INTRODUCTION

Iatrogenic movement disorders refer to movement disorders that occur due to treatment-related adverse effects. Although iatrogenic movement disorders are most often associated with medication, i.e., tardive disorders, a wide range of interventions, either medical or surgical, have been implicated in their generation. These can include chemotherapeutic and anesthetic agents, antipsychotics, radiotherapy, and neurological and non-neurological surgeries [1-6].

In this context, movement disorders can occur following interventional procedures (Figure 1), including but not limited to radiotherapy [7], dental procedures [8], cardiac, cerebral and spinal surgeries [9] and deep brain stimulation (DBS) [6]. These disorders tend to be rare with an uncertain prevalence and incidence. The majority of cases are unexpected sequelae with variable phenomenology and latency, and they can often be far more disabling than the primary disease for which the procedure was performed. Owing to poor understanding and awareness of the problem, delays in diagnosing the condition are common, as is misdiagnosis as a functional movement disorder. At present, there is no established system of classification for these disorders, and the latency of onset is highly variable, even with the same underlying procedure (Figure 2). Furthermore, the underlying mechanism varies based on the causative procedure, with variability for the same phenomenology (Figure 3).

This narrative review aims to review the phenomenology, pathophysiology, and potential treatments of various movement disorders caused by radiotherapy and neurological and non-neurological surgical procedures. DBS-related movement disorders [6] are predominantly stimulation induced and have been extensively reviewed elsewhere. They are therefore not included in the present review.

POST RADIOTHERAPY MOVEMENT DISORDERS

Radiotherapy is an important modality of treatment in various neurological diseases, such as tumors and arteriovenous malformations (AVMs). However, radiation can often cause significant neurological injury owing to damage to normal tissue. Post radiation adverse effects have been previously categorized into immediate, subacute (< 6 months) and delayed (> 6 months) [5]. While immediate and subacute complications may be reversible, delayed complications are considered to be permanent [5]. Almost all core movement disorders, i.e., parkinsonism, dystonia, tremor, myoclonus, and ataxia, have been reported post radiotherapy (Table 1). Although the exact site of injury for each of these phenomena may vary, immediate complications are suggested to be due to disruption of the blood–brain barrier by endothelial apoptosis, which leads to vasogenic edema and increased intracranial pressure. Subacute complications are proposed to occur due to demyelination, and delayed complications may occur through damage to the vasculature, i.e., loss of normal vessels or progressive fibrosis with or without neovascularization [5].

Post radiotherapy parkinsonism

Post radiotherapy parkinsonism can occur within a wide latency range, from between a few weeks and 39 years post radiotherapy [7], and to date, only a few cases have been reported (Table 1). Except for a single case that presented with tremordominant parkinsonism [10], all other cases presented with akinetic-rigid parkinsonism [7,11,12]. Magnetic resonance imaging (MRI) in subacute cases show predominantly globus pallidus hyperintensities, whereas in delayed onset cases, diffuse white matter hyperintensities consistent with radiation encephalopathy are evident. In addition, dopamine transporter scans show decreased uptake in the putamen [7]. The underlying pathophysiology may differ based on the time of onset of the movement disorder. In subacute postradiotherapy parkinsonism, the suggested mechanism is vasogenic edema, whereas hypoxia-induced vasculopathy is suggested for delayed (more than 2 months) post radiotherapy parkinsonism [11,12]. Treatment with levodopa is usually unsatisfactory owing to the post synaptic pathology of post radiation parkinsonism [7,12]. However, it may rarely be levodopa responsive [10,11] and reversible [11].

Post radiotherapy dystonia

Postradiotherapy dystonia primarily comprises cervical, oromandibular (OMD) and segmental dystonia, with occurrence close to the site of radiotherapy (Table 1) [13-15]. Similar to post radiotherapy parkinsonism, there is variable latency in the onset of post radiotherapy dystonia, which can range from 3 weeks to 5 years.

Post radiotherapy cervical dystonia has been described in patients who received radiotherapy for laryngeal [15] and lung [14] carcinoma. In these patients, tonic muscular activity and co-contraction of the affected muscles consistent with dystonia were observed on electromyography (EMG) with the absence of neuropathic or myopathic potentials. Imaging is usually normal; however, in one case with post radiotherapy cervical dystonia, spinal MRI showed hyperintensities in the cervical spine from the C3 to C6 segments without mass effect [13]. It is imperative to differentiate dystonia from contractures wherein atrophy of the affected muscles is seen rather than hypertrophy.

Post radiotherapy OMD has been reported following radiotherapy for nasopharyngeal carcinoma [13]. In both reported cases, patients developed jaw-closing dystonia with involvement of the masseters after a latency of 3 weeks to 3 months, and EMG showed co-contraction of the affected muscles (masseter and platysma), consistent with dystonia [13]. Post radiotherapy OMD is suggested to be a peripheral injury-related movement disorder, wherein mild but repeated injury to the trigeminal nerve due to focal radiotherapy leads to reorganization of its somatosensory representation in the thalamus. Another postulated mechanism in these cases is the involvement of the pons due to its close proximity to the radiation field. The pons has a central pattern generator function, and its involvement can lead to the generation of altered impulses to higher subcortical structures, leading to abnormal movements such as dystonia [13].

Finally, post radiotherapy segmental dystonia involving the shoulder and trunk has been described in 3 patients who received radiotherapy for breast carcinoma [16]. These patients presented with pain and decreased range of motion of the involved region, and EMG showed involuntary motor potential firing and myokymic discharges [16].

All forms of post radiotherapy dystonia respond poorly to anti dystonic drugs, including benzodiazepines, baclofen, and biperiden. However, they respond favorably to botulinum toxin injections, which is the drug of choice for post radiotherapy dystonia [13,16].

Post radiotherapy myoclonus

Post radiotherapy myoclonus has been reported to be either orthostatic [17] or spinal [18-20], with a variable latency ranging from 4 weeks to 6 years (Table 1). Post radiotherapy orthostatic myoclonus has been described in two patients who underwent wholebrain irradiation for meningioma and frontal right lobe gliosarcoma, with latency varying from subacute to chronic [17]. Both patients demonstrated high-amplitude short bursts on EMG recordings from the tibialis anterior, quadriceps and hamstrings when standing; these bursts were absent when patients were seated. Radiation-induced damage to the supplementary motor area and prefrontal cortex was suggested to contribute to the origin of myoclonus [17], which was reported to be unresponsive to levetiracetam, levodopa and clonazepam.

Post radiotherapy spinal myoclonus has been reported in 3 cases to date, with latency periods ranging from 3 months to 6 years post-radiotherapy. In all reported cases, patients received radiotherapy that involved the spinal cord: specifically, the cervical cord [20], thoracic cord [18,20], craniospinal cord and whole cord [19]. Myoclonus was observed in areas surrounding the sites of radiotherapy. The severity was variable, with the myoclonus severe enough to lead to an acetabular fracture in one case [20]. In another case, due to a long latency of 6 years, a functional etiology was initially considered. The possibility of postradiotherapy myoclonus was only considered following the absence of Bereitschafts potential associated with the movements [19]. Imaging was reported to be normal in all reported cases, and no specific basis for myoclonus was reported. However, based on the improvement with GABAergic drugs in 2 of the cases, the possibility of underlying post radiation hyperexcitability may be considered [18]. Intrathecal morphine may be beneficial in cases of unresponsiveness to clonazepam, dantrolene or valproate [20].

Post radiotherapy tremor

Post radiotherapy tremor can occur either as a palatal tremor or Holmes tremor, following radiotherapy directed toward the pons and midbrain via gamma knife radiosurgery (GKRS) for AVMs [21,22] or after whole-brain irradiation [23].

In contrast to other post radiotherapy movement disorders, post radiotherapy tremor, either palatal or Holmes, has a relatively shorter range of latency (2 weeks–3.5 months). Both reported cases of post radiotherapy palatal tremor were found to have hypertrophic olivary degeneration [21]. A variable imaging observation was reported in the post radiotherapy Holmes tremor. While a hyperintense lesion of the red nucleus was observed in the case that underwent GKRS for the AVM [22], no obvious lesion of the red nucleus was observed following whole-brain irradiation [23]. In the latter, it is possible that following irradiation, contraction of the hamartoma led to a distortion of the mesencephalon, which in turn produced a Holmes tremor [23]. No specific treatment was reported for the palatal tremor, whereas the post-GKRS Holmes tremor responded well to amantadine and trihexyphenidyl, and the post-whole-brain irradiation Holmes tremor completely resolved following surgical resection of the hamartoma.

Post radiotherapy ataxia

Postradiotherapy ataxia is predominantly reported following whole-brain irradiation for metastatic cancer [24-28]. The latency can range from 5 months to several years post-radiotherapy. Patients may also present with progressive dementia, ataxia, and urinary incontinence, which may resemble normal pressure hydrocephalus [28]. Radiation-induced leukoencephalopathy is considered to contribute to ataxia, and no specific treatment has been recommended, with corticosteroids and ventriculoperitoneal shunting offering incomplete improvement [28].

POST-SURGICAL MOVEMENT DISORDERS

Non neurological procedures

Dental procedures

Oromandibular dystonia (OMD) is a well-reported form of post-dental procedure movement disorder, and a vast variety of procedures have been implicated. These include dental extraction [29-33], ill-fitting dentures [33-35], oral surgery [36], dental implants [37], root canal treatment [33], gingivectomy [33], apicoectomy, ostectomy, TMJ arthroscopic surgery and occlusal alteration (Table 2) [38-41]. A higher prevalence has been reported among women between 40 and 70 years of age, with post procedural latency ranging from a few hours to a few years. OMD may progress to laryngospasm [34], or involvement of the tongue and neck may result in segmental distribution, rarely becoming generalized dystonia [42]. The basis for post-dental procedure OMD may be similar to that of peripheral trauma-induced dystonia [31], wherein peripheral trauma can lead to an altered somatotropic organization in the thalamus with subsequent changes in subcortical circuits, which leads to altered transmission within the basal ganglia. A few patients report transient improvement with sensory tricks, and botulinum toxin injections provide satisfactory improvement. Some patients have a history of bruxism predating the OMD; thus, it is uncertain whether such patients have a predisposition to developing OMD following the dental procedure. Facial dyskinesias (jaw opening, closing spasms, blepharospasm) have also been reported following dental procedures, with latency periods of a few days to a year following the procedure [31].

Cardiothoracic surgeries

Aortic surgery

Progressive supranuclear palsy (PSP)-like syndrome, i.e., Mokri syndrome, was first described in 2004 [43]. Occurring after aortic surgery, this relatively uncommon syndrome is characterized by a triad of supranuclear gaze palsy, dysarthria and gaze disturbance (Table 3) [43-56]. Although it is suggested that there is a higher prevalence of this syndrome in men, this is likely due to the higher prevalence of thoracic aortic aneurysms and abdominal aortic dissections in men.

The disease is biphasic, with immediate and latent phases. In the immediate phase, supranuclear gaze palsy with mild gait disturbance, dysarthria and tremulousness can be seen. This initial phase improves or stabilizes within a few weeks. Subsequently, after a latency of a few months, progressive supranuclear down-gaze palsy with ataxic gait, dysarthria and dysphagia can develop [43]. Impairment of horizontal gaze has been more commonly reported than vertical gaze impairment [43].

One possible explanation postulated for Mokri syndrome is the use of profound hypothermia (12.5°C to 30°C) during aortic surgeries in comparison to other cardiac surgeries [44]. Although hypothermia is considered a neuroprotective strategy, patients may develop ischemia if rewarming is carried out rapidly. Furthermore, this ischemia may further impact patients who develop hyperglycemia during hypothermia. Additionally, improper acid-base management can lead to cerebral edema. All these factors can lead to vasoconstriction and impaired microcirculation [44]. Another proposed mechanism is multiple emboli in the posterior circulation; however, structural imaging has been found to be normal in most cases [47]. While AV-1451 tau PET was normal in one case, fluorodeoxyglucose-positron emission tomography (FDG-PET) demonstrated the ‘pimple sign,’ which is consistent with PSP; however, the DAT scan was normal [44]. Mokri syndrome is unresponsive to levodopa and has a poor prognosis.

Cardiopulmonary bypass

Post-pump chorea refers to choreiform movements that occur in children who undergo major cardiac surgery needing cardiopulmonary bypass and deep hypothermia circulatory arrest (DHCA) [57]. This entity was first described in 1960 [58], and the incidence of post-pump chorea varies between 1–18 [59]. This is a rare entity, as evidenced by a recent study by Ahn et al. [60], who identified 2 patients with adult-onset post-pump chorea out of 5,338 adults who underwent cardiopulmonary bypass. Although more common in children, it may be seen in adults following pulmonary endarterectomy, aortic arch and valve replacement surgeries [61]. Chorea is usually generalized and occurs after a latency of one day to a week post-surgery. Apart from generalized chorea, orofacial dyskinesia, dysphagia, loss of tone and dysarthria can occur [62]. Risk factors can be young age (children), prolonged duration of cardiopulmonary bypass, longer duration of total circulatory arrest, hypothermia, and duration of aortic clamping [60,63].

The proposed mechanism is cerebral vasoconstriction due to hypocapnia and alkalosis during rewarming and increased blood viscosity. Hypothermia can also result in marked cerebral vasoconstriction leading to ischemic insult. The globus pallidus interna (GPi) and striatum are vulnerable to hypoxic damage, which results in abnormal movements. MRI shows bilateral basal ganglia hyperintensities in the caudate, putamen and globus pallidus. FDG-PET indicates hypometabolism in the bilateral basal ganglia [64]. The course of this condition is variable. It has been transient in some patients and subsided after treatment with neuroleptics and dopamine blockers. In other cases, it has been severe and irreversible, with cognitive deficits and disability [65,66]. GPi DBS with good outcome has been reported in a case with disabling post-pump chorea [67]. No differences in age, sex or surgical findings were observed in adults with post-pump chorea who had a good outcome versus those who had a bad outcome. However, initial MRI signal changes in the caudate and putamen have been associated with a poor outcome [60].

Neurological procedures

Ventriculoperitoneal shunt

Post-ventriculoperitoneal shunt parkinsonism usually occurs secondary to shunt malfunction rather than the procedure itself. It is more commonly observed in patients with obstructive hydrocephalus secondary to aqueductal stenosis [68]. The latency can be from 3 days to 24 years after the initial shunt placement and often follows repeated episodes of shunt failure (Table 4) [69-75]. In the case of shunt malfunction, hydrocephalus leads to pressure over the basal ganglia circuits, leading to decreased dopaminergic output, which can lead to the development of acute parkinsonian symptoms [70]. Specifically, for obstructive hydrocephalus, both bottom-up and top-down damage from the pressure gradient between the infratentorial and supratentorial space is suggested to contribute to parkinsonism [68]. The common manifestations are symmetrical parkinsonism with bradykinesia, rigidity and hypophonia. However, parkinsonism may also be asymmetrical [68]. Tremor is uncommon but has been previously reported [69].

Decreased cerebral blood flow to the basal ganglia was observed in cases who underwent single-photon emission computerized tomography (SPECT) [70]. In a few cases with hydrocephalus, simple revision of the shunt abated the symptoms of parkinsonism, suggesting a component of reversible compression of basal ganglia. In cases of obstructive hydrocephalus, endoscopic third ventriculostomy might be beneficial [68]. Repeated episodes of shunt blockage may induce irreversible damage that may not improve with shunt surgery alone and may need levodopa therapy. This condition is levodopa responsive, and the prognosis is usually good. In a few cases, eventual withdrawal of levodopa has been possible [68,70,76].

Aneurysmal coiling

Similar to parkinsonism that develops following ventriculoperitoneal shunting, parkinsonism has been associated with aneurysmal coiling, although it is more likely due to mechanical compression of structures by the aneurysm or cyst that developed post-coiling rather than a direct complication of coiling. To date, two cases of hemiparkinsonism subsequent to aneurysm coiling have been described [77,78]. In the first case, hemiparkinsonism developed four weeks following coiling of a posterior cerebral artery aneurysm, and compression of the midbrain by the aneurysm sac was implicated in the genesis of parkinsonism [77]. In the other case, hemiparkinsonism developed 15 months post-coiling of an anterior cerebral artery aneurysm, and the compression of the ventrolateral cerebral peduncle by the aneurysmal sac was implicated for parkinsonism [78]. In both cases, the parkinsonism was responsive to trihexyphenidyl [77] and levodopa-carbidopa [78].

Spinal surgery

Post-spinal surgery-associated movement disorders are a type of peripherally induced movement disorder that occur in close anatomical relationship to the operated segment. Most patients may experience pain before the onset of symptoms. Occurring more frequently after surgery of the cervical cord than other segments, a wide range of movement disorders can be observed, including tremor, focal dystonia, paroxysmal kinesigenic dystonia, and spinal myoclonus (Table 5) [9,79,80]. The latency period is also highly variable and may range from days to years post-surgery. As with post-dental procedure OMD, peripheral injury-induced changes have been implicated in the pathogenesis of post-spinal surgery movement disorders. Clonazepam has been reported to be variably beneficial. However, botulinum toxin injections may prove to be useful in focal conditions.

CONCLUSIONS

As radiotherapy- and surgical procedure-related movement disorders are a diagnosis that is presumed based on an antecedent relationship after the procedure, it is necessary to understand the limitations of an inaccurate diagnosis. First, the frequency of occurrence is rare, various factors (radiation intensity, period, etc.) exist within one type of procedure, and the spectrum of the latency period from procedure to occurrence is wide. A few disorders, such as post-pump chorea, are transient; however, the majority are progressive with unsatisfactory response to medication. Awareness of this entity by the treating physicians and proper pre procedure neurological evaluation and counseling is necessary to ensure identification of new-onset, post procedure movement disorders.

Notes

Conflicts of Interest

The authors have no financial conflicts of interest.

Funding Statement

None.

Author Contributions

Conceptualization: Pramod Kumar Pal. Data curation: Bharath Kumar Surisetti, Shweta Prasad. Formal analysis: Bharath Kumar Surisetti, Shweta Prasad. Investigation: Bharath Kumar Surisetti, Shweta Prasad. Methodology: Pramod Kumar Pal. Supervision: Vikram Venkappayya Holla, Nitish Kamble, Ravi Yadav, Pramod Kumar Pal. Validation: Vikram Venkappayya Holla, Nitish Kamble, Ravi Yadav, Pramod Kumar Pal. Visualization: Bharath Kumar Surisetti, Shweta Prasad. Writing—original draft: Bharath Kumar Surisetti, Shweta Prasad. Writing—review & editing: Vikram Venkappayya Holla, Nitish Kamble, Ravi Yadav, Pramod Kumar Pal.

Figure 1.

Classification based on phenomenology. A variety of phenomenologies can be seen in movement disorders which are associated with radiotherapy and surgical procedures. With the exception of ataxia which is reported only post radiotherapy, all others are phenomenologies are seen with multiple causes. VP, ventriculoperitoneal.

Figure 2.

Classification based on latency. There is high variability observed in the latency of onset, even with the same underlying procedure and phenomenology.

Figure 3.

Classification based on underlying mechanism. The underlying mechanisms can be broadly classified as direct injury to the brain/spinal cord to the specific region or via diffuse hypoxic/ischemic injurt, or due to brain changes induced by peripheral injury. PKD, paroxysmal kinesigenic dyskinesia; VP, ventriculoperitoneal.

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References

Citations

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