The Dysarthria-Clumsy Hand Syndrome: A Distinct Clinical Entity Related to Pontine Infarction Jonathan D. Glass, MD, Allan I. Levey, MD, PhD, and Jeffrey D. Rothstein, MD, PhD Using magnetic resonance imaging, we studied 6 patients with the dysarthria-clumsy hand syndrome. All were found to have pontine infarctions contralateral to the symptomatic side. Clinically, these patients exhibited dysarthria; “clumsiness,” characterized by dysmetria, dysrhythmia, dysdiadochokinesia and sometimes truncal and gait ataxia; and mild ipsilateral weakness. Previous clinical-anatomical correlations for this syndrome are limited by inconsistencies in clinical diagnostic criteria and low-resolution imaging methods. In our patients, and in a review of the literature, the overwhelming majority of patients with the dysarthria-clumsy hand syndrome had pontine infarcts. We conclude that if rigid clinical criteria are used, the label of the dysarthria-clumsy hand syndrome predicts a lesion in the contralateral basis pontis. Glass JD, Levey AI, Rothstein JD. The dysarthria-clumsy hand syndrome: a distinct clinical entity related to pontine infarction. Ann Neurol 1990;27:487-494 Intriguing studies of patients with ipsilateral pyramidal and cerebellar signs have been reported sporadically under the titles of “The Dysarthria-Clumsy Hand Syndrome,” “Ataxic Hemiparesis,” and “Homolateral Ataxia and Crural Paresis.” Fisher 11-31 coined each of these terms to identify separate stroke syndromes based on different constellations of symptoms and signs, although it is clear from his most recent review 141 that the term ataxic hemiparesis is meant to replace the term homolateral ataxia and crural paresis. The clinical distinction between dysarthria-clumsy hand syndrome and ataxic hemiparesis is outlined in Table 1. The “clumsiness” and “ataxia” may look the same, as noted by Fisher l31, but the lack of dysarthria, prominent hemiparesis, and frequent sensory symptoms and signs in ataxic hemiparesis serve to distinguish the two syndromes. Numerous publications have suggested varied anatomical localizations responsible for the clinical syndromes, and these data have led to a generally accepted conclusion that both syndromes can be caused by a lesion of either the basis pontis or the internal capsule. This conclusion is based on evidence limited by two factors: (1) Some authors have used the labels “dysarthria-clumsy hand” and “ataxic hemiparesis” interchangeably, not adhering to Fisher’s original descriptions and thus confusing the clinical distinction. (2) There is virtually no pathological data available for anatomical confirmation of lesions. The majority of clinical-anatomical correlations have been based on computed tomographic (CT) images that are notoriously insensitive for detecting pathological conditions of the posterior fossa. High-resolution in vivo brain imaging by magnetic resonance scanning (MRI) is an invaluable tool for clinical-anatomical correlation, especially for diseases such as lacunar strokes, which have low mortality and thus provide few immediate specimens for pathological study. We collected a series of 6 patients who adhere to Fisher’s original description of the dysarthriaclumsy hand syndrome and found that all showed pontine infarction by MRI. A patient with ataxic hemiparesis had both pontine and capsular infarcts on MRI. We suggest that if rigid clinical criteria are used, the label of dysarthria-clumsy hand syndrome predicts a lesion in the contralateral basis pontis. From the Department of Neurology, The Johns Hopkins Hospital, Baltimore, MD. Received Jun 21, 1989, and in revised form Oct 23. Accepted for publication Oct 26, 1989. Address correspondence to Dr Glass, Neuropathology Laboratory, Pathology 509, The Johns Hopkins Hospital, 600 N. Wolfe Street, Baltimore, MD 21205. Methods Patients were selected from the inpatient populations of the three hospitals served by the Johns Hopkins Neurology program. All were examined by at least one of us. Inclusion into the study was made solely on the basis of the patients’clinical appearance; MRI data, even if available, were not considered in the selection of patients. Q i d clinical criteria were used in order to enhance the specificity of the clinical-anatomical correlation. Patients selected as having the dysarthria- Copyright 0 1990 by the American Neurological Association 487 Table 1 . Distinguishing Features between Dysarthria-Clumsy Hand and Ataxic Hemiparesis Dysarthria-Clumsy Hand Ataxic Hemiparesis Dysarthria Hemiparesis Moderate to severe Mild (if any) “pyramidal” weakness Clumsinesdataxia Ipsilateral clumsiness characterized by dysmetria, dysrhythmia, dysdiadochokinesia, and frequently gait ataxia None None Moderate, frequently leg weakness > arm weakness > face weakness Similar to dysarthria-clumsy hand Sensory Frequent ipsilateral paresthesias, sometimes with objective sensory signs +I - tongue deviation on protrusion, palatal weakness, and Babinski sign Other Table 2. Summary of Clinical Findings Patient No. Age (yr) HTN, DM 1 63 + 2 72 3 5 6 57 63 37 49 + 7 59 + 4 + + + + + Dysarthria UMN VII ++ ++ ++ ++ +++ ++ + + + + + + + Tongue Deviation Palate Deviation Weakness Babinski Sign Lesion Location + + Pons Pons + + + + + + + + ++ + + + Pons Pons Pons Pons Pondcapsule HTN = hypertension; DM = diabetes mellitis; UMN VII = central facial paresis; + = present; + + = moderate impairment; + + + = severe impairment. clumsy hand syndrome met the following criteria: (1) dysarthria without dysphasia; (2) unilateral ‘‘central’’ facial weakness with ipsilateral clumsiness appearing as a cerebellar-type ataxia (dysmetria, dysrhythmia, dysdiadochokinesia, gait ataxia), with mild or no weakness; and (3) no sensory symptoms or signs. Other findings were variable (Table 2). MRI scans were done 2 to 7 days after the onset of symptoms using either 0.4- or 1.5-tesla machines and standard acquisition settings and times. Results Six patients with the dysarthria-clumsy hand syndrome were identified. There were 4 women and 2 men with a mean age of 57 years (range, 37-72 years). All patients were found by MRI to have paramedian pontine lesions. One patient with ataxic hemiparesis had both a pontine and a capsular lesion. Case Reports A 63-year-old, right-handed woman complained of sudden onset of thick speech and unstable walking. She noticed severe difficulty with writing and signing a check and described her right hand as “clumsy.” On examination she was awake, alert, and oriented. Blood pressure was 220/110 mm Hg and there were bilateral carotid bruits. Speech was thick and slow without dysphasia. There was a PATIENT 1. 488 Annals of Neurology Vol 27 N o 5 May 1990 right “central” facial paresis. Tongue and palate movements were normal. Appendicular strength was normal except for minimal (545) weakness of the finger abductors in the right hand. Deep tendon reflexes (DTRs) were symmetrical and normally active except for bilaterally diminished ankle jerks. She had a right Babinski sign. Results of a sensory exam were normal. O n the right, finger-to-nose (FIN)and heel-toshin (HTS) movements were dysmetric and rapid alternating movements (pronatiodsupination RAM) were slow and irregular. Gait was wide based and she fell to the right. Brain CT scan on the day of admission had a normal appearance. A MRI scan the following day showed an abnormal high-intensity signal on T2-weighted images in the left paramedian basis pontis (Fig 1). PATIENT 2. A 72-year-old, right-handed diabetic man had difficulty walking after arising from bed and complained of “weakness” of his right side and a “thick tongue.” H e had a “stroke” 1 year previously, with right-sided weakness but no speech difficulties. O n examination he was awake and oriented but slow to respond. H e recalled only one of four cities in 5 minutes but performed well with the remainder of the bedside mental status testing. Speech was thick but there was no dysphasia. There was mild right facial weakness. Strength was normal and DTRs were symmetrical. Plantar reflexes were flexor bilaterally. There was a mild sensory polyneuropathy. H e performed poorly on FTN,HTS, and RAM on the right. Gait was wide based but steady. Fig 1. Patient 1. Figures 1 through 6are horizontal plane MRls h-ougb $bepons, revealing wried degrees of paramdian infarction contralateral to the patients’ symptomatic side. Brain CT scan on the day of admission was normal. MRI done on the third hospital day showed a left paramedian pontine infarct (Fig 2). PATIENT 3. A 5 7-year-old, right-handed hypertensive woman noted the gradual onset over an hour of weakness in the right leg and then thick, slow speech late one evening before going to bed. The next morning her symptoms persisted, with additional complaints of difficulty using her right hand and a headache in the left occipital region. When examined later that morning her blood pressure was 150190 mm Hg; there were no bruits or murmurs. Mental status was clear, and speech was dysarthric but not dysphasic. There was a “central” facial paresis and palatal and tongue weakness on the right. She had a mild right hemiparesis (4/5, arm weakness > leg weakness). Tendon reflexes were symmetrical and there was a right Babinski reflex. Results of a sensory examination were normal. She had poor RAM and an intention tremor on the right. Gait was more unsteady than could be expected from the degree of weakness. Brain CT scan on the day of admission was normal. MRI on the third hospital day showed a left paramedian pontine infarct (Fig 3). PATIENT 4 . A 63-year-old, right-handed alcoholic, hypertensive man noticed weakness of his right arm and leg when arising from a chair. He complained of a bifrontal headache and his family noted a right facial droop and slurred speech. His symptoms had largely resolved when he was first examined. Blood pressure was 160/100 mm Hg. Speech was dysarthric but not dysphasic. The right nasolabial Fig 3. Patient 3 . Glass et al: Dysarthria-Clumsy Hand 489 Fig 4.Patient 4. Fig 5 . Patient 5 . fold was flat and the tongue and palate were normal. There was a right pronator drift and mild (4 +/5) weakness of the right triceps and wrist extensors. Tendon reflexes were brisker on the right and plantar reflexes were flexor. H e had a mild stocking and glove peripheral neuropathy. RAMS were dysrhythmic and slow and on ETN testing he had mild dysmetria on the right. Gait was wide based and he could not tandem walk. Brain CT scan on the day of admission was normal. On hospital day 7 an MRI showed extensive infarction of the left paramedian basis pontis (Fig 4). she had a grade 2 cardiac ejection murmur. Speech was slow and thick but there was no dysphasia. Mental status was normal. Saccadic eye movements were hypermetric to the right. She had weakness of the right lower face and the right side of her tongue. Also present were a right pronator drift, mild (4 +/5) weakness of the intrinsic muscles of the right hand, and minimal weakness of the right hamstrings and foot dorsiflexors. Tendon reflexes were brisker on the right and there were bilateral Babinski reflexes. She had a mild stocking polyneuropathy. She performed poorly on RAM and ETN on the right and her gait was broad based and unsteady. Brain CT scan on admission was normal. Head MRI on day 2 showed a left paramedian pontine infarct (Fig 6). PATIENT 5. A 37-year-old, right-handed woman with a history of migraine headaches experienced the sudden onset of speech difficulty right-sided weakness, and headache in the left temporal region. Her blood pressure was 120/70 mm H g and a general exam revealed normal findings. She had severe dysarthria but no deficit in language. There was a right “central” facial paresis and the tongue deviated to the right. Palatal elevation was symmetrical. She had a moderate right hemiparesis (arm 3/5, leg 4 5 ) with symmetrical DTRs and a Babinski sign on the right. Findings on sensory examination were normal. Bilateral dysmetria and dysrhythmia were present, much more severe on the right. Gait was wide based and ataxic. Brain CT scan and lumbar puncture on admission revealed normal findings. Head MRI on day 2 showed a left paramedian pontine lesion consistent with infarction (Fig 5). PATIENT 6. A 49-year-old, right-handed woman with a long history of poorly controlled diabetes and hypertension awoke with slurred speech and an inability to walk. Her symptoms resolved over 1 hour but recurred 24 hours later and persisted. Her blood pressure was 140/90 mm Hg and 490 Annals of Neurology Vol 27 No 5 May 1990 PATIENT 7. A 59-year-old, right-handed hypertensive woman complained of sudden “heaviness” in the right arm and leg, unsteady walking, and a “clumsy” right hand. She had no difficulties with her speech. On examination, her mental status and speech were normal; blood pressure was 150/85 mm Hg. There was minimal flattening of the right nasolabial fold and other cranial nerves were normal. She had a right hemiparesis, with the leg (3/5) weaker than the arm (4+ 15). Tendon reflexes were symmetrical and plantar reflexes were flexor. Results of the sensory examination were normal. She exhibited past pointing on FTN and dysrhythmic RAM in the right upper extremity. Gait was not tested. Several hours after admission the right hemiparesis progressed to hemiplegia. A brain CT scan was normal. She was then started on continuous intravenous infusion of heparin. Her weakness began to improve after 24 hours and improved to baseline by 72 hours. Examination again confirmed dysmetria on the right. Head MRI on day 7 showed lacuna lesions in the left corona radiata and left pons (Fig 7 ) . Fig 6. Patient 6. Fig 7. Patient 7 , who bad ataxic bemiparesis. Small infarcts are seen in the pons and internal capsule, both contralateral to the symptomatic side. Discussion Since Fisher’s original articles describing syndromes with unilateral pyramidal and cerebellar signs 11-31, there have been numerous case reports of similar patients, bearing the titles of “dysarthria-clumsy hand,” “ataxic hemiparesis,” and “homolateral ataxia and crural paresis.” Though Fisher’s case descriptions served to separate these patients into at least two distinct groups, several authors have used the terms interchangeably or have chosen to lump all cases under the label of “ataxic hemiparesis” 15-10]. Some authors have added qualifiers such as “hypesthetic” 1111, “painful’’ 1121, or with “trigeminal” weakness 15, 131, cresting new categories of “ataxic hemiparesis.” Since nearly all publications suggest clinical-anatomical correlations, the specificity of the labels, necessarily based on clinical symptoms and signs, is quite important. Inconsistent applications of these labels have made the literature on this topic confusing and nonspecific, serving to support Landau’s recent conclusion that the term ataxic hemiparesis has “. . . no operational meaning, and no utility at all” 1141. Using Fisher’s original description of the dysarthriaclumsy hand syndrome, we studied 6 consecutive patients using MRI in an attempt to define an anatomical site where a lesion would produce the associated symptoms and signs. We made a point of clinically separating these patients from those with ataxic hemiparesis (homolateral ataxia and crural paresis) as defined by Fisher’s original report of 14 patients Clf. Distinguishing features of ataxic hemiparesis are tran- Glass et al: Dysarthria-Clumsy Hand 491 Table 3. Previous Reports of Dysarthria-Clumsy Hand and Ataxic Hemiparesis” As Reportedb Author(s) Year AH# Fisher and Cole 111 Fisher I21 Fisher I31 Spertell and Ransom 1251 Perman and Racy 1381 Bendheim and Berg 1291 Sakai et al. 151 Ichikawa et al. I261 Iragui and McCutchen 1231 Schnapper 161 Tuhrim et al. 1411 Jabbari et al. 1351 Jacome 171 Jokelainen and Pike I201 Kobatake and Shinohara 181 DeRenzi et al. 1161 Sage and Lepore 191 Van Buggenhout 1421 Biller and Scardigh I301 Bougousslavsky et al. 1121 Donati et al. I331 Huang and Lui 1241 Huang and Chan I171 Mori et al. 1191 Tredici et al. I211 Delgado et al. 1311 DeVries and Sno 1321 Mori et al. I371 Verma and Maheshwari I111 Sakai et al. 1181 Schleimer et al. 1401 Ambrosetto 1131 Koppel and Weinberger I361 Nabatame et al. 1221 Roy 111 et al. I391 Huang et al. 1341 1965 1967 1978 1979 1980 1981 1981 1982 1982 1982 1982 1983 1983 1983 1983 1983 1983 1984 1984 1984 1984 1984 1984 1984 1983 1985 1985 1985 1986 1986 1986 1987 1987 1987 1987 1988 14 Reevaluatedb*‘ D-CH AH D-CH Method 3 1 Clinical Pathological Pathological 1 CT 14 3 3 2 1 CT CT 1 1 1 1 “trigemid weak” 1 1 CT 1 1 1 1 CT CT CT CT 1 1 1 1 1 1 1 1 1 CT 1 2 2 2 3 2 2 1 2 1 2 1 “pain” 4 5 1 1 1 4 4 1 1 1 1 1 1 1 1 1 5 2 ‘‘numbness” 1 3 1 n/a 1 n/a 2 1 1 1 “trigeminal weak” 1 1 1 1 2 1 3 3 1 2 CT 1 (no VII) 1 CT CT CT CT CT CT CT CT CT CT CT CT CT CT CT CT CT CT CT CT MRI CT/MRI CT Location Pons (1) Pons Capsule Capsule Midbrain (leukemia) Pons Capsule Capsule Pons Pons Capsule Capsule CO~OM radiata Pons Capsule Corona radiata (2), capsule (1) Pons Corona radiata Thalamus Capsuldcorona AH: capsule (4); “ D - C H no lesion (1) Pons Capsule Capsule Pons Capsule AH:capsule(4), pons(1); D-CH: putamen(3) Thalamus Pons Capsule Pons Pons Pons Cerebellum Pons ”Terms in quotations refer to qualifiers in case descriptions. bNumber of patients. ‘Revised diagnosis after review of published case histories. AH = ataxic hemiparesis or homolateral ataxia and crural paresis; D-CH = dysarthria-clumsy hand syndrome; n/a = case histories not published. Table 4. Clinical-AnatomicalCorrelation in Previous Reports As Published Localization Pons AH 19 Capsulelcorona Other Totals 29 4 53 D-CH 3 2 4 9 Reevaluated AH 9 D-CH” 11 24 4 37 3 1 15 “Note: 3 patients with D-CH had no reported anatomical correlation. AH = ataxic hemiparesis; D-CH = dysanhria-clumsy hand. sient paresthesias; more prominent hemiparesis, with the leg frequently being weaker than the arm and face; and relative lack of dysarthria. All of our patients who were labeled as having dysanhria-clumsy hand syndrome had lesions consistent with small infarcts (lacunes) in the paramedian basis pontis contralateral to the symptomatic side. Patient 7 was diagnosed as having ataxic hemiparesis and was included for comparison. Our data support Fisher’s original pathological findings ~ 2 and ) suggest that the dysarthria-clumsv hand syndrome is usually caused by a lesion of the paramedian basis pontis. The current literature, however, does not support this hypothesis, with more than half the cases reported correlated with lesions outside the pons (Table 3). Because of the question of seman- 492 Annals of Neurology Vol 27 No 5 May 1990 tics in labeling patients, we reviewed all published case histories and relabeled them based on more rigid criteria as dysarthria-clumsy hand, ataxic hemiparesis, or neither (Table 4). Patients for whom there was insufficient data for clear diagnosis were left as the authors’ original designation. It is interesting that no patient reported to have “dysarthria-clumsy hand” was relabeled while 9 patients with “ataxic hemiparesis” were redesignated to have dysarthria-clumsy hand, supporting the view that authors have tended to group all patients under the general term of ataxic hemiparesis. After reevaluation, in only 3 of 15 patients was dysarthria-clumsy hand correlated with lesions outside the pons. Our analysis of other authors’ published material must be interpreted with caution because we did not examine the patients nor did we review their charts and radiological images. However, these data are useful for the interpretation of our data in comparison with others. This series of patients focuses only on clinicalanatomical correlations in the dysarthria-clumsy hand syndrome. There is no doubt that lesions of the basis pontis cause other neurological syndromes, including some that may resemble the dysarthria-clumsy hand syndrome (i.e., “ataxic hemiparesis”). It remains debatable which system(s) is (are) responsible for the motor abnormalities in patients with the dysarthria-clumsy hand syndrome Ll51. Clinically, our patients with pontine lesions showed signs suggestive of cerebellar dysfunction. Corticospinal tract findings were not prominent and did not appear to be a significant cause of the “clumsiness” in our patients. This further supports the view 18, 9, 11, 16-28) that there is disruption of cerebellar pathways accounting for at least some, if not all, of the symptoms. It remains unclear why a unilateral pontine lesion, which should equally affect nuclei and crossing fibers, does not give bilateral cerebellar signs. One patient (Patient 5) in this series did have bilateral ataxia. Her signs, however, were notably asymmetrical, raising the same functional question. Our conclusions are: (1) The dysarthria-clumsy hand syndrome is distinguishable from other syndromes of unilateral pyramidal and cerebellar signs. (2) The most likely anatomical location for a lesion causing the dysarthria-clumsy hand syndrome is the contralateral basis pontis. Strict adherence to clinical criteria coupled with the wide availability of MRI technology will enable clinicians to quickly test this hypothesis. ~~ ~ The authors would like to thank Dr Constance Meyd for her helpful discussion. Presented in part at the meeting of the American Neurological Association, October 2-5, 1988, Philadelphia, PA. References 1. Fisher CM, Cole M. Homolateral ataxia and crural paresis: a vascular syndrome. J Neurol Neurosurg Psychiatry 1965;28: 48-55 2. Fisher CM. A lacunar stroke: the dysarthria-clumsy hand syndrome. Neurology 1967;17:614-6 17 3. Fisher CM. Ataxic hemiparesis: a pathologic study. Arch Neurol 1978;35:126-128 4. Fisher CM. Lacunar strokes and infarcts: a review. Neurology 1982;32:871-876 5. Saki T, Murakami S , Ito K. Ataxic hemiparesis with trigeminal weakness. Neurology 1981;31:635-636 6. Schnapper RA. 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