~
Sciences, 1977, 34: 267-278
C) Elsevier Scientific Publishing Company, Amsterdam - Printed in The Netherlands

Join,hal of the N

267

GLOBAL SPATIAL DISORIENTATION
Clinico-Pathologic Correlations

CARLOS S. K ~SE*,JUAN F. TRONCOSO, JAIME E. COURT, JORGE F. TAPIA and JAY
P. MOEIR

Departments of Neurology ( CSK, JFT, JEC, JFT) and Neuropathology ( CSK), Catholic University,
Santiago ( CMle), and Harvard Medical School and the Massachusetts General Ho.vpilal f Neurology
Department) (JPM), Boston, Mass. (U.S.A.)

(Received 7 May, 1977)

SUMMARY
Two patients presenting with the acute onset of bilateral parietal lobe damage
showed initially the features of Balint's :;yndrome. ~'-fter most of its manifestations had
cleared, both patients exhibited severe disorders of spatial orientation: acoust!:" atax m,
inability to localize objects in space. In addition, I patient showed a topographical
disorientation and abnormalities of whole b3dy movements. This patient came to
post-mortem examination, which revealed bilateral and fairly symmetrical old and
recent infarctions of the superior parietal lobules.
In the light of these observations and previous reports, it is suggested that the
reported abnormalities of whole h..~d.y movements can be explained on the basis of a
visuo-motor intrahemispheric disconnection due to the bilateral lesion of the dorsal
l~trietai lobe. In addition, the global spatial disorientatior, i~ analyzed and is thought
to be the manifestation of a derangement of a specific function centered in the parietal
lobe. Moreover, it is pointed out that topographic disorientation does not require the
concomitant failure of oculomotor mechanisms for its production.
The topography of the anatomical lesion is considered in relation to current
conzepts on brain damage after severe hypotension and cardiac arrest. It is concluded
that this group of patients is most likely at risk of developing behavioural abhornudities akin to the ones here reported.

ncrltom.~noN
- The terla "Vilaial. Disorientation" was introduced by Holmes (1918) to refer
*o a d e f e r in Slattiai"~ t i o n
of objects and their distances by sight. A number of
* PluNgt addl,ud:.ld[llaldmlel~ Otmral ~ ,

;tkma, MaL e~tt4.u:g~, wkm r q ~

~

Neurology Department, Fruit SUeet,

be requeued.

268
additional behaviourai defects have been reported a m o n g the so-caUed "disorders o f
~patial orientation" (Benton 1969) and include: (a) inability to localize objects in space
and to estimate their size and distance from the observer; (b) impaired m e m o r y for the
location of objects or places; (c) inability to trace a path or follow a route; (d) reading
and counting disabilities; (e) incapacity to relate spa0ally separated objects or events
~to each other; tf) visuo-constructive abnormalities.
In a number o f the reported cases, these abnormafities in spatial orientation
have been associated with severe oculomotor disturbances (Holmes 1918; Holmes and
Horrax 1919). The underlying pathological process in this last group has always been
a bilateral lesion of the posterior half o f the brain. O n the other hand, there have been
reports o f " p u r e " forms o f spatial disorientation, without concomitant oculomotor
abnormafities (Meyer 1900; Paterson and Zangwill 1945). In these, the responsible
brain lesion has been clinically localized as unilateral in the right temporo-parietal
~.~ea or bilateral affecting the occipital lobes.
We are reporting 2 cases which showed a combination o f permanent spatial
disorientation with transient oculomot,~r disturbances. One o f them came to postmortem examination allowing us to establish the anatomical bases o f the permanent
behavioural abnormalities. Also, some ideas on the probable pathogenesis o f such
disturbances are discussed.
REPORT OF CASES
Case I (M.V.V. (HSR No. 141002))

A 63-year-old right-handed female, with 6 years of primary education, was tint seen in our
neurology service (Santiago, Chile) in December, 1973. In 1967, a carcinoma of the cervix had been
diagnosed and treated with radiotherapy, without ~ .
On the evening of 26 December, 1973, the patient suddenly complained of ~vere diffm¢ head.
ache followed by profuse vomiting and ~-veral generalized seizures. On admission to the Emerpncy
Ward, her pulse was regular (80/rain), BP 180/100 mm Hg, temperature 35 °C and she had regular
respirations. Her carotid pubes were full and without bruits. The ileneral physical examination was
otherwise unremarkable. Neurological examination: she was in deep coma with a weak ~
to
noxious stimuli and with pinpoint pupils which cont _r~_t_~dweakly to light. The eyes were oonjngately
deviated to the fight and showed an incomplete deviation to the left on the doll's head manoeuvre.
The 4 extremities were hypotonic with depl~tsed deep tendon reflex~ and bilaterld flexor plantar
responses. She could, however, move all 4 extremities in a groc~ly symn~qrical way. A first lumbar
puncture was traumatic. (hemorrhagic CSF, clear after centrifugation, with abundant fresh red blood
cells).
On examination 24 hr later, she nmudned in coma but showed some ralmmes to noxious
stimuli. The face was symmetrical, the ocular deviation to the right had dbaEpeared and the extraocular movements were full on the doll's head manoeuvre. Shec.ould move both lowerextrendties
(withdrawal) in response to painful stimuli, whereas the Upper extremitiesmo~ bandy with the same
stimuli. The deep tendon reflexes w~re still diffusely ~
and the planter re~xml~ nmaticod
flexor. A second lumbar puncture yielded clear CSF with a protein content of 37 m~100 ml, slucme
of 67 rag/100 ml and 5 mononuclear oelh/mma. By the third hospital day, ~ e became alert and cooperative. Her speech was normal without l~xaphasic egrort, and she could follow comnmnds and
repeat to dictation without mlstakes. Howev~, a striking abnorn~ity could he ~
ip her vireo.
motor behaviour. Her eyes were co.mtantlymovtng in a alow Im~lunpredictable wando¢i~ way, and
when an object was put in :.he pedpltecy of her vimalfleid, dm acted as if ~lteoouldnot see it ~ could
not fix her eyes on it. W~henher attention was c i t Y ' t o this i~pherally ~
:object, she would
attempt its localization by moving her head more than her e y a in 8 ~
faahion until abe would
finally "see" the object afte~ variable inta'tah, t d ~ ~ ; i t : ~ ,
She W l t l ~ 4 o ~ i ) W
a
slowly moving object with her eyes, bl~ her ~ ~ ~ ~ w ~ - ¢ f l a l t ~ i n
a l l ~
oa om~.
•

,

269
mand. She thus behaved as if she wew. having the so.called "psychic paralysis of visual fixation", a
dist~rbma:e which, t o l g ¢ l ~ with "optic ataxia" and "'visual inattention", forms the triad of Balim's
syndrome (Bafint t909}.
In addltioo to this abnormal behaviour regarding extraocular movements and wsual pursuit
functinn~ she also showed featut~ which sug~sted visuo-motor incoordination. When the patient
was asked to touch an object held in front of her with either hand, she first had to fix her vision on i t,
t h ~ she tried to touch the object. However, she consistently fai~,ed because her hand would stop a few
cm in front, behind or to the side of the object, but never close enough to touch it. This contraste.'l
with her perfectly normal ability to touch different parts of her body with eyes closed. In addition,
her motor coordination was also normal, without evidence of cerebellar ataxia.
Another deficit she showed at this s t a p was an inability to perceive visually more dam one object
at a time, an abnormality which has been considered to be a visual attention defect in ~atients ~ith
visual disorientation (Godwin-Austen 1965). This abnormal behaviour contrasted with a normal visual
acuity and fields, and full extrancular movements.
In addition to the abnormalities in the visually-mediated motor acts, she was also unable to
localize properly or gxasp an object guided by its characteristic noise with eyes closed. When a keychain or whistle were the auditory stimuli, she would orient her head and hand in the wrong direction,
even to the opposite side. These abnormalities occurred in the setting of normal auditory function
under bedside testing conditions: symmetric aerial and osseous auditory perception, non-lateralized
Weber's sign and no extinction on double simultaneous stimulation.
The motor strength, tone, deep tendon reflexes and plantar responses were normal and symrnctrical, as were the superficial and deep sensory functions. Stereo~osis was preserved, but she
showed an abnormality in the perceptiorl and integration of her body-scheme in the form of a left
somatoagnosi~. She also had a dysgraphia and constructional apraxia. The verbal arithmetic calculation, dlght-left orientation and finger order sense were preserved. Her reading abilities for individual words and short sentences were spared.
When she started walking 3 weeks later, a different set of abnormalities became apparent.
When walking, she would behave as a blind person. Her sight would be directed beyond the immediate
obstacles, her right arm would be stretched in :{'ront of her to detect obstacles, and she would bump
frequently into thin~ suf;h u chairs, tables, etc. Wht n she was asked t~, identify these objects, she
would name them correctly without hesitation, showi.lg an absence of ag,~osic features in the visual
e~phere. She had a severe spatial disorientation that w~s apparent in most of her restricted activities.
When placed in the corridor, she was unable to find he, way back to her room, and would take several
different paths in all possible directions until she would finally take the right one. Being in her room
(which had 6 beds), she was unable to find her bed. When she would finally get in it, she would lie in
the wronlg orientation with respect to its long axis, even in a transverse position (Fig. I). After many
~ f u l
attemp~ s to correct her postition trying several different approaches, including a com..
pletely upside-down one, she would react catastrophically.
When she was placed in front of a chair (which she would immediately recognize as such) and
asked to sit down, she would hesitate and then get in several abnormal sitting positions. These included
sitting facing the back of the chair, sitting on the very edge of it, and sometimes "sitting" in the air by

.

FiB. 1, Case l..Abmcm~ ~,4a:debod__y, ' ~ o ~ t s
pendiculady to the ions ~ of the bed.

. .o-j[~.~

-,

•

on attempting to get in her bed. lying down per-

270

Fig. 2. View of the brain from above, showing bilateral dor.~o-medial parietal lobe infarction, hemorrhagic medially and pale laterally.
the side c

he chair, occasionally falling down. At this stage she was able to name two or more different

objects simultaneously presented to her, but she had trouble in determining their position relative to
each other.
Her appreciation of lengths (a few cm long objects, or distances (s.-,veral meters) was adequate.
Her orientation in time, memory for recent and remote events, p r c r a i judi~naent capacities and general behaviour (excluding the activities that essentially require spatial orientation) were within normal
limits. A standard electroencephalogram (EEG) showed diffuse slow wave 0hera) activity without
foca: abnormalities or spike discharges. Urinalysis, blood glucose and BUN were normal.
She was discharged after I month in the hospital and at that time the symptomatic triad of
B~.lint's syndrome had cleared. The constructional apraxia and left somatoagnosia had also disappeared, but the abnormalities related to spatial disorientation ,acre unchanl~L This distmaoan~
was still present 2½ months after discharge. When walking in the s aeets, she would frequently lose her
way to fami,aar places or her way back home. This incapacity was disabling to the extent that it made
her refuse to go out unaccompanied. On examination, she was still unable to give tl',¢ relative spatial
location of several different objects presented to her simultaneously. Her inability to find her way inside the hospital, inside the examining room, or to position her body on the examining strctch¢ was
unchanged.

271

Fig. 3. Extension of the infarcts on to ~he m~dial aspect of the hemispheres. Above: right hemisphere,
belch1: left hemisphe~.

272

Fig. 4. Coronal sections of the hemisphere, from the spleaium of the corpus ¢allmum towards the
occipital poles (posterior aspect of the sections shown). Bilateral softening of the superior parietal
Iobules, more extensive on the left, hemorrhagic on the. right.
Being in this state, 4 months alter her initial illness, otte afternoon she suddenly complained
of severe diffuse headache and collapsed. On admission she appeared in deep coma without reaction
to painful stimuli. Pupils were 4 mm in diameter and reactive. There was no movement in the extremities and she had bilateral Babinski signs. She died 24 hr after admission.
Post-mortem study (Autopsy A-427)
General autopsy

The relevant findings were: cardiac hypertrophy, bilateral confluent bro~hopneumonia, ahd
widespread arterio- and arteriolosclerosi~.
Central nervous system
Gross. Upon removal of the brain, the dural venou~ sinus~ appeared normally patent. The

fresh brain weighed 1,200 g. The arteries at the base of the brain showed moderate athero~ler~is.
On external inspection, the cerebral hemispheres showed a bilateral softening of the pax~etal
lobes, more on the left, with a distinct lw,morrl~agic component (Fig. 2). On both sides, the infarcted
area ended abruptly at the level of the parieto-c~cipittl fissure, both on the medial and lateral aspects
of the hemispherer., leaving the occipital lobes comldetely intact. The anterior margin of the infarct
was at the level of the calloso-marginal fissure on the light and I cam in front of this Essure on the left,
involving medially the gyrus cingulus and all ~he wecuneus on the flight, and the posterior one-third
of the paracentrai iobule, the whole precuneus and the poster<or one-third of the gyrtut cinl~dus on
the left (Fig. 3). On their lateral aspects, the infarcts involved the whole extemion of the superior
parietal lobules, sparing completely the angular and supran.arllinal gyri.
The coronal cuts of the cerebral hemispheres showed the large infarcts on the medial and lateral
surfaces of both parietel lobes, which appear, d hemorrhagic medially and l ~ e on the periphery
(laterally). The hemonbagic component was more prominent on the fight parietal lobe. The sections
made from a level anterior to the splenium of the corpus callosum toward.~ the par/eto-occipital jura:-

273

Fig. 5. Sups:[[or parietal Iobule cortex. Extensive necrosis of the middle layers ("p~eudolaminar"),
infiltrated by macrophages, with capillary neoformation. Old necrosis of adjacent areas, with heavy
astrocytic reaction. Hematoxylin and eosin, , 80.
tion disclosed successive involvement of the following structures in a:: antero-posterior direction:
gyrus cingulus bilaterally, posterior one-third of the p~raccntral Iobul¢ on the left, precuneus bilaterally and superic.r parietal iobule bilaterally (Fig. 4). The white matter softening at these levels was les~
prominent and was restricted to a band of inf.'.,rcted sabcortica] white matter without signs of cavitation.
The r~ore posterior sections which included the confluence of parietal, temporal and occipital
lobes, showed the infarcts restricted only to the parietal lobes, sithout involvement below the level cf
the parieto-occipital fissure. On the other hand, the sections showing the lateral ~spects of the infarct~
disclosed lesions restricted only to the su~rior parietal iobules, neve reaching beyond the intrapari~.
tal sulcus towards the angular and supramarginal gyri, which appeared spared in their comple=e
antero-posterior extension.
Microscopic. Sections from rr,uhiple areas of cerebral cortex, white matter, basal ganglia, cerebellum and brai, stem were stained witl:, hematoxylin-.-~sin and some of them with the Verhoeff-Van
Gie,.;on t,--chnique for elastic fibres. The microscopic lesions were confined to the areas macroscopicalb,
affected, and they consisted of areas of cereb,-'al infarction which were of two different locations an,~
ages:

274

a normal ~

and white nmttm', ~:, " i,. .~:::;~"
"-::-i.
~:i.:-:!./.:-j."
..:-:.'':ii~,
::;--.:~-~::: !~:..~~i!".:;:~:.:~.
i.-~:
I

the ~ . s p ~ ,

o f t ~ m ; ~ ~ ~ ~ . ~

and showedab.adm~tloci.of~ c O ~ o f
infarct was located at the I X t l ~ . . ~
day.o~ ~
~'~u~o~. ~ ~

of m~ou~ m~-r~ o ~ u ~ ~

~

m~~.

~ ~ i ~ - ~ n
mdMo~c~ltL ~

of the J . ~ . . ~ "
~
~"~.
~:~m

~

m

or ~

type Of

I m d . ~
* 3-4e~l evi. e" ~ . or~my k ~

.....

Case 2 (M.M.P. (HSR No. 141534))
A 28-year-old risht-handed knmle wi!'h 2 years of , e m n d ~ education, who had always enjoyed good health,
O n 19 September, 1973, It ~
was l~'fmmed under.Bmend anaesthesia in an
o..ide ~q,~mz. ~n~

~

zmmopmuiveperiod~ h ~ q ~ u i ~ . ~ , b e e t 3O~ ~ d

had a cardiorespimtory arrest of _~m.k_nowndurationfrom which she ~ . w i t h
open-ch~ cardiac m.ssasg. She was left in deep ~
~
and.with bilateral Babimki dsm. Over the foDowiag.
days her state ofcomciomnms prosmnivdy improved, mul after 3 wwlm she was able to mopemte
for physical rehabilitation, Three months after the csrdiofespiraiory arrest she was sent to out, neurolog,/service in Santiago (Chile) for evaluation,
On neurological examination, she was alert and well odlemed is to time, ~
and penmn. Her
speech was normal in articulation, compmhemion, repetition sad intonation. She .had a marked
dysgraphia and constructional apraxla. However. she did not disdme a fixed pettem ofinattention
for a particular part of the v~ual space. Her visual acutty was hard to trot, but the was able to point
to the presence ofa I mm diameter dot at 30 cm distance. The visual fields were reduced (about 15 to
20°) in a concentric way bilaterally, Verbal aritlm~ic calculation, riilht-loft orientation and finller
order sense were preserved.
T.he characteristic features of Bzlint's syndron,, were pcesent. When an object was placed in
front of her, she showed a long delay in orientinll her gaze towards it. She teacr,h ~ for the object with
the use of head movements rather than eye movements. Whea she was,sited to touch witheither hand
the object she had already seen, her perfornmnce was ~ r y iL-~_~_q'ate, as she Would dillct ..her finBer
to the sides of the object, n:ver being able to touch it correctly. This contrasted with her perf0rmm~
on the fir'get-to-nose test for motor coordination, in whith she would always touch her nose m : m a t d y
but not the examiner's finger. She also had an occasional visual alin0sia for objects, which w a e readily
recognized by palpation.
Both the visual object-agnosia and the elements of Balint's syndrome detmd over the following
weeks, leaving her with a distinct defect in the vbual percept!on of spatial relationships.
Was Iraable to establish the relativeposition of xveral o b ~
Or fillun~ :both i n . . ~ : I t m l , ~
arrangements. On the other hand, she also had a.dea~ ~ _ ~
inthe.~l~tiM ~ ~
o f ~ i
~muli:.despite normal and ~ m m e t r k aud/te~..~
~ :~b,l
~.~. ~ ! ~ :
nen me sound o f a familia- object was produced, nround.her and Sh¢, w M : ~ t O : ~
her e~s/
os~.. and point to the place from which the smmd:wrt ~ . : d ~ e
~alwa~
i~
~ .the.W m q
irectlon,even opposite to the ammd.,
- . .~ : . : . : • : .
.i~:/..:..:,...~::!~.
• ~:::...~.~:/.:.
:.:...
in contrast with these striking abnmnmlitim , I m ' t o P o l l n n l ~ . m : U d ~ i o n . ~ : . ~ t ~ .
!
ax.m of her body properly inn ~ : m "
bed.. w U dm.~.~:~i:~:~'.:~~\~:
mmat.,o.n was nornml, except for very mild ~ s ~ : i n
tl~ ~ i i ~ " .u~_"Of~

~i~Rit

t'- t
,.ratorYte~l~of the bloodsi!d, ut~ae,,wet,e ~
~ , ~ i ~ ' ~ ; ~
~
ne a-wave d~sclmrl~ •
. " ~ ~/i-'.-:..!:i " :::;'~:- .....
-:-~!:~::::i.,i!.i~;~::::~i.ii.i::~~;:..-';4,,~:~:ii;:::~i::
..::...~.
permanent 0efic~ts left were t h e ~ : a l m l : ~ ~ : : ~ : . ~ i , . . . / ~

275
DISCUSSION

Both our patients presen~ed with fairly similar clinical pictures, although of
different severity. They initiallypresented with the features of Balint's syndrome.
At a second stage, as the former elements cleared, they showed severe abnormalities
in spatial orientation which persisted unchanged for long periods of time.
Abnormalities in spatial orientation
Different forms and degrees of spatial disorientation were prominent clinical
features in our patients. They both showed a striking inability to appreciate the spatial
relationships of several objects in horizontal or vertical arrangements. This was observed at a time when their extraocular movements were normal (voluntarily and on
pursuit), their visual fields were full and their naming abilities for common objects
were intact. Although the testing of the above functions was ~fformed at the bedside
~thout instrumental recording of extraocular movements, it seems reasonable to
assume that the basic perceptual visual functions were essentially intact. This suggests
that the reported abnormality represents an agnosic deficit witi-, specificity for spatial
relationships.
The second variety of spatial disorientation shown by both patients consisted
in their inability to localize and grasp an object guided by its characteristic noise, the
so-called "acoustic ataxia". It occurred despite grossly normal audition and ability
to recognize the object by its sound with eyes closed. Due to technical limitations, o,~r
auditory testing conditions did not include audiograms and binamal testing. However,
we believe that the localization deficit is not due to auditory imbalan,.e. Ahhcagh
auditory localization defects do occur with bilateral hemispheric lesions, they are
located in the vicinities of the auditory cortex in the temporal lobe.,. (Doig 1972). in
our Case I the only areas involved pathologically were the parietal lo~es, On the other
hand, it is unlikely that our second case had bilateral temporal lobe involvement, as
this situation, when associated with auditory perceptive ~isorders, is accor~panied by
overt language problems (Lhermitte, Chain, Ercoureqe, Ducarne, Piilon and Chedru
197 I). In addition, this parle", did not show other signs of temporal lobe in volvement,
such as memory defects (Scoville and Miiner 1957).
In our cases and in 1 of Holmes' (1918), "acoustic ataxia" was present together
with gross disturbances of orientation in the visual sphere. We regard it as another
non-specific manifestation of these patients' disturbances in the perceptk "~ of spatial
relationships. According to Critchley (1953), this function normally requires the interplay of multiple sensory data, mainly visuo-tactile but also auditory, vestibular and
olfactory. The integration and coordination of these sensory data in the intact parietal
lobes leads to a normal spatial perception. In the setting of parietal lobe damage, the
loss of this multisensorial integrative function produces the spatial disorientation which
w e propose should more properly be called "global spatial disorientation" on
account ofthe multiplicity of the sensory data involved.
One of the most striking of the forms ~-f spatial disorientation here reported was
the topogap~© disturbance shown by o,x Case 1. She became disoriented in both

276
familiar and unfamiliar surroundings, thus resembling simi'l~r cases reported by
Meyer (1900) and Paterson and ZangwiU (1945). Their cases (1 in Paterson and Zangwill's and 2 in Meyer's reporlm) were c"hnically diagnosed as having sustained right
temporo-parietaL right occipital and left occipital lesions, respectively. The pathologically verified third case of Meyer's had bilateral occipital lesions. Brain (1941) has stated
t.hat topographic disorientation is an abnormality that arises independently from other
forms of visual disorientation and from visual object-agnosia. Our case seems to
prove this contention, as this abnormality wa-~present at a time when the oculomotor
disturbances and most of the visual disorientation features had already cleared.
With regard to the pathologic bases for such disturbances, our case showed a
sharply demarcated area of old infarction which was restricted to the medial and superior portions of both parietal lobes, with sparing of the inferior parietal lobules and
occipital lobes. At the time of her death, the remaining behavioural abnormalities were
the global spatial disorientation and the topographic disorientation, in addition to
abnormalities in whole body movements, which will be considered in the next section.
Gur pathological findings contrast with Holmes' (1918) with regard to the role played
by the inferior parietal lobule and occipital lobe in these disturbances. His conclusions
on the location of the bullet-produced lesions were mostly based on craniometric
estimations, in relation to the entrance and exit points. On the basis of that information,
he concluded that the most constantly injured areas were the inferior parietal Iobule
bilaterally and, to a lesser extent, the occipital lobes. From our data we can conc',ude
that the involvement ofthese areas is not a pre.requisite for the existence of topographic
and global spatial disorientation, which may occur on the sole basis of upper bi-parietal
disease.
Abnormalities in whole body movements
Our Case I presented a very striking abnor~nality when asked to perform acts such
as sitting in a chair or lying in her bed. These acts were slow and hesistant, but essentially
correct in the several intermediate stages, becoming grossly abnormal at the moment
of their adaptatio', to the visual stimulus (chair or bed). This contrasted with her ability
to perform normally in other acts requiring axial body movements, such as walking
or standing from the sitting or recumbent position. Similarly preserved were her
abilities to grasp with either hand objects placed in front of her, and to adopt different
body postures on verbal command. This kind of abnormality is rarely observed in
clinical practice and we have been unable to find detailed descriptions ofcases like ours
in the literature.
The abnormal whole body movements in our case corresponded to poor adaptation to the visually-perceived stimulus towards which they were directed. One explanation for such a defect woulc~be one similar to Balint's "optic ataxia", which has
been interpreted as due to a disconnection between visual and frontal motor areas
(Holmes 1918; Rondot aed de Recondo 1974; Boiler, Cole, Kim, Mack and paotwaran
! 975). However, in our case the visuo-motor incoordination involved axial rather than
limb movements. Its pathogenesis could also be p m t u l ~ on the basis of a disconnection between visual an-~ frottial .,ttotor a t e ~ prodaoed by the. lq:lqperbi, p6tietal

277
lesion. However, the anatomical substrate for the performance of normal axial movements is not at all clear. Geschwind (1965, 1975) postulates that the main efferent
pathway for axial movements would be different from the mostly pyramidal control
of independent limb movements and could be represented by the bundle of TOrcl:. in
the macaque, it originates from the posterior aspect of the superior temporal gyrus
and ends in the vermis of the cerebellum, through an intermediate stage in the dofsolateral pontine nuclei (Peele 1961). Although this is a well-known structure in primates,
its existence is controversial in man. However. it could be speculated, along with the
arguments given by Geschwind (1965), t h ~ our patient's remarkable axial motor
abnormafity was due to an interruption of the connections between visual cortex and
the posterior aspects of the superior temporal gyrus bilaterally. Such an isolation of
the latter structure from visual but not from auditory inputs would account for her
specific deficit. However, this selective involvement of "visuall)-guided whole body
movements" with sparing of her abilities to name common objects and read short
sentences, would imply that the pathways from visual cortex to superior temporal
gyri (and thence to T~irck's bundle) would be different from the commonly accepted
ones that subserve visual-verbal connections (visual cortex, visual association areas,
angular gyrus, Wernicke's area) (Geschwind 1965). The bilateral sparing of the inferior
parietal Iobule in our case would thus account for her preserved naming and reading
abilities. The selective involvement of both superior parietal Iobules associated with
her abnormal "visually-guided whole body movements" could mean that the pathways
normally subserving this last function travel from visual cortex via the superior
parietal lobule to the superior temporal gyrus bilaterally. This speculative proposition
clearly requires confirmation with further detailed clinico-anatomical studies and
experimental observations.

Pathogenests of brain damage
The clinical and pathological data in Case i are suggestive of brain damage of
a vascular aetiology, but the clinically suspected embolic origin of the lesions could
not be pathologically verified, if the hemispheric lesions in this case are analyzed from
the standpoint of their topographic distribution, they closely correspond with the
lesions usually found in cases of so-called "low-flow infarcts" produced by profound
systemic hypotension or cardiac arrest (Mohr 1969). In this situation, Lindenberg
(1963) has proposed the existence of .~ topographic hierarchy of susceptibility to
ischaemic damage of the brain, the first areas to be involved being the dorsal parietal
regions, in relation to the borderzones between the middle and •osterior cerebral
arteries.
From these data we can assume that our Case 2, who sustained bilateral brain
damage after cardiac arrest, most likely presented a pattern of bi-hemispheric infarction
similar to the one pathologically verified in C a ~ !. Although they differed in the severity of the clinical abnormalities shown, they were essentially c:omparable regarding
the type of behavioural disturbances presented. On the basis of their clinical and
probable anatomical similarities, it can be concl:Jded that "global spatial disorientafioa" pro~bly r e p r m ~ t s a syndrome of upper bi-parietai damage. This calls for the

278
necessity of careful behaviound stud; ~ in the g r o w i q popular/on o f l ~ i e n t s surviving
profound hy potension and cardiam arrest in the I m m m ~ e r a o f improved gmmscitativefacilities.
REFERENCES
Balint, R. (i.q~) S.u~tmdJd~mqj des "Schauam'; ~
Amxie., rtundichc St~.m~ din"Auf'mm~:~mkeit, M~gw. P.~j~tda:. Neurol., 25: $1.-81.
Benton, A. L. (1969) Disorders of ~
~tiou.
In: P. J. Vinkca and G. W. B,-uyn (Eds.),/'/and.
book of Cli~c~ Newe4ofy, Vat. 3 ( IJ~order~rof H~gher Nervous A~'tvlty), Anuterdera, North.
Holland PubL Co.~ pp. 212-228.

Boiler, F., M. Cole, Y. IGrn, J. L. Mack n ~ C. Patawaran (1975) Optic ataxia-- Clinical.ra_4,_'_aleqli~
correlations with the ~
7. Neurol. Neurosurf. PsycMat., 38: 9M-958.
Brain, W. R. (19~1) Visual deKmentatiou with special ~
to lesions of the right cerebral he.
misplmre, Brain,, 64: 244-272.
Critchley, M. (!953) The Par/ad/.ahes, Hafnm" Publ. Co., New York, Chapter 10.
Doll, J. A. (1972) Auditory and vestibular function and d ~ .
In: M. Cxitchley, J. L. O ' l . a ~
and B. Jennett (Eds.), Sclemiflc Fosmdattom of Neurololy, F. A. Davis Co., Plfi!m__d~_phia, Pa.,
Sect. 5, pp. 138-147.
Geschwind, N. (1965) Disconnexion syndromes in animals and man, Brain, 88:237-294 and 585.-4544.
Geschwind, N. (197S) The aprax~ - - Neural ~
of dismdev~ of learned movements,
Amer. Sci., 63: 188-195.
Godwin-Austen, g. B. (1965) A case of visual disorientation.J, NeuroL Newe,u~. Psycblat.,28:
453-458.
Holmes, G. (1918) Disturbances of visual orientation, Brlt. J. Opbthal., 2:449-468 and 506-516.
Holmes, G. and G. Hotrax (1919) Distm'lmnom of spatial orientation and visual attention, with Ires
of stereoscopic vision, Arch. Neuroi. PzycMal. (Chic.), 1 : 385-407.
Lhermitte, F., F. Chain, R. Esc.ourelie, B. Ducarnc, B. Pillon and F. ~
(1971) I~ttgledes troublea
perceptifs auditifs dam lea I~iom 14mrtporala bilatAh'alee, Rev. ncuro/., 124: 329-351.
Lindenberg, R. (1963) Patterns ofCN$ vtdnerability in acute hypoxia, indudin| anaesthesia accidents.
In: J. P. Schad~ and W. H. McMem:mey (Eds.), Selective Vulnerability of the Brain in Hypoxae.
mia, B. H. Biackwell, Oxford.
Meyer, O. (1900) Ein- trod doppelseidlle homonyme Hemianopsie wit Oricntirunlpmt6runlDen,
Mschr. Psychiat. NeuroL, 8: 440-456.
Mohr, J. P. (1969) Distal field infarction, Neurolosy ( M ~ . ) ,
19:279 (Abstract).
Paterson, A. and O. L. Zangwill (1945) A aute of topollraphical disorientation assorted with a unilateral cerebral lesion, Bra/n, 68: H;8-212.
Peele, T. (1961) The NeuroamatomicalB ~ for CIImtcal NmmdoSy, M~3raw.Htll, New York, N.Y.
Rondot, P. and J. de R¢¢oudo (1974) lttaxie opfique - - Trouble de la ¢omdinstion visuo-mot:i~,
Brain Res., 71 : 367-375.
Scoviile, W. B. and B. Milner (1957) ~
of re0ent memory after bilateral ~
lesions,
J. Neurol. Neurosurg. Psychiat., 20: 11-21.