Not All Who Stagger are Drunk: Ocular and Gait Abnormalities in a Young Adult
Poster #: 055
Session/Time: B
Author:
Jacob Givonetti Knapp, BA
Mentor:
Barry John Knapp, MD
Research Type: Case Report
Abstract
INTRODUCTION:
Wernicke encephalopathy is a debilitating neurological disorder caused by a depletion of Vitamin B1 (thiamine), which is a critical component of cellular metabolism. Namely, it plays a vital role as a coenzyme in the production of ATP. Wernicke encephalopathy most acutely affects the nervous system and can lead to widespread neuronal cell death. The most prevalent demographic affected are those with chronic alcohol use disorder, since alcohol impairs the dietary absorption of thiamine. Typical neurological symptoms include a triad of ocular dysfunction, uncoordinated muscle movements, and altered mental status. Nystagmus - the most common presentation ¬- is characterized by rapid, involuntary movement of the eye. In this case report, we investigate an atypical Wernicke encephalopathy patient: one who presents with prominent nystagmus but lacks a history of chronic alcohol use.
CASE INFORMATION:
A 31-year-old woman presented to the emergency department for the third time in four weeks with vomiting, unstable gait, and odd behavior. She had a history of chronic nausea and vomiting. She denied any history of alcohol use. Physical exam showed vertical nystagmus (Video), hyperreflexia, ataxia and an odd affect. CT and MRI of the brain were normal. Labs were normal except for a Vitamin B1 (thiamine) level of 30 nmol/L (reference range 78-185 nmol/L). The patient was diagnosed and treated for Wernicke's encephalopathy with thiamine 500 mg every six hours for five days. She was discharged on hospital day eight on oral thiamine supplementation.
DISCUSSION:
Wernicke encephalopathy presents a challenge for clinicians: it manifests most commonly as a consequence of chronic alcoholism, but its presentation is nearly indistinguishable from that of acute alcohol intoxication. The classic Wernicke encephalopathy triad is ocular dysfunction, ataxia, and altered mental status, but the complete triad is found in less than one third of patients. Therefore, a patient with known alcohol use disorder presenting with symptoms of altered mental status and uncoordinated muscle movements could likely be suffering from intoxication, but Wernicke encephalopathy cannot reasonably be excluded as a contributory factor without labs. When nystagmus occurs in conjunction with altered mental status or ataxia - as in this patient - suspicion for Wernicke encephalopathy should be raised. In this patient, the nystagmus presents vertically (Video), but it can also present horizontally. Ocular dysfunction may be the only reliable clinical presentation that can readily be differentiated from alcohol intoxication. Moreover, not all Wernicke encephalopathy patients have a history of alcohol use. In this patient, the thiamine deficiency manifested as a result of chronic malnutrition. Malnutrition is a less common cause of Wernicke encephalopathy in the United States and therefore may be under-recognized in this patient population by clinicians.
CONCLUSION:
Wernicke encephalopathy is a severe neurological disorder that can result in irreversible cognitive impairment in the absence of early recognition and prompt thiamine replacement. Recognition of ocular dysfunction - such as nystagmus - in these patients is crucial to distinguish from alcohol intoxication. A history of chronic alcohol use is common, but Wernicke encephalopathy should not be disregarded in its absence, especially in the setting of severe malnutrition.
Wernicke encephalopathy is a debilitating neurological disorder caused by a depletion of Vitamin B1 (thiamine), which is a critical component of cellular metabolism. Namely, it plays a vital role as a coenzyme in the production of ATP. Wernicke encephalopathy most acutely affects the nervous system and can lead to widespread neuronal cell death. The most prevalent demographic affected are those with chronic alcohol use disorder, since alcohol impairs the dietary absorption of thiamine. Typical neurological symptoms include a triad of ocular dysfunction, uncoordinated muscle movements, and altered mental status. Nystagmus - the most common presentation ¬- is characterized by rapid, involuntary movement of the eye. In this case report, we investigate an atypical Wernicke encephalopathy patient: one who presents with prominent nystagmus but lacks a history of chronic alcohol use.
CASE INFORMATION:
A 31-year-old woman presented to the emergency department for the third time in four weeks with vomiting, unstable gait, and odd behavior. She had a history of chronic nausea and vomiting. She denied any history of alcohol use. Physical exam showed vertical nystagmus (Video), hyperreflexia, ataxia and an odd affect. CT and MRI of the brain were normal. Labs were normal except for a Vitamin B1 (thiamine) level of 30 nmol/L (reference range 78-185 nmol/L). The patient was diagnosed and treated for Wernicke's encephalopathy with thiamine 500 mg every six hours for five days. She was discharged on hospital day eight on oral thiamine supplementation.
DISCUSSION:
Wernicke encephalopathy presents a challenge for clinicians: it manifests most commonly as a consequence of chronic alcoholism, but its presentation is nearly indistinguishable from that of acute alcohol intoxication. The classic Wernicke encephalopathy triad is ocular dysfunction, ataxia, and altered mental status, but the complete triad is found in less than one third of patients. Therefore, a patient with known alcohol use disorder presenting with symptoms of altered mental status and uncoordinated muscle movements could likely be suffering from intoxication, but Wernicke encephalopathy cannot reasonably be excluded as a contributory factor without labs. When nystagmus occurs in conjunction with altered mental status or ataxia - as in this patient - suspicion for Wernicke encephalopathy should be raised. In this patient, the nystagmus presents vertically (Video), but it can also present horizontally. Ocular dysfunction may be the only reliable clinical presentation that can readily be differentiated from alcohol intoxication. Moreover, not all Wernicke encephalopathy patients have a history of alcohol use. In this patient, the thiamine deficiency manifested as a result of chronic malnutrition. Malnutrition is a less common cause of Wernicke encephalopathy in the United States and therefore may be under-recognized in this patient population by clinicians.
CONCLUSION:
Wernicke encephalopathy is a severe neurological disorder that can result in irreversible cognitive impairment in the absence of early recognition and prompt thiamine replacement. Recognition of ocular dysfunction - such as nystagmus - in these patients is crucial to distinguish from alcohol intoxication. A history of chronic alcohol use is common, but Wernicke encephalopathy should not be disregarded in its absence, especially in the setting of severe malnutrition.