(Stroke. 1997;28:1761-1764.)
© 1997 American Heart Association, Inc.
Articles |
Pure or Predominant Sensory Stroke Due to Brain Stem Lesion
From the Department of Neurology, University of Ulsan, Asan Medical Center, Seoul, South Korea.
Correspondence to Jong S. Kim, MD, Department of Neurology, Asan Medical Center, Song-Pa PO Box 145, Seoul 138-600, South Korea.
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Abstract |
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Background and Purpose Pure or predominant hemisensory symptoms can be seen in patients with brain stem stroke. However, there have been no reports in which sufficient numbers of patients were studied with detailed descriptions on the sensory patterns and imaging findings.
Methods We describe 17 patients presenting with pure or predominant hemisensory symptoms due to brain stem stroke in whom CT scan and/or MRI identified appropriate lesions.
Results Eleven patients had an infarct and 6 had a hemorrhage. Aside from sensory deficit, the majority had dizziness and gait ataxia. Fifteen patients had paramedian dorsal pontine lesions associated with pure or predominant lemniscal sensory involvement, often in the cheiro-oral (n=4) or leg dominance (n=4) patterns. The lesions of the former group tended to be located more medially compared with those of other patients, which is in agreement with the sensory topography of the pontine lemniscal sensory tract. Bilateral facial or perioral sensory symptoms were noted in 6 patients. One patient with a dorsolateral pontine lesion had selective spinothalamic modality impairment, while one with a lateral midbrain infarct had sensory deficit of all modalities.
Conclusions Pure or predominant brain stem sensory stroke is most often produced by small infarcts or hemorrhages in the paramedian dorsal pontine area and may be differentiated from thalamic pure sensory stroke by the following characteristics: frequent association of dizziness/gait ataxia, predominant lemniscal sensory symptoms, occasional leg dominance or cheiro-oral pattern, and frequent bilateral perioral involvement.
Key Words: brain stem • cerebrovascular disorders • pons • sensory stroke
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Introduction |
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Pure sensory stroke (PSS) is defined when there are predominantly hemisensory symptoms without other major neurological signs.1 2 3 Although PSS is most commonly caused by lesions affecting the thalamus, it can also be produced by small strokes occurring in nonthalamic regions, including the pons, internal capsule/corona radiata, and cortico-subcortical area.4
However, despite the presence of sporadic case reports of PSS due to brain stem stroke,5 6 7 8 9 10 11 12 13 the clinical and radiological characteristics of brain stem PSS have not yet been sufficiently studied. In this article we describe 17 patients with brain stem stroke who presented with pure or predominantly hemisensory symptoms and correlate the clinical pattern with radiological findings.
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Subjects and Methods |
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At Asan Medical Center, we examined 17 patients who presented with pure or predominantly hemisensory symptoms due to brain stem stroke between August 1990 and August 1996. All but 2 patients were examined by one of us (J.S.K.) within 7 days after the onset. Some patients who additionally exhibited gait ataxia and clumsiness of the affected limbs (or a sense of weakness) were included in our study because these neurological deficits may be at least partly attributed to the patients' sensory impairment. Patients with minor ophthalmic signs (transient nystagmus or internuclear ophthalmoplegia) were also included, but those with hemiparesis of IV/V or worse were excluded. Isolated trigeminal sensory deficit due to brain stem lesions14 15 16 17 18 was not considered in the present study. All patients underwent CT scan (n=8) and/or magnetic resonance imaging (MRI) (n=14), which showed lesions considered appropriate to the clinical findings.
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Results |
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The clinical features of the patients are summarized in the Table
.
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Demographic Features and Risk Factors
There were 17 patients (13 men and 4 women) ranging in age from 52
to 71 (mean, 61) years. Eleven patients had small infarcts, and 6 had
hemorrhages. Risk factors for vascular disease included
hypertension in 14, diabetes mellitus in 4, current cigarette smoking
in 6, habitual alcohol drinking in 3, and
hypercholesterolemia in 5. None had emboligenic
cardiac disease.
General Clinical Features
In 3 patients, sensory symptoms were the only manifestation of
stroke, whereas minor nonsensory symptoms and signs were present in
the others: dizziness in 14 patients (2 of whom had transient whirling
vertigo), gait ataxia in 12, mild limb ataxia in 4, transient fine
horizontal nystagmus in 4, transient internuclear ophthalmoplegia in 1,
and mild dysarthria in 5.
Sensory Patterns and Topography
Paresthesia (numbness or tingling sensation), the initial and main
complaint in all patients, usually started at a part of the body (hand
or foot) and then spread to other parts. Objective sensation remained
intact in 5 patients. In 2 (patients 7 and 15), however, who were
examined more than 1 week after onset, the initial absence of objective
sensory deficit was not unequivocal. Objective sensory impairment, when
present, was always mild to moderate in degree. In 7 patients,
lemniscal sensation (vibration and/or position) was selectively
impaired, whereas 1 (patient 8) showed a selective deficit of
spinothalamic sensation (pinprick and temperature). In
3 patients (patients 5, 16, and 17), both modalities were impaired, but
lemniscal sensory deficit was dominant in patients 5 and 17.
The patients' sensory topography is summarized in the Table
. Four
(patients 1 through 4) had sensory symptoms limited to perioral (or
facial)-hand area (cheiro-oral syndrome), and 1 (patient 5) had sensory
symptoms limited to the contralateral hand. Others (12 patients) had
hemisensory symptoms, including arm, leg, trunk, and face;
sensory deficit was predominant in the leg (as compared with the arm
and face) in 4 (patients 6 through 9). Overall, 6 (patients 1 through 3
and 11 through 13) had sensory symptoms on the bilateral perioral or
facial area.
Radiological Localization and Clinical-Radiological
Correlation
Imaging findings are shown in Fig 1, and the largest lesion diameter (in millimeters) is recorded in the
Table. Lesions detected by MRI are presented when both CT and
MRI were performed. Fifteen patients had paramedian dorsal pontine
lesions, 1 (patient 8) had a relatively large infarct in the
dorsolateral pons, and 1 (patient 17) had an infarct in the lateral
midbrain. Four (patients 3, 8, 11, and 12) had relatively large lesions
(longest diameter of >10 mm), and others had small lesions
(Table).
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To make a clinical-radiological correlation we measured the distance
(in millimeters) between the center of the 4th ventricle and that of
the lesion (Fig 2C) in patients with
paramedian dorsal pontine small lesions (n=13; Table). The measurement
was performed by one of the authors (Y.H.B.), who was blinded to the
sensory topography of the patients. The median distance was 5.0 mm
in patients with cheiro-oral syndrome or restricted symptoms of the
hand (patients 1, 2, 4, and 5) and 5.9 mm in others. Statistical
analysis was not carried out because of the small number of
cases in each group.
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One patient underwent conventional angiography, and 6 had MR angiography. The results were all within normal limits, except for 2: patient 17, with a lateral midbrain lesion, showed a tight stenosis in the midbasilar level, and patient 16 showed diffuse atherosclerotic changes without significant focal stenosis in the basilar artery. ECG findings were all negative, and transthoracic and transesophageal echocardiography performed in 3 patients showed normal results.
Follow-up Findings
Two patients (patients 8 and 9) were not followed up after
discharge. Follow-up periods of other patients ranged from 1 to 18
months. In all patients, the nonsensory neurological manifestations
resolved within a few days or weeks, but the sensory symptoms remained
longer. Sensory symptoms completely or almost completely resolved in 5
patients but improved only partially in others, who usually had
persistent paresthesia in the acral body parts (Table 1). In 2
(patients 14 and 15) the paresthesia worsened, became painful, and was
often exacerbated by cold weather or fatigue, mimicking the so-called
"thalamic pain syndrome."
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Discussion |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Our 17 patients presented with prominent hemisensory symptoms without other major neurological deficits. The most frequent minor nonsensory symptoms and signs were dizziness and gait ataxia. Rarely present were transient whirling vertigo and nystagmus, possibly caused by involvement of the medial longitudinal fasciculus and related structures. The patients' frequent gait ataxia and occasional limb ataxia could have been produced by an involvement of the pontocerebellar fibers, but might also have been caused by proprioceptive sensory deficit. Mild dysarthria can also be caused by involvement of the pontocerebellar fibers but could possibly be attributed to involvement of the corticobulbar fibers that were reported to be preferentially located in the dorsomedial part of the corticospinal tract.19 However, these nonsensory symptoms and signs were mild and of short duration, whereas the hemisensory symptom remained a predominant clinical manifestation in all the patients.
All our patients presented with paresthesia, a sign suggestive of involvement of the lemniscal sensory pathway.20 The early-onset paresthesia, along with dominant or selective lemniscal sensory deficit, strongly suggests that the involvement of the medial lemniscus in the paramedian dorsal pontine region is the main mechanism of sensory symptoms in our series. Imaging findings were also consistent with this.
Although reported previously,4 21 pure lemniscal sensory
deficit is quite uncommon in thalamic lesions.4 This is
probably due to the fact that while the lemniscal sensory tract tends
to converge onto a limited part of the ventral posterior nuclei of the
thalamus, spinothalamic fibers are widely projected
to various thalamic nuclei, including the posterior nuclei, the
intralaminar nuclei, and the ventral posterior nuclei,22
and are thus more vulnerable to a pathological lesion. However, in the
pons, the medial lemniscus is located in the dorsal tegmentum in the
medial-lateral direction, whereas the spinothalamic
tract is compactly localized in the lateral-posterior side of the
medial lemniscus22 23 (Fig 2). The preferential
involvement of the paramedian pontine area by small infarcts and
hemorrhages24 may explain the frequent involvement
of the lemniscal sensory system in our series. Considering the location
of the lesion, the results of the vascular studies, and risk factor
profiles, hypertensive small-vessel changes are the likely pathogenesis
of the stroke in our patients with paramedian dorsal pontine lesions.
The paucity of other neurological signs in patients with relatively
large lesions (patients 3, 8, 11, and 12) remains unexplained.
Of particular interest in our study was occasional leg-dominance or cheiro-oral sensory pattern. These topographies may be related to relatively laterally or medially located lesions, respectively, because sensory projection from the face, arm, and leg has been shown to be arranged from a medial to a lateral direction in the pontine trigeminal-lemniscal tract.22 23 Consistent with this topography, our study illustrated that lesions producing a cheiro-oral sensory pattern tended to be located more medially than other lesions.
Also noteworthy was the frequent bilateral trigeminal (or perioral)
involvement in our patients. The explanation for this phenomenon would
be that the ascending trigeminal secondary fibers are located in the
most medial portion of the medial lemniscus and therefore may easily be
involved bilaterally by paramedian lesions25 26 (Fig 2).
However, involvement of the as yet ill-defined paramedian brain stem
pathways that subserve bilateral midline facial sensation may also be
responsible.27 28
Finally, we have found a patient with a somewhat laterally situated pontine lesion (Patient 8) presenting with isolated sensory deficit of spinothalamic modality. We also observed 1 patient (patient 17) with midbrain infarction that produced PSS, presumably due to artery-to-artery embolism. The results of imaging in this patient were again consistent with the location of sensory tracts laterally in the midbrain. Although midbrain stroke as a cause of PSS has been reported in the literature, our study illustrated that lateral pontine or lateral midbrain stroke should be considered a rare cause of PSS and may have a pathogenetic mechanism different from that of dorsal pontine PSS. Although the prognosis was generally excellent in our series, 2 patients developed uncomfortable and often painful paresthesia in the affected area. This sensory sequela was not differentiated from the so-called thalamic syndrome of Dejerine-Roussy, which reinforces a previous notion that the term "thalamic" is a misnomer.29
In summary, brain stem pure or predominant sensory stroke is usually caused by a paramedian dorsal pontine lesion. It may be differentiated from thalamic PSS by its frequent association with dizziness/gait ataxia, dominant lemniscal sensory modality impairment, occasional cheiro-oral or leg dominance sensory patterns, and frequent bilateral perioral sensory involvement.
Received May 1, 1997; revision received June 10, 1997; accepted June 10, 1997.
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