Samenvatting
A 41-year-old man was found unconscious at his home by a friend. He was
immediately admitted to the hospital through the emergency department. At the
emergency department he regained consciousness. He mentionned he had a
few alcoholic beverages the night before but otherwise clinical history was
negative. On physical examination swelling of the right orbital area was evident.
Further clinical history and laboratory tests were unremarkable. CT scan of the
brain showed the right periorbital swelling. Also noted was marked hypo density
of the globus pallidus bilaterally. These areas of hypodensity showed no
contrast enhancement. Next MRI of the brain was performed. On T2 weighted
images symmetric hyperintensity of the globus pallidus was seen bilaterally. On
diffusion weighted images strong hyperintensity was evident due to a reduction
in apparent diffusion coefficient reflecting cytotoxic edema. Due to the unusual
nature of these lesions further clinical history was obtained and the patient
admitted to the single use of ecstasy the night before he was admitted. Follow
up MRI after 3 weeks showed a decrease of signal intensity on T2 weighted
images of the central area of the globi pallidi consistent with the development of
liquefaction necrosis. After contrast administration there was marked
enhancement of T1 weighted images likely due to passage through the bloodbrain
barrier. On diffusion weighted images loss of hyperintensity was evident
and an increase in apparent diffusion coefficient was seen. Further clinical
evolution was unremarkable.
immediately admitted to the hospital through the emergency department. At the
emergency department he regained consciousness. He mentionned he had a
few alcoholic beverages the night before but otherwise clinical history was
negative. On physical examination swelling of the right orbital area was evident.
Further clinical history and laboratory tests were unremarkable. CT scan of the
brain showed the right periorbital swelling. Also noted was marked hypo density
of the globus pallidus bilaterally. These areas of hypodensity showed no
contrast enhancement. Next MRI of the brain was performed. On T2 weighted
images symmetric hyperintensity of the globus pallidus was seen bilaterally. On
diffusion weighted images strong hyperintensity was evident due to a reduction
in apparent diffusion coefficient reflecting cytotoxic edema. Due to the unusual
nature of these lesions further clinical history was obtained and the patient
admitted to the single use of ecstasy the night before he was admitted. Follow
up MRI after 3 weeks showed a decrease of signal intensity on T2 weighted
images of the central area of the globi pallidi consistent with the development of
liquefaction necrosis. After contrast administration there was marked
enhancement of T1 weighted images likely due to passage through the bloodbrain
barrier. On diffusion weighted images loss of hyperintensity was evident
and an increase in apparent diffusion coefficient was seen. Further clinical
evolution was unremarkable.
Originele taal-2 | English |
---|---|
Pagina's (van-tot) | 93-93 |
Aantal pagina's | 1 |
Tijdschrift | JBR-BTR |
Volume | 94 |
Status | Published - 1 nov 2011 |