Joint Program in Nuclear Medicine

Crossed Cerebellar Diaschisis

David A. Bader, MD
J. Stevan Nagel, MD

March, 14, 1995

Presentation

A 63 year old female had a left temporal glioblastoma diagnosed 15 months prior to the current admission. She underwent resection followed by chemotherapy and radiation therapy. A small recurrence, diagnosed by MRI, was treated with additional radiation therapy one year prior to the current presentation. Three months prior to the current presentation, she was admitted for a left frontoparietal craniotomy with subsequent right facial seizures, right hemiparesis, and dysarthria. A CT scan showed a ring enhancing mass in the posterior left frontal lobe, it was not possible to differentiate radiation necrosis from residual or recurrent tumor. MRI demonstrated enhancement characteristics of the frontal mass "suggestive" of infiltrating tumor. Thallium and HMPAO brain imaging was performed for further evaluation.

Imaging Technique

Studies were performed on a dedicated brain camera (ASPECT). Imaging with 3.0 mCi (111 MBq) Thallium-201 was performed first, followed by a perfusion study with 20.0 mCi (740 MBq) Tc-99m HMPAO without change in patient position. Technical parameters for the two studies were identical (except for the photopeaks) and included patient in supine position in dimly lit room, 10 minute delay to imaging following injection, 120 projections at 15 seconds per projection, 2D Butterworth filter with a cutoff of 0.95 cm and an order of 10, attenuation corrected (Chang method) reconstructed slices displayed on a 128x128 matrix as axial slices summed to 8.3 mm thickness. Coronal reconstructions were utilized as needed during image interpretation.

Imaging Findings

On the CT and Thallium brain images (27k bytes), the most cranial aspect of the ring enhancement (27k bytes, arrow) was thicker and showed increased Thallium activity (thin arrow) correlating with tumor recurrence. In addition, there was associated increased perfusion about the margins of the surgical site with a large central region of hypoperfusion corresponding to the known post-operative fluid collection.

Thallium and HMPAO perfusion brain scans (95k bytes) are shown together. The site of tumor recurrence (95k bytes, thin arrow) is again seen. There is a large area of decreased perfusion in the left supratentorial surgical bed (arrow heads). There was decreased perfusion to the contralateral (right) cerebellum (arrow). The cerebellum showed no abnormalities on the previous CT and MRI examinations.
(Brain scintigraphy courtesy of B. Garada)

Diagnosis

Recurrent glioblastoma

Discussion

The term "diaschisis" comes from the Greek meaning "shocked throughout". The term was introduced by von Monakow in 1914 and initially included 4 important aspects:
  1. remote functional changes,
  2. clinical diagnosis,
  3. gradual regression, and
  4. a "wave of diaschisis" following neuroanatomical pathways (Feeney).
The modern usage of the term includes depression of regional neuronal metabolism and cerebral blood flow caused by dysfunction in an anatomically separate but functionally related neuronal region (Brunberg). Many functional pathways have been investigated, and cortico-cerebellar is one specific type. It was first described by Baron in 1980 using PET imaging to demonstrate matched reduction in cerebral blood flow and oxygen extraction fraction in the contralateral cerebellum in patients with supratentorial ischemic stroke (Baron). The finding has been subsequently seen with SPECT perfusion imaging in many settings including: infarction, ischemia, tumor, hemorrhage and ateriovenous malformations. It is of particular interest to nuclear medicine physicians who perform brain imaging because it is seen in greater than 50%% of patients with well-defined hemispheric lesions and is usually otherwise anatomically and clinically occult (Brunberg).

The mechanism of the phenomenon is diminished excitatory trans-synaptic neuronal input into otherwise normal neurologic tissue with subsequent decrease in metabolic rate and alterations in blood flow (Reivich, Eckard, Brunberg). Many connections between the cerebral hemispheres and the cerebellum exist with the corticopontocerebellar being the most numerous and accounting for 40 times all other afferent sources combined (Eckard). Essentially instantaneous appearance of crossed cerebellar hypometabolism has been demonstrated with carotid temporary balloon occlusion (Brunberg, Eckard). Correlation with MRI by Tien has shown that crossed cerebellar atrophy can be seen after many years of symptoms, but no MRI abnormalities were seen with events less than several years in duration and all cases of cerebellar atrophy had associated supratentorial atrophy (Tien). The mechanism has been hypothesized to be due to transneuronal degeneration.

Clinical findings correlate poorly with cerebellar hypometabolism and seem related to the supratentorial disease (Tien). Additional evidence exists for functional cortico-cerebellar connections such as reversed crossed cerebellar diaschisis as well as crossed hemispheric diaschisis seen with cerebellar hemorrhage (Katsuragi, Park, Rousseaux).

Conclusions

Crossed cerebellar diaschisis represents the most consistent evidence of transneuronal depression in humans yet remains poorly understood in terms of pathophysiology, clinical correlations, and therapeutic implications (Feeney). It is of particular significance to the nuclear medicine physician as it is most often clinically and anatomically occult yet may frequently seen with SPECT cerebral perfusion studies.

References

  1. Baron JC, Bousser MG, Comar D, Castaigne. "Crossed cerebellar diaschisis" in human supratentorial infarction (abstract). Ann Neurol 1980; 8:128.
  2. Brunberg J, Frey K, Horton J, Kuhl. Crossed cerebellar diaschisis: occurrence and resolution demonstrated with PET during carotid temporary balloon occlusion. AJNR 1992;13:58-61
  3. Di piero V, Chollet F, Dolan RJ, Thomas DJ, Frackowiak R. The functional nature of cerebellar diaschisis. Stroke 1990; 21:1365-1369.
  4. Eckard DA, Purdy PD, Bonte F. Crossed cerebellar diaschisis and loss of conciousness during temporary balloon occlusion of the internal carotid artery. AJNR 1992; 13:55-57.
  5. Feeney D, Baron JC. Diaschisis. Stroke 1986; 17:817-830.
  6. Katsuragi M, Torigoe R, Nishihara H. Disappearance of crossed cerebellar diaschisis after convulsion in a patient with a putaminal hemorrhage. Clinical Nuclear Medicine 1994; 19:651-2.
  7. Park CH, Kim SM, Streletz LJ, Zhang J, Intenzo C. Reverse crossed cerebellar diaschisis in partial complex seizures related to herpes simplex encephalitis. Clinical Nuclear Medicine 1992; 17:732-735.
  8. Reivich M. Crossed cerebellar diaschisis (commentary). AJNR 1992; 13:62-64.
  9. Rousseaux M, Steinling M. Crossed cerebellar diaschisis in unilateral cerebellar lesions. Stroke 1992; 23:511-514.
  10. Tien RD, Boyd CA, Crossed cerebellar diaschisis and crossed cerebellar atrophy: correlation of MR findings, clinical symptoms, and supratentorial diseases in 26 patients. AJR 1992; 158:1155-1159.

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J. Anthony Parker, MD PhD, Tony_Parker@bidmc.harvard.edu