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 »  Introduction
 »  Case report
 »  Results
 »  Discussion
 »  References

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Year : 2002  |  Volume : 50  |  Issue : 1  |  Page : 102-4

A case of emotional facial palsy with ipsilateral anterior inferior cerebellar artery territory infarction.

Department of Neurology, Postgraduate Institute of Medical Education and Research, Chandigarth, India.

Correspondence Address:
Department of Neurology, Postgraduate Institute of Medical Education and Research, Chandigarth, India.
[email protected]

  »  Abstract

Emotional facial palsy (EFP) commonly results from anterolateral thalamic or striatocapsular infarcts. Its occurrence in brainstem lesions is uncommon, with previously reported cases being restricted to superior cerebellar artery infarction (3 cases). We report an unusual case of EFP ipsilateral to an anterior inferior cerebellar artery infarction, which opens new insights into the facial corticobulbar tract pathway.

How to cite this article:
Khurana D, Sreekanth V R, Prabhakar S. A case of emotional facial palsy with ipsilateral anterior inferior cerebellar artery territory infarction. Neurol India 2002;50:102

How to cite this URL:
Khurana D, Sreekanth V R, Prabhakar S. A case of emotional facial palsy with ipsilateral anterior inferior cerebellar artery territory infarction. Neurol India [serial online] 2002 [cited 2021 Jan 18];50:102. Available from:

   »   Introduction Top

Emotional facial palsy (EFP) refers to weakness of facial movements during emotions like smiling or weeping, while voluntary movements do not show any deficit. EFP has been described in association with lesions in the contralateral supplementary motor area,[1] striatocapsular region, thalamlus and subthalamus, Parkinson's plus syndrome and postencephalitic parkinsonism.[2],[3],[4],[5] EFP associated with pontine infarction is rare in occurrence. Three patients with EFP in association with superior cerebellar artery (SCA) infarction have been previously reported.[6] We report a case of EFP in association with anterior inferior cerbellar artery infarction - an entity not previously described.

   »   Case report Top

A 20 year old male presented with recurrent episodes of vomiting, dizziness, along with nasal regurgitation of fluids and slurring of speech. Examination revealed ocular dipping, right sided emotional facial palsy [Figure 1a] and [Figure 1b], right palatal weakness, an extensor plantar on the left side, ataxic gait, scanning speech, with dysdiadochokinesis, intention tremor and dysmetria on the right upper limb. Cranial MRI, showed an infarct in the right cerebellum and right lower dorsal pons suggestive of right anterior inferior cerebellar artery infarction [Figure - 2].

   »   Discussion Top

EFP has been characteristically associated with anterolateral thalamic infarction (tuberothalamic artery ischemia),[7],[8] although lesions of posterior thalamus and frontal lobe with sparing of the anterolateral thalamus have been described.[2] The occurrence of EFP in the latter cases has been linked to the interruption of the connections between the thalamus and the frontal or mesial temporal lobes.[2],[5] These anterior fronto-thalamo-pontine connections descend in the anterior limb of the internal capsule. EFP in association with subthalamic and dorsal midbrain tumors has been attributed to the involvement of a small fibre bundle within the dorsal midbrain tegmentum.[5],[9] The occurrence of EFP in pontine lesions has been linked to dorsolateral pontine tegmentum infarction, conforming to the superior cerebellar artery territory.[6] The uniformity with which EFP precludes classic vascular midbrain lesions like Benedikt's or Weber's syndrome as well as rostral pontine lesions is possibly linked to the ventral location of these lesions.[2],[10]
Classically, a lesion rostral to the upper mid pons results in a contralateral supranuclear facial paresis, while ipsilateral facial paresis of the infranuclear type results from lesions of inferolateral pons.[11],[12] The occurrence of a supranuclear facial paresis in a lesion of the lower pons, as in our case, needs to be reckoned with. It has been hypothesized that the facial corticobulbar tract fibres may dissociate from the pyramidal tracts at the pontomedullary junction and descend caudally to atleast the middle medullary levels, before most of them cross to the opposite facial nucleus.[13] The occurrence of a contralateral supranuclear facial paresis commonly results from the involvement of these descending pathways rather than the ascending pathways. Terao et al postulated that the facial CBT descend upto the upper medullary level and determined that supranucelar facial palsy was more common in lesions of lower pons and upper medulla than middle or lower medullary lesions.[14] The facial CBT can thereby be considered to be constituted by looping fibres which decussate in the upper medulla. The occurrence of an ipsilateral EFP in our case, however, may be representative of the involvement of the ascending pathways. It has been deemed that the corticofacial fibres course down the mediodorsal portion of the base of pons and the volitional and emotional fibres possibly converge below the middle one-third of the pons.[15] If the explanation of the
ipsilateral EFP in our case holds good, it would imply that the fibres for the emotional and volitional control follow a distinct course even after their decussation. This case offers further insight into the course of the central pathways of the facial cortico-bulbar tracts.


  »   References Top

1.Gelmers HJ : Non-paralytic motor disturbance and speech disorders : the role of supplementary motor area. J Neurol Neurosurg Psychiatry 1983; 46 : 1052-1054.   Back to cited text no. 1    
2.Hopf HC, Muller-forell W, Hopf NJ : Localization of emotional and volitional facial paresis. Neurology 1992; 42 : 1918-1923.   Back to cited text no. 2    
3.Bogousslavsky J, Regli F, Uske A : Thalamic infarcts : Clinical syndromes, etiology and prognosis. Neurology 1988; 38 : 837-848.   Back to cited text no. 3    
4.Trosch RM, Sze G, Brass LM et al : Emotional facial paresis with striatocapsular infarction. J Neurol Sci 1990; 98 : 195-201.   Back to cited text no. 4    
5.Wilson SAK : Some problems in neurology. II. Pathological laughing and crying. J Neurol Psychopathol 1924; 4 : 299-333.   Back to cited text no. 5    
6.Hopf HC, Fitzek C, Marx J et al : Emotional facial paresis of pontine origin. Neurology 2000; 1217.   Back to cited text no. 6    
7.Bogousslavsky J, Regli F, Assal G : The syndrome of unilateral tuberothalamic artery territory infarction. Stroke 1988; 17 : 434-441.   Back to cited text no. 7    
8.Graff-Radford NR, Eslinger PJ, Damasio H et al : Nonhemorrhagic thalamic infarction : Clinical, neurophysiological and electrophysiological findings in four anatomical groups defined by computerized tomography. Brain 1985; 108 : 485-516.   Back to cited text no. 8    
9.Nothnagel H : Zin Diagnose der Sehhugelerkrankugen. Z Klin Med 1989; 24 : 424-430.   Back to cited text no. 9    
10.Hopf HC, Tettenborn B, Krainer G : Pontine supranuclear facial palsy. Stroke 1990; 21 : 1754-1757.   Back to cited text no. 10    
11.Kuypers HGJM : Corticobulbar connections to the pons and lower brain stem in man. An anatomical study. Brain 1958;81 : 364-88.   Back to cited text no. 11    
12.Tenny AB, Saper CB : Organization of the facial projection in the monkey : A reconsideration of the upper motor neuron facial palsy. Neurology 1987; 37 : 930-939.   Back to cited text no. 12    
13.Currier RD: The medial medullary syndrome. J Univ Mich Med Cent 1976; 42 : 96-104.   Back to cited text no. 13    
14.Terao S, Miura N, Takeda A et al : Course and distribution of facial corticobulbar tract fibres in the lower brain stem. J Neurol Neurosurg Psychiatary 2000; 69 : 262-265.   Back to cited text no. 14    
15.Urban PP, Wicht S, Marx J et al : Isolated voluntary facial paresis due to pontine ischemia. Neurology 1998; 50 : 1859-1862.   Back to cited text no. 15    


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