Journal of Neurology, Neurosurgery and Psychiatry 1990;53:797-799

797

SHORT REPORT

Paramedian thalamic and midbrain infarcts
associated with palilalia
Yuzuru Yasuda, Ichiro Akiguchi, Masashi Ino, Hidehiko Nabatabe, Masakuni Kameyama

Department of
Neurology, Kyoto City
Hospital
Y Yasuda
Department of
Neurology, Faculty of
Medicine, Kyoto
University
I Akiguchi
M Ino
H Nabatabe
Department of
Neurology, Sumitomo
Hospital, Japan
M Kameyama
Correspondence to:
Dr Y Yasuda, Department of
Neurology, Kyoto City
Hospital, HigashiTakadacho, Mibu,
Nakagyoku, Kyoto 604,
Japan.
Received 7 July 1989 and in
revised form 25 September
1989.

Accepted 11 October 1989

Abstract
sides (right 8 mm, left 6 mm), and light reacA patient with paramedian thalamic and tion was absent. Bilateral ptosis was seen, and
midbrain infarcts developed palilalia.
his eyes were divergent. Eye movement was
restricted in all directions, except for a slight
Palilalia is a speech abnormality characterised medial gaze. Convergence was absent. Doll's
by compulsive repetition of a phrase or word head and Bell's phenomena were not seen.
and was first described by Souques in 1908.' Other cranial nerves were normal. Although
Reports of palilalia are rare and the cause is deep tendon reflex was normal, Babinski sign
unknown. Clinical and neuropathological was elicited on the right side. Though muscle
findings by Boller et al2 concluded that it is strength was normal in the extremities, musassociated with a disturbance of the extra- cle tone was decreased. Finger-to-nose test
pyramidal system.
and heel-to-knee test were clumsy and marked
Patients with paramedian thalamic lesions hypermetria was observed. He showed
show altered consciousness, ocular motility marked ataxic gait, but could walk a short
changes, abnormal movements, memory dis- distance unaided.
turbance, and aphasia.' We observed a
When his speech was not repetitious it was
patient with palilalia for four months. MRI slow and indistinct. When he became repetishowed infarcts in the medial thalami, sub- tious, the rate of speech gradually increased,
thalami and midbrain on both sides, but no the loudness reduced, and finally he began to
other lesions. We present the first report of whisper. A syllable or word was involuntarily
paramedian thalamic and midbrain infarcts repeated five to ten times in spontaneous
associated with palilalia.
speech or in reply to a question; repetition of
phrases being more infrequent than that of
syllables or words. This patient's palilalia was
Case report
rarely noticed when he repeated words spoken
A 62 year old man fell while walking in the to him by the examiner. Slight perseveration
garden on 5 June 1986. Paraesthesia devel- was seen. Literal and verbal paraphasia was
oped from the left cheek to the left corner of not present. When asked, for example, how
his mouth and he became blind in the left eye. his condition was, his answer was "guai-guaiHe did not complain of vertigo, nausea or guai-guai-guai ima-ima-ima-ima toku-tokuvomiting and was admitted to hospital as an toku-tokuni ii-desu" (guai = condition, ima
emergency. On admission he was comatose
= now, tokuni = especially, ii = good, desu
and showed flaccid tetraplegia. He had dila- = a particle).
tated non-reactive pupils. Doll's head
Despite marked ataxia and photophobia, his
movements were absent. Two days later, he writing was preserved. Right left disorienbegan to improve gradually. Neurological tation, apraxia and agnosia were absent.
examination revealed bilateral cerebellar Wechsler Adult Intelligence Scale verbal IQ
ataxia, oculomotor nerve palsy, lack of spon- was 83, but a performance test could not be
taneity, and amnesia. Deep tendon reflexes, carried out because of his ataxia. Recent verpower and sensation were normal. Babinski bal and visual memories were moderately dissign was noted on the right side. Muscle tone turbed, and immediate ones only slightly.
was decreased. Ten days later, he began to say
Laboratory findings including complete
his name and speak simple words. Two mon- blood count and serum calcium, blood urea
ths later, he began to show compulsive repeti- nitrogen, creatinine phosphokinase, alkaline
tion of syllables, words, or phrases, and was phosphatase, and glutamic oxalacetic transtransferred to our hospital.
aminase were normal. Electrocardiogram
On admission, physical examination was showed sinus bradycardia.
normal except for the pulse rate which was 46/
The basic rhythm on EEG was 7 Hz theta
min. Neurologically he was apathetic, and and 8-9 Hz alpha waves, and sporadic 4-5 Hz
continued to lie in bed if other instructions theta waves were seen bilaterally. A vertebral
were not given. He could however understand
angiography showed no stenosis of basilar
questions and eat food in a sitting position artery, thalamogeniculate artery, posterior
with help. His pupils were dilated on both choroidal artery, and thalamoperforating

798

Yasuda, Akiguchi, Ino, Nabatabe, Kameyama

Figure MRI. A.B:
Partial saturation (TR =
400 ms, TE = 25 ms),
C.D: Spin echo (TR =
2500 ms, TE = 80 ms).
Bilateral infarcts in the
medial thalami,
subthalami, and midbrain.

artery. MRI showed infarcts in the medial words spoken to him by the examiner. The
thalami, subthalami and midbrain on both repetition was not restricted to the first or last
sides (fig), but no other lesions. Somato- syllable, and can therefore be differentiated
sensory evoked potentials (SEP) showed no from stammering or logoclonia. As the patient
abn-ormality. Brainstem evoked response spoke, the rate of speech gradually increased,
showed delayed latency of V-waves on both the loudness reduced, and finally he began to
sides (6-4 ms) and I-V time was prolonged whisper. This phenomenon is called "palilalie
(4-7 ms), which showed a disturbance of the aphone", which was first described by Marie
midbrain.
and Levy in 1922."
The palilalia gradually disappeared and was
Patients with paramedian thalamic lesions
almost imperceptible by December 1986. show reduced voice volume,4 dysarthria,5 perHowever, the patient's speech remained slow severation,4 5 7 8 confusion,6 confabulation,6 and
and unsteady. Cerebellar ataxia was slightly a tendency to echolalia.7 This reduced voice
improved, but there was no improvement in volume4 is similar to palilalie aphone," but
oculomotor palsy, ptosis, and mydriasis.
compulsive repetition of phrases or words has
not been reported in patients with paramedian
thalamic lesions. Therefore previously reporDiscussion
ted abnormalities of speech and language with
Palilalia has been described' as a speech dis- paramedian thalamic lesions' differ from
order characterised by compulsive repetition of palilalia.
a phrase or word. Marie and Levy9 described
The mechanism of palilalia is thought to be
the characteristics as: (1) compulsive repetition derived from the disturbance of accommodaof several short phrases or words or, more than tion of pronunciation by extrapyramidal dystwo occasions; (2) monotonous speech and a function, which is based on the findings that
tendency to shorten phrases; (3) initial explo- the basal ganglia were often involved in cases
sive speech with the speed gradually increasing with palilalia at necropsy. For example, several
but becoming quieter. Reports of palilalia are infarcts were seen bilaterally in the putamen,
rare although several exist in the literature; a the caudate and the subthalamic nucleus in one
case with apoplexy by Souques,' one with of Pick's cases.'2 Another of Pick's cases
pseudobulbar palsy by Dupre and showed widespread loss of cells in the caudate
Savoureaux,"' one with Parkinsonism by Marie and lenticular nuclei.'2 Critchley's case showed
and Levy,"l one with Parkinson's disease small lacunae in the basal ganglia and pons. " A
by Pick,'2 one with Alzheimer's disease by case described by Contamin et al showed
Frey,'3 and one with falx meningioma by bilateral atrophy of globus pallidus, subAlajouanine."4 The common characteristics in thalamic nucleus and substantia nigra.'6 Boller
these reports is that palilalia was often seen in et al observed that palilalia fluctuated with
spontaneous speech but rarely seen in repeti- chorea in familial cases that showed extensive
tion and reading.
intracranial calcifications involving the basal
Palilalia must be differentiated from stam- ganglia on both sides, and proposed that palimering, logoclonia, and echolalia. Stammering lalia is caused by bilateral lesion in inhibitory
is characterised by difficulty in producing the motor circuits.2 Thus most cases with
next expected sound; logoclonia by repetition have bilateral lesions of the basal palilalia
ganglia.
of the last syllable of the words, and echolalia is However, cases with cerebral hemisphere
on
the automatic repetition ofthe words addressed both sides,12 or one with one cerebellar hemito the patient. In this case repetition of syl- sphere and several areas of the corpus callolables, words, and phrases were noted and sumj° have been reported.
repetition was mostly observed in spontaneous
MRI showed infarcts in the medial
speech and rarely when the patient repeated the subthalami, and midbrain on both sides,thalami,
but no

Paramedian thalamic and midbrain infarcts associated with palilalia

lesions in the basal ganglia, cerebral hemispheres or cerebellar hemispheres in this case.
The dentato-rubro-thalamic tracts were
involved on both sides. Within the thalamus,
not only intralaminar-parafascicular-centromedian nuclei but also postero-medial nuclei
may be partially involved. From the literature
and our case we propose that a specific localised
lesion is not necessary for the development of
palilalia. Disturbance of nuclei in the subthalami, basal ganglia and thalami, and their
projection areas namely widespread extrapyramidal dysfunction, may cause palilalia.
1 Souques MA. Palilalie. Rev Neurol (Paris) 1908;16:340-9.
2 Boller F, Boller M, Denes G, et al. Familial palilalia.
Neurology 1973;23:1117-25.
3 Castaigne P, Lhermitte F, Buge A, et al. Paramedian
thalamic and midbrain infarcts: Clinical and neuropathological study. Ann Neurol 1981;10:127-48.
4 Stuss DT, Guberman A, Nelson R, et al. The neuropsychology of paramedian thalamic infarction. Brain and

Cognition 1988;8:348-78.

5 Graff-Radford NR, Eslinger PJ, Damasio AR, et al. Nonhemorrhagic infarction of the thalamus: Behavioral,

799
anatomic, and physiologic correlates. Neurology 1984;34:
14-23.
6 Bogousslavsky J, Regli F, Uske A. Thalamic infarcts.
Clinical syndrome, etiology, and prognosis. Neurology

1988;38:837-48.

7 Fensore C, Lazzarino LG, Nappo A, et al. Language and
memory disturbances from mesencephalothalmic infarcts.
A clinical and computed tomography study. Eur Neurol

1988;28:51-6.

8 Crosson B. Role of the dominant thalamus in language: a
review. Psychol Bull 1984;96:491-517.
9 Marie P, Levy G. Un singulier trouble de la parole: la
palilalie. Monde Med 1925;35:329-44.
10 Dupre E, Savoureaux L. Palilalie chez une pseudo-bulbaire.
Rev Neurol (Paris) 1914;27:453-6.
11 Marie P, Levy G. Palilalie et syndrome parkinsonien par
encephalite epidemique. Rev Neurol (Paris) 1922;29:
6-80.
12 Pick A. Die Palilalie, ein Teilstuck striarer Motolittasstorungen. Abhandl Neurol Psychiatr Psychol 1921;13:178-224.
13 Frey E. Beitrage zur Klinik und pathlogischen Anatomie der
Alzheimerschen Krankheit. Z Gesamte Neurol Psychiatr

1914;27:397-434.

14 Alajouanine Th, Castaigne P, Sabouraud 0, et al. Palilalie
paroxystique et vocalisations iteratives au cours de crises
epileptiques par lesion interessant l'aire motorice supplementaire. Rev Neurol (Paris) 1959;101:685-97.
15 Critchley M. On palilalia. J Neurol Psychopathol 1927;8:
3-32.
16 Contamin F, Escourolle R, Nick J, et al. Atrophic pallidonigro-luysienne. Syndrome akinetique avec palilalie,
rigidite oppositionelle et catatonie. Rev Neurol (Paris)
1971;24:107-20.