ClinicaVScientific Notes
Vomiting out of proportion to dizziness in
ischemic brainstem strokes
C.M. Fisher, MD
At the onset of ischemic strokes involving the lower brainstem,
vomiting may be prominent when dizziness and other neurologic
abnormalities are minimal or absent. Errors in interpretation may
result in the misdiagnosis of a gastrointestinal disorder. The
stroke literature does not clearly refer to this clinical point. The
present note draws attention to the phenomenon both for practical
diagnostic reasons and to illustrate a distinct form of vestibular
vomiting.
Case I. A 52-year-old hypertensive, diabetic man with a history of myocardial infarction awakened at 1 AM with nausea and
vomiting. He vomited hourly until arrival a t the Emergency Department a t 8 AM. He had no history of dizziness, headache, abdominal pain, or diarrhea. On examination the man was alert and
afebrile; his abdomen felt normal; and his neurologic status was
intact except for peripheral neuropathy. His blood pressure was
220/118 mm Hg. Blood chemistry test results were normal. Nifedipine (sublingual), promethazine, and hydralazine (intravenous)
were administered. Acute gastroenteritis was suspected and the
man was admitted to the Medical Service.
On day 1 further vomiting occurred and the man requested
medication for headache once. By 10 PM, 12 hours after admission,
his blood pressure fell to 110/60 mm Hg; he became diaphoretic
and reported that, momentarily, the door appeared to slant sideways and his wife, standing near the bed, looked like she was
upside down. Examination within 15 minutes showed no new
abnormality. Vision was chronically impaired by diabetic retinopathy treated with laser and the fundi could not be seen. The
vomitus was coffee-ground and the differential diagnoses included
gastrointestinal bleeding. There had been no dizziness. A CT scan
of the head was normal. On day 2 nausea continued with occasional vomiting. On returning to bed after voiding, the patient was
dizzy briefly, for the first time, and “the world tilted like it did last
night.” His blood pressure, treated vigorously, was 135/70 mm Hg.
On days 3 and 4 nausea continued with occasional vomiting and,
for the second time, medication was requested for headache. Hypertensive encephalopathy was considered. On day 5 hoarseness
and dysphagia appeared abruptly, and in the following 12 hours a
complete lateral medullary syndrome developed. The man’s restlessness precluded satisfactory MRI scanning. Respiratory complications followed and cardiac arrest occurred 12 hours later. An
autopsy was not performed. Thrombosis of the left vertebral artery was suspected.
Comment. In the incipient stage, intractable nausea and
vomiting were quite out of proportion to dizziness. Headache, neither persistent nor severe, was ascribed to hypertension. Tilted
vision and upside-down vision, although infrequently reported in
the literature, would probably have led a neurologist to the right
diagnosis.
Case 2. A 70-year-old hypertensive man, while traveling on a
commercial airliner, vomited forcefully six times in 20 minutes.
He sat with his eyes closed; he was pale, diaphoretic, and cold. On
arrival after 2 112 hours he walked, with support, to a wheelchair.
He disclaimed dizziness. His blood pressure was 165/85 mm Hg.
Examination a t the Emergency Department was normal and the
man was admitted to the Medical Service with the diagnosis of
gastroenteritis. Forty-eight hours later transient diplopia occurred
and a neurologic consultant found a fine, rapid, horizontal nystagmus on gaze to the right, a slower, coarser nystagmus on gaze to
the left; the nystagmus subsided after 24 hours. An MRI scan and
vertebrobasilar angiogram were normal. Occlusion of a basilar
artery penetrating branch was the presumed diagnosis.
Discussion. In labyrinthine (end organ) disorders, nausea and
vomiting are generally proportionate to dizziness (vertigo). This
relationship does not always hold for ischemic lesions in the brainstem vestibular system, as these two cases illustrate. With ischemic lesions the vestibular deficit may be less restricted to one
side, thereby preventing the relative contralateral overactivity
that underlies end organ dizziness, the sum total of the disturbed
afferent impulses resulting in a pattern that stimulates the vom-

iting center with little or no
There is some parallel with
the dynamic neural arrangement in motion sickness.
Upside-down vision might be interpreted somewhat analogously.’J Normally, objects are still seen as correctly oriented when the
observer is in a n upside-down position, indicating a complex compensatory brain process involving vestibular function. Brainstem
ischemia must create a n abnormal neural pattern that is comparable, and that is interpreted as the environment being visually
upside down, since all other sensory information, somatosensory
and proprioceptive, indicates that the body is not upside down.
From the Neurology Service, Massachusetts General Hospital, Boston, MA.
Received March 13, 1995. Accepted in final form April 27, 1995.
Address correspondence and reprint requests to Dr. C.M. Fisher, Neurology
Service, Massachusetts General Hospital, Boston, MA 021 14.

References
1. Young LR. Perception of the body in space: mechanisms. In: Brookhart
JM,Mountcastle VB,Darian-Smith I, eds. Handbook of physiology, vol
111, part 2. Bethesda, M D American Physiological Society, 1984:10231066.
2. Goldberg JM, Fernandez C. The vestibular system. In: Brookhart J M ,
Mountcastle VB,Darian-Smith I, eds. Handbook of physiology, vol LLL,
part 2. Bethesda, MD: American Physiological Society, 1984:977-1022.
3. Ropper AH. Illusion of tilting of the visual environment. J Clin Neuroophthalmol 1983;3:147-1 51.

Transient hemiballismhemichorea due to an
ipsilateral subthalamic nucleus infarction
S. Crozier, MD; S. Lehkricy, MD, PhD; P. Verstichel, MD;
C. Masson, MD; and M.Masson, MD
Hemiballism usually results from vascular lesions of the subthalamic nucleus (STN), its afferent or efferent pathways, or its projection areas (thalamus, striatum, and lenticular nucleus). Most
often, the lesions are contralateral to the abnormal limb, but there
may be ipsilateral lesions (review reference 1).Precise correlation
between the ipsilateral lesion and the abnormal movements is
uncertain, because the lesions are usually multiple and often bilateral. We report a case of transient hemiballismhemichorea
that occurred with an isolated ischemic lesion of the ipsilateral
STN.
C a s e report. A 63-year-old man, without previous history of
neurologic or systemic disease, was awakened on May 5, 1994, by
a sudden onset of abnormal movements of the left side of the body.
Involuntary movements involved the proximal aspect of the upper
and lower limbs and were violent, irregular, and associated with
flexion and rotation. There were also irregular choreic movements
of the left hand. All these movements were exaggerated when the
patient was speaking. Muscle tone was decreased in the affected
limbs. General physical examination was normal except for elevated blood pressure (180/100 mm Hg).
Investigation revealed normal serum analysis, including lipids
and coagulation factors. Antiphospholipid antibodies were negative. Cardiac echography, B-mode carotid and vertebral ultrasonography, and Holter study were also normal.
Chlorpromazine (50 mg/day), introduced the first day, resulted
in great reduction of abnormal movements over the next 24 hours.
Then, only rare movements of wide range persisted.
CT scan performed the first day was normal. Postcontrast MRI
scan, 5 days after the onset of abnormal movements, showed a
small enhancement in the left subthalamic area. Follow-up MRI
examination, performed at 3 months, confirmed the presence of an
isolated small infarction (45 mm3) within the left subthalamic
area (figure). The stereotaxic coordinates of the center of the lesion (calculated using three-dimensional T1-weighted sections, 2
T, 1.7 mm thick) were as follows: 3 mm below the anterior commissure-posterior commissure (AC-PC) line, 2 mm behind the
midline of the AC-PC line (25 mm length), and laterally 10 mm
from the midline (width of the third ventricle, 3 mm). These coordinates corresponded to those of the subthalamic nucleus.*
Discussion. Because the previously reported cases of hemiballism, presumably caused by ipsilateral lesions, had multiple or
bilateral lesions,’ the temporal sequence of onset of abnormal
Copyright 0 1996 by the American Academy of Neurology 267

References
1. Dierssen G, Gioino GG, Coopper IS. Participation of ipsilateral hemisphere lesions in t h e pathology of hemichorea and hemiballismus. Neurology 1961;11:894-898.
2. Hassler R. In: Schaltenbrand G, Bailey P, eds. Introduction to stereotaxis with a n atlas of the human brain, vol 2. Stuttgart, Germany:
Thieme, 1977:plates 1-57.
3. Hoogstraten MC, Lakke JPWF, Zwartz MJ. Bilateral ballism: a rare
syndrome: review of the literature and presentation of a case. J Neurol
1986233:25-29.
4. Moersch FP, Kernohan JW.Hemiballismus-a clinicopathologic study.
Arch Neurol Psych 1939;41:365-372.
5. Laitinen LV, Bergenheim AT, Hariz MI. Leskell's posteroventral pallidotomy in the treatment of Parkinson's disease. J Neurosurg 1992;
76:53-61.
6. Carpenter MB, Carleton SC, Keller JT, Conte P. Connections of the
subthalamic nucleus in the monkey. Brain Res 1981;224:1-29.
7. Lavoie B, Parent A. Pedunculopontine nucleus in the squirrel monkey:
projections to the basal ganglia as revealed by anterograde tract-tracing
methods. J Comp Neurol 1994;344:210-231.

Figure. Postcontrast coronal TI-weightedMRI showing a
hypointense area (infarction) in the left subthalamic nucleus area (arrow).
movements and appearance of the lesion was not established unequivocally.
Cases of ipsilateral hemiballism have also occurred after neurosurgical lesions of the thalamus in Parkinson's disease.' In
these patients, the onset of abnormal movements was chronologically related to the production of the lesion in one or the other
hemisphere, but all had previous contralateral stereotaxjc thalamic lesions.
Hoogstraten et a13reported a case of biballism due to a unilateral lesion; and to our knowledge, Moersch and Kernohad reported the only case of hemiballism related to a n isolated ipsilateral lesion of the basal ganglia. This patient had severe left-sided
hemiballism associated with ipsilateral STN infarction, without
contralateral basal ganglia lesion, on histologic examination.
In the present case, neuroimaging studies showed that the
abnormal movements were contemporary with the infarction, as
the lesion initially enhanced after contrast administration and
enhancement disappeared a t 3 months. Stereotaxic analysis located the infarction within the ipsilateral STN and no other lesion
was present.
The pathophysiology of hemiballism is still poorly understood.
Even less understood is ipsilateral hemiballism. Based on their
model of stereotaxic thalamic lesions in parkinsonian patients,
Dierssen et a l l have postulated that a previous contralateral lesion was necessary for the occurrence of hemiballism secondary to
the ipsilateral lesion. In these patients, the ipsilateral lesion
played a "triggering" role combined with the previous contralateral basal ganglia lesion, resulting in the expression of the abnormal movements. In our patient, the presence of a preexisting
contralateral basal ganglia lesion, which was too small to detect
on MRI scans, cannot be excluded. The possibility that the STN
exerts a bilateral control of motor function may represent another
explanation to the Occurrence of ipsilateral hemiballism. This is
supported by unilateral stereotaxic neurosurgery in Parkinson's
disease frequently resulting in bilateral improvement of abnormal
movement^.^ Anatomic pathways related t o this bilateral control
are unknown. To our knowledge, there is no evidence of crossed
subthalamopallidal projections or intersubthalamic connections!
The pedunculopontine nucleus, however, which is involved i n motor functions, is bilaterally connected to the STN.' Whether these
pathways play a role in the production of ipsilateral hemiballism
remains to be determined.
Acknowledgment
We thank Professor J. Feger for his useful comments and suggestions.
From the Departments of Neurology fDrs. Crozier, Verstichel, C. Masson,
and M. Masson) and Radiology (Dr. Lehericy), Hipital Beaujon. Clichy,
France.
Received February 16, 1995. Accepted in final form May 4. 1995.
Address correspondence and reprint requests to Dr. Verstichel, Service de
Neurologie, H6pital Beaujon, 921 10 Clichy. France.

268

Copyright 0 1996 by the American Academy of Neurology

Headaches after inadvertent lumbar puncture
during bone marrow harvest
Frank Lieberman, MD, and Subhash Gutati,MD
Headaches in a cancer hospital are common and often require
extensive diagnostic evaluation to exclude metastatic intracranial
disease or infection. However, one does not expect to encounter
headache in an individual with no other neurologic illness who
donates bone marrow. We have seen two patients develop positional headaches, which were typical of low pressure headaches
occurring after lumbar puncture, after bone marrow harvest. In
both patients, the headaches resolved without specific therapy.
Case reports. Patient 1. A 44-year-old woman underwent
elective bone marrow harvest to provide marrow for a n HLA compatible sibling. She was morbidly obese. For several years, she
suffered diffuse headache on awakening that would abate as she
stood up and began her daily activities. The physician performing
the bone marrow harvest noted the patient's obesity obscured the
usual landmarks. When the surgical drapes were removed, several puncture marks were noted over the lateral sacrum. When
the patient awoke from general anesthesia, she complained of
severe headache accompanied by nausea and several episodes of
vomiting. Sitting upright exacerbated the headache, which was
relieved by lying supine. These new headaches were clearly different from the early morning headaches she had reported a t the
time of admission. Neurologic examination several hours after the
headaches began demonstrated anisocoria with the right pupil
being 3mm and the left 2.5mm. There was no papilledema. The
cranial nerve examination was otherwise normal and the remainder of the neurologic exam was unremarkable. The headaches
gradually abated over 5 days, and the anisocoria resolved.
Patient 2. A 50-year-old woman with stage IV diffise T-cell
lymphoma underwent bone marrow harvest to obtain stem cells
for autologous bone marrow rescue after high-dose chemotherapy.
Before the harvest, performed under general anesthesia, she had
no neurologic complaints. The procedure was uneventful and the
patient resumed normal activity. Severe band-like headache,
which radiated into the nuchal region, began 48 hours later. The
headache pain was worsened by sitting or standing and relieved
by lying flat. The patient visited the emergency room after these
headaches persisted unchanged for several days. Neurologic examination was unremarkable. The needle marks from the marrow
aspiration were visible, including a puncture mark 3 cm left of the
midline over the sacrum. A brain magnetic resonance imaging
(MRI) scan, performed with and without gadolinium 10 days after
the headaches began, was unremarkable. The headaches remitted
after 2 weeks.
Discussion. Positional headache is a frequent complication of
diagnostic lumbar puncture' and a well-recognized, although infrequent, complication of epidural anesthesia.2 The headache improves when the patient lies flat and is exacerbated by sitting or
standing. The headache is caused by low spinal fluid pressure due
to leakage of CSF from the thecal sac. Symptoms and signs of
cranial nerve dysfunction, including diplopia, tinnitus, facial
numbness, and anisocoria, occur? MRIs of patients with low pressure headache sometimes demonstrate diffuse meningeal enhancement and downward brain displacement.' Rarely, subdural

Transient hemiballism/hemichorea due to an ipsilateral subthalamic nucleus infarction
S. Crozier, S. Lehericy, P. Verstichel, et al.
Neurology 1996;46;267-268
DOI 10.1212/WNL.46.1.267-a
This information is current as of January 1, 1996
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