plasmy in members of both families, including the 2
mothers. Single mtDNA deletions, occurring in a
mother and her son, were previously reported 1131,
but they differed in the 2 patients by size and localization, making direct transmission of the mutation unlikely.
Since in all our patients deletions were present in
different tissues, the origin of heteroplasmy must be
traced back to a somatic mutation occurring at a stage
earlier than organogenesis. In mouse C141 and Xenopus
laevis 1151 embryos, mtDNA content increases tremendously during organogenesis. As a result, enormous amplification could occur even of a single deleted mtDNA, which because of its smaller size,
replicates faster than wild-type mtDNA. Furthermore,
the rapid cell proliferation will promote mitotic segregation, “loss” of mutant mtDNAs in the extrafetal
structures, and negative selection of respiratory-deficient cells. These can be important clues to understanding the variability in the quantitative distribution
of the heteroplasmic mtDNAs in different clinical
phenotypes.

References
1. Anderson S, Bankier AT, B a r d BG, et al. Sequence and
organization of the human mitochondrial genome. Nature
1981;290:457-465
2. Holt IJ, Harding AE, Morgan-Hughes JA. Deletions of mitochondrial DNA in patients with mitochondrial myopathies. Name 1988;331:717-719
3. Zeviani M, Moraes CT, DiMauro S, et al. Deletions of mitochondrial DNA in Kearns-Sayre syndrome. Neurology 1988;
38: 1339-1346
4. Moraes CT,DiMauro S , Zeviani M, et al. Mitochondrial DNA
deletions in progressive external ophthalmoplegia and KeamsSayre syndrome. N Engl J Med 1989;320:1293-1299
5. Poulton J, Deadman ME, Gardiner RM. Duplication of mitochondrial DNA in mitochondrial myopathy. Lancet 1989;l:
236-240
6. Rotig A, Colonna M, Bonnifont JP, et al. Mitochondrial DNA
deletions in Pearson’s marrow/pancreas syndrome. Lancet,
1989;1:902-903
7. Zeviani M, Servidei S, Gellera C, et al. An autosomal dominant
disorder with multiple deletions of mitochondrial DNA starting
at the D-loop region. N a m e 1989;339:309-311
8. Saiki RK, Gelfand DH, Stoffel S, et al. Primer-directed enzymatic amplification of DNA with a thermostable DNA polymerase. Science 1988;239:487-491
9. Winship PR. An improved method for directly sequencing
PCR-amplified material using dimethyl sulphoxide. Nucleic
Acids Res 1989;17:1266
10. Pavlakis SG, Rowland LP, DeVivo DC, et al. Mitochondrial
myopathies and encephalomyopathies. In: Plum F, ed. Contemporary neurology. Philadelphia: FA Davis, 1988:95-433
11. Tome FMS, Fardeau M. Ocular myopathies. In: Engel AG,
Banker BQ, eds. Myology: basic and clinical, vol2. New York:
McGraw-Hill, 1986:1327-1347
12. Schon EA, RiRitzuto R, Moraes CT, et al. A direct repeat is a
hotspot for large-scale deletion of human micochondrial DNA.
Science 1989;244:346-349
13. Ozawa T, Yoneda M, Tanaka M, et al. Maternal inheritance of

deleted mitochondrial DNA in a family with mitochondrial myopathy. Biochem Biophys Res Commun 1988;154:1240-1247
14. Piko’ L, Taylor KD. Amounts of mitochondrial DNA and abundance of some mitochondrial gene transcripts in early mouse
embryos. Dev Biol 1987;123:364-374
15. Chase JW,Dawid IB. Biogenesis of mitochondria during
Xenopus lawis development. Dev Biol 1972;27:504-518

Dissociated Neglect
Behavior Following
Sequential Strokes in the
Right Hemisphere
Kirk R. Daffner, MD, Geoffrey L. Ahern, MD, PhD,
Sandra Weintraub, P h D , and M-Marsel Mesulam, M D

A 42-yeax-old woman suffered two focal right hemisphere strokes, sequentially damaging different components of a proposed cerebral network for the spatial distribution of attention. Her first stroke was centered in
the right frontal lobe and resulted in left hemispatial
neglect
but only for tasks that emphasize exploratorymotor components of directed attention. A second
stroke occurred 20 days later in the parietal lobe and led
to the emergence of perceptual-sensory aspects of neglect. This case strongly supports the existence of a distributed anatomic-functional network subserving diattention.
Daffner KR, Ahern GL, Weinuaub S, Mesulam M-M.
Dissociated neglect behavior following
sequential strokes in the right hemisphere.
A n n Neurol 1990;28:97-101

Unilateral neglect is a common and dramatic sequel of
right hemisphere injury. It reflects a fundamental disruption in the distribution of directed attention and
manifests itself clinically as a failure to recognize, respond to, and explore stimuli located within the left
hemispace 11-31. While the occurrence of neglect was
originally believed to reflect parietal lobe disease 14,
51, subsequent reports have clearly shown that lesions
elsewhere in the right hemisphere may result in a similar clinical picture 16-12}.
From the Bullard and Denny-Brown Laboratories, the Division of
Behavioral Neurology and Neuroscience of the Harvard Neurology
Department, and the Charles A. Dana Research Institute of the
Beth Israel Hospital, Boston, MA.
Received Sep 21, 1989, and in revised form Jan 5 , 1990. Accepted
for publication Jan 17, 1990.

Address correspondence to Dr Daffner, Behavioral Neurology
Unit, Beth Israel Hospital, 330 Brookline Avenue, Boston, MA
02215.

Copyright 0 1990 by the American Neurological Association

97

Several authors have accounted for the various behavioral components of neglect and the multiplicity of
underlying lesion sites on the basis of a distributed
cerebral network 11, 2, 13, 141. According to one of
these theories, directed spatial attention is subserved
by a distributed cerebral network with three cortical
components { 1, 27. The relationship between the anatomical site of the lesion within this network and the
clinical features of the resultant neglect behavior is
incompletely understood. We recently had the opportunity to investigate a patient who had had two sequential right hemisphere strokes involving separate anatomical components of the attention network. Each
stroke resulted in different behavioral deficits that
were in keeping with the proposed organization of this
network.

Case Report
A 42-year-old right-handed woman with a history of severe
hypertension and thrombotic thrombocytopenic purpura (in
remission) developed acute neurological deficits. She had full
visual fields, normal extraocular movements, a left facial
palsy, and mild left upper-extremity weakness. The left plantar response was extensor. Pin prick and light touch sensations were intact. There were mild and inconsistent deficits
in position sense, graphesthesia, and stereognosis in the left
upper extremity.
The patient was alert, oriented, and appropriately motivated. Judgment, insight, and abstract reasoning were intact.
Digit span was 6 forward and 5 in reverse. Tasks requiring
sustained vigilance, divided attention, memory, language,
and analogical reasoning were done well.
The major abnormalities on mental state testing were
noted in tasks of directed attention and complex perceptual
processing. She was given two types of spatial attention tasks,
emphasizing either perceptual-sensory or exploratory-motor
processes. The perceptual components were assessed by
tests for sensory extinction. The patient was presented with
multiple trials of sensory stimulation in each of the three
major modalities. Six stimuli were right sided, 6 were left
sided, and 6 were bilateral and simultaneous, presented randomly. She was errorless in the tactile modality, and exhibited left-sided extinction in only 1 of the 6 trials of bilateral
auditory stimulation. There was no visual extinction, but she
exhibited allesthesia, by mislocating the stimulus to the right
in 1 of 6 unilateral left-sided visual stimulation trials. In summary, after the first stroke, the degree of sensory neglect for
the left hemispace was minimal.
The exploratory-motor components were tested by two
instruments. On a random letter cancellation task [15, 16),
using her unaffected and preferred right hand, she marked
only stimuli located within the right margin of the test sheet
(Fig 1). The second test to assess the exploratory-motor aspects of neglect was based on a manual spatial exploration
task [16]. The patient was blindfolded and asked to search by
palpation for a small plastic pin fixed to a cork-covered
board. There were 9 trials conducted in each hemispace,
using each hand. The patient took significantly longer to
locate a target in the left hemispace than in the right. Using
her unaffected right hand, she required a mean of 18 seconds

98 Annals of Neurology Vol 28 No 1 July 1990

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side of the page.

in the left hemispace versus 10 seconds in the right hemispace ( p < 0.05, one-tailed Wilcoxon signed ranks test).
Even when using her modestly paretic left upper extremity,
she consistently crossed over the midline to begin her search
on the right side of the board, and required 47 seconds to
locate a target on the left side versus 26 seconds on the right
( p < 0.05). The severity of exploratory-motor neglect revealed by these two tests contrasted sharply with the very
mild tendency for sensory extinction.
Other tests of complex perceptual function revealed salient deficits. For example, she performed in the severely
impaired range (7/30) on the Judgment of Line Orientation
Test 1171, the Block Designs subtest of the Wechsler Adult
Intelligence Scale-Revised (raw score, 17; scaled score, 6)
[18f,the Facial Recognition Test (35154) 1191, and the Mental Rotation subtest of the Luria-Nebraska Neuropsychological Battery (6110) [20].
A cranial computed tomographic scan revealed an infarction in the right frontal lobe within the distribution of the
middle cerebral artery, largely involving the middle frontal
gyms and including the frontal eye fields (Fig 2). Extensive
vascular, cardiac, and hematological tests failed to reveal a
specific cause for the stroke.
Examination 1 week later demonstrated mild improvement of motor strength. Repetitive trials of sensory stimdation revealed no extinction in any modality. On the random
letter cancellation task, she exhibited some improvement but
still missed about half (12130) of the targets on the left side
of the test sheet. At this stage of partial recovery, the dissociation between the exploratory-motor and perceptual-sensory
components of neglect became even more obvious.
Two weeks after discharge, she came to the emergency
room complaining of a right frontal headache and an episode
of visual clouding of her right eye. Her elementary neurological examination revealed a left facial palsy and weakness of
the left upper extremity. There was no hemianopsia. Pin,
temperature, light touch, and vibratory sensations were intact. She exhibited marked astereognosis and agraphesthesia
in the left hand.

F i g 3. Coronal magnetic resonance imaging MRI (Tl-weighted
image) revealing the second stroke in the right posterior parietal
lobe, including the inferior parietal lobaule. The right side of the
head is on the lej9 side of the scan. Arrows demarcate the infa.ct.
Fig 2.Axial computed tomographic scan aft.. the first stroke,
demonstrating an infarction in the right frontal lobe (demarcated
&y arrows), largely inzdwing the middle frontal gyus and inclnding the frontal eyefields. The right side ojthe head is on the
leJt side of the scan.

Repeat administration of the sensory stimulation trials revealed prominent neglect and allesthesia. In the visual and
auditory modalities, she made no mistakes when presented
unilateral stimuli; however, she exhibited left-sided extinction on bilateral simultaneous stirnulation in 4 of 6 trials in
the visual modality and in all 6 trials in the auditory modality.
She made no errors when given unilateral right-sided and
bilateral simultaneous tactile stimuli but exhibited allesthesia
by mislocating to the right side 3 of 6 tactile stimuli presented on the left side. Thus, extinction was particularly
prominent in the two modalities, auditory and visual, which
are most closely associated with the extrapersonal space. In
comparison with the first stroke that yielded left-sided extinction in only 8% of the bilateral simultaneous stimulation
trials in the visual and auditory modalities, the second stroke
increased the frequency of these errors to 83%.
Repeat administration of the two exploratory-motor tasks
demonstrated the reemergence of severe deficits. For example, on the random letter cancellation test, she missed all
30 stimuli on the left. Performance on the Judgment of Line
Orientation Test (8130) and Block Designs (raw score, 6;
scaled score, 4 ) remained severely impaired.
A computed tomographic scan revealed a new right posterior parietal stroke with a hemorrhagic component. The infarct included the inferior parietal lobule and was Confirmed
by a follow-up magnetic resonance imaging Scan (Fir: 1).
Discussion
Many theories have been proposed to account for neglect. Some have emphasized its sensory manifesta-

tions. For example, Denny-Brown [21) argued that
parietal lobe damage leads to deficits in sensory integration (amorphosynthesis), resulting in neglect of the
contralateral hemispace. Bender 1221 invoked a process of perceptual rivalry through which sensory input
to a lesioned hemisphere is degraded and “extinguished’’ when competing with simultaneous input to
the intact hemisphere. Others have argued that neglect
reffects distortion of the internal mental representation
of extrapersonal space [23, 241. Heilman and colleagues [13, 14, 251 have described a neuroanatomical
system involving cortical-limbic-thalamic-reticular cornponents that lead to preparatory activation or arousal
toward meaningful stimuli in the contralateral hemispace.
A review of neglect syndromes in monkeys and humans suggested that several cerebral regions provide
an integrated network for the mediation of directed
attention [l, 2). The three cortical components of this
network are the posterior parietal lobe, frontal eye
fields, and the cingulate gyrus. In addition to delineating these anatomical regions, three major behavioral
components of attention were also identified as follows: (1) A sensory component provides an internal
representation of extrapersonal space. Dysfunction of
this component yields extinction, allesthesia, and perceptual misrepresentations. (2) A motor component
coordinates scanning and exploratory behavior. Dysfunction of this component is manifested as impaired
scanning, searching, and orienting. (3) A limbic cornponent regulates the spatial distribution of motivationd valence. Dysfunction of this component can lead
to an emotional devaluation of events occurring in the
opposite hemispace.

Brief Communication: Daffner et al: Dissociated Neglect Behavior 9!9!

It was hypothesized that specific parts of the anatomical network provided the underlying substrate for
the different behavioral aspects of directed attention.
The parietal component was linked with the perceptual-sensory aspects, the frontal component with the
exploratory-motor aspects, and the cingulate component with the motivational aspects. Although studies
with experimental animals have tended to support
these relationships, pertinent evidence has been difficult to gather in humans. The special nature of our
patient’s clinical course allowed us to address this issue.
Sequential and relatively selective damage to two components of the attention network created the appropriate circumstances for a dissociation of her neglect behavior.
The first stroke sustained by our patient yielded an
infarction in the frontal lobe including the frontal eye
fields. At that time, the patient demonstrated severe
left-sided neglect on two tasks that emphasize the exploratory-motor components of directed attention but
not on tasks that emphasize its perceptual-sensory
components. The patient’s second stroke involved the
right posterior parietal lobe, including the inferior
parietal lobule. At that time, the patient developed
marked sensory-perceptual aspects of neglect in the
form of multimodal extinction. Even this patient, however, demonstrates the existence of a strong physiological linkage among the various components of this network, since the exploratory-motor deficits reemerged
with increased intensity after her second stroke in the
parietal lobe.
Consideration of the different components of neglect is important when evaluating patients. Our patient’s performance after the first stroke (severe exploratory neglect with minimal sensory extinction)
demonstrates that sensory extinction cannot be viewed
simply as a subtle form of neglect as some have
claimed. Tests that emphasize one component of directed attention may be normal in the face of marked
abnormalities in tasks that emphasize other components [3, 9, 16, 26, 271. The absence of primary visual
and auditory sensory loss or oculomotor deficits illustrates that neglect does not result from a combination
of elementary sensory-motor deficits but reflects a disorder of complex attention.
Even after the first stroke, the neuropsychological
deficits exhibited by our patient were not limited to
hemispatial neglect. She did poorly on visual-perceptual and spatial rotational tasks. The existence of such
additional deficits is in keeping with the network approach to the localization of complex behavior. This
approach suggests that cortical areas subserving a
complicated behavior such as attention are also components of intersecting networks subserving other
complex neuropsychological functions. The unique circumstances of this patient’s clinical history further support the conclusion that directed spatid attention is
100 Annals of Neurology Vol 28 No 1 July 1990

subserved by a cerebral network containing several
anatomically distributed but neurally interconnected
components, each specializing in a different aspect of
this behavior.
We thank Betsy Sherry, MD, who initially evaluated this patient,
and Jill Kaplan, MD, and Steven Schacter, MD, who managed her
care during the second admission. We appreciate the assistance of
Joan Guinnessey, who helped administer some of the tests, Jonathan
Kleefield, MD, and Gerald OReilly, MD, who reviewed her
radiological scans, and Jim Stoddard, who provided technical assistance.

References
1. Mesulam M-M. Attention, confusional states, and neglect. In:
Mesulam M-M, ed. Principles of behavioral neurology. Philadelphia: F A Davis, 1985:125-168
2. Mesulam M-M. A cortical network for directerl attention and
unilateral neglect. Ann Neurol 1981;10:309-325
3. Weintraub S, Mesulam M-M. Neglect: hemispheric specialization, behavioral components and anatomical correlates. In: Boller F, Grafman J, eds. Handbook of Neuropsychology, vol 2.
Amsterdam: Elsevier Science Publishers, 1989:357-374
4. Denny-Brown D, Chambers RA. The parietal lobe and behavior. Proc Assoc Res Nerv Ment Dis 1958;36:35-117
5. Critchley M. The parietal lobes. London: Edward Arnold, 1953
6. Damasio AR, Damasio H, Chui HC. Neglect following damage
to frontal lobe or basal ganglia. Neuropsychologia 1980;18:
123-132
7. Heilman KM, Valenstein E. Frontal lobe neglect in man. h-eud o g y 1972;22:660-664
8. Watson RT, Valenstein E, Heilman KM. Thalamic neglect: possible role of the medial thalamus and nucleus reticularis in behavior. Arch Neurol 1981;38:50 1-506
9. Vallar G, Perani D. The anatomy of unilateral neglect after right
hemisphere stroke lesions: a clinicdCT scan correlation study
in man. Neuropsychologia 1986;24:609-622
10. Stein S, Volpe BT. Classical “parietal” neglect syndrome after
subcortical right frontal lobe infarction. Neurology 1983;33:
797-799
11. Hier DB, Davis KR, Richardson EP, Mohr JP. Hypertensive
putaminal hemorrhage. Ann NeuroI 1977;1:152-159
12. Healton EB, Navarro C, Bressman S, Brust JCM. Subcortical
neglect. Neurology 1982;32:?76-778
13. Heilman KM, Watson RT, Valeristein E. Neglect and related
disorders. In: Heilman KM, Valenstein E, eds. Clinical neuropsychology. New York Oxford University Press, 1985:243294
14. Heilman KM, Valenstein E. Mechanisms underlying hemispatial
neglect. Ann Neurol 1979;5:166-170
15. Weintraub S, Mesulam M-M. Visual hemispatial inattention:
stimulus parameters and exploratory strategies. J Neurol
Neurosurg Psychiatry 1988:5 1:1481-1488
16. Weintraub S, Mesulam M-M. Right cerebral dominance in spatial attention: further evidence based on ipsilateral neglect. Arch
Neurol 1987;44:621-625
17. Benton AL, Varney NR, Hamsher K deS. Visuospatial judgment: a clinical test. Arch Neurol 1978;35:364-367
18. Wechsler D. Manual for the Wechsler adult intelligence scale.
New York: The Psychological Corporation, 1955
19. Benton AL, Hamsher K deS, Varney NR, Spreen 0. Contributions to neuropsychological assessment. New Yo&: Oxford
University Press, 1983
20. Golden CJ, Hammeke TA, Purisch AD. Manual for the LuriaNebraska neuropsychological battery. Los Angeles: Western
Psychological Services, I980

21. Denny-Brown D, Meyer JS, Hornstein S. The significance of
perceptual rivalry resulting from parietal lobe lesion. Brain
1952;75:434-471
22. Bender MD. Extinction and precipitation of cutaneous sensation. Arch Neurol Psychiatry 1945;54:1-9
23. Bisiach E, Luzzatti C, Perani D. Unilateral neglect, representational schema and consciousness. Brain 1979;102:609-618
24. Bisiach E, Luzzatti C. TJnilateral neglect of representational
space. Cortex 1978;14:129-133
25. Heilman KM, Bowers D, Coslett HB, et al. Directional hypokinesia: prolonged reaction times for leftward movements in
patients with right hemisphere lesions and neglect. Neurology
1985;35:855-859
26. Barbieri C, De Renzi E. Patterns of neglect dissociation. Behav
Neurol 1989;2:13-24
27. Zarit SH, Kahn RL. Impairment and adaptation in chronic disabilities: spatial inattention. J Nerv Ment Dis 1974;159:63-72

Positron Emission
Tomography in Shy-Drager
Syndrome
Mohit H. Bhatt, MD, DM,
Barry J. Snow, MBChB, FRACP,
W. R. Wayne Martin, MD, FRCPC, Sandra Cooper, RN,
and Donald B. Calne, DM, FRCP, FKCPC

motor neuron deficits El]. Parlunsonism is an important manifestation of SDS [l-31. With the availability
of {'8F)6-fluoro-1-dopa (6-FD) and positron emission
tomography (PET), the functional integrity of the nigrostriatal pathway can be studied in vivo. Striatal 6F D uptake has been shown to be depressed in presynaptic nigrostriatal dopaminergic disorders such as
idiopathic parkinsonism [4-71. T h e purpose of this
study was to evaluate presynaptic nigrostriatal function
in parkinsonism of SDS by using 6-FD PET.

Patients and Methods
Patient I
A 52-year-old man had a 4-year history of limb rigidity,
impotence, incontinence of urine, chronic constipation, and
multiple syncopal attacks. On examination he had postural
hypotension (2201130 supine, 70150 standing). Kgidity,
bradgkinesia, hypomimia, and hand tremor were present.
His voice was monotonous and hypophonic. He had brisk
tendon reflexes and bilateral extensor plantar responses. He
scored 35 on the Columbia scale, which measures overall
motor deficits in parkinsonian patients. Head computed tomographic (CT) scan was normal. Levodopdcarbidopa (2501
25 mg four times daily) and bromocriptine (20 mdday) did
not improve his parkinsonism.
Patient 2

We studied the nigrostriatal dopaminergic pathway in 3
patients with Shy-Drager syndrome, by using positron
emission tomography and ['8F]6-fluoro-l-dopa to determine whether their parkinsonism correlated with impaired functional integrity of the presynaptic nigrostriatal pathway. One patient had short duration of
disease, mild parkinsonism, and a normal positron emission tomographic scan, suggesting pathological changes
functionally distal to the nigrostriatal pathway. T w o patients with longer duration of disease had more severe
parkinsonism and reduced ['*F}Gfluoro-1-dopa uptake,
suggesting impaired nigrostriatal dopaminergic function with progression of Shy-Drager syndrome.
Bhatt MH, Snow BJ, Martin WRW, Cooper S,
Calne DB. Positron emission tomography
in Shy-Drager syndrome.
Ann Neurol 1990;28:101-103
Shy-Drager Syndrome (SDS) is characterized by autonomic failure with any combination of parkinsonism,
pyramidal dysfunction, cerebellar ataxia, and lower

From the Belzberg Laboratory of Clinical Neuroscience, Division of
Neurology, University of British Columbia, and UBCiTRIUMF
PET Program, Vancouver, Canada.
Received Nov 26, 1989, and in revised form Jan 9, 1990. Accepted
for publication Jan 17, 1990.
Address correspondence to Dr Calne, Department of Medicine,
Division of Neurology, 221 1, Wesbrook Mall, Vancouver, British
Columbia, V6T 1W5, Canada.

A 52-year-old woman had a 4-year history of unclear speech
and bradykinesia She suffered multiple syncopal attacks.
Two years after the onset of her disease she developed incontinence of urine and feces. On examination there was a
postural drop in blood pressure (130190 supine, 80/60 standing). She had rigidity, marked bradykinesia, hypomimia, and
a fine postural hand tremor. Her Columbia score was 53. She
had emotional lability, an active jaw jerk, brisk tendon
reflexes, and bilateral extensor plantar responses. Head
CT scan and magnetic resonance imaging were normal.
Levodopdcarbidopa (250125 mg four times daily) and
bromocriptine (15 mg1day) did not help her.

Patient 3
A 72-year-old woman had a 6-month history of unsteady
gait, multiple syncopal attacks, and incontinence of urine and
feces. On examination, she had a postural drop in blood
pressure (1801110 supine, 55/30 standing) with hypomimia,
cogwheel rigidity, bradykinesia, and bilateral spasticity. Her
Columbia score was 28. She could not walk tandem. Rectal
examination revealed a gaping, patulous anus. Head
scan
was normal. Levodopdcarbidopa (250125 mg three times
daily) was not helpful.
There were 14 normal control subjects (age range, 22-80
yr; mean, 45.5 yr). They were asymptomatic, neurological
examination was normal, and none was taking medication.
The data collection scheme for both groups (control subjects
and patients) was identical, and a standard protocol for PET
scanning approved by the University of British Columbia
Ethics Committee was followed.

Methods
PET studies were performed with the University of British
ColumbiaiTRIUMF positron emission transaxial tomog-

Copyright 0 1990 by the American Neurological Association

101