Journal of Neurology, Neurosurgery, and Psychiatry 1984;47: 1016-1019

Transient inaccuracy in reaching caused by a posterior
parietal lobe lesion
JOSE M FERRO
From the Neurobehavioral Unit, Centro de Estudos Egas Moniz, Department of Neurology, Hospital de Santa
Maria, Lisbon, Portugal

A transient disturbance of manual reaching in both hemispaces associated with a small
contralateral posterior perietal lobe (area 7) lesion is described. This defect was increased when
the patient tried to reach without viewing of the affected arm. Inacurate reaching is a distinct
syndrome from visuomotor or optic ataxia, and is interpreted as a failure in guiding the arm
towards specific sites of the space.
SUMMARY

Inaccurate reaching and manual ataxia are consistent findings after posterior parietal lesions in the
monkey.'-' This defect is confined to the limbs contralateral to the lesion. In humans unimanual reaching defects affecting both visual fields are very rare
and unilateral posterior parietal lesions usually produce visuomotor ataxia of one or both hands in the
contralateral half-field.'-' Tzavaras and Masure,'"
Levine, Kauffman and Mohr,'3 Perenin et al14
described patients who were mostly impaired when
they tried to reach with the contralesional arm into
both half-fields. Misreaching was interpreted by
Levine et al'4 as due to a loss of posterior parietal
neurons subserving a supramodal function of integration of visual and upper extremity sensory and
motor information.
We report a patient who had a similar but transient disorder of reaching caused by a small ischaemic
left posterior parietal lesion.
Case report
A 73-year-old right-handed woman came to the
emergency room of our hospital complaining of speech
disturbance, incoordination of her right hand and of bumping obstacles with her right limbs. These symptoms had
suddenly appeared four hours before. Blood pressure was
110-80 mmHg and general physical examination was negative. Neurological examination disclosed fluent speech with
abundant circumlocutions and some verbal paraphasias.
Understanding of oral commands and naming were
Address for reprint requests: Jost M. Ferro, M.D.,
Neurobehavioral Unit, Centro de Estudos Egas Moniz, Hospital de
Santa Maria, 1600 Lisboa, Portugal.
Received 25 October 1983, and in revised form 7 March 1984.
Accepted 10 March 1984.

impaired but repetition was normal. There was a right
homonymous hemianopia, flattened right naso-labial fold,
an old left peripheral facial palsy and a questionable right
extensor plantar response. Limb strength, tonus and deep
tendon reflexes were symmetrical. Manual reaching was
disturbed with the right hand in both hemispaces and to a
minor degree with the left hand in the right hemispace.
(We use the term hemispace in the sense defined by Heilman and Valenstein:"I the space to one side of the midline
of the body).
Routine blood counts and serum chemistry examinations
were normal except for an abnormal response on a glucose
loading test.
Formal neuropsychological evaluations were carried out
on the 3rd, 7th and 10th days of illness. On the 3rd day
after onset language disturbance assessed with a standardised aphasia battery'6 was very mild: spontaneous speech
was fluent and anomic, confrontation naming was moderately impaired (10 out of 16 objects). Aural comprehension and word and sentence repetition were normal. The
patient showed very severe alexia, agraphia and contructional disability: she could neither read or copy (with either
hand) letters and her own name, nor copy (with either
hand) simple drawings. Her performance on the Benton
Fogel Test of three-dimensional constructional praxis was
very poor: she scored 4/29 and presented "closing-in"
phenomenon. She showed no bucco-facial or limb apraxia,
but she was somewhat clumsy when manipulating objects
with the right hand. She still presented a right homonymous hemianopia and right threat reflex was absent. Visual
fixation, spontaneous conjugate eye movements, slow and
saccadic pursuit were normal. Optokinetic nystamus was
diminished to the right. Right hand strength and sensation
were normal. However, even with free eye and head
movements, when she attempted to reach for visual
targets, (for example, trying to grasp the examiner's index
finger with her index finger and thumb) her right hand
performance was impaired in both hemi-spaces, while the
left hand performance was accurate. When free eye

1016

1017
Transient inaccuracy in reaching caused by a posterior parietal lobe lesion
movements were not allowed, by having the patient fixat- longer present, except for some hesitancy when pointing to
ing the examiner's nose while trying to grasp visual targets
presented in the left hemi-space (this testing could not be
performed in the right hemi-space owing to right
hemianopia), the right hand performance deteriorated
while the left hand was still accurate. Errors in reaching
showed no predominant direction. The right hand stopped
some centimeters around the target and then a final corrective movement was made. On other occasions the right
hand bumped the examiner's arm and then groped and
palpated in order to reach the target. Intention tremor or
other involuntary movements were never observed. Pointing to body parts with the right hand was slightly disturbed
even with open eyes, but to a less extent than pointing
toward extrapersonal targets. Right hand reaching
improved after repeated attempts or after the left hand had
first grasped the target, and was more accurate when trying
to reach a stationary than a moving target.
The patient's condition continued to improve within the
next few days. Her speech disturbance had completely
cleared by the 7th day of illness. Speech was fluent without
anomia or paraphasias. Confrontation naming was normal
(16/16). Performance on an abbreviated form of the Token
test was 100% correct (22/22). Reading and drawing were
unimpaired. When writing she tended to separate letters,
by leaving blank spaces between them, a feature that has
been described in spatial dysgraphia.'8 Performance on the
Benton-Fogel test was only borderline impaired (22/29).
Performance on tests of right-left orientation, digitognosia
and gesture recognition were within normal limits. The
right visual field defect was restricted to a peripheral crescent. Right hand reaching was also improved. This defect
was inconstant, disappearing with practice or if free eye
movements were allowed, but was still present in both
hemispaces when visual fixation was required. As stated
above, the patient's arm and hand movement suffered a
final correction when the hand stopped after approaching
the target in a wrong direction. This correction was probably dependent on external feedback based on the viewing
of the affected limb. To evaluate the role of this feedback
the patient was given the following test, adapted from
Levine et al: 13 the projecting limbs were excluded from the
patient's view by covering them with a large cardboard
with several holes where pinheads were introduced. This
cardboard was placed in front of the patient at midthoracic level. The patient was requested to touch, on the
undersurface of the board, the lower edge of a pinhead he
was seeing on the upper surface of the board. While the left
hand (LH) was remarkably accurate, the right hand (RH)
inaccurate reaching was strikingly increased, demonstrating the corrective effect of vision upon the movement of
the affected limb. We used the Purdue Pegboard and a
visuomotor rotor pursuit test (Pursuit Rotor MK4, Forth
Instruments Ltd) in order to quantify the right hand defect.
Although hand grip (measured with a dynamometer) and a
tapping test gave comparable results for both hands, the
performance of the RH was inferior to that of the LH on
the Purdue Pegboard (time to range a row of pegs: RH =
164", LH = 120') and on the visuo-motor pursuit task
(mean total time on target on five trials of 20" each: RH =
7.39 + 4-13 sec, LH = 3.99 + 2-40, t = 1-59, p < 005).
By the 10th day the right-hand reaching disorder was no

rapidly moving targets. The RH had regained its usual
superiority on the Purdoe Pegboard (RH = 67", LH =
79") but was still slightly slower on the visuomotor pursuit
task (RH = 2 95 + 1-20; LH = 2-66 + 1*07; NS). The
CT-scan disclosed a discrete ischaemic lesion involving a
small area of the left posterior parietal cortex (Brodman's
area 7) and subjacent white matter, (fig). The lesion could
be traced in three consecutive cuts, each being 1 cm thick.

Fig Cl scan demonstrating a sma
involving the left superior parietal I

Discussion

This woman presented a transient disturbance of
reaching with the right hand associated with a small
contralateral superior parietal lobe lesion. During
the first few days of disease signs of involvement of
surrounding areas were also present: alexia and
agraphia, severe constructional disability and fluent
(transcortical sensory) aphasia.
In humans, posterior parietal lobe lesions can
cause visuo-motor ataxia of one or both hands in the
contralateral hemifield.8- " Following a posterior
parietal lobe lesion, monkeys became impaired
when trying to reach with the contralateral arm in
both half-fields of extrapersonal space.'7 Tzavaras
and Masure'2 (case 1), Levine et al" and Perenin et
all4 (case 2) recently described a corresponding
human syndrome. As in our case, Levine's and
Perenin' s patients also had posterior parietal lesions.
The disturbance of manual reaching displayed by
our patient can be interpreted either as a visuomotor

1018

disconnection or as a failure in guiding the arm
toward specific sites of the space. Although a right
hemianopsia was present during the first days of disease, it cannot be considered the cause of this defect,
as reaching was incorrect in both hemispaces, and in
the right one even with free eye movements.
Moreover the patient's reaching behaviour suggested that vision could improve her performance.
In fact, after an initial incorrect movement toward
the target, vision-guided terminal correction was
made to grasp it. The importance of this visual correction and of viewing the moving limb was demonstrated by the increased reaching innaccuracy when
the patient tried to reach without viewing of the
affected arm. This effect, that was also present in
Levine's case, is in agreement with the fact that, in
monkeys, the reaching disturbance is aggravated in
the dark.3 6 It also stresses that this patient's trouble
was not due to a visuomotor disconnection but to a
disturbance in commanding operations with the contralateral limb towards specific points of the space.
This is in accordance with electrophysiological evidence. Several researchers found, in the posterior
parietal lobe of the behaving monkey, cells that had
no apparent sensory input but were extremely active
when the animal reached into the immediate
extrapersonal space to obtain or to manipulate an
object of motivational interest.'920 About 20% of
these cells are active with contralateral movements
towards either half of the space.'9 Loss of these cells,
caused by a posterior parietal lobe lesion, can
explain the patient's inacurate reaching.
In visuomotor ataxia and in the patient described
by Tzavaras and Masure,'2 both the initial arm projection and the terminal visually guided movement
to the target were affected. In Levine's'3 and our
case, if vision of the moving arm was allowed, the
final adjustment to the target was correct. This
adjustment needs intact striate visual cortex,2' while
arm projection seems to depend more on parietal
cortex (area 7), that receives visual information
indirectly from the peristriate area, the pulvinar and
the superior colliculus.22 The visually guided terminal adjustment may depend on direct intact
occipito-frontal connexions,2' or visual indirect
input to non-damaged portion of the posterior
parietal lobe. Indeed, by means of a parietal
leucotomy severing occipito-frontal connexions,
Haaxma and Kuypers23 produced a disturbance of
visual guidance of hand and arm movements but
leaving the arm projection unaffected.
Tzavaras and Masure'2 and Perenin et all4 suggested that defects of visuo-motor coordination may
present different aspects accordingly to the hemispheric side of lesion. Right hemispheric lesions
would produce "field-effect", that is, direct and

Ferro

crossed optic ataxia in the contralateral hemifield,
while left-sided lesions would cause "hand-effect",
that is, a disturbance of reaching with the contralateral hand in both hemifields. Unilateral reaching
defects affecting both fields were caused by left vascular lesions in Tzavaras and Masure,'2 Perenin et
al'4 and in the present case, and by a right hemispheric tumour in Levine's report.'3 However, left
hemispheric lesions can also produce a hemifield
effect.8 Reports of unilateral reaching defects are,
at the present time, too few to enable a confirmation
of the suggestions of Tzavaras and Masure 2 and
Perenin et al.'4
This case also illustrates the compensatory
mechanisms that help manual reaching: (a) viewing
of the moving arm enables a final corrective movement and is probably dependent on occipito-frontal
connexions; (b) allowance of free eye movements,
either because central vision increases the visual
input to the parietal cortex or because gaze movements provide extraretinal spatial information, via
mesencephalon, superior colliculus and pulvinar; (c)
grasping the target with the opposite hand, gives an
external clue (view of the moving arm) and proprioceptive feedback that helps in visuo-spatial localisation; (d) practice; (e) a stationary target.
While in Levine's patient the lesion was a large
parietal tumour, in our patient the ischaemic area
was quite small. This may account for the rapid
recovery that was probably dependent on the
remaining spared area of left posterior parietal lobe.
In monkeys the effect of removal of the posterior
parietal lobe is also transient, lasting about 15 days,
but the extent of the lesions did not appear to be the
only factor in this rapid recovery, that could be
accelerated by practice.24
We thank Dr Medina for performing the CT scan,
Dra Angela Gongalves for assistance in testing and
M FRtima Pereira for typing. This work was supported in part by a grant from the Gulbenkian
Foundation.
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