Truncal Contrapulsion in Claude’s Syndrome
Year: 2025
Type: article
Study design: Case Report
Abstract: Sir, Claude’s syndrome refers to the association of unilateral oculomotor and/or trochlear palsy of midbrain origin with contralateral ataxia.[1] Truncal lateropulsion, is a compelling sensation of being pulled toward one side. Truncal ipsipulsion has been described primarily in Wallenberg syndrome and may occur with lesions that involve the peripheral vestibular system, cerebellum, or basal ganglia.[2] Truncal contrapulsion has been reported in both pontomesencephalic and thalamic lesions.[3] However, truncal contrapulsion in Claude’s syndrome has not been described previously. We report a case of Claude’s syndrome with truncal contrapulsion caused by a mesencephalic infarction. A 34-year-old man with a 2 year history of hypertension presented with sudden onset of drooping of right eyelid with diplopia and falling to the left side. He had vertical diplopia, which was binocular and was more on looking toward the left side. He could stand only by holding onto the side rails of his bed; however, on attempting to stand by releasing his hands, the patient immediately fell to the left side because of instability characterized by marked left -sided pulsion. His blood pressure was 180/80 mmHg at admission and his heart rate was 78 beats/minute. He was alert and fully oriented, with no impairment of higher functions. He showed complete ptosis of the right eye. The right pupil was dilated and sluggishly reactive to light. In the right eye, only abduction was possible with complete impairments of adduction, elevation, and depression. The function of the right trochlear nerve was determined to be abnormal from absent intorsion of the right eye on attempted downward gaze. In the left eye, all movements were normal. Other cranial nerves were found to be normal on examination. He could not stand without support due to leftward falling. Left-sided limb ataxia was present. The muscle tone of the extremities was normal. The muscle strength of the trunk and extremities was normal. The deep tendon reflexes were normal, with no pathological reflexes. Superficial sensation, joint position senses, and vibratory senses were not impaired. The clinical features of right-sided oculomotor and trochlear nerve palsy with left-sided ataxia and truncal contrapulsion to left indicated a diagnosis of Claude’s syndrome. An electrocardiogram and complete blood counts and chemistry did not reveal any abnormal findings. Diffusion MRI revealed an acute infarction in the right medial midbrain [Figures 1-3]. MR angiography was normal. Findings from two-dimensional echocardiography were normal. Hypercoagulabilty work up and antinuclear antibodies were negative. He was started on Aspirin 150 mg, Atorvastatin 40 mg, and other supportive measures including physiotherapy and gait training.Figure 1: Diffusion-weighted MRI—axial cut showing hyperintensity involving right medial midbrainFigure 2: Coronal diffusion-weighted imaging showing hyperintensity involving right paramedian midbrainFigure 3: Coronal ADC images showing low values in the right paramedian midbrainClaude’s syndrome was first described by Henry Claude in 1912 as ipsilateral complete ophthalmoplegia with contralateral ataxia. His patient had a paramedian mesencephalic infarction with involvement of superior cerebellar peduncle, medial half of red nucleus, and medial longitudinal fasciculus and oculomotor nerve fascicles. Later, Claude and Levi Valenci in their modified description included sensory impairment and trochlear nerve involvement. Our patient had features of ipsilateral oculomotor palsy and trochlear palsy and contralateral ataxia, which are classical of Claude’s syndrome. However, our patient had a truncal contrapulsion, which is not described so far in Claude’s syndrome. Truncal lateropulsion is a well-known sign of Wallenberg syndrome.[4,5] Truncal lateropulsion is attributed to lesions in the lateral medulla, flocculonodular lobe,[6] reticular formation,[7] red nucleus of midbrain,[8] cerebellar peduncles, or olivocerebellar fibers at the level of inferior cerebellar peduncle.[9] Pulsion in thalamic lesions is believed to interrupt the projections that run from the ventrolateral nucleus of the thalamus to the medial portion of the precentral gyrus where the trunk and leg are represented. The involvement of the fastigial projections through which the thalamus receives information from the vestibulocerebellum is the presumed mechanism of thalamic pulsion. Contralateral pulsion in mesodiencephalic lesion is due to the disruption of the ascending fibers in the crossed cerebellothalamic tract.[5] It has been reported that the vestibulothalamic, dentatorubrothalamic, and fastigiothalamic fibers join the thalamic fascicle adjacent to the red nucleus and that interruption of any of these fibers can cause lateropulsion.[5] Truncal lateropulsion without limb ataxia reflects an impairment of vestibulospinal postural control caused by a lesion of the descending lateral vestibulospinal tract, whereas body lateropulsion with limb ataxia reflects the consequence of impaired or absent proprioceptive information caused by a lesion of the ascending dorsal spinocerebellar tract. The lateral vestibulospinal tract is considered to play an important role in the maintenance of posture by exerting strong excitatory influences on the extensor muscles and inhibitory influences on the flexor muscles.[10] Thus, interruption of the lateral vestibulospinal tract decreases extensor muscle tone of the trunk and lower limb on the side of the lesion, which is likely to cause ipsilateral axial lateropulsion. Declaration of patient consent The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.
Source: Neurology India
Authors: S Sheetal, P Byju
Institution: Pushpagiri Medical College
Language: English
Subfield: Neurology
Field: Neuroscience
Domain: Life Sciences
Open Access status: hybrid
OpenAlex ID: W4407798828