Neuro-radiology

Neuroradiology(1993) 35:92-96

9 Springer-Verlag1993

Infantile panthalamic infarct with a striking sonographic finding:
the "bright thalamus"
H. S. Wang 1 and S. C. Huang 2
Departments of Paediatrics, 1ChangGung MemorialHospital at Taipei, and Chang GungMedicalCollege,Taiwan,
2Chang GungMemorialHospitalat Kaohsiung,Republic of China
Received: 12 February1991

Summary. A "bright thalamus" is not uncommonly observed in cranial sonograms of asphyxiated neonates,
but not those of older infants. Three infants, aged
9-14 months, developed acute onset of seizures and disturbance of consciousness after a minor prodromal illness.
Bilateral thalamic infarcts were demonstrated by ultrasonography and CT. One patient expired from causes not directly related to the infarcts; the other two survived with
severe neurological sequelae.
Key words: Bright thalamus - Thalamic infarct - Infantile
panthalamic infarct - Ultrasonography - Computed tomography - Paediatric neuroradiology

Involvement of the thalamus in asphyxiated term or preterm neonates is not uncommon [1-9], and is manifest on
sonograms as a "bright thalamus" due to markedly increased echogenicity [10-14]. The pathological changes
include infarction, haemorrhage, calcification and status
marmoratus [15]. However, in older infants, thalamic infarcts severe enough to be seen sonographically as a symmetrical, diffusely "bright thalamus" are rarely reported
in the English literature, to the best of our knowledge.
Three previously normal infants presenting with acute
encephalopathy due to infarction of the whole thalamus
are described.

Case reports
Case 1

A 9-month-old girl was well until 4 days prior to admission
when she developed a cough, vomiting, and irritability.
Two days later, she had sudden, repeated generalized
seizures, and soon became stuporous. Examination 2 days
later showed a rectal temperature of 38.1~ pulse rate
144/min, respiratory rate 58/min, blood pressure
107/68 mmHg, and body weight 7.8 kg. The anterior fontanelle was tense and bulging. The mucosae were mildly

dry, but the skin did not appear dehyrated. Heart sounds
were regular without murmur. She was semicomatose.
Deep tendeon reflexes were diffusely increased. No focal
weakness could be found. The blood pressure was normal
throughout admission. Blood analysis, including gases,
was normal, as was the cerebrospinal fluid. Ultrasonography showed mild dilatation of both lateral ventricles
and markedly increased echogenicity of the thalamus bilaterally, which appeared conjoined into one mass obliterating the third ventricle (Fig. i a). CT showed hypodensity of both thalami with no abnormal contrast
enhancement. The patient could reach for objects and had
a social smile i week after admission. Repeat sonography
and CT showed almost no change, except for mild enlargement of the lateral ventricles (Fig. lb, c). Initially
discharged without antiepileptic drugs, the patient was
readmitted 2 months later for recurrent seizures and
placed on phenobarbitone 30 mg/day. Developmental retardation was noted. Subsequently, she had two episodes
of clustered attacks in spite of good compliance with the
phenobarbitone. The final attack resulted in her death
8 months after the onset of her illness. Pathological examination of the brain showed mature thalamic infarcts.

Case 2

A previously healthy 10-month-old girl developed mild
fever and a runny nose 2 days before admission. On the
day of admission, she had several episodes of vomiting
and diarrhoea; urine volume fell. Repetitive generalized
convulsions occurred several hours later. Examination
showed a rectal temperature of 37.8~
pulse rate
164/rain, respiratory rate 43/min and blood pressure
92/65 mmHg. The anterior fontanelle was flat. The mucosae were mildly dry, but the skin was not dehyrated; heart
sounds were normal. She was semicomatose and responded to deep pain only. No sign of increased intracranial pressure, meningitis nor any focal neurological deficit
was found. Her blood pressure remained normal
throughout the admission. Laboratory tests of blood and

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Fig.la--e. Case 1. a Initial sonogram showingmarkedlyincreased echogenicityof both thalami which appear as a single mass. b A study
6 dayslater was almostthe same exceptfor enlargementof the lateral ventricles, c Follow-up13 dayslater

cerebrospinal fluid showed no significant abnormality.
The EEG revealed diffuse low voltage delta waves. Cranial sonography showed markedly increased echogenicity
in both thalami (Fig. 2 a), and CT revealed low density in
the thalamus and periventricular areas bilaterally
(Fig.2b). Carotid and vertebral angiography performed
2 days later showed no vascular occlusion. She remained
severely handicapped 16 months after the onset of her illness. Follow-up sonography showed less hyperechogenicity in the thalamic region and mild dilatation of the lateral ventricles (Fig.2c). Decreased size of the thalamic
and periventricular infarcts was demonstrated on CT
10 days after the onset (Fig. 2 d).

Case 3

A previously normal 14-month-old girl developed mild
fever 3 days and vomiting 1 day prior to admission. Her
fluid intake and urinary output decreased. On the day of
admission, she had diarrhoea followed by a generalized
seizure. Physical examination showed that she was afebrile with pulse rate 128/min, respiratory rate 44/rain and
blood pressure 98/64 mm Hg. The anterior fontanelle was
flat, the mucosae were dry and the skin appeared dehydrated. The heart sounds were normal. She was semicomatose, but no sign of increased intracranial pressure,
meningitis, or focal neurological deficit could be found.
Investigations were normal, apart from serum AST:
164 units/l; BUN: 31 mg%; PT and PTT: 17 s (control
12.7) and > 100 s (control 31.8) respectively and blood
ammonia: 292 gg % (normal 40-110 gg %); 2 days after
admission these values all returned to normal apart from
the AST, which dropped to 60 units/1 5 days after admission. Sonography showed marked hyperechogenicity
of both thalami (Fig. 3 a). CT showed hypodensity of both
thalami and mild dilatation of the lateral ventricles
(Fig.3b). Blood pressure was normal throughout the
course. Her consciousness did not improve much. Ten
months after onset, she had spontaneous eye opening but
no visual following. She moved limbs aimlessly and did

not respond socially. Follow-up sonography showed less
hyperechogenicity of the thalami and the appearance of
brain atrophy (Fig. 3 c). Gradually decrease in size of the
thalamic infarcts was demonstrated on CT scan 1 and
1.5 years after the onset of the illness (Fig. 3 d).

Discussion
In adults, thalamic infarction is usually unilateral and lacunar [16]. Some cases of bilateral paramedian thalamic
infarction may result from occlusion of a thalamosubthalamic perforating artery which supplies the medial thalamus on both sides, as reported in adults with underlying
risk factors of hypertension or atherosclerosis [17-21].
Deep cerebral venous thrombosis causing symmetrical,
diffuse thalamic infarcts has been demonstrated by CT
and/or MRI in a few cases [22-24], but the margins of thalamic infarcts seen on CT were not as sharp and clear-cut
as in our cases.
The three patients reported here had acute onset of
seizures and disturbed consciousness beginning after a
few days of non-specific minor illness. Their ages at the
onset of disease were 9, 10 and 14 months. Central nervous system infection, intoxication, Reye's syndrome, and
haemorrhagic shock syndrome were all excluded by the
clinical course and laboratory findings. No risk factor for
thromboembolism existed, except minimal fluid depletion [25]. CT showed no direct signs of deep cerebral venous thrombosis [24]. A normal anion gap excluded the
possibility of organic acidaemia. Since the clinical course
in the two survivors showed neither deterioration nor recurrence, the possibility of an inborn error of metabolism
was considered remote.
The clinical course of the three patients was quite
similar; all had minor prodromal disease causing poor
oral intake and increased G1 loss. A component of dehydration is possible as two patients had diminished urine
output, and one had transiently marked elevation of
AST, PT, PTT, ammonia and BUN which was considered
as evidence of the ischaemic insult being caused by circu-

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Fig.3a-d. Case 3. a Sonogram at
onset showed markedly increased
echogenicity of both thalami.
b Initial CT showed hypodensity
of both thalami and periventricular areas.
c Sonogram 6 days later showed
fading of the bright thalamus.
d CT 6 months later showed the infarct to have decreased in area

latory insufficiency. These patients had no evidence of
low blood pressure before or after their change of consciousness. Nevertheless, a relative circulatory insufficiency or impending shock may have existed. The patients' condition was not considered severe until the
onset of seizures. Their circulatory status could have
been further compromised with the occurrence of
seizures.
Possible causative factors may have been excessive metabolic requirements and relative vascular insufficiency of
those thalamic areas which were infarcted. Symmetrical,
diffuse thalamic infarction, so-called status marmoratus,
is not u n c o m m o n in survivors of neonatal asphyxia [9]. In
the newborn period, the thalamus is particularly vulnerable to hypoxaemia and/or ischaemia because of its high
metablic requirement [26]. Rorke [27] suggested that selective damage to the thalamus or deep grey nuclei might
be the result of diminution of blood flow in branches of
basal penetrating vessels or of selective neuronal vulnerability. Our patients could have sustained episodes of partial and total asphyxia which injured the thalamus in particular as Myers suggested [28].

4
Fig.2a-d. Case2. a Sonogram at onsetshowed markedlyincreased
echogenicity of both thalami, b Initial CT showed low density within both thalami and the periventricular areas, c Sonogram 2 weeks
later showed fading of the bright thalamus, d Decrease in the area
of the thalamic low density was shown on CT 10 days after the onset

The outstanding appearance of a "bright thalamus" on
sonography may serve as a landmark of profound asphyxial damage [10-14], not onyl in postasphyxial neonates but
also in infants with acute encephalopathy, as in our patients. Their prognoses were grave. Early, adequate hydration of infants with poor intake and increased gastrointestinal loss may help to avoid this tragedy.

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Dr. H.-S. Wang
Department of Pediatrics
Chang Gung Memorial Hospital
199, Tung-Hua North Road
Taip ei, Taiwan 10 591
Republic of China