Neuropsychiatric Masquerades: Diagnosis and Treatment

February 19, 2016

A focus on the differential of CNS disorders that present with neuropsychiatric symptoms, their presentations, and guidelines for treatment.

Premiere Date: February 20, 2016
Expiration Date: August 20, 2017

This activity offers CE credits for:

1.Physicians (CME)
2. Other

ACTIVITY GOAL

This article focuses on the differential of CNS disorders that present with neuropsychiatric symptoms, their presentations, and guidelines for treatment.

LEARNING OBJECTIVES

At the end of this CE activity, participants should be able to:

• Describe the interplay between CNS disorders and psychiatric symptoms

• Identify the primary CNS disorders that can masquerade as neuropsychiatric illness

• Explain the differential for these disorders as well as how such disorders might present

TARGET AUDIENCE

This continuing medical education activity is intended for psychiatrists, psychologists, primary care physicians, physician assistants, nurse practitioners, and other health care professionals who seek to improve their care for patients with mental health disorders.

CREDIT INFORMATION

CME Credit (Physicians): This activity has been planned and implemented in accordance with the Essential Areas and policies of the Accreditation Council for Continuing Medical Education (ACCME) through the joint providership of CME Outfitters, LLC, and Psychiatric Times. CME Outfitters, LLC, is accredited by the ACCME to provide continuing medical education for physicians.

CME Outfitters designates this enduring material for a maximum of 1.5 AMA PRA Category 1 Credit™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Note to Nurse Practitioners and Physician Assistants: AANPCP and AAPA accept certificates of participation for educational activities certified for 1.5 AMA PRA Category 1 Credit™.

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It is the policy of CME Outfitters, LLC, to ensure independence, balance, objectivity, and scientific rigor and integrity in all of their CME/CE activities. Faculty must disclose to the participants any relationships with commercial companies whose products or devices may be mentioned in faculty presentations, or with the commercial supporter of this CME/CE activity. CME Outfitters, LLC, has evaluated, identified, and attempted to resolve any potential conflicts of interest through a rigorous content validation procedure, use of evidence-based data/research, and a multidisciplinary peer-review process.

The following information is for participant information only. It is not assumed that these relationships will have a negative impact on the presentations.

Yelizaveta Sher, MD, has no disclosures to report.

Renee Garcia, MD, has no disclosures to report.

José R. Maldonado, MD, has no disclosures to report.

Jonathan M. Silver, MD, (peer/content reviewer) reports that he is Course Director of a neuropsychiatry course for PGY III residents in the department of psychiatry at the New York University School of Medicine; he is a reviewer for the Colorado Traumatic Brain Injury Trust Fund Research Grant Program; he is Chair of the Data and Safety Monitoring Board for A Multicenter, Parallel-Group, Randomized, Double-Blind, Placebo-Controlled Trial of Amantadine Hydrochloride for the Treatment Of Chronic TBI Irritability Aggression: A Replication Study (National Institute on Disability and Rehabilitation Research [NIDRR]) and for the Multicenter Evaluation of Memory Remediation After Traumatic Brain Injury With Donepezil (NIDRR).

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It is important for psychiatrists to be aware of the variety of CNS disorders that present with neuropsychiatric symptoms, masquerading as mental illness. A high level of suspicion and the correct identification of the underlying process are paramount to treatment. This article focuses on the key differential of such disorders, common and important presentations, and guidelines for treatment.

CNS disorders and psychiatric symptoms or conditions can interplay in several ways: comorbidity (eg, depression and epilepsy); CNS conditions that present with psychiatric symptoms (eg, agitation in dementia); psychiatric conditions that present with neurologic and other physical symptoms (eg, conversion disorder); and, finally, psychiatric symptoms that appear as an adverse effect of treatment for CNS disorders (eg, depression as an adverse effect of levetiracetam for treatment of epilepsy).

Multiple CNS disorders can present with psychiatric symptoms or as comorbidities with psychiatric symptoms. These CNS disorders include headaches, seizures, traumatic brain injury (TBI), delirium, neurodegenerative disorders, major neurocognitive disorders, limbic encephalitis, CNS infections, tumors, and substance-related disorders (Table 1). Multiple other systemic (ie, metabolic, endocrine, autoimmune, and infectious) processes can also affect the CNS but are not covered in this article in their entirety (see Tables 2 to 6 for the full differential). The proper work-up and correct identification of the underlying process rely on accurate history taking, careful mental status examination, neurologic examination, obtaining collateral information, and supporting laboratory and imaging data.

Delirium

One of the most common CNS disorders that presents with psychiatric symptoms, especially in a hospital setting, is delirium. In one study, 42% of hospitalized elderly patients who were referred for psychiatric consultation to evaluate depression were in fact delirious.1 Delirium is a syndrome of neuropsychiatric symptoms driven by the underlying medical illness or substance-induced dysregulation. This acute or subacute organic mental syndrome is characterized by the cardinal symptom of attention deficit as well as disturbance of consciousness, global cognitive impairment, disorientation, perceptual disturbance, changes in psychomotor activity and sleep-wake cycle, and fluctuation in symptom severity. It is caused by transient disruption of normal neuronal activity due to disturbances of systemic physiology.

Delirium includes 3 motoric types: hyperactive, hypoactive, and mixed. The hyperactive type, which is marked by agitation, hyperactivity, aggressiveness, hallucinations, and delusions, is frequently recognized by primary care providers because of its disruption of clinical care. However, the hypoactive type-which is characterized by decreased reactivity, motor and speech retardation, and facial inexpressiveness and which constitutes the majority (up to 65%) of delirium cases-is often missed or mistaken for depression.2 Because of dysphoric and restricted affect, decreased engagement and cooperation with care providers, and at times endorsed suicidality, patients with hypoactive delirium can appear depressed.

The clinical history (acute/subacute onset of symptoms, symptom fluctuation, comorbid medical and neurologic conditions), careful mental status examination (with the help of screening tools such as the Delirium Rating Scale-Revised 98 [DRS-R-98]), and neurologic examination (with the inclusion of primitive reflexes) often clarify the diagnosis of hypoactive delirium. In addition, a review of medications that can precipitate and perpetuate delirium (eg, anticholinergic medications, benzodiazepines, opiates) and pertinent laboratory values (eg, electrolyte abnormalities, renal and/or hepatic dysfunction, anemia) help identify contributors to delirium and guide appropriate treatment.

CASE VIGNETTE 1

A 74-year-old woman with a history of hypertension and diabetes is admitted to the hospital for right hip replacement. Postoperatively, her surgical team becomes increasingly concerned about her mood: she has been crying all the time, sleeping most of the day, refusing to work with rehabilitation services, not eating well, and endorsing a desire to “just give up.” A psychiatric consultation reveals significant disorientation to place and year and a belief that her family has “abandoned” her.

She cannot maintain attention during the assessment and falls asleep repeatedly. Physical examination demonstrates multiple primitive reflexes. A diagnosis of hypoactive delirium prompts a medical work-up that reveals a urinary tract infection. She is started on a 7-day course of ciprofloxacin and low-dose risperidone nightly. Over the next few days, her mental status progressively improves and risperidone is tapered off.

 

Major neurocognitive disorder

While delirium is frequently the culprit when a patient presents with acute neuropsychiatric decompensation in the hospital, major neurocognitive disorders, previously known as dementias, are important to consider, especially in elderly patients with subacute or prolonged neuropsychiatric decompensation. According to DSM-5, major neurocognitive disorder is diagnosed when there is evidence of significant cognitive decline that interferes with independence and impairment in cognitive performance; this decline does not occur exclusively in the context of delirium and is not better explained by another mental disorder. In addition to cognitive changes, many patients with major neurocognitive disorders have changes in affect, thought process, and behavior.

Alzheimer disease (AD) is the leading cause of major neurocognitive disorders; it is estimated to occur in 50% to 75% of those with dementia.3 Up to 88% of affected patients eventually have neurocognitive disorder–associated behavioral and psychiatric symptoms, including affect dysregulation, psychosis, and agitation. Of note, hallucinations in AD are more commonly visual compared with primary psychotic conditions, and delusions are often based in the faulty memories. Although antipsychotics have a black box warning regarding increased mortality and stroke in patients with dementia and psychosis and/or agitation, some patients might benefit from short-term carefully monitored administration of atypical antipsychotics.4 Acetylcholinesterase inhibitors, NMDA antagonists, and SSRIs might also be helpful with symptoms of agitation and restlessness.3

Frontotemporal dementia

Frontotemporal dementia (FTD) is a heterogeneous group of conditions with prominent early behavioral disinhibition. The mean age of onset is 52.8 years, and there is a striking male preponderance (14:3).3 It is divided into 3 clinical variants: frontal or behavioral variant, progressive non-fluent aphasia, and semantic aphasia. Patients with FTD often present first with behavioral alterations: either disinhibition and overactivity, or apathy and blunted affect.

The frontal variant of FTD is characterized by the insidious onset of personality changes, disinhibition, mood instability, behavioral abnormalities, and poor insight, associated with atrophy of the frontal lobes. Speech output is often impaired and progresses to mutism with time. The most noticeable cognitive deficits are impairment of executive function and working memory.

Progressive non-fluent aphasia is associated with asymmetric atrophy of the left hemisphere and is marked by agrammatic nonfluent speech and decreased speech output leading to mutism. Behavioral symptoms appear later.

Semantic aphasia is associated with bilateral atrophy of the middle and inferior cortices and is characterized by loss of word meaning and knowledge. Patients present with fluent speech, but impaired naming, less specific wording and, unappreciated by them, difficulty with comprehension. Behavioral symptoms may appear at any stage.

Brain imaging is helpful in distinguishing AD from FTD based on the difference in hypometabolism: temporoparietal regions are affected in AD and frontotemporal regions in FTD. Because there is evidence of less cholinergic deficit and more serotonergic disturbance in FTD compared with AD, serotonergic agents (such as SSRIs) might have a greater role than cholinergic agents in managing behavioral symptoms.

Dementia with Lewy bodies

Dementia with Lewy bodies represents up to 20% of all cases of major neurocognitive disorders. It is characterized by cortical and subcortical cognitive impairments; affected patients have worse visuospatial and executive functioning than those with AD.4 The diagnosis is based on the presence of a major neurocognitive disorder and an additional 2 of 3 features: spontaneous parkinsonism, hallucinations, and daily fluctuation in cognition.

Visual hallucinations consist of fully formed, detailed, 3-dimensional objects, people, or animals. Auditory hallucinations are uncommon. Patients with dementia with Lewy bodies often have REM parasomnia due to the loss of normal muscle atonia during REM sleep. When coupled with dream content, this results in aberrant muscle activity during dreams, ranging from increased muscle tone to acting out complex behaviors. REM sleep behavior disorder (RBD) can precede the onset of the neurodegenerative disorders by years and even decades, and can serve as a precursor.5 In fact, including RBD in diagnostic consideration of the disease significantly improves the sensitivity of the diagnosis. In addition, low dopamine transporter uptake on single-photon emission CT improves the sensitivity and specificity of the diagnosis of dementia with Lewy bodies compared with AD.

Dementia with Lewy bodies represents up to 20% of all cases of major neurocognitive disorders.

Acetylcholinesterase inhibitors might be helpful with cognition and hallucinations due to the cholinergic deficits in Lewy body disease. Avoid antipsychotics because patients with this disease are very sensitive to dopamine blockers as a result of dopamine deficiency. However, low-dose quetiapine or clozapine might be considered for those with persistent disturbing psychotic symptoms.

Other presentations

Other important dementias to consider include vascular dementia, chronic traumatic encephalopathy, and rapidly progressive dementias. In addition, mild cognitive impairment (MCI) is common in elderly patients: from 3% to 19% of adults older than 65 years are affected.6 It is defined as a cognitive decline greater than expected for an individual’s age but which does not yet interfere with activities of daily living. However, MCI is a risk factor for dementia, and at least 50% of patients with MCI progress to dementia within 5 years. Poor performance on delayed recall and executive function tests indicates a high risk of progression to dementia. In addition, behavioral symptoms, such as anxiety, depression, irritability and apathy, are often present in patients with MCI.

If there are any concerns about a patient’s cognition, the clinician should assess the patient with such validated measures as the Montreal Cognitive Assessment, which can be a first step in the cognitive evaluation.

Epilepsy

Seizures are another important CNS process that may have a neuropsychiatric presentation. Epilepsy represents a significant risk factor for the development of psychiatric symptoms. In addition, seizures can present with changes in mood, behavior, and thought process.

Epilepsy is the second most common neurologic disorder after headaches. At least 50 million people worldwide have recurrent, non-provoked seizures; age-adjusted rates range from 0.2% to 4.1%.7 The International League Against Epilepsy correlates clinical seizure type with ictal and interictal EEG changes. Generalized seizures manifest immediately and spread bilaterally through the cerebral cortex, resulting in loss of consciousness with no preceding motor or perceptual experience. The most common form of generalized seizures is tonic-clonic or grand mal seizures. Absence seizures or “staring spells” are another type of generalized seizures in children. These seizures are associated with loss of consciousness for only a few seconds, without a motor phase; they are usually characterized by bilateral and synchronous spike waves of 3 to 4 Hz amplitude.

Focal (partial) or localization-related seizures start in a specific focus, usually the cortex. They can be simple partial seizures, with no alteration of consciousness, or complex partial seizures, with altered consciousness. Moreover, they can have secondary generalization. Finally, status epilepticus is a continuous seizure state with 2 or more superimposed seizures and is a medical emergency.

Temporal lobe epilepsy

While the nomenclature of temporal lobe epilepsy is no longer officially recognized by the International League Against Epilepsy, it is helpful when used descriptively. Temporal lobe epilepsy-which arises from the hippocampus, parahippocampal gyrus, amygdala, and the neocortex on the outer surface of the temporal lobe-occurs in 80% of patients with localization-related epilepsy and is more commonly correlated with psychiatric presentations and comorbidities. Temporal lobe seizures are usually preceded by an aura (80% of cases), with a variety of psychiatric and somatosensory symptoms, including sensations of déjà vu and/or jamais vu, fear, visual illusions, unusual smells and tastes, depersonalization, and derealization. Ictal states are characterized by automatisms (eg, lip-smacking, chewing, swallowing, picking) and a trance-like state with semireactivity to the environment and no recollection of the events. The postictal period consists of confusion or dysphasia that lasts minutes to hours; on rare occasions it can last for days.

Frontal lobe epilepsy

The clinical presentation of frontal lobe epilepsy includes contralateral clonic movements, unilateral or bilateral tonic motor activity, and complex automatisms. The seizures are commonly nocturnal, abrupt in onset, short in duration, and associated with little or no postictal confusion. The yield of a surface EEG may be limited because of the difficulty in detection of mesial or basal foci. Some patients may be misdiagnosed as having nonepileptic events (ie, pseudo-seizures) because of their complicated motor movements and the failure of a surface EEG to capture the epileptiform correlates.

Occipital and parietal seizures

Occipital seizures are much less common than those of temporal or frontal origin. They usually manifest in visual hallucinations or illusions; forced blinking or eyelid flutters at the beginning have been described as well. Parietal seizures are the least common and are usually associated with sensory alterations, visuospatial disorientation, and apraxias.

Nonconvulsive status epilepticus

Nonconvulsive status epilepticus is an important entity to consider when a patient is evaluated for mental status changes. It is defined as a change in mental processes and behavior in association with continuous epileptiform changes on an EEG, without major motor signs, that lasts for at least 30 minutes. A clinical or EEG response to antiepileptic drug treatment helps confirm the diagnosis.

The changes in mental processes may be as subtle as a change in sense of humor or as severe as a coma. Nonconvulsive status epilepticus can be accompanied by very subtle neurologic findings, such as nystagmus, subtle tremor, or myoclonus; thus, a careful observation and neurologic examination are important to establish a correct diagnosis. Risk factors include a recent history of convulsive seizures; tumors; stroke; electrolyte abnormalities; and conditions and medications that predispose to posterior reversible encephalopathy syndrome, such as immunosuppressants, hypertensive crisis, preeclampsia, and eclampsia.

Epilepsy is the second most common neurologic disorder after headaches. At least 50 million people worldwide have recurrent, non-provoked seizures.

Psychosis in epilepsy

The incidence of psychosis in epilepsy ranges from 4% to 27%.8,9 Psychotic symptoms in epilepsy are categorized according to their temporal relationship to the seizures as ictal, postictal, or interictal psychoses. Ictal psychosis occurs concurrently with epileptic discharges and can last seconds to minutes and up to a few days to weeks when manifested as nonconvulsive status epilepticus. Symptoms include visual or auditory illusions and hallucinations, affective changes, agitation, fear, paranoia, notions of depersonalization/derealization, and a sense of autoscopy or “of someone behind.”

Postictal psychosis occurs in 2% to 8% of patients with epilepsy.8 It is characterized by a lucid interval of 2.5 to 48 hours (up to 1 week) between the last seizure and the onset of psychosis. It might be accompanied by some clouding of consciousness and psychotic symptoms (eg, delusions, hallucinations, catatonia), as well as prominent affective symptoms. First-rank schizophrenia and negative symptoms are absent. The initial symptoms include elevated mood or emotional lability, derealization, and irritability. Symptoms usually resolve within hours (up to 70 hours), aided by low-dose antipsychotic treatment. There might be an increase in the frequency of secondarily generalized tonic-clonic seizures that precedes the onset of postictal psychosis. Nonconvulsive status epilepticus should be considered and ruled out in some cases. Postictal psychosis is a self-remitting condition in most cases, but patients in the midst of it can be violent and agitated. Acute treatment includes benzodiazepines and antipsychotics with seizure management with anticonvulsants.

Chronic interictal psychosis occurs between seizures and most commonly manifests as schizophrenia-like psychosis. It emerges 10 to 15 years after the onset of epilepsy in 2% to 10% of patients and is virtually indistinguishable from schizophrenia. First-rank criteria symptoms are usually absent, and there are more negative symptoms of isolation, affective blunting, and social drift. There is a special, but not exclusive relationship with temporal lobe epilepsy. No specific treatment guidelines exist for schizophrenia-like psychosis of epilepsy, and it is treated in line with well-established protocols for primary schizophrenia and related psychotic illnesses.10

CASE VIGNETTE 2

A 61-year-old man with hypertension is brought to the emergency department because of changes in his mood and behavior. His family explains that during the past 3 days the patient seemed confused and disorganized and said that he did not want to live any longer. A psychiatric consultation is obtained for suicidal ideation. The patient is disoriented, overwhelmed, and perplexed with tangential and disorganized thought processes. He states that he “can no longer go on like this.” He complains of headache and blurry vision. His examination reveals bilateral grasp and palmomental reflexes. His blood pressure is 195/95 mm Hg.

Because of the patient’s confusion and physical complaints and findings, medical and neurologic consultations are also obtained. A head CT scan shows no acute abnormalities. EEG monitoring reveals epileptic events. The diagnosis is hypertensive emergency with nonconvulsive seizures. Within 3 days of treatment with blood pressure medication and anticonvulsant agents, his mental status normalizes and he exhibits euthymic mood with no suicidal ideation.

 

Traumatic brain injury

TBI is a significant individual and public health problem worldwide. Approximately 5.3 million people (2% of the US population) live with disabilities resulting from a TBI.11 Originally TBI severity was based on the Glasgow Coma Scale, in which the lowest post-resuscitation score of 3 to 8 is severe TBI, 9 to 12 is moderate, and 13 to 15 is mild. Although this scoring is useful for predicting mortality, it is not as helpful for predicting level of disability and neurobehavioral outcomes.

The American Congress of Rehabilitation Medicine created a more useful definition of mild TBI, which requires loss of consciousness of 30 minutes or less, posttraumatic amnesia of 24 hours or less, and any alteration of mental state at the time of injury or a focal neurologic deficit, in addition to a score of 13 to 15 on the Glasgow Coma Scale.11

Patients with TBI can present with depression, apathy, fatigue, difficulty with concentration, mania, anxiety, irritability, agitation, and aggression, as well as psychosis and substance use disorders.

TBI causes primary and secondary damage, which leads to neurologic dysfunction and neuropsychiatric sequelae. Primary damage consists of immediate insults, such as skull fractures, brain hemorrhages, and diffuse axonal injury caused by shearing forces. Secondary damage often begins at the time of the injury but progresses over time. Biochemical changes are a part of the secondary damage. In the acute phase after the injury, an increase in brain metabolism results in excess activity of multiple neurotransmitters, including acetylcholine, dopamine, norepinephrine, and glutamate, which can be neurotoxic and lead to apoptosis and neuronal dysfunction. This stage is followed by the subacute phase of reversal and biochemical hypoactivity, which contributes to multiple neuropsychiatric presentations. As a result of primary and secondary damage, patients with TBI often present with cognitive, mood, and behavioral complaints.

In the acute setting during hospitalization, agitation in patients with TBI is frequently a pressing symptom. Posttraumatic amnesia is common in patients who were comatose following a TBI and then regained consciousness.12 This subtype of delirium is characterized by generalized cognitive disturbances with confusion, disorientation, retrograde amnesia, inability to store new memories, and sometimes agitation and delusions. Treatment includes behavioral interventions, ensuring the patient feels safe and calm, limiting disturbing and distracting sensory inputs, and frequent orientation.

The use of antipsychotics has been controversial. Animal studies have suggested worse outcomes on motor tasks as well as delays in cognitive recovery.12 However, this concern should be weighed against the risks of severe agitation. In the acute setting, antipsychotics might be an appropriate and indicated intervention. If antipsychotics are warranted, atypical antipsychotics (especially quetiapine and aripiprazole) with less dopamine blockade and potentially less proglutamatergic activity are preferred. Valproic acid can also be considered, especially given its antiglutamatergic, anti-inflammatory, antiapoptotic, and neuroprotective effects.13 Depending on the patient and the situation, other potentially beneficial interventions for agitation are beta blockers, alpha-2 agonists, stimulants, amantadine, and antidepressants.12,14

After a TBI, psychiatric disorders are common. However, it is difficult to establish a direct causal relationship because premorbid psychiatric disorders2 increase the risk of TBI; common third factors, such as substance abuse, are frequently involved; and TBI causes not only structural and biochemical changes but also psychosocial effects.11 Patients with TBI can present with depression, apathy, fatigue, difficulty with concentration, mania, anxiety, irritability, agitation, and aggression, as well as psychosis and substance use disorders.

Well-designed studies on the treatment of neuropsychiatric symptoms following TBI are lacking. The main principle in the pharmacologic treatment of these patients is to “start low and go slow.” For depression, SSRIs, such as sertraline, citalopram, and escitalopram, are the first choice. For anxiety, buspirone and SSRIs might be effective with limited adverse effects. Amantadine can be helpful for cognitive recovery, concentration, and irritability. Stimulants can help with arousal, apathy, and fatigue. Anticonvulsants, such as carbamazepine and valproic acid, can be effective for irritability, agitation, and mania. Most importantly, patients with TBI should undergo careful evaluation and monitoring and be offered a wrap-around array of rehabilitation and therapeutic services.

Other disorders

Headaches

Findings indicate increased comorbidity between migraines and psychiatric syndromes, including mood and anxiety disorders.15,16 The presence of an anxiety spectrum disorder may be a risk factor for migraine chronification (ie, transition from episodic to chronic migraines).15 It is important to appreciate that vestibular migraines-characterized by episodic symptoms of dizziness, imbalance, and nausea-are frequently mistaken for panic attacks. In fact, psychiatric disorders are found in approximately 65% of patients with vestibular migraine.17 Theories that explore this relationship have been investigated, including serotonin dysfunction, estrogen levels, and hypothalamic-pituitary-adrenal axis dysregulation.

Autoimmune encephalitis

Although autoimmune encephalitis (AE) was initially thought to be rare, new data suggest that this condition is actually more common but is infrequently tested for.18 Paraneoplastic AE is a constellation of symptoms that are the consequence of humoral factors (hormones or cytokines) excreted by tumor cells or by an immune response against the tumor itself. The most common cancers associated with paraneoplastic AE are breast, lung, lymphatic system, ovary, pancreas, and prostate. In almost 50% of cases no tumor is identified. The symptoms of AE may be grouped into 4 categories: seizures, memory problems, cognitive dysfunction (of which memory disturbances are prominent), and mood (eg, depression) and behavioral changes (eg, personality changes, irritability). Symptoms often appear before a primary tumor has been identified.

The diagnosis of AE requires a high level of suspicion, especially in cases of atypical psychiatric presentation. The diagnosis is made more certain with the presence of antineuronal antibodies, which often allows for early detection of the associated tumor. Because of the possibility of herpes simplex virus encephalitis as part of the differential diagnosis, most patients with subacute AE are treated with acyclovir. If identified, malignancies are treated according to the standard of care for the primary cancer diagnosis (eg, surgical resection, chemotherapy, radiation therapy). There is still no standard of care with regard to immunotherapy. The most commonly used treatments are intravenous corticosteroids (eg, methylprednisolone), plasmapheresis, and/or intravenous immunoglobulin. In cases of poor or no response, cyclophosphamide and/or rituximab may be considered.

Infections

A multitude of infectious processes can present with neuropsychiatric symptoms, including neurocysticercosis, tuberculosis, pediatric autoimmune neuropsychiatric disorder associated with streptococcal infection, Lyme disease, herpes encephalitis, hepatitis C, and HIV infection. A comprehensive history; mental status, cognitive, neurologic, and physical examinations; and additional complaints (eg, headache, neck stiffness) and risk factors usually lead to the correct diagnosis.

CASE VIGNETTE 3

A 62-year-old Navy veteran with a history of hypothyroidism, obstructive sleep apnea, and poorly controlled diabetes complicated by neuropathy presents to his primary care physician. He reports increased difficulty in walking and shooting pains in both of his lower extremities over the past 2 months, which has led him to feel depressed about his health. He states that he can no longer trust anyone, and as a result he prefers to be alone.

His physical examination is significant for hyporeflexia, upper extremity hypotonia, and pupillary abnormality. These new-onset neurologic symptoms prompt serum and cerebrospinal fluid (CSF) studies, which reveal lymphocytosis, elevated protein, and a positive CSF VDRL test. Neurosyphilis is diagnosed, and the patient is admitted for a 14-day course of intravenous penicillin.

 

Conclusions

Psychiatrists often serve as a gateway to a correct diagnosis in patients with a neuropsychiatric presentation. Neuropsychiatric symptoms are common in many disorders of the CNS, as well as in systemic metabolic, endocrine, autoimmune, and infectious processes that affect the CNS. Psychiatrists are consulted for the diagnosis and management of these symptoms. Detailed neurocognitive and neurologic examinations, medical history from the patient and collateral providers, and knowledge of disorders that present with neuropsychiatric symptoms allow the psychiatrist to develop a comprehensive differential. Collaboration with other services and further laboratory, imaging, and EEG work-up when necessary will help with making the correct diagnosis and planning appropriate treatment.

 

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Disclosures:

Dr Sher is Assistant Clinical Professor of Psychiatry, Dr Garcia is Clinical Instructor in Psychosomatic Medicine, and Dr Maldonado is Associate Professor of Psychiatry, Internal Medicine, Surgery and Law, Stanford University Medical Center, Stanford, Calif.

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