.Movement Disorders
Vol. 1. NO. 4. pp. 27! -274, 1986
8 1986 Movement Disorder Society

Case Report

Focal Asterixis Caused by a Small
Putaminal Hemorrhage
Jose M.Trejo, Santiago Gimknez-Roldh, and Angel Esteban
Department of Neiirology and Division of Clinical Neurophysiology, Hospital Provincial,
Madrid, Spain

Summary: Unilateral asterixis and mild pure motor hemiparesis contralateral
to a small putaminal hemorrhage were observed in a 74-year-old hypertensive
man. The motor deficit proved to be rapidly reversible, but the focal asterixis
remained for some time as the only sign of the intracranial hemorrhage. This
case suggests that altered striopallidal inhibitory input to the thalamus probably disturbed the circuit subserving the maintenance of postural tone. Key
Words: Asterixis-Putamen-Pure
motor hemiparesis-Intracranial
hemorrhage.

Asterixis is a brief lapse of postural tone that is most commonly observed while
the patient holds his hands outstretched. The phenomenon is usually bilateral
when there is an underlying metabolic disorder. Unilateral asterixis occurs after
focal damage to any of a number of brain structures, including the mesencephalon, thalamus, frontal and parietal lobes, as well as the pons and internal capsule
(1,2). It has been postulated that these structures subserve a cortico-subcortical
circuit that is involved in the maintenance of postural tone (3). To the authors'
knowledge, however, focal asterixis secondary to a putaminal Iesion has not been
described previously and wouId implicate the striaturn as a functional member of
this circuit.

CASE REPORT
A 74-year-old hypertensive man was admitted 24 h after the sudden onset of
weakness of his right limbs and slight speech impairment. He was fully alert and
could express himself without aphasic speech, although he did exhibit some articulatory defects. On examination, he had a minimal right hemiparesis and could
walk without help. There was some flattening of the right nasoIabia1 fold, and the
Address correspondence and reprint request to Dr. S . Gimenez-Roldkn at Department of Neurology, Hospital Provincial, Doctor Esquerdo 42, Madrid-28007, Spain.

2 71

272

J . M . TREJO ET AL.

right plantar response was extensor. The findings on sensory examination were
normal, including proprioception, and there was no evidence of neglect. With
hands outstretched, rapid and brief lapses of posture of his right hand were revealed by a downward falling movement; this was observed with the hand either
in a supine or a prone position. The abnormal movement was not rhythmic and
occurred at a frequency of about 40 per minute. This frequency remained unchanged when the patient's eyes were closed, and even though he was fully aware
of the involuntary jerks, he was unable to prevent them.
An electrophysiological examination by means of surface electrodes on the
flexor and extensor muscles of the forearm showed that during the postural
lapses, there was complete interruption of muscle activity, involving both agonist
and antagonist muscle groups. Such periods when electrical activity was absent
were irregular, lasting up to a maximum of 100 ms. They were not recorded in the
biceps and triceps muscles of the ipsilateral limb. Cortical somatosensory evoked
potentials to median nerve stimulation were normal bilaterally.
Any systemic metabolic abnormality was excluded by appropriate laboratory
tests. A computed tomography (CT) scan of the head demonstrated a small hemorrhage that was mostly confined to the left putamen, though slightly extending
into the globus pallidus as well. It was about I cm in transverse diameter, with
minimal surrounding edema and no midline shift. Three weeks later, it had been
completely reabsorbed, leaving a small area of hypodensity (Fig. 1).
Forty-eight hours after its onset, the hemiparesis began to subside, and 7 days
later, muscle strength was back to normal, though the patient still exhibited some
slowness of his right hand in opposing the thumb to the other fingers. The focal
asterixis, however, persisted, decreasing over the following 2 weeks and disappearing 2 months after onset. By that time, he had fully recovered manual dexterity.

DISCUSSION
This patient suffered from a pure motor hemiparesis that was secondary to a
small contralateral putaminal hemorrhage (4). In most cases, putaminal hemorrhages are fatal or leave severe focal motor deficits, particularly when their size is
large (5). Neurological deficits associated with small hemorrhages may be completely reversible (6,7). We believe that the slight initial motor impairment in our
patient, followed by rapid recovery, was a precondition for the focal asterixis to
manifest itself in the limbs involved; presumably, it might have been absent in a
dense hemiplegia. Other authors have reported the appearance of asterixis in parallel to recovery of the associated motor deficit (8). and in a number of instances,
focal asterixis was not associated with any motor deficit (9, 10). It is interesting to
note that for some weeks the focal asterixis was the only demonstrable neurological abnormality resulting from the intracranial hemorrhage. Encroachment into
the thalamus and internal capsule by the hemorrhage itself is therefore an unlikely
explanation for the asterixis in this case ( 1 I , 12).
The most common sites at which a focal lesion produces unilateral asterixis are

Movement Disorders, Vol. I , No. 4, I986

FOCAL AS TERIXIS

273

FIG. 1. A smafl left-sided hemorrhage. mainly involving the putamen, as found on admission, is
shown in A. Three weeks later, it has been completely reabsorbed, leaving a small low-density area
(arrow) (B).

the mesencephalon (131, the thalamus ( 1 1,121 and the parietal and frontal lobes
(1). Shahani and Young (1) postulated that these interconnected brain structures
comprise a circuit necessary for the maintenance of postural tone. Our observations would indicate that the striatum is also involved in this system and participates in maintaining postural tone. Limited damage to the striopallidal complex
probably impaired GABAergic inhibitory output to the thalamus and from there
to the motor cortex. Some authors (9). on the other hand, interpret focal asterixis
as a localized inattention failure secondary to a disturbance of sensory integration
in the mesencephalon, thalamus, or parietal cortex. This mechanism is unlikely in
our patient, as careful examination disclosed no sensory deficit and the somatosensory evoked potentials were also in keeping with an undamaged sensory
pathway.
Focal asterixis may be encountered after localized damage to the central
nervous system, involving an)' of a number of different structures, and the putamen should be considered another potential site. In the present case, the associated motor deficit regressed, while the focal asterixis remained for some time as
the only neurological impairment secondary to the lesion caused by the putaminal hemorrhage.

Mowmerrt Disorders. Vol. I , No. 4 , I986

274

J . M . TREJO ET AL.

REiFmNCES
1. Young RR, Shahani BT. Asterixis: One type of negative myocfonus. Adv Neurol 1986;43:137-55.
2 . Kudo Y, Fukai M, Yamadori A. Asterixis due to pontine haemorrhage. J Neurol Neurosurg Psychiarry 1985;48:487-9.
3. Shahani BT, Young RR. Asterixis: a disorder of the neural mechanism underlying sustained
muscle contraction. In: Shahani M, ed. The motor system: neurophysiology and muscle mechanisms. Amsterdam: North Holland, 1977:301-6.
4. Tapia JF, Kase CS, Sawyer RW, et al. Hypertensive putaminal haemorrhage presenting as pure
motor hemiparesis. Stroke 1983;14:505-6.
5 . Hier DB, Davis KR,Richardson EP Jr, et al. Hypertensive putaminal haemorrhage. Ann Neurol
1977;1:152-9.
6. Brusa A, Piccardo A, Meneghini S,et al. Cerebral haemorrhages presenting as reversible clinical
entities. Ital J Neurdl Sci 1982;4:333-7.
7. Scott WR, Miller BR. Intracerebid haernorrhage with rapid recovery. Arch Neurol 1985;42:
I33-6.
8. Davalos A, Titus F, Cervera J, et al. Asterixis unilateral: un signo de lesiones focales cerebrales.
Rev Neurol (Barcelona) 1982;lO:127-31.
9. Degos JD, Verroust J, Bouchareine A, et al. Asterixis in focal brain lesions. Arch Neurol
1979;36:705-7.
10. Santamarfa J, G nu s F, Martinez J, et al. Asterixis en lesiones focales del sistema nervioso central. Rev Clin ESP 1983;168:37-9.
11. Donat JR. Unilateral asterixis due to thalamic hemorrhage. Neurology 1980;30:83-4.
12. Massey EW, Goodman JC, Stewart C, et al. Unilateral asterixis: motor integrative dysfunction in
focal vascular disease. Neurology 1979;29:1188-90.
13. Bril V, Sharpe JA, Ashby P. Midbrain asterixis. Ann Neurol 1979;6:362-4.

Movement Disorders, Vol. I . No. 4, 1986