Thalamic Syndrome and Cortical Hypoperfusion on Technetium-99m HM-PAO Brain SPECT

Sep 15, 2026

Six patients with thalamic pain and dysesthesia due to vascular lesions in or near the thalamus were studied using HM-PAO brain SPECT. Lesion localization by brain CT was categorized into anterior medial and posterior lateral thalamic regions. Three patients with near-thalamic lesions showed decreased regional cerebral perfusion (rCP) in the ipsilateral cortex, whereas three with thalamic lesions demonstrated symmetrical cortical radioactivity. Findings were interpreted as loss of thalamic afferent activating stimuli leading to reduced cortical neuronal activity and consequent hypoperfusion, with remote thalamic damage and cortical deregulation not excluded.

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Thalamic Syndrome and Cortical Hypoperfusion on Technetium-99m HM-PAO Brain SPECT

Patients and Methods

Results

# Thalamic Syndrome and Cortical Hypoperfusionon Technetium-99m HM-PAO Brain SPECT Myung Sik Lee,Il Saing Choi and Tae Sub Chung¹ The six patients included in this study had painful dysesthesia,resulting from vascular lesions in or nearthe thalamus,confirmed by computerized tomography(CT)brain scan.Using hexamethyl propyleneamine ox-ime(HM-PAO)single photon emission computed tomographiy(SPECT)brain scanning,regional cerebral perfu-sion(rCP)was demonstrated.In contrast to three patients with lesions near the thalamus who showed symmetricalcortical radioactivity,the other three patients with thalamic lesions revealed decreased rCP in the ipsilateralcerebral cortex on HMPAO brain SPECT.We thought that the loss ofafferent activating stimuli from the thalamusled to decreased cortical neuronal activity and the following hypoperfusion.In patients with thalamic syndromeresulting from thalamic lesions,the role of the remote effect of the thalamic damage and consequent corticalderegulation in the development of thalamic pain and/or neuropsychological symptoms cannot be excludedcompletely. Key Words:Thalamic syndrome,HM-PAO brain SPECT,cortical hypoperfusion. Spontaneous pain and painful overreaction to ex-ternal stimuli resulting from lesion confined to the cen-tral nervous system(CNS)was named as“centralpain(CPY”(Riddoch 1938). Although stroke involving ventral posterolateralthalamus is the leading cause of CP(Martin 1969),other lesions,regardless of the level,ocated in or verynear the pain transmitting pathway could lead to CP(Riddoch 1938;Fields and Adams 1974).Since Dejerneand Roussy provided formal accounts of“Le syndromethalamique”in 1906,many possible pathogeneseshave been proposed (Fields 1987),but no one couldexplain all the features of the CP. Although positron emission tomography(PET)demonstrated cortical hypometabolism and itstopographical correlations in patients with thalamicinfarction(Baron et al.1986),the absence of corticalderegulation in a case of thalamic syndrome wasreported.They concluded that deregulation of thethalamus itself,not the corticothalamic or thalamocor-tical loop,leads to thalamic syndrome (Laterre et al. Received January 9,1989Accepted March 2,1989 Department of Neurology,Yongdong Severance Hospital,YonseiUniversity College of Medicine. Department of Radiology',Yonse University Colege ofMedicine. Address reprint equests to Dr.M S Lee,Department of Neuro-logy,Yongdong Severance Hospital,Yonsei University College ofMedicine,Seoul,Korea,137-270 1988). And so,we evaluated cortical perfusion with HM-PAO brain SPECT in six patients with thalamicsyndrome. ## PATIENTS AND METHODS The mean age of the two men and four womenincluded in this study was 54.5 years (range 47-64).All had spontaneous pain and painful dysesthesia op-posite to the lesion side on brain CT scan,which oc-curred one to ten months after a stroke.At the timeof the occurence of painful dysesthesia,chest x-ray,blood cell count,routine blood study,and electrocar-diography showed no abnormalities. The patients were evaluated by two neurologistsand the results were summarized in Table 1.Therewas no evidence of peripheral neuropathy on physicaland laboratory examination. We evaluated brain CT scans,which were doneat the time of the cerebrovascular accidents(CVA)and/or a few days before performing HM-PAO brainSPECT,to localize the lesion.The thalamic lesion wasdivided into the anterior medial part,which projectsto the frontoparietal lobe,and the posterior lateralpart,wich projects to the temporoparietal lobe(Fields1987). We performed SPECT by the following method.Eluting with 0.5 ml normal saline,(Eluent for du Pont | Patient | Sex/Age,yr | Character &location
of the lesion | | Latent period
after stroke | Cutaneous
hyperesthesia | Spontaneous
pain | Deep sense
impairment | Chorea | Dysarthria | Motor
deficit | Babinski
sign | | --- | --- | --- | --- |

FAQs

How were thalamic lesions and symptom timing characterized before imaging?

Brain CT scans were reviewed to localize lesions, and the painful dysesthesia occurred one to ten months after stroke. Chest X-ray, blood cell counts, routine blood studies, and electrocardiography showed no abnormalities at symptom onset.

What imaging approach was used to assess cortical perfusion?

Cortical perfusion was evaluated with Technetium-99m HM-PAO brain SPECT. After intravenous injection, axial and coronal reconstructions were produced for regional cerebral perfusion assessment.

What perfusion differences were observed between groups based on lesion location?

Patients with lesions near the thalamus showed decreased rCP in the ipsilateral cerebral cortex. In contrast, patients with lesions in the thalamus demonstrated symmetrical cortical radioactivity.

Sep 15, 2026

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