Case Study: A 41 year-old male with no previous medical problems presented with two short episodes of unconsciousness and transient ptosis. The patient returned to normal within several hours of presentation. The patient had no mood or personality changes after the event and bedside testing showed no evidence of cognitive changes or memory difficulties. A MRI scan of his brain showed an acute bilateral thalamic infarct.

Conclusions: This is only the second known described case with complete resolution of symptoms following bilateral paramedian thalamic infarction. This case also demonstrates that physicians should consider a bilateral thalamic infarct in the differential diagnosis when a patient presents with only transient unconsciousness and transient third nerve dysfunction.

Bilateral thalamic infarction most commonly occurs in patients who have an anomalous perfusion to the thalamus. The four arteries that supply blood to each thalamus are the paramedian, inferolateral, tuberothalamic, and posterior choroidal arteries. An anomalous paramedian artery is most commonly identified in people who suffer from a bilateral thalamic infarction. The paramedian artery arises from the P1 segment of the posterior cerebral artery.⁽⁸⁾ While each paramedian artery normally arises from each P1 segment, some people have both paramedian arteries anomalously arise from one common P1 trunk. This anatomic variant is known as the artery of Percheron.⁽⁸⁾ Bilateral paramedian thalamic infarction is due to this rare anatomical variant in which a single lesion may affect both thalami. The lesion may be atherothrombotic or embolic in nature. The following case demonstrates a clinical variation of the usually described features and outcome of a bilateral paramedian thalamic infarct.

The patient was admitted to the intensive care unit (ICU) for monitoring. By the time he arrived in the ICU (3 hours from presentation), he was fully communicating and his neurologic exam was normal except his lower extremity reflexes remained brisk bilaterally and he continued to have bilateral Babinski signs. The following day, he was extubated without difficulty. He subsequently underwent an electroencephalogram (EEG) which was also normal. The patient continued to do extremely well while in the hospital without any episodes of alteration in consciousness. An MRI with diffusion weighted images was performed three days after the event. It showed a discrete increase in signal in the thalami bilaterally on both diffusion weighted images and fluid-attenuated inversion recovery (FLAIR) sequences. Also, a corresponding dark area on the apparent diffusion coefficient (ADC) map was present. These imaging findings were consistent with an acute bilateral ischemic infarct of the thalamus (Figure 1). The patient subsequently had an extensive evaluation which showed a normal sedimentation rate, thiamine level, cholesterol level, thyroid function, antinuclear antibody level, and syphilis studies. An echocardiogram was also performed which showed no abnormalities.

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Figure 1: A) Diffusion weighted image showing restricted diffusion in both thalami B) ADC map showing corresponding dark areas in both thalami C) FLAIR image showing increased signal in both thalami

The patient continued to do well throughout his hospital course with a normal exam except for bilaterally brisk lower extremity deep tendon reflexes. During the hospitalization, the patient’s mood was pleasant and appropriate toward the staff as well as his family. Bedside cognitive testing revealed the patient had fluent speech and was able to follow all commands. His cognition appeared intact with a mini-mental status of 30/30. The patient had no difficulty in naming common and uncommon objects. Remote memory was tested and found to be intact (with assistance from his wife for verification). Furthermore, the patient’s fund of knowledge appeared normal after questioning him on current and past major political figures. He also successfully interpreted several proverbs. Lastly, his visual-spatial-constructional ability was determined to be normal after correctly drawing a clock figure.

The patient’s family felt there was no change in his personality or memory after the stroke. The patient was discharged home on aspirin therapy one week after his bilateral paramedian thalamic infarct in good condition. The patient was contacted six months after his hospital admission. The patient had no complaints and was working. The patient’s family reported no personality changes and no noticeable memory difficulties. Due to the fact that the patient was a member of a health maintenance (HMO) insurance plan, he was not able to be followed-up at our center for formal neuropsychological testing.

Our case presents several important clinical feature variations which differ from previously reported cases of bithalamic infarction. First, our patient did not have the vertical gaze paresis. Vertical gaze paresis has been noted in many prior case reports as being associated with the decreased level of consciousness in bilateral paramedian thalamic infarction. Instead, our case had a transient partial third nerve dysfunction in which there was a dilated pupil only. Second, our patient demonstrates that a bilateral paramedian infarct may present with loss of consciousness for a very limited time (minutes to few hours). This is much different than what previous case reports in the literature had reported.^(2,9) In fact, there have been many case reports citing that patients had difficulty in maintaining a normal conscious state for at least several days. The purported mechanism for the decreased level of consciousness is due to affected midline thalamic nuclei. These nuclei are a rostral extension of the reticular activating system.⁽²⁾ Third, our patient also demonstrates that a person with bilateral paramedian thalamic infarct may have a lack of pervasive retrograde or anterograde amnesia after the event and no subsequent behavior or personality changes. This differs from most prior case reports, such as the report by Winocur et al, who described anterograde amnesia with the syndrome of bilateral paramedian infarction.⁽¹⁰⁾ Finally, in contrast to the Kumral et al. case series in which 7 of the 8 cases with bilateral paramedian infarction had known causes (5 patients had longstanding diabetes or hypertension with presumed small artery disease while 2 patients had a potential cardiac source of embolism)⁽⁵⁾, our patient was relatively young, had no known risk factors, and had a negative workup. Furthermore, our patient did not have any less common conditions such as lupus, syphilis, cysticercosis, fungal infection, or thiamine deficiency. This is in contrast to the association made by Roitberg et al. who reported these less common disorders may be an underlying cause of a bithalamic infarct.⁽⁷⁾

This case demonstrates a departure from many prior case reports with regard to the clinical manifestations of a bilateral thalamic paramedian infarct. As this entity can easily be missed by CT scan in the acute phase, it is important to consider this type of infarct in the differential diagnosis of patients with otherwise unexplained transient impairment of consciousness (even without the classical vertical gaze paresis). Physicians should be alert to the possibility that transient loss of consciousness coupled with a transient third nerve palsy may be a presentation of bilateral thalamic infarction.

Recived by: Nov.21.2005
Revised by: Jun.21.2005
Accepted :  Dec.12.2005

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