Elsevier

Brain and Development

Volume 21, Issue 5, 1 July 1999, Pages 307-311
Brain and Development

Original article
Gastrointestinal manifestations in children with cerebral palsy

https://doi.org/10.1016/S0387-7604(99)00025-XGet rights and content

Abstract

We describe the prevalence and nature of gastrointestinal (GI) symptoms in 58 children affected by cerebral palsy (range: from 6 months to 12 years of age) referred to a pediatric neurology outpatient clinic.

In each patient we assessed (GI) symptoms and defined the associated GI functional or structural abnormalities. Furthermore, we tried to correlate the type of GI dysfunction with findings on computed tomography (CT) or magnetic resonance imaging (MRI) of the brain. Our results showed that 92% of children with cerebral palsy had clinically significant gastrointestinal symptoms. Swallowing disorders were present in 60% of patients, regurgitation and/or vomiting in 32%, abdominal pain in 32%, episodes of chronic pulmonary aspiration in 41% and chronic constipation in 74%. Dysfunction of the oral and/or pharyngeal phase of swallowing was found in 28 of 30 (93%) patients with swallowing disorders. Of the 45 patients with symptoms suggesting gastroesophageal reflux, 41 (91%) had an abnormal pH-monitoring and/or esophagitis. Furthermore, a significant delay in the scintigraphic gastric emptying of liquids was found in 12 of 18 patients (67%) and an abnormal esophageal motility in 11 of the 18 (61%) investigated patients. In 25 patients with chronic constipation evaluation of colonic transit showed a delay at level of the proximal segments of the colon in 13 (52%), at level of the left colon and rectum in 9 (36%) and in 3 (12%) at level of the rectum only. Computed tomography and/or magnetic resonance imaging were normal in 5 (9%) and abnormal in 53 (91%) of the 58 children with cerebral palsy. No GI symptom was significantly associated with any kind of abnormal neuroimaging.

In conclusion, children with cerebral palsy exhibited diffuse GI clinical manifestations, mostly due to disorders of GI motility. The GI symptoms seemed not to be related to any specific finding on CT or MRI of the brain.

Introduction

The survival of children with severe central nervous system damage has created a major challenge for medical care [1], [2]. Numerous clinical reports, in small series of patients, have indicated that brain damage may result in gastrointestinal (GI) dysfunction. Dysphagia, dysfunctional feeding patterns, vomiting and chronic constipation have all been reported in neurologically impaired children [3], [4], [5], [6]. Usually, all these symptoms are not specifically evaluated and/or related to any particular syndrome of perinatal brain damage. Cerebral palsy refers to a group of chronic, non progressive disorders of movement, posture, and tone due to a central nervous system damage during early development. The prevalence of cerebral palsy is approximately 2 per 1000 live births [1], [2]. The proportion of the different types of cerebral palsy varies from series to series, the spastic type being invariably the most frequent, while periventricular leukomalacia and/or cortical/cerebral atrophy stand out as the main neuropathological substrates [2], [7], [8], [9].

The aims of our study were to document gastrointestinal pathology in a series of patients with cerebral palsy and to possibly correlate GI symptoms with findings on neuroimaging studies.

Section snippets

Subjects and methods

From September 1995 to May 1997 gastrointestinal symptoms were evaluated in 58 consecutive children (M/F:25/33; Meanage+SD: 5.2+4.9 years) with cerebral palsy referred to a pediatric neurology outpatient clinic. The degree of functional brain impairment was defined on the basis of the IQ level, according to DSM-IV [10]. The type and distribution of the cerebral palsy were categorized according to the definitions proposed by Hagberg et al [11].

Clinical features in our patients with cerebral

Results

Fifty-three out of 58 (91%) children affected by cerebral palsy had gastrointestinal symptoms of at least 6 months’ duration. Clinical GI manifestations in our patients are reported in Table 3. Computed tomography and/or magnetic resonance imaging gave were normal findings in five of the 58 (9%) patients. Three of the five patients with normal neuroimaging did not show GI symptoms. Abnormal neuroimaging findings included: ventricular dilation in 14 (24%) patients, periventricular leukomalacia

Discussion

Our results indicate that, when appropriate diagnostic techniques are employed, children with cerebral palsy, particularly in its most severe form, show a multitude of gastrointestinal motility dysfunctions, which may be responsible for significant morbidity. The high prevalence of GI functional abnormalities among retarded children may not be generally recognized: however, early recognition could allow for specific therapy for the GI disorder.

GI motor dysfunctions are known to occur frequently

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