Question:

Diffuse post-hypoxic leukoencephalopathy (DPHL) is characterized by:
1. a clinical monophasic presentation.
2. a permanent deterioration after the initial event.
3. a presentation characterized by akynetic-mutism or a Parkinsonian syndrome.
4. a known genetic mutation.
5. a good depiction of the imaging findings by CT.





Answer:

The correct answer for the question "Diffuse post-hypoxic leukoencephalopathy (DPHL) is characterized by:" is:

3. a presentation characterized by akynetic-mutism or a Parkinsonian syndrome.



Explanation
1. a monophasic presentation. [Patients typically present a biphasic pattern]

2. a permanent deterioration after the initial event. F [Patients typically present a biphasic pattern: full or near-full recovery after an initial event]

3. a presentation characterized by akynetic-mutism or a Parkinsonic syndrome.   [Two distinct forms of neurological deterioration have been described, namely akynetic-mutism … or Parkinsonism ]

4. a known genetic mutation. [represents one uncommon sub-type of acquired leukoencephalopathy ]

5.  a good depiction of the imaging findings by CT.  [CT scan may show diffuse supra-tentorial white matter hypodensity although this abnormality is usually very subtle and may be difficult to detect]



From the manuscript:
Delayed leukoencephalopathy after acute carbon monoxide intoxication
Radiology Case. 2014 May; 8(5):1-8


This article belongs to the Neuro section.




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From the manuscript

Delayed leukoencephalopathy after acute carbon monoxide intoxication

Free full text article: Delayed leukoencephalopathy  after acute carbon monoxide intoxication

Abstract
Delayed leukoencephalopathy is an uncommon complication of hypoxic-ischemic events of different etiologies, including carbon monoxide intoxication. We present a case of a 40-year-old male patient who was admitted with rapidly progressive neurocognitive and behavioral deficits. There was a history of accidental carbon monoxide intoxication one month before, presenting with loss of consciousness and short hospitalization, followed by a complete clinical recovery. The imaging studies in the delayed phase depicted confluent, symmetric supra-tentorial white matter lesions in keeping with diffuse demyelinization. Restricted diffusion and metabolite abnormalities in magnetic resonance proton spectroscopy were also seen. The diagnosis of CO-mediated delayed post-hypoxic leukoencephalopathy was assumed after exclusion of other mimickers. Hyperbaric oxygen therapy was tentatively performed and the patient had a favorable clinical and radiological evolution.






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