Bilateral, Neurologia i Neurochirurgia Polska od 2012
[ Pobierz całość w formacie PDF ]
CASE REPORT/OPIS PRZYPADKU
Bilateral paramedian thalamic infarction with hypothalamic dysfunction
Obustronny udar wzgórza zdysfunkcj¹ podwzgórza
Ewa Papuæ, Joanna Wojczal, Zbigniew Stelmasiak, Konrad Rejdak
Chair and Department of Neurology of Medical University of Lublin, Poland
Neurologia i Neurochirurgia Polska 2012; 46, 3: 279-283
DOI: 10.5114/ninp.2012.29135
Abs t r ac t
St res zc zen ie
Unilateral thalamic lesions cause transient or permanent
behavioral, sensory and oculomotor disturbances; bilateral
lesions of thalamus result in more severe and longer lasting
symptoms. We present an atypical case of bilateral parame-
dian thalamic infarct with concomitant hypothalamic dys-
function. The only risk factor of ischaemic stroke found in
the patient was a short lasting episode of atrial fibrillation.
Bilateral paramedian thalamic infarcts may result from occlu-
sion of one paramedian thalamic artery, which arises from
the posterior cerebral artery, either with separated or with
a common trunk, thus supplying the thalamus bilaterally.
Independently of anatomical variants of thalamus blood sup-
ply, the most probable cause of infarct in our patient was uni-
lateral or bilateral occlusion of the posterior cerebral artery
by cardioembolism, probably in the course of basilar artery
occlusion. Hypothalamic dysfunction may accompany tha la-
mic infarcts; thus hypothalamo-pituitary function should be
routinely assessed in bithalamic infarcts.
Key worrdss::ischaemic stroke, bilateral thalamic infarct, hypo-
thalamic dysfunction.
Jednostronne udary wobrêbie wzgórza mog¹ byæ przyczyn¹
przemijaj¹cych lub trwa³ych zaburzeñ zachowania, objawów
czuciowych lub zaburzeñ ga³koruchowych. Obustronne uda-
ry wzgórza skutkuj¹ zwykle bardziej nasilonymi i d³u¿ej
trwaj¹cymi objawami. Wniniejszym artykule zaprezentowa-
no przypadek obustronnego udaru wzgórza z jednoczesn¹
dysfunkcj¹ podwzgórza. Jedynym czynnikiem ryzyka udaru
niedokrwiennego mózgu, jaki stwierdzono u pacjenta, by³
krótkotrwa³y epizod migotania przedsionków. Obustronne
udary wzgórza mog¹ byæ wynikiem zamkniêcia jednej têtni-
cy przyœrodkowej wzgórza, odchodz¹cej od têtnicy tylnej
mózgu albo w postaci dwóch osobnych ga³êzi, albo te¿ jed-
nego wspólnego pnia, zaopatruj¹cego jednak wzgórze obu-
stronnie. Niezale¿nie jednak od wariantów anatomicznych
unaczynienia wzgórza najbardziej prawdopodobn¹ przyczyn¹
udaru niedokrwiennego uprzedstawionego pacjenta by³o jed-
nostronne lub te¿ obustronne zamkniêcie têtnicy tylnej mózgu
przez materia³ zatorowy, prawdopodobnie w przebiegu
zamkniêcia szczytu têtnicy podstawnej. Dysfunkcja pod-
wzgórza mo¿e towarzyszyæ udarom wzgórza, autorzy suge-
ruj¹ wiêc, aby funkcja uk³adu podwzgórzowo-przysadkowe-
go by³a rutynowo oceniana w przypadku obustronnych
udarów wzgórza.
S³³owa klluczowe:: udar niedokrwienny, obustronny udar wzgó-
rza, dysfunkcja podwzgórza.
Correspondence address: Ewa Papuæ, MD, PhD, Department of Neurology, Medical University of Lublin, 8 Jaczewskiego St., 20-954 Lublin, Poland,
phone: +48 81 724 47 20, fax: +48 81 724 45 40, e-mail: ewapap@yahoo.pl
Received: 19.01.2011; accepted: 27.09.2011
279
Neurrollogiia ii Neurrocchiirrurrgiia Pollsska 2012; 46, 3
Ewa Papuæ, Joanna Wojczal, Zbigniew Stelmasiak, Konrad Rejdak
circulation. The patient was referred to the department
of toxicology, where toxic causes of coma were exclud-
ed. Before admission to the toxicology department, he was
con sulted by aneurologist, and brain computed tomog-
raphy (CT) was performed afew hours after disease onset,
which revealed no brain abnormality; the patient’s blood
pressure on first neurological examination was normal.
The second brain CT performed on day 2 after disease
onset (< 48 hours) revealed no pathology again. On the
3
rd
day he was referred to our Department of Neurolo -
gy to continue diagnostics. Neurological examination per-
formed on admission revealed acomatose patient (Glas-
gow Coma Scale – 3 points) with equal pinpoint pupils
unreactive to light and discrete right hemiparesis, right-
sided Babiñski sign was also present. The patient
remained comatose for 3 days, after which he recovered
consciousness but presented pathological sleepiness.
From the 4
th
day, the consciousness was fully recovered,
but the patient presented hypersomnia, amnesia, transcor-
tical aphasia, vertical gaze palsy and discrete right
hemiparesis; his reflexes were decreased in the right limbs.
On the brain magnetic resonance imaging (MRI) per-
formed on the 4
th
day after the disease onset, bi-thala-
mic ischemic lesions in the paramedian territories were
found (hyperintense lesions in T2-weighted and FLAIR
sequences located bilaterally in the paramedian thalamus)
(Figs. 1A and 1B). Brain angio-CT scans were performed
Introduction
Acute bilateral infarction of the thalamus is not acom-
mon condition as it represents 0.6% of first-ever acute
ischemic strokes [1], but is usually associated with spe-
cific neurological and neuropsychological symptoms.
As the tha lamus is one of the strategic regions of the
human brain, the knowledge of its functions and clini-
cal consequences of its lesions is vital [1-3]. Vascular
lesions destroy thalamic nuclei in different combinations
producing sensorimotor and behavioral syndromes de -
pending on the nuclei involved. Unilateral thalamic lesions
cause transient or permanent behavioral, sensorial or ocu-
lar motor disturbances; bilateral lesions of the thalamus
result in more severe and longer lasting symptoms and
complete recovery in these cases is rare [4]. Bilateral para-
median thalamic infarctions account for one third of all
paramedian infarcts [5]. Here, we discuss an atypical case
of acute bilateral paramedian infarct with concomitant
hypothalamic dysfunction.
Case report
Afifty-eight-year-old man with sudden onset of vig-
ilance disturbances, without previous history of conco -
mitant disorders, was found by his family in the morn-
ing in a comatose state with preserved breathing and
A
B
Fiig.. 1..Magnetic resonance imaging of the patient with bilateral thalamic infarct. Axial FLAIR images (A) and T1-weighted images (B) are shown. Sites of lesion are
indicated by arrows
280
Neurrollogiia ii Neurrocchiirrurrgiia Pollsska 2012; 46, 3
Bilateral paramedian thalamic infarction with hypothalamic dysfunction
subsequently (to exclude cerebral deep venous throm-
bosis), revealing afilling defect of both P1 segments of
posterior communicating arteries. Complete blood cell
count, biochemical profile, and urinalysis were within nor-
mal limits. Thiamine deficiency, cerebral lupus and tox-
o plasmosis were excluded. Additionally, we performed
transcranial Doppler and duplex sonography of the carotid
and vertebral arteries, 12-lead electrocardiography (ECG),
24-hour ECG monitoring, and transthoracic and trans-
esophageal echocardiography. Neither transthoracic nor
transesophageal echocardiography revealed pathology.
Only 24-hour ECG monitoring revealed one paroxys-
mal short-lasting episode of atrial fibrillation, which re -
mained unnoticed by the patient. Blood coagulation (in -
cluding mutation of factor V, antithrombin, and lupus
anticoagulant) were normal.
Results of more detailed blood tests revealed hypothy-
roidism, secondary to hypothalamo-pituitary dysfunction;
serum free T4 (fT4) and free T3 (fT3) levels were low-
ered, and the thyroid stimulating hormone (TSH) lev-
el was undetectable. The patient also presented ACTH,
cortisol, gonadotropin, dehydroepiandrosterone (DHEA)
and testosterone deficiency. The prolactin and growth hor-
mone levels were within normal limits. After aweek, the
patient also presented symptoms of diabetes insipidus.
Repetitive measurement of blood electrolytes revealed
hypernatremia; urinalysis demonstrated adilute urine with
a low specific gravity.
In the follow-up period the patient required substitu-
tional treatment with hydrocortisone, thyroid hormones and
oral preparations of vasopressin analogues. On brain MRI,
no structural damage of the pituitary gland were found,
but the presence of multihormonal deficiency indicated loss
of function of upper centers in the hypothalamus.
On discharge from hospital, the patient presented
amnestic syndrome, reduced verbal fluency and vertical
gaze paresis. Although the memory and concentration
improved, 6 months after stroke onset the patient did not
regain his premorbid levels. He was referred for inten-
sive cognitive neurorehabilitation.
but it may differ substantially [7]. Percheron distingu -
ish ed three variants of this artery. The paramedian arte -
ries can arise as apair from each P1 section (type I), but
they also may arise from one P1 portion of the posterior
cerebral artery either with separated (type IIa) or with
acommon trunk (type IIb), thus supplying the thalamus
bilaterally [8]. In type III, we observe an arcade of thal-
amic perforators branching from an artery which connects
both P1 segments. The paramedian artery supplies ava-
riable part of the thalamus, but usually the dorsome dial
nucleus, internal medullary lamina and the intralaminar
nuclei: central lateral, centromedian and parafascicular.
Sometimes lateral dorsal, lateral posterior and ventral ante-
rior nuclei may also be supplied. In the absence of tube -
rothalamic artery, the paramedian artery assumes that ter-
ritory as well. Percheron’s artery (tuberothalamic artery,
TTA) originates from the middle third of the posterior
communicating artery and may be visualized in vivo by
superselective early angiography; we did not attempt to
verify its presence because it could have carried a high
risk because of the state of the patient.
Our patient was unusual, because he presented con-
comitant hypothalamic dysfunction. Normally, the TTA
and the paramedian artery are two arteries responsible
for the vascular supply of posterior parts of the hypo-
thalamus where the sympathicoexcitatory tract has its ori-
gin [9]. For this reason, infarction in the hypothalamic
region occurs rarely and when it happens the clinical and
radiological damage is often limited [10]. In our case
angio-CT scans of brain vessels revealed abilateral fill-
ing defect in posterior communicating arteries; thus we
hypothesize that in our patient the paramedian artery was
responsible for blood supply to the posterior part of the
hypothalamus, and its occlusion resulted in bilateral thal-
amic infarct with hypothalamic dysfunction. Usually para-
median artery occlusion results from occlusion of the P1
portion of the PCA as avariant of tip basilar artery (BA)
occlusion, or is subsequent to tip BA occlusion. Cases of
concurrent infarction in the paramedian and tuberothal-
amic territory are rare in the literature [11]. Neverthe-
less, independently of anatomical variants of thalamus
blood supply, the most probable cause of infarct in our
patient was occlusion of the P1 segment of the PCA, uni-
lateral or bilateral, in the course of BA top occlusion,
resolved by the 4
th
day, which was seen in angio-CT scans.
Bilateral infarction in the paramedian artery territo-
ry may result in disorientation, confusion, hypersom-
nolence, deep coma, ‘coma vigil’ or akinetic mutism and
severe memory impairment often accompanied by eye mo -
vement abnormalities [12]. Anterograde and retrograde
Discussion
The typical cause of bilateral paramedian thalamic
infarcts is an occlusion of the paramedian thalamic artery
resulting in loss of consciousness or somnolence at stroke
onset, subsequent concentration and orientation deficits
as well as memory deficits [6]. The paramedian artery
arises from the P1 section of the posterior cerebral artery,
281
Neurrollogiia ii Neurrocchiirrurrgiia Pollsska 2012; 46, 3
Ewa Papuæ, Joanna Wojczal, Zbigniew Stelmasiak, Konrad Rejdak
memory deficits and apathy are typical, as well as im pul-
sive, aggressive behaviors, emotional blunting, loss of
initiative and absence of spontaneous mental activities.
Never theless, complete recovery from bilateral parame-
dian thalamic infarction has also been reported [4]. It is
worth not ing that bilateral and left-sided infarcts have
worse outcome than right-sided ones [13]. The main struc-
tures involved in patients with memory deficits are the
mamillothalamic tract, internal medullary lamina and dor-
somedial nucleus [4,6], although there are some data sug-
gesting that the latter is not involved in memory deficits
[14]. Loss of psychic activation and thalamic dementia
are probably caused by interruption of the striatal-ven-
tral pallidal-thalamic-frontomesial limbic loop [2,15].
Typical oculomotor signs resulting from lesions in the
paramedian artery territory may cause complete or par-
tial vertical gaze paresis, loss of convergence, bilateral
intranuclear ophthalmoplegia, miosis and sometimes into-
lerance to bright light [6]. Lesions of the medial thala -
mus disrupt the corticofugal fibers that lead from motor
and premotor cortices to the nuclei of the midbrain, which
are responsible for vertical gaze (up and down); they also
disrupt the fibers to the rostral nucleus of the medial
longitudinal fasciculus responsible for downgaze [16].
In our patient, we observed at the beginning acomplete
vertical gaze paresis, which improved with time; after
8 weeks the patient presented apartial vertical gaze pare-
sis. Nevertheless, the prognosis of full recovery of ver-
tical eye movements is poor [3].
The most frequent causes of stroke in patients with
bilateral thalamic involvement are firstly lacunar strokes
(small vessel disease), and secondly embolic ones (artery
to artery embolism, cardioembolism) [1,6]. In our case
no history of concomitant disorders was present, but asin-
gle episode of atrial fibrillation confirmed in 24-hour
ECG was found; therefore the most probable cause of bi-
thalamic stroke seems to be embolus to the tip of the basi-
lar artery with subsequent occlusion of the paramedian
artery. However, it is worth noting that bilateral thala-
mic infarcts may rarely be symptomatic of cerebral deep
venous thrombosis [17], which we excluded by angio-CT
and brain MRI angiography. It is also worth noting that
in paramedian infarcts acardioembolic source is more fre-
quent than in other thalamic infarcts [6]. Atrial fibrilla -
tion and atrial flutter remain the most frequent causes of
cardioembolic stroke, but they usually escape from stan-
dard ECG or Holter monitoring [18].
To conclude, hypothalamic dysfunction may be asym-
p tom of damage of the area adjacent to the thalamus,
resulting from occlusion of the variants of the parame-
dian artery or tuberothalamic artery. Therefore hypo-
thalamo-pituitary function should be routinely assessed
in bithalamic infarcts.
Disclosure
Authors report no conflict of interest.
References
1. Kumral E., Evyapan D., Balkir K., et al. Bilateral thalamic in -
farction. Clinical, etiological and MRI correlates.
Acta Neurol Scand
2001; 103: 35-42.
2. Engelborghs S., Marien P., Pickut B.A., et al. Loss of psychic
self-activation after paramedian bithalamic infarction.
Stroke
2000;
31: 1762-1765.
3. ThurtellM.J., HalmagyiG.M. Complete ophthalmoplegia – an
unusual sign of bilateral paramedian midbrain-thalamic infarction.
Stroke
2008; 39: 1355-1357.
4. Krolak-Salmon P., Croisile B., Houzard C., et al. Total recovery
after bilateral paramedian thalamic infarct.
Eur Neurol
2000; 44:
216-218.
5. Emond H., LandisT., Perren F. From amaurosis fugax to asym -
ptomatic bithalamic infarct.
J Neurol
2009; 256: 1007-1008.
6. Bogousslavsky J., Regli F., Uske A. Thalamic infarcts: clinical
syndromes, etiology, and prognosis.
Neurology
1988; 38: 837-848.
7. Percheron G. The anatomy of the arterial supply of the human
thalamus and its use for the interpretation of the thalamic vas cular
pathology.
Z Neurol
1973; 205: 1-13.
8. PercheronG. Les arteres du thalamus humain, II : arteres et teri -
toire thalamiques paramedians de l’artere basilaire communicante.
Rev Neurol
(
Paris
) 1976; 132: 309-324.
9. Perren F., Clarke S., Bogousslavsky J. The syndrome of combin -
ed polar and paramedian thalamic infarction.
Arch Neurol
2005;
62: 1212-1216.
10. Azabou E., DerexL., Honnorat J., et al. Ipsilateral ptosis as main
feature of tuberothalamic artery infarction.
Neurol Sci
2009; 30:
69-70.
11. Castaigne P., Lhermitte F., Buge A., et al. Paramedian thalamic
and midbrain infarcts: clinical and neuropathological study.
Ann
Neurol
1981; 10: 127-148.
12. Graff-Radford N.R., Damasio H., YamadaT., et al. Non hemorr -
hagic thalamic infarction: clinical, neuropsychological and elec -
tro physiological findings in four anatomical groups defined by
computerized tomography.
Brain
1985; 108: 485-516.
13. Hermann D.M., Siccoli M.S., Brugger P., et al. Evolution of
neurological, neuropsychological and sleep-wake disturbances after
paramedian thalamic stroke.
Stroke
2008; 39: 62-68.
14. Graff-Radford N.R., Tranel D., VanHoesenG., et al. Diencephalic
amnesia.
Brain
1990; 113: 1-25.
15. Bogousslavsky J., Regli F., Delaloye B., et al. Loss of psychic self-
activation with bithalamic infarction.
Acta Neurol Scand
1991; 83:
309-316.
16. LeighR.J., Zee D.S. The neurology of eye movements.
FA Davis
,
Philadelphia 1983.
282
Neurrollogiia ii Neurrocchiirrurrgiia Pollsska 2012; 46, 3
Bilateral paramedian thalamic infarction with hypothalamic dysfunction
17. Bell D.A., Davis W.L., Osborn A.G., et al. Bithalamic hyper -
intensity on T2-weighted MR: vascular causes and evaluation
with MRI angiography.
AJNR
1994; 15: 893-899.
18. Jabaudon D., Sztajzel J., Sievert K., et al. Usefulness of ambula -
tory 7-day ECG monitoring for the detection of atrial fibrillation
and flutter after acute stroke and transient ischemic attack.
Stroke
2004; 35: 1647-1651.
283
Neurrollogiia ii Neurrocchiirrurrgiia Pollsska 2012; 46, 3
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CASE REPORT/OPIS PRZYPADKU
Bilateral paramedian thalamic infarction with hypothalamic dysfunction
Obustronny udar wzgórza zdysfunkcj¹ podwzgórza
Ewa Papuæ, Joanna Wojczal, Zbigniew Stelmasiak, Konrad Rejdak
Chair and Department of Neurology of Medical University of Lublin, Poland
Neurologia i Neurochirurgia Polska 2012; 46, 3: 279-283
DOI: 10.5114/ninp.2012.29135
Abs t r ac t
St res zc zen ie
Unilateral thalamic lesions cause transient or permanent
behavioral, sensory and oculomotor disturbances; bilateral
lesions of thalamus result in more severe and longer lasting
symptoms. We present an atypical case of bilateral parame-
dian thalamic infarct with concomitant hypothalamic dys-
function. The only risk factor of ischaemic stroke found in
the patient was a short lasting episode of atrial fibrillation.
Bilateral paramedian thalamic infarcts may result from occlu-
sion of one paramedian thalamic artery, which arises from
the posterior cerebral artery, either with separated or with
a common trunk, thus supplying the thalamus bilaterally.
Independently of anatomical variants of thalamus blood sup-
ply, the most probable cause of infarct in our patient was uni-
lateral or bilateral occlusion of the posterior cerebral artery
by cardioembolism, probably in the course of basilar artery
occlusion. Hypothalamic dysfunction may accompany tha la-
mic infarcts; thus hypothalamo-pituitary function should be
routinely assessed in bithalamic infarcts.
Key worrdss::ischaemic stroke, bilateral thalamic infarct, hypo-
thalamic dysfunction.
Jednostronne udary wobrêbie wzgórza mog¹ byæ przyczyn¹
przemijaj¹cych lub trwa³ych zaburzeñ zachowania, objawów
czuciowych lub zaburzeñ ga³koruchowych. Obustronne uda-
ry wzgórza skutkuj¹ zwykle bardziej nasilonymi i d³u¿ej
trwaj¹cymi objawami. Wniniejszym artykule zaprezentowa-
no przypadek obustronnego udaru wzgórza z jednoczesn¹
dysfunkcj¹ podwzgórza. Jedynym czynnikiem ryzyka udaru
niedokrwiennego mózgu, jaki stwierdzono u pacjenta, by³
krótkotrwa³y epizod migotania przedsionków. Obustronne
udary wzgórza mog¹ byæ wynikiem zamkniêcia jednej têtni-
cy przyœrodkowej wzgórza, odchodz¹cej od têtnicy tylnej
mózgu albo w postaci dwóch osobnych ga³êzi, albo te¿ jed-
nego wspólnego pnia, zaopatruj¹cego jednak wzgórze obu-
stronnie. Niezale¿nie jednak od wariantów anatomicznych
unaczynienia wzgórza najbardziej prawdopodobn¹ przyczyn¹
udaru niedokrwiennego uprzedstawionego pacjenta by³o jed-
nostronne lub te¿ obustronne zamkniêcie têtnicy tylnej mózgu
przez materia³ zatorowy, prawdopodobnie w przebiegu
zamkniêcia szczytu têtnicy podstawnej. Dysfunkcja pod-
wzgórza mo¿e towarzyszyæ udarom wzgórza, autorzy suge-
ruj¹ wiêc, aby funkcja uk³adu podwzgórzowo-przysadkowe-
go by³a rutynowo oceniana w przypadku obustronnych
udarów wzgórza.
S³³owa klluczowe:: udar niedokrwienny, obustronny udar wzgó-
rza, dysfunkcja podwzgórza.
Correspondence address: Ewa Papuæ, MD, PhD, Department of Neurology, Medical University of Lublin, 8 Jaczewskiego St., 20-954 Lublin, Poland,
phone: +48 81 724 47 20, fax: +48 81 724 45 40, e-mail: ewapap@yahoo.pl
Received: 19.01.2011; accepted: 27.09.2011
279
Neurrollogiia ii Neurrocchiirrurrgiia Pollsska 2012; 46, 3
Ewa Papuæ, Joanna Wojczal, Zbigniew Stelmasiak, Konrad Rejdak
circulation. The patient was referred to the department
of toxicology, where toxic causes of coma were exclud-
ed. Before admission to the toxicology department, he was
con sulted by aneurologist, and brain computed tomog-
raphy (CT) was performed afew hours after disease onset,
which revealed no brain abnormality; the patient’s blood
pressure on first neurological examination was normal.
The second brain CT performed on day 2 after disease
onset (< 48 hours) revealed no pathology again. On the
3
rd
day he was referred to our Department of Neurolo -
gy to continue diagnostics. Neurological examination per-
formed on admission revealed acomatose patient (Glas-
gow Coma Scale – 3 points) with equal pinpoint pupils
unreactive to light and discrete right hemiparesis, right-
sided Babiñski sign was also present. The patient
remained comatose for 3 days, after which he recovered
consciousness but presented pathological sleepiness.
From the 4
th
day, the consciousness was fully recovered,
but the patient presented hypersomnia, amnesia, transcor-
tical aphasia, vertical gaze palsy and discrete right
hemiparesis; his reflexes were decreased in the right limbs.
On the brain magnetic resonance imaging (MRI) per-
formed on the 4
th
day after the disease onset, bi-thala-
mic ischemic lesions in the paramedian territories were
found (hyperintense lesions in T2-weighted and FLAIR
sequences located bilaterally in the paramedian thalamus)
(Figs. 1A and 1B). Brain angio-CT scans were performed
Introduction
Acute bilateral infarction of the thalamus is not acom-
mon condition as it represents 0.6% of first-ever acute
ischemic strokes [1], but is usually associated with spe-
cific neurological and neuropsychological symptoms.
As the tha lamus is one of the strategic regions of the
human brain, the knowledge of its functions and clini-
cal consequences of its lesions is vital [1-3]. Vascular
lesions destroy thalamic nuclei in different combinations
producing sensorimotor and behavioral syndromes de -
pending on the nuclei involved. Unilateral thalamic lesions
cause transient or permanent behavioral, sensorial or ocu-
lar motor disturbances; bilateral lesions of the thalamus
result in more severe and longer lasting symptoms and
complete recovery in these cases is rare [4]. Bilateral para-
median thalamic infarctions account for one third of all
paramedian infarcts [5]. Here, we discuss an atypical case
of acute bilateral paramedian infarct with concomitant
hypothalamic dysfunction.
Case report
Afifty-eight-year-old man with sudden onset of vig-
ilance disturbances, without previous history of conco -
mitant disorders, was found by his family in the morn-
ing in a comatose state with preserved breathing and
A
B
Fiig.. 1..Magnetic resonance imaging of the patient with bilateral thalamic infarct. Axial FLAIR images (A) and T1-weighted images (B) are shown. Sites of lesion are
indicated by arrows
280
Neurrollogiia ii Neurrocchiirrurrgiia Pollsska 2012; 46, 3
Bilateral paramedian thalamic infarction with hypothalamic dysfunction
subsequently (to exclude cerebral deep venous throm-
bosis), revealing afilling defect of both P1 segments of
posterior communicating arteries. Complete blood cell
count, biochemical profile, and urinalysis were within nor-
mal limits. Thiamine deficiency, cerebral lupus and tox-
o plasmosis were excluded. Additionally, we performed
transcranial Doppler and duplex sonography of the carotid
and vertebral arteries, 12-lead electrocardiography (ECG),
24-hour ECG monitoring, and transthoracic and trans-
esophageal echocardiography. Neither transthoracic nor
transesophageal echocardiography revealed pathology.
Only 24-hour ECG monitoring revealed one paroxys-
mal short-lasting episode of atrial fibrillation, which re -
mained unnoticed by the patient. Blood coagulation (in -
cluding mutation of factor V, antithrombin, and lupus
anticoagulant) were normal.
Results of more detailed blood tests revealed hypothy-
roidism, secondary to hypothalamo-pituitary dysfunction;
serum free T4 (fT4) and free T3 (fT3) levels were low-
ered, and the thyroid stimulating hormone (TSH) lev-
el was undetectable. The patient also presented ACTH,
cortisol, gonadotropin, dehydroepiandrosterone (DHEA)
and testosterone deficiency. The prolactin and growth hor-
mone levels were within normal limits. After aweek, the
patient also presented symptoms of diabetes insipidus.
Repetitive measurement of blood electrolytes revealed
hypernatremia; urinalysis demonstrated adilute urine with
a low specific gravity.
In the follow-up period the patient required substitu-
tional treatment with hydrocortisone, thyroid hormones and
oral preparations of vasopressin analogues. On brain MRI,
no structural damage of the pituitary gland were found,
but the presence of multihormonal deficiency indicated loss
of function of upper centers in the hypothalamus.
On discharge from hospital, the patient presented
amnestic syndrome, reduced verbal fluency and vertical
gaze paresis. Although the memory and concentration
improved, 6 months after stroke onset the patient did not
regain his premorbid levels. He was referred for inten-
sive cognitive neurorehabilitation.
but it may differ substantially [7]. Percheron distingu -
ish ed three variants of this artery. The paramedian arte -
ries can arise as apair from each P1 section (type I), but
they also may arise from one P1 portion of the posterior
cerebral artery either with separated (type IIa) or with
acommon trunk (type IIb), thus supplying the thalamus
bilaterally [8]. In type III, we observe an arcade of thal-
amic perforators branching from an artery which connects
both P1 segments. The paramedian artery supplies ava-
riable part of the thalamus, but usually the dorsome dial
nucleus, internal medullary lamina and the intralaminar
nuclei: central lateral, centromedian and parafascicular.
Sometimes lateral dorsal, lateral posterior and ventral ante-
rior nuclei may also be supplied. In the absence of tube -
rothalamic artery, the paramedian artery assumes that ter-
ritory as well. Percheron’s artery (tuberothalamic artery,
TTA) originates from the middle third of the posterior
communicating artery and may be visualized in vivo by
superselective early angiography; we did not attempt to
verify its presence because it could have carried a high
risk because of the state of the patient.
Our patient was unusual, because he presented con-
comitant hypothalamic dysfunction. Normally, the TTA
and the paramedian artery are two arteries responsible
for the vascular supply of posterior parts of the hypo-
thalamus where the sympathicoexcitatory tract has its ori-
gin [9]. For this reason, infarction in the hypothalamic
region occurs rarely and when it happens the clinical and
radiological damage is often limited [10]. In our case
angio-CT scans of brain vessels revealed abilateral fill-
ing defect in posterior communicating arteries; thus we
hypothesize that in our patient the paramedian artery was
responsible for blood supply to the posterior part of the
hypothalamus, and its occlusion resulted in bilateral thal-
amic infarct with hypothalamic dysfunction. Usually para-
median artery occlusion results from occlusion of the P1
portion of the PCA as avariant of tip basilar artery (BA)
occlusion, or is subsequent to tip BA occlusion. Cases of
concurrent infarction in the paramedian and tuberothal-
amic territory are rare in the literature [11]. Neverthe-
less, independently of anatomical variants of thalamus
blood supply, the most probable cause of infarct in our
patient was occlusion of the P1 segment of the PCA, uni-
lateral or bilateral, in the course of BA top occlusion,
resolved by the 4
th
day, which was seen in angio-CT scans.
Bilateral infarction in the paramedian artery territo-
ry may result in disorientation, confusion, hypersom-
nolence, deep coma, ‘coma vigil’ or akinetic mutism and
severe memory impairment often accompanied by eye mo -
vement abnormalities [12]. Anterograde and retrograde
Discussion
The typical cause of bilateral paramedian thalamic
infarcts is an occlusion of the paramedian thalamic artery
resulting in loss of consciousness or somnolence at stroke
onset, subsequent concentration and orientation deficits
as well as memory deficits [6]. The paramedian artery
arises from the P1 section of the posterior cerebral artery,
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Neurrollogiia ii Neurrocchiirrurrgiia Pollsska 2012; 46, 3
Ewa Papuæ, Joanna Wojczal, Zbigniew Stelmasiak, Konrad Rejdak
memory deficits and apathy are typical, as well as im pul-
sive, aggressive behaviors, emotional blunting, loss of
initiative and absence of spontaneous mental activities.
Never theless, complete recovery from bilateral parame-
dian thalamic infarction has also been reported [4]. It is
worth not ing that bilateral and left-sided infarcts have
worse outcome than right-sided ones [13]. The main struc-
tures involved in patients with memory deficits are the
mamillothalamic tract, internal medullary lamina and dor-
somedial nucleus [4,6], although there are some data sug-
gesting that the latter is not involved in memory deficits
[14]. Loss of psychic activation and thalamic dementia
are probably caused by interruption of the striatal-ven-
tral pallidal-thalamic-frontomesial limbic loop [2,15].
Typical oculomotor signs resulting from lesions in the
paramedian artery territory may cause complete or par-
tial vertical gaze paresis, loss of convergence, bilateral
intranuclear ophthalmoplegia, miosis and sometimes into-
lerance to bright light [6]. Lesions of the medial thala -
mus disrupt the corticofugal fibers that lead from motor
and premotor cortices to the nuclei of the midbrain, which
are responsible for vertical gaze (up and down); they also
disrupt the fibers to the rostral nucleus of the medial
longitudinal fasciculus responsible for downgaze [16].
In our patient, we observed at the beginning acomplete
vertical gaze paresis, which improved with time; after
8 weeks the patient presented apartial vertical gaze pare-
sis. Nevertheless, the prognosis of full recovery of ver-
tical eye movements is poor [3].
The most frequent causes of stroke in patients with
bilateral thalamic involvement are firstly lacunar strokes
(small vessel disease), and secondly embolic ones (artery
to artery embolism, cardioembolism) [1,6]. In our case
no history of concomitant disorders was present, but asin-
gle episode of atrial fibrillation confirmed in 24-hour
ECG was found; therefore the most probable cause of bi-
thalamic stroke seems to be embolus to the tip of the basi-
lar artery with subsequent occlusion of the paramedian
artery. However, it is worth noting that bilateral thala-
mic infarcts may rarely be symptomatic of cerebral deep
venous thrombosis [17], which we excluded by angio-CT
and brain MRI angiography. It is also worth noting that
in paramedian infarcts acardioembolic source is more fre-
quent than in other thalamic infarcts [6]. Atrial fibrilla -
tion and atrial flutter remain the most frequent causes of
cardioembolic stroke, but they usually escape from stan-
dard ECG or Holter monitoring [18].
To conclude, hypothalamic dysfunction may be asym-
p tom of damage of the area adjacent to the thalamus,
resulting from occlusion of the variants of the parame-
dian artery or tuberothalamic artery. Therefore hypo-
thalamo-pituitary function should be routinely assessed
in bithalamic infarcts.
Disclosure
Authors report no conflict of interest.
References
1. Kumral E., Evyapan D., Balkir K., et al. Bilateral thalamic in -
farction. Clinical, etiological and MRI correlates.
Acta Neurol Scand
2001; 103: 35-42.
2. Engelborghs S., Marien P., Pickut B.A., et al. Loss of psychic
self-activation after paramedian bithalamic infarction.
Stroke
2000;
31: 1762-1765.
3. ThurtellM.J., HalmagyiG.M. Complete ophthalmoplegia – an
unusual sign of bilateral paramedian midbrain-thalamic infarction.
Stroke
2008; 39: 1355-1357.
4. Krolak-Salmon P., Croisile B., Houzard C., et al. Total recovery
after bilateral paramedian thalamic infarct.
Eur Neurol
2000; 44:
216-218.
5. Emond H., LandisT., Perren F. From amaurosis fugax to asym -
ptomatic bithalamic infarct.
J Neurol
2009; 256: 1007-1008.
6. Bogousslavsky J., Regli F., Uske A. Thalamic infarcts: clinical
syndromes, etiology, and prognosis.
Neurology
1988; 38: 837-848.
7. Percheron G. The anatomy of the arterial supply of the human
thalamus and its use for the interpretation of the thalamic vas cular
pathology.
Z Neurol
1973; 205: 1-13.
8. PercheronG. Les arteres du thalamus humain, II : arteres et teri -
toire thalamiques paramedians de l’artere basilaire communicante.
Rev Neurol
(
Paris
) 1976; 132: 309-324.
9. Perren F., Clarke S., Bogousslavsky J. The syndrome of combin -
ed polar and paramedian thalamic infarction.
Arch Neurol
2005;
62: 1212-1216.
10. Azabou E., DerexL., Honnorat J., et al. Ipsilateral ptosis as main
feature of tuberothalamic artery infarction.
Neurol Sci
2009; 30:
69-70.
11. Castaigne P., Lhermitte F., Buge A., et al. Paramedian thalamic
and midbrain infarcts: clinical and neuropathological study.
Ann
Neurol
1981; 10: 127-148.
12. Graff-Radford N.R., Damasio H., YamadaT., et al. Non hemorr -
hagic thalamic infarction: clinical, neuropsychological and elec -
tro physiological findings in four anatomical groups defined by
computerized tomography.
Brain
1985; 108: 485-516.
13. Hermann D.M., Siccoli M.S., Brugger P., et al. Evolution of
neurological, neuropsychological and sleep-wake disturbances after
paramedian thalamic stroke.
Stroke
2008; 39: 62-68.
14. Graff-Radford N.R., Tranel D., VanHoesenG., et al. Diencephalic
amnesia.
Brain
1990; 113: 1-25.
15. Bogousslavsky J., Regli F., Delaloye B., et al. Loss of psychic self-
activation with bithalamic infarction.
Acta Neurol Scand
1991; 83:
309-316.
16. LeighR.J., Zee D.S. The neurology of eye movements.
FA Davis
,
Philadelphia 1983.
282
Neurrollogiia ii Neurrocchiirrurrgiia Pollsska 2012; 46, 3
Bilateral paramedian thalamic infarction with hypothalamic dysfunction
17. Bell D.A., Davis W.L., Osborn A.G., et al. Bithalamic hyper -
intensity on T2-weighted MR: vascular causes and evaluation
with MRI angiography.
AJNR
1994; 15: 893-899.
18. Jabaudon D., Sztajzel J., Sievert K., et al. Usefulness of ambula -
tory 7-day ECG monitoring for the detection of atrial fibrillation
and flutter after acute stroke and transient ischemic attack.
Stroke
2004; 35: 1647-1651.
283
Neurrollogiia ii Neurrocchiirrurrgiia Pollsska 2012; 46, 3
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