BRAIN INJURY, 1998, VOL. 12, NO . 8, 697±

701

Ca se Stud y
Gerstmann’s syndrome associated with chronic
subdural haematoma: a case report
S. MAESHIMA, Y. OKUMURA,
K . N A K AI, T. ITA K UR A and N . K O M A I
Department of Neurological Surgery, Wakayama Medical College, Wakayama, Japan
(Received 11December 1996; accepted 25 January 1997)
We report a patient who exhibited Gerstmann’s syndrome in association with a chronic subdural
haematoma. A 71-year-old right-handed woman presented with mild right arm and leg weakness that
began 2 weeks prior to admission. Neurological examination on admission revealed a mild right
hemiparesis. Neuropsychological examination revealed right± left disorientation, finger agnosia, agraphia, and acalculia, but no language disturbance. A computerized tomographic (CT) scan revealed a
large left frontoparietal, extra-axial hypodense fluid collection containing scattered hypodense foci. A
left parietal evacuation of the haematoma was performed. Following surgery the patient dramatically
improved. We suggest that the direct compression by the chronic subdural haematoma or a hemispheric pressure difference caused Gerstmann’ s syndrome. This is an unusual report of a Gerstmann’s
syndrome following chronic subdural haematoma.

Introd uctio n
Gerstmann’ s syndrome consists of right± left disorientation, finger agnosia, agraphia,
and acalculia [1,2]. The lesion has been localized to the left parietal cortex including
the angular and second occipital gyrus, supramarginal gyrus, and superior parietal
lobule [3,4]. Constructional apraxia and mild aphasia can also occur in Gerstmann’ s
syndrom e.
Patients with a chronic subdural haematoma often have cognitive impairm ents,
which may not be severe enough to meet the criteria for the clinical diagnosis of
dementia. Rarely, aphasia can also be a presenting symptom of subdural haematomas [5,6]. However, to our knowledge, Gerstmann’ s syndrome has not been previously reported. We desribe a patient with Gerstmann’ s syndrome due to a
subdural haematoma, and then discuss its possible pathogenesis.

Ca s e rep or t
A 71-year-o ld right-handed woman presented with a 2-week history of right arm
and leg weakness. She denied headache, nausea, and vomitting. She had 9 years of
formal education. She had no history of hypertension, stroke, transient ischaemic
attacks, seizures, or alcoholism.
Physical examination on admission revealed a blood pressure of 150/90 mmHg
and a pulse of 66 per minute. No carotid bruits or cardiac murmur was present.
Correspondence to: Shinichiro Maeshima, MD, PhD, Department of Neurological Surgery,
Wakayama Medical College, 27 Nanabancho, Wakayama 640, Japan
0269± 9052/98 $12 ´ 00 Ñ

1998 Taylor & Francis Ltd.

S. Maeshima et al.

698

On neurological examination she was alert and cooperative. Her cranial nerve
examination was normal. Examination of the extremities showed mild pronator
drift of the right upper extremity but good strength on individual muscle group
testing and normal tone. Sensory testing to pin, touch, vibration, position, graphaesthesia, and stereognosis was normal. Finger-to-nose and heel± shin testing
were normal. Gait was grossly normal.
On neuropsychological examination her attention was relatively intact (digit
span, seven forward and four backward) Language testing did not reveal any impairment in spontaneous speech such as word-finding difficulties or paraphasic errors.
Prosody was preserved. Repetition was not impaired. Naming of objects in the
room and elements of the examiner’s clothing and body parts was performed with
better than 90% accuracy. Comprehension was unimpaired, as demonstrated by
appropriate verbal responses to questions and correct execution of simple and multiple step directives. Striking right± left confusion was noted. Any tasks that required
right± left discrimination led to hesitation, frustration, and repeated errors in execution. She was unable to identify digits on either hand. She could not reliably name
the digits and made frequent errors in attempting to follow commands instructing
her to identify or utilize a specific digit on her own hand or on the hand of the
examiner. She was aware of her difficulty and was frustrated by it. She also was
unable to perform any calculations. Even very simple calculations, such as adding
12 + 13 or subtracting 93 7, could not be carried out. Her performance did not
improve with the use of pencil and paper. Reading was not impaired. The patient
could read sentences out loud correctly. She was able to write with either hand, but
demonstrated spelling errors and omissions (Figure 1a).

-

Figure 1. Dictation and copy in the patient. (a) The patient was able to write with either hand but had numerous
spelling errors and omissions. (b) Three days following sugery she dramatically improved. She could write accurately
without minor errors.

Gerstmann’s syndrome due to subdural haematoma

699

Scores on cognitive tests were as follows: the Mini-mental state, 23/30: Osaka
Memory Scale (the Japanese version of the Wechsler Memory Scale), 45/100; word
fluency test, 6/min; and Rave’s CPM , 18/36. The GBS scale was 12 points,
showing a deterioration of motor function and intellectual deficits (Table 1).
Computerized tomography (CT) of the head revealed a large left frontoparietal,
extra-axial hypodense fluid collection containing scattered hyperdense foci (Figure
2).
Clinical course
The patient underwent a left parietal trepanation and evacuation of a haematoma on
11 August 1996.
Three days following surgery she improved clincially. She could write without
minor errors (Figure 1b), and her hemiparesis was resolved. The results of neuropsychological examinations peformed 7 days following surgery were also markedly
improved. A follow-up CT on the 7th postoperative day demonstrated only mild
residual fluid and little mass effect. Neuropsychological exam inations performed 1
month following surgery demonstrated continued improvement.
D is cu s s io n
In our patient, finger agnosia and right± left disorientation were prominent symptoms. Her agraphia, characterized by paragraphia with misspellings and syntax
errors, and spatial dysgraphia (poor word alignment across a page) were mild.
Her acalculia also was severe. These features are commonly associated with
Gerstmann’ s syndrome.
Table 1.

Neuropsychological examination results and GBS scale scores
11 August

16 August

5 September

4 December

Mini-mental state (/30)
Word fluency (/min)
Raven’ s CPM (/36)
Osaka Memory Scale (/100)
Information
Mental control
Story recall
Digit span
Visual reproduction
Associated learning
Delayed recall

23
6
18
45
7
6
6
10
5
9
2

28
8
21
59
9
6
10
9
5
17
3

28
8
21
65
9
9
10
10
10
12
5

28
11
22
57
9
9
10
11
0
13
5

GBS scale
Motor
Intellectual
Emotion
Others

12
8
4
0
0

4
1
3
0
0

2
0
2
0
0

2
0
2
0
0

Mean (SD) compaired with 20 age-matched controls
Mini-mental state:
28´4 ( 2´0)
Osaka Memory Scale: 71´9 ( 8´0)
Word fluency:
12´0 ( 1´9)

700

S. Maeshima et al.

Figure 2. Computerized tomography (CT) of the head revealed a large left frontoparietal, extra-axial hypodense
fluid collection containing scattered hyperdense foci.

Subdural haematomas, caused by haemorrhage from bridging veins between the
dura and arachnoid, are usually associated with head trauma. The blood typically lies
near the frontal and parietal convexities, and in some cases is bilateral. Patients
usually complain of a headache, and they may have cognitive impairment, aphasia
and a hemiparesis contralateral to the haematoma. Gerstmann’ s syndrome is uncommon. Patients with Gerstmann’ s syndrome typically have a lesion which involves
either the angular gyrus or the subcorical white matter posterolateral to the posterior
horn of the left lateral ventricle. The resolution of our patients’ Gerstmann’ s syndrome following haematoma evacuation suggests a causal relationship. The postoperative CT scan showed no other responsible cerebral infarction or mass lesion.
Daly et al. [7] have suggested that mass lesions can cause neurological symptoms
by mechanical stimulation of the cortex followed by a spreading depression of
cerebral electrical activity [8]. However, this mechanism would be too diffuse to
cause focal symptoms. Direct compression, or a hemispheric pressure difference
created by the chronic subdural haematoma [9], would also be too widespread.
We cannot exclude the possibility that these diffuse processes may have induced the
expression of an otherwise subclinical focal lesion. Otherwise our patient would
have had a mild cognitive impairment due to a diffuse brain lesion.
McLaurin [10] has recognized that subdural haematomas may compromise
regional cerebral blood flow by indirectly shifting the anterior and posterior cerebral
arteries. The size of the haematoma, however, does not necessarily determine
symptoms, nor have most of the reported patients had significant midline shift or
syndromes suggesting anterior or posterior cerebral artery ischaemia. The haematoma in our patient would not be expected to cause a shift of intracranial structures
leading to contralateral compression of the left frontoparietal lobe.

Gerstmann’s syndrome due to subdural haematoma

701

Since patients can respond dramatically to surgical evacuation of a subdural
haematoma, physicians should be aware that, in addition to strokes and tumours,
chronic subdural haematoma may lead to Gerstmann’ s syndrome, prior to progressing to dementia.
Referenc es
1. G ERSTMANN , J.: Fingeragnosie und isolierte Agraphie, ein neues Syndrom. A Gesamte Neurol
Psychiatrie , 108: 381± 402, 1927.
2. G ERSTMANN , J.: Syndrome of finger agnosia, disorientation for right and left, agraphia and acalculia. Archives of Neurology and Psychiatry, 44: 398± 408, 1940.
3. M AESHIMA , S., F UNAHASHI , K., U EMATSU , Y. et al.: Gerstmann’s syndrome due to the subcortical
hemorrhage in the left parietooccipital lobe. Brain Science and Mental Disorders (Tokyo). 5: 47± 52,
1994.
4. M AESHIMA , S., K AJIWARA, T., D OHI , N. et al.: Gerstmann’s syndrome associated with left posterior
cerebral artery occlusion. A case report. Neurological Medicine (Tokyo), 36: 159± 162, 1992.
5. M C K ISSOCK , W., RICHARDSON , A. and B LOOM , W. H.: Subdural hematoma: a review of 389 cases.
Lancet, 1, 1365± 1369, 1960.
6. D ELL, S. O., BATSON , R., K ASDON , L. et al.: Aphasia in subdural hematoma. Archives of Neurology,
40, 177± 179, 1983.
7. D ALY, D. D., SVIEN , H. J. and Y OSS , R. E.: Intermittent cerebral symptoms with meningiomas.
Archives of Neurology, 5, 287± 293, 1961.
8. LEAO , A. A. P.: Spreading depression of activity in the cerebral cortex. Journal of Neurophysiology, 7,
359± 390, 1944.
9. SYMON , L., P ASZTOR, E., D ORSCH , N. W. C. et al.: Differential pressures recorded in acute epidural
expanding lesions. Correlation with local cerebral blood flow by hydrogen clearance in baboons.
In T. W. Langfitt, L. C. McHenry, M. Reivich et al. (editors): Cerebral Circulation and Metabolism
(Springer-Verlag, New York, pp. 235± 237, 1975.
10. M C LAURIN, R. L.: Contributions of angiography to pathophysiology of subdural hematomas.
Neurology, 15, 866± 873, 1965.