Lazarus phenomenon in a brain-dead patient: a case report

Abstract

Background

Brain death is defined as the irreversible cessation of all cerebral and brainstem functions, confirmed through clinical examination and, when necessary, ancillary testing. While the diagnostic criteria are well established, certain spinal reflexes, such as the Lazarus phenomenon, can complicate clinical examinations and lead to diagnostic uncertainty. Most reported cases describe predominant upper-limb movements; however, atypical variants involving truncal or lower-limb responses have rarely been reported.

Case presentation

We report the case of a 33-year-old Iranian man with cerebellar hemangioblastoma who developed transtentorial herniation and fulfilled all clinical criteria for brain death. Brain death determination was performed independently by two neurologists 6 h apart after exclusion of sedative exposure, metabolic disturbances, neuromuscular blockade, and hypothermia. Apnea testing demonstrated an increase in PaCO₂ from 39 to 64 mmHg without spontaneous respiratory effort. During examination, reproducible reflex movements were triggered by passive neck flexion and painful stimulation, consisting predominantly of bilateral hip and knee flexion with lower-limb adduction, accompanied by limited upper-extremity flexion. These findings were interpreted as spinal reflex activity consistent with an atypical lower-limb-predominant Lazarus phenomenon.

Conclusion

This variation reinforces the importance of recognizing spinal reflexes in brain-dead individuals and underscores the need for awareness of such findings to avoid misinterpretation. Clinicians must distinguish these movements from indicators of residual brain function to ensure accurate and timely determination of brain death.

Supplementary Information

The online version contains supplementary material available at https://doi.org/10.1186/s13256-026-06331-1.

Background

Brain death is defined as the irreversible and complete cessation of all brain activity, including the functions of the brainstem [1]. Despite this, brain-dead patients may exhibit spontaneous or reflex movements, many of which are categorized as spinal reflexes. Among these, the most striking is “Lazarus phenomenon,” a complex reflex that typically involves bilateral flexion of arms toward the chest, adduction of the shoulders, and crossing of the hands [2, 3]. In this report, we present a variation of Lazarus sign observed in a brain-dead patient and discuss the potential mechanisms underlying this reflex.

Case presentation

A 33-year-old Iranian man with no significant past medical and psychological history and normal family history presented to the hospital with complaints of headache for the last 2 months and new-onset dizziness. Further investigations, including a magnetic resonance imaging (MRI) study, revealed a cerebellar hemangioblastoma. Given the imaging findings and his chief complaint, a digital subtraction angiography (DSA) was scheduled to further evaluate the tumor. The DSA was performed under local anesthesia through right femoral artery puncture with 6 F femoral sheath and by Seldinger technique. At selective injection of both vertebral arteries, evidence of an arterial tumoral blush fed by left posterior inferior cerebellar artery (PICA) was visible (in favor of left cerebellar hemangioblastoma). After tumor vascular mapping, embolization was performed successfully. Main feeders of the lesion were selectively micro-catheterized and one vial of ONYX was injected through the left PICA in order to occlude feeders. The follow-up DSA showed near-complete occlusion of the malformation, and the patient was discharged in stable condition. However, 2 days later, he experienced a sudden progressive decline in consciousness. Upon return to the hospital, his Glasgow Coma Scale (GCS) was reported to be 3; therefore, the patient was immediately intubated according to standard protocols.

CT imaging revealed severe hydrocephalus, compression of the fourth ventricle, and downward trans-tentorial herniation secondary to the cerebellar mass.

Potential confounding conditions for brain-death determination were excluded. The patient was normothermic, had no exposure to sedatives or neuromuscular blocking agents, and laboratory evaluation revealed no major metabolic or electrolyte abnormalities. Brain-death assessment was performed independently by two qualified neurologists 6 h apart in accordance with institutional protocol. The apnea test was performed using preoxygenation and oxygen insufflation through the endotracheal tube; baseline PaCO₂ was 39 mmHg and increased to 64 mmHg without spontaneous respiratory effort.

During neurological examination, a reproducible complex motor pattern was observed in response to passive head flexion and painful stimulation of the limbs (Video 1). The movements consisted predominantly of bilateral adduction of the lower extremities with flexion of the hips and knees, accompanied by limited flexion and abduction of both upper limbs. Each episode lasted for several seconds and recurred with repeated passive neck flexion. No purposeful or brain-mediated motor responses were identified. Through this, the patient was maintained on a norepinephrine infusion, in accordance with standard intensive care management, to support mean arterial pressure to avoid neurogenic shock and loss of central sympathetic outflow.

Following confirmation of brain death, the patient’s next-of-kin consented for organ donation, and the patient’s liver, both kidneys, and left cornea were donated. A timeline of the patient’s symptoms, interventions, and outcomes is presented in Fig. 1.

Fig. 1.

Patient timeline from first presentations to confirmed brain death

Discussion

Brain death is defined as the irreversible cessation of all cortical and brainstem activity, and its diagnosis requires the exclusion of confounding conditions that could mimic this state. The core clinical criteria for brain death include coma, absence of brainstem reflexes, and the lack of spontaneous respiration. Once these criteria are met, the individual is considered legally and clinically dead [1, 4, 5]. Brain death is identified by fulfilling all the following criteria: (1) no response to maximal external stimulation; (2) pupils fixed at mid-size or dilated, nonreactive to light; (3) absence of corneal, oculocephalic, and oculovestibular reflexes; (4) no facial motor response to painful stimuli; (5) absence of the gag reflex upon bilateral stimulation of the posterior pharynx; (6) no cough reflex during deep tracheal suctioning; (7) no brain-mediated motor response to painful limb stimulation; (8) no spontaneous respiration during an apnea test with pH < 7.30 and PaCO₂ ≥ 60 mm Hg. When the full clinical examination cannot be completed, ancillary tests such as cerebral blood flow imaging or electrophysiologic studies may be employed [1].

In our case, despite fulfilling all clinical criteria for brain death, the patient exhibited a reproducible motor response pattern, consistent with the Lazarus phenomenon described in the literature. This phenomenon characterized by complex spinal reflex movements in brain-dead individuals has been documented in approximately 2% of cases [6]. The classical Lazarus phenomenon involves bilateral arm flexion across the chest, shoulder adduction, and hand crossing [7]. In our patient, however, the pattern differed slightly, involving flexion and adduction in both lower limbs in response to passive head flexion or painful stimuli. Other post-brain death literature has mentioned reflexes involving the lower limb (such as toe flexion sign and proximal lower limb reflexes), but none included the simultaneous movement of upper limbs [8, 9].

The differential diagnosis of these movements includes spinal automatisms, triple flexion response, and decerebrate or decorticate posturing. We excluded the latter since decerebrate and decorticate posturing are brainstem functions and the absence of all brainstem reflexes in our patient contradicts this possibility [10]. Spinal automatisms are defined as spontaneous, ongoing, and sometimes sustained rhythmic movements that occur without any identifiable external trigger [6]. In our patient, the movements were neither spontaneous nor sustained; they were consistently and reproducibly evoked only by a specific stimulus and stopped promptly upon stimulus cessation, thereby excluding an automatism. The triple flexion response, on the other hand, is a classic spinal withdrawal reflex characterized by simultaneous flexion of the hip, knee, and ankle in response to a painful stimulus applied to the foot [11]. Our patient’s movements differed in two critical ways. First, our triggering stimulus was passive and not a painful foot stimulus. Second, the observed response included adduction of the lower limbs in addition to flexion of the hips and knees, which is not typical of the pure flexor synergy of the triple flexion reflex. Moreover, the involvement of both upper and lower limbs in a single, temporally synchronized pattern further distinguishes this phenomenon from the isolated, segmental response of the triple flexion reflex. In this case, preserved brain function was excluded because the patient fulfilled all accepted clinical criteria for brain death, including absent brainstem reflexes and a positive apnea test. The reproducible and stimulus-induced nature of the movements, together with the absence of any purposeful response, strongly supports a spinal cord–mediated mechanism rather than supraspinal activity.

Such movements are attributed to spinal cord–mediated reflexes, independent of cerebral function [7, 12]. While individual variability in spinal circuitry likely explains differences in reflex patterns, our findings fall within the spectrum of spinal reflex phenomena observed in brain-dead patients. Reports indicate that 13–75% of brain-dead patients may display some form of limb movement or reflex [7, 13], and in pediatric cases, 22.6% showed either reflex or spontaneous motor activity [14]. Initially, it was believed that hypoxia (e.g., during an apnea test) was associated with this phenomenon; however, the occurrence of the Lazarus phenomenon in normoxic conditions has challenged this theory [12, 15]. Another theory proposes that spinal cord compression, especially during passive neck flexion, may trigger these reflexive motor responses [3].

Conclusion

This case highlights a notable variation of the Lazarus phenomenon, distinguished by prominent lower limb involvement, which is rarely emphasized in existing literature. This pattern suggests that spinal reflex pathways in the lumbosacral region may also play a significant role in spinal reflexes. Recognition of such atypical reflex patterns is important to prevent misinterpretation during brain-death evaluations and underscores the need for broader awareness of the diverse manifestations of spinal reflexes in brain-dead individuals.

Abbreviations

GCS

Glasgow Coma Scale

MRI

Magnetic resonance imaging

DSA

Digital subtraction angiography

PICA

Posterior inferior cerebellar artery

Author contributions

D.S and R.M. collected data of the case and drafted the manuscript. T.K. designed work, reviewed, edited and approved the manuscript.

Funding

No funding was received for this study.

Data availability

The data supporting this study are available from the corresponding author upon reasonable request.

Declarations

Ethics approval and consent to participate

Ethics approval is held to be unnecessary by Iran University of Medical Sciences, as this is a single, rare case encountered during clinical practice.

Consent for publication

Written informed consent was obtained from the patient’s next of kin (his father) to publish this case report in accordance with the journal’s patient consent policy. A copy of the written consent is available for review by the Editor-in-Chief of this journal.

Competing interests

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript.