Paroxysmal Kinesigenic Dyskinesia and Cervical Disc Prolapse With Cord Compression: More Than a Coincidence?

LETTERS FIGURE 3.

MRI of the Brain Showing Multiple Embolic Phenomenon

substances parenterally and present with neuropsychiatric symptoms undergo detailed neuropsychiatric assessment, including appropriate imaging. Tih-Shih Lee, M.D., Ph.D. Psychiatry and Behavioral Science, Duke University Beng Yeong Ng, M.B.B.S., M.Med.(Psych) Department of Psychiatry, Singapore General Hospital References

rectly and indirectly lead to damage of the brain vasculature and parenchyma. To the best of our literature search we have not found published information pertaining to embolic phenomenon associated with parenteral burprenorphine. Of great interest also is the observation that such gross radioimaging findings did not correlate commensurately with significant, overt neuropsychiatric impairment. Instead the clinical symptoms appeared to abate with time. Multiple embolic infarcts in the brain have been associated with aortic arch atheroma, atrial fibrillation, atrial myxoma and aneurysm, cardiomyopathy, infective endocarditis, carotid artery, and cardiac procedures.4 The pattern of infarction has been reported to depend on embolic load, type, composition, and size of particles. Such particles include air bubbles, calcified particles, fibroelastomic tissue, and platelet fibrin particles.5 Hence it

can be inferred that the particulate size and constituents of ground buprenorphine and the water used may have a bearing on the embolic infarct. It is conceivable that a large injection of powdered drug could cause a shower of particulate emboli in the brain. It would not always be possible to distinguish whether the embolic phenomenon is caused by or associated with this patient’s subacute endocarditis or the parenteral buprenorphine or both, which, in our view, is most likely the case. Moreover, temporally it is likely that the multiple episodes occurred over several months and the neuropsychiatric and radiologic sequalae were due to a cumulation of multiple successive insults. More investigation is merited to understand the etiology, pathophysiology and treatment of multiple particulate embolism due to intravascular injection of substances. We also recommend that patients who abuse

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1. Chua SM, Lee TS: Abuse of prescription buprenorphine, regulatory controls and the role of the primary physician. Ann Acad Med Singapore 2006; 35:492–495 2. Yeo AK, Chan CY, Chia KH: Complications relating to intravenous buprenorphine abuse: a single institution case series. Ann Acad Med Singapore 2006; 35:487–491 3. Nasreddine ZS, Chertkow H, Phillips N, et al: The Montreal Cognitive Assessment (MoCA): a brief cognitive screening tool for detection of mild cognitive impairment. Neurology 2004; 62:A132 4. Wein TH, Bornstein NM: Stroke prevention: cardiac and carotid-related stroke. Neurol Clin 2000; 18:321–341 5. Babikian VL, Caplan LR: Brain embolism is a dynamic process with variable characteristics. Neurology 2000; 54:797– 801

Paroxysmal Kinesigenic Dyskinesia and Cervical Disc Prolapse With Cord Compression: More Than a Coincidence? To the Editor: Paroxysmal kinesigenic dyskinesia (PKD) is a relatively rare neurological condition which is characterized by sudden, brief (seconds to 5 minute) attacks of involuntary movements which are precipitated by sudden voluntary movement.1 Although often inherited in an autosomal dominant pattern, the pathophysiology of the disease remains largely unknown.2

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LETTERS Besides evidence supporting the paroxysmal kinesigenic dyskinesia as a form of epilepsy or basal ganglia disorder, many patients with symptomatic movement disorders have also been associated with a focal lesion.1 These reported lesions are distributed widely from the cerebral cortex to the spinal cord and make the pathophysiological correlation difficult. A 43-year-old male was admitted because of paroxysmal abnormal movements. There was no family history of paroxysmal movement disorders, seizures, or epilepsy. Ictal electroencephalograms of his attacks without loss of consciousness or a seizure were normal. The neurologic examination demonstrated choreiform movements of proximal and distal parts of the right arm and fingers, especially when he moved his right arm suddenly. But interestingly, the same dyskinetic movements did not appear when the patient was asked to get up from the sitting position and walk or when the patient was resting quietly or moved his other limbs. These movements appeared suddenly and lasted for 15–30 seconds. His face and the other upper limbs were not affected. Motor examination showed mild right monoparesis (grade 4/5) and minimally increased tone and hyperreflexia with no clonus on the right upper extremity. Systemic and blood examination was otherwise unremarkable. Magnetic resonance imaging (MRI) of cervical spine revealed multiple prolapsed discs at the C34, C4-5, C5-6 and C6-7 levels; severe cord compression was more prominent at the C5-6 level (Figure 1 and Figure 2). Brain MRI scan did not show any abnormalities. Interictal electroencephalograms were normal. Electroneuromyography suggested mild C7-8 radix involvement but the electrophysiologic evidence of posterior column abnormality on

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somatosensory evoked potential examination was not shown. The patient was treated with carbamaze-

FIGURE 1.

pine, 100 mg twice daily, which was remarkably effective in stopping the attacks.

Sagittal T2-Weighted Magnetic Resonance Image of the Cervical Spine Showing Multiple Disk Prolapses at the C3-4, C4-5, C5-6 and C6-7 Levels

Note the significant cord compression at the C5-6 level.

FIGURE 2.

Axial Section at C5-6 Level Showing Significant Cord Compression

J Neuropsychiatry Clin Neurosci 20:2, Spring 2008

LETTERS Discussion The modulation of movement at spinal level is thought to be in a computerized manner whereas the supraspinal and the peripheral afferent inputs are well integrated into the evolution of the movement.3 Altered sensory input (in particular proprioceptive pathways), abnormal processing of both input and output signals in the spinal interneurons, and increased excitability of the spinal motor neurons have been hypothesized to play an important role in the development of movement disorders in cervical cord lesions. Although we have excluded possible epileptic phenomena, it seemed very interesting that a small dosage of carbamazepine was remarkably effective in stopping the attacks. This may be explained on the basis of altered sodium channels due to the extrinsic cord compression as suggested by previous experimental studies.4,5 However, the anticonvulsant agents that are preferable by spinal dysesthesias with their potential effect on ion channels could also suggest the role of spinal channel blockage in controlling these dyskinesias. This case emphasizes that spinal cord compression may also be considered in every patient with the clinical symptoms of cervical disk prolapse and movement disorders. Burak Yulug, M.D. Mustafa Bakar, M.D. Department of Neurology, University of Uludag, Bursa, Turkey ¨ zer H, M.D. Haluk O Mu¨slu¨m Yilmaz, M.D. Sifa Hospital Neurology and Neurosurgey, Outpatient Clinic, Izmir, Turkey ¨ nlu¨, M.D. Bu¨lent U Aydin Hospital Neurology, Outpatient Clinic, Izmir, Turkey

References

1. Demirkiran M, Jankovic J: Paroxysmal dyskinesia: clinical features and classification. Ann Neurol 1995; 38:571–579 2. Bennett LB, Roach ES, Bowcock AM: A locus for paroxysmal kinesigenic dyskinesia maps to human chromosome 16. Neurology 2000; 54:125–130 3. Prochazka A, Mushahwar VK: Spinal cord function and rehabilitation: an overview. J Physiol 2001; 533:3–4 4. Fehlings MG, Agrawal S: Role of sodium in the pathophysiology of secondary spinal cord injury. Spine 1995; 20:2187–2191 5. Schwartz G, Fehlings MG: Evaluation of the neuroprotective effects of sodium channel blockers after spinal cord injury: improved behavioral and neuroanatomical recovery with riluzole. J Neurosurg 2001; 94:245–256

Clozapine-Induced Delirium To the Editor: Clozapine, an atypical antipsychotic, remains the “gold standard” for patients with treatment-resistant schizophrenic symptoms. The hematological, metabolic changes, sedation, and lowering of seizure threshold of clozapine is well known, but the occurrence of clozapine-induced delirium has been less reported. Case Report Mr. M is a 44-year-old male with an 18-year history of schizophrenia characterized by somatic delusion, delusion of persecution, and episodes of aggressive behaviors with impaired occupational functioning. He was untreated for 16 years. His medical history was negative. For the past 20 months, he had been reasonably stable on risperidone, 6 mg/day. Following a stressor, he had worsening of psychotic symptoms and had episodes of aggressive behaviors with deteriorating occupational functioning. Risperidone was increased to 9 mg/day, however, he did not show much change in his mental state. Consid-

J Neuropsychiatry Clin Neurosci 20:2, Spring 2008

ering his long-term illness and worsening of symptoms in spite of an adequate dose of risperidone, clozapine was considered. At the time of admission for initiation of clozapine, his baseline, complete blood count, liver function test, and ECG were normal. His vital signs were as follows: BP 120/80, pulse 79 bpm. His neurological examinations were normal. On day one of admission, risperidone was reduced to 6 mg/day and clozapine was initiated with 25 mg/day. On the subsequent days, risperidone was reduced by 2 mg/ day and clozapine was increased by 25 mg/day until he reached 100 mg/day. Five days after admission, he was on clozapine, 50 mg in the morning and 75 mg in the night, and his orientation and level of consciousness were stable. On day six with the same dose of clozapine, he became confused, disoriented, and his recent memory was impaired. He was agitated, intermittently answered questions inappropriately, and was unable to follow commands. His vital signs were BP 110/75, pulse 89 bpm; ECG, electrolytes and glucose were normal. His neurological examinations were normal. Clozapine was stopped on day seven and his agitation secondary to delirium was managed with lorazepam and haloperidol injections. Two days after stopping clozapine, his delirium resolved completely. He was started with olanzapine, 5 mg, on day 10 and the dose was gradually increased to 15 mg/day. Two months after starting on olanzapine, Mr. M returned to his work and did not show any signs of delirium, however, continued to harbor delusions. Comment Clozapine-induced delirium has been reported to have an incidence between 2.1%–10%.1,2 Many physicians may be unaware of clozapine-

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