Limits...
Preserving brain function in a comatose patient with septic hyperpyrexia (41.6   ° C): a case report

View Article: PubMed Central - PubMed

ABSTRACT

Background: Pyrexia is a physiological response through which the immune system responds to infectious processes. Hyperpyrexia is known to be neurodegenerative leading to brain damage. Some of the neurotoxic effects of hyperpyrexia on the brain include seizures, decreased cognitive speed, mental status changes, coma, and even death. In the clinical management of hyperpyrexia, the goal is to treat the underlying cause of elevated temperature and prevent end organ damage.

Case presentation: This case illustrates a 39-year-old white American man referred from another medical facility where he had undergone an upper gastrointestinal tract diagnostic procedure which became complicated by blood aspiration and respiratory distress. During hospitalization, he developed a core body temperature of 41.6 °C (106.9 °F) leading to cognitive decline and coma with a Glasgow Coma Score of 3. Levetiracetam and amantadine were utilized effectively for preserving and restoring neurocognitive function. Prior studies have shown that glutamate levels can increase during an infectious process. Glutamate is an excitatory neurotransmitter that is utilized by the organum vasculosum laminae terminalis through the neuronal excitatory system and causes an increase in body temperature which can lead to hyperpyrexia. Similar to neurogenic fevers, hyperpyrexia can lead to neurological decline and irreversible cognitive dysfunction. Inhibition of the glutamate aids a decrease in excitatory states, and improves the brain’s regulatory mechanism, including temperature control. To further improve cognitive function, dopamine levels were increased with a dopamine agonist.

Conclusions: We propose that a combination of levetiracetam and amantadine may provide neuroprotective and neurorestorative properties when administered during a period of hyperpyrexia accompanied by any form of mental status changes, particularly if there is a decline in Glasgow Coma Score.

No MeSH data available.


Related in: MedlinePlus

Computed tomography scan of brain without contrast showing brain atrophy disproportionately advanced for patient’s age. Arrows pointing to areas of atrophy
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
getmorefigures.php?uid=PMC5304390&req=5

Fig1: Computed tomography scan of brain without contrast showing brain atrophy disproportionately advanced for patient’s age. Arrows pointing to areas of atrophy

Mentions: As an antiepileptic agent, levetiracetam functions by binding to neuronal synaptic vesicle glycoprotein 2A and inhibiting presynaptic calcium channels which leads to decreased cell excitation [11]. Prolonged excitatory states with glutamate release from brain neurons occur in anoxic-hypoxic brain injury via unregulated release of neurotransmitters from the vesicles where they are normally stored [16]. In hyperpyrexia, the excitatory states with continuous release of neurotransmitters further induce necrosis which usually can be noticed on CT imaging within 14 days of initial injury [17, 18] (Fig. 1). As further necrosis occurs, more glutamate is released from damaged neurons causing more excitatory states in the brain causing further cognitive decline and coma due to excitatory neuronal states. Excitogenicity caused by the release of glutamate after any form of brain injury occurs due to reactive oxygen stress, which occasionally causes epileptogenic foci in patients [19, 20]. In this case, our patient had hypoxic ischemic brain injury and brain atrophy as seen on CT imaging. Levetiracetam inhibits glutamate transmission through presynaptic P/Q-type calcium channels thus decreasing neuronal excitation [21]. The inhibition of glutamate release in our patient’s brain led to improvement and preservation in brain function by decreasing excitatory states in his brain and assisting in improved fever regulation. Hence, we theorize that the inhibition of action potential via utilization of levetiracetam halted the progression of neuronal damage in this patient thus preserving cognitive function despite a temperature of 41.6 °C (106.9 °F).Fig. 1


Preserving brain function in a comatose patient with septic hyperpyrexia (41.6   ° C): a case report
Computed tomography scan of brain without contrast showing brain atrophy disproportionately advanced for patient’s age. Arrows pointing to areas of atrophy
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC5304390&req=5

Fig1: Computed tomography scan of brain without contrast showing brain atrophy disproportionately advanced for patient’s age. Arrows pointing to areas of atrophy
Mentions: As an antiepileptic agent, levetiracetam functions by binding to neuronal synaptic vesicle glycoprotein 2A and inhibiting presynaptic calcium channels which leads to decreased cell excitation [11]. Prolonged excitatory states with glutamate release from brain neurons occur in anoxic-hypoxic brain injury via unregulated release of neurotransmitters from the vesicles where they are normally stored [16]. In hyperpyrexia, the excitatory states with continuous release of neurotransmitters further induce necrosis which usually can be noticed on CT imaging within 14 days of initial injury [17, 18] (Fig. 1). As further necrosis occurs, more glutamate is released from damaged neurons causing more excitatory states in the brain causing further cognitive decline and coma due to excitatory neuronal states. Excitogenicity caused by the release of glutamate after any form of brain injury occurs due to reactive oxygen stress, which occasionally causes epileptogenic foci in patients [19, 20]. In this case, our patient had hypoxic ischemic brain injury and brain atrophy as seen on CT imaging. Levetiracetam inhibits glutamate transmission through presynaptic P/Q-type calcium channels thus decreasing neuronal excitation [21]. The inhibition of glutamate release in our patient’s brain led to improvement and preservation in brain function by decreasing excitatory states in his brain and assisting in improved fever regulation. Hence, we theorize that the inhibition of action potential via utilization of levetiracetam halted the progression of neuronal damage in this patient thus preserving cognitive function despite a temperature of 41.6 °C (106.9 °F).Fig. 1

View Article: PubMed Central - PubMed

ABSTRACT

Background: Pyrexia is a physiological response through which the immune system responds to infectious processes. Hyperpyrexia is known to be neurodegenerative leading to brain damage. Some of the neurotoxic effects of hyperpyrexia on the brain include seizures, decreased cognitive speed, mental status changes, coma, and even death. In the clinical management of hyperpyrexia, the goal is to treat the underlying cause of elevated temperature and prevent end organ damage.

Case presentation: This case illustrates a 39-year-old white American man referred from another medical facility where he had undergone an upper gastrointestinal tract diagnostic procedure which became complicated by blood aspiration and respiratory distress. During hospitalization, he developed a core body temperature of 41.6 °C (106.9 °F) leading to cognitive decline and coma with a Glasgow Coma Score of 3. Levetiracetam and amantadine were utilized effectively for preserving and restoring neurocognitive function. Prior studies have shown that glutamate levels can increase during an infectious process. Glutamate is an excitatory neurotransmitter that is utilized by the organum vasculosum laminae terminalis through the neuronal excitatory system and causes an increase in body temperature which can lead to hyperpyrexia. Similar to neurogenic fevers, hyperpyrexia can lead to neurological decline and irreversible cognitive dysfunction. Inhibition of the glutamate aids a decrease in excitatory states, and improves the brain’s regulatory mechanism, including temperature control. To further improve cognitive function, dopamine levels were increased with a dopamine agonist.

Conclusions: We propose that a combination of levetiracetam and amantadine may provide neuroprotective and neurorestorative properties when administered during a period of hyperpyrexia accompanied by any form of mental status changes, particularly if there is a decline in Glasgow Coma Score.

No MeSH data available.


Related in: MedlinePlus