomy. 
She had significant cognitive impairment, had a longstanding indwelling catheter because of 
urinary incontinence and was incontinent of faeces. She also had depression and had recently 
ceased mianserin because of vomiting. Her current medications were: ranitidine 150 mg b.d., 
cisapride 10 mg t.d.s., salbutamol 5 mg nebule q.i.d. and sodium chromoglycate nebules 20 
mg daily. She was admitted because of fever, tachycardia, tachypnoea and right basal 
crackles on chest auscultation. The chest X-ray was consistent with aspiration pneumonia. 
She was treated with oral antibiotics and improved over 5 days. On the sixth day of 
admission, she developed a new fever to 39°C and hypotension. She died the following day. 
Autopsy revealed colonic pseudo-obstruction and megacolon. There was also right lower 
lobe bronchopneumonia and pulmonary oedema of both lower lobes. 
  Case 3: A 35-year-old woman had a history of multiple sclerosis for 11 years. She had 
severe disability attributable to her multiple sclerosis, including severe dysarthria, postural 
tremor of the upper limbs and urinary incontinence. She was unable to walk or perform any 
of the activities of daily living. Her multiple sclerosis initially followed a relapsing-remitting 
course, but over the last 3 years her disease had entered a secondary progressive phase, for 
which she was commenced on methotrexate 7.5 mg weekly. She had iron deficiency anaemia, 
although no cause was found for this. Her medications were: penicillin V 500 mg q.i.d., 
ferrous sulphate 350 mg daily, methotrexate 7.5 mg weekly, folic acid 5 mg weekly, 
amitriptyline 25 mg nocte, propantheline 15 mg q.i.d. and propranolol 40 mg b.d. She was 
admitted following an episode of severe vomiting. Clinical findings were consistent with a 
left lower lobe aspiration pneumonia. She was successfully treated with intravenous 
antibiotics followed by oral antibiotics and was discharged home. Four months later, the 
patient died. A coronial autopsy revealed adynamic ileus leading to intestinal pseudo-
obstruction and showed the typical lesions of multiple sclerosis. 
 The diagnosis of multiple sclerosis depends on clinical criteria aided by laboratory 
investigations, including examination of the cerebrospinal fluid, magnetic resonance imaging 
of the brain and spinal cord, and electrophysiological testing. Severe multiple sclerosis can 
result in quadriparesis, cognitive impairment, visual loss, brain stem syndromes, cerebellar 
dysfunction, bowel, bladder and sexual dysfunction (1). 
 Multiple sclerosis is often associated with gastrointestinal dysfunction. In one series 
of 280 patients, 43% described constipation (defined as two or fewer bowel motions per week, 
a need for digital manipulation of the rectum to pass bowel motions or the use of laxatives at 
least once per week) and 51% had one or more episodes of faecal incontinence, thus giving an 
incidence of 68% for any bowel dysfunction (2). This was more likely to be found with 
coexisting bladder dysfunction. In another study, autonomic symptoms (including symptoms 
of urinary, sexual, sudomotor, gastrointestinal and cardiovascular dysfunction) were seen in 
79% (3). There was a relationship between the presence of gastrointestinal symptoms and 
more severe multiple sclerosis. 
 We could find only two previously published case reports of intestinal pseudo-
obstruction in multiple sclerosis, and individual patient demographics were not available 
(4,5). There has also been one report of acute myelitis presenting as intestinal pseudo-
obstruction. In this case, the diagnosis of pseudo-obstruction was made after laparotomy and 
histological examination of resected bowel. The diagnosis of myelitis was based on clinical 
grounds (progressive paralysis which spontaneously resolved in the absence of a 
compressive lesion) in the presence of an elevated cerebrospinal fluid white cell count (6). 
Furthermore, there have been rare reports of gastroparesis associated with multiple sclerosis, 
characterized by a severe delay in gastric emptying (7-9). 
 Intestinal pseudo-obstruction represents a functional, not mechanical, obstruction. 
Clinical manifestations include nausea, vomiting, intermittent or chronic abdominal 
distension, weight loss, abdominal pain and diarrhoea or constipation. The diagnosis is made 
by a combination of clinical, radiographic, manometric and pathological findings. 
Radiographic findings are of dilation of the small or large bowel on plain films, in the absence 
of a demonstrated luminal obstruction. Manometry can reveal absent peristalsis. Pathological 
features consist of alteration of neural or muscle cell mass or morphology. Causes include 
drugs, connective tissue diseases, diabetes mellitus and hypothyroidism (4,10,11). Intestinal 
pseudo-obstruction can be distinguished from toxic megacolon by the presence of systemic 
toxicity and histological evidence of severe inflammation of the colonic smooth muscle layer 
in the latter (12) . Colonic pseudo-obstruction may be associated with similar changes in the 
oesophagus, stomach or small intestine; hence oesophageal manometry may be a useful 
adjunct to diagnosis (10). 
 The gastrointestinal tract is innervated by parasympathetic and sympathetic nerve 
fibres. The vagal and pelvic nerves (parasympathetic) provide both excitatory and inhibitory 
stimuli whereas the sympathetic trunks are inhibitory (13). We propose that central nervous 
system lesions due to multiple sclerosis could produce pseudo-obstruction in a number of 
ways. First, a medullary lesion involving the dorsal nucleus of the vagus nerve or its 
intramedullary nerve fibres could result in loss of excitatory stimulation to the myenteric 
plexus innervating the gut from the oesophagus through to the transverse colon. A lesion in 
the sacral spinal cord involving the parasympathetic preganglionic sacral efferents, which 
innervate the descending colon, sigmoid colon and rectum, may cause similar effects. Second, 
interruption of visceral afferent pathways within the spinal cord may interrupt reflex 
pathways or perception of visceral distension. Finally, lesions involving interneurones or 
descending tracts in the spinal cord or brainstem could lead to disinhibition of sympathetic 
activity or a decrease in parasympathetic activity, with a resultant reduction in intestinal 
motility (14). The anticholinergic effects of our patients' medications (amitriptyline, mianserin 
and propantheline) may also have contributed to the development of pseudo-obstruction. 
 The clinical course of intestinal pseudo-obstruction is usually chronic or relapsing. 
Initial medical treatments include prokinetic agents, such as cisapride or metoclopramide, 
intravenous fluids or antibiotics. Surgery may be used to form a defunctioning stoma or 
bypass, or for resection of severely affected segments. Unfortunately, the response to therapy 
is often disappointing (10) . 
 In conclusion, intestinal pseudo-obstruction is an infrequently recognized 
complication of multiple sclerosis with significant morbidity and mortality, and with limited 
treatment options. A high index of clinical suspicion is necessary to diagnose this 
complication. 
  
References  
  
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5.     Feldman S. Paralytic ileus complicating multiple sclerosis. Harefuah 1977; 92: 203-5. 
6.     Williams HT, Turner DT. Acute myelitis presenting as spastic colonic ileus. Br J Surg 1972; 59: 918. 
7.     Graves MC. Gastric outlet obstruction in a patient with multiple sclerosis. Ann Neurol 1981; 10: 397-8. 
8.     Gupta YK. Gastroparesis with multiple sclerosis. JAMA 1984; 252: 42. 
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10.     Schuffler MD, Rohrmann CA, Chaffee RG, Brand DL, Delaney JH, Young JH. Chronic intestinal pseudo-
obstruction. Medicine 1981; 60: 173-96. 
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Intestinal Pseudo-Obstruction Complicating Multiple Sclerosis

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Intestinal Pseudo-Obstruction Complicating Multiple Sclerosis

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