Adina Bowe, MD

The effect of sepsis survivorship on cognition is a substantially under-recognized public health problem.¹ Sepsis survivorship has implications for patients’ families and the health care system.² Research has demonstrated that older patients may develop impaired cognition and functional capacity after severe sepsis³; limited evidence shows neurocognitive decline in non-geriatric patients.³  There are no reports of exacerbation of psychiatric illness after severe sepsis or septic shock, and existing literature indicates that the causative factors, epidemiology, and predisposition that may worsen psychiatric illness after septic shock are poorly defined.

Case: Sepsis-induced cognitive decline?

Following an intensive care admission for septic shock, Mr. J, age 49, presents to the outpatient behavioral medicine department with worsening mood, lethargy, agitation, suicidal ideations, hallucinations, and poor work performance for 10 months. He was diagnosed with major depressive disorder 13 years prior, but has no history of hospitalization for psychiatric illness. His depressive symptoms respond well to paroxetine, 60 mg/d.  Subsequently, Mr. J becomes delusional, has intense command hallucinations, and attempts suicide, resulting in hospitalization. Neuropsychological testing reveals dementia and significant psychiatric distress, including elevated levels of depression and suicidal ideation. He is stabilized with duloxetine, 90 mg/d, and quetiapine, 50 mg/d. Two years later, Mr. J still exhibits cognitive and psychiatric disturbances.

Long-term results

The underlying mechanism of septic shock on the brain may be similar to the mechanisms that exacerbate psychiatric illnesses.  This case validates the use of neuropsychological testing in septic shock survivors and encourages recognition of the effect septic shock has on neuropsychiatric illness.

Disclosure
The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers
of competing products.

References

1. Iwashyna TJ, Ely EW, Smith DM, et al. Long-term cognitive impairment and functional disability among survivors of severe sepsis. JAMA. 2010;304(16):1787-1794.

2. Safdieh J. Cognition after sepsis. Neurology Alert. 2010; 29(4):30-31.

3. Williams GS. Older severe sepsis survivors are at risk for cognitive and developmental disability. Pulmonary Reviews. 2010;15(12):17-18.

The effect of sepsis survivorship on cognition is a substantially under-recognized public health problem.¹ Sepsis survivorship has implications for patients’ families and the health care system.² Research has demonstrated that older patients may develop impaired cognition and functional capacity after severe sepsis³; limited evidence shows neurocognitive decline in non-geriatric patients.³  There are no reports of exacerbation of psychiatric illness after severe sepsis or septic shock, and existing literature indicates that the causative factors, epidemiology, and predisposition that may worsen psychiatric illness after septic shock are poorly defined.

Case: Sepsis-induced cognitive decline?

Following an intensive care admission for septic shock, Mr. J, age 49, presents to the outpatient behavioral medicine department with worsening mood, lethargy, agitation, suicidal ideations, hallucinations, and poor work performance for 10 months. He was diagnosed with major depressive disorder 13 years prior, but has no history of hospitalization for psychiatric illness. His depressive symptoms respond well to paroxetine, 60 mg/d.  Subsequently, Mr. J becomes delusional, has intense command hallucinations, and attempts suicide, resulting in hospitalization. Neuropsychological testing reveals dementia and significant psychiatric distress, including elevated levels of depression and suicidal ideation. He is stabilized with duloxetine, 90 mg/d, and quetiapine, 50 mg/d. Two years later, Mr. J still exhibits cognitive and psychiatric disturbances.

Long-term results

The underlying mechanism of septic shock on the brain may be similar to the mechanisms that exacerbate psychiatric illnesses.  This case validates the use of neuropsychological testing in septic shock survivors and encourages recognition of the effect septic shock has on neuropsychiatric illness.

Disclosure
The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers
of competing products.

References

1. Iwashyna TJ, Ely EW, Smith DM, et al. Long-term cognitive impairment and functional disability among survivors of severe sepsis. JAMA. 2010;304(16):1787-1794.

2. Safdieh J. Cognition after sepsis. Neurology Alert. 2010; 29(4):30-31.

3. Williams GS. Older severe sepsis survivors are at risk for cognitive and developmental disability. Pulmonary Reviews. 2010;15(12):17-18.

The effect of sepsis survivorship on cognition is a substantially under-recognized public health problem.¹ Sepsis survivorship has implications for patients’ families and the health care system.² Research has demonstrated that older patients may develop impaired cognition and functional capacity after severe sepsis³; limited evidence shows neurocognitive decline in non-geriatric patients.³  There are no reports of exacerbation of psychiatric illness after severe sepsis or septic shock, and existing literature indicates that the causative factors, epidemiology, and predisposition that may worsen psychiatric illness after septic shock are poorly defined.

Case: Sepsis-induced cognitive decline?

Following an intensive care admission for septic shock, Mr. J, age 49, presents to the outpatient behavioral medicine department with worsening mood, lethargy, agitation, suicidal ideations, hallucinations, and poor work performance for 10 months. He was diagnosed with major depressive disorder 13 years prior, but has no history of hospitalization for psychiatric illness. His depressive symptoms respond well to paroxetine, 60 mg/d.  Subsequently, Mr. J becomes delusional, has intense command hallucinations, and attempts suicide, resulting in hospitalization. Neuropsychological testing reveals dementia and significant psychiatric distress, including elevated levels of depression and suicidal ideation. He is stabilized with duloxetine, 90 mg/d, and quetiapine, 50 mg/d. Two years later, Mr. J still exhibits cognitive and psychiatric disturbances.

Long-term results

The underlying mechanism of septic shock on the brain may be similar to the mechanisms that exacerbate psychiatric illnesses.  This case validates the use of neuropsychological testing in septic shock survivors and encourages recognition of the effect septic shock has on neuropsychiatric illness.

Disclosure
The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers
of competing products.

References

1. Iwashyna TJ, Ely EW, Smith DM, et al. Long-term cognitive impairment and functional disability among survivors of severe sepsis. JAMA. 2010;304(16):1787-1794.

2. Safdieh J. Cognition after sepsis. Neurology Alert. 2010; 29(4):30-31.

3. Williams GS. Older severe sepsis survivors are at risk for cognitive and developmental disability. Pulmonary Reviews. 2010;15(12):17-18.

Interictal psychosis of epilepsy (IPE) is schizophrenia-like psychosis associated with epilepsy that cannot be directly linked to an ictus. IPE often is indistinguishable from primary schizophrenia. This phenomenon commonly occurs in patients with a history of temporal lobe epilepsy (TLE); in those with frequent seizures; and in patients with a long history of epilepsy (>10 years).¹ Interictal psychosis rarely precedes seizure activity² and few cases have been reported. The epidemiology and clinical characteristics of IPE are poorly defined.³ We recently treated a patient with suspected IPE.

Mr. R, age 18, presented to our emergency department with his mother, who stated that her son was behaving strangely and had slow speech for 4 days. He had decreased social interaction, reduced appetite, poor hygiene, decreased sleep, and auditory hallucinations. Mr. R demonstrated hypervigilance and paranoia. He repeatedly checked rooms in his house for intruders. Mr. R also expressed suicidal ideation and exhibited cognitive decline of memory, attention, and fund of knowledge. His physical exam, routine laboratory investigations, CT, and MRI were within normal limits. Urine drug screen was positive for marijuana. We made a clinical diagnosis of acute psychosis.

Mr. R was admitted and started on ziprasidone, titrated to 160 mg/d; however, he could not tolerate this medication because of orthostatic hypotension. We discontinued ziprasidone and started risperidone, titrated to 4 mg/d. By day 4 Mr. R remained psychotic and marijuana intoxication was ruled out. EEG demonstrated rare intermittent left temporal sharp slow wave discharges and sharply contoured slow waves. This suggested an underlying seizure disorder, although Mr. R had no history of seizure.

The psychosis resolved 3 weeks later with risperidone, 2 mg/d, risperidone long-acting injection, 25 mg every 2 weeks, and carbamazepine, 400 mg/d. Mr. R was discharged home on these medications. He was noncompliant with treatment and continued to smoke marijuana. Four months later, Mr. R was rehospitalized for strange behavior. When seen in the outpatient clinic for follow-up, Mr. R admitted that he had his first witnessed seizure before his last hospitalization. Mr. R was restarted on risperidone, 4 mg/d, and risperidone long-acting injection, 25 mg every 2 weeks. To increase compliance, we switched carbamazepine to divalproex sodium extended-release, 500 mg/d. He remains stable, but continues to smoke marijuana.

Our case illustrates that IPE may be a presenting feature of TLE. Because IPE may occur in patients who do not have a history of TLE, EEG monitoring should be considered in the workup of new-onset psychosis.

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Interictal psychosis of epilepsy (IPE) is schizophrenia-like psychosis associated with epilepsy that cannot be directly linked to an ictus. IPE often is indistinguishable from primary schizophrenia. This phenomenon commonly occurs in patients with a history of temporal lobe epilepsy (TLE); in those with frequent seizures; and in patients with a long history of epilepsy (>10 years).¹ Interictal psychosis rarely precedes seizure activity² and few cases have been reported. The epidemiology and clinical characteristics of IPE are poorly defined.³ We recently treated a patient with suspected IPE.

Mr. R, age 18, presented to our emergency department with his mother, who stated that her son was behaving strangely and had slow speech for 4 days. He had decreased social interaction, reduced appetite, poor hygiene, decreased sleep, and auditory hallucinations. Mr. R demonstrated hypervigilance and paranoia. He repeatedly checked rooms in his house for intruders. Mr. R also expressed suicidal ideation and exhibited cognitive decline of memory, attention, and fund of knowledge. His physical exam, routine laboratory investigations, CT, and MRI were within normal limits. Urine drug screen was positive for marijuana. We made a clinical diagnosis of acute psychosis.

Mr. R was admitted and started on ziprasidone, titrated to 160 mg/d; however, he could not tolerate this medication because of orthostatic hypotension. We discontinued ziprasidone and started risperidone, titrated to 4 mg/d. By day 4 Mr. R remained psychotic and marijuana intoxication was ruled out. EEG demonstrated rare intermittent left temporal sharp slow wave discharges and sharply contoured slow waves. This suggested an underlying seizure disorder, although Mr. R had no history of seizure.

The psychosis resolved 3 weeks later with risperidone, 2 mg/d, risperidone long-acting injection, 25 mg every 2 weeks, and carbamazepine, 400 mg/d. Mr. R was discharged home on these medications. He was noncompliant with treatment and continued to smoke marijuana. Four months later, Mr. R was rehospitalized for strange behavior. When seen in the outpatient clinic for follow-up, Mr. R admitted that he had his first witnessed seizure before his last hospitalization. Mr. R was restarted on risperidone, 4 mg/d, and risperidone long-acting injection, 25 mg every 2 weeks. To increase compliance, we switched carbamazepine to divalproex sodium extended-release, 500 mg/d. He remains stable, but continues to smoke marijuana.

Our case illustrates that IPE may be a presenting feature of TLE. Because IPE may occur in patients who do not have a history of TLE, EEG monitoring should be considered in the workup of new-onset psychosis.

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.

Interictal psychosis of epilepsy (IPE) is schizophrenia-like psychosis associated with epilepsy that cannot be directly linked to an ictus. IPE often is indistinguishable from primary schizophrenia. This phenomenon commonly occurs in patients with a history of temporal lobe epilepsy (TLE); in those with frequent seizures; and in patients with a long history of epilepsy (>10 years).¹ Interictal psychosis rarely precedes seizure activity² and few cases have been reported. The epidemiology and clinical characteristics of IPE are poorly defined.³ We recently treated a patient with suspected IPE.

Mr. R, age 18, presented to our emergency department with his mother, who stated that her son was behaving strangely and had slow speech for 4 days. He had decreased social interaction, reduced appetite, poor hygiene, decreased sleep, and auditory hallucinations. Mr. R demonstrated hypervigilance and paranoia. He repeatedly checked rooms in his house for intruders. Mr. R also expressed suicidal ideation and exhibited cognitive decline of memory, attention, and fund of knowledge. His physical exam, routine laboratory investigations, CT, and MRI were within normal limits. Urine drug screen was positive for marijuana. We made a clinical diagnosis of acute psychosis.

Mr. R was admitted and started on ziprasidone, titrated to 160 mg/d; however, he could not tolerate this medication because of orthostatic hypotension. We discontinued ziprasidone and started risperidone, titrated to 4 mg/d. By day 4 Mr. R remained psychotic and marijuana intoxication was ruled out. EEG demonstrated rare intermittent left temporal sharp slow wave discharges and sharply contoured slow waves. This suggested an underlying seizure disorder, although Mr. R had no history of seizure.

The psychosis resolved 3 weeks later with risperidone, 2 mg/d, risperidone long-acting injection, 25 mg every 2 weeks, and carbamazepine, 400 mg/d. Mr. R was discharged home on these medications. He was noncompliant with treatment and continued to smoke marijuana. Four months later, Mr. R was rehospitalized for strange behavior. When seen in the outpatient clinic for follow-up, Mr. R admitted that he had his first witnessed seizure before his last hospitalization. Mr. R was restarted on risperidone, 4 mg/d, and risperidone long-acting injection, 25 mg every 2 weeks. To increase compliance, we switched carbamazepine to divalproex sodium extended-release, 500 mg/d. He remains stable, but continues to smoke marijuana.

Our case illustrates that IPE may be a presenting feature of TLE. Because IPE may occur in patients who do not have a history of TLE, EEG monitoring should be considered in the workup of new-onset psychosis.

Disclosure

The authors report no financial relationship with any company whose products are mentioned in this article or with manufacturers of competing products.