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AB Clincopathologic Conference (CPC) 5/20/2016

AB Clincopathologic Conference (CPC) 5/20/2016. Neurology Resident : Thomas Shoemaker,MD Pathologist: Geoffrey Murdoch,MD. History.

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AB Clincopathologic Conference (CPC) 5/20/2016

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  1. ABClincopathologic Conference (CPC)5/20/2016 Neurology Resident: Thomas Shoemaker,MD Pathologist: Geoffrey Murdoch,MD

  2. History • HPI: 82 year old male with a history of DM c/b neuropathy, lumbar stenosis, possible CIDP, and remote TBI with associated seizure disorder who was being evaluated for gait dysfunction. • 4/13: elective ACDF C3-C6. In Rehab had episode of unresponsiveness, beleieved to be seizure • 4/20: Another episode of unresponsiveness, believed again to be a seizure • 4/21: EEG- No seizure, no epielpetiform discharges

  3. History • 5/2: Another episode of unresponsiveness. Suspected seizure. Repeat EEG, no epilpetiform discharges. AEDs adjusted. • 5/4: Plan for discharge home, but in evening, condition called for unresponiveness. Multiple Rounds of CPR and vasoactive medications. Unsuccessful. Time of death 5/5/16 • Cause of death: CV vs status

  4. Seizures? • Remote history of Seizures, per EMR • Neuro note from 11/2015: He has history of seizure disorder after her to traumatic brain injury in the Korea war. He has been on phenytoin since then and has not had any seizure for many many years. He continues to be on phenytoin. He is not sure about the phenytoin level.

  5. Seizures? • Remote history of Seizures, per EMR • Neuro note from 11/2015: He has history of seizure disorder after her to traumatic brain injury in the Korea war. He has been on phenytoin since then and has not had any seizure for many many years. He continues to be on phenytoin. He is not sure about the phenytoin level.

  6. EEG 4/21

  7. EEG 4/21 • INTERPRETATION: This EEG is probably within normal limits, predominantly drowsy, and asleep. This slowing in the background may be related to drowsy and sleep state. There were no epileptiform discharges seen in this recording

  8. EEG 5/2

  9. EEG 5/2 • INTERPRETATION: Abnormal EEG because of diffuse slowing indicating diffuse cerebral dysfunction such as seen in patients with encephalopathy. There were no epileptiformdischarges seen in this recording.

  10. Examination-Prehospital • Mental Status: Normal • CN: Normal • MOTOR: • Motor • Tone is increased in upper and lower extremities. • Upper extremity: • - R: Arm abduction/ Forearm flexion/ Forearm extension/ Wrist flexors/ Wrist extensors/ Interossei, significant atrophy in the APB • 4/5 4+/5 4+/5 4+/5 4+/5 4+/5 • - L: Arm abduction/ Forearm flexion/ Forearm extension/ Wrist flexors/ Wrist extensors/ Interossei, moderate atrophy and APB • 4/5 4+/5 4+/5 4+/5 4+/5 4/5 • Lower extremity: • - R: Hip flexion/ Knee flexion/ Knee extension/hip abductor/hip abductor/ Dorsi flexors/ Plantar flexors • 5/5 5/5 5/5 5/5 5/5 4/5 5-/5

  11. Examination • Deep Tendon Reflexes • Deep tendon reflexes are slightly asymmetric in the upper extremities but present bilaterally, knee and ankle reflexes are absent. Toes are mute in the right and upgoing on the left. Hoffman negative. No ankle clonus. • Sensation • Decreased to pinprick, temperature and light touch in bilateral lower extremity up to mid thigh and bilateral upper extremity up to the elbows. Abnormal proprioception in the toes and ankles bilaterally as well as fingers. Absent vibratory sensation in the metatarsophalangeal, ankles and knees. Decreased to vibratory sensation in the fingers. • Coordination:Difficultywith finger to nose mainly secondary to shoulder problem • Stance and Gait: Able to stand up from the chair using his arms pulling himself up. Walks with cane. Very unsteady

  12. T1 SAG

  13. FLAIR

  14. GRE

  15. Predicted Pathology-TBI • Predicted Gross pathology: • Brief Discussion of why • Predicted Micro pathology: • Brief Discussion of why

  16. Predicted Pathology-Status • Neuropathological findings reported following fatal cases of status epilepticus (SE) include: • neuronal loss or injury in hippocampal CA1, CA3 and the hilus (the dentate granule cells may be spared), amygdala (corticomedial and basolateral nuclei), neocortex (mid-cortical layers), the entorhinal cortex, Purkinje cell layer of the cerebellum, mamillarybodies, the dorsal medial nuclei of the thalamus and basal ganglia. • Nneuronaldamage may be predominantly unilateral in some cases and with histories of prolonged hemi-convulsions cerebral hemiatrophy can eventually occur with striking unilateral laminarnecrosisof the second to fourth cortical layers. • Neuronal loss, however, is not an inevitable consequence of status epilepticus.

  17. Prelim Autopsy • Overall the most likely cause of immediate death in this patient is due to hypertensive and atherosclerotic cardiovascular disease. Supported by coronary artery disease, cardiomegaly, and an aorta with athermanous plaques. No gross evidence of myocardial infarction was noted, however microscopic examination demonstrates_____ Also this patient had CHF supported by the biventricular dilated cardiomyopathy, pulmonary edema, and congested organomeglay. Preliminary autopsy findings did not reveal any relationship with seizure activity clinically described in this patient, therefore neuropathy report will be key to clarify this issue.

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