Brain Neurorehabil.  2014 Sep;7(2):143-146. 10.12786/bn.2014.7.2.143.

Early Recurrent Right Basal Ganglia Infarction after Intravenous Thrombolysis for Left Basal Ganglia Infarction Management

• Ji HM
• Suh JH
• Won YH
• Yoon TS

• KMID: 1797649
• DOI: http://doi.org/10.12786/bn.2014.7.2.143

Abstract

A 43-year-old man with no notable medical history was admitted due to sudden onset dysarthria and right side weakness. The man was diagnosed with acute infarction of left basal ganglia (BG) and uncontrolled diabetes mellitus (DM). After 9 hours post the thrombolysis, mental change and left side weakness symptoms were newly observed, and the man was additionally diagnosed with acute infarction in right BG.The man showed symptoms of quadriplegia and was fed through nasogastric tube. He showed motor aphasia, and no signs of phonation, but showed some indications of intact cognition. After rehabilitation therapies, the man showed marginal improvement in motor function, but still lacked any meaningful changes functionally. This is the first case of symmetric bilateral BG infarction, which one-sided infarction additionally occurred within 24 hours post the treatment of contralateral infarction through thrombolysis. Also,the features observed were atypical while the patient has no previous external causes related with bilateral BG infarction.

Keyword

basal ganglia; recurrent stroke; thrombolytic therapy

MeSH Terms

Adult
Aphasia, Broca
Basal Ganglia*
Cognition
Diabetes Mellitus
Dysarthria
Humans
Infarction*
Phonation
Quadriplegia
Rehabilitation
Thrombolytic Therapy

Figure

• 

  Fig. 1 Brain MRI diffusion-weighted image revealed the acute cerebral infarction in left basal ganglia at theemergency room (A). After 9 hours from thrombolysis, right basal ganglia infarction is newly appeared (B).

Reference

1. Ko MH, Kim YH, Seo JH. Clinical and neuropsychological characteristics of patients with stroke of the basal ganglia. J Korean Acad Rehabil Med. 1997; 21:652–657.

2. Schwartz A, Hennerici M, Wegener OH. Delayed choreoathetosis following acute carbon monoxide poisoning. Neurology. 1985; 35:98–99.

3. Yu FC, Lin SH, Lin YF, Lu KC, Shyu WC, TsaoWL . Double gaps metabolic acidosis and bilateral basal ganglion lesions in methanol intoxication. Am J Emerg Med. 1995; 13:369–371.

4. Fukamachi A, Horikoshi T, Nagaseki Y, Sasaki H, Nukui H. Symmetrical bilateral low-density lesions in the areas of supply by heubner's arteries after aneurysm surgery. Acta Neurochir (Wien). 1987; 84:89–92.

5. Georgiadis D, et al. Early recurrent ischemic stroke in stroke patients undergoing intravenous thrombolysis. Circulation. 2006; 114(3):237–241.

6. Daras MD, Orrego JJ, Akfirat GL, Samkoff LM, Koppel BS. Bilateral symmetrical basal ganglia infarction after intravenous use of cocaine and heroin. Clin Imaging. 2001; 25:12–14.

7. den Heijer T, Ruitenberg A, Bakker J, Hertzberger L, Kerkhoff H. Bilateral caudate nucleus infarction associated with variant in circle of willis. BMJ Case Rep. 2009; 2009:bcr2006112656.

8. Comoglu S, Ozen B, Ozbakir S. Methanol intoxication with bilateral basal ganglia infarct. Australas Radiol. 2001; 45:357–358.

9. Lim JK, Yap KB. Bilateral caudate infarct--a case report. Ann Acad Med Singapore. 1999; 28:569–571.

10. Devere TR, Lee AG, Hamill MB, Phasin D, Orengo-Nania S, Coselli JS. Acquired supranuclear ocular otor paresis following cardiovascular surgery. J Neuroophthalmol. 1997; 17(3):189–193.

11. Chung PW, Moon HS, Song HS, Kim YB. Ocular motor apraxia after sequential bilateral striatal infarctions. J Clin Neurol. 2006; 2:134–136.