(Stroke. 1997;28:649-651.)
© 1997 American Heart Association, Inc.
Articles |
Isolated Pontine Infarctions With Prominent Ipsilateral Midfacial Sensory Signs
From the Servicio de Neurología, Hospital Ramón y Cajal, Madrid, Spain.
Correspondence to Jaime Masjuan, Servicio de Neurología, Hospital Ramón y Cajal, Crta de Colmenar Viejo km 9.101, 28034 Madrid, Spain.
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Abstract |
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Background Pontine infarctions may produce combined motor, sensory, cerebellar, and cranial nerve dysfunction. Midline sensory complaints and facial pain are uncommon.
Case Descriptions Three patients are described with hypoesthesia and numbness of the midline facial area associated with dysarthria and contralateral hemiparesis due to pontine strokes. MRI demonstrated isolated ipsilateral ischemic infarctions of the ventral pons.
Conclusions Pontine infarctions can produce diverse sensory features. Ipsilateral midfacial sensory defect has been rarely reported. The clinicoanatomic basis for the ipsilateral midfacial sensory defect described is unknown. Involvement of the dorsal trigeminothalamic tract or fiber tracts related to central regions of the face, located in the medial part of the midbrain, could help to explain these data. The symptoms could be due to direct damage or to edema resulting from the infarct. In some patients, midfacial sensory complaints, particularly of the ala nasi, could be an early sign of major pontine deficits and may be important to determine appropriate treatment.
Key Words: brain stem infarction • pons • sensory stroke • vertebrobasilar stroke
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Introduction |
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Diverse clinical syndromes related to pontine infarctions have been reported since the last century, when the classic pontine syndromes of Millard-Gubler and Foville were described.1 The development of MRI studies has contributed to establish good clinicoanatomic correlations and to discover new clinical features. Combined motor, sensory, cerebellar, and cranial nerve dysfunction is a common feature of pontine strokes. Several sensory complaints have been reported. Facial pain near the eye or limited to isolated spots on the forehead, nose, or cheek is not a common symptom of pontine lesions and when typical is virtually diagnostic of lateral medullary ischemia.2 We identified three patients with unilateral acute pontine infarctions who developed a peculiar sensory defect characterized by hypoesthesia and numbness of the ipsilateral midfacial area, particularly of the ala of the nose (Fig 1
).
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Case Reports |
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Case 1
A hypertensive 67-year-old man had a sudden onset of dysarthria, dysgeusia, right hemiparesis, and numbness of the left part of his nose. Examination 3 hours later disclosed a blood pressure of 180/100 mm Hg, a regular pulse, dysarthria, bilateral reactive miosis, fragmentation of smooth pursuit movements, and horizontal nystagmus. The subject had a right hemiparesis sparing the face and right Babinski sign. Marked decreased perception of pinprick was noted in the left cheek, left ala of the nose, and right arm and leg. No dysmetrias were found. Laboratory studies, electrocardiogram, chest roentgenography, and duplex ultrasound of the extracranial carotid and vertebral arteries were normal. MRI disclosed lacunar infarcts in the cerebral hemispheres and an ischemic infarct in the left pons (Fig 2
). The sensory defect resolved in a few days. Eight
months later, mild right hemiparesis and dysarthria persisted.
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Case 2
A hypertensive 75-year-old man suddenly developed numbness in the
right frontonasal region, which lasted a few hours. He was hospitalized
15 days later when he suddenly felt dizzy followed by nausea,
dysarthria, and left hemiparesis. Examination shortly after disclosed
that his blood pressure was 110/60 mm Hg and his pulse was regular. He
was alert but dysarthric. There were no ocular abnormalities except
miotic reactive pupils. He had a left flaccid hemiplegia sparing the
face. Perception of pinprick was diminished in the midfacial right
region, particularly in the ala of the nose. No other sensory defects
were noted. Laboratory studies, electrocardiogram, chest
roentgenography, and duplex ultrasound of the extracranial carotid and
vertebral arteries were normal. MRI showed a right ventral pons
infarction and another small infarction near the tegmental area (Fig 3). The sensory defect had disappeared by the end of the
first week. Six months later a mild left hemiparesis persisted.
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Case 3
A hypertensive 68-year-old man suffered four consecutive episodes
of throbbing pain in the ala of the nose and upper lip. Each episode
lasted 15 minutes. The last episode was immediately followed by
dysarthria and right hemiparesis. Two hours later, the examination
disclosed a blood pressure of 160/90 mm Hg and a regular pulse. The
subject's speech was dysarthric, and he had right hemiparesis sparing
the face. Pinprick sensation was diminished in the left ala of the nose
and upper lip. No other sensory defects were noted. Laboratory studies,
electrocardiogram, chest roentgenography, and duplex ultrasound of the
extracranial carotid and vertebral arteries were normal. MRI disclosed
a left pons infarction in the paramedian penetrating arteries
territory, with probable extension to the tegmental area (Fig 4). The sensory defect lasted 3 days. One year later,
right hyperreflexia was the only finding on examination.
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Discussion |
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We have described three patients with a curious sensory complaint characterized by numbness and hypoesthesia of the midline facial area due to an ischemic lesion in the ipsilateral pons. In two subjects numbness was subjectively noted, and the other subject had several episodes of throbbing pain in the ala nasi. Other common clinical features were dysarthria and contralateral hemiparesis sparing the face. No explanation was found for the latter.
Isolated pontine infarctions are not unusual and cause diverse sensory complaints.3 Pontine lacunes4 or hemorrhages5 6 can produce pure sensory strokes or manifest themselves as trigeminal neuropathy.7 8 9 10 Helgason and Wilbur11 described 10 patients with acute pontine infarction and specific sensory findings. Kim12 reported eight cases of pontine strokes with diverse patterns of restricted acral sensory syndrome. However, sensory complaints in the midline facial area are very uncommon clinical patterns, since to our knowledge only Reutens13 has described a patient with burning oral and midfacial pain as an early sign of the locked-in syndrome due to a pontine ventral infarction.
Pain or dysesthesias are uncommon in acute brain ischemia with the exception of the lateral medullary syndrome, which frequently produces pain in the ipsilateral eye or face at the onset of the stroke. This is probably related to involvement of sensory neurons in the nucleus of the descending tract of the trigeminal nerve.14 Paramedian ischemic lesions of the pons may cause sensory alterations in the face. Caplan and Gorelick15 described three patients with a curious variety of facial pain ("salt and pepper on the face") as a prominent and acute symptom. They attributed it to ischemia of medial structures of the brain stem. No anatomic documentation was available.
The clinicoanatomic basis for the temporary ipsilateral midfacial sensory defect is unknown. Lesions above the pontine level can produce bilateral midfacial sensory symptoms, as Kim16 has reported recently. In the patients we have described, MRI disclosed supratentorial lesions only in case 1; the rest of the clinical and MRI findings make this explanation unlikely. The contralateral sensory deficit of the arm and leg in case 1 may be due to dysfunction of the medial lemniscus, but this does not explain the facial sensory complaint. The ischemic lesions we described were located in the rostral part of the ventral pons, without involvement of the dorsolateral structures (trigeminal principal nucleus or spinotrigeminal tract).The tegmental area could be affected in cases 2 and 3. Midfacial symptoms may be mediated by fiber tracts related to central regions of the face, particularly the oral and nasal areas, which are located in the medial part of the midbrain, near the aqueduct.17 Alternatively, ipsilateral facial symptoms could be due to the involvement of uncrossed fibers of the dorsal trigeminothalamic tract, although these fibers usually convey sensations from the mandibular division.18 However, the tegmental area in case 1 was not affected, which makes these explanations unlikely in this case.
The symptoms could be due to direct damage or to edema resulting from the infarct. Although the latter could explain the resolution of the sensory complaints in a few days, in two of the patients the sensory alteration preceded the definite stroke. This fact, associated with the reports of Caplan and Gorelick15 and Reutens,13 in which facial complaints occurred before major pontine infarctions, indicates that in some patients midfacial sensory features can be an early sign of major pontine deficits. This may be important to recognize to determine appropriate treatment. Little is known about the somatotopic organization of these sensitive tracts. This report may contribute to the knowledge of their anatomic and somatotopic distribution.
Received September 23, 1996; revision received November 12, 1996; accepted November 21, 1996.
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