This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kim, J. S. Articles by Bae, Y. H. Search for Related Content PubMed PubMed Citation Articles by Kim, J. S. Articles by Bae, Y. H.

(Stroke. 1997;28:1761-1764.)
© 1997 American Heart Association, Inc.

Articles

Pure or Predominant Sensory Stroke Due to Brain Stem Lesion

Jong S. Kim, MD; Yeong H. Bae, MD

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.

	Abstract

Top Abstract Introduction Subjects and Methods Results Discussion References

 
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

	Introduction

Top Abstract Introduction Subjects and Methods Results Discussion References

 
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.

	Subjects and Methods

Top Abstract Introduction Subjects and Methods Results Discussion References

 

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 lesions^{14 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.

	Results

Top Abstract Introduction Subjects and Methods Results Discussion References

 
The clinical features of the patients are summarized in the Table.

View this table: [in this window] [in a new window]   Table 1. Clinical Features of the 17 Study Patients

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).

View larger version (93K): [in this window] [in a new window]   Figure 1. Imaging results in the patients. Number on each indicates patient number. Numbers 1, 3, and 12, CT scan; 5 and 6, T1-weighted MRI; others, T2-weighted MRI.

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.

View larger version (17K): [in this window] [in a new window]   Figure 2. Important structures and schematic drawing of the lesion. A=lesion producing leg dominance pattern, B=lesion producing bilateral perioral-hand pattern, and C=distance between center of the 4th ventricle and lesion.

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."

	Discussion

Top Abstract Introduction Subjects and Methods Results Discussion References

 
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 lemniscus^{22 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 lesions^{25 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.

	References

Top Abstract Introduction Subjects and Methods Results Discussion References

 

1. Fisher CM. Pure sensory stroke involving face, arm and leg. Neurology.. 1965;15:76-80.
2. Fisher CM. Thalamic pure sensory stroke: a pathological study. Neurology.. 1978;28:1141-1144.[Abstract/Free Full Text]
3. Fisher CM. Pure sensory stroke and allied conditions. Stroke.. 1982;13:434-447.[Abstract/Free Full Text]
4. Kim JS. Pure sensory stroke: clinical-radiological correlates of 21 cases. Stroke.. 1992;23:983-987.[Abstract/Free Full Text]
5. Tuttle PV, Reinmuth OM. Midbrain hemorrhage producing pure sensory stroke. Arch Neurol.. 1984;41:794-795.[Medline] [Order article via Infotrieve]
6. Ono S, Inoue K. Cheiro-oral syndrome following midbrain haemorrhage. J Neurol.. 1985;232:304-306.[Medline] [Order article via Infotrieve]
7. Araga S, Fukada M, Kagimoto H, Takahashi K. Pure sensory stroke due to pontine hemorrhage. J Neurol.. 1987;235:116-117.[Medline] [Order article via Infotrieve]
8. Azouvi PH, Tougerron A, Hussonois C, Schouman-Claeys E, Bussel B, Held JP. Pure sensory stroke due to midbrain haemorrhage limited to the spinothalamic pathway. J Neurol Neurosurg Psychiatry.. 1989;52:1427-1428.[Abstract]
9. Hommel M, Besson G, Pollak P, Borgel F, Le Bas JF, Perret J. Pure sensory stroke due to pontine lacune. Stroke.. 1989;20:406-408.[Abstract/Free Full Text]
10. Iwasaki Y, Kinoshita M, Ikeda K, Takayama K, Shiojima T. Pure sensory stroke and cheiro-oral syndrome. J Neurol.. 1989;236:186-187.[Medline] [Order article via Infotrieve]
11. Alvarezc-Sabin J, Montalban J, Tintore M, Codina A. Pure sensory stroke due to midbrain hemorrhage. J Neurol Neurosurg Psychiatry.. 1991;54:843. Letter.
12. Deleu D, Waele JD, Buisseret T. Dorsolateral pontine hemorrhage producing pure sensory stroke. Eur Neurol.. 1992;32:222-224.[Medline] [Order article via Infotrieve]
13. Shintani S, Tsuruoka S, Shiigai T. Pure sensory stroke caused by a pontine infarct: clinical, radiological, and physiological features in four patients. Stroke.. 1994;25:1512-1515.[Abstract]
14. Holzman RNN, Zablozki V, Yang WC, Leeds NE. Lateral pontine tegmental hemorrhage presenting as isolated trigeminal sensory neuropathy. Neurology.. 1987;35:637-643.[Abstract/Free Full Text]
15. Berlit P. Trigeminal neuropathy in pontine hemorrhage. Eur Neurol.. 1989;29:169-170.[Medline] [Order article via Infotrieve]
16. Kim JS. Trigeminal sensory symptoms due to midbrain lesions. Eur Neurol.. 1993;33:218-220.[Medline] [Order article via Infotrieve]
17. Kim JS, Lee MC, Kim HG, Suh DC. Isolated trigeminal sensory change due to pontine hemorrhage. Clin Neurol Neurosurg.. 1994;96:168-169.[Medline] [Order article via Infotrieve]
18. Nakamura K, Yamamoto T, Yamashita M. Small medullary infarction presenting as painful trigeminal sensory neuropathy. J Neurol Neurosurg Psychiatry.. 1996;61:138.[Medline] [Order article via Infotrieve]
19. Tohgi H, Takahashi S, Takahashi H, Tamura K, Yonezawa H. The side and somatotopical location of single small infarcts in the corona radiata and pontine base in relation to contralateral limb paresis and dysarthria. Eur Neurol.. 1996;36:338-342.[Medline] [Order article via Infotrieve]
20. Kim JS, Kim HG, Chung CS. Medial medullary syndrome: report of 18 new patients and a review of the literature. Stroke.. 1995;26:1548-1552.[Abstract/Free Full Text]
21. Sacco RL, Bello JA, Traub R, Brust JC. Selective proprioceptive loss from a thalamic lacunar stroke. Stroke.. 1987;18:1160-1163.[Abstract/Free Full Text]
22. Martin JH. Anatomical substrate for somatic sensation. In: Kandel ER, Schwartz JH, eds. Principles of Neural Science. 2nd ed. New York, NY: Elsevier; 1986:301-315.
23. Heines DE. Neuroanatomy and Atlas of Structures, Sections and Systems. 2nd ed. Berlin, Germany: Urban & Schwartzenberg; 1987:158-163.
24. Kim JS, Lee JH, Lee MC. Small primary intracerebral hemorrhage: clinical presentation of 28 cases. Stroke.. 1994;25:1500-1506.[Abstract]
25. Matsumoto S, Kaku S, Yamasaki M, Imai T, Nabatame H, Kameyama M. Cheiro-oral syndrome with bilateral oral involvement: a study of pontine lesions by high resolution magnetic resonance imaging. J Neurol Neurosurg Psychiatry.. 1989;52:792-794.[Abstract]
26. Kim JS. Restricted acral sensory syndrome following minor stroke: further observation with special reference to differential severity of symptoms among individual digits. Stroke.. 1994;25:2497-2502.[Abstract]
27. Kim JS. Bilateral perioral sensory symptom after unilateral stroke: Does it have a localizing value? J Neurol Sci.. 1996;140:123-128.[Medline] [Order article via Infotrieve]
28. Nashold BS Jr, Wilson WP, Slaughter DG. Sensations evoked by stimulation in the midbrain of man. J Neurosurg. 1969;30:14-24.[Medline] [Order article via Infotrieve]
29. Leijon G, Boivie J, Johansson I. Central post-stroke pain-neurological symptoms and pain characteristics. Pain.. 1989;36:13-25.[Medline] [Order article via Infotrieve]

This article has been cited by other articles:

				J. S. Kim Patterns of sensory abnormality in cortical stroke: Evidence for a dichotomized sensory system Neurology, January 16, 2007; 68(3): 174 - 180. [Abstract] [Full Text] [PDF]

				J. S. Kim Internuclear ophthalmoplegia as an isolated or predominant symptom of brainstem infarction Neurology, May 11, 2004; 62(9): 1491 - 1496. [Abstract] [Full Text] [PDF]

				H. Russmann, F. Vingerhoets, J. Ghika, P. Maeder, and J. Bogousslavsky Acute Infarction Limited to the Lenticular Nucleus: Clinical, Etiologic, and Topographic Features Arch Neurol, March 1, 2003; 60(3): 351 - 355. [Abstract] [Full Text] [PDF]

				K. Johkura, S. Matsumoto, A. Komiyama, O. Hasegawa, and Y. Kuroiwa Unilateral Saccadic Pursuit in Patients With Sensory Stroke : Sign of a Pontine Tegmentum Lesion Stroke, November 1, 1998; 29(11): 2377 - 2380. [Abstract] [Full Text] [PDF]

This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kim, J. S. Articles by Bae, Y. H. Search for Related Content PubMed PubMed Citation Articles by Kim, J. S. Articles by Bae, Y. H.