Publication date: Mar 5, 2020 Publication description: Utah ACP Chapter Presentation of an individual with a pathologic lumbar fracture who developed PRES in the setting of hypercalcemia, a known rare risk factor for PRES. Symptoms resolved with the correction of hypercalcemia. Multiple myeloma was ultimately diagnosed. Understanding the risk factors for PRES allows for appropriate treatment and resolution in symptoms.

1. When Back Pain leads to
Posterior Reversible Leukoencephalopathy Syndrome
Jon Akstinas, OMS-III; Emily Anderson, OMS-III; Matthew Fabiszak, DO
Introduction
Posterior Reversible Leukoencephalopathy Syndrome (PRES) is a
rare neurological condition characterized radiographically by edema
of the posterior cerebral hemispheres within the subcortical white
matter and clinically with headache, confusion, visual symptoms
and/or seizures. There are many factors that may lead to PRES
such as hypertension, immunosuppressive agents and renal
disease.1
This case highlights PRES in the setting of hypercalcemia of
malignancy due to multiple myeloma and hypertension (HTN).
Clinical Course
Case Description
History of Present Illness:
A 73 year old White female with past medical history of chronic low
back pain, depression, and remote history of breast cancer status
post bilateral mastectomy presented to Dixie Regional Medical
Center with complaint of intractable low back pain. Mild
hypertension was noted on initial vitals. Physical examination was
pertinent for point tenderness in the low back as well as evidence of
dehydration.
Diagnostic Data:
Labs were remarkable for calcium of 14.1 mg/dL, ionized Ca 1.74
mg/dL (nml 1.03-1.25), potassium 2.6 mg/dL, serum creatinine 1.5
mg/dL, gamma gap of 5.3.
CT of abdomen and pelvis was negative for acute process.
MRI of the lumbar spine revealed a compression fracture of L1.
Due to intractable pain requiring IV pain medications, admission
was recommended.
Discussion
PRES is best radiographically visualized with T2 FLAIR MRI with
involvement in the posterior portions of the brain (posterior parietal
and occipital lobes, cerebellum, pons).2 This may be due to a lower
concentration of adrenergic receptors, possibly leading to less local
blood pressure control.3
Multiple mechanisms have been proposed, including cerebral blood
pressure auto-dysregulation, ischemia, and endothelial dysfunction,
but pathogenesis remains unclear.
We suggest that our patient’s hypercalcemia crisis played a
significant role in her development of PRES as her encephalopathy,
seizures, and visual deficits clinically improved or resolved with
normalization of her hypercalcemia despite still continuing to
aggressively promote normalization of blood pressure. Indeed, it
has been demonstrated that hypercalcemia can induce vasospasm
due to actin-myosin coupling.4
Although the mechanisms behind PRES remain poorly understood,
the mainstay of treatment involves controlling the inciting factors.
Furthermore, this case supports hypercalcemia as an alternative
etiology of PRES in a patient with a seemingly unrelated chief
complaint.
Antihypertensives, bisphosphonates, and calcitonin were
promptly started. Her HTN remained modestly controlled
throughout her admission and calcium levels normalized within
48 hours. PRES symptoms of encephalopathy and seizures
seemed to resolve simultaneous to calcium correction. She
experienced visual field deficits that continued to improve
throughout the course of admission.
Ultimately, Multiple Myeloma was diagnosed as the etiology of
her hypercalcemia and pathologic fracture.
Fig 1: Patient’s T2 Flair with PRES in bilateral occipitoparietal regions.
Conclusion
• The mainstay of treatment of PRES involves recognizing and
controlling inciting factors.
• This case highlights a unique example of PRES with
hypercalcemia of malignancy as an inciting factor.
References
1.Bolanthakodi, Nandakrishna, et al. “Posterior Reversible Encephalopathy
Syndrome Due to Hypercalcaemia: A Rare Cause.” BMJ Case Reports, vol. 12,
no. 2, Feb. 2019, p. bcr-2017-223415, 10.1136/bcr-2017-223415. Accessed 9 Feb.
2020.
2.Algahtani, Hussein, et al. “Posterior Reversible Encephalopathy Syndrome.” The
Neurohospitalist, vol. 7, no. 1, 18 Sept. 2016, pp. 24–29,
10.1177/1941874416665762. Accessed 8 Feb. 2020.
3.Beausang-Linder, Marianne, and Anders, Bill. “Cerebral Circulation in Acute
Arterial Hypertension-Protective Effects of Sympathetic Nervous Activity.” Acta
Physiologica Scandinavica,
4.Nilsson, Inga-Lena, et al. “Endothelial Vasodilatory Function and Blood Pressure
Response to Local and Systemic Hypercalcemia.” Surgery, vol. 130, no. 6, Dec.
2001, pp. 986–990, 10.1067/msy.2001.118368. Accessed 9 Feb. 2020.
Initial treatment included IV fluids for volume repletion, acute kidney
injury, and hypercalcemia. A TLSO brace was fitted and a palliative
pain medication regimen was prescribed. It was felt that the patient
demonstrated HTN due to pain.
PTH was ordered on admission and returned with physiologic
suppression. With the past medical history of breast cancer and
concern for pathologic fracture, CT of the chest was also obtained
but was without significant process. Pain palliation was still a
concern with marked HTN. She began exhibiting new onset
encephalopathy followed by a brief tonic-clonic seizure. MRI of the
brain was obtained which revealed PRES.
Fig 2: Symptom Timeline with Serum Calcium levels and Blood Pressure
Onset Encephalopathy and Seizures Resolved