The wilting widow’s masquerading illness

Current Psychiatry. 2008 August;07(08):68-74

August 1, 2008|Current Psychiatry

Mrs. D seems depressed since being treated for sepsis, and she has abrupt episodes of unresponsiveness and confusion. What’s causing these events?

EVALUATION: Continuing decline

The emergency room staff learns Mrs. D has a history of vague auditory hallucinations and has developed more overt paranoia, including thoughts that police may be out to harm her. She has difficulty responding to questions and can not offer details of her history; her speech is soft and her thought process appears slowed.

Mrs. D is admitted to the inpatient psychiatry service. Her family reports that she has episodes of disorientation, poor memory, staring, and paranoia about the police that last minutes to 1 hour.

Clinical Point

Although Mrs. D’s symptoms might be psychogenic, somatization disorders rarely develop late in life

On initial examination, she is poorly oriented. MMSE is 12/30, indicating a dramatic change in cognition from a week ago, and language impairment severely affects bedside cognitive testing. Her speech is perseverative: she repeats the phrase, “yes, very good, uh hum.” Later, she has difficulty speaking clearly. She attempts to answer questions but her speech is garbled. She can follow commands but cannot speak or do verbal repetitions.

On a subsequent examination 1 hour later, her speech difficulties are variable. She cannot speak fluently, has limited ability to repeat phrases, and cannot follow simple verbal commands. These symptoms persist only minutes. Mrs. D slowly becomes more conversant but appears tired. During the next few hours she is disoriented and tries to walk into the nursing station. Other repetitive activity includes putting on/taking offmultiple layers of clothing.

The authors’ observations

Clinical Point

A normal EEG does not guarantee the absence of recent seizures

Although EEG is important for distinguishing an atypical psychiatric presentation from seizures, carefully consider the patient’s history and symptoms before you look to the EEG for diagnosis because:

A normal EEG does not guarantee the absence of recent seizures; a standard scalp EEG can miss epileptiform changes that may occur earlier in the ictal phase.⁹
EEG abnormalities may occur in normal subjects.

O’Sullivan¹⁰ recommended performing an EEG only in the presence of an “organic factor,” such as a recent known or suspected convulsion, recent head trauma with more than momentary loss of consciousness, or a known CNS disorder. Exam findings that warrant EEG include:

visual, olfactory, or tactile hallucinations
mutism
catatonia
poor memory not due to inattention
episodic aphasia, apraxia, or agnosia.

Because only 50% to 70% of patients with recurrent seizures will have epileptiform activity on a single interictal EEG,¹¹ repeat studies are useful, especially if they include activation procedures and sleep deprivation.

Mrs. D’s confusion level and speech abnormalities varied over time. Her speech arrest early in the admission appeared to be a Broca’s or expressive aphasia because she comprehended commands but was unable to speak. Later, her speech exhibited a mixed transcortical aphasia pattern—she was unable to speak or comprehend, but retained some ability to repeat. The changing aphasia patterns and the often abrupt starting and stopping of these symptoms were the clues that an active process was occurring, suggesting that seizures should be considered.

DIAGNOSIS: Irrefutable EEG evidence

Mrs. D receives another neurology consult. An EEG shows spike and wave discharges in both frontal lobes consistent with nonconvulsive status epilepticus (NCSE). During these bursts, the neurologist notes speech arrest and altered alertness. Phenytoin loading is administered as a single 800-mg oral dose followed by 100 mg twice daily, and Mrs. D is transferred to the neurology unit for further stabilization.

The authors’ observations

When evaluating whether a psychiatric presentation reflects an underlying general medical or neurologic disorder—including seizures—consider the clinical features outlined in Table 2.¹²

In Mrs. D’s case, several factors supported the diagnosis of depression. She had numerous depressive symptoms, including depressed mood, social withdrawal, low energy, poor sleep, and “scattered mind,” which the psychiatrist interpreted as poor concentration. Interestingly, she attributed her dramatic episode of mutism and unresponsiveness in the hospital to being depressed. Mrs. D also had a personal and family history of depression; she had experienced a possible major depressive episode in her late 20s but was never treated, and her brother had depression.

Several features of her presentation were atypical, however, and suggested a medical etiology. Her family described the onset of her symptoms as abrupt, and she declined rapidly. Mrs. D’s concern about her estate had no connection with reality, and she became more psychotic. The dramatic episode of decreased responsiveness that led to her intubation was both peculiar and brief.

Clinical Point

Changing aphasia patterns and abrupt starting/stopping of symptoms were clues that an active process was occurring

Following the initial neurologic consultation, the medical team did not carefully consider seizure because Mrs. D appeared depressed. The neurology team was quick to ascribe her episodes as psychosomatic and mood-related after an episode occurred in the presence of Mrs. D’s daughter. The psychiatry consultants did not uncover major conflicts or psychological crises that could explain her presentation but also focused heavily on her depressive history.

References

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