Dear Sirs,

Neurological disease may present with respiratory dysfunction. This presentation is also well recognized for stroke although the precise mechanisms responsible for respiratory problems are poorly understood. Diagnosis of respiratory dysfunction resulting from diaphragmatic paresis after stroke has been reported but few data are available about the effects of stroke on the diaphragmatic function. It is commonly thought that respiratory muscles are under bilateral hemispheric control although diaphragmatic excursion reduction and cases of diaphragmatic paralysis on the hemiplegic side have been reported in stroke patients [1, 2]. We report a case of a patient with unilateral diaphragmatic palsy contralateral to the hemiparetic side.

A 65-year-old woman awoke with vomiting, dizziness and left hemiparesis. There was no history of recent trauma of the neck or the chest or recent surgery. On admission, her pulse rate was 80 beats/min, blood pressure was 110/60 mm Hg, and respirations were 15/min and regular. The patient denied dyspnea. The neurological examination showed a normal mental status. Her speech was dysarthric. The visual fields were intact; pupils were equal, with a normal light reflex; and ocular movements were full and smooth, without nystagmus. A mild left hemiparesis was present involving the face. There were no sensory deficits to touch, pain, temperature, vibration, or position sense. There was no ataxia on either side. No abnormality was demonstrated on brain computed tomography performed in the acute stage. Extensive laboratory investigations including hematological and biochemical parameters were unremarkable. Electrocardiogram, echocardiogram and carotid Doppler studies were normal. Chest radiograph revealed an elevated right hemidiaphragm (Fig. 1a). The brain magnetic resonance imaging (MRI) showed an area of increased signal intensity on T2 weighted or FLAIR images involving the paramedian region of the right pons (Fig. 2). The lesion showed focal restricted diffusion by using MRI diffusion-weighted imaging. The disturbance of neurological symptoms gradually improved. Complete resolution of diaphragmatic elevation and no hemiparesis were detected on day 60 of follow-up (Fig. 1b).

Fig. 1
figure 1

a Chest radiograph shows an elevated right hemidiaphragm. b. Repeat chest radiograph 2 months later showing resolution of the hemidiaphragm elevation

Fig. 2
figure 2

MRI of the brain depicting an acute infarct involving the paramedian region of the right pons

The diaphragm is considered to contribute up to 60–70% of the total ventilation at rest, in both sitting and supine positions. Hemidiaphragmatic paralysis results in a vital capacity decrement of 10–30%, with the most substantial decrements seen in the supine position [3]. Breathing can be activated either automatically or volitionally [4]. The exactly cortical motor representation of respiratory muscles is not completely understood and there is no clear evidence of cerebral dominance for diaphragm function [5]. The descending pathways of the voluntary system are associated with the corticospinal tracts in the brainstem and upper cervical cord [6].

Several studies have suggested impairment of voluntary activation of the diaphragm in cortical or subcortical unilateral lesions in patients with stroke. Furthermore, assessment of diaphragmatic movements or corticodiaphragmatic pathway in ischemic stroke patients has showed abolishment or retardation of diaphragm contraction [79].

In humans, most studies suggested that respiratory muscles are voluntarily activated via bilateral symmetric pyramidal projections [9, 10]. Nevertheless, patients with acute ischemic stroke with unilateral lesions of the brain may develop contralateral diaphragmatic dysfunction; therefore, this diaphragmatic paresis is observed ipsilateral to the hemiplegic side. Only a few cases of ipsilateral diaphragmatic paralysis associated to unilateral brain lesions have been reported [11]. In a recent report, hemidiaphragm dysfunction was noted in a group of stroke patients. The diaphragmatic paresis observed in some patients may be due to ipsilateral diaphragmatic innervation [12].

In the case reported, the reversible diaphragmatic dysfunction developed contralateral to the hemiparetic side. This finding supports that in some patients the ipsilateral innervation of the diaphragm is more prominent than contralateral projections.