Systematic Reviews
Copyright ©The Author(s) 2024.
World J Clin Cases. Oct 16, 2024; 12(29): 6285-6301
Published online Oct 16, 2024. doi: 10.12998/wjcc.v12.i29.6285
Table 2 Cases of delayed-post hypoxic leukoencephalopathy reported
Ref.
Year of publication
Age
Gender
Cause of hypoxia
Comorbidities
Symptomatology
Time to onset of symptoms
Neuroimaging findings
Other neurodiagnostics
Therapeutic interventions
Complications
Outcomes
Aljarallah and Al-Hussain[7]201519MBenzodiazepine overdoseNoneComatose 21 daysT2WI: Diffusely increased signal intensity in cerebral white matter. DWI/ADC: Diffuse and symmetric diffusion restriction within the subcortical cerebral white matter and the right globus pallidus. T1WI: Patchy enhancement within cerebral white matterEEG: Diffuse slowing at 2-3 HzOsmolar therapyTonsillar herniation and brain deathDeath (23rd day of hospitalization)
Arciniegas et al[8]200424MOpioid and benzodiazepine overdoseNA21 daysExecutive dysfunctionT2WI: Diffusely increased signal intensity in cerebral white matterNAAmantadineNADid not return to baseline
Arimany et al[9]201743MHeroin overdoseSchizoaffective disorderAkinetic mutism and ataxia21 daysT2WI: Diffuse and symmetric increase in T2 signalNASupportiveNASignificant improvement at 16 weeks after overdose
Beeskow et al[10]201851FCarbon monoxide poisoningHypertension, obesity, sleep apnea syndrome, and depressionAgitation, reduced psychomotor activity, strange behavior. Progressed to mutism21 daysT2WI: Diffusely increased the T2 signal of the bilateral cerebral hemispheres and the basal gangliaNASupportiveNADischarged from neurological rehabilitation in 6 weeks. At nine months improvement in leukoencephalopathy with cerebral atrophy
Betts et al[11] 201246-59--Benzodiazepine overdose, ETOH abuseCognitive decline, speech disturbance, and memory loss17 days, 24 days, and 5 daysT2WI: Diffusely increased T2 signal of the bilateral cerebral hemispheres, including the globus pallidi. MRS: Decreased NAA, increased Cho/Cr ratioEEG: Diffuse slowingSupportiveNASignificant improvement in one patient. Persistent memory dysfunction in other two patients
Brovelli et al[12] 202255FOpioid intoxicationNonePsychomotor slowing, apathy, cognitive decline, akinetic mutism14 daysT2WI: Diffusely increased T2 signal within the frontal regions. DWI/ADC: The corresponding diffusion restriction was confirmed on the ADC maps EEG: Global slowingLogopedic and physiotherapic treatmentNoneAwake and collaborative, with mild hypomimia and decreased spontaneous speech upon discharge
Cardona Quiñones et al[13]202226MOpioid intoxication with cardiac arrestNoneAnton-Babinski syndromeFew daysT2WI: Bilateral cerebral hemisphere hyperintensities including corpus callosumNASupportiveNoneNA
Chachkhiani et al[14]202246MOpioid intoxication with respiratory failureHepatitis C, substance use disorder, mesial temporal lobe epilepsyPsychomotor agitation and abulia27 daysT2WI: Bilateral cerebral hemisphere hyperintensitiesEEG: Diffuse polymorphic delta activity. CSF: Normal High dose IVMP, and amantadine NoneDischarged on day 48 with mild abulia and day 138 with a normal clinical exam, except hyperreflexia. Radiographic resolution of cerebral white matter disease
Chen et al[15]202264MNitrite poisoning. Comatose on initial presentationNoneCognitive decline and mental and behavioral abnormalities60 daysT2WI: Hyperintensities of the bilateral cerebral hemisphere, involving the basal ganglia and the thalamus. DWI/ADC: Corresponding diffusion restriction involving NASupportiveNoneDid not regain functional independence at 6-month follow-up
Choi et al[16]201337MTraumatic cervical cord injuryNoneAkinetic mutism7 daysT2WI: Bilateral fronto temporal and basal ganglia hyperintensities NASupportiveNoneAt 2 months of follow-up, they continued to show cognitive disability and disorientation
Fong et al[17]201961FBenzodiazepine overdoseNoneNeuropsychiatric symptoms41 daysT2WI: Confluent cerebral white matter changes DWI/ADC: Associated diffusion restrictionEEG: Generalized slowing. CSF: NormalSupportiveNoneClinical improvement at follow-up (MoCA: 26/30). Repeat neuroimaging at 3 months showed improvement
Garzón-Hernández et al[18]202268MSevere acute respiratory syndrome-coronavirus 2related hypoxiaNoneUnresponsiveness17 daysT2WI: Confluent cerebral white matter hyperintensities. SWI: Cerebral microbleedsEEG: isolated polymorphic delta waves in the frontal region without epileptiform activitySupportiveNoneDischarged to rehab on day 30 of hospitalization
Geraldo et al[19]201461MCarbon monoxide poisoningNoneDisorientation, incoherent speech, and behavior disturbances39 daysT2WI: Confluent cerebral white matter hyperintensitiesCSF: NormalHyperbaric oxygen therapy (90 minutes daily sessions, 100 % oxygen at 2.5 atmospheres with a total of 40 sessions)NoneMild to moderate improvement and discharged to a rehabilitation facility
Gottfried et al[20]199436MOpioid overdoseNAQuadriparesis, myoclonic jerks, encephalopathy, cognitive decline24 daysT2WI: Increased supratentorial white matter signal. Hyperintense foci within globus pallidi. MRS: Decreased NAA; elevated choline and elevated lactateNANANASignificant improvement
Hakamifard et al[21]202139MOpioid (methadone) overdoseSubstance use disorderAphasia and decreased level of consciousnessApproximately 30 daysT2WI: Confluent cerebral white matter hyperintensitiesCSF: NormalVitamin E 400 mg/day, vitamin C 1000 mg/day, magnesium-sulfate 1000 mg/day and vitamin B complexNoneSignificant improvement in two months
Hamlin et al[22]202029 MOpioid overdoseSubstance use disorderMalignant catatonia, paroxysmal sympathetic hyperactivityApproximately 30 daysT1WI and T2WI: Confluent hyperintensities involving the bilateral centrum semiovaleEEG: No epileptiform dischargesPropranolol, clonidine, and lorazepamAkinetic mutism and sympathetic hyperactivity after electroconvulsive therapy (ECT)Moderate improvement in 30 days
Hori et al[23]199113Asphyxiation NAPseudobulbar paralysis, choreoathestosis7 daysLesion involving the putamen and caudate nucleiNANANASignificant improvement at 1.5 years
Hsiao et al[24]200411-79Carbon monoxide poisoning NACognitive impairment, akinetic mutism, and parkinsonism 14-45 daysT2WI: Increased signal within the subcortical white-matter, basal ganglia, and globus pallidusNANANAModerate to considerable improvement
Huarcaya-Victoria[25]201837 FCarbon monoxide poisoning NoneProgressive psychomotor agitation, catatonia, and cognitive declineApproximately 30 daysT2WI: Confluent cerebral white matter hyperintensitiesNAHyperbaric oxygen therapy (29 feet for one hour, 2.2 absolute atmospheres, 20 sessions). Aripiprazole and diazepam for the management of catatoniaNoneSignificant improvement and discharge to rehabilitation facility
Huisa et al[26] 201319, 32--Opioid overdoseNADecreased level of arousal, and encephalopathy58 days and 112 daysT2WI: Confluent cerebral white matter hyperintensities. ADC: Diffusion restriction in both cases with normalization at follow-up in case twoNANANAPersistent deficits in both cases
Jang et al[27]201750MCarbon monoxide poisoning NoneMyoclonus, dysarthria, decreased level of consciousness26 daysT2WI: Bilateral basal ganglia hyperintensities. DTT: Dysconnectivity involving the ascending reticular activating systemNASupportiveNoneDischarge to rehabilitation facility six weeks from initial presentation. No significant improvement
Jayakrishnan et al[28]202168FMyocardial infarctionHypertension, hyperlipidemia, and myocardial infarctionDrowsiness, behavioral changes, urinary incontinence21 daysT2WI: Diffuse hyperintensities involving the cortex. ADC: Diffusion restriction involving the basal gangliaNASupportiveNoneDischarge to hospice
Jingami et al[29] 202447MOpioid intoxicationNoneDecreased level of consciousness20 daysT2WI: Confluent cerebral white matter hyperintensities. N-isopropyl-(123I)-p-iodoamphetamineCSF: Elevated myelin basic protein 135.5 pg/mLHyperbaric oxygen (2.0 ATA, 60 minutes, 63 total)NoneImprovement in mini-mental status exam from unmeasurable to 15 on day 40 of hospitalization
Kim et al [30]200254-71Carbon monoxide poisoningNAMemory loss, confabulations, and akinetic mutism1-4 weeksT2WI: Confluent white matter hyperintensities in the brainNANANA4 patients with significant improvement
Law-ye et al[31]201858MCarbon monoxide poisoningNoneEncephalopathy14 daysT2WI: Confluent white matter hyperintensities in the brain. ADC: Diffusion restriction in the corresponding area CSF: NormalSupportiveNoneSignificant improvement
Lee et al[32]200171FBenzodiazepine overdoseNoneEncephalopathy14 daysT2WI: Confluent cerebral white matter hyperintensitiesCSF: Normal. EEG: Diffuse delta wave pattern SupportiveNoneSignificant improvement with discharge to rehabilitation facility on day 47
Lou et al[33]200962FCardiac arrest after gastrointestinal hemorrhageNAAkinetic mutism, rigidity14-21 daysT2WI: Confluent cerebral white matter hyperintensities involving the globus pallidi, and basal ganglia NANANANo significant improvement
Manjunath et al[34]202176MAcute respiratory distress syndromeNACognitive declineFew weeksT2WI: Confluent cerebral white matter hyperintensities. ADC: Diffusion restriction in corresponding areaNASupportiveNoneSignificant clinical improvement over 3 months. With significant radiographic improvement in 4 months
Mazo et al[35]202066MCarbon monoxide poisoningNoneEncephalopathy12 daysT2WI: Increased signal within the bilateral globus pallidusCSF: NormalSupportiveNoneNo significant improvement
Meyer et al[36]201343FBenzodiazepine overdoseNoneEncephalopathy--T2WI: Confluent cerebral white matter hyperintensities. MRS: High peak for choline and creatinineEEG: Generalized slowingSupportiveNoneSignificant improvement in a few months
Mittal et al[37]201038MPolysubstance abuseNAEncephalopathy, akinetic mutism21 daysT2WI: Confluent cerebral white matter hyperintensitiesNASteroids and antioxidantsNoneSignificant improvement
Molloy et al[38]200640FOpioid overdoseNAAgitation, echolalia17 daysT2WI: Confluent cerebral white matter hyperintensities. ADC: With associated restricted diffusionCSF: NormalSupportiveNoneSignificant improvement over 6 months
Newburn et al[39]202419MBenzodiazepine overdoseDevelopmental delay Cognitive decline--DSIR: High signal in the white matter of the brainNASupportiveNoneMild improvement
Newburn et al[39]202420MSuicide attempt (hanging) Substance abuseCognitive decline--DSIR: High signal in the white matter of the brainNASupportiveNoneMild improvement
Nzwalo et al[40]201155FBenzodiazepine overdoseNAAkinetic mutismNAT2WI: Confluent cerebral white matter hyperintensitiesCSF: NormalSupportiveNANo significant improvement
Pfaff et al[41]202281MUnilateral internal carotid artery occlusionAcute myeloid leukemia, hypertension, hyperlipidemiaEncephalopathy13 daysT2WI: Increased signal within the left centrum semiovaleNASupportive; mechanical thrombectomyNoneClinical and radiographic improvement on day 92 of hospitalization
Quinn et al[42]201456FOpioid overdoseSchizoaffective disorder, cirrhosisCatatonia21 daysT2WI: Confluent cerebral white matter hyperintensitiesEEG: generalized polymorphic theta waves, 2-3 Hz delta waves, and superimposed beta waves ECT, methylprednisoloneNoneNo significant improvement
Rozen et al[43]201259--Opioid overdoseNAAkinetic mutism21 daysT2WI: Confluent cerebral white matter hyperintensities including the globus pallidiNAIV MagnesiumNoneSignificant improvement
Salazar et al[44]201254MOpioid overdoseNAEncephalopathy, and rigidity21 daysT2WI: Confluent cerebral white matter hyperintensities. ADC: Diffusion restriction involving the globus pallidiNALevodopa for rigidityNoneSignificant improvement
Singu et al[45] 201766MLeft main coronary artery occlusionHypertension, hyperlipidemia, diabetes mellitus, myocardial infarctionAphasia, dysexecutive syndrome35 daysT2WI: Cerebral white matter hyperintensities involving the L MCA territory. ADC: Corresponding region hypointense. SPECT: 60%-70% decrease in CBF CSF: Elevated protein SupportiveNoneModerate improvement
Smolinsky et al[46]201816FTraumatic brain injuryNoneEncephalopathy8 daysDWI/ADC: Restricted diffusion involving right frontoparietal lobes, right temporal lobe, and left parietal lobe, and corpus callosumNoneAmantadineNoneMild improvement
Tahir and Islam[47] 202143METOH abuseNoneEncephalopathy6 daysDWI/ADC: Diffusion restriction involving the bilateral centrum semiovaleCSF: Normal. EEG: Paroxysmal epileptiform activity SupportiveNoneDeath
Tainta et al[48]201843MPolysubstance abuseSchizophreniaDecreased level of consciousness21 daysT2WI: Confluent cerebral white matter hyperintensities. DWI/ADC: Diffusion restriction involving the bilateral centrum semiovaleNASupportive NoneSignificant improvement in 2.5 months
Tan and Teo[49]202364MCarbon monoxide poisoningNAPsychomotor agitation7 daysT2WI: Hyperintensities involving the bilateral globus pallidus NASupportiveNoneNA
Tormoehlen et al[50]201346FCarbon monoxide poisoningNAPseudobulbar affect14 daysT2WI: Confluent cerebral white matter hyperintensitiesNASupportiveNAUnknown
Wallace et al[51]200928MPolysubstance abuseETOH abuseEncephalopathy 35 daysT2 BLADE: Hyperintensities involving the bilateral centrum semiovaleEEG: NormalSupportiveVentilatory and hemodynamic support Significant improvement at 12 months
Wang and Yang[52]200315MSubstance abuseNASeizures, dysphagia, dystonia, and altered mental statusNAT2WI: Bilateral globus pallidi hyperintensitiesNASupportiveNANA
Weinberger et al[53]199434--Benzodiazepine overdoseNAEncephalopathy, hyperreflexia, clonus, primitive reflexes, and frontal lobe release sign24 daysIncreased signal within the supratentorial white matterNANANAPersistent cognitive decline
Zamora et al[54]201564MCardiopulmonary arrestNAPsychomotor agitation23 daysT2WI: Confluent cerebral white matter hyperintensities. ADC: Increased signal less extensive than T2WINANANoneModerate improvement
Zamora et al[54]201532MOpioid abuseNAEncephalopathy32 days
T2WI: Confluent cerebral white matter hyperintensities. ADC: More extensive than T2WI NANANoneSignificant improvement
Zamora et al[54]201563FPolysubstance abuseNAAkinetic mutism35 daysT2WI: Confluent cerebral white matter hyperintensities.ADC: Matched signal to T2WI NANANoneSignificant improvement
Zamora et al[54]201565MPolysubstance abuseNAEncephalopathy14 daysT2WI: Confluent cerebral white matter hyperintensities. ADC: Increased signal less extensive than T2WINANANoneSignificant improvement
Zamora et al[54]201559FOpioid abuseNACatatonia14 daysT2WI: Confluent cerebral white matter hyperintensities. ADC: Matched signal to T2WINANANoneDeceased
Shprecher et al[55]200839-56--Polysubstance abuseNACatatonia, memory loss, disorientation, encephalopathy31 days-38 weeksT2WI: Confluent cerebral white matter hyperintensities. ADC: Diffusion restriction in 2 cases. MRS: Decreased NAANANANANo significant improvement