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Case Study
Class: END 2463
by: Mais Mujarkesh
Instructor: Stacy Pedigo
A 57 y/o Female with PMH significant for:
• HCV cirrhosis [hepatitis C].
• HCC [hepatocellular carcinoma]: a cancer arising from
the liver.
• HTN [hypertension].
• DM [diabetes mellitus].
Family Medical History:
• Uncle- Heart failure.
• Grandfather- DM, HTN.
Pt was presented to ED on 5/22/13 and admitted till
5/28/13 with AMS and abdominal pain.
She was diagnosed with ascites, hepatic hydrothorax, and
colitis. She was treated with rocephine and azithromycin.
Then was discharged.
• The pt end up being re-admitted on 5/29/13 to the ER
with AMS, hallucination, and combative behavior. She
was treated with Zoloft after she was evaluated by a
psychiatrist and was discharged.
Few days later, family noticed that pt was confused, which
continued to worsen.
On 6/4/13 Pt was brought back to ED, she was treated with
cipro and transferred to TSICU for further evaluation
were she witnessed a generalized tonic clonic seizure.
No tongue biting, bowel or bladder incontinence was
noticed.
She then was treated with Keppra for the seizure.
Diagnostic Tests
• CT scan of the head (6/5/13):
was negative for acute abnormalities.
MRI Brain (6/11/13):
Persistent cortical edema in the right lateral parietal lobe,
insula, and anterior temporal lobe. Persistent signal
abnormality in the ventral medial thalamus. ADC
changes have resolved and there is no abnormal
enhancement. Findings may represent evolution of
encephalitis, post ictal changes. Findings are not typical
of acute or subacute ischemia.
EEG
Electroencephalogram was requested to investigate for
seizure tendency. A routine adult EEG was recorded
digitally, utilizing the International 10-20 electrode
placement system with the patient awake and asleep.
On (6/24/13) The pt was presented to the EEG department
in a confused state.
Slow ODR.
Pt appears asleep.
Notice the unilateral periodic PLEDs on the right.
During Photic stimulation.
Periodic lateralized epileptiform discharges over the right parietal occipital region.
Periodic unilateral PLEDs continued throughout the EEG.
EEG Results
The background consists of 6 Hz frequency activity.
PLEDs [Periodic lateralized epileptiform discharges]
were seen over the right parietal occipital region at a
frequency of 1 Hz. Upon sleep, the patient continued to
have PLEDs over the right parietal occipital region.
Photic stimulation was performed and triggered no
specific abnormalities.
This encephalogram is considered abnormal due to
moderate generalized slowing along with the unilateral
periodic discharges [PLEDs] over the right parietal
occipital region with increased risk for seizure from this
area.
More Diagnostic Tests
• MRI (7/9/13):
There has been spread of the previously described
pathologic process into new areas, specifically the right
occipital lobe.
The lack of any encephalomalacia change in the previously
affected areas exclude the diagnosis of stroke or post
ictal change.
All suggestive of hepatic encephalopathy.
• CT scan of abdomen (7/15/13):
1. Hepatic cirrhosis. [is a chronic degenerative disease in
which normal liver cells are damaged and are then
replaced by scar tissue.]
2. Enlargement masses in segment 7 and 4B, concerning
for HCC.
Patient’s condition
• The pt was following simple commands, until
she was decompensated again with concern
for pneumonia, was intubated and started on
Fentanyl drip. Without significant
improvement in mental status.
Treatment
1. Continue antibiotic for acute episode of
infection.
2. Continue to aggressively treat hepatic
encephalopathy.
3. Continue Vimpat, Keppra, and Trileptal for
seizure.
Final Report
• On 7/27/13
The pt was unresponsive to verbal and tactile stimuli, pupils
were fixed and dilated, and no spontaneous respiration
were noted. Peripheral pulses were absent and no heart
beat on auscultation.
PLEDs
Was first discovered by Chatrian and colleagues in 1964 .
“PLEDs are periodically recurring paroxysmal discharges
of sharp waves, spike-waves, or complex discharges
consisting of mixed theta-delta waves arising from one
hemisphere or a relatively restricted area within one
hemisphere.” (Yamada, and Meng , pg207)
This discharge in EEG is seen in patient’s with:
1. acute cerebral infarct.
2. herpes simplex encephalitis.
3. other types of encephalitis [infectious mononucleosis].
“PLEDs are often caused or seen in acute ischemic
stroke, tumors, hemorrhages or infection.”
http://www.sharecare.com/question/what-are-pleds
• According to (Tyner, Knott, and Mayer 156) Most of the
time patients with history of tumors, and spikes in their
EEG will have seizures.
• In aggressive growing tumors we might see periodic
lateralized Epileptiform discharges.
“High grade tumors were more likely to be associated
with high amplitude focal slowing, diffuse slowing,
background attenuation, IRDA, PLEDs.”
http://epilepsygroup.com/epilepsy-research-detail5-60-9/abst-2073.htm
• Seizures often occur acutely in patients with PLEDS
discovered on a routine EEG.
• http://emedicine.medscape.com/article/1139025-overview#a30
In conclusion
• EEG has been an invaluable tool in diagnosing
neurological abnormalities such as brain tumors.
• It helps in localizing the affected area of the brain based
on the EEG study. For example, the area of the tumors
can be isolated, but the exact type cannot be known.
• I believe that the patient above with her medical history,
had disturbances in the right hemisphere of the brain
causing the seizure and then the epileptic discharge to
be seen during the encephalogram test.
“PLEDs have been reported to be usually associated with an
acute process and occur early during the course of illness.”
http://www.jsnm.org/files/paper/anm/ams203/ANM20-3-11.pdf
reference Page
Yamada, and Meng, Practical Guide for Clinical Neurophysiologic Testing.
EEG, Lippincott Williams & wilkins. 2010.
Tyner, Knott, and Mayer, Fundamentals of EEG TECHNOLOGY, Lippincott,
1989. Print.
http://www.sharecare.com/question/what-are-pleds
http://epilepsygroup.com/epilepsy-research-detail5-60-9/abst-2073.htm
http://www.jsnm.org/files/paper/anm/ams203/ANM20-3-11.pdf
http://epilepsygroup.com/epilepsy-research-detail5-60-9/abst-2073.htm

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final Case Study1

  • 1. Case Study Class: END 2463 by: Mais Mujarkesh Instructor: Stacy Pedigo
  • 2. A 57 y/o Female with PMH significant for: • HCV cirrhosis [hepatitis C]. • HCC [hepatocellular carcinoma]: a cancer arising from the liver. • HTN [hypertension]. • DM [diabetes mellitus].
  • 3. Family Medical History: • Uncle- Heart failure. • Grandfather- DM, HTN. Pt was presented to ED on 5/22/13 and admitted till 5/28/13 with AMS and abdominal pain. She was diagnosed with ascites, hepatic hydrothorax, and colitis. She was treated with rocephine and azithromycin. Then was discharged.
  • 4. • The pt end up being re-admitted on 5/29/13 to the ER with AMS, hallucination, and combative behavior. She was treated with Zoloft after she was evaluated by a psychiatrist and was discharged.
  • 5. Few days later, family noticed that pt was confused, which continued to worsen. On 6/4/13 Pt was brought back to ED, she was treated with cipro and transferred to TSICU for further evaluation were she witnessed a generalized tonic clonic seizure. No tongue biting, bowel or bladder incontinence was noticed. She then was treated with Keppra for the seizure.
  • 6. Diagnostic Tests • CT scan of the head (6/5/13): was negative for acute abnormalities. MRI Brain (6/11/13): Persistent cortical edema in the right lateral parietal lobe, insula, and anterior temporal lobe. Persistent signal abnormality in the ventral medial thalamus. ADC changes have resolved and there is no abnormal enhancement. Findings may represent evolution of encephalitis, post ictal changes. Findings are not typical of acute or subacute ischemia.
  • 7. EEG Electroencephalogram was requested to investigate for seizure tendency. A routine adult EEG was recorded digitally, utilizing the International 10-20 electrode placement system with the patient awake and asleep. On (6/24/13) The pt was presented to the EEG department in a confused state.
  • 9. Pt appears asleep. Notice the unilateral periodic PLEDs on the right.
  • 10. During Photic stimulation. Periodic lateralized epileptiform discharges over the right parietal occipital region.
  • 11. Periodic unilateral PLEDs continued throughout the EEG.
  • 12. EEG Results The background consists of 6 Hz frequency activity. PLEDs [Periodic lateralized epileptiform discharges] were seen over the right parietal occipital region at a frequency of 1 Hz. Upon sleep, the patient continued to have PLEDs over the right parietal occipital region. Photic stimulation was performed and triggered no specific abnormalities.
  • 13. This encephalogram is considered abnormal due to moderate generalized slowing along with the unilateral periodic discharges [PLEDs] over the right parietal occipital region with increased risk for seizure from this area.
  • 14. More Diagnostic Tests • MRI (7/9/13): There has been spread of the previously described pathologic process into new areas, specifically the right occipital lobe. The lack of any encephalomalacia change in the previously affected areas exclude the diagnosis of stroke or post ictal change. All suggestive of hepatic encephalopathy.
  • 15. • CT scan of abdomen (7/15/13): 1. Hepatic cirrhosis. [is a chronic degenerative disease in which normal liver cells are damaged and are then replaced by scar tissue.]
  • 16. 2. Enlargement masses in segment 7 and 4B, concerning for HCC.
  • 17. Patient’s condition • The pt was following simple commands, until she was decompensated again with concern for pneumonia, was intubated and started on Fentanyl drip. Without significant improvement in mental status.
  • 18. Treatment 1. Continue antibiotic for acute episode of infection. 2. Continue to aggressively treat hepatic encephalopathy. 3. Continue Vimpat, Keppra, and Trileptal for seizure.
  • 19. Final Report • On 7/27/13 The pt was unresponsive to verbal and tactile stimuli, pupils were fixed and dilated, and no spontaneous respiration were noted. Peripheral pulses were absent and no heart beat on auscultation.
  • 20. PLEDs Was first discovered by Chatrian and colleagues in 1964 . “PLEDs are periodically recurring paroxysmal discharges of sharp waves, spike-waves, or complex discharges consisting of mixed theta-delta waves arising from one hemisphere or a relatively restricted area within one hemisphere.” (Yamada, and Meng , pg207)
  • 21. This discharge in EEG is seen in patient’s with: 1. acute cerebral infarct. 2. herpes simplex encephalitis. 3. other types of encephalitis [infectious mononucleosis]. “PLEDs are often caused or seen in acute ischemic stroke, tumors, hemorrhages or infection.” http://www.sharecare.com/question/what-are-pleds
  • 22. • According to (Tyner, Knott, and Mayer 156) Most of the time patients with history of tumors, and spikes in their EEG will have seizures. • In aggressive growing tumors we might see periodic lateralized Epileptiform discharges. “High grade tumors were more likely to be associated with high amplitude focal slowing, diffuse slowing, background attenuation, IRDA, PLEDs.” http://epilepsygroup.com/epilepsy-research-detail5-60-9/abst-2073.htm
  • 23. • Seizures often occur acutely in patients with PLEDS discovered on a routine EEG. • http://emedicine.medscape.com/article/1139025-overview#a30
  • 24. In conclusion • EEG has been an invaluable tool in diagnosing neurological abnormalities such as brain tumors. • It helps in localizing the affected area of the brain based on the EEG study. For example, the area of the tumors can be isolated, but the exact type cannot be known. • I believe that the patient above with her medical history, had disturbances in the right hemisphere of the brain causing the seizure and then the epileptic discharge to be seen during the encephalogram test. “PLEDs have been reported to be usually associated with an acute process and occur early during the course of illness.” http://www.jsnm.org/files/paper/anm/ams203/ANM20-3-11.pdf
  • 25. reference Page Yamada, and Meng, Practical Guide for Clinical Neurophysiologic Testing. EEG, Lippincott Williams & wilkins. 2010. Tyner, Knott, and Mayer, Fundamentals of EEG TECHNOLOGY, Lippincott, 1989. Print. http://www.sharecare.com/question/what-are-pleds http://epilepsygroup.com/epilepsy-research-detail5-60-9/abst-2073.htm http://www.jsnm.org/files/paper/anm/ams203/ANM20-3-11.pdf http://epilepsygroup.com/epilepsy-research-detail5-60-9/abst-2073.htm