Case Report

A case of tactile agnosia with a lesion restricted to the postcentral gyrus
Bruno Estañol, José Fidel Baizabal-Carvallo, Horacio Sentíes-Madrid
Department of Neurology and Psychiatry, The National Institute of Medical Sciences and Nutrition, Salvador Zubirán, Mexico City, Mexico

Tactile agnosia has been described after lesions of the
primary sensory cortex but the exact location and extension
of those lesions is not clear.
We report the clinical features and imaging findings in a
patient with an acute ischemic stroke restricted to the primary
sensory area (S1). A 73-year-old man had a sudden onset
of a left alien hand, without left hemiparesis. Neurological
examination showed intact primary sensory functions, but
impaired recognition of shape, size (macrogeometrical) and
texture (microgeometrical) of objects; damage confined to the
post-central gyrus, sparing the posterior parietal cortex was
demonstrated on MRI. An embolic occlusion of the anterior
parietal artery was suspected as mechanism of stroke.
Tactile agnosia with impaired microgeometrical and
macrogeometrical features’ recognition can result from a
single lesion in the primary sensory cortex (S1) in the right
parietal hemisphere, sparing other regions of the cerebral
cortex which presumably participate in tactile object
recognition.
Key words: Sensory cortex, stroke, tactile agnosia.

Introduction
Although much has been written on the subject of
tactile agnosia since the time of the classical description
by Dejerine, (“syndrome sensitif cortical”),[1,2] it is not
clear what is the exact nature of the clinical deficit
when the lesion is confined to the post-central gyrus
or primary sensory area. In this regard it has been
difficult also to decide what signs may be attributed
to the damage of the primary sensory area (Brodmann
areas 1,2 and 3) and what signs may be attributed to the
posterior parietal areas (Brodmann areas 5 and 7). The

present case affords a unique opportunity to evaluate
the effects of damage to the primary sensory area.

Case Report
A 73-year-old man had the sudden onset of the
sensation that the left hand did not belong to him. He
also noticed difficulty in recognizing objects with that
hand. There was no weakness of the face, the left upper
or lower extremity.
He was examined 48 h after the onset of symptoms.
He had no hemianopia, limb weakness, hyper-reflexia
of the left upper extremities and no Babinski sign.
The sensory examination of the hand was as follows:
Pinprick sensation was equal in both hands; cold and
warm sensations were normal with water tubes at
20 and 37 degrees Celsius respectively. Two points
discrimination was 1 mm in the tips of the fingers of
both hands; vibratory sensation was found to be equal
in both hands, threshold sensitivity for vibration in the
left hand was 2/50, and in the right hand was 2/50 (BIOTHESIOMETER Biomedical Instruments Co, Newbury,
Ohio), considering a normal threshold of 2/50 to 4/50.
Position sense was normal in the distal and proximal
joints of the fingers; barognosis was equal in both
hands. There was decreased recognition of numbers
and letters written in the palm of the left hand (17 out
of 20 times could not recognize a number or a letter).
There was decreased recognition of the shape, size
(macrogeometrical) and texture (microgeometrical) of
an object placed on the palm of the left hand and rolled
over the fingers (7 out 10), could not recognize the
object placed in the palm of the left hand and examine
it with the fingers either passively or actively (13 out
15). There was extinction with bilateral simultaneous
stimulation at the tip of the fingers on the left hand

Dr. Bruno Estanol
The National Institute of Medical Sciences and Nutrition, Salvador Zubirán, Vasco de Quiroga, No 15, Col Secc XVI , Tlalpan , C.P. 14000, México City, Mexico.
E-mail: bestanol@hotmail.com

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Estañol, et al.: Tactile agnosia with primary sensory cortex lesion

50% of times. There was a marked difficulty in bringing
an object placed in the palm of the left hand into the
tip of the fingers with the eyes closed (tactile apraxia).
There was also a marked difficulty recognizing the
direction of a tip of a pencil running in the palm of the
left hand or in the left fingers; all these clinical deficits
were not found on the right side. Decreased amplitude
of the cortical somatosensory evoked potential with
left median nerve stimulation was found on the right
side. There was absence of the long latency responses
in the abductor pollicis brevis on the affected side
with stimulation of the median nerve at the wrist. We
reexamined the patient one and six months later and
found identical signs.
A brain MRI was performed 48 h after the onset of
symptoms, showing ischemic damage confined to the
post-central gyrus and a small lesion in the prefrontal
cortex [Figure 1]. The main lesion was confined to
the areas 1, 2 and 3 of Brodmann or S1 and spared
the posterior parietal cortex areas 5 and 7, secondary
sensory cortex (S2), and the medial part of S1 cortex.
The patient was a physician who had training in internal
medicine and psychiatry. He had no history of arterial
hypertension, diabetes, dyslipidemia, stroke or transient
ischemic attacks, but had a history of intense cigarette
smoking and alcohol abuse. Atrial fibrillation was
excluded with ECG and 72-h cardiac rhythm monitoring.
US showed non-ulcerated bilateral atheromas at the origin
of both internal carotid arteries with stenosis less than
50% by NASCET. No further studies were performed
because the patient refused. He died a year later of
pneumonia and no autopsy was performed.

Discussion
The main findings in this case are related to the
clinical deficits that result in lesions restricted to
the primary sensory cortex (S1). Recently, some
authors have pointed out that the underlying failure
in tactile agnosia is mainly impaired perception of
microgeometrical properties (such as textures) of objects
due to lesions in the primary sensory cortex (SI) and
that macrogeometrical properties (such as shape and
size) are recognized in the secondary somatosensory
area (SII) and the posterior parietal cortex in a parallel
processing fashion. [3,4] However, our patient had
problems with the recognition of both properties (micro
and macrogeometrical) of objects with a lesion restricted
to SI which suggests that at least in some individuals all
these functions could be impaired with a single lesion
in the primary sensory cortex.
It has been suggested that a right hemisphere lesion
with sparing of right SI cortex produces a deficit in
exploratory motor procedures that results in a pure
tactile apraxia without agnosia, which can produce
a deficit in tactile object recognition (TOR) when
472

Figure 1: FLAIR axial section of the brain showing a hyperintense lesion
confined to the post-central gyrus on the right hemisphere. There is a
small lesion in the prefrontal cortex

the patient explores objects passively (spontaneous
exploration) and not actively (manually or verbally
guided exploration).[5] Interestingly, our case presented
features of tactile apraxia, even though the lesion was
confined to a single area in the post-central gyrus.
Using functional magnetic resonance imaging
(MRI) in healthy subjects, it has been shown that
the right superior parietal cortex is specifically
activated by kinaesthetic attention during tactile object
discrimination.[6] Also, functional MRI in healthy
subjects has been used to demonstrate that TOR involves
the calcarine cortex, inferior parietal lobule, inferior
frontal gyrus and superior frontal gyrus polar region,
and may utilize visual systems to access an internal
object representation with a lexical strategy of naming
the objects being examined.[7] One possible explanation
for the topography of the stroke is an occlusion of the
anterior parietal artery, which is usually a branch of
the inferior division of the middle cerebral artery. We
suspected artery-artery embolism from the right carotid
plaque as mechanism for arterial occlusion.

References
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2.
3.

4.

Dejerine J. Sémiologie des affections du systéme nerveux. Masson
Editeurs 1914. p. 915-8.
Caselli RJ. Rediscovering tactile agnosia. Mayo Clin Proc
1991;66:129-42.
Bohlhalter S, Fretz C, Weder B. Hierarchical versus parallel processing
in tactile object recognition: A behavioural-neuroanatomical study of
aperceptive tactile agnosia. Brain 2002;125:2537-48.
Burton H, Sinclair RJ. Attending to and remembering tactile stimuli:
A review of brain imaging data and single-neuron responses. J Clin
Neurophysiol 2000;17:575-91.
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Estañol, et al.: Tactile agnosia with primary sensory cortex lesion

5.
6.

Valenza N, Ptak R, Zimine I, Badan M, Lazeyras F, Schnider A.
Dissociated active and passive tactile shape recognition: A case study
of pure tactile apraxia. Brain 2001;124:2287-98.
Stoeckel MC, Weder B, Binkofski F, Choi HJ, Amunts K, Pieperhoff P, et
al. Left and right superior parietal lobule in tactile object discrimination.
Eur J Neurosci 2004;19:1067-72.

7.

Deibert E, Kraut M, Kremen S, Hart J Jr. Neural pathways in tactile
object recognition. Neurology 1999;52:1413-7.

Accepted on 05-10-2008
Source of Support: Nil, Conflict of Interest: None declared.

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There is no data on follow-up of these patients.
Authors’ Reply: The follow up of patients have been included in the results section [Page 3, para 2]
Authors should highlight the relation of complication to duration of diabetes.
Authors’ Reply: The complications as seen in our study group has been included in the results section [Page 4, Table]

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