Accepted Manuscript
Rehabilitation Course and Specification of Dysmetria of a Patient with Ataxia,
Dysmetria and Hemiparesis Following a Stroke in the Corona Radiata: A Case
Presentation
Monir Mohar, MD, Kosandra Hartman, BS, Bronwyn Long, BA, Peter Lee, MD, Adrian
Didita, MD, Eric L. Altschuler, MD, PhD
PII:

S1934-1482(18)30058-3

DOI:

10.1016/j.pmrj.2018.01.008

Reference:

PMRJ 2052

To appear in:

PM&R

Received Date: 31 October 2017
Revised Date:

17 January 2018

Accepted Date: 21 January 2018

Please cite this article as: Mohar M, Hartman K, Long B, Lee P, Didita A, Altschuler EL, Rehabilitation
Course and Specification of Dysmetria of a Patient with Ataxia, Dysmetria and Hemiparesis Following a
Stroke in the Corona Radiata: A Case Presentation, PM&R (2018), doi: 10.1016/j.pmrj.2018.01.008.
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Rehabilitation Course and Specification of Dysmetria of a Patient with Ataxia,
Dysmetria and Hemiparesis Following a Stroke in the Corona Radiata: A Case
Presentation

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Monir Mohar1, MD, Kosandra Hartman2, BS, Bronwyn Long3, BA, Peter Lee1, MD,
Adrian Didita1, MD, Eric L Altschuler1*, MD, PhD
1

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Department of Physical Medicine and Rehabilitation, Metropolitan Hospital, New York,
NY, 10029, USA
2
Geisinger Commonwealth School of Medicine, Scranton, PA, 18510, USA
3
New York Medical College, Valhalla, New York, 10595, USA

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*To whom correspondence should be addressed:
Eric L Altschuler, MD, PhD
Metropolitan Hospital
1901 First Avenue
New York, NY, 10029, USA
email: altschue@nychhc.org
Phone: (212) 423-6448
Fax: (212) 423-6326

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We have no financial or other conflicts.

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Rehabilitation Course and Specification of Dysmetria of a Patient with Ataxia, Dysmetria
and Hemiparesis Following a Stroke in the Corona Radiata: A Case Presentation

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Abstract
We present a case of a patient with ataxia, dysmetria and hemiparesis following a stroke in the
corona radiata. The patient had an excellent clinical course with near resolution of symptoms in
two and a half weeks, and returned and back to work fully duty and full-time a couple of weeks
later. We use a video of severeal neurological tests to demonstrate and characterize the
dysmetria. Interestingly, a key characteristic of the dysmetria appears to be different from that
seen in patients with dysmetria arising from a cerebellar, thalamic or pontine lesion. We propose
a possible neurophysiologic mechanisms—damage to and redundancy of part of the
corticopontine portion of the cerebellar circuit located in the corona radiata—respectively
responsible for this condition and recovery. We also discuss how a simple noninvasive study of
patients with ataxia and dysmetria secondary to corona radiata, thalamic, pontine and possibly
other brain lesions may be helpful in elucidating the contribution of pontocerebellar fibers and
other structures to motor control.

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Introduction
For more than 100 years [1-5] and perhaps back into the 19th century [6] physicians have
recognized that lesions to midbrain structures can cause clinical cerebellar type symptoms such
as ataxia and dysmetria. These deductions were particularly remarkable because imaging of the
brain in a living human was not available until more than half of a century later. Far from being
an interesting and valid, but arcane corner of neurology, such non-cerebellar ataxia-dysmetria
syndromes are not uncommon and may be of great relevance to the consultant and inpatient
physiatrist. Recently, the rehabilitation courses of patients with ataxia and dysmetria secondary
to a thalamic [7] and pontine lesion [8] have been described. Here, we describe the case and
rehabilitation course of a patient with ataxia, dysmetria, and hemiparesis secondary to a lesion in
the corona radiate. We also discuss and demonstrate with a video the difference between the
dysmetria in this patient and that encountered in patients with lesions in the thalamus [7], pons
[8] or cerebellum [9].
Case Presentation
A 55 year-old female with past medical history of poorly controlled hypertension and
hyperthyroidism noticed right upper extremity and lower extremity numbness upon waking,
progressing to impaired right-hand dexterity and gait with foot drop. After admission, on hospital
day 2, MRI revealed a small acute infarct in the left parietal corona radiata (Figure 1). Upon
physiatry evaluation, on day 5 after admission, she displayed right ataxic hemiparesis with 4/5
shoulder, 3+/5 hip flexion/extension, and 2/5 dorsi/plantar flexion strength, positive Romberg
sign, right upper extremity dysmetria, inability to perform manipulation tasks and a steppage gait
that required a rolling walker. Re-evaluation on day 8 revealed continued discoordination and
weakness with some improvement in right upper extremity dexterity and ambulation endurance.
On admission to acute rehabilitation on the tenth day after the original admission to the hospital
the patient’s blood pressure was still not controlled. Her strength was 4+/5 for right hip flexion
and bicep flexion/extension. The patient had persistent right upper extremity dysmetria,
dysdiadochokinesia and ataxic gait. Internal medicine was consulted and the blood pressure was
eventually brought into the high normal range necessitating five antihypertensive medications.

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Four days after admission to acute rehabilitation the patient had only dysmetria in the right arm
with the lack of a smooth trajectory starting about halfway through the reaching task(Video 1)
and a mild to moderate deficit in a task of tapping the right heel on the left mid-shin (Video 2)
[10]. On discharge home from acute rehabilitation sixteen days after being admitted for her
stroke, she was independent with activities of daily living and ambulating without an assistive
device. On follow-up a month after discharge from acute inpatient rehabilitation the patient was
doing well with no falls or other problems and had returned to work full time to her job in line
food service. Trace dysmetria remained and ambulation was mildly slow with a slightly wide
based gait.

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Discussion
We describe the case of a patient with ataxia, dysmetria, and hemiparesis following stroke in the
corona radiata. All of these deficits improved rapidly and the patient was discharged home. She
has only residual ataxia and dysmetria, and trace hemiparesis, allowing her to return back to
work.

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It has been appreciated [11] that there is usually significant improvement with corona radiata
ataxia-dysmetria syndrome. This is relevant for physiatrists because with such a stroke, the
patients have a rapid recovery and may be able to go back to work. Our patient worked as a food
server and returned to work without restrictions. Had she been in a position requiring more
dexterity and use of fine motor skills, further study may be warranted as to residual risk from
ataxia or dysmetria.

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Features of the three non-cerebellar ataxia-dysmetria syndromes are given in Table 1. There are
a number of important implications of this for the physiatrists (Figure 2). Physicians, therapists,
patients, and family members should be aware that a patient could have significant gait
impairment despite little or no hemiparesis. During the first week or two following stroke, a
patient’s gait is usually not significantly improved such that they can be discharged home. We
have found that a walker is invaluable initially, and usually, if not always, the patient progresses
to ambulating with a cane or without an assistive devise in only a couple of weeks. In a stroke
affecting a patient’s non-dominant side, the dysmetria is usually not symptomatic. As mentioned,
returning to work is a strong possibility for these patients. Returning to a job with more
significant occupational hazards remains in question and is worthy of future study.
Table 1
Features of the three non-cerebellar ataxia dysmetria syndromes

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Corona radiata ataxiadysmetria-hemiparesis

Pontine ataxia-dysmetriahemiparesis

Thalamic ataxiadysmetria

Ataxia

Present

Present

Present

Dysmetria
(smooth
trajectory
lost)

50% of way through
reaching process

30%

75%

Hemiparesis

Mild to Moderate

Mild

Absent

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Recovery

Full or near full
typically in 1-2 weeks.

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Interestingly the “dysmetria” seen with corona radiata, thalamic or pontine lesions is not true
dysmetria – the word is derived from Greek, meaning “wrong length” – because the patient is
able to reach the target. This is in contrast patients with cerebellar lesions who typically do not
reach the target. There is also difference in reaching patterns in patients with non-cerebellar
lesion for the finger-nose-finger (FNF) test: Patients with corona radiata lesions lose a smooth
trajectory about 50% through the reaching process. Patients with pontine lesions lose smooth
trajectory within the first 30% of the reaching task, but in patients with thalamic lesions, smooth
reaching is maintained until the final 20-25% of end range reaching.

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For the patient described in this case as well as in the prior recent cases [7, 8] and older work
[11-19], lesions were secondary to hypertension. Given the prevalence of hypertension,
especially in the aging population, we expect the number of cases of these non-cerebellar ataxia
dysmetria syndromes to increase.

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The pontine ataxia-dysmetria hemiparesis syndrome is a good analog for a study done in
monkeys. Using isotope tract tracing in rhesus monkeys, Schmahmann and colleagues
demonstrated that a lesion to decussating pontocerebellar fibers caused contralateral dysmetria.
They suggest that unmasking of redundant or reorganization of pontocerebellar fibers is
responsible for the rapid clinical recovery [20]. There is no animal model of which we are aware
for the corona radiata ataxia-dysmetria-hemiparesis syndrome. We propose that our patient
sustained damage to the corticopontine portion of the cerebellar circuit located in the corona
radiata, accounting for the (at first thought) paradoxical contralateral cerebellar-like signs seen in
this case (Figure 3). Based on this patient’s improvement, we suspect the corona radiata has a
redundant organization similar to the pontocerebellar fibers that are suspected to contribute to
pontine ataxia-dysmetria recovery. Diaschisis could also play a role in recovery from corona
radiata legions. There is no animal model for the thalamic ataxia-dysmetria syndrome. The
known neural pathways shown in Figure 3 explain the lack of hemiparesis in the thalamic ataxiadysmetria syndrome and also why the dysmetria is on the side contralateral to the thalamic
lesion. The clinical finding of dysmetria at end range in the reaching process in patients with a
thalamic lesion suggests that cells in the thalamus or tracts passing through the thalamus are
needed or “come online” at terminal reaching. Dysmetria starts earlier in the process of reaching
in patients with pontine lesions presumably due to efferent tract damage, but we do currently
have an explanation as to why dysmetria seems to start later in reaching process in patients with
coronoa radiata lesions than patients with pontine lesions. These clinical findings can be tested
and studied in animal models. We would also predict that lesions to other parts of the pathway
show in Figure 3 might have distinct clinical findings.

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Full or near full in
Full or near full ~1-2 weeks
~2-4 weeks depending
(mild hemiparesis);
on extent of hemiparesis. often good recovery in 2-4 weeks
(moderate hemiparesis)

Animal lesion studies are difficult and increasingly no longer possible to perform. So further
study of the corona radiata ataxia-dysmetria-hemiparesis may come from study of human
patients. With current technology, most patients have a high quality MRI and good clinical
workup following stroke. Combining that with high quality video, reaching can be studied quite

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easily in these patients, even without any other equipment and compared to patients with
cerebellar lesions. Improved characterization of the intricacies of FNF test findings seen in
different non-cerebellar ataxia-dysmetria syndromes may allow physicians to better localize
lesions and support imaging studies through physical exam. Fortuitously we have a, safe, easy,
non-invasive task from which much can be learned in less than an hour of a patient performing
controlled reaching tests.

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2. Nicolescu J, Cretu V, Demetresco L. Syndrome de l'artere cerebrale anterieure.
Monoplegie crurale droite avec symptomatologie cerebelleuse preponderante. Bull. Soc.
Med. Hop. Bucarest 1920; 10. Synopsis in Rev. Neurol. 1932; 1: 563.

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3. Alajouanine, T., and Lemaire, A. Tumeur de la region para-centrale posterieure avec
symptoms 'pseudo-cerebelleux'. Rev. Neurol. 1925; 1: 71-75.

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4. Iragui VJ, McCutchen CB. Capsular ataxic hemiparesis. Arch Neurol 1925;39: 528-9.

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5. Garcin R, Lapresle J. Syndrome sensitif de type thalamique et a topographie cheiro-orale
par lesion localisee du thalamus. Rev Neurol 1954; 90: 124-9.

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6. Bruns, L. (1892). Ueber storungen des gleichgewichtes bei stirnhirn- tumoren. Dtsch.
med. Wschr., 18, 138-140.

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7. Menard R, Shah A, Metzger C, Altschuler EL. Thalamic dysmetria. PM&R 2016; 8:291292.

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8. Li S, Hartman K, Surapaneni K, Altschuler EL. Rehabilitation of the Pontine AtaxiaDysmetria Syndrome. PM R. 2017; 9(6):636-638.

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9. Bodranghien F, Bastian A, Casali C, et al. Consensus Paper: Revisiting the Symptoms
and Signs of Cerebellar Syndrome. Cerebellum. 2016; 15: 369-391.

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10. Fisher CM. Quantitation of deficits in clinical neurology. Trans Am Neurol Assoc.
1969;94: 263-5.

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Conclusion
Patients with corona radiata infarcts may present with ataxia, dysmetria and hemiparesis but
follow a different clinical course with faster and more complete functional recovery than patients
with cerebellar or cortical lesions. Formal study of dysmetria in these patients, and patients with
other non-cerebellar lesions may improve understanding the role of pontocerebellar fibers and
other midbrain structures in motor control.

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(b)

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Figure 1 Acute stroke seen (arrow) in the left corona radiata. (a) Diffusion weighted image.
(b) Apparent diffusion coefficient MRI image.

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Figure 2 Algorithm for diagnosis and treatment of non-cerebellar ataxia-dysmetria syndromes.

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Figure 3 Simplified corticocerebellar pathways involved in non-cerebellar ataxia-dysmetria
syndromes. The schematic shows how a lesion in the right corona radiata, pons or thalamus can
cause left limb dysmetria and ataxia. A lesion to the right corona radiata or pons will also cause
hemiparesis on the left side of the body via damage to the corticospinal tracts. Damage to the
thalamus is predicted not to cause hemiparesis.

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Video 1 Normal reaching in the unaffected left arm. Non-smooth trajectory starting about
halfway in the reaching process in the affected right arm. (The patient gave written informed
consent for use of the videos.)

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Video 2 Twelve taps in four seconds by the unaffected left leg. Only eight taps in seven seconds
by the affected right leg.

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