Neurologic Sequellae of Nutritional Deficiencies 03

Topic: Imaging

Created on Wednesday, September 24 2008 by jdmiles

Last modified on Wednesday, September 24 2008.

 
        A) Thiamine
 
        B) Vitamin C
 
        C) Folate
 
        D) Penicillin
 
        E) Glucose
 

 

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This question was created on September 24, 2008 by jdmiles.
This question was last modified on September 24, 2008.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

ANSWERS AND EXPLANATIONS

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A) thiamine

This answer is correct.

This FLAIR MRI shows hyperintensity in the medial thalamic nuclei, which is characteristic of Wernicke encephalopathy and Korsakoff dementia. The typical symptoms of Wernicke encephalopathy include ophthalmoparesis, nystagmus, ataxia, and a change in mental status characterized by confusion and apathy. Wernicke encephalopathy and Korsakoff dementia are both due to a deficiency of thiamine (vitamin B1), and both are more common in alcoholics. Treatment of Wernicke encephalopathy requires administration of thiamine. Adams and Victor recommend 50mg IV and 50mg IM immediately, followed by 50mg IM daily.  (See References)

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B) vitamin C

This answer is incorrect.

The patient's imaging and history are consistent with Wernicke encephalopathy. Vitamin C is not the definitive treatment for this disorder.  (See References)

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C) folate

This answer is incorrect.

The patient's imaging and history are consistent with Wernicke encephalopathy. Folate is not the definitive treatment for this disorder.  (See References)

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D) penicillin

This answer is incorrect.

The patient's imaging and history are consistent with Wernicke encephalopathy. Penicillin would not be indicated in this nutritional deficiency disorder.  (See References)

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E) glucose

This answer is incorrect.

The patient's history and imaging are consistent with Wernicke encephalopathy. Administration of glucose, prior to the administration of thiamine, is absolutely contraindicated. The process of glycolysis consumes thiamine. Giving the patient glucose while he still has a thiamine deficiency could worsen his condition, and could be fatal.  (See References)

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References:

1. Victor, M., and Ropper, A.H. (2001). Adams and Victor's Principles of Neurology, 7th Edition. McGraw-Hill, New York.
2. Rowland, L.P. (Ed) (2000). Merritt's Neurology, 10th Edition. Lippincott Williams & Wilkins, Philadelphia.
3. So, Y.T., and Simon, R.P. (2004). Deficiency diseases of the nervous system. In Bradley, W.G., Daroff, R.B., Fenichel, G.M., and Jankovic, J. (Eds.). Neurology in Clinical Practice, Fourth Edition. Butterworth Heinemann, Philadelphia, pp. 1693-1708.
4. Koguchi, K., Nakatsuji, Y., Abe, K., and Sakoda, S. (2004). "Wernicke's encephalopathy after glucose infusion." Neurology, 62(3) 512. (PMID:14872047)

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imaging
Neurologic Sequellae of Nutritional Deficiencies 03
Question ID: 092408140
Question written by J. Douglas Miles, (C) 2006-2009, all rights reserved.
Created: 09/24/2008
Modified: 09/24/2008
Estimated Permutations: 30240