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Arquivos de Neuro-Psiquiatria

Print version ISSN 0004-282XOn-line version ISSN 1678-4227

Arq. Neuro-Psiquiatr. vol.63 no.4 São Paulo Dec. 2005 

Facial sensory symptoms in medullary infarcts


Sintomas sensitivos na face em infartos medulares



Adriana Bastos ConfortoI; Fábio Iuji YamamotoI; Cláudia da Costa LeiteII; Milberto ScaffI; Suely Kazue Nagahashi MarieI

INeurology Division, Hospital das Clínicas, São Paulo University, São Paulo SP, Brazil (HC/FMUSP)
IIRadiology Department, HC/FMUSP




OBJECTIVE: To investigate the correlation between facial sensory abnormalities and lesional topography in eight patients with lateral medullary infarcts (LMIs).
METHOD: We reviewed eight sequential cases of LMIs admitted to the Neurology Division of Hospital das Clínicas/ São Paulo University between July, 2001 and August, 2002 except for one patient who had admitted in 1996 and was still followed in 2002. All patients were submitted to conventional brain MRI including axial T1-, T2-weighted and Fluid attenuated inversion-recovery (FLAIR) sequences. MRIs were evaluated blindly to clinical features to determine extension of the infarct to presumed topographies of the ventral trigeminothalamic (VTT), lateral spinothalamic, spinal trigeminal tracts and spinal trigeminal nucleus.
RESULTS: Sensory symptoms or signs were ipsilateral to the bulbar infarct in 3 patients, contralateral in 4 and bilateral in 1. In all of our cases with exclusive contralateral facial sensory symptoms, infarcts had medial extensions that included the VTT topography. In cases with exclusive ipsilateral facial sensory abnormalities, infarcts affected lateral and posterior bulbar portions, with slight or no medial extension. The only patient who presented bilateral facial symptoms had an infarct that covered both medial and lateral, in addition to the posterior region of the medulla.
CONLUSION: Our results show a correlation between medial extension of LMIs and presence of contralateral facial sensory symptoms.

Key words: ventral trigeminothalamic tract, spinal trigeminal nucleus, ischemic stroke, Wallenberg syndrome.


OBJETIVO: Investigar a correlação entre alterações de sensibilidade na face e topografia lesional em oito pacientes com infartos bulbares laterais (IBLs).
MÉTODO: Revisamos oito casos seqüenciais de IBLs admitidos na Divisão de Clínica Neurológica do Hospital das Clínicas da Universidade de São Paulo entre julho de 2001 e agosto de 2002, exceto por um caso que havia sido admitido em 1996 e estava sendo seguido em 2002. Todos os pacientes foram submetidos a ressonância magnética de encéfalo, incluindo seqüências pesadas em T1, T2 e FLAIR. As ressonâncias foram avaliadas por investigadores que não tiveram acesso às características clínicas. Avaliaram-se as extensões dos infartos em relação às topografias presumidas dos tratos trigeminotalâmico ventral (TTV), espinotalâmico lateral, trigeminal espinhal e do núcleo trigeminal espinhal.
RESULTADOS: Sintomas ou sinais sensitivos foram ipsilaterais ao infarto bulbar em 3 pacientes, contralaterais em 4 e bilaterais em 1. Em todos os casos de comprometimento exclusivo da sensibilidade da hemiface contralateral, os infartos tiveram extensões mediais que incluíram a topografia do TTV. Em casos de anormalidades sensitivas faciais exclusivamente ipsilaterais, os infartos afetaram as porções lateral e posterior do bulbo, com pouca ou nenhuma extensão medial. O único paciente que apresentou sintomas faciais bilaterais tinha um infarto comprometendo as porções medial e lateral, além da região posterior do bulbo.
CONCLUSÃO: Nossos resultados mostram uma correlação entre extensão medial de IBLs e presença de sintomas sensitivos faciais contralaterais.

Palavras-chave: trato trigeminotalâmico ventral, núcleo trigeminal espinhal, síndrome de Wallenberg.



Wallenberg’s syndrome (WS) is usually caused by infarction of the lateral portion of the medulla, more often caused by vertebral artery (VA) disease1-3. In classical WS, pain and temperature sensation loss on the face is ipsilateral to the lesion in the medulla. However, contralateral and bilateral sensory abnormalities may also occur4-7.

In neuroanatomical descriptions of the brain stem, the descending spinal nucleus/tract (DSN/T) and the ventral ascending tract of the trigeminal nerve or ventral trigeminothalamic tract (VTT) are located in the posterolateral medulla1,4. The VTT is positioned adjacent to the medial lemniscus or medial to the lateral spinothalamic tract (LST) in the dorsomedial corner of the inferior olive (Fig 1)4. DSN/T lesions are associated with decrease in pain and temperature sensation on the ipsilateral face, while injuries to the VTT crossing fibers produce diminished sensation on the contralateral face4,8. Thus, it would be expected that infarcts extending medially and anteriorly in the dorsolateral medulla would cause pain and temperature sensory loss on the contralateral face, opposite to the side of the lesion.



Some studies reported lateral medullary infarcts (LMIs) to be more medially located in patients with contralateral facial pain/temperature sensory loss than in those with ipsilateral facial sensory abnormalities4,9 but others did not confirm these findings8. We have investigated the correlation between facial sensory abnormalities and involvement of the VTT topography in eight patients with medullary infarcts (MIs).



There were 5 men and 3 women ranging in age from 40 to 64 years (one less than 45 years), admitted to the Neurology Division of Hospital das Clínicas/ São Paulo University between July, 2001 and August, 2002 except for one patient who had been admitted in 1996 and was still been followed in 2002. Vascular risk factors were arterial hypertension (n=4), diabetes mellitus (n=2), smoking (n=6) and Chagas’ disease (n=1)10. All of the patients were evaluated by the Neurology Division staff. Side and type of sensory findings on the face, arm and/or leg, as well as other neurological symptoms and signs were reviewed. Investigation included biochemical and serological testing, electrocardiogram, chest radiography, echocardiogram, cervical Doppler ultrasound, cranial computed tomography (CT), magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA). Digital subtraction angiography (DSA) and transcranial Doppler were performed in 4 and 2 patients, respectively. Patients less than 45 years were submitted to exhaustive haematologic, immunologic and cerebrospinal fluid analysis. Criteria of the Lausanne Stroke Registry were used to define presumed causes of infarction11.

All patients were submitted to conventional brain MRI including axial T1-, T2-weighted and Fluid attenuated inversion-recovery (FLAIR) sequences from a 1.5-T MR unit (GE Signa System, General Electric). Diffusion-weighted images (DWI) were performed in 3 patients.

The investigator evaluated MRI lesional topography based on transverse anatomical templates of the medulla oblongata4 (Fig 1, left) was blind to patient history and neurological examination. Two lines were drawn on the transverse MRI section demonstrating the MI. Line 1 divided each hemi-medulla in anterior and posterior regions. Line 2 bisected Line 1, dividing the hemi-medulla in medial and lateral regions. Medullary sections were also classified as rostral (massive bulging of the restiform body), middle (bulging of the inferior olive) and caudal (relatively round shape without bulging of the lateral surface)3.



There were 4 right and 4 left MIs. Characteristics of the 8 cases are shown in the Table. All of the patients had sensory abnormalities: 7 patients had pain and/ or temperature hypesthesia and 4 patients had facial paresthesias. Deep sensation was normal in all of them. Sensory symptoms or signs were ipsilateral to the bulbar infarct in 3 patients (37.5%), contralateral in 4 (50%) and bilateral in 1 (12.5%).



In all of the patients with facial sensory abnormalities ipsilateral to the lesion (Cases 1-3), MIs included lateral and posterior medullary regions. In Cases 1 and 2, infarcts had also slight medial extensions. In all of the patients with contralateral facial symptoms or signs (Cases 4-7), infarcts had greater medial extension than in Cases 1-3 (Fig 2, Table). In Case 8, the patient had bilateral facial symptoms and the lesion also extended medially in the medulla (Fig 1, right).



The middle portion of the medulla was affected in all infarcts. In cases 1, 3 and 8, there was also involvement of the caudal medulla (Fig 2). Two of these patients had exclusive ipsilateral facial symptoms and the other patient, bilateral symptoms. Unilateral cerebellar infarcts, ipsilateral to the bulbar lesion, were present in Cases 2-5 and bilateral infarcts, in Case 8. Glossopharyngeal and vagus nerve involvement was present in 6 of these cases (85.7%); miosis and ptosis occurred in 5 (71.4%); limb and/or gait ataxia were found in 3 (42.8%).

VA atherosclerosis was the presumed mechanism of infarction in all of the 3 patients with ipsilateral facial sensory symptoms. Atherosclerosis was the presumed mechanism in 1 of the patients with contralateral symptoms (Case 4). In the other 4 patients, mechanisms were undetermined but VA or posterior inferior cerebellar artery (PICA) dissections were considered probable candidate stroke mechanisms in 3 patients (Cases 5, 7 and 8).



Our findings suggest that contralateral facial sensory abnormalities are related to medial extension of the infarct and lack of contralateral symptoms, to absence of medial involvement in agreement with other reports4,9. Case 8 presented a truncal sensory level. Such a finding has been previously reported in LMIs4. Case 3 had arm paresthesias ipsilaterally to the LMI. This pattern of sensory abnormality has also been described9.

Based on current neuroanatomical information and meticulous neurological evaluation, Currier and colleagues12 associated sensory symptoms contralateral to the LMI to ventral and dorsoventral syndromes. More than twenty years later, Matsumoto and colleagues4 correlated imaging findings and neurological symptoms, concluding that patients with LMIs and contralateral facial symptoms had lesions more medially located than those with ipsilateral sensory defects. In a patient with bilateral facial symptoms, lesions encopassed both DSN/T and VTT projections. In four patients with medullary infarcts confirmed by MRI, two had ipsilateral , one contralateral and one, bilateral sensory abnormalities. On the other hand, Chia and colleagues did not find an association between LMI location and side of facial sensory abnormalities4,8. They reported 53.8% of ipsilateral and 46,2% of contralateral facial sensory loss in 13 patients. Likewise, in a series of 130 patients with pure LMIs, no significant correlations were found between horizontal patterns of infarction and ipsilateral or contralateral sensory symptoms6. Ipsilateral, contralateral and bilateral facial symptoms or signs were described respectively in 26%, 25% and 8% of the patients. Comparisons were made between 5 groups of lesions. In 3 of these groups ("typical", "large" and "ventral"; n=59) lesions extended medially and therefore, potentially involved the VTT while in the other 2 groups ("lateral" and "dorsal", n=9), VTT topography was spared. Specific comparisons between facial sensory symptoms and infarcts involving or not the VTT topography were not performed. However, if the data from the first 3 groups had been pooled and compared with combined results from the last 2 groups, facial symptoms in lesions potentially encopassing VTT topography would be contralateral or bilateral in 42/59 (71.2%) patients and ipsilateral in 17/59 (28.8%), while in lesions sparing the VTT, contralateral or bilateral symptoms would occur in 1/9 (11.1%) and ipsilateral symptoms, in 8/9 patients (88.9%).

Different criteria for classification of lesional topography may partially explain discrepancies in the literature. However, differences in mechanisms of stroke and anatomical PICA and VA variations may also contribute to conflicting results in different series of patients. The lateral medulla is more often supplied by perforating branches from the VA, and less frequently through the medial PICA branch or the proximal basilar artery3,9,13. It has been suggested that the speed of vascular lesion development as well as collateral blood flow have a major role in defining imaging and clinical characteristics in MIs3. In the present series, VA atherosclerosis was the probable cause in 2 patients with ipsilateral facial involvement and the possible mechanism in the third case. Among 5 cases with contralateral or bilateral sensory loss, VA or PICA dissections were considered likely stroke mechanisms in 3 patients.

Sensory symptoms and signs have been found to be the most common neurological manifestation in LMIs6,14. Our results confirm the correlation between medial extension of the infarct involving VTT topography, and side of facial sensory symptoms, as previously described4. Simultaneous comparisons between side of sensory facial symptoms, topography of medullary lesions and presumed causes of stroke according to complete neurovascular investigation should be performed in a larger series of patients in order to determine whether characteristics of facial sensory symptoms and signs can also be related to LMI mechanisms.



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Received 9 March 2005, received in final form 24 August 2005. Accepted 5 September 2005.



Dra. Adriana Bastos Conforto - Neurology Department / Hospital das Clínicas / São Paulo University - Avenida Dr. Enéas de Carvalho Aguiar 255/5131 - 05409-011 São Paulo SP - Brasil. E-mail:,

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