Locked-in syndrome post snake bite: a rare presentation

Kutiyal, Aditya Singh; Malik, Chetanya; Hyanki, Gitika

doi:10.1177/0049475517726262

Cited by 5 publications

(5 citation statements)

References 6 publications

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“…We grouped substances with greater than five cases into separate descriptive tables. Snake envenomation (Table 1) [7][8][9][10][11][12][13][14][15][16] was the most frequent cause of a brain death mimic, followed by baclofen (Table 2) [17][18][19][20][21][22][23][24][25][26][27], tricyclic antidepressants (TCA) ( Table 3) [28][29][30][31][32][33][34] and bupropion (Table 4) [5,6,[35][36][37][38][39][40]. We grouped all cases with three or fewer cases into Table 5 [41][42][43][44][45][46][47][48...…”

Section: Resultsmentioning

confidence: 99%

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Toxicologic Confounders of Brain Death Determination: A Narrative Review

2020

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The aim of this narrative review is to describe the toxicologic confounders of brain death currently reported in the literature to offer guidance for physicians assessing brain death after a toxic exposure. We established an a priori definition of a "brain death mimic" as an unresponsive, intubated patient missing some, but not all brainstem reflexes. We completed a review of the literature utilizing MEDLINE and EMBASE to find case reports of patients of all ages in English, French, and Spanish meeting the criteria and hand searched the references of the results. We recorded xenobiotic dose, duration of physical exam suggesting brain death, and how the cases failed to meet full brain death criteria, when available. Fifty-six cases representing 19 different substances met the a priori definition of brain death mimic. Xenobiotic toxicities included: snake envenomation (13), baclofen (11), tricyclic antidepressants (8), bupropion (7), alcohols (4), antiepileptic agents (3), barbiturates (2), antidysrhythmics (2), organophosphates (2), and one case each of magnesium, succinylcholine, tetrodotoxin, and zolpidem. All patients except one survived to discharge and the majority at their baseline physical health. The most common means by which the cases failed brain death examination prerequisites was via normal neuroimaging. The xenobiotics in this review should be considered in cases of poisoning resulting in loss of brainstem reflexes and addressed before brain death determination. Brain death diagnosis should not be pursued in the setting of normal cerebral imaging or incomplete evaluation of brain death prerequisites.

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Section: Resultsmentioning

confidence: 99%

“…Depressed DTR. Extensor plantar response Neuroimaging Normal CT Normal MRI Normal MRA Diffuse background slowing, no epileptiform changes Extubated at 36 h Discharged day 6 Recovery to baseline health [ 16 ] 26/M 48 h “Areflexia”. Absent pupillary, corneal, and oculocephalic reflexes.…”

Section: Resultsmentioning

confidence: 99%

Toxicologic Confounders of Brain Death Determination: A Narrative Review

2020

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“…• Conversion disorders 94 • Late-stage amyotrophic lateral sclerosis 95 • Severe cases of Guillain-Barré syndrome 31,96,97 (also reported as a complication of SARS-CoV-2 98 ) • Snake bites [99][100][101] • Supratentorial traumatic lesions 13…”

Section: Aetiologies Leading To Infarction/other Damage Of the Ponsmentioning

confidence: 99%

Locked-in syndrome revisited

Schnetzer

McCoy

Bergmann

et al. 2023

Ther Adv Neurol Disord

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The locked-in syndrome (LiS) is characterized by quadriplegia with preserved vertical eye and eyelid movements and retained cognitive abilities. Subcategorization, aetiologies and the anatomical foundation of LiS are discussed. The damage of different structures in the pons, mesencephalon and thalamus are attributed to symptoms of classical, complete and incomplete LiS and the locked-in plus syndrome, which is characterized by additional impairments of consciousness, making the clinical distinction to other chronic disorders of consciousness at times difficult. Other differential diagnoses are cognitive motor dissociation (CMD) and akinetic mutism. Treatment options are reviewed and an early, interdisciplinary and aggressive approach, including the provision of psychological support and coping strategies is favoured. The establishment of communication is a main goal of rehabilitation. Finally, the quality of life of LiS patients and ethical implications are considered. While patients with LiS report a high quality of life and well-being, medical professionals and caregivers have largely pessimistic perceptions. The negative view on life with LiS must be overthought and the autonomy and dignity of LiS patients prioritized. Knowledge has to be disseminated, diagnostics accelerated and technical support system development promoted. More well-designed research but also more awareness of the needs of LiS patients and their perception as individual persons is needed to enable a life with LiS that is worth living.

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“…We read the case report of Kutiyal et al. 1 with great interest and would like to comment on the pathophysiology and bed side diagnostic aspects of locked-in syndrome (LIS) based on our earlier experiences 2 as well as making some suggestions.…”

mentioning

confidence: 99%

“…Thus, paralysis is not reversed immediately with antivenom as observed in this case. 1 Clinical recovery is usually slow in krait envenomation and takes approximately 3–5 days after exposure to the toxin, but neuromuscular function and reinnervation recover in general by a week.…”

mentioning

confidence: 99%