extrapyrimidal sympoms - Nursing Case Study

Pathophysiology

• Primary mechanism: Extrapyramidal symptoms (EPS) primarily arise due to dopamine receptor blockade, especially D2 receptors, in the nigrostriatal pathway. This pathway is crucial for coordinating voluntary movement, and its disruption leads to symptoms like tremors, rigidity, and bradykinesia.

• Secondary mechanism: Imbalance between dopamine and acetylcholine in the basal ganglia further exacerbates motor disturbances. Reduced dopamine activity allows for unopposed cholinergic activity, contributing to muscle stiffness and other motor control issues.

• Key complication: Persistent EPS can lead to tardive dyskinesia, a condition characterized by involuntary, repetitive movements, emphasizing the importance of monitoring and managing antipsychotic medications effectively.

Patient Profile

Demographics:

45-year-old female, office manager

History:

• Key past medical history: Schizophrenia diagnosed 10 years ago, hypertension

• Current medications: Haloperidol, Lisinopril

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Involuntary muscle movements and stiffness

• Key symptoms: Tremors in both hands, muscle rigidity, bradykinesia, anxiety

• Vital signs: Blood pressure 150/95 mmHg, heart rate 92 bpm, respiratory rate 20 breaths per minute, temperature 37.2°C (99°F)

Section 1

New Diagnostic Results:

Following the initial assessment, further diagnostic evaluations were undertaken to better understand the extent and potential progression of the patient's extrapyramidal symptoms. A complete blood count (CBC), comprehensive metabolic panel (CMP), and serum drug levels were ordered to rule out other causes of the symptoms and assess the therapeutic levels of Haloperidol. The CBC and CMP results were largely unremarkable, except for a slight elevation in creatinine at 1.4 mg/dL, potentially indicating decreased renal clearance. This finding necessitates careful consideration of medication metabolism and excretion. Serum Haloperidol levels revealed a concentration at the upper therapeutic range, suggesting that while the medication is within acceptable limits, its dose might be contributing to the severity of the EPS.

An MRI of the brain was conducted to exclude other neurological conditions that could mimic or exacerbate the current symptoms. The neuroimaging results showed no acute intracranial abnormalities, confirming that the involuntary movements and muscle stiffness are primarily attributable to the medication’s effect on the nigrostriatal pathway. With these insights, the clinical team is prompted to consider modifying the patient’s treatment regimen. Adjusting the Haloperidol dosage or switching to an alternative antipsychotic with a lower EPS profile, such as an atypical antipsychotic, could potentially alleviate the patient's symptoms while still effectively managing her schizophrenia. This decision will require a delicate balance between controlling psychiatric symptoms and minimizing adverse motor effects, underscoring the importance of collaborative care involving psychiatry, neurology, and primary care.

Section 2

Change in Patient Status:

Following the decision to adjust the patient's treatment regimen, the clinical team opted to taper down the Haloperidol dose and initiate a low dose of an atypical antipsychotic, Risperidone, known for its lower incidence of extrapyramidal symptoms. Over the course of the next few days, the patient was closely monitored for both psychiatric stability and any changes in motor symptoms. Initially, there was a slight improvement in the rigidity and tremors, suggesting a positive response to the medication adjustment. However, the patient began to exhibit increased restlessness and mild agitation, which raised concerns about the onset of akathisia, a potential side effect of the new medication.

As the week progressed, the patient's vital signs remained stable; blood pressure was 120/80 mmHg, heart rate at 78 bpm, and respiratory rate at 16 breaths per minute. Despite these stable vitals, the patient reported experiencing persistent insomnia and episodes of palpitations. A subsequent ECG was ordered to rule out any cardiac involvement, which returned normal results. However, the persistence of restlessness and insomnia prompted the team to reassess the current medication plan. The possibility of adjusting the Risperidone dosage or introducing adjunctive therapy, such as a beta-blocker or benzodiazepine to manage the akathisia symptoms, was considered.

This change in the patient’s status necessitated a multidisciplinary approach to ensure comprehensive management of her symptoms. The team engaged in collaborative discussions with psychiatry to evaluate the risk-benefit ratio of the current treatment. The primary goal remained to balance the effective management of schizophrenia symptoms while minimizing adverse effects. The ongoing dialogue between the clinical team and the patient was crucial to address her concerns and preferences, ensuring an individualized treatment plan that aligns with her overall health needs and quality of life.

Section 3

As the team continued to monitor the patient's response to the modified treatment regimen, it became apparent that the management of akathisia was becoming increasingly challenging. Despite the initial stability in psychiatric symptoms, the patient's restlessness and agitation persisted, impacting her quality of life. In response to these developments, the healthcare team decided to initiate a low-dose beta-blocker, Propranolol, to address the akathisia while continuing Risperidone at the current dose. This intervention aimed to alleviate the movement disorder without compromising the control of her schizophrenia symptoms.

Following the introduction of Propranolol, the patient reported a modest reduction in restlessness and a slight improvement in her sleep pattern, although insomnia was still present. During routine assessments, the patient's vital signs remained stable, with a heart rate of 72 bpm and blood pressure at 115/75 mmHg, indicating that the beta-blocker was well-tolerated. However, the persistence of insomnia prompted further investigation, leading to the decision to conduct a sleep study to assess potential underlying sleep disorders exacerbated by medication changes.

Results from the sleep study revealed that the patient was experiencing periodic limb movements during sleep (PLMS), a condition that can contribute to disrupted sleep and daytime fatigue. This new complication introduced an additional layer of complexity to her management, requiring further adjustment of her treatment plan. The clinical team considered the possibility of adding a low-dose benzodiazepine at bedtime to manage both the akathisia and PLMS, while continuing to engage with the patient to ensure her treatment aligns with her personal goals and preferences. This decision highlighted the need for ongoing clinical reasoning and collaboration to address the multifaceted nature of her symptoms effectively.

Section 4

Following the decision to introduce a low-dose benzodiazepine at bedtime, the patient initially experienced some relief from the periodic limb movements during sleep (PLMS), which led to a noticeable improvement in her sleep quality. Over the next few weeks, the patient reported feeling more rested upon waking, and her daytime fatigue diminished slightly. Despite these positive changes, the healthcare team remained vigilant, understanding the potential risks associated with benzodiazepine use, particularly in a patient with a complex psychiatric and movement disorder history.

During a routine follow-up visit, the patient's vital signs continued to be stable, with a heart rate of 70 bpm and blood pressure at 110/70 mmHg. However, she expressed new concerns about experiencing occasional muscle stiffness and mild tremors, particularly in the mornings. This prompted the clinical team to reevaluate her medication regimen, considering the potential for these symptoms to be indicative of emerging Parkinsonism as a complication of continued antipsychotic therapy. A thorough neurological examination was conducted, revealing mild bradykinesia and rigidity, suggesting that the extrapyramidal symptoms were evolving despite previous interventions.

In response to these findings, the clinical team faced the challenge of balancing the control of her schizophrenia symptoms with the management of her extrapyramidal side effects. They discussed the possibility of adjusting the antipsychotic medication to one with a lower risk of inducing Parkinsonism, while weighing the benefits of non-pharmacological interventions such as physical therapy to address the muscle stiffness and tremors. The team emphasized the importance of involving the patient in these discussions, ensuring that her preferences and concerns are central to the decision-making process. This approach underscored the need for ongoing clinical reasoning and adaptability as the patient's care plan continued to evolve in response to her changing clinical status.

Section 5

In the weeks following the adjustment of the patient’s antipsychotic medication to one with a lower propensity for inducing Parkinsonism, the clinical team remained vigilant in monitoring her response. During a follow-up evaluation, the patient reported feeling less muscle stiffness and noted a reduction in her morning tremors, indicating a positive initial response to the medication change. However, she also mentioned experiencing occasional dizziness and a slight increase in anxiety, symptoms that were new and concerning. The team attributed these changes to the recent medication switch and considered the need for further adjustments.

To gain more insight into the patient’s condition, comprehensive lab work was ordered, including a complete blood count, metabolic panel, and serum drug levels. The results revealed a slight electrolyte imbalance, with low sodium levels at 132 mmol/L, which could be contributing to the dizziness. Additionally, the serum drug levels indicated that the antipsychotic was within the therapeutic range, suggesting that her symptoms were not due to overmedication. These findings prompted the team to consider increasing her fluid intake while closely monitoring her sodium levels to address the hyponatremia without compromising her psychiatric stability.

As the clinical team continued to navigate these complexities, they engaged the patient in a detailed discussion about her treatment goals and preferences. Emphasizing a collaborative approach, they explored options such as modifying her diet to manage electrolyte levels, adjusting her benzodiazepine dosage to alleviate anxiety, and incorporating relaxation techniques to improve overall well-being. This ongoing dialogue not only empowered the patient but also reinforced the need for dynamic clinical reasoning and adaptability in managing her evolving condition. The healthcare team recognized that continuous monitoring and patient-centered care would be crucial in preventing further complications and ensuring optimal outcomes.