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Buccofacial apraxia without aphasia due to a right parietal lesion.

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neurological disease. There is no support for cerebral
vasospasm as the cause because cerebral blood flow
remains normal with moderate or even severe hypoglycemia El}. Underlying brain disease may rarely
come to light with hypoglycemia. One report describes
a patient with HH in whom surgical correction of a
carotid lesion stopped subsequent hypoglycemia from
producing contralateral hemiplegia [S]. In animals, ligation of the middle cerebral artery and subsequent
hypoglycemia may produce contralateral paralysis,
which resolves when the hypoglycemia is corrected
{ S } . The rarity of underlying brain disease revealed by
hypoglycemia is demonstrated in this series, in which
detectable brain disease was found in only 1 of the 16
patients. In Patient 6, gross and microscopic examination of the brain showed no focal disease despite
prominent focal neurological symptoms in life. Postmortem examination of similar patients also failed to
demonstrate focal brain lesions {9]. The right-sided
predilection as well as the alternating character of the
hemiplegia also argue against an underlying brain disease. Finally, hemiplegic hypoglycemia occurs in patients who are not expected to have underlying brain
disease, such as those with insulinoma {9}, children
{31, and patients receiving insulin shock for schizophrenia {lo]. The diagnosis of HH is best not ruled
out until a blood glucose level is available, as a response to glucose treatment alone may not be
sufficiently specific. Rapid confirmation of hypoglycemia using a capillary blood sample is an adequate indication for glucose treatment while awaiting a more reliable sample. If the diagnosis is suspected or confirmed,
reduction of the dose of insulin or oral hypoglycemic
agents may be used as a diagnostic trial. If successful,
this may avoid the occurrence of irreversible neurological deficits and save unnecessary and risky investiga:ions.
References
1. Agardh C-D, RosCn 1, Ryding E: Persistent vegetative state with
2.
3.
4.
5.
6.
7.
8.
high cerebral blood flow following profound hypoglycemia.
Ann Neurol 14:482-486, 1983
Gale EAM, Tattersall RB: Unrecognized nocturnal hypoglycaemia in insulin-treated diabetics. Lancet 1:1049-1052, 1979
MacDonald JT, Brown DR: Acute hemiparesis in juvenile insulin-dependent diabetes mellitus (JIDDM). Neurology (Minneap) 29~893-896, 1979
Malouf R, Brust JCM: Hypoglycemia: causes, neurological manifestations, and outcome (abstr). Ann Neurol 12:110, 1982
Meyer JF, Porrnoy HD: Localized cerebral hypoglycemia
simulating stroke. Neurology (Minneap) 8:601-614, 1958
Montgomery BM, Pinner CA, Newberry SC: Transient hypoglycemic hemiplegia. Arch Intern Med 114:680-684, 1964
Penman WA, Johnson JK: Recurrent hemiplegia due to hypoglycemia. Postgrad Med J 58:501-502, 1982
Portnoy HD: Transient “ischemic” attacks produced by carotid
stenosis and hypoglycemia. Neurology (Minneap) 152330432,
1965
5 12
9. Richardson JC, Chambers BM, Heywood PM: Encephalopathies of anoxia and hypoglycemia. AMA Arch Neurol 1:
178-190, 1959
10. Wortis J, Bowman KM, Orenstein LL., Rosenbaum IJ: Further
experiences at Bellevue Hospital with the hypoglycemic insulin
treatment of schizophrenia. Am J Psychiatry 94:153-158, 1937
Buccofacial Apraxia
without Aphasia Due to a
Right Parietal Lesion
Joel H. Kramer, PsyD, Dean C. Delis, PhD,
and Tsutomu Nakada, MD
~
~~~~~~~~~~~~~~~~~
Buccofacial praxis in right-handers is thought to be
mediated by the left hemisphere. We present the case of
a right-handed man without family history of sinistrality who exhibited a buccofacial apraxia following a unilateral right parietal infarction. Other findings such as
intact language, visuospatial impairment, and hemiinattention are more characteristic of right posterior
lesions.
Kramer JH, Delis DC, Nakada T:
Buccofacial apraxia without aphasia
due to a right parietal lesion.
Ann Neurol 18:512-514, 1985
Buccofacial apraxia in right-handers is generally considered to result from lesions in the left hemisphere
[3}. Reports of buccofacial apraxia in right-handers following right-hemisphere damage are particularly uncommon. Nathan [S} cited five articles published prior
to 1914 that described lesions in the right hemisphere
producing “facial apraxia.” The patient’s handedness
was not always stated, however, and the lesions were
described as being extensive or in the frontal lobes. To
our knowledge, a buccofacial apraxia following a righthemisphere lesion in a right-hander (“crossed apraxia”)
has not been reported since 1914. We report a case of
buccofacial apraxia in a right-handed man following a
unilateral right posterior lesion.
Case Report
A 62-year-old retired school teacher was admitted because
of a left-sided weakness. One day prior to admission his wife
From the Martinez VA Medical Center, 150 Muir Rd, Martinez,
CA 94553.
Received Mar 18, 1985, and in revised form Apr 16. Accepted for
publication Apr 18, 1985.
Address reprint requests to Dr Kramer, Psychology Service (1IbB),
VA Medical Center, 150 Muir Rd, Martinez, CA 94553.
A
B
Fig I . Patient’s copy (A) of a daisy (B).
had found him on the floor. At that time he had a “droopy
left face” and was unable to move the left side of his body.
The patient was right-handed and had no known family history of sinistrality.
O n admission, neurological examination revealed weakness of the left arm and milder weakness of the left leg.
Results of cranial nerve examination were unremarkable except for a mild left central facial weakness and a ptosis of the
right eye. Results of the sensory examination were normal.
Deep tendon reflexes were symmetrical with bilateral flexor
plantar responses.
Expressive speech was intact except for a mild dysarthria
and a flattening of melodic line. O n the Boston Diagnostic
Aphasia Examination, the patient’s comprehension, confrontation naming, repetition, reading, and writing abilities were
intact. His verbal IQ on the Wechsler Adult Intelligence
Scale (WAIS) was 116 (85th percentile). His performance
on the Wechsler Memory Scale was also above average (75th
percentile).
O n testing of buccofacial praxis, the patient could not follow commands to cough, swallow, grin, whistle, blow out a
match, suck through a straw, or protrude his tongue, despite
indications that he understood the commands. The patient
was equally unable to imitate these movements. Errors consisted of either verbal substitutions for the requested motor
act (e.g., he said “cough” when trying to cough), or inability
to initiate the movement. Bilateral testing of limb praxis was
precluded by the patient’s left hemiparesis. With his right
arm and hand, he could perform such movements as saluting
and flipping a coin, but made body-part-as-object errors on
commands to comb his hair, shave, and saw wood; on one
occasion he perseverated on a prior movement. H e correctly
imitated these limb gestures when they were performed by
the examiner and was able to use objects such as a comb.
The patient’s visuospatial abilities were evaluated with
drawing tasks and the Performance subtests from the WAIS.
His drawings, block designs, and puzzle constructions revealed marked spatial disorganization, loss of configuration,
and absence of three-dimensional perspective. His copies of
a daisy (Fig 1) and the Rey-Osterreith Complex Figure indicated a left hemi-inattention. Right-left discrimination and
map orientation were also impaired. His WAIS Performance
I Q was at the 1lth percentile (PIQ = 84).
Fig 2 . Computed tomographic scan showing a low-density area
in the right parietal and frontal lobes. This area extended into
the right corona radiata.
Computed tomographic (CT) scanning of the brain revealed a low-density area in the right parietal and frontal
lobes with extension into the right corona radiata consistent
with an infarct of the right postcentral and anterior parietal
region (Fig 2). No other cerebral lesions were discovered.
Discussion
It has been thought that the right hemisphere does not
play a major role in buccofacial praxis (31. In righthanded individuals the major repository for motor
learning is considered to be in the left hemisphere { 1,
61. The model of apraxia proposed by Geschwind 111
and others 13, 61 suggests that apraxic syndromes result from destruction of kinesthetic motor engrams or
from their disconnection from primary motor areas.
Thus, the lesions thought to produce apraxia are in the
left hemisphere, corpus callosum 111, or right premotor regions [l, 31. Buccofacial or limb apraxia associated with right posterior lesions is very uncommon
and has only been reported in left-handers 14, 7, 101.
Most of our patient’s neurological and neuropsychological findings were consistent with his right
posterior lesion (e.g., left hemiparesis, left hemiinattention, spatial disorganization). His inability to execute learned facial movements was unexpected, however. His symptoms cannot be attributed to language
Case Report: Kramer et al: Buccofacial Apraxia
5 13
disturbance or motor weakness because linguistic skills
and complex oral movements such as speech were intact. It is equally unlikely that there was left hemisphere involvement; his prior neurological history was
unremarkable and his CT scan was normal on the left
side. Our patient’s case thus illustrates a buccofacial
apraxia following a right posterior lesion in a righthander .
In our patient, buccofacial praxis either was lateralized to the right hemisphere or was bilaterally represented. It is possible that the cerebral organization for
praxis within his right hemisphere “mirrored” the organization most typically found when praxis is subserved by the left hemisphere. The evidence for this is
equivocal. Some structures of the left hemisphere
thought to be critical for buccofacial apraxia such as the
frontal and central opercula [9} were infarcted in our
patient’s right hemisphere. However, other areas such
as the anterior insula and the first temporal convolution were intact, and there were no indications of abnormal asymmetries on CT scans. The mechanisms by
which our patient’s anomalous cerebral organization
for praxis developed are also uncertain. A related
question is whether his right parietal lobe represented
the primary area for buccofacial praxis or whether it
played a secondary but still critical role.
It has been known for some time that language and
right-handedness are not invariably linked in the left
hemisphere. In right-handers without a family history
of sinistrality, crossed aphasia occurs following right
hemisphere compromise in only 2% of the cases [a}.
In contrast, variance in the association of praxis and
right-handedness when the left hemisphere is compromised has rarely been observed 171. The present case
indicates that variability in cerebral organization for
buccofacial praxis can occur, resulting in a “crossed
apraxia” for buccofacial movements. The presence of a
“crossed apraxia” in a patient with intact verbal skills
also lends support for theories of cerebral organization
that dissociate praxis and language [ 5 ] .
References
1. Geschwind N: The apraxias: neural mechanisms in disorders of
learned movement. Am Sci 63:188-195, 1975
2. Hecaen H , Albert ML: Human Neuropsychology. New York,
Wiley, 1978
3. Heilman K. Apraxia. In Heilman K, Valenstein E (eds): Clinical
Neuropsychology. New York, Oxford University Press, 1972
4. Heilman KM, Coyle HM, Gonyea EF, Geschwind N: Apraxia
and agraphia in a left-hander. Brain 9621-28, 1973
5. Kertesz A, Hooper P: Praxis and language: the extent and variety of apraxia in aphasia. Neuropsychologia 20:275-286, 1982
6. Leipmann H: Die linke Hemisphire und das Hindelin. Munch
Med Wschr 49:2375-2378, 1905
7. Margolin DI: Right hemisphere dominance for praxis and lefthemisphere dominance for speech in a left-hander. Neuropsychologia 18:715-719, 1980
514
8. Nathan PW. Facial apraxia and apraxic dysarthria. Brain
70:442-478, 1947
9. Tognolo G, Vignolo LA: Brain lesions associated with oral
apraxia in stroke patients: a clinico-neuroradiologicalinvestigation with the CT scan. Neuropsychologia 18:257-272, 1980
10. Valenstein E, Heilman KM: Apraxic agraphia with neglectinduced paragraphia Arch Neurol 36:506-508, 1979
a-1 Antitrypsin
Phenotvoes- in
DernyeGnating Disease:
An Association between
Demyelinating Disease
and the Allele PiM3
P. A. McCornbe, FRACP, P. Clark, PhD,
J. A. Frith, MB, S. R. Hammond, FRACP,
G. J. Stewart, FRACP, J. D. Pollard, FRACP,
and J. G. McLeod, FRACP
a-1 Antitrypsin, the major circulating protease inhibitor, has more than thirty alleles that can be
identified by electrophoresis. In addition to its role as a
protease inhibitor, a-1 antitrypsin may regulate the immune response. As there is evidence that both the
inflammatory polyneuropathies and multiple sclerosis
have an immune basis, and that genetic factors influence
susceptibility, we have determined the a-1 antitrypsin
phenotypes (protease inhibitor types) of 63 patients with
Guillain-Barre syndrome, 52 patients with chronic inflammatory demyelinating polyneuropathy, and 178 patients with multipIe sclerosis. In all 3 groups there was a
significant increase in the proportion of patients with
the protease inhibitor type M3 allele.
McCombe PA, Clark P, Frith JA, Hammond SR,
Stewart GJ, Pollard JD, McLeod JG: a-1
Antitrypsin phenotypes in demyelinating disease:
an association between demyelinating disease and
the allele PiM3. Ann Neurol 18:514-516, 1985
a-1 Antitrypsin or a-1 proteinase inhibitor, an acutephase reactant, functions as a protease inhibitor {b}
and also may regulate the immune response 191. It is
From the Department of Medicine, University of Sydney, New
South Wales 2006, Australia.
Received Ju1 30, 1984, and in revised formJan 14, 1985. Accepted
for publication Jan 25, 1985.
Address reprint requests to Dr McLeod.
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