Psychosomatics 48:461-466, November-December
doi: 10.1176/appi.psy.48.6.461
© 2007 Academy of Psychosomatic Medicine
Antiemetics, Akathisia, and Pregnancy
Mark T. Wright, M.D.
Received October 9, 2006; revised October 26, 2006; accepted November 1, 2006. From the Dept. of Psychiatry and Behavioral Medicine, Medical College of Wisconsin, Milwaukee, WI. Send correspondence and reprint requests to Mark T. Wright, M.D., Dept. of Psychiatry and Behavioral Medicine, Medical College of Wisconsin, 8701 Watertown Plank Rd., Milwaukee, WI 53226. e-mail: mwright{at}mcw.edu
© 2007 The Academy of Psychosomatic Medicine
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ABSTRACT
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Gastrointestinal disorders are common in pregnant women. These disorders are often treated with antiemetic medications that block central dopaminergic neurotransmission. Dopamine antagonists can cause akathisia. Hormonal changes and other factors may place pregnant women at increased risk for the development of severe antiemetic-induced akathisia. The mental symptoms that can accompany akathisia can be misinterpreted as primary mental illness. The author reports on the case of a pregnant woman who attempted to injure herself after developing severe antiemetic-induced akathisia.
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INTRODUCTION
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Gastrointestinal disorders are common in pregnant women, with up to 85% experiencing gastroesophageal reflux disease (GERD) and/or nausea and vomiting of pregnancy (NVP).1,2 NVP usually begins during the first 8 weeks of gestation. Severe NVP is termed hyperemesis gravidarum and occurs in 0.5%–2% of pregnancies.2 Hyperemesis gravidarum can lead to significant maternal dehydration and weight loss and occasionally to life-threatening conditions related to vomiting and malnutrition, such as esophageal rupture and Wernicke’s encephalopathy. NVP is probably undertreated; it is the most common reason for hospital admission in early pregnancy.2 GERD and NVP can be prevented and treated with a number of nonpharmacological and pharmacological interventions.1–4 Dopamine antagonists, such as the benzamides trimethobenzamide and metoclopramide, the phenothiazines promethazine and prochlorperazine, and the butyrophenone droperidol are commonly prescribed for NVP despite a paucity of randomized, controlled trials in this population.2
Akathisia is an extrapyramidal movement disorder characterized by a subjective sense of restlessness and associated movements.5,6 Individuals with akathisia often experience severe inner tension and a need to move, most prominently experienced in the legs. This subjective experience is associated with restless movements, including an inability to remain lying or seated, pacing in place (tasikinesia), leg-crossing and uncrossing, and shifting weight from foot to foot.5,6 Akathisia can be associated with a variety of mental symptoms, including anxiety, fear, panic, anger, rage, depression, psychosis, and depersonalization.7–11 An association between suicidality and aggression and medication-induced akathisia has been reported, but the nature of this association is unclear.10,12–18 Mental symptoms and violent ideation or behavior often lead to individuals with akathisia being misdiagnosed with primary mental disorders. Akathisia can be seen with diseases associated with impairment in dopaminergic neurotransmission, such as Parkinson’s disease, but it is most commonly caused by dopamine-antagonist medications. Akathisia can occur acutely after treatment with a dopamine antagonist; tardive akathisia, a phenomenon analogous to tardive dyskinesia, can occur after long-term use of a dopamine antagonist.6 Akathisia associated with dopamine-blocking antipsychotic/mood-stabilizing medications is well known to psychiatrists. Akathisia can also be seen with serotonergic antidepressants, possibly as a result of serotonin’s inhibitory effect on dopaminergic neurotransmission.19 In addition to psychotropic medications, akathisia can be seen with dopamine-blocking medications used in other areas of medicine. Dopamine-antagonist antiemetics, such as prochlorperazine and promethazine are known to cause akathisia.20,21 Metoclopramide has been reported to cause akathisia in pregnant women.22,23 What follows is an illustrative case report of a woman with hyperemesis gravidarum who developed severe antiemetic-induced akathisia and subsequently harmed herself.
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Case Report
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A 22-year-old Hispanic woman developed severe nausea and vomiting during the first 6 weeks of her seventh pregnancy. She had had mild nausea with her previous pregnancies, but never used antiemetic medication. At approximately 6 weeks estimated gestational age (EGA), the patient’s primary physician prescribed ranitidine 150 mg. twice per day, prochlorperazine 10 mg. per day, and promethazine 25 mg. 4 times per day, as needed.
Around the time she began taking these medications, the patient developed episodes lasting several hours to a full day characterized by severe restlessness and a need to move. The patient said that she would alternately sit, lie down, pace, and run, with minimal relief. When asked about associated symptoms, she reported a tremor, hot and cold flashes, sweats, palpitations, shortness of breath, and dizziness. The patient said that when her symptoms were severe she cried and felt "not peaceful," "possessed," and "desperate." She also reported feeling depressed in association with these symptoms. She denied having any hallucinations.
Two days before her admission, the patient was seen at another hospital for dehydration and depression with mild suicidal ideation. She was given intravenous fluids and a prescription for an antidepressant and sent home. After returning home, the patient’s severe distress continued, and this led her to jump from a third-story balcony. When evaluated by paramedics at the scene, the patient was found to be alert and oriented and to have a Glasgow Coma Scale score of 15 (best score). Hospital evaluation revealed a viable 9-week estimated gestational age (EGA) pregnancy and a compression fracture of the first lumbar vertebra. A pulmonary embolus in the upper lobe of the right lung was incidentally noted. When seen by the psychiatry service and questioned about her jump, the patient said that she jumped impulsively, hoping that this would terminate her intense restlessness. The patient explained that she thought severe pain or seeing her own blood would lessen her restlessness; she denied jumping in an attempt to kill herself or harm her fetus.
In reviewing past psychiatric symptoms, the patient reported a history of childhood sexual abuse and said that, in the past, she had had distressing memories of her abuse while having intercourse with her ex-husband. She reported ongoing mild distress with reminders of her abuse, and minor flashbacks during arguments with her boyfriend; she denied other posttraumatic stress disorder (PTSD) symptoms, including nightmares, hypervigilance, and an excessive startle response. The patient felt that distress related to her abuse had greatly lessened in recent years, and she remarked that she had seen one of her abusers on several occasions and felt no distress. The patient’s past psychiatric history was also notable for an overdose of aspirin at age 12 in the face of situational stress. She said that this had led to a short stay in a psychiatric hospital, where she did not receive any psychotropic medications.
The patient’s earlier medical history also included GERD, one spontaneous abortion, and two surgical abortions. She reported smoking three packs of cigarettes per week for 5 years, but said she had stopped smoking 6 weeks before her admission because of her pregnancy. She also acknowledged sporadic alcohol and cocaine use but said that she had had neither in 3 weeks.
The patient’s family history was positive for "schizophrenia" in a sister and "depression" in the patient’s mother (who also has diabetes mellitus) and aunt (during treatment for cancer). The family history was negative for anxiety and suicide.
The patient had three children, ages 9, 7, and 5 years. She was "excited" about her pregnancy. The patient reported that the father of her fetus was very controlling and mildly physically abusive, and she was somewhat reluctant to continue her relationship with him.
Physical and mental status examination revealed an obese young woman. She was alert and cooperative. Her affect was mildly dysphoric. Her speech was normal. No psychotic signs were noted. Laboratory testing revealed a mild microcytic anemia, a thyroid-stimulating hormone (TSH) level of 0.249 (normal range: 0.350–5.500 mIU/mL), and a toxicology screen positive for opiates (given because of spine pain).
The patient was given a working diagnosis of medication-induced movement disorder, not otherwise specified (DSM–IV: 333.90). Mild improvement in her restlessness was noted when she was given Valium 2 mg. Her nausea and vomiting were initially treated with droperidol, but after a working diagnosis of medication-induced akathisia was made, the patient was switched to ondansetron with good results. The patient was treated with enoxaparin for her pulmonary embolus. On the 3rd hospital day, the patient was deemed medically stable. Because her intense restlessness led to impulsive self-harm, and because the restlessness had not totally resolved, it was decided that psychiatric hospitalization would be in the best interest of both the patient and her fetus. She agreed, and was transferred to an inpatient psychiatric unit.
The patient was readmitted 10 days later with shortness of breath. She was taking fluoxetine 20 mg. per day and trazodone 50 mg. at bedtime; she had not been compliant with her anticoagulant medication. The patient was noted to have no thyromegaly. She was again found to be anemic. Her TSH was low, at 0.186; her free T4 was 1.11, and her free T3 was 2.8, both normal values. When the patient was discharged 3 days after admission, her fluoxetine had been increased to 40 mg. per day, and her trazodone had been increased to 100 mg. at bedtime by her primary physicians. She was given dolasetron for nausea.
Nine days later, the patient was again admitted with nausea and vomiting, complicated by dehydration and hypotension. She again complained of anxiety, depression, and restlessness, but denied suicidal ideation. She had recently been evaluated in a psychiatric emergency facility; the results of that evaluation were unknown. The patient was still taking fluoxetine and trazodone. She had been unable to fill her prescription for dolasetron. Lab studies revealed a microcytic anemia, a blood-urea nitrogen of 2, ketonuria, and a TSH within normal limits, at 0.426 mIU/mL. Cranial CT scan was negative. The patient was started on an iron supplement at this time.
Five months later, the patient was taking fluoxetine, enoxaparin, and hydrocodone, and was using diphenhydramine and dolasetron for nausea and vomiting. At 36 weeks EGA, labor was induced, and the patient delivered a male infant without difficulty.
Differential Diagnosis
The differential diagnosis of our patient’s neuropsychiatric illness included a number of disorders. The patient was initially thought to have panic attacks and depression precipitated by her situational stressors. PTSD was also considered, given the patient’s report of sexual abuse in childhood and subsequent reexperiencing symptoms, as well as her ongoing abusive relationship. Psychosis and culture-bound syndromes were considered when the patient stated that she felt "possessed." We considered a nicotine-withdrawal syndrome, given the patient’s report that she had abstained from smoking for several weeks. Borderline personality disorder was considered, given the history of two episodes of impulsive self-harm. Anxiety caused by hypoxia from pulmonary emboli was considered, as was anxiety due to hyperthyroidism.
Our patient received a diagnosis of antiemetic-induced akathisia for several reasons. Her core symptoms were severe restlessness and a need to move, complaints that are central to akathisia. The patient had never experienced these symptoms before and felt that they were ego-alien.18 The patient’s symptoms correlated with the use of phenothiazine antiemetics known to cause akathisia and could have been worsened by the droperidol she received while hospitalized. Although the patient endorsed several symptoms seen with panic attacks and depression, this picture was not felt to be inconsistent with a diagnosis of akathisia even though patients with akathisia have been known to report symptoms of panic and depression.8,9,22 The long duration of the patient’s episodes of distress was not suggestive of panic attacks. The patient did have a history of PTSD symptoms but felt that these symptoms were minimal at the time that her episodes of restlessness began.
She denied hallucinations and had no clear signs of psychosis on examination. Nicotine withdrawal was felt to be unlikely since her symptoms began approximately 2 weeks after she had stopped smoking. Although the patient’s TSH was low, her physical examination and other thyroid laboratory tests were not consistent with hyperthyroidism. Women with hyperemesis gravidarum often have high levels of human chorionic gonadotropin (hCG), and hCG, which is structurally similar to TSH, can cause increased secretion of thyroid hormones and a related decrease in TSH release.24
Are Pregnant Women at Increased Risk for Akathisia?
A number of factors may place pregnant women at increased risk for the development of severe medication-induced akathisia with mental symptoms. Relationship problems and other social factors associated with pregnancy can cause significant stress,25 and stress-induced anxiety and depression could be amplified by the severe distress often associated with akathisia. Pregnancy is a time of increased iron requirements, and many pregnant women develop iron deficiency. Studies mainly involving patients with mental disorders have suggested a negative correlation between serum-iron status and medication-induced akathisia, but conflicting results have been reported.26–30 Folate deficiency has been correlated with restless legs syndrome (RLS), a syndrome similar to akathisia, in pregnant women,31 and could also predispose to the development of medication-induced akathisia. Since many women abstain from use of substances after learning they are pregnant, the risk of substance-withdrawal is elevated in this population; the anxiety and dysphoria associated with some of these syndromes may be significantly worsened by the distress that can accompany akathisia. Approximately 25% of pregnant smokers stop smoking at some time during pregnancy, and most of these stop during the first trimester.32 Nicotine-withdrawal is associated with a decrease in mesolimbic dopaminergic activity,33 and a recent study suggested that a decrease in striatal dopaminergic activity might also take place.34 This decrease in dopaminergic activity could cause dysphoria and motoric agitation that could be worsened by a dopamine-antagonist antiemetic.
Several lines of evidence suggest that the hormonal changes of pregnancy could inhibit nigrostriatal and other dopaminergic neurotransmission and make pregnant women more susceptible to medication-induced akathisia. In animal studies, estrogen has been shown to block tuberoinfundibular dopamine release as well as dopamine agonist-induced acetylcholine accumulation in the striatum.35–37 In clinical studies, estrogen has been shown to decrease the efficacy of dopamine agonists in treating prolactinomas.38 In population studies of patients with schizophrenia, women have been shown to have a later age at onset than men, to have a second onset peak around the time of menopause, and to have improvement of symptoms with pregnancy; all of these findings could indicate an inhibitory effect of sex hormones on dopaminergic neurotransmission.39 Pregnancy has been shown in some studies to have a negative effect on the symptoms of Parkinson’s disease,40 and progesterone has been associated with parkinsonism.41 Pregnant women are at increased risk for the development of RLS.42 It has been estimated that up to 26% of pregnant women develop RLS or a worsening of preexisting RLS. The risk for RLS increases into the third trimester and then drops significantly at delivery. Although RLS can be associated with iron deficiency, the improvement in pregnancy-related RLS after delivery and its attendant blood loss argues against iron deficiency as the sole etiology; decreasing hormone levels are likely the cause of postpartum improvement. Individuals with RLS may be at increased risk for the development of medication-induced akathisia,43 possibly because of a shared underlying pathogenesis (e.g., decreased dopaminergic neurotransmission). A case report of dystonia occurring in early pregnancy44 also supports the idea of impaired dopaminergic neurotransmission. Estrogen has also been shown to increase medication-induced parkinsonism.45–47 It should be emphasized, however, that the relationship between sex hormones and dopaminergic neurotransmission is a complex one, and some studies have suggested facilitation of dopaminergic activity by these hormones.48
If estrogen has a negative effect on nigrostriatal and tuberoinfundibular dopaminergic activity, this could have an effect on locomotion and maternal behaviors via multiple pathways (Figure 1). Impaired nigrostriatal dopaminergic neurotransmission could cause an increase in motor activity, as seen in akathisia. Decreased tuberoinfundibular dopamine release increases prolactin,49 and prolactin has a significant effect on the hypothalamic medial preoptic area (mPOA) in pregnancy.50 In rat studies, the mPOA has been shown to send projections to the ventral tegmental area51 and the pedunculopontine nucleus,52 areas that play important roles in locomotion. The mPOA has been shown in animals to be crucial for the production of maternal behaviors such as nesting, foraging, and protection of offspring from predators.53 An increase in locomotor readiness may underlie all of these behaviors. Given this, it is possible that an ability to decrease dopaminergic neurotransmission during pregnancy has been favored by natural selection, since this could result in behaviors conducive to the rearing of offspring. The development of antiemetic-induced akathisia in pregnant women may serendipitously reveal a physiological process integral to childrearing.
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FIGURE 1. Possible Routes by Which Pregnancy-Related Hormonal Changes Might Affect Dopaminergic Activity, Locomotion, and Maternal Behavior
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Treatment of Akathisia in Pregnancy
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Treatment of antiemetic-induced akathisia in pregnant women should begin with lowering the dose or discontinuation of the offending medication. Fortunately, newer antiemetics, such as dolasetron, ondansetron, and granisetron, are now available; these medicines are well tolerated in pregnancy, and because they are serotonin (5HT3)-receptor (and not dopamine-receptor) antagonists, they do not cause akathisia.
Medications used in the treatment of pregnancy-related GERD and NVP also include ginger, pyridoxine, H1-blockers (e.g., doxylamine), H2-blockers, and proton-pump inhibitors.1,2 Because drug-induced akathisia can be severe and persist for some time after the offending drug is stopped,9 some patients may require pharmacologic treatment of akathisia. Benzodiazepines, antihistamines, anticholinergic medications, beta-blockers, and dopamine agonists have been used traditionally to treat drug-induced acute akathisia. The effectiveness of these medications is unclear, however,54–56 and some drugs (e.g., benzodiazepines) may pose risks to the fetus that would contraindicate their use.
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CONCLUSION
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Professionals involved in the care of pregnant women should be aware when treating nausea and vomiting that older antiemetic medications such as metoclopramide and the phenothiazine antiemetics are central dopamine blockers and can cause akathisia. Factors associated with pregnancy may place women at increased risk for medication-induced akathisia. Medication-induced akathisia should be included in the differential diagnosis of neuropsychiatric disorders in pregnancy, and proper diagnosis is essential, since some psychotropic medications, like selective serotonin reuptake inhibitors (SSRIs), could worsen akathisia. Akathisia can cause severe distress, and pregnant women with akathisia are at risk for harming themselves and their fetuses. Because a thorough cost/benefit analysis, in which drug efficacy, side effects, cost, and teratogenic risks has yet to be done, a universal recommendation to treat pregnant women only with 5HT3-blocking antiemetics should not be made now. Before prescribing dopamine-blocking antiemetics for pregnant women, however, physicians should screen for risk factors for severe akathisia and closely monitor patients treated with these medications.
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ABSTRACT
INTRODUCTION
