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"Found down": Patient with lesions impacting globus pallidus and hippocampus following suspected drug overdose.

Abstract

Our patient presented with the chief complaint of "found down" likely secondary to drug overdose. Patients found in this state present with an unclear history leading to difficulty in diagnosis and treatment. As drug overdose is a growing epidemic in this state and country, it is important to consider both apparent and less evident effects of end-organ damage caused by anoxia following overdose. We suggest including neurocognitive disorders in the differential diagnosis, especially in patients "found down" for indeterminate periods of time. As these disorders are not always initially apparent, Magnetic Resonance Imaging (MRI) and neuropsychological testing can be used to further characterize both disease process and prognosis.

Introduction

The chief complaint of "found down" is often listed for patients that present to the emergency department after being discovered unconscious. They often present with little or no collateral history. This type of patient is a unique challenge with respect to diagnosis, triage, and treatment as they are not able to provide contributory history surrounding their current condition. A common cause is unintentional drug overdose associated with substance use disorder. This is an important issue as the epidemic of overdose deaths and substance use disorders (SUD) in both West Virginia and the United States is growing.

In the event of an overdose, end-organ damage often occurs. Many different organ systems can be impacted, including the brain. Identification of advanced neurologic sequelae is an important part of the diagnosis, treatment, and long-term prognosis following an incident in which the patient presents in an unconscious state. MRI and neuropsychological testing can be used as important tools in detailing specific neurologic deficits. We present a case unique for a "found down" patient determined to have concurrent bilateral globus pallidus lesions as well as bilateral blood breakdown products and atrophy in the hippocampus with deficits in implicit and explicit memory that correlate to the sites of neuroanatomical injury.

Case Presentation

A 29 year-old male with history of alcohol, tobacco, and benzodiazepine use disorders was "found down" after an overdose that may have included bath salts, benzodiazepines, and alcohol. He had a history of multiple alcohol-related incarcerations. He had been a pharmacy student a few years earlier, but being unable to complete schooling, had been working as a roadside flagman. He was discovered unresponsive and hypothermic and was intubated and admitted to the intensivecare unit (ICU). He regained consciousness and respiratory function approximately 16 hours later and was transferred to our facility the following day. He was a poor historian, confused, and was unable to place events linearly in time. Prior to the episode, he had been depressed and anxious secondary to multiple life stressors. Urine Drug Screen (UDS) at outside facility was positive for benzodiazepines, and he was started on an Ativan taper. No compounds that are common ingredients in bath salts were tested. At the outside facility, there were non-specific lab abnormalities that indicated end organ damage from hypoxia.

During his hospital stay, the patient had persistent problems with confusion and short-term memory according to both the patient and his mother. Magnetic Resonance Imaging (MRI) with and without contrast showed mild parenchymal loss which was disproportionate to the patient's age, bilateral symmetrical cavitary lesions in the globus pallidus measuring 7.5mm (See Figure 1), and staining by blood breakdown products and volume loss involving both hippocampi (See Figure 2).

Neuropsychological testing a month after this injury indicated significant cognitive deficits with specific difficulty consolidating new memories, both motor/procedural based memory, and explicit memory. He showed some confabulation and limited insight into his problems. He also showed evidence of frontal lobe dysfunction. Following his one-month evaluation, he was able to return home in close custody of his mother. This pattern of deficits remained at a three-month re-evaluation. This unique finding of anterograde amnesia with loss of procedural memory that correlates imaging has not been characterized to our knowledge. The patient was unable to recall events surrounding his presentation at any point during hospitalization or follow-up. He believed memory difficulties or an "asthma attack" were responsible for his hospitalization.

On discharge, it was recommended that he have close supervision initially as a means of assessing functional ability due to limited insight into his condition and anterograde amnesia. He was discharged on fish oil with rationale of neuroprotective effects of [omega]3 fatty acids.

[FIGURE 1 OMITTED]

Discussion

Our patient's unconsciousness was likely secondary to hypoxia, although etiology is unclear due to a murky history. Difficulty in defining the etiology in "found down" patients can cause problems in triage, diagnosis, and treatment that may increase morbidity and mortality. (1) The diagnosis and specific deficits were identified using MRI and neuropsychological testing.

[FIGURE 2 OMITTED]

The rates of drug overdose in West Virginia and the United States have grown to epidemic levels. From 1999 to 2004, the rates of unintentional drug poisoning increased 68% nationwide, and West Virginia experienced the largest increase in mortality rates at 550%. (2) SUD was involved in 14% of medical and 26% of psychiatric admissions. (3,4) Given our patient's presenting state and history, his "found down" condition was most likely secondary to either overdose or long-term SUD. His prognosis would have been more severe had he not presented to medical care when he did.

In West Virginia, sedatives and opiates are the most common drugs associated with overdose and are often used with alcohol. (2) Abuse of these drugs can have dangerous results including respiratory depression, loss of consciousness, coma, and death. Anoxia from opiate and sedative abuse can lead to end-organ damage impacting any organ system. While our patient initially showed widespread endorgan damage, it resolved after medical stabilization. However, findings on MRI and neuropsychiatric testing persisted.

Hypoperfusion and subsequent hypoxia, the most likely cause in this case, and small vessel disease are the most common causes of lacunar strokes. Other diagnostic considerations that could have resulted in this type of end-organ damage are bath salt intoxication and carbon monoxide poisoning. Bath salts have been shown to cause a decrease in hippocampal neurotransmitter levels and working memory in animal models. (5,6) Stimulants present in bath salt formulations have been shown to reduce working memory performance in a rodent model. (5) Carbon monoxide intoxication is most known for causing basal ganglia lesions on neuroimaging and has been shown to cause other changes such as widespread atrophy and decreased hippocampal volume. (7,8,9)

Difficulty consolidating and learning new explicit information is consistent with bilateral hippocampal loss, and difficulty learning procedural aspects of motor tasks is consistent with bilateral basal ganglia lesions. (10) Left hippocampal lesions have been seen to cause both retrograde and anterograde amnesia, although they are less likely to cause difficulties in long-term memory or recall difficulties. (11-14) Regions of the hippocampus are particularly sensitive to ischemia and oxidative stress. Some research suggests that microhemorrhages of the hippocampi cause sublethal inflammation that may lead to neuronal dysfunction. (15) The globus pallidus is involved in extrapyramidal motor coordination, and bilateral lesions are commonly associated with carbon monoxide intoxication, but can also result from oxygen or glucose deprivation due to high-energy requirements. (16,17) This is the first case we are aware of that has such discrete lesions in two different locations (globus pallidus and hippocampus) that correlate with clinical deficits in explicit memory (hippocampus) and procedural memory (globus pallidus). Use of other drugs such as heroine, cocaine, opiate, or MDMA have been associated with bilateral globus pallidus lesions, (18,19) and bilateral hippocampal atrophy has also been shown with chronic ecstacy use. (16)

Treatment in our patient was largely supportive with considerations for monitoring the patient upon discharge. [omega]3 fatty acids were started as they have been shown to reduce oxidative stress and apoptotic changes in the hippocampus in rat models of ischemic brain damage. (20,21) It is also important to consider the risks of our patient for continued SUD. Given his decreased memory capacity and secondary changes in both social and occupational contexts, it is likely that depression and anxiety may put him at an increased risk to have continued SUD.

Conclusion

Drug overdose can have a variety of both apparent and less evident effects of end-organ damage. We suggest including neurocognitive disorders in the differential, especially in patients "found down" for indeterminate periods of time. MRI and advanced neuropsychological testing can also be considered in order to better characterize long-term prognosis.

References

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(3.) Mordal J, Bramness JG, Holm B, Morland J. Drugs of abuse among acute psychiatric and medical admissions: laboratory based identification of prevalence and drug influence. Gen Hosp Psychiatry. 2008; 30(1):55-60.

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(5.) den Hollander, Bjorner, et al. Long-term cognitive and neurochemical effects of "bath salt" designer drugs methylone and mephedrone. Pharmacology, Biochemistry and Behavior; 103 (2013): 501-509.

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(11.) Maeshima S, et al. Memory impairment caused by cerebral hematoma in the left medical temporal lobe due to ruptured posterior cerebral artery aneurysm. BMC Neurology. 2014; 14:44

(12.) Spiers HJ, Maguire EA, Burgess N. Hippocampal Amnesia. Neurocase. 2001; 7: 357-382.

(13.) Arai N, Shikai C, Fuse S, Shimpo T. Severe amnesia after a restricted lesion in the left hippocampal body. J Neurol Neurosurg Psychiatry. 2006; 77: 1196-1198.

(14.) Kito S, Nakigima T, Koga Y. Amnesia duet o left hippocampal hemorrhage. Int Psychogeriatr. 2008; 20: 643-644.

(15.) Nishimura N, Schaffer CB. Big Effects From Tiny Vessels: Imaging the Impact of Microvascular Clots and Hemorrhages on the Brain. 2013; 44 [suppl 1]: S90-92.

(16.) Alquist, CR, et al. Bilateral globus pallidus lesions. J La State Med Soc. 2012; 164(3): 145-146.

(17.) Ho, VB, et al. Bilateral basal ganglia lesions: pediatric differential considerations. Radiographics. 1993; 13(2): 269-292.

(18.) Kadi R., et al. Bilateral lesions of the globus pallidus in a young woman. JBR-BTR; vol 97 issue 2 (2014): 118-120.

(19.) Ruis C, et al. Cognitive disorders after sporadic ecstacy use? A case report. Neurocase (2014) [Epub ahead of print].

(20.) Cosar, M, et al. The neuroprotective effect of fish n-3 fatty acids in the hippocampus of diabetic rats. Nutr Neurosci. 2008; 11(4): 161-166.

(21.) Zendedel, A, et al. Omega-3 polyunsaturated fatty acids ameliorate neuroinflammation and mitigate ischemic stroke damage through interactions with astrocytes and microglia. J Neuroimmunol. 2015; 278: 200-2011.

Blair Suter, MD

West Virginia University School of Medicine

Mark W. Haut, PhD, ABPP

Chair of Department of Behavioral Medicine and Psychiatry at West Virginia University School of Medicine

Jeffery Hogg, MD

Department of Radiology at West Virginia University School of Medicine

Patrick Marshalek, MD

Department of Behavioral Medicine and Psychiatric at West Virginia University School of Medicine

Corresponding Author: Blair Suter, MD, Riley Hospital for Children, 705 Riley Hospital Drive, Riley 5867, Indianapolis, IN 46202. Email: suterbc@gmail.com.
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Title Annotation:Case Report
Author:Suter, Blair; Haut, Mark W.; Hogg, Jeffery; Marshalek, Patrick
Publication:West Virginia Medical Journal
Article Type:Clinical report
Date:May 1, 2017
Words:2000
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