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Neurocase: The Neural Basis of Cognition
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Post Graphemic Impairments Of Writing: The Case Of
Micrographia
Gianfranco Denes

a b

, Matteo Signorini

a b c

& Chiara Volpato

a c

a

Dept. of Neurology, Venice Hospital , Venice, Italy

b

Dept. of Science of Language, Ca’ Foscari Venice University , Venice, Italy

c

AfaR - Fatebenefratelli Hospital , Venice, Italy
Published online: 16 Feb 2007.

To cite this article: Gianfranco Denes , Matteo Signorini & Chiara Volpato (2005) Post Graphemic Impairments Of Writing: The
Case Of Micrographia, Neurocase: The Neural Basis of Cognition, 11:3, 176-181, DOI: 10.1080/13554790590944636
To link to this article: http://dx.doi.org/10.1080/13554790590944636

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Neurocase (2005) 11, 176–181
Copyright © Taylor & Francis Inc.
ISSN: 1355-4794 print
DOI: 10.1080/13554790590944636

Post graphemic impairments of writing:
The case of micrographia
Neurocase

GIANFRANCO DENES1,2, MATTEO SIGNORINI1,2,3, and CHIARA VOLPATO1,3
1

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Dept. of Neurology, Venice Hospital, 2Dept. of Science of Language, Ca’ Foscari Venice University,
and 3AFaR - Fatebenefratelli Hospital, Venice, Italy

Micrographia (MG), an acquired impairment of writing characterized by diminution of letter size, coupled with slowing and loss of
accuracy, is most frequently observed in the course of degenerative disease of basal ganglia, such as Parkinson’s Disease. Only a few cases
of MG without concomitant extrapyramidal signs have been described, mostly following vascular lesion of the left basal ganglia.
In this article we report an isolated pattern of MG following an extensive traumatic cerebral lesion centered in the left basal ganglia. The
nature of this impairment is analyzed according to a cognitive model of writing and interpreted as a specific example of peripheral
dysgraphia.

Introduction
Any cognitive model of writing includes central and peripheral
processes (Caramazza, 1988; Ellis, 1988a). Central processes
involve a number of functionally, if not anatomically, distinct
components, whose task is to retrieve stored spellings in the
central lexicon, or to convert phonological representations
into orthographic representations sublexically.
The final product of these processes is then temporarily
stored in the graphemic buffer (Caramazza et al., 1987;
Schonauer and Denes, 1994), whose task is to maintain the
activation level of the identity and order of letter sequences
for the time needed for the sequential assignment of formatspecific information.
Peripheral processes are involved in the task of translating
the distinct specific letter representations into specific letter
names or letter shapes, via letter name or letter shape conversion processes (Ellis, 1988b; Rapp and Caramazza, 1997).
These processes can dissociate, as shown by the patient
reported by Chialant, Domoto-Reilly, Proios and Caramazza
(2002), that had intact oral spelling, but severely impaired written spelling. Ellis (1982) proposed that at least two stages below
the graphemic level should be identified in the production of
handwriting, the allographic and the graphomotor levels.
The allographic representation is a quasi-spatial representation of each letter form. B, b, are all allographs of the
same grapheme, which can be selectively used by a person
handwriting according to the needs and rules. The errors at
this stage are characterized either by case substitution

Received 28 April 2004, accepted 6 January 2005.
Address correspondence to Dr. Gianfranco Denes, Dept. of
Neurology, Ospedale Civile di Venezia, Campo SS Giovanni e Paolo
30122, Venezia, Italy. E-mail: denes@unive.it.

(De Bastiani and Barry, 1989) or visually similar letters substitution (Ellis 1988). Selective deficits in writing upper case
(Trojano and Chiacchio, 1994) or lower case (Patterson and
Wing, 1997) letters and words are often assumed to reflect
the existence of independent representations of cursive and
print style. Silveri (1996) reported a patient who was much
better in writing cursive than uppercase print. The opposite
dissociation was reported by Hanley and Peters (1996),
whose patient was much more severely impaired at writing in
lower case than in upper case letters.
The second stage is the retrieval of the graphic motor
program (Van Galen, 1980), which will guide the movement
of the pen specifying the sequence, direction and relative
size of the strokes to be produced. The information about
abstract spatio-temporal movement aspects, such as size,
sequence, position and direction of strokes necessary to
write letters, is included in graphic motor programs: these
programs, independent from the muscle group necessary for
the movement execution, don’t, however, specify parameters
of an absolute stroke size or duration, and are distinct from
motor programs involved in other limb movements (Ellis
1982, 1988). Patients, whose impairment is assumed to lie at
the level of the graphic motor program, often write shapes
that are not real letters. Baxter and Warrington (1986)
described a nonapraxic patient with intact oral spelling, who
was unable to write even single letters, his errors involving
writing incorrect, incomplete letters and forms which looked
like fusions of two letters. In contrast their patient could
flawlessly copy written texts. The opposite dissociation was
present in the patient described by Cipolotti and Denes
(1989), who showed a pattern of spared spontaneous and
impaired writing on copy, coupled with severe limb and constructional apraxia.
The final stage of the motor control system of handwriting
consists of the translation of the graphic motor programs into

177

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Micrographia Following Focal Lesion
sequences of graphic motor commands; a deficit of the system
ascribed to generate graphic innervatory patterns results in
a defective control of force, amplitude and speed of writing.
The most frequent example of peripheral dysgraphia is the
writing impairment present in Parkinson’s Disease (PD),
a degenerative disorder of the brain, characterized by
a degeneration of the dopaminergic nigrostriatal neurons of the
basal ganglia, resulting in akynesia, rigidity and tremor (Mardsen and Obeso, 1994). Writing of PD patients, consequent to an
impairment of control and speed, results in a combination of
hypometria and bradykinesia, the first impairment giving rise to
a reduction of letter size, Micrographia (MG), and the second to
an increased length and loss of accuracy. MG includes progressive diminution of letter size as the subject continues to write, in
addition to overall smallness. MG must be distinguished from
“the fine, dainty style, sometimes observed in the handwriting
of the learned” (Pick, 1903). The presence (10–15% of PD
patients) and severity of MG is neither related to the occurrence
of other extrapiramidal symptoms, such as tremor, rigidity and
bradikynesia, nor to the degree of severity of illness.
In some cases MG has been described in isolation or not in
the context of PD. Since Pick's seminal observation (1903) of
isolated MG following a syphilitic infarct of the left thalamus,
this symptom has been reported following a lesion different
from the condition usually linked to PD. MG has been
described following lesions, mostly of vascular origin, of the
left basal ganglia including putamen, globus pallidus, thalamus
or substantia nigra (Scolding and Lees, 1994; Pullicino et al.,
1994; Kim et al.,1998; Derkinderen et al., 2002; Nakamura
et al., 2003; Troyer et al., 2004), sometimes as the only clinical
manifestation (Martinez-Vila et al., 1988), in other cases with
concomitant mild deficits of expressive language and verbal
memory (Pullicino et al., 1994), attentional disorders (Troyer
et al., 2004) or focal dystonia (Münchau et al., 2000); a pattern
of MG and hypophonia has been described in a case of extensive
cerebral vein thrombosis (Murray et al., 2000) or associated to
the dysarthria-clumsy hand syndrome (Noda et al., 1994).
Finally, MG has been reported following a parietal lobe lesion
in Multiple Sclerosis (Scolding and Lees, 1994).
The underlying reasons for a motor disorder such as MG are
not clear: from the anatomical point of view, basal ganglia
structures exert their influence on motor behavior through
connections to frontal premotor areas via a major reentrant basal
ganglia-thalamo-cortical motor loop (Alexander et al.,1986).
Operating as a functional unit, this neural network plays a
critical role in controlling movement force, speed and
amplitude. According to the influential force impulse
model of handwriting proposed by Wing (1978), changes
in letter height can be produced by altering applied force
(amplitude or duration) or interpose interval. On this basis,
Margolin and Wing (1983), and Demirci et al.(1997)
proposed that MG could be caused by the combined effect
of reduced kinesthesia and reduced motor output. Finally
MG in PD has been interpreted as a manifestation of a
generalized hypometria evident in other tasks such as
drawing (Longstaff et al., 2003).

In the present article, starting from the description of a case
of MG following head trauma (pistol shot) in the left basal
ganglia, we'll try to clarify the nature of MG.

Case report
P.P is a 43- year- old right-handed woman, with a university
degree in business administration, working as a tax consultant.
Previous medical history was unremarkable until the age of 40
when, in the course of a depressive episode, she attempted suicide, shooting her head with a gun. The patient was admitted to
a neurosurgical unit and operated on, but the bullet was not
removed from her brain. After an initial state of coma, the
patient started to improve and was discharged 15 days later in
good condition and in antiepileptic prophylaxis (Phenobarbital
100 mg a day) that the patient followed for about one year.
She resumed her work four months later, her only complaint being a change of writing, that became micrographic, a
mild dystonic position of the fourth and fifth fingers of the
right hand and, to a lesser degree, of the right foot.
A cerebral MRI (June 2001) showed the following pattern:
a bullet is located in the left basal ganglia; given, however, its
high density, the bullet provokes many artifacts A large
proencephalic cavity is situated close to the bullet, in the
region corresponding to the head of caudate and lenticular
nucleus. A wide area of cortico-subcortical atrophy involves
the right frontal lobe in the region corresponding to the entry
hole of the bullet (Figure. 1).
The patient was seen in our clinic three years after the
trauma, at the age of 43. Neurological examination showed a
slight dystonic position of the ring and little fingers of the
right hand and of the toe of the right foot, but no other evidence of dystonia. Muscle tone was normal and she could
easily perform rapid movements of alternating fingers. Power
and reflexes were normal. Plantars were flexor. Arm swing
was normal. Cranial nerve examination was normal, with
normal facial mimic and no gaze abnormalities.

Neuropsychological examination
The patient was fully alert, cooperative and her mood was
normal. Her score on the WAIS-R Test (Wechsler 1974) was
normal (Full-scale IQ 132). Executive Functions: her performance on attention tests was above average: digit span forward 7 (n.v.≥3.75, Orsini et al., 1987), spatial span (Corsi
Test) 5 (n.v.3.50, Orsini et al., 1987). Category naming following semantic and phonemic cueing was normal: semantic
30 (n.v.≥25), phonemic 32 (n.v.≥17) (Novelli et al., 1986). In
a shortened version of the Tower of London Test (Shallice,
1982) her performance was 4/4 correct.
Memory: episodic and semantic memory in every day life
were normal as proved by her successful working activity.
On the Wechsler Memory Scale (Wechsler, 1945) she
obtained a Memory Quotient of 143.

178

Denes, Signorini and Volpato
movement variability (Longstaff et al., 2003) in writing tasks,
we explored several variables such as spontaneous writing
versus writing on copy and the use of different allographs and
characters.
Writing to dictation. The patient was asked to write to
dictation a short text, two lists of 20 high frequency words,
and two lists of nonwords of different length (two-four syllables), half in cursive and the other half in capital letters.

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Writing from copy. A similar list was presented to the patient,
whose task was to copy it in the same and double dimension.
The stimuli to be processed were written in Times New
Roman Character, corpus 16 (capital letters) and Lucida
Handwriting, corpus 16 (cursive letters).
Transcoding. The patient was asked to translate a similar list
written in block letters in italics and vice-versa.
Drawing from copy. The patient was asked to copy 30 items
from Benton’s Visual Retention task (Benton, 1945).
Copying of Japanese characters. The patient was asked to
copy a list of ten Japanese words, approximately two centimeters in height, under three conditions: same size, double
size and half size.
Fig. 1. Cerebral MRI showing a bullet located in the left basal
ganglia. A large proencephalic cavity is situated close to the bullet,
in the region corresponding to the head of caudate and lenticular
nucleus. A wide area of cortico-subcortical atrophy involves the
right frontal lobe in the region corresponding to the entry hole of
the bullet.

Follow-up
The patient was required to repeat all the tasks on a follow-up
evaluation after six months.

Results
Her performance on an Italian version of Aachener
Aphasie Test (Luzzatti et al., 1991) was flawless: spontaneous
speech, repetition, naming, oral and written comprehension,
reading were normal. Apart form MG (vide infra) her written
production was normal, from the orthographic, lexical and
syntactic point of view. Oral and written calculation was
flawless.
The patient was submitted to an Apraxia Battery, tapping Ideatory, Ideomotor and Limb-kinetic Apraxia (Denes et al., 1998),
currently in use in our Unit, and her performance was perfect.

Experimental section
Methods
The patient was submitted to a series of graphic tasks,
tapping her skills in processing alphabetic and non-alphabetic
material, such as drawing and copying meaningful and meaningless pictures. In order to investigate if MG was a consequence of a strategy to maintain accuracy in order to reduce

Alphabetic tasks
Writing to dictation
Writing was fluent, composed of well written letters, the style
of writing being the same as before the trauma except for the
MG: a definite pattern of MG was evident both on writing in
capital letters and in cursive, without any difference in writing
sentences or single words. Her MG pattern was compared
with a sample of her handwriting before the accident: the size
of actual writing was about one-third of the previous writing
size, for example, the height of the cursive f was 14 mm.
before the trauma and 5 mm in MG writing. In contrast with
PD patients the height of the letters was the same throughout
the text, without progressive tendency to diminution and with
good accuracy (Figure. 2).
Transcoding
MG was evident in translating block letters into cursive and
vice versa.

179

Micrographia Following Focal Lesion

Writing on copy
MG was evident only on copying cursive, while copying of
words in capital letters was normal. In the double dimension
copy task the correct dimension was evident only in copying
capital letters.
Non alphabetic tasks
Writing arabic numbers
The patient’s production was correct, but micrographic.
Drawing on copy
The patient copied the drawings flawlessly, following the
model size.
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Copying of Japanese characters
The patient’s performance was flawless and the dimension of
her production strictly followed the model.
Follow up
At the follow-up control, six months later, the patient
reported that she could write in normal dimensions using capital letters, a strategy that she adopted in everyday writing.
On testing, MG was evident only in cursive writing.

Discussion

Fig. 2. (a) Spontaneous writing of P.P. before the trauma;
(b) spontaneous writing of P.P. 3 years after the trauma; (c)
spontaneous writing of a patient with Parkinson’s Disease and MG;
(d) P.P: Writing to dictation in cursive and capital letters; (e) P.P.:
writing from copy of non-alphabetical signs. Note the accuracy of
P.P.’s MG compared with PD’s MG.

In this study we report the case of a highly educated patient
who, following an extensive lesion of the left basal ganglia of
traumatic origin (gunshot), developed a definite pattern of
MG, its only accompanying deficit being a very mild dystonia
of right hand and foot; in particular, unlike other cases of MG
following focal lesion, there was not hypophonia (Murray
et al., 2000; Nakamura et al., 2003), or clumsiness of hand
movements.
At variance with the MG present in PD, P.P.’s writing was
not distorted, and did not show a progressive reduction in
writing size as the length of the text to be produced increased,
her MG pattern being constant throughout the text. This latter
finding excludes that her MG was secondary to an increase of
processing load, consequent to the increased coordination
and control of fingers, wrist and arm during writing and the
processing of future words, or increased extension of the wrist
joint, as the execution of the writing progresses to the right
across the page (Van Gemmert et al., 2001).
Actual production of letters in handwriting is dependent
upon a graphic motor plan, which specifies the appropriate
sequence of strokes, while graphic innervatory patterns
specify their relative size. Only a few cases are reported in
the literature where a detailed analysis of isolated MG is
provided: Troyer et al. (2004) reported a case of MG, following a left basal ganglia lesion of ischemic origin, context

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180
dependent, thus appearing only on spontaneous writing, but
not when copying sentences or drawing: they interpreted
this dissociation as an effect of task difficulty (spontaneous
writing requires the generation and expression of ideas,
while copying has no demands on generation or expressive
language). P.P.’s MG was present both in cursive and capital letters (spontaneous writing and dictation), in writing
texts and single words and persisted even when she had to
copy in large dimensions. Her production was fluent, syntactically and semantically correct, as was her spontaneous
language. P.P. was able to retrieve and produce the appropriate sequence of strokes, she respected the difference in
size in writing capital letters at the beginning of text and
sentences and the cursive writing in the remaining words.
This finding clearly shows that the patient has an intact graphemic code, her only writing impairment being an inability
to form the appropriate letter size. Similarly to the patient of
Troyer et al. (2004), spontaneous drawing, drawing form
copy and copying of non-alphabetical graphic signs (Japanese
characters), were flawless, without any tendency to size
reduction.
At the follow-up, MG was present only in cursive writing,
while spontaneous writing in capital letters, as well as copying of cursive, was of normal size.
This dissociation could be ascribed to the work of different
processes used in handwriting: automatic and controlled:
writing in cursive, the usual, everyday writing, is a fast,
familiar process; in addition, the production of the single letters
of a word to be written requires an anticipation process that
could vary according to the subsequent letter; on the other
hand, writing words in capital letters is a less frequent, slower
process and the composition of the letters is not influenced by
the presence of preceding or subsequent letters. It is not
unreasonable to postulate that cursive writing requires less
conscious attention to the mechanic output, while writing in
capital letters, copying and drawing require more visual
control; this in turn could exert a positive influence in modifying the writing size reduction. While MG present in PD
patients is easily interpreted as an epiphenomenon of a diminution of force, with secondary changes in timing and in
some subjects to the effect of tremor (Margolin and Wing,
1983), the question of the underlying deficit in pure MG is far
from being resolved: most of the published reports are merely
descriptive and do not deal with this problem.
Two possible answers could be offered, one based on the
presence of a subtle motor deficit not evident in other tasks,
whose execution does not require such a fine degree of motor
control as in writing. Pullicino et al. (1994) and more
recently Nakamura et al. (2003) suggest that a disruption of
the connections between basal ganglia and frontal lobes could
play a major role in the pathogenesis of MG due to the damage
of one of the frontal-subcortical motor circuits. The second
hypothesis, more attractive from a cognitive point of view,
postulates a specific role of the basal ganglia in the process of
choosing and realizing the appropriate size of the letters to be
written, once the graphomotor plan is realized.

Denes, Signorini and Volpato
Finally, of particular interest was the normality of P.P.’s
cognitive functions: there is considerable evidence that
damage to the basal ganglia is frequently associated with
both direct effects and indirect effects due to the interruption of the frontal- subcortical circuits and consequent
effects on frontal lobe functions. Thus, it could be easily
predicted that our patient should have been affected by cognitive deficits similar to those found in frontal lobe-damaged
patients such as impairments of executive functions
(impaired attention, working memory, planning, etc.). (For
a summary see Faglioni, 1999). More than her normal to
superior performance in the tests to which the patient was
submitted in the course of the present work, particularly
indicative of the normality of her cognitive skills was her
highly successful professional activity as head of an important
tax consultant firm.
The implication of such a pattern of cognitive normality,
despite the gross anatomical lesion, is intriguing and we cannot
offer a reasonable explanation. Only multiple single case
studies (Shallice, 1988) can help to disentangle the problem
of selective deficit or sparing of cognitive functions in
patients with basal ganglia lesions.

References
Alexander GE, DeLong MR, Strick PL. Parallel organization of functionally
segregated circuits linking basal ganglia and cortex. Annual Review of
Neuroscience 1986; 9: 357–81.
Baxter DM, Warrington EK. Ideational agraphia: A single case study. Journal of Neurology, Neurosurgery and Psychiatry 1986; 49: 369–74.
Benton AL. A visual retention test for clinical use. Archives of Neurology
and Psychiatry 1945; 54: 212–6.
Caramazza A. Some aspects of language processing revealed through the
analysis of acquired dysgraphia: The lexical system. Annual Review
of Neuroscience 1988; 11: 395–421.
Caramazza A, Miceli G, Villa G, Romani C. The role of the Graphemic
Buffer in spelling: Evidence from a case of acquired dysgraphia. Cognition 1987; 26: 59–85.
Chialant D, Domoto-Reilly K, Proios H, Caramazza A. Preserved orthographic length and transitional probabilities in written spelling in a
case of acquired dysgraphia. Brain and Language 2002; 82: 30–46.
Cipolotti L, Denes G. When a patient can write but not copy: Report of a
single case. Cortex 1989; 25: 331–7.
De Bastiani P, Barry C. A cognitive analysis of an acquired dysgraphic
patient with “allographic” writing disorder. Cognitive Neuropsychology 1989; 6: 25–41.
Demirci M, Grill S, McShane L, Hallett M. A mismatch between kinesthetic and visual perception in Parkinson's disease. Annual Neurology
1997; 41: 781–8.
Denes G, Mantovan MC, Gallana A, Cappelletti JY. Limb-kinetic apraxia.
Movement Disorders 1998; 13: 468–76.
Derkinderen P, Dupont S, Vidal JS, Chedru F, Vidailhet M. Micrographia
secondary to lenticular lesions. Movement Disorders 2002; 17: 835–7.
Ellis AW. Spelling and writing (and reading and speaking). In: Ellis AW,
editor, Normality and pathology in cognitive function. London:
Academic Press, 1982.
Ellis AW. Reading, writing and dyslexia. Hove, UK: LEA Publishers,
1988a.
Ellis AW. Normal writing processes and peripheral acquired dysgraphias.
Language and Cognitive Processes 1988b; 3: 99–127.

Downloaded by [FU Berlin] at 08:26 26 November 2014

Micrographia Following Focal Lesion
Faglioni P. The frontal lobe. In: Handbook of clinical and experimental
neuropsychology. Denes G, Pizzamiglio E, editors. Hove: Psychology
Press, 1999; 525–570
Hanley JR, Peters S. A dissociation between the ability to print and write
cursively in lower-case letters. Cortex 1996; 32: 737–45.
Kim JS, Im JH, Kwon SU, Kang JH, Lee MC. Micrographia after thalamomesencephalic infarction: evidence of striatal dopaminergic hypofunction. Neurology 1998; 51: 625–7.
Longstaff MG, Mahant PR, Stacy MA, VanGemmert AW, Leis BC, Stelmach
GE. Discrete and dynamic scaling of the size of continuous graphic
movements of parkinsonian patient and elderly controls. Journal of
Neurology, Neurosurgery and Psychiatry 2003; 74: 299–304.
Luzzatti C, Willmess K, De Bleser R. Aachener Aphasie Test. Firenze,
Italy: Organizzazioni Speciali 1991.
Margolin DI, Wing AM. Agraphia and micrographia: clinical manifestations
of motor programming and performance disorders. Acta Psychologica
(Amst) 1983; 54: 263–83.
Marsden CD, Obeso JA. The functions of the basal ganglia and the paradox
of stereotaxic surgery in Parkinson's disease. Brain 1994; 117: 877–97.
Martinez-Vila E, Artieda J, Obeso JA. Micrographia secondary to lenticular
haematoma. Journal of Neurology Neurosurgery and Psychiatry 1988;
51: 1353.
Münchau A, Mathen D, Cox T, Quinn NP, Marsden CD, Bhatia KP. Unilateral lesions of the globus pallidus: Report of four patients presenting
with focal or segmental dystonia. Journal of Neurology, Neurosurgery
and Psychiatry 2000; 69(4): 494–8.
Murray BJ, Llinas R, Caplan LR, Scammell T, Pascual-Leone A. Cerebral
deep venous thrombosis presenting as acute micrographia and hypophonia. Neurology 2000; 54: 751–3.
Nakamura M, Hamamoto M, Uchida S, Nagayama H, Amemiya S, Okubo S,
Tanaka K. A case of micrographia after subcortical infarction: Possible
involvement of frontal lobe function. European Journal of Neurology
2003; 10: 593–6.
Noda S, Itoh H, Goda S. Micrographia due to focal cerebral lesions as
seen in the dysarthria-clumsy hand syndrome. Neurology 1994; 44:
150–1.
Novelli G, Papagno C, Capitani E, Laiacona M, Vallar G, Cappa SF. Tre
test clinici di ricerca e produzione lessicale: Taratura su soggetti
normali. Archivio di Neurologia, psichiatria e psicologia 1986; 47:
477–505.
Orsini A, Grossi D, Capitani E, Laiacona M, Papagno C, Vallar G. Verbal and
spatial memory span: normative data from 1355 adults and 1112 children. Italian Journal of Neurological Sciences 1987; 85: 39–48.

181
Patterson K, Wing AM. Processes in hand-writing: A case for case. Cognitive Neuropsychology 1997; 6: 1–23.
Pick A. Ueber eine eigenthumliche Schreibstorung, Mikrographie, in Folge
cerebraler Erkrankung. Prag Med Wochenschr 1903; 28: 1–4. Quoted
by LeWitt PA. Micrographia after thalamo-mesencephalic infarction.
Neurology 1999; 52: 1921–2.
Pullicino P, Lichter D, Benedict R. Micrographia with cognitive dysfunction: “Minimal” sequelae of a putaminal infarct. Movement Disorders
1994; 9: 371–3.
Rapp B, Caramazza A. From graphemes to abstract letter shapes: levels of
representation in written spelling. Journal of Experimental Psychology
and Human Perception Performance 1997; 23: 1130–52.
Schonauer K, Denes G. Graphemic jargon: A case report. Brain and Language 1994; 47: 279–99.
Scolding NJ, Lees AJ. Micrographia associated with parietal lobe lesion in
multiple sclerosis. Journal of Neurology, Neurosurgery and Psychiatry
1994; 57: 739–41.
Shallice T. Specific impairments of planning. Philosophical transactions of
the Royal Society of London. Series B, Biological Sciences 1982; 298:
199–209.
Shallice T. From neuropsychology to mental structure. Cambridge University
Press, 1988.
Silveri MC. Peripheral aspects of writing can be differentially affected by
sensorial and attentional defect: evidence from a patient with afferent
dysgraphia and case dissociation. Cortex 1996; 32: 155–72.
Trojano L, Chiacchio L. Pure dysgraphia with relative sparing of lower-case
writing. Cortex 1994; 30: 499–501.
Troyer AK, Black SE, Armillo ML, Moscovitch M. Cognitive and motor
functioning in a patient with selective infraction of the basal ganglia:
evidence for decrease non routine response selection and performance.
Neuropsychologia 2004; 42: 902–911.
Van Galen, GP. Handwriting and drawing: A two stage model of complex
motor behaviour. In Stelmach G, Requin S, editors. Tutorials in motor
behavior. Amsterdam; North Holland, 1980.
Van Gemmert AW, Teulings HL, Stelmach GE. Parkinsonian patients
reduce their stroke size with increased processing demands. Brain and
Cognition 2001; 47: 504–12.
Wechsler D. A standardized memory scale for clinical use. Journal of Psychology 1945; 19: 87–95.
Wechsler D. Adult Intelligence Scale. Firenze, Italy: Organizzazioni Speciali, 1974.
Wing A. Response time in handwriting. In: Stelmach GE, editor. Information processing in motor control and learning. New York: Academic Press, 1978.