Corticosteroids in posterior reversible encephalopathy syndrome: Friend or foe? A systematic review

Table 2 Cases of posterior reversible encephalopathy syndrome determined to have corticosteroids as a causal agent

Case No.	Ref.	Age (year)	Sex	Clinical sequela	BP (mmHg)	MRI findings	Vessel imaging	CSF studies	Cause	LOS (days)	Management	Outcomes
1	No author[23], 2016	33	F	Subarachnoid hemorrhage	N/A	Although no magnetic resonance imaging and vessel imagining was performed, cranial imaging showed hypodense areas in small acute infarcts and temporal, parieto, and occipital regions. Later, a repeat cranial imaging showed delineation of hypodensities in temporal-parieto-occipital regions	N/A	N/A	Methylprednisolone pulse therapy	Not specified but > 11	For seizures, anticonvulsants were administered. For SLE hydrocortisone along with mycophenolate mofetil. The patient was treated for pneumonia and underwent hemodialysis	Follow up: Normal brain parenchyma revealed by CT a year later. Outcome: Less edematous and seizures stopped
2	Alexander et al[24], 2013	16	M	Three episodes of tonic clonic seizures, tubulitis, and increased systolic blood pressure	220	FLAIR MRI revealed bilateral multifocal subcortical hyperintensities in the parietal lobe. Furthermore, there was relative sparing in the left frontal lobe, which means that there were less severe hyperintense lesions there. There was involvement/lesions of the deep white matter of the ganglionic region and of the right internal capsule. Areas with high signal intensities reveal vasogenic edema, as shown by increased ADC values	N/A	N/A	Higher doses of tacrolimus, corticosteroids, and being of a young age were factors causing PRES. Additionally, an extended period of uremia before transplantation led to PRES	9	The patient received five oral antihypertensive drugs. This included antiepileptic levetiracetam and minoxidil. The dose of tacrolimus was increased	Follow up: 6 weeks later had complete resolution of brain abnormalities. Outcome: Fully recovered
3	Camara-Lemarroy et al[25], 2015	22	F	Renal decline, severe bilateral occipital headache, seizures, confusion, hyperreflexia, reduced visual acuity	170/100	A T2 FLAIR of the occipital, parietal, and frontal lobes (subcortical) revealed bilateral hyperintensities. These findings are indicative of vasogenic edema with no diffusion restriction observed in DWI	N/A	N/A	Immunosuppressive therapy: Pulses of pulses of methylprednisolone	8	Hemodialysis, immunomodulation analgesic, IV diazepam (10 mg), IV nitroglycerin, IV phenytoin	Follow up: N/A. Outcome: After 24 hours, the patient recovered completely, the seizures stopped
4	Chennareddy et al[26], 2013	17	F	Case 1: Headache, blurry vision, and tonic-clonic seizures	Case 1: 110/70	Case 1: FLAIR hyperintense signal in the left occipital lobe. DWI: Showed no restriction in the left occipital lobe	N/A	N/A	Case 1: Endothelial dysfunction caused by SLE and pathologic dysregulation of cerebral blood flow that was exacerbated by methylprednisolone (in enhancing the vascular tone) caused PRES	Case 1: Estimated 5 days	Case 1: Analgesics and anticonvulsants	Follow up for Case 1: N/A. Outcome for Case 1: No flare-up of lupus, no more seizures, decreased headaches, well
5	Chennareddy et al[26], 2013	16	F	Case 2: Headache, blurred vision	Case 2: 120/70	Case 2: A hyperintense signal in the bilateral occipital areas that was suggestive of PRES	Case 2: N/A	Case 2: N/A	Case 2: N/A	Case 2: Estimated 7 days	Case 2: N/A	Follow up for Case 2: N/A. Outcome for Case 2: Headache went away, nephritis absent, and well
6	Wee et al[27], 2020	19	M	Epilepticus, altered sensorium, HTN	170/116	The non-contrasted CT scan revealed hypodensities of white matter at the bifrontal, bilateral occipital, left cerebellum and left parietal lobe. Also, contrast CT did not reveal venous thrombosis	N/A	N/A	Methylprednisolone	10	For aspiration pneumonia, intravenous antibiotics and antiepileptics along with intermittent hemodialysis were administered	Follow up: N/A. Outcome: His GCS value returned to normal after one week in the ICU
7	Ding et al[28], 2015	40	M	HTN, headache, two episodes of generalized tonic-clonic seizures	159/93	High signals seen on T2-weighted, FLAIR MRI, DWI, ADC. Comparable signals on T1 and enhanced sequence in the bilateral parieto-occipital lobes	N/A	Unrevealing	Methylprednisolone	Approximately 7	Irbesartan and edaravone. A week later, he continued antihypertensive drugs with a tapering dose of methylprednisolone	Follow up: N/A. Outcome: Neurological symptoms improved. MRI showed a significant decrease in abnormal signals
8	Fujita et al[29], 2008	23	F	Fever, headache, fatigue, vomiting, tonic-clonic seizures	180/120	T2WI/ADC: Increased bilateral parietal lobes. However, there were no significant signal alterations in DWI. Contrast MRI showed hyperintense signals on T2 and FLAIR images in the bilateral temporal–parietal–occipital lobes, left frontal lobe, and left cerebellar hemisphere. MRI showed more hyperintense signals on T2 and FLAIR images in the bilateral temporal–parietal– occipital lobes and left cerebellar hemisphere	The MRA did not show abnormalities in the cerebrovascular system except for a less important flow signal from the left vertebral artery. This is indicative of involvement of disease with the left vertebral artery. Cerebral angiography revealed no intracranial aneurysm	Normal	Pulse dose methylprednisolone	60	Diazepam, phenytoin, and nifedipine; Cyclophosphamide plasmapheresis; Thiopental; Betamethasone; Oral prednisolone; high-dose; methylprednisolone	Follow up: N/A. Outcome: A physical examination revealed no neurological deficits and CRP became negative, seizures disappeared
9	Fukuyama et al[30], 2011	6	M	Generalized seizures, drowsiness, cortical blindness	157/110	MRI revealed high signal intensities in the posterior medial frontal regions consistent with vasogenic edema. ADC mappings and DWI revealed restricted diffusion in focal areas that were again consistent with vasogenic edema	N/A	Before developing PRES, patient had normal CSF levels	Methylprednisolone was listed as a risk factor for PRES in this patient. Also, the patient most likely developed PRES due to HSCT that included mPSL	N/A	mPSL, BMT, methotrexate, FK506, magnesium, intravenous nicardipine, myeloid engraftment, mycophenolate mofetil, VPA	Follow up: The patient died from gastrointestinal hemorrhagic shock. Outcome: N/A
10	Gera et al[31], 2014	5	F	Headache, cortical blindness, seizure	180/100	MRI revealed lesions in the parietal and occipital lobe	N/A	N/A	3 pulses of methylprednisolone	N/A	For renal disease and renal failure, timely correction of fluid electrolyte was performed along with acid base balance. For hypertension, antihypertensives and nitroglycerin drips were administered. IV albumin was administered for hypoalbuminemia. Lastly, HUS was treated using plasma exchanges and methylprednisolone medication dose adjustment	Follow up: Cranial images were normal after 4-5 weeks. Outcome: Recovery of complete renal and neurological function
11	El Hage et al[32], 2021	15	M	Seizure, headache, HTN	210/136 during PRES max. 150/82	T2WI: Increased subcortical and bilateral occipital, parietal, and superior frontal areas	N/A	N/A	Corticosteroid was listed as a precipitating factor	N/A	Antihypertensives and antiepileptic medications	FU: Brain MRI was normal after three months. Outcome: Recovered
12	İncecik et al[33], 2013	8	M	Headache, confusion, seizures, HTN	150-90 - 160/100	T2WI: Increased signal in the bilateral parieto-occipital lobe and left frontal lobe	N/A	N/A	Pulse IV methylprednisolone; HTN	N/A	Levetiracetam, pulse dose IVMP	Follow up: N/A. Outcome: Neurological symptoms improved and after 15 days, MRI showed significant reversal
13	Irvin et al[34], 2007	48	F	Disoriented, agitated, autonomic instability, HTN	190/100	T2WI: Diffuse cortical and subcortical white matter signal abnormality in a symmetric bilateral distribution involving predominantly the occipital areas, superior frontal areas, the cerebellum, and some focal areas of the thalamus bilaterally, not evident on T1-weighted images	Same as left	Normal limits	Dexamethasone-induced PRES	N/A	Trazodone and zolpidem, and a single dose of haldol	Follow up: A repeat brain MRI 4 days later showed improving PRES. Outcome: Hospice was started and she did not receive radiation therapy to the brain
14	Ismail et al[35], 2021	57	F	N/A	N/A	T2WI: Bihemispheric and extensive symmetric diffusion impairment (parieto-occipital, temporal, cerebellar, frontal, and temporal) hypersignal (cortical and subcortical)	N/A	N/A	Methylprednisolone	N/A	Levetiracetam and valproate	Follow up: N/A. Outcome: Died from PRES and confirmed from autopsy
15	Kamezaki et al[36], 2012	62	F	High fever	180/118	T2WI: High signal intensity in the pons, cerebral hemisphere, basal ganglia, thalamus bilaterally. T2 star-weighted images show low intensity signals in the right thalamus. Diffusion-weighted images reveal high signal intensity in the same region	N/A	Normal	Chemotherapeutic agents which included methylprednisolone were listed as a possible factor	120	Unspecified but rehabilitation was used	Follow up: MRI revealed complete resolution of lesions. Outcome: N/A
16	Kamo et al[37], 2019	51	F	Abducens palsy left eye, left-sided dysesthesia, dysarthria	202/127	MRI of the brain on DWI revealed isointense area in the pons. Additionally, it revealed a circumscribed hyperintense area on both the ADC and FLAIR. DWI, ADC map and FLAIR imaging showed vasogenic edema caused by PRES	N/A	N/A	IV methylprednisolone	N/A	Nicardipine with tranexamic acid and glycerol were administered. Plasmapheresis	Follow up: N/A. Outcome: Final NIHSS lowered to 3. From therapy, blindness improved to light perception. Sensory disturbance on the left side and cerebellar ataxia of both the lower and upper limbs persisted
17	Khan et al[38], 2018	Patient 1: N/A; M Note: The mean age of all patients was 7 years	M	HTN; Note: Seizures and altered mental status were symptoms for > 90% of the symptoms for > 90% of cases although it was not specifically stated which cases had which symptoms	N/A	MRI revealed abnormalities in parietal cortex	N/A	WBC: 0; RBC: 1000; Cyto: Neg	Dexamethasone	N/A	Levetiracetam, methotrexate	Follow up: Alive. Outcome: Symptom resolution and PRES scan done after treatment showed resolvement
18	Khan et al[38], 2018	Patient 2: N/A	M	N/A	N/A	MRI revealed abnormalities in the parietal cortex and subcortical region	N/A	WBC: 1; RBC: 3; Cyto: Neg	Dexamethasone, steroid-induced hypertension that might lead to PRES	N/A	Levetiracetam, methotrexate	Follow up: Alive. Outcome: Symptom resolution and PRES scan after treatment showed resolvement
19	Khan et al[38], 2018	Patient 3: N/A	M	HTN	N/A	MRI revealed abnormalities in parietal cortex, subcortical region, and anterior cortex	N/A	WBC: 0; RBC: 2; Cyto: Neg	Dexamethasone, steroid-induced hypertension that might lead to PRES	N/A	Methotrexate	Follow up: Dead. Outcome: No symptom resolution and no PRES scan done after treatment
20	Khan et al[38], 2018	Patient 4: N/A	F	HTN	N/A	MRI revealed abnormalities in parietal cortex, subcortical region, and anterior cortex	N/A	WBC: 1; RBC: 1; Cyto: Neg	Dexamethasone	N/A	Levetiracetam, methotrexate	Follow up: Alive. Outcome: Unimproved
21	Khan et al[38], 2018	Patient 5: N/A	F	HTN	N/A	MRI revealed abnormalities in parietal cortex, subcortical region, and anterior cortex	N/A	WBC: 0; RBC: 0; Cyto: Neg	Dexamethasone	N/A	Levetiracetam,methotrexate	Follow up: Deceased. Outcome: No symptom resolution and no PRES scan done after treatment
22	Khan et al[38], 2018	Patient 8: N/A	M	HTN	N/A	MRI revealed abnormalities in the parietal cortex	N/A	WBC: 0; RBC: 1000; Cyto: Neg	Dexamethasone, steroid-induced hypertension that might lead to PRES	N/A	Phenytoin, methotrexate	Follow up: Dead. Outcome: No symptom resolution and no PRES scan done after treatment
23	Khan et al[38], 2018	Patient 9: N/A	M	N/A	N/A	MRI revealed abnormalities in the parietal cortex and anterior cortex	N/A	WBC: 0; RBC: 2000; Cyto: Neg	Dexamethasone, steroid-induced hypertension that might lead to PRES	N/A	Levetiracetam	Follow up: Alive. Outcome: Symptom resolution but PRES scan didn’t show resolution after treatment
24	Khan et al[38], 2018	Patient 10: N/A	M	HTN	N/A	MRI revealed abnormalities in parietal cortex, subcortical region, and anterior cortex	N/A	WBC: 0; RBC: 0; Cyto: Neg	Dexamethasone, steroid-induced hypertension that might lead to PRES	N/A	Methotrexate	Follow up: Alive. Outcome: Symptom resolution but no PRES scan done after treatment
25	Khan et al[38], 2018	Patient 11: N/A	M	HTN	N/A	MRI revealed abnormalities in parietal cortex, subcortical region, and anterior cortex	N/A	WBC: 0; RBC: 0; Cyto: Neg	Dexamethasone, steroid-induced hypertension that might lead to PRES	N/A	Levetiracetam, phenytoin, and methotrexate	Follow up: Alive. Outcome: Symptom resolution and PRES scan after treatment showed resolvement
26	Khan et al[38], 2018	Patient 14: N/A	M	HTN	N/A	MRI revealed abnormalities in the parietal cortex and anterior cortex	N/A	WBC: 5; RBC: 35; Cyto: Neg	Dexamethasone, steroid-induced hypertension that might lead to PRES	N/A	Phenytoin, methotrexate	Follow up: Dead. Outcome: No symptom resolution and no PRES scan done after treatment
27	Khan et al[38], 2018	Patient 15: N/A	M	HTN	N/A	MRI revealed abnormalities in the parietal cortex and anterior cortex	N/A	WBC: 0; RBC: 0; Cyto: Neg	Dexamethasone, steroid-induced hypertension that might lead to PRES	N/A	Phenytoin	Follow up: Alive. Outcome: Symptom resolution but no PRES scan done after treatment
28	Khan et al[38], 2018	Patient 18: N/A	M	HTN	N/A	MRI revealed abnormalities in the parietal cortex	N/A	WBC: 2; RBC: 1; Cyto: Neg	Dexamethasone, steroid-induced hypertension that might lead to PRES	N/A	Phenytoin, methotrexate	Follow up: Alive. Outcome: Symptom resolution and PRES scan done after treatment showed partial resolvement
29	Khan et al[38], 2018	Patient 19: N/A	F	HTN	N/A	MRI revealed abnormalities in the parietal cortex	N/A	N/A	Dexamethasone, steroid-induced hypertension that might lead to PRES	N/A	Phenytoin, methotrexate	Follow up: Dead. Outcome: No symptom resolution and no PRES scan done after treatment
30	Khanjar et al[39], 2018	Patient 1: 34	F	Tonic-clonic seizures, headache, decreased vision, HTN. All patients reported headache and impaired vision	Case 1: 190/100; Cases 2, 3 and 4: N/A	T2WI: Patchy multi-focal increased signal within the parietal-occipital cortical and subcortical areas bilaterally	N/A	N/A	PRES was caused by the initiation of immunosuppressive therapy, mostly due to pulse methylprednisolone therapy	6	Management of blood pressure and seizures along with mechanical ventilation	Follow up: N/A. Outcome: Successfully managed
31	Khanjar et al[39], 2018	Patient 2: 23	F	Tonic-clonic seizures, HTN, and renal decline	N/A	T2WI: Patchy multi-focal increased signal within the parietal-occipital cortical and subcortical areas bilaterally	N/A	N/A	PRES was caused by the initiation of immunosuppressive therapy, mainly due to pulse methylprednisolone therapy	16	Intubation, antihypertensives, antiepileptics, mechanical ventilation	Follow up: N/A. Outcome: Improved dramatically
32	Khanjar et al[39], 2018	Patient 3: 41	F	N/A	N/A	T2WI: Patchy multi-focal increased signal within the parietal-occipital cortical and subcortical areas bilaterally	N/A	N/A	PRES was caused by the initiation of immunosuppressive therapy, mostly due to pulse methylprednisolone therapy	16	Intubation, hemodialysis, antihypertensive, antiepileptic, mechanical ventilation	Follow up: N/A. Outcome: Complete resolution
33	Khanjar et al[39], 2018	Patient 4: 29	F	Seizures, diffuse alveolar hemorrhage, hemophagocytic lymphocytosis	N/A	MRI indicated PRES	N/A	N/A	PRES was caused by the initiation of immunosuppressive therapy, mainly due to pulse methylprednisolone therapy	20	Rehab, mechanical ventilation	Follow up: N/A. Outcome: Patient required rehab but eventually recovered
34	Kitamura et al[40], 2022	84	F	Fatigue, mental status deteriorated, leg numbness	1288/58	A DWI and MRI revealed vasogenic oedema after showing mild hyperintensity and higher signal of an ADC map of the parietal, bilateral occipital, frontal cortex, midbrain, and subcortical white matter. FLAIR-MRI findings also revealed an increased signal intensity of the previously mentioned regions, suggesting PRES	N/A	N/A	Methylprednisolone pulse therapy, prednisolone	At least 53 days	Rituximab, IV immunoglobulin, plasma exchange, hemodialysis, eculizumab, meningococcal vaccination, prednisolone was reduced	Follow up: 8 month follow up showed no relapse. Outcome: 56 days after admission. MRI showed PRES was resolved
35	Kumar and Rajam[41], 2011	6	M	HTN, absence of visual fixation, seizures, cortical blindness, fever, macular rash	N/A	T2WI: bilateral focal hyperintensities in the occipital lobes involving cortical and subcortical white matter during the acute phase; mild diffuse brain atrophy	N/A	N/A	Pulse methylprednisolone therapy; HTN due to steroids	Approximately 3-4 months	High dose oral prednisolone; second course of methylprednisolone; cyclosporine, etoposide and dexamethasone (HLH-2004 protocol); ventilation	Follow up: N/A. Outcome: Full neurological recovery, no existing illness, disease control due to cyclosporine
36	Kurahashi et al[42], 2006	4	F	Lethargic, convulsions, coma	160/100	T2WI: hyperintensities in the white matter of the bilateral occipital lobes	CSF no abnormalities	N/A	Methylprednisolone	At least 67 days	Intravenous hydrocortisone, continuous inhalation of b-2 stimulator, and additional oxygen; Sevoflurane; Furosemide; nicardipine, phenobarbital, and mannitol	Follow up: She presents no neurological sequelae 2 years after the event. Outcome: FLAIR image on the 67th hospital day shows resolution of hyperintensities
37	Dar et al[43], 2015	51	F	Seizure, headache, HTN	N/A	MRI of the spine showed long segment myelitis. MRI of the brain revealed bilateral diffuse white matter edema and faint restricted diffusion in the subcortical and cortical regions. This was suggestive of PRES	N/A	N/A	IV methylprednisolone and IV vitamin B12	N/A	Treatment with methylprednisolone and dexamethasone for 1 month	Follow up: Alert and coherent during activities. Outcome: Recovered significantly
39	Mimura et al[44], 2023	73	F	Consciousness deteriorated	140/80	FLAIR MRI showed multiple lesions with high signal intensity	N/A	N/A	Steroid administration increases blood pressure due to fluid retention and can be a risk factor for the development of PRES	At least 11 days	Intravenous methylprednisolone oral prednisolone; Rituximab; Intravenous administration of nicardipine and fluid removal by hemodialysis	Follow up: N/A. Outcome: blood pressure decreased and her consciousness improved dramatically
40	Morrow et al[45], 2015	53	F	Insomnia, dizziness, general malaise, and a headache, holocephalic headache	199/110	T2 hyperintensities were found in the cervical cord and brain that are suggestive of MS, same MRI results as six months earlier. In addition, there was an abnormal T2 signal in the posterior occipital, posterior white matter extending to the vertex, and in both thalami. Along with the new lesions, mild local sulcal effacement was observed. They found no diffusion restrictions based on the lesions. Overall, the findings were indicative of a diagnosis of PRES	N/A	N/A	Corticosteroids, HTN	N/A	High dose CR. 1250 mg oral prednisone. Hydrochlorothiazide and amlodipine. Labetalol and amlodipine	Follow up: 1 month follow-up neurologically stable. Outcome: One month later, the signal change resolved in the posterior cerebral hemispheres, consistent with the resolution of PRES
41	Nguyen et al[46], 2009	32	F	Nausea, seizures, dizziness, forgetfulness	112/85	MRI revealed multifocal areas of increased non-enhancing T2-Weighted FLAIR signals. This was found within the white matter of both hemispheres	N/A	N/A	Dexamethasone	N/A	Aprepitant, palonosetron, lorazepam, oral dexamethasone, rescue prochlorperazine, ondansetron, prochlorperazine, diphenhydramine, Dronabinol, diazepam, and fosphenytoin	Follow up: 1 month MRI showed full resolution. Outcome: Returned to baseline in one week. Dexamethasone doses were tapered and eventually discontinued
42	Ozkok et al[47], 2012	22	F	HTN	N/A	MRI from T2-weighted and FLAIR revealed lesions in the bilateral cortical occipital lobe	N/A	N/A	Hypertension and methylprednisolone were listed as the highest risk factors	Approximately 14	3 times a week, hemodialysis and antihypertensive treatment with amlodipine and doxazosin	Follow up: Her renal functions failed to improve and became anuric. However, she had no respiratory symptoms. Outcome: PRES resolved within 2 weeks
43	Shibata et al[48], 2022	51	F	Headache, tonic-clonic seizures	205/107	FLAIR sequences MRI revealed a bilateral occipital subarachnoid hemorrhage, parenchymal hemorrhage in the left occipital lobe, and hyperintense lesions of the subcortical white matter of both occipital lobes. The lesion in the left occipital lobe showed hyperintensity on the ADC map suggesting vasogenic edema	MRA: A partial resolution of signal change and vasoconstrictions in the bilateral middle cerebral arteries and posterior cerebral arteries	N/A	Intravenous methylprednisolone pulse	12	Diazepam, phenytoin, levetiracetam, antihypertensive therapy	Follow up: N/A. Outcome: Discharged without any neurological deficits
44	Sinha and Hurley[49], 2008	16	F	Disorientation, motor apraxia, blurred vision, headache	150/80-160/90	Axial FLAIR and turbo spin echo T-2 weighted images revealed increased signal intensity in the occipital and left parietal regions. DWI and ADC images did not reveal any restricted diffusion pattern	N/A	N/A	PRES was linked to corticosteroid	N/A	Cyclophosphamide and high oral dose	Follow up: MRI taken 6 weeks after starting treatment revealed resolution of the lesions. Outcome: N/A
45	Stârcea et al[50], 2018	10	F	Seizures, respiratory distress, bilateral amaurosis, drooling, renal decline	120/65	T2FLAIR/DWI: Cortical hyperintensity in the parietal lobe, indicating damage to white matter; white matter damage; degeneration with diffuse demyelination in the parietal and posterior occipital lobes	N/A	Normal	Immunosuppressive therapy: Methylprednisolone	N/A	Mechanical ventilation, blood transfusions, platelet concentrate, antibiotic therapy, continuous veno-venous hemofiltration, nifedipine, clonidine, dialysis	Follow up: 6 months. Outcome: No neurological problems, fully recovered, regular hemodialysis sessions
46	Swarnalatha et al[51], 2012	11	F	Generalized tonic clonic seizures	110/60	MRI of the brain revealed asymmetrical bilateral T2-weighted and FLAIR revealed hyperintense lesions in subcortical location of parieto-occipital, cortical, temporal lobes, cerebellum, and bilateral thalami indicative of PRES	N/A	CSF fluid analysis showed protein: 15 mg/dL, 3 cells/hpf, glucose: 56 mg/dL	Corticosteroid was listed as a possible factor leading to vasogenic edema, a characteristic of PRES	N/A	The patient was treated with antiepileptics and her dose was reduced to half of prednisolone	Follow up: N/A. Outcome: Recovered in 48 hours after the treatment listed in the left column
47	Tsukamoto et al[52], 2012	28	F	Generalized tonic-clonic convulsions with loss of consciousness	150/100	Both FLAIR and DWI MRI revealed cortical and subcortical hyperintensities in the occipital lobes, left thalamus, and bilateral frontal lobe. ADC revealed high signal intensities in the lesions of T2 shine through	The MRA did not reveal vascular abnormalities	The CSF was normal without any infiltration of leukemic cells	Induction chemotherapy which included prednisone. It was also stated that corticosteroids along with l-asparaginase and vincristine may cause PRES	N/A	Nifedipine was used to control blood pressure and midazolam was used as an anticonvulsant. Consolidation therapy and intrathecal administration. Underwent BMT for ALL	Follow up: Completely recovered from PRES without leukemia relapse. Outcome: MRI revealed significant resolution of lesions but still had difficulty walking, leg pain, and somnolence
48	Ulutaş et al[53], 2020	39	M	Tonic clonic seizures, severe headaches, HTN	160/110	White matter Hyperintense vasogenic edema lesions were found primarily on the right side of the posterior brain, as revealed by T2-weighted sequences	N/A	Nerve conduction studies and CSF analysis both revealed dysautonomic inflammatory demyelinating polyneuropathy and albuminocytologic dissociation, respectively	Patient developed PRES because of intensive immunosuppressive treatment that consisted of CyC and pulse steroid therapy	N/A	The patient was treated with antiedema therapy and antiepileptics. To control blood pressure, parenteral antihypertensive agents were administered	Follow up: Passed away. Outcome: No clinical improvement
49	Vernaza et al[54], 2021	34	F	Holocranial pulsatile cephalalgia with photophobia, headache, tonic-clonic seizure	N/A	In both T2-weighted and FLAIR scans, there were hyperintensities in the cerebellar corticosubcorctical and parieto-occipital regions	Angiography and computed tomography showed a suboccluding thrombus in the right internal jugular vein and mild subarachnoid hemorrhage in both sides of the frontal lobe	No lumbar puncture	Methylprednisolone; immunosuppressive treatment	17 days	Cyclosporine, IV artesunate, chloroquine and primaquine	Follow up: Died due to multiorgan failure. Outcome: 5 days later in the emergency department. Patient complained of gastrointestinal problems
50	Yang et al[55], 2022	Patient 1: 48	F	Sleepiness, diplopia	120/74	Lesions found in the parietal and occipital lobe	N/A	N/A	Intravenous methylprednisolone was found to be an inducing factor for PRES	N/A	No treatment for PRES	Follow up: N/A. Outcome: Partial brain lesion resolution
51	Yang et al[55], 2022	Patient 2: 53	F	Headache, giddiness	Normal (not specified)	Lesions found in the temporal, parietal, and occipital lobe	N/A	N/A	Intravenous methylprednisolone was found to be an inducing factor for PRES	N/A	Unknown	Follow up: N/A. Outcome: Unknown
52	Yang et al[55], 2022	Patient 3: 35	F	Sleepiness, Visual impairment, delirium	N/A	Lesions found in the temporal lobe	N/A	N/A	Intravenous methylprednisolone was found to be an inducing factor for PRES	N/A	Unknown	Follow up: N/A. Outcome: Partial brain lesion resolution
53	Yang et al[55], 2022	Patient 4: 48	F	Epilepsy, visual impairment	N/A	Lesions found in the semiovale, temporal and occipital lobe of the center	N/A	N/A	Intravenous methylprednisolone was found to be an inducing factor for PRES	N/A	Reduction/tapering of IVMP	Follow up: N/A. Unknown
54	Yang et al[55], 2022	Patient 5: 51	F	Headache	202/127	Lesions found in the brain stem	N/A	N/A	Intravenous methylprednisolone was found to be an inducing factor for PRES	N/A	Antihypertension and plasma exchange	Follow up: N/A. Complete resolution of brain lesion
55	Zekić et al[56], 2017	18	F	The patient had fever, leg oedema, lupus nephritis, acute arthritis, and malaise	160/100	Transverse sequence T2 and FLAIR magnetic resonance imaging revealed subcortical and cortical hyperintensities of the right frontal lobe and both sides of the parietal brain lobe	N/A	No abnormalities were found by brain CT scans, cytological and bacteriological analysis of the CSF	Intravenous pulse therapy with methylprednisolone	N/A	Antihypertensive, antiedema, and antiepileptic therapy	Follow up: 1 year. Successfully delivered a child and was in complete clinical remission due to SLE. Outcome: Full neurological recovery
56	Zhang et al[57], 2018	22	F	Sudden epileptic attacks, onset of seizures, HTN	190/130	MRI of cranium revealed vasogenic edema at both sides of the parietal region, occipital parietal regions, and centrum ovale	N/A	The CSF pressure was observed as 330 mm H2O, the protein level was normal, the white blood cell count was 0 cell/mm3, and no signs of infection	Intravenous methylprednisolone 80 mg daily induced hypertension which caused PRES	N/A	Corticosteroid impulse therapy was not administered. Drugs were administered to decrease intracranial pressure, intravenous drugs to lower blood pressure, anmidazolam for sedation	Follow up: N/A. Outcome: Recovered the next day after starting treatment

BP: Blood pressure; MRI: Magnetic resonance imaging; CSF: Cerebrospinal fluid; LOS: Length of stay; SLE: Systemic lupus erythematosus; CT: Computerized tomography; ADC: Apparent diffusion coefficient; PRES: Posterior reversible encephalopathy syndrome; DWI: Diffusion-weighted imaging; GCS: Glasgow coma scale; ICU: Intensive care unit; HTN: Hypertension; T2WI: T2-weighted imaging; MRA: Magnetic resonance angiography; CRP: C-reactive protein; mPSL: Methylprednisolone; HUS: Hemolytic uremic syndrome; IVMP: Intravenous methylprednisolone pulse; WBC: White blood cell; RBC: Red blood cell; Cyto: Cytology; CR: Creatinine; ALL: Acute lymphoblastic leukemia; N/A: Not applicable.