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Acute Bithalamic Infarct Manifesting as
Sleep-Like Coma: A Diagnostic Challenge
ASNR 2015
Abstract No: 1839
Ruth Eliahou1, Eitan Auriel2, Tamir Ben Hur3, J Moshe Gomori1, Asaf Honig3
Departments of 1Radiology and 3Neurology,
Hadassah-Hebrew University Medical Center, Jerusalem, Israel
2Department of Neurology, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel
Disclosure Statement
• The authors report no conflicts of interest
Background
• Acute bilateral thalamic infarction (BTI) may present without
localizing signs, as sleep-like coma (SLC)
• SLC is defined as a hypersomnolence state, ranging from easily
arousable with stimulation to nonarousable with deep sleep
• SLC may lead to delayed diagnosis & treatment
– Late ER arrival, since the patient may appear to be sleeping
– A challenging diagnosis, since the differential includes toxic/
metabolic/ infectious causes as well as brain hemorrhage, tumor
• Delayed treatment of BTI may result in sequelae such as severe
“thalamic dementia” with behavioral and cognitive manifestations;
ataxia, tremor, dysphasia
Background
• The thalamus contains gray matter nuclei that serve as a relay
between the cerebral hemispheres and the brainstem
• Neuronal circuits of the reticular activating system (RAS), which has
a major role in consciousness and regulation of sleep and
wakefulness, also relay signals via the paramedian thalamus
• Given the strategic role and location of the thalamus, even small
thalamic strokes can mimic cortical strokes and result in significant
cortical deficits
• Paramedian insults may hamper connectivity to the RAS, and may
manifest as a decreased level of consciousness and SLC
Thalamic Blood Supply
• Dual blood supply
• Anterior circulation
– Polar artery, arising from the Pcom, ICA
• Posterior circulation (predominant)
– Medial: paramedian arteries, arising
from P1
– Ventrolateral: thalamogeniculate
arteries, arising from P2
– Posterior: posterior choroidal artery,
arising from P2
Renard et al, Behavioral Neurol
2014; article ID 154631
Thalamic Blood Supply Paramedian Arteries
(~78%)
(~22%)
http://radiopaedia.org/images/604
• The Percheron artery is a normal variant of the thalamic paramedian penetrating
arteries
• It has a solitary arterial trunk, arising from the P1 segment of one of the PCAs
• It supplies the paramedian thalami and the rostral midbrain bilaterally
• Its occlusion results in bilateral paramedian thalamic infarctions with/without
midbrain infarction
Percheron G, Z Neurol 1973;205:1–13
Purpose
• To review cases of BTI manifesting as SLC,
with different mechanisms
• To emphasize the critical role of timely
imaging, diagnosis, and management,
“time is brain”
• To illustrate other clinical entities with
bithalamic involvement that may mimic BTI
Methods
• We retrospectively reviewed files of 8 patients
admitted to the ER between 2006–2014 with a
clinical presentation of SLC and a diagnosis of BTI
• The Institutional Review Board approved this study
and waived the requirement for informed consent
Diagnostic Algorithm
Diagnostic protocol to SLC
1. Blood tests : Na ++ levels to r/o hyponatremia and extrapontine
myelinolysis; CRP to r/o encephalitis
2. Full toxic screen
3. Give thiamine in case of Wernicke Korsakoff syndrome
4. Emergent CT
– Hi resolution noncontrast
TIME IS
– CTA
BRAIN !
– CTV
however CT, CTA, CTV are frequently normal
in cases of BTI
5. Emergent diffusion-weighted MRI
Results
• 8 patients
– Sudden onset SLC, minimal response to painful stimuli
– Other localizing findings suggestive of acute stroke were scarce
• Differential diagnosis: systemic toxicity, ischemic injury, intracranial
hemorrhage, neoplastic disease, infectious process, hyponatremia,
Wernicke-Korsakoff syndrome
• Emergent head CT showed normal brain tissue in 6
– CTA: normal in 4, PCA cutoff in 2
– DWI-MRI: symmetric bilateral thalamic DWI hyperintense lesions with
variable degrees of brainstem involvement
• Emergent CT showed previous contralateral thalamic infarct in 1
– CTA: normal
– DWI-MRI: new ipsilateral infarct
• CT revealed bithalamic edema and expansion in 1
– CTV: thrombosis of the straight sinus
– DWI-MRI: negative
– FLAIR: marked bithalamic edema
Patients
Age /
Sex
Risk factors
Imaging findings
Treatment
Time:
symptom
onset
ER arrival
Time:
ER
admission
treatment
Late
outcome
Mechanism
68 / F
Diabetes
CT, CTA, CTV: normal
DWI-MRI: BTI
Conservative+
ventilation
>3h
1.5h
Severe
thalamic
dementia,
ataxia, tremor
Small vessel
disease
55 / M
Diabetes
HTN
CT, CTA, CTV: normal
DWI-MRI: BTI
Conservative
1.5h
1h
Marked
improvement,
short-term
memory
deficit
Small vessel
disease
88 / F
Atrial
fibrillation
CT, CTA, CTV: normal
DWI-MRI: BTI
Iv- tPa
0.5h
1.2h
Full recovery
Embolic
77 / M
Atrial
fibrillation
CT, CTA, CTV: normal
DWI-MRI: BTI
Conservative
>3h
Delayed dx in
ER
Severe
thalamic
dementia,
ataxia
Embolic
Patients
Age
/
Sex
Risk
factors
Imaging findings
Treatment
Time:
symptom
onset
ER arrival
Time:
ER
admission
treatment
Late
outcome
Mechanism
74 /
M
None
CT, CTV: normal
CTA: PCA-P2 occlusion, VA
atherosclerotic changes
DWI-MRI: BTI + post
circulation shower of emboli
Conservative
>3h
1h
Severe
thalamic
dementia,
ataxia
Embolic –
artery to
artery
60 /
M
Cardiac
mural
thrombus
CT, CTV: normal
CTA: PCA-P1 occlusion
DWI-MRI: BTI
Conservative
INR=2.2 C/I for IVtPa
1.5h
1h
Ataxia,
motor
sensory
dysphasia
Embolic
60 /
M
DM
HTN
s/p left
thalamic
infarct (4
mo)
CT: Old left thalamic infarct
CTA, CTV: normal
DWI-MRI: acute right
thalamic infarct
Conservative
2h
Delayed dx in
ER >3h
Severe
memory
impairment,
impaired
visualspatial skills
Sequential
58 /
F
None
CT: bithalamic hypodensity ,
expansion
CTA: normal
CTV: straight sinus
thrombosis
DWI-MRI: normal
appearance
FLAIR: bithalamic edema
Neuro-endovascular:
DAVF repair
1h
1h
Full
recovery
Deep sinus
vein
thrombosis
due to DAVF
Case 1
88-year-old woman. ER arrival within 1 hr of sudden onset.
Underlying atrial fibrillation, severe generalized flaccid paralysis,
bilateral Babinsky, skew deviation
Rx:CTV:
IV-tPA initiated 1 hr after ER arrival
CT, CTA,
DWI-MRI:
unremarkable
BTI
extending to
midbrain
Outcome: Full recovery of symptoms
Case 2
68-year-old woman. Sudden onset of severe generalized flaccid paralysis.
Arrival to ER >3h after symptom onset, delayed due to snow
BTI
CT, CTA:DWI-MRI:
unremarkable
Rx: Conservative
+ ventilation
Outcome: Severe thalamic dementia, ataxia,
rubral tremor
Case 3
60-year-old male with acute SCL. Arrival at ER <3 hr from symptom onset. S/P left
thalamic stroke 16 weeks prior. Late referral to Neurology, delayed imaging,
delayed diagnosis.
CT: old left
thalamic
infarct;
normal
appearance
right
thalamus
Rx: Conservative
Outcome: Severe memory impairment
2 d later, CT
shows BTI
(different
ages)
DWI-MRI:
new right
thalamic
infarct
Case 4
74-year-old male, acute SCL. ER arrival 3.5 hr after onset, family
thought patient sleeping.
CT:
unremarkable
CTA: Right P2
occlusion, VA
atherosclerosis
DWI-MRI: Right
PCA territory
infarct, bilateral
cerebellar infarcts
Rx: Conservative
suggesting shower
of emboli
Outcome: Severe thalamic dementia, ataxia
Case 5
60-year-old man with acute ataxia and dysarthria proceeding to SLC. S/P cardiac
catheterization (1 week). Known cardiac apex thrombus, under anticoagulation, INR
2.2. Arrival at ER within 1 hr, diagnosis within 1 hr.
CT: normal
DWI-MRI:
BTI
extending caudally
to the left medial
temporal lobe
CTA: left P1 cut
off
Rx: Conservative. IV tPa contraindicated
due to INR=2.2 and recent mural MI
Outcome: ataxia, motor & sensory dysphasia
Case 6
58-year-old woman, SLC. ER arrival within 1 hr. DAVF repair within 4 hr.
CT: bithalamic
hypodensity &
expansion
CTV: straight
sinus thrombusis
Rx: IV Heparin and prompt DAVP
endovascular repair Conservative
Late
DSA: DAVF of the
internal maxillary
outcome:
Full recovery artery and vein of
DWI-MRI: normal
FLAIR: bithalamic
Galen (arrowhead)
edema
with venous drainage
(arrow)
Results: Mechanisms of BTI
• Small vessel disease: 2
• Embolic: 4
– Cardioembolic 3
– Artery to artery 1
• Sequential thalamic stroke 1
• Deep sinus vein thrombosis 1
Treatment
• Conservative management in 6/8 patients
– IV fluids
– Oxygen
– Antiplatelet load anticoagulation (coumadin or
heparin) until echo confirmed no cardiac thrombus
– Continuous cardiac monitoring to r/o atrial
fibrillation
• IV tPa in 1/8
• Endovascular repair of DAVF in 1/8
Results: Late Outcome
Time from symptom onset
+ Time to diagnosis
≤ 3 hours
> 3 hrs
• Full recovery: 2 patients
• Marked improvement, short-term memory issues: 1
patient
• Mild ataxia, motor & sensory dysphasia: 1 patient
• Severe thalamic dementia: 3 patients
• Severe memory loss, severe impairment visual-spatial
skills: 1 patient
Time is brain
Conclusions
• Urgent diagnosis of stroke is essential to preserve
neurological function
• Diagnosis in a patient presenting with sleep-like coma is
challenging
• Diagnostic algorithm should include EMERGENT CT, CTA,
CTV, followed by EMERGENT DWI-MRI
• We cannot control time from symptom onset to ER arrival
• We must control time from ER arrival to diagnosis and
intervention!
Radiological Differential Diagnosis
for Bithalamic Pathology
Case illustrations:
Metabolic and toxic processes, infection, and
neoplasia with bithalamic involvement
Case 1: A 15 year old girl with a 3 week history of severe headache
and vomiting
Expansile FLAIR hyperintense nonenhancing infiltrative bithalamic mass with
secondary occlusion of the third ventricle and obstructive hydrocephalus
Dx: Bilateral thalamic glioma
Case 2: 62 year old man with mild cognitive impairment and
tremor
Calcium deposits in the basal ganglia and thalami. T1 hyperintensity on
precontrast T1, no enhancement in T1+ Gad
Dx: Fahr disease
Case 3: 34 year old man with progressive ataxia, dysmetria, dysarthria
Bithalamic T2/FLAIR hyperintensity
T2 shows Bilateral hypertrophic olivary
degeneration
Dx: Mitochondrial Disease:
POLG GENE MUTATION-RELATED
DISORDER
Case 4: 2.5 year old girl who had drowned, prolonged apnea, resuscitated
Non contrast CT showing bithalamic hypodensities
T2/FLAIR showing hyperintensity in the basal ganglia and thalami
Dx: Hypoxic ischemic injury
Case 5: 53 year old man, 2-week history of rapid cognitive decline,
walking difficulty, weakness, rt hemiparesis
Restricted diffusion
and FLAIR
hyperintensity in
the basal ganglia,
thalami, corpus
callosum
Ill-defined
enhancement of
the right caudate
head
Dx: Viral encephalitis
Case 6: 79 year old woman found unresponsive at home
Initial CT unremarkable.
Restricted diffusion consistent with
acute infarction of the superior
cerebellar and posterior cerebral artery
territories, including the brainstem and
median thalami.
MRA showed lack of flow-related
enhancement in the posterior
circulation
Dx: Top of the basilar syndrome
Case 7: 20 year old man with progressive tremor and ataxia
Kayser-Fleischer
ring on clinical
examination
T2/ FLAIR hyperintensity in the basal ganglia, lateral thalami
Dx: Wilson disease
Case 8: 52 year old woman, alcoholic, with ataxia, altered
consciousness, abnormal eye movements
Axial FLAIR: hyperintensity and restricted diffusion in both
thalami and to lesser degree in heads of both caudate nuclei
Dx: Wernicke encephalopathy
http://www.ajronline.org/doi/full/10.2214/AJR.08.1585
Case 9: 28 year old woman after rapid correction of hyponatremia
Axial FLAIR ; hyperintensity involving basal ganglia,
both thalami, pons
Dx: osmotic myelinolysis
http://www.ajronline.org/doi/full/10.2214/AJR.08.1585
Case 9: 70 year old man with cognitive deterioration
Axial DWI MRI: restricted diffusion in
caudate nuclei and thalami, prominent
cortical ribboning
Dx: Creutzfeldt-Jakob disease
http://www.ajronline.org/doi/full/10.2214/AJR.08.1585
Case 10: 32 year old man with hypertension, presented with
headache, seizures, and visual disturbance
Axial FLAIR: symmetric hyperintensity in
posterior white matter and both thalami
Dx: posterior reversible
encephalopathy syndrome (PRES)
http://www.ajronline.org/doi/full/10.2214/AJR.08.1585
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