Parkinsonian syndrome after cardiac arrest: and neurochemical changes

Werner Verslegers*, Roeland Crols*, Manfred van den Kerchove*, Werner de Potter* *, Brigitte Appel* * *, and Armand Lowenthal*

Introduction

Extrapyramidal (parkinsonian) syndromes with mental enfeeblement as one of the different posthypoxic syndromes are classically described in textbooks 1'2. After an extensive review of the literature, pure Parkinson syndromes in young adults who survived a cardiac arrest were not found. We will now report such a case who did survive, with a discussion of the CT, MRI and some CSF changes.

Case report

A 21-year-old man, physically fit but addicted on intravenous street drugs for more than three years, decided to kick off at home. He was found in his own vomit, unconscious and cya- notic, by family members. The elapsed period of time in between is unknown. During his trans- port to the hospital he developed after aspira- tion of vomitus, a sudden cardiac arrest. Cardiac action was restored after five minutes. After 24 hours, he regained consciousness, but was aki- netic and hypertonic. There was no history of a head trauma. After 3 days, he showed a full- blown Parkinson syndrome consisting of: my- driasis, diminished blinking, expressionless face, dysarthric speech with poor voice volume, micrography, generalized severe rigidity with

Summary

Following a cardiac arrest, a 21-year-old man developed a Parkinson syndrome. This was due to, as shown by brain computerized to- mography (CT) and magnetic resonance imag- ing (MRI), symmetrical infarctions of the basal ganglia, especially the globi pallidi. The levels of homovanillic acid (HVA) in the CSF were lower than normal, pointing to a possible alter- ation of the central dopaminergic activity. An alteration of the opioid system may also be supposed because of the extremely high levels of methionine-enkephalin (Met-Enk).

Key words: Cardiac arrest, basal ganglia in- farction, methionine enkephalin, dopamine beta-hydroxylase.

pillow sign, impairment of postural reflexes with slight propulsion and flexor spasms of all toes. There were no pyramidal, cerebellar or menin- geal signs. Only a slight improvement of his rigid gait was noted during the first two weeks: his balance improved, there was less anteropulsion but he took still small shuffling steps. Biochem- ical and toxicologic screening, chest X-rays, ECG, EEG, evoked potentials, regional cere- bral blood flow and neuropsychologic assess- ment were all normal. EMG detected an irreg-

* Department of Neurology, Algemeen Ziekenhuis Middelheim, Lindendreef 1, 2020 Antwerp and Laboratory of Neuroche- mistry, Born-Bunge foundation, University of Antwerp (UIA), Universiteitsplein 1, 2610 Wilrijk, Belgium, * * Laboratory of Pharmacology, Department of Medicine, University of Antwerp (UIA), Universiteitsplein 1, 2610 Wilrijk, Belgium, * * * De- partment of Neuroradiology, A lgemeen Ziekenhuis Middelheim, Lindendreef 1, 2020 Antwerp, Belgium.

Address for correspondence and reprint requests: IV. Verslegers, Laboratory of Neurochemistry, Born-Bunge foundation, University of Antwerp (UIA), Universiteitsplein 1, 2610 Wilrijk, Belgium.

Accepted 4.3.88

Clin Neurol Neurosurg 1988. Vol.90-2. 177

Fig. 1. CT showing symmetrical infarctions of the globi pallidi.

ular tremor of 8 to 12 c/s. CT performed two months after his cardiac arrest demonstrated symmetrical low density areas in the globi pallidi (Fig. 1). MRI after 65 days detected more exten- sive lesions (Fig. 2a, 2b). After two months without medication and showing for at least six weeks a clinical 'status-quo', a lumbar puncture was performed: normal cytology, slightly in- creased protein content of 48 rag% (normal 15-45 mg%) with a serumlike agar gel electro- pherogram, low dopamine beta-hydroxylase (D[3H) 0.49 U/ml (0.5-1.3 U/ml) and HVA 23.0 ng/ml (25.7-76.7 ng/ml), normal 5-hydroxyin- dole acetic acid 32.6 ng/ml (11.4-38.9 ng/ml) and 3-methoxy-4-hydroxyphenylethyleneglycol (MHPG) 11.1 ng/ml (5.8-11.7 ng/ml) and very high levels of Met-Enk 693.7 pg/ml (5.2-35.0 pg/ml). After the lumbar puncture treatment with L-dopa up to 1000 mg daily, associated with benserazide (250 mg) was started. No improve- ment was noted, but the flexor spasms of the toes responded well to quinine sulfate 600 mg

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daily. Now, two years later, no changes in his Parkinson syndrome can be observed.

Discussion

In contrast to our case, the reported anoxic en- cephalopathies with basal ganglia lesions did not occur as a 'pure form' but also affected other cerebral structures. These concern mostly elder- ly subjects with an already precarious cerebral perfusion, or young adults after respiratory de- pression due to drug overdose (morphine, methadone, phenobarbital) 3, intoxications, hanging 4, hypoglycemia, anesthesia accidents, shock, and status epilepticus 3. In these condi- tions, postmortem examination demonstrated widespread necrotic loci of the white and gray matter, diffuse and perivascular demyelinisa- tion and neurocellular degeneration. Although the basal ganglia are to be considered 'at risk' in acute and chronic ischemic-hypoxic situations due to their localisation at boundary zones of perfusion, cases of an advanced stage of a pure Parkinson syndrome in young adults following a cardiac arrest were not found in the literature. In our case, a post-ischemic parkinsonism clear- ly followed a cardiac arrest. Similar pure Parkin- son syndromes have only been described follow- ing carbon monoxide 5, cyanide 6 and methanol 7 intoxications, following head traumas 8 and in multiple basal ganglia infarcts due to arterio- sclerosis 9. Comparable pallidal lesions as in our case, detected by CT, have been described in the just previous mentioned conditions and af- ter hanging, in Wilson's, Hallervorden-Spatz' and Leigh's disease s. MRI showed more exten- sive lesons than CT: an additional pathological signal was detected in the posterior part of the putamen. The multiecho technique indicated a cystic transformation of these structures.

MPTP as a contributing factor in developing parkinsonism seems unlikely in our patient, since administration of MPTP does not result in infarctions of the basal ganglia, and the patient's friends exposed to the same drugs did not devel- oped any parkinsonian signs. Furthermore our patient's parkinsonism was predominantly of the hypertonic-akinetic type and the MHPG- levels in the CSF were normal.

In our case HVA, the major catabolic product of dopamine, was decreased in the CSF. This is

Fig. 2. Transverse MRI examination, single slice multiecho procedure (TR 1500/TE,30,60,90,...240). a. showing a bilateral low signal intensity of the globus pallidus and the posterior part of the putamen in the first echo, b. a high signal intensity of the same lesions was seen in the third echo.

felt to reflect lower dopamine metabolism with- in the central nervous system and is compatable with his severe Parkinson manifestations. D[3H originates from central noradrenergic neurons. Therefore, in this case, an impairment of central noradrenergic transmission may exist because of the decreased D~H activity found in the CSF and the extremely high levels of Met-Enk, which can cause an inhibition of central nor- adrenergic activity. Furthermore, an alteration of the opioid system can be presumed taking into account the high levels of Met-Enk. In- creased levels have been reported in early stages of Parkinson's disease 1~ but never as high as in our case.

Acknowledgements

This work was supported by the 'Fonds voor Geneeskundig Wetenschappelijk Onderzoek' (grant nr. 3.00019.86), the 'Ministerie voor Nationale Opvoeding en Nederlandse Cul- tuur', the 'Nationale Loterij' (grant nr. 9.0017.83), the 'Concerted Action U T A . ' nr. 84/89-68, the University of Antwerp and the Born-Bunge foundation.

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