# Situation: A 22-year-old man with a first episode of psychosis is admitted to an acute psychiatric unit. He receives haloperidol 5 mg intramuscularly (IM) for severe agitation and is then started on oral haloperidol. On day 12, two days after his oral haloperidol dose was increased, he paces the hallway, rocks from foot to foot while standing, and cannot stay seated through a meal. He says, "My legs won't let me sit still." His hallucinations have decreased. Which problem is MOST likely?

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> subject: Nursing Practice V — Care of Clients with Maladaptive Patterns of Behavior; Care of Clients with Life-Threatening Conditions, Acute Multi-Organ Problems, High Acuity and Emergency Situations

## 문제

Situation: A 22-year-old man with a first episode of psychosis is admitted to an acute psychiatric unit. He receives haloperidol 5 mg intramuscularly (IM) for severe agitation and is then started on oral haloperidol.

On day 12, two days after his oral haloperidol dose was increased, he paces the hallway, rocks from foot to foot while standing, and cannot stay seated through a meal. He says, "My legs won't let me sit still." His hallucinations have decreased. Which problem is MOST likely?

## 보기

1. Anxiety from worsening psychosis
2. Tardive dyskinesia from dopamine blockade
3. Akathisia from dopamine blockade **✔ 정답**
4. Parkinsonism from dopamine blockade

**정답: 3**

## 해설

Akathisia is a subjective inner restlessness with an urge to move, often felt in the legs, appearing days to weeks after starting or increasing an antipsychotic. Timing after a dose increase and improving psychosis point to a drug effect rather than anxiety. It can raise suicide risk and is reported for dose reduction or other treatment.

## 심화 해설

Core mechanism

Haloperidol is a first-generation antipsychotic whose primary action is dopamine D2 receptor blockade. In the nigrostriatal pathway, this blockade produces the spectrum of extrapyramidal symptoms (EPS): acute dystonia, drug-induced parkinsonism, akathisia, and tardive dyskinesia [2]. The patient’s presentation—pacing, rocking foot-to-foot, inability to remain seated, and the statement “My legs won’t let me sit still”—is the classic motor picture of akathisia. Akathisia is defined by a subjective feeling of inner restlessness accompanied by an observable urge to move, most often experienced in the legs. [3][4]

Why this is akathisia, not anxiety or worsening psychosis

The timing is decisive. The patient’s oral haloperidol dose was increased two days before the restlessness appeared, and akathisia typically emerges days to weeks after initiation or dose escalation of an antipsychotic [4]. Equally important, his hallucinations have decreased. Worsening psychosis would not selectively improve positive symptoms while producing isolated motor restlessness; a drug-induced effect is far more consistent with this clinical trajectory. Anxiety from psychosis is a possible consideration, but the objective motor signs—pacing, shifting weight, inability to stay seated through a meal—are more specific for akathisia than for anxiety alone.

Differentiating the EPS subtypes

| Feature | Akathisia | Parkinsonism | Tardive dyskinesia |
| --- | --- | --- | --- |
| Onset after dose change | Days to weeks | Days to weeks | Months to years |
| Core motor sign | Restlessness, pacing, inability to sit still | Bradykinesia, rigidity, tremor, shuffling gait | Involuntary choreoathetoid movements (face, tongue, limbs) |
| Subjective distress | Marked inner restlessness and urge to move | Usually less prominent subjective urge to move | Often less distressing or unnoticed by patient |
| Response to dose reduction | Often improves | Often improves | May persist or worsen |

Key point! The patient’s dominant symptom is an urge to move with visible motor restlessness, not slowness, rigidity, or involuntary writhing movements. That pattern is akathisia, not parkinsonism or tardive dyskinesia.

Pathophysiology link to the basal ganglia

Akathisia has been linked to dopamine D2 receptor blockade in the basal ganglia . Functional imaging in a case of clinically manifest akathisia demonstrated bilateral putaminal hypermetabolism on [18F]FDG PET, supporting the view that akathisia is not simply a psychological reaction but a neurobiological consequence of altered basal ganglia activity . This helps explain why the symptom can be so distressing and why it may not respond to reassurance alone.

Clinical significance for nursing care

Akathisia is not a minor nuisance. It is associated with significant distress, can impair treatment adherence, and has been linked to increased suicide risk. [2][4] In a patient already vulnerable during a first psychotic episode, unrecognized akathisia may be misinterpreted as agitation or worsening illness, leading to an inappropriate antipsychotic dose increase. The correct nursing response is to recognize the motor pattern, report it promptly, and advocate for dose reduction or a medication change rather than additional antipsychotic dosing. Standard treatments such as benzodiazepines or anticholinergics may fail in severe cases, and adjunctive options such as low-dose mirtazapine have been reported to improve treatment-resistant akathisia [4]. Watch out! Increasing the haloperidol dose to treat what appears to be agitation would likely worsen akathisia, because the underlying mechanism is dopamine blockade rather than undertreated psychosis.References (research sources)

- [2]Traditional Chinese Medicine Interventions for Antipsychotic-Induced Extrapyramidal Symptoms: A Data Mining-Based Integrative Review of Prescription Patterns and Evidence.Research articleQin Y, Gao L, Tong J, Sun X, Zhou Y. (2026) · DOI: 10.2147/ndt.s608799

- [3]Antipsychotic-induced akathisia in delirium: A systematic review.Meta-analysis/systematic reviewForcen FE, Matsoukas K, Alici Y (2016) · DOI: 10.1017/S1478951515000784

- [4]Reassessing mirtazapine and akathisia: A case report on its efficacy in treating severe, treatment-resistant akathisia and a review of the evidence.Case reportChidiac M, Elhusein B, Gajebasia N. (2024) · DOI: 10.1177/2050313x241299947

## 임상 시나리오

Acute Akathisia After Antipsychotic Dose IncreaseRecognition and Management in Inpatient Psychiatry
Akathisia typically emerges days to weeks after starting or increasing an antipsychotic, especially with high-potency agents like haloperidol. The classic presentation includes pacing, rocking from foot to foot, inability to remain seated, and a subjective report such as "my legs won't let me sit still."

Differentiate from worsening psychosis by noting that positive symptoms have improved while motor restlessness appeared after a dose escalation. Anxiety alone lacks the objective motor signs of akathisia. Tardive dyskinesia occurs after months to years, and parkinsonism presents with bradykinesia and rigidity rather than restlessness.

CautionAkathisia is associated with an increased risk of suicide and treatment nonadherence. Assess for subjective distress, reduce the antipsychotic dose if clinically feasible, or consider adjunctive treatment such as a beta-blocker or anticholinergic.

## 핵심 개념

- **Akathisia** — Subjective inner restlessness with an observable urge to move, often felt in the legs, occurring days to weeks after starting or increasing an antipsychotic.
- **Extrapyramidal symptoms (EPS)** — Movement disorders caused by dopamine D2 receptor blockade in the nigrostriatal pathway, including dystonia, parkinsonism, akathisia, and tardive dyskinesia.
- **Haloperidol** — First-generation antipsychotic with potent dopamine D2 receptor blockade, associated with a high risk of extrapyramidal symptoms.
- **Tardive dyskinesia** — Late-onset EPS characterized by involuntary choreoathetoid movements, typically emerging after months to years of antipsychotic exposure.
- **Drug-induced parkinsonism** — EPS subtype presenting with bradykinesia, rigidity, and resting tremor due to dopamine blockade in the nigrostriatal pathway.

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