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C.N.S.
Toxic & Metabolic Diseases
Mohamed Zaitoun
Assistant Lecturer-Diagnostic Radiology
Department , Zagazig University Hospitals
Egypt
FINR (Fellowship of Interventional
Neuroradiology)-Switzerland
zaitoun82@gmail.com
Knowing as much as
possible about your enemy
precedes successful battle
and learning about the
disease process precedes
successful management
Toxic & Metabolic Diseases
1-Liver Disease
2-Hypoglycemia
3-Hypoxic Ischemic Encephalopathy
4-Methanol Poisoning
5-Carbon Monoxide
1-Liver Disease :
a) Mechanism
b) Radiographic Findings
a) Mechanism :
-Most patients have a history of chronic
cirrhosis resulting in nitrogenous waste
products crossing the blood brain barrier
and causing long-term toxic brain damage
b) MRI Findings :
-Bilateral regions of signal hyperintensity in
the lentiform nucleus and substantia nigra
on T1
-These regions of abnormally high signal
intensity at T1 are related to the
accumulation of manganese in patients
with hepatic encephalopathy and may be
encountered also in welders and
recipients of hyperalimentation therapy
T1 at the level of the basal ganglia (arrowheads in a) and substantia
nigra (arrows in b) show bilateral symmetric regions of
hyperintensity in these structures
Hepatic cirrhosis in a 55-year-old man , T1 shows symmetric
hyperintense foci in the globus pallidus (arrows)
2-Hypoglycemia :
-The extent of brain damage depends on the
severity and duration of hypoglycemia and
clinical presentation includes seizures , focal
neurologic deficits and coma
-Characteristic MR imaging findings of severe
hypoglycemia include bilateral T2
prolongation in the cerebral cortex ,
hippocampi and basal ganglia
-The abnormal areas are typically hyperintense
on diffusion-weighted
(a) T2 , (b) diffusion show diffuse hyperintensity and restricted diffusion in
the heads of the caudate nuclei (arrowheads in a) , lentiform nuclei
(arrows in a) and cerebral cortex with sparing of the subcortical white
matter and thalamus
3-Hypoxic Ischemic Encephalopathy :
a) Etiology
b) Radiographic Features
a) Etiology :
-HIE of the brain in adults may be the result
of circulatory or respiratory failure from
causes including cardiac arrest , drowning
or asphyxiation
b) Radiographic Features :
1-CT :
-Shows diffuse edema , decreased attenuation of
the cortical gray matter with loss of normal gray
matter white matter differentiation and bilateral
decreased attenuation of the basal ganglia and
thalamus (same distribution as hypoglycemia)
but the brainstem and cerebral white matter are
typically spared
-The (reversal sign) may be seen in which there is
higher attenuation in the white matter reversing
the normal relative attenuation between white
matter and gray matter , diffuse cerebral
damage results in a lower attenuation compared
with the cerebellum and brainstem which are
relatively spared resulting in the (white
cerebellum sign)
(a) NECT reveals bilaterally symmetric hypoattenuating areas in the thalamus
(arrowheads) , caudate nuclei (black arrows) and globus pallidus (white
arrows) , (b) CT scan obtained through the posterior fossa shows that the
relatively spared cerebellum has higher attenuation than do the damaged
hypoattenuating supratentorial structures (white cerebellum sign)
2-MRI :
-The earliest finding at MR imaging (after 2
hours) is increased signal intensity of the
affected areas on diffusion-weighted images
-T2 shows subtle increased signal intensity and
swelling of the affected areas usually 24
hours or more after the insult
-Delayed postanoxic leukoencephalopathy may
result in diffuse T2 prolongation in the
subcortical white matter
(a) FLAIR shows symmetrical T2 prolongation in the bilateral
putamina , heads of the caudate nuclei & to a lesser extent in the
globi pallidi , (b) DWI shows marked diffusion hyperintensity within
the globi pallidi (arrows)
(a) T2 shows bilaterally symmetric hyperintense areas in the thalamus
(white arrowheads) , basal ganglia and cerebral cortex , Black
arrowheads = caudate nuclei , arrows = lentiform nuclei , (b) Obtained
at a higher level more clearly depicts diffuse cortical involvement
4-Methanol Poisoning :
-Can present with optic neuritis as the first
symptom
-Hemorrhagic necrosis of the putamen &
white matter edema may follow
Methanol poisoning in a 41-year-old man who presented with altered
mental status and retrobulbar pain , CT+C shows hypoattenuating
areas in the lentiform nuclei (arrows) , corpus callosum , and
subcortical deep white matter in the frontal and parietooccipital
regions (arrowheads)
5-Carbon Monoxide :
-Typically causes symmetric T2 prolongation
and restricted diffusion of the globus
pallidus
-Carbon monoxide poisoning in a 33-year-old man who was found in a
coma after a suicide attempt , (a) T2 , (b) FLAIR obtained 4 weeks after
the poisoning depict symmetric hyperintense foci in the globus pallidus
(arrows) , symmetric hyperintense areas in the deep white matter
(arrowheads in b) are consistent with delayed leukoencephalopathy
Diagnostic Imaging of Cerebral Toxic & Metabolic Diseases

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Diagnostic Imaging of Cerebral Toxic & Metabolic Diseases

  • 2. Mohamed Zaitoun Assistant Lecturer-Diagnostic Radiology Department , Zagazig University Hospitals Egypt FINR (Fellowship of Interventional Neuroradiology)-Switzerland zaitoun82@gmail.com
  • 3.
  • 4.
  • 5. Knowing as much as possible about your enemy precedes successful battle and learning about the disease process precedes successful management
  • 6. Toxic & Metabolic Diseases 1-Liver Disease 2-Hypoglycemia 3-Hypoxic Ischemic Encephalopathy 4-Methanol Poisoning 5-Carbon Monoxide
  • 7. 1-Liver Disease : a) Mechanism b) Radiographic Findings
  • 8. a) Mechanism : -Most patients have a history of chronic cirrhosis resulting in nitrogenous waste products crossing the blood brain barrier and causing long-term toxic brain damage
  • 9. b) MRI Findings : -Bilateral regions of signal hyperintensity in the lentiform nucleus and substantia nigra on T1 -These regions of abnormally high signal intensity at T1 are related to the accumulation of manganese in patients with hepatic encephalopathy and may be encountered also in welders and recipients of hyperalimentation therapy
  • 10. T1 at the level of the basal ganglia (arrowheads in a) and substantia nigra (arrows in b) show bilateral symmetric regions of hyperintensity in these structures
  • 11. Hepatic cirrhosis in a 55-year-old man , T1 shows symmetric hyperintense foci in the globus pallidus (arrows)
  • 12. 2-Hypoglycemia : -The extent of brain damage depends on the severity and duration of hypoglycemia and clinical presentation includes seizures , focal neurologic deficits and coma -Characteristic MR imaging findings of severe hypoglycemia include bilateral T2 prolongation in the cerebral cortex , hippocampi and basal ganglia -The abnormal areas are typically hyperintense on diffusion-weighted
  • 13. (a) T2 , (b) diffusion show diffuse hyperintensity and restricted diffusion in the heads of the caudate nuclei (arrowheads in a) , lentiform nuclei (arrows in a) and cerebral cortex with sparing of the subcortical white matter and thalamus
  • 14. 3-Hypoxic Ischemic Encephalopathy : a) Etiology b) Radiographic Features
  • 15. a) Etiology : -HIE of the brain in adults may be the result of circulatory or respiratory failure from causes including cardiac arrest , drowning or asphyxiation
  • 16. b) Radiographic Features : 1-CT : -Shows diffuse edema , decreased attenuation of the cortical gray matter with loss of normal gray matter white matter differentiation and bilateral decreased attenuation of the basal ganglia and thalamus (same distribution as hypoglycemia) but the brainstem and cerebral white matter are typically spared -The (reversal sign) may be seen in which there is higher attenuation in the white matter reversing the normal relative attenuation between white matter and gray matter , diffuse cerebral damage results in a lower attenuation compared with the cerebellum and brainstem which are relatively spared resulting in the (white cerebellum sign)
  • 17. (a) NECT reveals bilaterally symmetric hypoattenuating areas in the thalamus (arrowheads) , caudate nuclei (black arrows) and globus pallidus (white arrows) , (b) CT scan obtained through the posterior fossa shows that the relatively spared cerebellum has higher attenuation than do the damaged hypoattenuating supratentorial structures (white cerebellum sign)
  • 18. 2-MRI : -The earliest finding at MR imaging (after 2 hours) is increased signal intensity of the affected areas on diffusion-weighted images -T2 shows subtle increased signal intensity and swelling of the affected areas usually 24 hours or more after the insult -Delayed postanoxic leukoencephalopathy may result in diffuse T2 prolongation in the subcortical white matter
  • 19. (a) FLAIR shows symmetrical T2 prolongation in the bilateral putamina , heads of the caudate nuclei & to a lesser extent in the globi pallidi , (b) DWI shows marked diffusion hyperintensity within the globi pallidi (arrows)
  • 20. (a) T2 shows bilaterally symmetric hyperintense areas in the thalamus (white arrowheads) , basal ganglia and cerebral cortex , Black arrowheads = caudate nuclei , arrows = lentiform nuclei , (b) Obtained at a higher level more clearly depicts diffuse cortical involvement
  • 21. 4-Methanol Poisoning : -Can present with optic neuritis as the first symptom -Hemorrhagic necrosis of the putamen & white matter edema may follow
  • 22. Methanol poisoning in a 41-year-old man who presented with altered mental status and retrobulbar pain , CT+C shows hypoattenuating areas in the lentiform nuclei (arrows) , corpus callosum , and subcortical deep white matter in the frontal and parietooccipital regions (arrowheads)
  • 23. 5-Carbon Monoxide : -Typically causes symmetric T2 prolongation and restricted diffusion of the globus pallidus
  • 24. -Carbon monoxide poisoning in a 33-year-old man who was found in a coma after a suicide attempt , (a) T2 , (b) FLAIR obtained 4 weeks after the poisoning depict symmetric hyperintense foci in the globus pallidus (arrows) , symmetric hyperintense areas in the deep white matter (arrowheads in b) are consistent with delayed leukoencephalopathy