72ournal ofNeurology, Neurosurgery, and Psychiatry 1995;58:732-734

SHORT REPORT

Volitional type of facial palsy associated withpontine ischaemia

Rudolf T6pper, Christoph Kosinski, Michael Mull

Department ofNeurologyR TopperC KosinskiDepartment ofNeuroradiology,Technical UniversityofAachen, Aachen,GermanyM MullCorrespondence to:Dr Rudolf Topper,Department of Neurology,Pauwelsstrasse 30, 52057Aachen, Germany.Received 15 December 1994Accepted 8 February 1995

AbstractA dissociation between voluntary andemotional facial innervation is describedin a patient with a pure motor stroke dueto a unilateral ischaemic pontine infarc-tion. Voluntary facial innervation of thecontralateral orbicularis oris muscle wasaffected whereas emotionally inducedinnervation of the same muscle wasspared. This report provides evidencethat fibres conveying voluntary and emo-tional commands are still separated inthe pons. Whereas corticobulbar tractscarry the information for voluntary facialinnervation, efferents from the amygdalaand the lateral hypothalamus are candi-dates for the somatomotor aspects ofemotions.

(7 Neurol Neurosurg Psychiatry 1995;58:732-734)

Keywords: volitional facial paresis; pontine ischaemia

In patients with the volitional type of centralfacial palsy facial involvement is most pro-

nounced during voluntary contractionwhereas emotionally triggered contractionsare preserved or at times even exaggerated onthe paretic side.' In the emotional type offacial palsy the opposite phenomenon can beseen: whereas voluntary triggered contrac-tions are normal, there is facial impairmentduring emotionally triggered movements.Automatic voluntary dissociation is notrestricted to muscles supplied by the facialnerve: in the bilateral anterior opercular syn-drome automatic voluntary dissociation isalso seen in masticatory muscles supplied bythe trigeminal nerve, in the tongue, and inmuscles involved in swallowing.2 Whereas thevolitional type of facial palsy is thought to becaused by a lesion in the motor cortex or inthe corticobulbar pathways, lesions in thebasal ganglia, the hypothalamus, or the thala-mus can cause an emotional facial palsy.3 Theprecise neuroanatomical basis of automaticvoluntary dissociation, however, hasremained obscure. It is not clear at what levelabove the facial nucleus fibres conveying voli-tional and emotional information converge.We describe a patient who had an ischaemic

Figure 1 Volitionalfacial paresis when patientwas asked to bare his teeth(A). Symmetric movementwith emotional responses(laughing) (B). ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~.:!.~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~....~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~.732

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Volitional type offacial palsy associated with pontine ischaemia

Figure 2 T2 weightedMRI (SE 3-0 sf90 ms) inaxial (A) and sagittal (B)planes. Hyperintense lesionof the right upper pons isvisible consistent withanteromediallanterolateralpontine infarction. Notethe typical wedge shapedlesion in the sagittal plane(B) that spares the pontinetegmentum.

B

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stroke in the upper pons; he presented with avolitional type of facial paresis indicating thatthe pathways subserving volitional and emo-tional input on to the facial nucleus are stillanatomically separated in the upper pons.

Case reportA 57 year old man was admitted to the neu-rology department because of a central pare-sis of his left arm and leg with sudden onset.His medical history was unremarkable. Therewas no trauma preceding the episode. Onneurological examination the patient was alertand oriented. He had a facial paresis with rel-ative sparing of the upper portion of the face.When asked to bare his teeth there wasdrooping of the angle of the left side of hismouth (fig 1A). On involuntary contraction,however, there was symmetric innervation ofthe muscles of the mouth (fig 1 B). Theremainder of the cranial nerve examinationwas unremarkable; specifically there was nodisturbance of oculomotor function. He had a3/5 paresis of the left arm and leg withreflexes being more pronounced on the left.Babinski's sign was positive on the left, nega-tive on the right side. Cerebellar and sensoryfunction were normal.A brain CT obtained eight hours after the

onset of symptoms showed no brainstemlesion. Fourteen days after the event MRIshowed a large hyperintense lesion of theright upper pons on T2 weighted images (fig2A and B). This lesion respected the midline,had contact with the ventral circumference,and spared the lateral pontine border and thepontine tegmentum.

Extracranial and transcranial Dopplersonography showed no evidence of stenosis ordissection of extracranial or accessible cranialarteries. Transthoracic and transoesophagealechocardiography was also unremarkable.A diagnosis of an anteromedial/anterolat-

eral ischaemic pontine infarction with voli-tional facial paresis was made.

DiscussionA dissociation of volitional and emotionalfacial nerves was found in this patient with aunilateral pure motor stroke due to ischaemiain the pons. This finding may provide newinformation on the neuroanatomical organisa-tion of facial innervation. Voluntary motorimpulses from the motor cortex descendthrough the internal capsule and either makedirect connections with the facial nucleusor terminate in the pontine reticularformation.45 The pathway by which emo-tional commands reach the facial nucleus isnot clear in humans. Information from theamygdala and the lateral hypothalamus,which are thought to be involved in the gen-eration of emotions, reach the brainstem viathe medial forebrain bundle and the dorsallongitudinal fasciculus.6 Unlike corticobulbartracts the amygdala and the lateral hypothala-mus do not have direct projections to themotor nuclei of the facial nerve but sendaxons to the lateral tegmentum whereintemeurons for the facial nerve are located.7These polysynaptic pathways are consideredto form an anatomical basis for somatomotorcomponents of affective behaviour48 and aretherefore likely candidates for conveyingemotional responses to the facial nucleus.That a lesion of these tracts to the lateraltegmentum may cause an emotional facialparesis has already been postulated byWilson.9 The dissociation in our patient can,therefore, be explained by a pyramidal tractlesion in the upper pons that disrupts thecorticobulbar fibres to the facial nucleuswhereas efferents from the amygdala and thelateral hypothalamus to the lateral tegmentalarea are spared. Because emotional facialresponses such as laughter and crying involvestereotyped bilateral innervation of facialmuscles'0 it can be argued that the efferents

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Topper, Kosinski, Mull

from the amygdala and the hypothalamus areorganised bilaterally. In our patient onecould, therefore, postulate that emotionalinformation reached the facial nucleus via theundamaged ipsilateral fibres. This hypothesisis, however, contradicted by the overwhelm-ing majority of patients with hemisphericlesions of descending motor tracts in whomthere is both a volitional and an emotionalfacial palsy. The voluntary and emotionaltype of innervation of the facial nucleus there-fore seems to follow a common pattern withbilateral projections to the muscles of theupper two thirds of the face and unilateralprojection to the lower third.

We thank Professor Noth and Professor Poeck for criticalreading of the manuscript.

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2 Weller M. Anterior opercular cortex lesions cause dissoci-ated lower cranial nerve palsies and anarthria but noaphasia: Foix-Chavany-Marie syndrome and "automaticvoluntary dissociation" revisited. Neurol 1993;240:119-208.

3 Hopf HC, Miiller-Forell W, Hopf NJ. Localization ofemotional and volitional facial paresis. Neurology1992;42:1918-23.

4 Brodal A. Neurological anatomy in relation to clinical medi-cine. 3rd ed. New York: Oxford University Press,1981:660-3.

5 Holstege G, Kuypers HGJM. Propriobulbar fibre connec-tions to the trigeminal, facial, and hypoglossal motornuclei. I. An anterograde degeneration study in the cat.Brain 1977;100:239-64.

6 Nieuwenhuys R, Voogd J, van Huijzen C. The humancentral nervous system. New York: Springer, 1988:293-364.

7 Holstege G. Subcortical limbic systems projections. In:Paxinos G, ed. The human nervous system. San Diego:Academic Press, 1990:261-86.

8 Crosby EC, Dejonge BR. Experimental and clinical stud-ies of the central connections and central relations of thefacial nerve. Ann Otol Rhinol Laryngol 1963;72:735-55.

9 Wilson SAK. Some problems in neurology. No II: patho-logical laughing and crying. J3ournal of Neurology andPsychopathology 1924;16:299-333.

10 Poeck K. Pathological laughter and crying. In: Vinken PJ,Bruyn GW, Klawans HL, eds. Handbook of clinicalneurology. Vol 45. Amsterdam: Elsevier, 1985:219-25.

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